1. family and parenting
2. motherhood
3. pregnancy

1
CHAPTER 13
OBSTETRICS
Pregnancy
In women with regular menstrual cycles, a history of one or more missed cycles (periods) is
suggestive of pregnancy. Associated symptoms include fatigue, nausea/vomiting, breast tenderness,
frequent urination (caused by the enlarged uterus compressing the bladder), and “quickening” (first
movements of a fetus felt in utero at 16-20 weeks). Calculate the EDC (estimated date of
confinement) by adding 7 days to the first day of the last normal menses and subtracting 3 months.
Signs
Spider angiomata (branched capillaries on the skin, shaped like a spider) and blotchy or patchy palmar
erythema (more than 50-60% of patients), regress after delivery.
Striae gravidarum (stretch marks) develop in 50% of pregnant woman.
Hyperpigmentation of nipples, areola, umbilicus, axillae, perineum and midline of lower abdomen
(linea nigra). Breast enlargement due to increased hormone levels, which later causes release of
colostrum (thin, yellowish fluid seeping from the nipple) and lactation.
Other common signs and symptoms include lightheadedness, backache, dyspnea, urinary symptoms
(frequency, urgency, and incontinence), hemorrhoids, heartburn, ankle swelling, varicose veins,
abdominal cramping and constipation.
Fetal heart tones can be heard via auscultation (bell side of stethoscope) at or beyond
18-20 weeks of gestation.
Pregnancy tests can be used in the field. Most are nearly as accurate (97-99%) as a laboratory test on
serum.
Assessment: Palpation of fetal parts and the appreciation of fetal movement and heart tones are
diagnostic.
2
Anatomy
Placenta
Transfer of gases
Transport of nutrients
Excretion of wastes
Hormone production
Protection
Umbilical cord
Connects placenta to fetus
Two arteries
One vein
Amniotic Sac
Membrane surrounding fetus
Fluid originates from feral sources
500 - 1000 cc (after 20 weeks)
Rupture produces watery discharge
Terminology
Antepartum - before delivery
Postpartum - after delivery
Prenatal - occurring before the birth
Natal - connected with birth
Gravida - number of pregnancies
Para - number of pregnancies carried to full term
Abortion - number of pregnancies that ended before full term
Primigravida - woman who is pregnant for the first time
Primipara - woman who has given birth to her first child
Multiparous - woman who has given birth multiple times
Gestation - period of time for intrauterine fetal development
Fetal Growth Process
End of third month
Sex may be distinguished
Heart is beating
Every structure found at birth is present
End of fifth month
Fetal heart tones can be detected
Fetal movement may be felt by mother
3
End of sixth month
May be capable to survive if born prematurely
Middle of tenth month
Considered to have reached full term
Expected date of confinement (EDC)
Vaginal Delivery
Symptom:
When: Labor is defined as progressive dilation of the uterine cervix in association with repetitive
uterine contractions resulting in complete dilation (10 cm) and effacement (thinning) of the cervical os.
Normal labor is a continuous process.
First stage: Onset of cervical changes and uterine contractions through full dilation and effacement
of cervix
Second Stage: Full cervical dilation and delivery of the infant
Third Stage: Interval between the delivery of the infant and delivery of the placenta
Fourth Stage: Recovery of the uterus after delivery of the placenta
Supplies: 1% Lidocaine without epinephrine (approx. 20-30cc), sterile gloves (several pairs), gauzebandages and prep solution, 2-0, 3-0, and 4-0 absorbable suture (Vicryl or Chromic) for the repair,
scissors or a scalpel to make the episiotomy incision, sterile (or clean) towels, suction device (bulb
syringe), suture forceps, and needle holders
4
Procedure
During the First Stage of Labor:
1. Assess mother’s gestational age by asking the date of the first day of her last normal
menstrual period, subtracting 3 months and adding 7 days (40 weeks +/- 2 weeks). Palpate and
measure the height of the uterine fundus (top) from the pubic bone. Up to about 36 weeks, this
distance in centimeters approximates gestational age (i.e., 32 cm from pubic bone to top of fundus
equals approx. 32 weeks gestational age). If not >36 weeks by dates or measurement, see Preterm
Labor section.
2. Listen for fetal heart tones. Normal rate is approximately 160 beats/minute. Periodically
reassess during labor. The rate normally decreases during contractions but should recover.
3. Encourage the mother to walk as gravity and motion will encourage cervical dilation.
4. Read this section and others related to birth (Episiotomy, Breech Delivery, etc.).
5. Periodically assess progression of labor by timing contractions. Eventual delivery is likely
when contractions are <3 minute apart.
6. Check the birth canal with a sterile gloved hand once before birth to ensure the cervix is fully
dilated and effaced.
During the Second Stage of Labor:
1. As the cervix progresses to complete dilation, place the patient in the dorsal lithotomy
position (patient
is on her back with her thighs flexed on the abdomen). Women from some cultures may prefer to
squat.
2. With each contraction the patient should be urged to push and the care provider should perform
perineal massage.
3. As the fetal head crowns (i.e., distends the vaginal opening), consider an episiotomy if
massage has failed to stretch the tissue adequately. An episiotomy facilitates delivery of a large
infant, or one with shoulder dystocia. It is better to cut an episiotomy than to have the baby tear
the perineal tissue into the rectum. See Episiotomy Procedure guide.
4. As crowning continues, it is very important to support the fetal head via a modified Ritgen
maneuver.
This is accomplished by placing one hand over the fetal head while the other exerts pressure
through the perineum onto the fetal chin. Use a sterile towel to avoid contamination of this hand
by the anus.
5. After the head is delivered, suction the nose and mouth with the bulb syringe.
6. Check the neck for the presence of a umbilical cord around it, which should be reduced if
possible.
If the cord is too tight, it should be doubly clamped and cut.
7. Place your hands on the chin and head, applying gentle downward pressure, delivering the
anterior shoulder. Avoid injury to the brachial plexus; avoid excessive pressure on the neck.
8. Deliver the posterior shoulder by upward traction on the fetal head.
9. Delivery of the body should occur easily (see figure 3-8).
10. Cradle the fetus in your arms, suction once again and the umbilical cord is clamped and cut.
If no clamps are available, suture may be used.
11. To avoid significant heat loss, dry the newborn completely and wrap in towels or blankets.
12. If the mother (or another person) can hold the baby safely, put the baby to the mother's breast.
This will help the uterus contract.
During the Third Stage of Labor:
Soon after delivery of the infant, the placenta will follow. Placental delivery is iminent when the
uterus rises in the abdomen, the umbilical cord lengthens, and a “gush” of blood is noted. AVOID
excessive traction on the umbilical cord to avoid uterine inversion (pulling the uterus “inside-out”)
which will cause profound blood loss and shock. Instead, wait up to 30 min. for spontaneous
delivery of the placenta.
5
2. If spontaneous placental separation does not occur, remove the placenta manually. Pass a
gloved hand into the uterine cavity and gently apply traction to the umbilical cord, using the side
of the hand to develop a cleavage plane between the placenta and the uterine cavity.
3. Inspect the placenta to ensure it is complete. Inspect the cord for the presence of the expected
two umbilical arteries and one umbilical vein.
4. After the delivery of the placenta, palpate the uterus to ensure that it has reduced in size and
become firmly contracted.
5. Inspect the birth canal in a systematic fashion. Evaluate lacerations of the vagina and/or
perineum and extensions of the episiotomy and repair if necessary (refer to Episiotomy section).
Normal delivery, Crowning of the Head
5
6
7
During the Fourth Stage of Labor:
1. The likelihood of serious postpartum complications is greatest in the first hour or so after
delivery. Palpate the uterus to ensure that it is firm. Repeat uterine palpation through the
abdominal wall frequently during the immediate postpartum period to ascertain uterine tone.
2. Monitor pulse, blood pressure and the amount of vaginal bleeding every 15 minutes for the
first hour, then every 30 min. for 3 hrs after delivery to identify excessive blood loss.
3. Manage pain with NSAIDS or low dose narcotics (i.e., Motrin 800 mg 1 tablet tid with food
or Tylenol
#3 1-2 tablets q 4-6 hrs).
4. Apply ice to the perineum for 20-30 minutes every 4-6 hrs to decreasing swelling after the
delivery.
What Not to Do:
Do not contaminate the birth canal prior to birth.
Do not allow the episiotomy to tear into the rectum. Do not forget to reduce umbilical cord.
Do not forget to suction the baby’s nose and mouth. Do not forget to clamp and cut the umbilical
cord.
Do not forget to clean and dry the baby. Do not forget to deliver the placenta.
Do not forget to repair an episiotomy and any tears. Do not forget to monitor the mother’s vital
signs.
Preterm Labor (PTL)
Introduction: Preterm birth as a result of preterm labor is the most common cause of infant morbidity
and mortality. Complications include respiratory distress syndrome (RDS), intraventicular hemorrhage
(IVH), necrotizing enterocolitis, sepsis, and seizures. Long term morbidity associated with PTL and
delivery includes chronic lung problems (bronchopulmonary dysplasia) and developmental
abnormalities. Preterm labor is defined as regular uterine contractions occurring with a frequency of
10 minutes or less between 20 and 36 weeks gestation, with each contraction lasting at least 30
seconds. When contractions are accompanied by cervical effacement (thinning), dilation (opening),
and/or descent of the fetus into the pelvis, it becomes increasingly difficult to stop labor.
The cause of preterm labor is unknown but many factors have been associated with it and some
include: dehydration, rupture of membranes, infections, uterine enlargement (twins), uterine distortion
(fibroids), and placental abnormalities (previa and abruption), smoking and substance abuse.
Approximately 10-15% of women will rupture the amniotic membrane around the fetus >1 hour
prior to the onset of labor. This is called premature rupture of membranes, or PROM. After PROM,
labor must begin promptly or infection will develop as bacteria ascend through the birth canal.
Delivery should be completed within 24 hours of PROM to avoid infection in fetus and mother. One
of the most important causes of early onset neonatal infection is group B streptococcus (GBS).
8
Symptoms: Menstrual-like cramps, low back pain, abdominal or pelvic pressure, painless uterine
contractions, and increase or change in vaginal discharge (mucus, watery, light bloody discharge).
Signs
Palpable uterine contractions; palpable cervical dilation and effacement
Lab: Urinalysis and a saline wet preparation to evaluate for bacterial vaginosis. Fern Test (amniotic
fluid dries on a slide to resemble the leaves of a fern plant) to assess for PROM.
Assessment: Assess for PTL risk factors, and treat those found.
Differential Diagnosis
Low back pain/spasm - palpate for back spasm; evaluate for associated neurological symptoms (leg
tingling,radiation, etc.)
Infection - evaluate for urinary tract infection (urinalysis, fever), GI infection (diarrhea, fever) and
vaginosis (saline wet prep).
Ureter/kidney stone - evaluate flank pain, fever; perform urinalysis
True labor - verify dates of last menstrual period.
PROM - history of vaginal gush or leak, positive Fern Test
Constipation - history of infrequent bowel movements; retained fecal material
Diarrhea - infection (above), food poisoning, and others.
Treatment
1. Arrest labor:
Magnesium sulfate, 4 gm loading dose over at least 5 minutes, followed by 2 gm/hour in a steady IV
drip. Watch for magnesium toxicity with diminished reflexes and respiratory depression. Counteract
with calcium gluconate 1 gm slow IV push over 2-3 minutes if magnesium toxicity is encountered.
Alternates: Terbutaline 0.25 mg SQ, q 1-4 hours x 24 hours, total dose not to exceed 5 mg in 24
hours. May also be given po in 2.5 - 7.5 mg doses q 1.5 - 4 hours. Target maternal pulse rate is > 100
and < 120 BPM Indomethacin (Indocin) 50 mg po (or 100 mg PR), followed by 25 mg po q 4-6 hours
for up to 48 hours. Watch for gastric bleeding, heartburn, nausea and asthma.
Maternal: Significant hypertension (see Preeclampsia section), antepartum hemorrhage, cardiac
disease. Fetal: Gestational age > 37 wks, fetal death, chorioamnionitis (intrauterine infection)
2. Prevent infection (PROM; PTL > 12 hours; history of UTI, vaginal infections in last 2 weeks):
Primary: Penicillin 5 million units IV initially, then 2.5 million units q 4 hrs until delivered
Alternates: Ampicillin 2 g IV q 4-6h or Rocephin may also be used, 1 gram IV q 12 hrs.
For those patients who are penicillin allergic, clindamycin 600 mg q 6 h or 900 mg q 8 h or
erythromycin 1-2 g q 6 h or vancomycin 500 mg q 6 h or 1000 mg q 12 h.
3. Help fetus mature: After postponing delivery, many fetuses less than 34 weeks gestation will
benefit from administering steroids to the mother. The effect of the steroids on the fetus is to
accelerate fetal lung maturity, lessening the risk of respiratory distress syndrome at birth.
Dexamethasone 6 mg IM q 12 hours x 4 doses.
9
Relief of Shoulder [Dystocia] lock
What: Shoulder dystocia is a labor complication caused by difficulty delivering the fetal shoulders.
Improperly relieving the dystocia can result in unilateral or bilateral clavicular fractures.
When: After delivery of the head, the fetus seems to try to withdraw back into the birth canal (the
“Turtle Sign”). Further expulsion of the infant is prevented by impaction of the fetal shoulders within
the maternal pelvis. Digital exam reveals that the anterior shoulder is stuck behind the pubic
symphysis. In more severe cases, the posterior shoulder may be stuck at the level of the sacral
promontory.
What To Do:
1. Check for nuchal cord (the umbilicus wrapped around the baby's neck) and relieve it.
2. Suction the infant’s mouth to clear the airway of amniotic fluid and other debris.
3. Do not apply excessive downward traction on the head to get the baby out. This action can
injure the nerves in the neck and shoulder (brachial plexus palsy) and must be avoided. While most
of these nerve injuries heal spontaneously and completely, some do not.
4. Otherwise cut a generous episiotomy following proper technique (see Episiotomy Procedure in this
chapter) unless a spontaneous perineal laceration has occurred, or if the perineum is very stretchy
and offers no obstruction.
5. Initially apply gentle downward traction on the chest and back initially to try to free the
shoulder. If this has no effect, do not exert increasing pressure. Try some alternative maneuvers to
free the shoulder.
6. Place the mother in the MacRobert’s position, and apply gentle downward traction on the baby
again.
Maneuver involves flexing the mother’s thighs tightly against her abdomen. This can be done by the
woman herself or by assistants. By performing this maneuver, the axis of the birth canal is
straightened, allowing a little more room for the shoulders to slip through.
7. If the MacRobert’s maneuver fails have an assistant apply downward, suprapubic (above the
bony pubic arch) pressure to drive the fetal shoulder downward, to clear the pubic bone. Again apply
coordinated, gentle downward traction on the baby.
8. If pressure straight down is ineffective, have the assistant apply it in a more lateral direction. This
tends to nudge the shoulder into a more oblique orientation, which usually provides more room for the
shoulder. Again apply coordinated, gentle downward traction on the baby.
9. Often, the baby’s posterior arm has entered the hollow of the sacrum. Reach in posteriorly,
identify the posterior shoulder, follow the humerus down to the elbow and identify the forearm.
Grasping the fetal wrist, draw the arm gently across the chest and then sweep the arm up and out of the
birth canal, freeing additional space and allowing the anterior shoulder to clear the pubic bone. Once
again apply coordinated, gentle downward traction on the baby.
10. An electric light bulb cannot be removed by simply pulling it out- it must be unscrewed. This
concept can be applied to shoulder dystocia problems. Rotate the posterior shoulder, allowing it to
come up outside of the subpubic arch. At the same time, bring the stuck anterior shoulder into the
hollow of the sacrum. Continue rotating the baby a full 360 degrees to rotate (unscrew) both shoulders
out of the birth canal.
Two variations on the unscrewing maneuver include:
Rotating/shoving the shoulder towards the fetal chest (“shoving scapulas saves shoulders”), which
compresses the shoulder-to-shoulder diameter, and
Rotating the anterior shoulder first rather than the posterior shoulder. The anterior shoulder may be
easier to reach and simply moving it to an oblique position rather than the straight up and down
position may relieve the obstruction.
Applying fundal pressure in coordination with the other maneuvers may, at times, be helpful. Applied
alone, it may aggravate the problem by further impacting the shoulder against the pubic symphysis.
10
12. If these measures fail, return to number 4 above and consider cutting or extending the
episiotomy, then progress through these maneuvers again. Do not attempt a C-Section. Since the
baby’s head is delivered, there should be no need to do so.
Breech Delivery
Breech presentation is an abnormality in which the buttocks or legs of the fetus, rather than the
head, appear first in the birth canal. There are several breech variations, including buttocks first,
one leg first or both legs first. “Frank breech” means the buttocks are presenting and the legs are
up along the fetal chest—the safest position for breech delivery. In any breech birth there are
increased risks of umbilical cord prolapse and delivery of the feet through an incompletely dilated
cervix, leading to arm or head entrapment. These risks are greatest when a foot is presenting
(“footling breech”).
When: Because of the risks of breech delivery, many breech babies are born by cesarean section (see
Cesarean section template) in developed countries. In operational settings, cesarean section may not be
available or may be more dangerous than performing a vaginal breech delivery. It is up to the care
team to decide which option will be the safest mode of delivery for both mother and infant.
What To Do:
1. The simplest breech delivery is a spontaneous breech. The mother pushes the baby out with
normal
bearing down efforts and the baby is simply supported until it is completely free of the birth
canal. These babies essentially deliver themselves. This works best with smaller babies, mothers who
have delivered in the past or frank breech presentation.
2. If a breech baby gets stuck halfway out or if you need to speed the delivery, perform an “assisted
breech” delivery. It is very helpful to have a second person assist you.
3. A generous episiotomy will give you more room to work, but may be unnecessary if the vulva is
very stretchy and compliant.
4. Grasp the baby so that your thumbs are over the baby’s hips. Rotate the torso so the baby is face
down in the birth canal. A towel can be wrapped around the lower body to provide a more stable grip.
5. Have your assistant apply suprapubic pressure to keep the fetal head flexed, expedite delivery and
reduce the risk of spinal injury.
6. Exert gentle outward traction on the baby while rotating the baby clockwise and then
counterclockwise a few degrees to free up the arms.
7. If the arms are trapped in the birth canal you may need to reach up along the side of the baby
and sweep them one at a time, across the chest and out of the vagina.
8. It is important to keep your hands low on the baby’s hips. Grasping the baby above the hips
could easily cause soft tissue injury to the abdominal organs including the kidneys.
9. During the delivery, always keep the baby at or below the horizontal plane or axis of the birth
canal. If you bring the baby’s body above the horizontal axis, you risk injuring the baby’s spine. Only
when the baby’s nose and mouth are visible at the introitus is it wise to bring the body up.
10. At this stage, the baby is still unable to breathe and the umbilical cord is likely occluded. Without
rushing, move steadily toward a prompt delivery. Place a nger in the baby’s mouth to control the
delivery of
the head. Try not to let the head “pop” out of the birth canal. A slower, controlled delivery is less
traumatic.
What Not To Do:
Do not assist too early. Only intervene if a breech baby gets stuck part way out of the pelvis.
Do not place hands too high on the abdomen. Keep hands low on the baby’s hips.
Do not raise baby above the horizontal plane until the nose and mouth are delivered.
11
ADVANCED
Cesarean Section
What: The delivery of a fetus by abdominal surgery (laparotomy) requiring an incision through the
uterine wall (hysterotomy).
When: Perform this procedure only when it is absolutely necessary, and is the only life saving measure
for mother or infant! The decision to perform a C-Section must be based on the health and stability of
the mother and fetus. Recognize that performing the procedure in the eld as an untrained provider is
extremely dangerous and will likely result in significant morbidity or mortality for both mother and
infant. If a C-Section is anticipated, prepare equipment and read this material, since the procedure
must often be performed emergently when vital signs become unstable.
12
The following are relative indications for cesarean delivery under field conditions:
1. Fetal Complications:
a. Non-vertex (not head first) such as a transverse lie or breech presentation. Attempt vaginal
delivery first. (See Breech Birth section).
b. Multiple gestation: triplets or greater, twins in which the first twin is not head first (vertex).
Attempt vaginal delivery of at least one fetus. (See Breech Birth section).
c. Large Fetus: Attempt vaginal delivery first.
d. Fetal distress: Fetal heart rate (<90 bpm) for more than 1 minute.
2. Placental Complications:
a. Placenta Previa (placenta lies over cervical os)
b. Placental Abruption (premature placental separation).
c. Although these conditions cannot be diagnosed in the field, any large vaginal hemorrhage during
labor, or hemorrhage accompanied by fetal distress should be reason to suspect them and consider
C-Section.
3. Uterine Complications:
a. Previous cesarean section with midline incision (classical).
b. Other surgery (e.g., for fibroids) where the uterine cavity was entered.
There is an increased risk for uterine rupture in this situation. C-Sections with low transverse
incisions are much less risky. Attempt vaginal delivery first.
4. Vaginal Complications:
a. Obstructive conditions (e.g., genital warts, cervical cancer). If noted, these conditions may
hinder dilation of the cervical os and descent of the fetus through the birth canal. Attempt vaginal
delivery first.
b. Vaginal Infections (e.g., Group B Strep, genital herpes). Delivering the infant through the
birth canal will greatly increase the baby’s risk of contracting these infections, which will likely
be deadly.
5. Maternal Complications: Any medical condition that worsens during labor in which a delayed
delivery would harm the mother (e.g., eclampsia).
6. Abnormal labor (failure to progress): Labor that does not progress (continued cervical changes
and fetal descent) over several hours endangers the fetus by increasing the risk of cord compression
and neurological damage.
Episiotomy and Repair
What: Incision of the perineum to enlarge the vaginal opening, and subsequent repair.
When: At the time of delivery, perform an episiotomy when 3-4 cm of fetal scalp is visible at the
vaginal opening. The most common practice is to repair the episiotomy after the delivery of the
placenta.
What You Need: 1% Lidocaine without epinephrine (approx. 20-30cc), sterile gloves, gauze bandages,
prep solution, 2-0, 3-0, and 4-0 absorbable suture (Vicryl or Chromic) for the repair, scissors or a
scalpel to make the episiotomy incision, suture forceps and needle holders.
What to Do:
Episiotomy: Indicated to assist in the delivery of a large infant or one with shoulder dystocia
after perineal
massage has failed to stretch the tissue adequately. It is better to cut an episiotomy than to have
the baby tear the perineal tissue into the rectum.
1. If no anesthesia has been given, administer 5-10 cc of Lidocaine along the midline of the
perineum and posterior vagina. Remember not to administer more than 50cc of Lidocaine total,
and to aspirate prior to injecting. If the perineum is very thin and well stretched, anesthesia
may not be necessary.
Place the first two fingers into the posterior vagina between the fetal head and the vaginal wall,
with one finger on either side of midline.
13
3. Cut between the fingers, through the vaginal wall and the perineum, but do not to incise the
anal sphincter or its capsule. (Figure 3-12)
4. If pressure from the fetal head does not control bleeding, press a 4x4 bandage against the
incised tissue to stop hemorrhage.
5. An alternate site for the episiotomy is the mediolateral position (approximately 4:30 on a clock
face).
Classifications of perineal episiotomies and lacerations
First Degree: Extends only through the vaginal and perineal skin
Second Degree: Extends deeply into the soft tissues of the perineum down to, but not including,
the external anal sphincter
Third Degree: Extends through the perineum and anal sphincter
Fourth Degree: Extends through the perineum, anal sphincter, and rectal mucosa to expose the
lumen of the rectum
First Degree Episiotomy or Laceration Repair
1. Test the area to be sutured for residual sensation. If necessary, administer Lidocaine into the
tissue as with typical wound repair.
I2. If the edges of lacerated tissue are less than 1 cm apart and not bleeding, repair is not
necessary.
3. Place the first stitch (2-0 or 3-0) 1 cm deep (proximal) to the end of the vaginal portion of the
episiotomy (or laceration) and tie it.
4. Continue with locking, continuous sutures 1 cm from each wound edge, 1 cm apart and 0.5 cm
deep through to the introitus or hymenal ring (or distal end of the laceration). Ensure the edges of
the hymenal ring lay approximated. Do not cut the suture in episiotomy repair.
5. With another suture, sew a running subcuticular suture from the anal end of the skin wound
back up toward the vagina to close the perineum.
6. Take the end of the suture back under the hymenal ring and tie it in the vagina.
Second Degree Episiotomy Repair:
1. Repair vaginal wound as in First Degree Repair down to the hymenal ring. Do not cut the
suture.
2. With another suture, sew 3 - 4 deep, interrupted stitches in the subcutaneous fascia, muscle
and fat of the perineum.
3. Take the suture from the vagina under the hymenal ring and approximate the edges of the
perineal fascia with continuous non-locking suture sewing toward the anus.
4. Sew a running subcuticular suture back up toward the vagina to close the perineum.
5. Take the end of the suture back under the hymenal ring and tie it in the vagina.
6. Do not suture any tear near the ureter without inserting a Foley catheter to avoid inadvertent
urethral closure.
Third and Fourth Degree Repair:
1. Reapproximate the rectal mucosa with interrupted, fine 4-0 sutures (usually two layers), taking
care not to puncture the mucosa and to leave the ends of the suture in the tissue, not the rectal
lumen.
2. Repair the torn ends of the doughnut-shaped anal sphincter with four well-spaced interrupted
sutures that traverse through the capsule of the muscle.
3. Then repair the wound as in a second-degree laceration or an episiotomy (above).
14
Management after Episiotomy
1. Apply ice to the affected area tid to control swelling.
2. Relieve pain with Tylenol #3 1-2 tabs po every 3-4 hours.
3. Pain may be an indication of a large hematoma or perineal cellulitis. Examine these areas
carefully if pain is severe or persistent.
4. Give stool softeners for approximately 7-14 days and direct increased intake of fiber and
water.
5. Do not give enemas.
What Not To Do:
Do not fail to restore anatomical features.
Do not use too many sutures.
Do not fail to achieve hemostasis.
15
Preeclampsia/Eclampsia
Preeclampsia is maternal hypertension accompanied by proteinuria or edema, seen from the 20th week
of gestation through delivery. If these symptoms are complicated by seizures or coma, the mother has
eclampsia. Hypertensive disorders are the most common medical complications of pregnancy.
Symptoms
Visual disturbances (usually irregular luminous patches in the visual fields after physical or mental
labor), headaches, nausea, vomiting, epigastric pain and generalized edema, seizures or coma.
Signs
Mild Preeclampsia (1 of the following):
1. Blood pressure changes (measure on two occasions at least 6 hours apart):
a. Systolic blood pressure (SBP) of 140 mm Hg or greater OR
b. Diastolic BP (DBP) of 90 mm Hg or greater (< 110) OR
Mean arterial BP (MAP) (calculated as 1/3 the difference between SBP and DBP, plus the DBP) of 105
mm Hg and/or an increase of 20 mm Hg over baseline
2. Proteinuria 2+ or > on a urine dipstick
3. Pathologic edema: generalized or involving the hands or face (Note: Moderate edema is a feature
of approx. 70-80% of normal pregnancies). Weight gain greater than 4 pounds/week in the third
trimester may be one of the first signs of preeclampsia.
Severe Preeclampsia (1 of the following):
1. Blood pressure changes (measure on two occasions at least 6 hours apart):
a. SBP of 160 mm Hg or greater OR
b. DBP of 110 mm Hg or greater
2. Proteinuria 3+ OR 4+ on dipstick
3. Severe edema, including pulmonary edema
4. Evidence of end organ compromise (cerebral or visual disturbances)
5. Persistent abdominal pain with nausea and vomiting.
May also see:
a. Oliguria (< 400 ml in 24 hr).
b. Decreased platelet count (thrombocytopenia <100,000)
c. Hyperreflexia
Eclampsia
Convulsions (seizures) during pregnancy with history of preeclampsia, or without other explanation.
2. Hypertension.
May also see weight gain, edema, proteinuria, visual disturbances, and right upper quadrant/epigastric
pain.
Treatment
Mild Preeclampsia:
1. Observe for worsening signs of the disease.
2. If patient’s condition does not progress, discharge and follow on a twice weekly basis.
3. In a field or remote setting, manage aggressively with dexamethasone 6 mg IM q 12 hours for a
total
of 4 doses to prevent fetal respiratory distress syndrome and maternal thrombocytopenia, and to
improve perinatal outcome in severe preeclampsia.
17
4. Give magnesium sulfate (to prevent seizures) by a controlled continuous infusion with a loading
dose of
4-6 gm in 100 ml over 15-20 min. followed by a continuous infusion of 2-3 gm/hr. Toxic levels
cause muscle weakness, respiratory paralysis, and cardiac arrest. Administer calcium gluconate 1 gm
slow IV push over 2-3 minutes to counteract magnesium toxicity.
Severe Preeclampsia:
With SBP > 180 mm Hg or the DBP > 110 mm Hg, the possibility of intracerebral damage increases
warranting antihypertensive medication. Give Hydralazine (Apresoline) 5-10 mg IV every 20 minutes
as indicated, or labetalol 20 mg IV q 10 min with a max dose of 300 mg, to reduce BP. Monitoring BP
q 5 minutes for at least 30 min. after giving the drug. Please note that some of the side effects with
labetalol are maternal tachycardia, headache and flushing.
Give magnesium sulfate as above.
Eclampsia:
1. Give magnesium sulfate as above.
2. Provide oxygen and airway support as needed.
3. Evacuate.
4. If evacuation not feasible deliver the fetus after seizure activity has abated.
5. If magnesium sulfate is not available, consider cesarean section as only option to save both mother
and fetus (see Cesarean Section procedure).
18
CHAPTER 14
Skin Disorders
Introduction to Dermatology
Classical Elements of the Clinical Approach to Dermatologic Disease Diagnosis and Disposition
Type of Skin Lesion
Primary Lesions
Macule: A circumscribed area of change in normal skin color that is flat and less than 1 cm in
diameter. Example: freckles.
Patch: A circumscribed area of change in normal skin color that is flat and > 1 cm in diameter.
Examples: café-au-lait spots, port-wine stains.
Papule: A solid lesion, usually dome-shaped, <1 cm in diameter and elevated above the skin.
Examples: verrucae, molluscum contagiosum.
Nodule: A solid lesion, usually dome-shaped, > 1 cm in diameter and elevated above the skin.
Examples: neurofibromas, xanthomas, and various benign and malignant growths.
Plaque: An elevation above the skin surface occupying a relatively large surface area in
comparison with its height. Frequently formed by a confluence of papules. Examples: lichen
simplex chronicus and psoriasis.
Vesicle: A circumscribed, thin walled, elevated lesion < 1 cm in diameter and containing fluid.
Examples: herpes, dyshydrotic eczema, varicella, and contact dermatitis
Bullae: A circumscribed, thin walled, elevated lesion > 1 cm in diameter and containing fluid.
Examples: burns, frostbite, pemphigus.
Comedone: Retained secretions of horny material within the pilosebaceous follicle. Examples:
open (blackheads) and closed (whiteheads), the precursors of the papules, pustules, cysts and
nodules of acne.
Pustule: A circumscribed elevation containing pus. Examples: sterile lesions as in pustular
psoriasis or bacterial as in acne and impetigo.
Cyst: A circumscribed, thick walled, slightly elevated lesion extending into the deep dermis and
subcutaneous fat. Examples: epidermal inclusion and pilar cysts.
Wheal/Hive: A distinctive white to pink or pale, red, edematous, solid elevation formed by local,
superficial, transient edema. They characteristically disappear yet may reappear within a period of
hours. Examples: dermographism, insect bites, and urticaria.
Telangiectasia: Blanchable (fades with fingertip pressure), small, superficial dilated capillaries.
Examples: rosacea, lupus erythematosus and basal cell skin cancer.
Purpura: Non-blanchable, purple area of the skin that may be flat/nonpalpable or raised/palpable.
Examples: hemorrhagic lesions of some fevers.
Secondary lesions represent evolution (natural) of the primary lesions.
Atrophy: Thinning and wrinkling of the skin resembling cigarette paper
Crusts (Scab): Dried serum, blood, or pus.
Erosion: Loss of part or all of the epidermisthat will heal without scarring.
Ulcer: Loss of epidermis and at least part of dermis that results in scarring.
Excoriation: Linear or hollowed-out crusted area caused by scratching, rubbing, or picking.
Lichenification: Thickening of the skin with accentuation of the skin lines.
Scales: Accumulation of retained or hyperproliferative layers of the stratum corneum
19
Scar: Permanent fibrotic changes seen with healing after destruction of the dermis.
Shape of Lesion
a. Annular: Ring shaped, round or circular
b. Nummular: Coin shaped
c. Oval: Oblong
d. Polycyclic: Rings within rings e. Polygonal: Geometric shaped f.
Serpiginous: Snake-like
Arrangement of the lesions in relationship to each other
a. Grouped Arrangement
i. Annular: Circular, round or like a ring
ii. Arciform: Shaped in curves
iii. Herpetiform: Like or in the shape of a herpetic lesion
iv. Linear: Geometrically forming a straight line
v. Reticulated: Net-like
vi. Serpiginous: Shape or spread of lesion in the fashion of a snake
b. Disseminated Arrangement: Diffuse involvement without clearly defined margins or scattered
discre telesion.
Distribution of Lesions
a. Isolated single lesions
b. Localized to specific body region
c. Universal over the entire body surface
d. Patterned
i. Sun-exposed areas
ii. Symmetrical
iii. Follicular based
iv. Flexure or extensor surfaces
Assessment:
Synthesize, integrate, and form a hypothesis by combining the history and the primary and
secondary characteristics of the lesion(s) together with their shape, arrangement and distribution.
Bacterial Skin Infections
Disseminated Gonococcal Infection
Gonococcemia is a systemic infection with Neisseria gonorrhoeae following the bloodborne spread
(dissemination) of the gram-negative diplococci from infected sites (1% of untreated cases).
Symptoms: Prodrome of fever and chills, anorexia, malaise during the 7 to 30 day incubation period.
May have migratory polyarthritis.
Signs
Lesions:
1.0 -5.0 mm erythematous macules (2 to 20 lesions) that evolve to slightly tender, deep-seated,
hemorrhagic pustules within 24-48 hrs; center may become necrotic; located on arms and hands more
often than legs or feet, in regions near the joint spaces.
Tenosynovitis of the extensors / flexors of the hands and feet is common.
20
Septic arthritis occurs with asym metrical, erythematous, hot, tender knee, elbow, ankle or
metacarpophalangeal joints.
Other organ systems may also be infected: hepatitis, carditis, meningitis, and others. Evaluate Lab:
Gram stain of mucosal surfaces may yield gram-negative diplococci; culture mucosal sites (80-90%
yield).
Differential Diagnosis: Meningococcemia (CNS effects); other bacteremias; psoriatic arthritis (plaque
lesions, multiple joints); systemic lupus erythematosus (multiple joints, multiple organ effects)
Treatment:
Primary: Ceftriaxone 1 gm IM or IV q 24 hrs
Alternative: Ceftizoxime or cefotaxime 1 gm IV q 8 hrs, or spectinomycin 2 gm IM q 12 hrs
After initial symptoms resolve, the uncomplicated patient should be treated for 1 week with oral
cefuroxime axetil 500 mg bid, or amoxicillin 500mg with clavulanic acid tid, or ciprofloxacin 500 mg
bid if patient is not pregnant.
Meningococcemia
Neisseria meningitides is a gram-negative coccus found in the nasopharynx of approximately 5 –
15% of the general population.
It invades the blood stream, causing acute meningococcal septicemia and meningitis.
Transmission is through person-to-person inhalation of droplets of infectious nasopharyngeal
secretions.
Symptoms: Prodrome of spiking fever, chills, myalgia, arthralgia; rash, photophobia, headache
Signs
Abnormal vital signs: high fever, tachypnea, tachycardia, mild hypotension; rash: small,
palpable, petechial lesions with irregular borders and pale gray, vesicular centers most commonly
observed on the trunk and extremities (but may be seen anywhere, including the palms, soles and
mucous membranes); posterior neck rigidity and tenderness with stretching; photophobia; altered
consciousness; severely ill patients may display ecchymosis and coalescence of the purpuric lesions
into bizarre shaped gray-to-black necrotic areas associated with disseminated intervascular
coagulation.
Lab: Gram stain scrapings from lesions to identify characteristic organism. Culture blood to identify
organism.
Differential Diagnosis: Rocky Mountain Spotted Fever, other rickettsial diseases, staphylococcal toxic
shock syndrome, enteroviral infections and acute bacteremia.
Treatment:
Primary: Cefotaxime 2.0 gm IV q 4-6 hrs + vancomycin 1.0 gm q 6-12 hrs
Alternate: Ceftriaxone 2 gm IV q 12 hrs + vancomycin 1.0 gm q 6-12 hrs
Erysipelas
Erysipelas is most commonly an acute, dermal and subcutaneously spreading cellulitis caused by
Group A beta-hemolytic Streptococcus pyogenes or Staph. aureus.
21
It is characterized by an erythematous, warm, raised, tender area of the skin. Inoculation is through a
break in the skin barrier (puncture, laceration,abrasion, surgical site) an underlying dermatosis (pitted
keratolysis, tinea, or stasis dermatitis/ulcer), or through the middle ear or nasal mucosa in children.
Symptoms: Prodrome of malaise, anorexia, fever and chills is occasionally observed. More common
is the rapid development of high fever and chills.
Signs
The primary lesion is a bright erythematous, edematous, raised, warm, tender plaque
with sharp, palpable leading margins.
The distribution of lesion varies from the face to the lower extremities. Usually seen with an associated
regional lymphadenopathy.
Lab: WBC count for infection
Differential Diagnosis: Early allergic or irritant contact dermatitis; fixed drug eruption; deep venous
thrombosis; thrombophlebitis; rapidly progressive necrotizing fasciitis (a well-demarcated dusky
purpuric lesion that is caused by thrombosis of the vessels, which is usually palpable).
Treatment:
Primary: Dicloxacillin 500 mg po q 6 hrs for early mild cases
Or nafcillin or oxacillin 2.0 grams IV q 4 hrs for more severe cases
Alternative: Erythromycin 500mg po q 6 hrs
Staphylococcal Scalded Skin Syndrome
Staphylococcal scalded skin syndrome is a fairly distinctive pediatric dermatosis caused by an
epidermolytic (epidermis-destroying) toxin.
The reason for the association with children appears to be related to the fact that most adults and
children over the age of 10 can localize, metabolize, and excrete the toxin more efficiently. They may
develop bolus impetigo instead, but will limit the hematogenous dissemination of the toxin. This
condition is most common in children 5 years of age and younger.
Symptoms: Prodrome: Fever, malaise, extreme irritability, and anorexia; irritable child with low-grade
fever.
Signs
Generalized macular erythema, with fine, stippled, “sandpaper” appearance, rapidly
progressing to a tender scarlatiniform phase over 24-48 hrs; spreads from the intertriginous and
perioral facial areas to the rest of the body.
22
The exfoliative phase is heralded by a characteristic perioral crusting that often cracks in a radial
fashion.
Within 48-72 hours, the upper epidermis may become wrinkled or slough off with light stroking of the
skin (Nikolsky’s sign).
Shortly thereafter, flaccid bullae and desquamation of the upper layers of the epidermis are noted
Unless subsequent infective processes are present, the entire skin will re-epithelialize with scarring
with in 2 weeks.
Lab: Staph aureus cultured only from colonized site of infection; umbilical stump, external ear canal,
conjunctiva, or nasal mucosa.
Diagnosis based on clinical criteria and verified by culture from a primary infection site.
Differential Diagnosis - Erythema multiforme, drug-induced toxic epidermal necrosis, and pemphigus
vulgaris. See related topics.
Treatment:
Primary: Supportive: Reliable home care, including cool baths or compresses and oral fluid
replacement.
Antibiotics: Dicloxacillin 30–50 mg/kg/day po in divided doses. In newborns and infants where
extensive sloughing has occurred: IV oxacillin 200 mg/kg/day q 4 hrs. Apply mupirocin ointment or
silver sulfadiazine (Silvadene) for more irritated and inflamed areas.
Impetigo Contagiosa
Impetigo is an acute, contagious, superficial infection caused by Staphylococcus aureus
(bolus/ulcerative), or group A beta-hemolytic streptococci (vesiculopustular), or both.
Although seen in all age groups, impetigo is most common in infants and children, occurring most
frequently on the exposed parts of the body, especially the face, hands, neck and extremities.
Predisposing factors include crowded living conditions, neglected minor wounds, and poor hygiene.
Symptoms: Itching, weeping lesions
Signs
Lesions: 1– 2 mm erythematous macules, which quickly develop into vesicles or bullae surrounded by
a narrow halo of erythema.
The vesicles rupture easily and release a thin, yellow, cloudy fluid which subsequently dries to a
characteristic “honey crust.”
Scattered, discrete lesions located most frequently on the exposed parts of the body, especially the
face, hands, neck and extremities.
Groups of lesions may have satellite autoinoculated lesions at the periphery . There may be associated
regional lymphadenopathy.
Lab: Gram stain of early vesicular lesions reveals gram-positive intracellular cocci in clusters or
chains.
Differential Diagnosis
Varicella, herpes simplex, bullous tinea, allergic contact dermatitis (see appropriate topics in this book).
Treatment
Primary: Dicloxacillin 250-500 mg po qid x 10 days
Alternative: Keflex (250 to 500 mg bid to tid); erythromycin (250 mg po qid)
23
Cutaneous Tuberculosis
Cutaneous tuberculosis (TB) commonly represents skin manifestations of underlying pulmonary TB.
It can also mean primary skin inoculation with TB, which is very rare.
It is an acid-fast, aerobic, gram-positive bacterium with both human and bovine forms.
Only about 1% of all TB patients will have skin lesions. Most cutaneous TB is indicative of
systemic TB infection and can be the first sign of TB, especially in patients with HIV infection.
Symptoms: Most are asymptomatic, some have a painless nodule progressing to painful ulcer, itching
is uncommon.
Signs
Primary skin inoculation: Non-tender, well-circumscribed ulcer; non-tender
lymphadenopathy (3-8 weeks later); these characteristics are the ulceroglandular complex
Cutaneous manifestations of pulmonary TB:
Variable presentations: boggy, indurated, erythematous skin and purulent ulcerations overlying infected
subcutaneous tissue and enlarged lymph nodes (scrofuloderma); brown-red papules, soft and applejelly like, most common on the face, ears, buttocks and breasts (lupus vulgaris); discrete, blue-red to
brown, tiny papules, some capped with minute vesicles, which burst to leave a crust and may affect
all body parts, but the trunk, thighs, buttocks and genitalia are predisposed
Differential Diagnosis
Primary Skin Inoculation - primary syphilis, tularemia, cat scratch disease, sporotrichosis, and others.
Cutaneous Manifestations of Pulmonary TB: extensive list including tertiary syphilis, deep fungal
infections, chronic granulomatous disease, leishmaniasis, sarcoidosis, squamous cell carcinoma, and
many others
Treatment
Primary: There are at least 13 different agents to choose from. Many organisms are multi-drug
resistant.
See Respiratory: TB section for details.
Medications: Some medications can be toxic, so periodic blood tests are necessary during treatment.
Leprosy (Hansen’s disease)
An inflammatory disease caused by infection with Mycobacterium leprae.
It may be localized to the skin only or may involve internal organs.
Infection of cutaneous nerves is very common.
Leprosy is endemic in India, sub-Saharan Africa, South and Central America, the Pacific Islands and
the Philippines. India, Myanmar and Nepal account for 70% of all the cases in the world. It is
found in the Southeastern US and Hawaii. Most patients in the United States have a history of
exposure to armadillos, a natural host for M. leprae.
Symptoms: Hypopigmented or reddish skin lesions with decreased or no sensation.
Signs: Circular patches and plaques with variable color including erythema, hyperpigmentation,
or hypopigmentation; tissue swelling with nodules or ulcerations; lesions are common on the face, ears,
and extremities.
24
Differential Diagnosis
Tinea corporis, mycosis fungoides, cutaneous TB, other causes of erythema nodosum (GI infections,
drug reactions, sarcoidosis, others).
Treatment
Dapsone, rifampin and clofazimine in combination as per specific protocols. Treatment lasts 6-12
months or longer. The relapse rate is very low (0.1% per year on the average).
Prevention: Isolate known patients until therapy is instituted.
Viral Skin Infections
Ecthyma Contagiosum
Ecthyma contagiosum infections (Milker's nodules, human orf) are caused by a genus of parapoxviruses which normally infect animals and only cause human infections when one handles infected
livestock or works in infested areas.
Symptoms
One usually reports a history of contact with ungulates (sheep, goats, yaks), or cattle.
After a 5 to 7 day incubation period one notes pruritus in an abraded area.
This lesion enlarges and becomes painful.
One may note systemic complaints of fever and chills on occasion.
Signs
In Milker’s nodule primary lesion is a deep erythematous papule (or small group of papules that
enlarges) gradually into a firm, smooth, hemispherical nodule varying in size up to 2 cm in diameter.
In human orf infections (HO) there are six classic clinical stages of the usually solitary lesion that last
approximately 1 week;
erythematous papular stage,
targetoid plaque with central crusting,
tender nodular, acute weeping nodular stage,
regenerative stage, and
regressive stage that heals without scaring.
The most common location is the dorsum of the index finger on the dominant hand due to handling
the livestock or items within the livestock area.
Other exposed skin sites of the arm, face, and leg are also at risk of infection.
Diagnosis based on clinical morphologic criteria and history of exposure to infected bovine or
ungulate livestock or livestock areas.
Differential Diagnosis
Erysipelas, erysipeloid, atypical mycobacterium, bacillary angiomatosis, cat-scratch disease,
leishmaniasis, pyogenic granuloma.
Treatment
Primary: Symptomatic treatment for pain and pruritus.
Alternative: Antibiotic for secondary wound infections.
25
Herpes Zoster (Shingles)
Herpes zoster is an acute, localized, recurrence of the varicella-zoster virus (VZV) most commonly
seen in patients over the age of 50. Less than 10% of cases are under the age of 20.
Symptoms
A prodrome of pain, tenderness, itching, burning, and/or tingling in a dermatomal distribution
precedes the eruption by 2-7 days.
Intense pain in the dermatome usually persists throughout the eruption and resolves slowly (post
herpetic neuralgia).
Constitutional symptoms of headache, fever and chills occur in approximately 5% of patients.
Signs
Erythematous papules or plaques, followed by umbilicated vesicles and bullae that commonly
evolve to pustules (progression over 48-72 hours) and crust over by 7-10 days; new lesions may
continue to appear for up to 1 week; lesions typically cluster in the distribution of a dermatome.
Lab: Tzanck smear of vesicle (undersurface of the vesicle or bullae has the highest yield) with
multinucleated giant epidermal cells.
Differential Diagnosis
Pain can be intense and may resemble that of cardiac disease, an acute abdomen or vertebral disk
herniation. The eruption of zoster can resemble allergic contact dermatitis, irritant contact
dermatitis or a localized bacterial infection.
Treatment
Primary: High dose oral acyclovir 800 mg po 5 times a day x 7 days.
Molluscum Contagiosum
Molluscum contagiosum is endemic in school age children through casual contact and spread of
the poxvirus.
Lesions are discrete, umbilicated, pearly, red papules.
Involvement of the diaper area, trunk, face, and axilla is common.
26
In the adult population, molluscum contagiosum is usually transmitted sexually, and may resolve
spontaneously after several months or may reappear.
HIV infected patients may have hundreds of small (2-3 mm) papules or develop giant 1-2 cm
lesions.
Symptoms
Asymptomatic, slow growing papules; commonly irritated by trauma or scratching, which can
cause local spreading and/or secondary infection.
Signs
Sharply circumscribed single or multiple superficial, pearly, dome-shaped papules with a
characteristic umbilication seen easily with a hand-held lens.
They initially present as pinpoint papules, increase slowly to 2-3 mm in size , and are often found
in the genital region.
Treatment
Primary: Treatment depends on location on body. Facial lesions should be treated less aggressively to
decrease the risk of scarring. Retinoid gel 0.01%-0.25% applied to affected area q hs will cause a
minor irritation to the lesion and works well for the face, as does potassium hydroxide topically.
Apply to lesion daily until cleared.
Alternative: Curettage, followed by imiquimod 5% cream applied to the lesion each day until
cleared.
Warts (including Venereal Warts)
The common wart is a benign growth in the epidermis seen in 7-10 % of the population. It is caused
by the human papilloma virus (HPV) and commonly presents as papules and plaques in school age
children. Some HPV strains have been associated with malignant transformation.
Symptoms: Usually slow growing; commonly irritated with minor trauma or excoriations
Signs
Verruca vulgaris:
Appear predominately on the dorsal aspect of the hands and periungual region of the nail, but may
occur anywhere.
They vary from solitary isolated lesions to vast numbers in any given individual.
The normal progression of the primary lesion is from a small, round, discrete, flesh colored papule to a
larger yellowish tan to black lesion that measures from several millimeters to a couple centimeters.
27
The surface of the lesion commonly takes on a rough finely papillomatous (verruciform) surface with
many characteristic “reddish-black seeds” (thrombosed capillary loops).
Verruca plana:
Appear predominately as smooth, flesh-colored to slightly tan, elevated papules, 2 to 5 mm in diameter,
with a round or polygonal base on the face, neck, arms, and legs.
In the bearded area of men and on the legs and axilla of women, irritation from shaving tends to
cause the warts to spread in linear arrays (Koebner effect)
Verruca plantaris: Appear initially as small, shiny, skin colored, sharply marginated papules that evolve
to plaques with a rough hyperkeratotic surface.
They commonly present over the weight bearing points of the foot and therefore are commonly tender
to palpation.
They may be distinguished from calluses by noting the loss of the normal dermography (skin lines) that
calluses usually retain. (see Podiatry: Plantar Warts). Venereal Wart / Condyloma Acuminatum: Appear
initially as tiny, pinpoint, flesh-toned, papules that may grow rapidly to cauliflower-like masses in any
region of the anogenital area and the oral mucosa.
Differential Diagnosis
Verruca vulgaris - seborrheic keratosis, lichen planus, simple callus, molluscum contagiosum,
carcinoma with verrucous (wart-like) appearance
Verruca plana - simple callus, foreign body, lichen planus, carcinoma with verrucous (wart-like)
appearance Venereal warts - condyloma lata (syphilis), intraepithelial neoplasm (Bowen’s disease),
invasive squamous cell skin cancer, molluscum contagiosum, lichen planus, skin tag
Treatment
Verruca vulgaris: Trim warts; apply liquid nitrogen to the lesion (for 5 seconds, slowly thaw, repeat x
1); or apply 40% salicylic acid to area once daily after trimming lesions; apply duct tape if unable to
keep acid on lesion; may need to treat for weeks until dermography (skin lines) returns.
Verruca plana: Trim warts; apply liquid nitrogen to the lesion for 5 seconds, slowly thaw, repeat x 1; or
apply 40% salicylic acid, retinoic acid, or cimetidine to the lesions as described above
Venereal Warts: Apply podophyllin (10-25%), imiquimod cream to the lesions as described above; or
apply liquid nitrogen as above.
28
Superficial Fungal Infections
Dermatophyte (Tinea) Infections
Ringworm - Tinea corporis
Jock itch - Tinea cruris Athlete’s foot - Tinea pedis
Some Dandruff - Tinea capitis Finger/Toenails - Tinea unguium
Dandruff of Beard - Tinea barbae/faciale
Palms and Soles - Tinea manuum
Dermatophyte infections are superficial, caused by fungi that invade only dead outer layers of the
skin or its appendages (stratum corneum, nails, hair).
Microsporum, Trichophyton and Epidermophyton are the genera most commonly involved.
Transmission of dermatophyte infections may be grouped into 3 main categories: from animals,
from the environment, and from one another. Infections are seen worldwide.
Symptoms: Rash, itching and flaking; severe cases: Painful, pruritic blisters.
Signs
Tinea corporis: Scaling, sharply demarcated plaque (with or without vesicles or pustules) with
central clearing and peripheral enlargement producing an annular configuration, commonly on
forearm and neck.
Tinea pedis: Various patterns: Slightly erythematous plague on the plantar surface of the foot; dry,
superficial, white scale is observed in an arciform pattern; moist patch of erythema, small fissures
and erosions usually localized to the third and fourth interdigital spaces and the lateral sole.
Tinea unguium (onychomycosis): Whitish/yellow/brown, thick, dry, subungual (under nail)
accumulation of friable keratin debris; the great toe is commonly affected first.
Tinea capitis: 3 main groups: Focal patch of alopecia with minimal scale and erythema; “Black
dot” appearance of broken of hair shafts also seen with minimal scale and erythema; kerion- a
boggy, purulent, inflamed group of pustules that is often tender to touch and heals with severe
scarring.
Tinea cruris: Similar to Tinea corporis but restricted to the intertriginous area of the groin.
Tinea barbae: Similar to Tinea corporis but restricted to the facial area.
Tinea manuum: Similar to Tinea corporis but restricted to the hands and feet.
Lab: KOH preparation for characteristic fungal hyphae.
Differential Diagnosis
Pityriasis rosea, discoid eczema, and psoriasis.
Diagnosis requires a KOH preparation
Treatment
Primary: Lac-Hydrin and Clotrimazole topically bid for 2-4 weeks for tinea pedis and
onychomycosis.
Lac-Hydrin decreases the dryness and increases the barrier properties of the skin.
Griseofulvin 500 mg bid with fatty meals (aids absorption) for 2 weeks for tinea corporis to 2 to 3
months for tinea capitis. Not effective against candidiasis or tinea versicolor.
Clotrimazole topical preparations (cream and solution) are effective against most fungal infections
when applied bid/tid to affected areas and washed off before reapplication.
Alternate: Itraconazole and terbinafine are not recommended in the field due to the inability to
properly evaluate side effects. A more effective treatment of onychomycosis is prevention and
topical ciclopirox nail lacquer (Penlac).
Note: Nystatin treats only candidal infections not dermatophytes
29
Pityriasis (Tinea) Versicolor
Pityriasis versicolor (tinea versicolor) is a chronic, asymptomatic fungal infection caused by
Pityrosporum orbicularis, a normal resident of the skin. The fine scales of this lesion are teeming with
hyphae and spores that transmit the disease. Factors that predispose to infection include warm humid
climate, genetic predisposition, high plasma cortisol levels (i.e., patients taking corticosteroids), serious
underlying disease or immunocompromise, pregnancy.
Symptoms: Asymptomatic to slightly pruritic depigmentation of skin.
Signs
White, tan, brown, or pink coalescing macules and patches with a fine scale; found most commonly on
the upper torso and neck (or face in children).
Lab: KOH prep of scales reveals numerous short, straight or ring-shaped hyphae.
Differential Diagnosis
Allergic contact or irritant dermatitis, various tinea, post inflammatory changes (hyper- or hypopigmentation), vitiligo (familial, autoimmune hypopigmentation, with only cosmetic effects).
Treatment
Primary: Ketoconazole 400 mg po with orange juice to aid in absorption, wait one hour, exercise,
leave sweat on body till the morning, then wash with selenium sulfide suspension. Repeat in one
week
Alternative: Fluconazole 200 mg po as above.
CELLULITIS:
A superficial bacterial infection of the skin and skin structures. Common in tropic regions.
Signs & Symptoms: Skin is red, hot and tender to the touch. Patient may have a mild/moderate fever.
No abscess is palpated in the SubQ tissue.
Treatment: Keflex, 250-500 mg every 6 hours. Alternative include: Cipro, 500 mg b.i.d. or Rocephin, 1
gram IV or IM every 24 hours. Warms soaks may help decrease symptoms. Evacuate if symptoms do
not improve within 24 hours of initiating treatment, if any high fever develops or if rash continues to
spread despite treatment.
30
Skin Cancer
(Basal & Squamous Cell Carcinoma, Malignant Melanoma)
Basal Cell Carcinoma (BCC)
BCC is by far the most common cancer in the world, with over 700,000 cases each year in
the U.S. alone.
Early detection and treatment are paramount in order to avoid extensive tissue destruction, damage
to adjacent structures, and complex surgery and reconstruction.
The good news is that this cancer is virtually 100% curable if approached early and properly.
Metastasis is very rare.
Sun exposure and fair complexion, light-colored hair and eyes are the main risk factors for skin
cancer.
Symptoms: Very slow-growing, small, pearly or waxy papule, usually in a sun-exposed area.
Sometimes the presenting complaint is that of a sore that will not heal. There may be a history of
trauma preceding the lesion.
Signs
Waxy or pearly papule (2-3mm diameter) that can grow to several cm over time; peripheral
telangiectasias (small, dilated blood vessels); superficial erosion; some lesions are lat scars, usually
without a history of trauma; sun-exposed areas are the most common sites: ears, periauricular skin,
eyelids and periocular skin, nose, cheeks, temples, forehead, upper chest and back, and arms and
forearms; can occur even in protected areas like the axilla, so skin exams should be thorough and
complete.
Differential Diagnosis - benign lichenoid keratosis, intradermal nevus, neurobroma, irritated
seborrheic keratosis, amelanotic melanoma, tricholemmoma. Differentiating these conditions in the
field is nearly impossible, since they require expert microscopic evaluation of a biopsy.
Treatment:
Freeze or store tumor in formaldehyde if possible for later study.
Prevention: Education about aggressive sun precautions is vital: avoid the sun during hours when the
individual’s shadow is shorter than their height; wear long sleeves, pants and broad-brimmed hats
(brim > 4 inches wide); apply sunscreen of SPF 30 or greater (with special attention to the nose, ears
and lips).
Squamous Cell Carcinoma (SCC)
SCC is the second most common skin cancer, affecting over 100,000 Americans each year.
The risk of metastasis is very real in invasive SCCs, especially on the lip or ear.
Rates of metastasis range from about 1-5 %.
Subjective: Symptoms
KAs grow rapidly, while SCCs usually are slow growing and much more common in sun-exposed
areas; usually painless lesion; history of chronic sun exposure is common, as is an inability to tan,
with many severe sunburns.
Signs
Red, scaly (hyperkeratotic) papules are most characteristic for SCC.
Size varies from a few mm to several cm.
SCC in situ can occur on the glans penis or within the foreskin, and usually has a soft, red, velvety
appearance, without hyperkeratosis (Bowen’s disease), since it arises from mucosa.
32
It is associated with a genital wart virus (HPV type 16) and can appear similar to genital warts, with
dark flat- topped verrucous papules.
Cervical and penile cancers are known to be caused by a genital wart virus.
KA has a distinctive appearance, similar to that of a volcano, with a central core of keratin surrounded
by domed, rolled borders, usually ranging in size from 1-3 cm. Metastatic SCC often presents with
palpable lymphadenopathy.
Differential Diagnosis - BCC, ulcers, chronic ulcerative herpes, benign adnexal tumors, contact
dermatitis, Bowen’s disease. Differentiating some of these conditions in the eld is nearly impossible,
requiring expert microscopic evaluation of a biopsy.
Treatment: Evacuate and refer to dermatology. If evacuation is not possible in the foreseeable future
(1-2 months—relatively slow growing tumor), perform full thickness excisions with wide margins (5
mm) all around the tumor. Freeze or store tumor in formaldehyde if possible for later study.
Prevention: Education about aggressive sun precautions is vital: avoid the sun during hours when the
individual’s shadow is shorter than their height; wear long sleeves, pants and broad-brimmed hats
(brim > 4 inches wide); apply sunscreen of SPF 30 or greater (with special attention to the nose, ears
and lips).
Malignant Melanoma
Incidence of malignant melanoma is rising faster than all other cancers in the United States.
The lifetime risk for developing melanoma in U.S citizens is currently 1 in 75 and rising, up from
about 1in 250 twenty years ago.
About 70,000 people in the U.S. develop melanoma each year, and about 7,000 die.
The 5-year survival rate is about 83% (double what it was 50 years ago), but since melanoma is
becoming more common, the death rate is still rising (3 per 100,000/year).
Melanoma is a killer, but is 100% curable with early detection and surgery.
Acral locations (hands and feet) are at risk for acral lentiginous melanoma. The nail beds and nail
matrix (which is just proximal to the cuticle and between the skin and the bone of the distal
phalanx) are also at risk, so have a high index of suspicion for pigmentation changes in these
areas.
Amelanotic melanomas are difficult to diagnose because they do not have much pigment and can
look nothing like the above description. Amelanotic melanomas can be flesh-colored or
hypopigmented papules or plaques and are often thought to be some other entity when they are
biopsied.
Symptoms
High-risk history: family history of melanoma, childhood history of sunburns, personal history of
many atypical nevi.
Signs
Use the mnemonic ABCD for lesion:
“A”–asymmetry,
“B”– border irregularity,
“C”–color variegation or change
“D”– diameter greater than 6mm.
33
The earliest of these is probably color variegation, and the colors red, white or blue are most
worrisome. Irregular areas which are very dark, or which become very light in color are also bad signs.
Asymmetry and border irregularity come from uncontrolled growth of abnormal melanocytes at the
edges of the lesion. Notched, grooved or scalloped borders are suspicious, and are usually apparent in
a lesion of 6mm diameter or more. Early melanomas tend to be flat with nodular components indicating
that the cancer is progressing, and a higher risk for metastasis. Lymphadenopathy may suggest
metastasis.
Differential Diagnosis: Seborrheic keratosis, pigmented basal cell carcinoma, atypical nevus, solar
lentigo.
Treatment: extreme care
Seborrheic Keratosis
Seborrheic keratosis is a very common pigmented, benign tumor that typically presents on the torso
after the age of 30.
Symptoms
Strong hereditary predisposition; slightly more common in males; rarely pruritic or painful unless
irritated or secondarily infected after trauma.
Signs
Lesion: 1 mm to 3 cm, round to oval, slightly elevated, “stuck-on” appearing, papule or
plaque with variable pigmentary change; surface of lesion commonly has “warty” (verrucoid)
appearance as it matures and grows; face, trunk and extremities are common sites.
Differential Diagnosis: Early lesions: actinic keratosis, nevus. Later lesions: malignant melanoma,
pigmented basal cell carcinoma. Differentiating these conditions in the eld can be very difcult
without expert microscopic evaluation of a biopsy.
Treatment: None is required for this benign lesion
Contact Dermatitis
The two main categories are allergic contact dermatitis (ACD) and irritant contact dermatitis (ICD).
The main difference is that an allergen will only cause problems such as dermatitis in those
sensitized to it.
Both ACD and ICD can be acute or chronic.
Plants such as poison oak can leave linear streaks of itchy, red papules and vesicles, corresponding
to the leafy contact made with the skin.
34
Nickel is the most common ACD causative agent, often affecting the earlobes, from earrings, or the
belly, from a belt buckle.
Neomycin is a very common cause of ACD (sensitizing almost 10% of all people exposed to it).
Beware of products containing neomycin, such as Neosporin ointment.
Some cases of detergent ICD arise from overly vigorous cleansing due to the mistaken notion that
there is a fungal infection or some type of infestation.
Symptoms
Various skin reactions including wheals, erythema, hives, edema, papules, vesicles and others,
depending on the product and level of sensitization. Geometric or linear arrangements implicate a
contactant substance.
Differential Diagnosis - other dermatitides such as atopic, seborrheic, xerotic, and stasis dermatitis,
as well as tinea, impetigo, erysipelas, cellulitis, or even Bowen’s disease (carcinoma in situ).
(See appropriate sections of this book).
Treatment:
1. AVOIDANCE IS KEY! Protective clothing can help, but a change of occupation, hobby or
substances used may be necessary.
2. Topical steroids are very useful, in higher potencies (fluocinonide or triamcinolone ointment),
in order to calm the skin while identifying offending agent.
3. For exudative, weeping areas, a soothing astringent (drying) treatment such as Domeboro
compresses bid/tid can help. Minimize wet-dry cycles and avoid over-cleansing the skin. In
generalized cases, bathe just every other day, with lukewarm water for less than 5 minutes. Use
only a mild cleanser like Cetaphil lotion or Dove Sensitive Skin soap. Avoid scrubbing the
affected areas.
4. Bland emollients like white petrolatum (Vaseline) or Crisco vegetable shortening will help
to moisturize and protect.
5. Oral antihistamines like Atarax (hydroxyzine) in doses of 25-50 mg tid/qid, or up to 100mg at
bedtime can alleviate much of the itch. The antipruritic effects of Atarax last 24 hours and the
drowsiness usually only lasts 8-10 hours, a decided advantage over Benadryl.
6. Oral steroids can be needed in the most severe cases, used in a tapering fashion for 3 weeks,
starting at 60 mg each morning for a week, then 40 mg for a week, then 20 mg for the last week.
Reserve oral steroids for the most widespread or bothersome cases. Three weeks of treatment is very
important in order to outlast the hypersensitivity reaction in the skin.
COMMON SKIN CONDITIONS
CUTANEOUS CANDIDIAS
LUPUS
35
ACNE
FUNGAL NAIL
INFECTION
SKIN HEMANGIOMA
HIVES
RUBEOLA
PSORIASIS
VITILIGO
SHINGLES
STASIS DERMATITIS
CARBUNCLE
36
SUBCUTANEOUS
CYST
Surgically removed encapsulated cyst. If a portion of the cyst is left behind, there is a good chance it
will return. 36
CHAPTER 14
Sexually Transmitted Diseases (STD)
CHAPTER 14
Sexually Transmitted Diseases (STD)
Consider evaluating for HIV antibody in 4-6 weeks when STDs ar treated
Urethral Discharges
Gonorrhea and chlamydia both present with urethral discharges.
Patients are often co-infected with both.
Neisseria gonorrhoeae causes gonorrhea and appears on Gram's stain as a clump of gram- negative
intracellular diplococci.
Asymptomatic infection can occur especially in the cervix, rectum and oropharynx.
Disseminated gonorrhea presents with infectious arthritis, tenosynovitis, and a characteristic gunmetal
blue skin lesion surrounded by a red halo, usually on the extremities (arthritis-dermatitis syndrome).
The incubation period is 2-14 days after exposu
Consider evaluating for HIV antibody in 4-6 weeks when STDs ar treated
Urethral Discharges
Gonorrhea and chlamydia both present with urethral discharges.
Patients are often co-infected with both.
Neisseria gonorrhoeae causes gonorrhea and appears on Gram's stain as a clump of gram- negative
intracellular diplococci.
Asymptomatic infection can occur especially in the cervix, rectum and oropharynx.
Disseminated gonorrhea presents with infectious arthritis, tenosynovitis, and a characteristic gunmetal
blue skin lesion surrounded by a red halo, usually on the extremities (arthritis-dermatitis syndrome).
The incubation period is 2-14 days after exposure.
Most nonspecific or non-gonococcal urethritis (NGU) and cervicitis is caused by Chlamydia
trachomatis, but Ureaplasma, genital Mycoplasma, Trichomonas and Herpes simplex are also
implicated.
These are some of the most common sexually transmitted diseases in the U.S. and a leading cause of
female infertility.
Infant eye and lung infections are consequent to maternal genital infection with Chlamydia.
Incubation period is 7-12 days after exposure.
A thick mucus discharge with pain on urination and genital ulcer should suggest Herpes simplex.
Incubation period is 2-12 days after exposure.
Symptoms
Male: Acute (< 3 days): Dysuria with discharge/without discharge- usually NGU Chronic (>10
days) urethral stricture
Female: Acute (< 3 days): Dysuria or frequent urination, vaginal discharge, pain with intercourse,
lower pelvic pain Chronic (>10 days): PID, infertility Either: Sub acute (3-10 days): Painful joints,
gun metal blue skin lesions (GC), tenosynovitis
Focused History: Have you had unprotected sex with a new partner in the past 6 weeks?
(incubation period 2 weeks for GC; longer for NGU)
Signs
Inspection: Acute (< 3 days): Purulent yellow to green discharge (both GC and chlamydia),
mucoid /scant discharge (more consistent with NGU), if oropharyngeal exposure, see red tonsils with
exudate (GC), Sub acute (3-10 days): Infection of periurethral glands, epididymitis, if disseminated
GC: red, tender swollen joints and tendon insertions, fever to 102ºF.
Palpation: Pelvic exam may show cervical movement tenderness
Lab: Gram stain: Urethral discharge shows gram-negative intracellular diplococci (low diagnostic
sensitivity in females), or many polymorphonuclear neutrophils but no organisms (NGU), pregnancy
test (drug selection).
Differential Diagnosis
Other causes of dysuria include: Trichomonas - malodorous discharge in females
Vaginal candidiasis - pruritus, white curd-like discharge
Herpes simplex - presence of mucoid discharge with skin ulcer
Urinary tract infection - usually frequency, urgency; sometimes hematuria
38
The arthritis-dermatitis syndrome of disseminated gonorrhea may resemble:
Meningococcemia - GC rash on extremities has distinctive bluish lesions surrounded by erythema
Lyme disease - E. migrans rash has larger, red lesions
Treatment:
Ceftriaxone 125 mg IM single dose AND azithromycin 1 gram po single dose
Cefixime 400 mg po single dose + doxycycline 100 mg po bid x 7 days ciprofloxacin 500 mg po
azithromycin 1 gm po single dose + ceftriaxone 125 mg IM single dose + erythromycin 500 mg qid
x 7 days
Azithromycin 2 gm in single dose (poor gastrointestinal tolerance) alone.
Pregnant patient: Use ceftriaxone or cefixime in a single dose AND erythromycin 500 mg po qid for
14 days. Do not use doxycycline in pregnant or nursing females.
Genital Ulcers
Genital ulcers have a wide variety of sexually transmitted causes.
Chancroid, caused by Hemophilus ducreyi, has been associated with an increased risk for HIV
transmission and may co-exist with other causes of genital ulcer (such as herpes infection).
The incubation period is 3-7 days. Granuloma inguinale (caused by gram-negative
Calymmatobacterium granulomatis) causes beefy red granulomas that progress slowly but can cover
the genitalia and heal slowly with scarring.
Patients can spread lesions to other areas through autoinoculation.
Incubation period is 1-12 weeks. Lymphogranuloma venereum (LGV), caused by variants of
Chlamydia trachomatis, starts as a painless vesicle or nodule that then ulcerates and heals.
Days to weeks later, regional lymph nodes become inflamed and tender.
Suppuration, scarring, systemic infection, chronic elephantiasis and rectal strictures have been seen in
untreated infection.
Caused by Treponema pallidum, syphilis is known as the “great imitator”.
Left untreated, up to 1/3 of patients will develop tertiary syphilis (CNS infection, aortic aneurysm,
gummas of the skin, bone and visceral organs).
Syphilis is curable in all stages but treatment may yield a Jarisch-Herxheimer reaction with fever,
rigors and intensification of the lesions 2-24 hours after initiating treatment.
Incubation period of primary stage syphilis is 10 days to 3 months.
Herpes is caused by Herpes simplex (HSV) type 1 and 2, both of which can cause genital ulcers.
HSV 1 is usually milder and often associated with oral sores, “fever blister”, keratoconjunctivitis and
encephalitis.
HSV 2 causes a more severe initial episode (fever, exudative pharyngitis, toxic appearance, multiple
genital lesions), and then recurs as a localized cluster of vesicles that ulcerate painfully. HSV2 is
associated with aseptic meningitis and radiculitis.
Symptoms
Painless ulcer: Syphilis, LGV, granuloma inguinale (Donovanosis)
Painful ulcer: Herpes simplex, chancroid, phagedenic ulcer (an otherwise painless ulcer secondarily
infected with bacteria)
Constitutional: Acute (1-3 days): Fever (in LGV and 1st episode HSV)
Specific: Acute (1-3 days): Generally starts as papule that ulcerates, HSV: Paresthesias can precede
outbreak, syphilis: rash including palms and soles Chronic (>1 month): LGV may be very chronic,
HSV often recurs
39
Signs
Inspection
HSV: Acute (1-3 days): Vesicles in clusters, 1st time may have fever Sub acute (3-10 days): Shallow
painful ulcer (often multiple) Chronic (>1 month): In AIDS patients- huge non-healing ulcers
Chancroid: Acute (1-3 days): Papules Sub acute (3-10 days): Painful, shaggy edged, deep ulcers;
suppurative regional adenopathy Chronic (>1 month):
Phimosis Granuloma Inguinale: Acute (1-3 days): Bright red, painless, satiny-surface, raised plaque,
often in folds between scrotum or labia and thighs Sub acute (3-10 days): The border of the ulcer
shows rolled edge
LGV: Acute (1-3 days): Painless vesicle or nodule that ulcerates and heals; may have fever Sub acute
(3-10 days): Groove sign (lymph node adheres above and below inguinal ligament) Chronic (>1
month): Chronic elephantiasis of genitals, rectal strictures, rectal fistula
Syphilis:
Acute (1-3 days): Painless ulcer with rolled border (chancre) heals without Rx in 3-6 weeks Chronic
(>1 month): Secondary syphilis: (see generalized 2-4 weeks after chancre, rash including palms and
soles; can also see flat genital warts, loss of hair, patches on the mucous membranes
Tertiary or late (5-20 years) syphilis: gummas (tumor like masses in skin/bone/viscera) neurologic
abnormalities- “neurosyphilis”: posterior column findings such as slapped foot gait, loss of deep
tendon reflexes, loss of position sense or hot/cold sense); also develop abnormal pupillary reflexes,
dementia Auscultation: Syphilis: In late syphilis may hear aortic regurgitation murmur
Palpation: Most patients with genital ulcers develop tender regional adenopathy
Lab: Gram’s stain pus from bubo (enlarged fluctuant node): large numbers of small gram negative
coccobacilli in a “school of fish” pattern (chancroid); Giemsa stain edge of tissue scraping from edge
of ulcer: intracytoplasmic bacilli in the macrophages (Donovan bodies) (Granuloma Inguinale);
Giemsa stain of tissue scraping at base of the ulcer (Tzanck smear): observe for multinucleated giant
cells (herpes); RPR (syphilis): may be negative during early stage, and should be repeated in 4-6
weeks.
The first symptom of primary syphilis is often a small , round, firm ulcer called a chancre ("shanker")
at the place where the bacteria entered your body.
mia via hematocrit; perform pregnancy test
Differential diagnosis: For many of these etiologies of AUB, physical findings will be minimal and
limited:
Bladder
Pubic symphisis
40
Chlamydia
Mode of Transmission
Oral / Anal / Vaginal Sex with an infected person
Symptoms:
Considered a silent disease with no apparent symptoms up to 2weeks from Infection
Those who do have symptoms may have an abnormal discharge (mucus or pus) from the vagina or
penis or experience pain while urinating. These early symptoms may be very mild.
TESTING:
Swab test is obtained by briefly placing a swab in the opening of the urethra at the tip of the penis; this
causes brief discomfort and a burning sensation
TREATMENT:
Antibiotics like Zithromax or Doxycycline
Chancroid
Treatment:
Primary: Antibiotics: Ceftriaxone 250 mg IM single dose, needle aspirate fluctuant nodes to avoid
rupture
Alternatives: Azithromycin 1 gm po single dose, erythromycin 500 mg po qid x 7 days or
ciprofloxacin 500 mg po bid for 3 days
Lymphogranuloma venereum (LGV)
Treatment:
Primary:
Antibiotics: Azithromycin 500 mg po qd x 7 days or 1 gm po each week for 4 doses; drain fluctuant
buboes by needle aspiration, avoid incision and drainage which can cause sinus tracts.
Alternatives: Doxycycline 100 mg po x 21-30 days, ceftriaxone 1 gm IM qd x 14 days, ciprofloxacin
750mg po qd x 21 days or erythromycin 1000 mg po bid x 21 days.
No Improvement/Deterioration: Drug resistant strains have been seen. Expect to see a treatment
response by seven days but prolonged therapy is needed to avoid relapse.
Granuloma inguinale
Treatment:
Primary: Azithromycin 500 mg po qd x 7 days or 1 gm po each week for 4 doses
Alternatives: Doxycycline 100 mg po x 21-30 days, ceftriaxone 1 gm IM qd x 14 days, ciprofloxacin
750 mg po qd x 21 days or erythromycin 1 gm po bid x 21 days
No Improvement/Deterioration: Drug resistant strains have been seen. Expect to see a treatment
response by seven days but prolonged therapy is needed to avoid relapse.
Herpes simplex
Treatment:
Primary: Acyclovir 400 mg q 8 hours x 10-14 days if initial episode, for 5 days if recurrence
Alternative: Valacyclovir 1000 mg q 12 hours x 10 days (use 500 mg po qd for 5 days for
recurrence), Famciclovir 250 mg po q 8 hours x 5-10 days (use 125 mg bid for 3-5 days for
recurrence)
41
Vaginal Trichomonas
Trichomonas vaginalis, a sexually transmitted fungus, is a common cause of abnormal vaginal
discharge.
The asymptomatic carrier rate in women is 10%.
Sexual partners should be treated.
Symptoms: Yellow-green discharge (may be frothy and malodorous but not usually fishy);
vulvovaginal irritation and burning; dysuria.
Signs: Characteristic discharge not always present; vulva may be edematous and inflamed; redness of
the cervix (“strawberry cervix”); tender vagina; no abdominal pain.
Lab: Vaginal pH: should be > 4.7 (test with urine dipstick); motile, flagellated trichomonads on wet
prep.
Differential Diagnosis
Bacterial vaginosis, gonorrhea or chlamydial infection, atrophic vaginitis, candida vaginitis
Treatment
Primary: Metronidazole 2 gm po X 1 or metronidazole 500 mg po bid x 7 days (95% cure rate)
Highly recommend GC/Chlamydia cultures - co-infection is common.
HIV
The highlight of the 20th century has been the pandemic of HIV/AIDS.
This disease has spread across all the continents, countries & races breaking all natural or manmade
barriers.
The human immunodeficiency virus (HIV) infects cells of the immune system,destroying or impairing
their function, leading to "immune deficiency."
The immune system is considered deficient when it can no longer fulfill its role of fighting infection
and disease.
Infections associated with severe immunodeficiency are known as "opportunistic infections," because
they take advantage of a weakened immune system.
The term AIDS applies to the most advanced stages of HIV infection, defined by the occurrence of any
of more than 20 opportunistic infections or HIV-related cancers.
How quickly does a person infected with HIV develop AIDS?
The length of time can vary widely between individuals.
42
Left untreated, the majority of people infected with HIV will develop signs of HIV-related illness
within 5-10 years.
Antiretroviral therapy (ART) can slow the disease progression by decreasing an infected person’s viral
load.
Acute HIV syndrome
50–70% of persons with HIV infection experience an acute clinical syndrome approximately 3–6
weeks after primary infection.
Usually persists for 1 to several weeks
Symptoms & Signs
General symptoms
Fever
Pharyngitis
Lymphadenopathy (70% of cases)
Headache/retro-orbital pain
Arthralgias/myalgias
Lethargy/malaise
Weight loss
Anorexia
Mucocutaneous ulceration
Nausea
Vomiting
Diarrhea
Neurologic
Meningitis
Encephalitis
Peripheral neuropathy
Myelopathy
Dermatologic
Erythematous maculopapular rash
Symptomatic disease
Symptoms can develop at any time during the course of HIV infection.
More severe and life-threatening complications of HIV infection occur in patients with a CD4+ T-cell
count <200/μL.
Persistent generalized lymphadenopathy
Fever persisting for >1 month
Involuntary weight loss of >10% of baseline
Diarrhea for >1 month in absence of explainable cause
HIV encephalopathy (AIDS dementia complex)
Aseptic meningitis
Myelopathy
Peripheral neuropathy
Myopathy
43
Secondary infectious diseases
Pneumocystis carinii pneumonia (m.c 80%)
Candida albicans (oral thrush, esophagitis)
Mycobacterium avium intracellulare (localized or disseminated infection)
Mycobacterium tuberculosis
Cryptococcus neoformans (meningitis, disseminated disease)
Toxoplasma gondii (encephalitis, intracerebral mass lesion)
Herpes simplex virus (severe mucocutaneous lesions, esophagitis)
Diarrhea due to Cryptosporidium species or Isospora belli
Bacterial pathogens (especially in pediatric cases)
KAPOSI’S SARCOMA
45
Secondary neoplasms
Kaposi’s sarcoma (cutaneous and visceral, more fulminant course than in non–HIV-infected patients)
Lymphoid neoplasms (especially B cell lymphomas of brain, marrow, GI tract) Organ-specific disease
What are antiretroviral drugs?
Antiretroviral drugs are used in the treatment and prevention of HIV infection.
They fight HIV by stopping or interfering with the reproduction of the virus in the body.
Standard antiretroviral therapy (ART) consists of the use of at least three antiretroviral (ARV) drugs to
maximally suppress the HIV virus and stop the progression of HIV disease.
In health care settings, transmission of HIV can be prevented through primary prevention measures
such as standard precautions, blood safety, injection safety, and safe waste disposal, as well as
secondary prevention measures, such as post-exposure prophylaxis for occupational or certain nonoccupational exposures to HIV such as in health-care settings, post-rape, and in case of condom
breakage.
31 anti retroviral drugs (ARVs) approved by the U.S. Food and Drug Administration (FDA) to treat
HIV infection.
These treatments do not cure people of HIV or AIDS. Rather, they suppress the virus, even to
undetectable levels, but they do not completely eliminate HIV from the body. By suppressing the
amount of virus in the body, people infected with HIV can now lead longer and healthier lives.
However, they can still transmit the virus and must continuously take antiretroviral drugs in order to
maintain their health quality.
46
CHAPTER 15
Gynecology
Female Pelvic Examination
When: As indicated per differential diagnosis, which primarily is for abdominal and pelvic
complaints. IMPORTANT DETAILS
Most females in the U.S. have one pelvic examination per year from the age of 18 to assess for
gynecologic malignancies or benign conditions such as uterine fibroids.
For females this examination is the most sensitive and fraught with concern. Discussion before
and after the exam what will happen and what was found.
It is necessary to discuss each part of the exam prior to its performance – prior to touching or
moving any structure
The exam should be performed expeditiously yet thoroughly.
A female chaperone is absolutely necessary for male examiners
Keep the patient as covered as possible.
If the examination targets the vulva ask the patient to undress only from the waist down.
Cover the abdomen with a sheet or drape.
As soon as the exam is done, allow the patient to dress.
What You Need:
For all exams: Good light source – preferably a mobile light, non-sterile gloves, water-soluble
lubricant, vaginal speculum of the correct size (small for patients who are virginal, medium Graves
are appropriate for most sexually active females and for parous women. Obesity may necessitate a
large Graves due to redundant tissue in the vagina). A speculum may be improvised out of two
spoons joined by a rubber band, or two bent spoons.
On certain exams: Culture medium for gonorrhea and chlamydia testing, large cotton-tipped
swabs, pH paper, screening test for fecal occult blood, set-up for wet mount and KOH prep (see
Lab Procedures).
What To Do:
Position the patient in low lithotomy. The head may be elevated 30-60° to allow the patient
visual access to the exam. If a lithotomy table with stirrups is not available, the patient may flex
her knees to her chest or an exam table can be improvised with a litter, litter stands, IV poles and
small battle dressings.
External Genitalia Examination:
Prior to touching the perineum inspect it visually. Observe for symmetry, bulges, rashes or
lesions If asymmetry or mass is noted these areas should be palpated to confirm mass,
induration or other abnormality.
Vaginal Examination:
Select the appropriate sized speculum. Speculum may be lubricated with warm water prior to
insertion. Remember to discuss the examination with the patient. Ask the patient to consciously
relax the muscles at the opening of the vagina.
47
Gentle downward pressure with the tip of the speculum or with the finger may help the patient
relax, although many times this is not necessary. Place the speculum at the opening of the vagina
and gently push it in and downwards until the vaginal apex is reached.
Insert the speculum obliquely through the introitus and then rotated to the horizontal plane. Always
control the speculum blades, holding them shut with one hand until the blades are opened as the
vaginal apex is reached.
Observe the vaginal sidewalls and the cervix.
Inspect vaginal discharge for quantity, color, consistency and odor.
Evaluate the cervix for erosion, lesion, infection, laceration, polyps, ulceration and tumors.
ADVANCED To perform cervical cultures for gonorrhea and chlamydia, place each swab into the
cervical os and allow to sit for 20-30 seconds. Replace in culture tube.
Assess vaginal pH by obtaining a sample of vaginal discharge from the sidewall or from any
pooled discharge in the posterior fornix using a small cotton swab.
Touch the cotton swab to the pH paper and look for color change. Obtain discharge samples for
KOH and wet mount with a similar technique. Blood or cervical mucus will be basic (high pH)
and will give false readings, so avoid these while sampling.
Bulging of the bladder and/or rectum into the vagina may be seen in patients with pelvic
relaxation. Women who have had children vaginally will have some relaxation of the rectovaginal
and vesicovaginal septum. The cervix may descend into the vagina with Valsalva.
Rectovaginal Examination:
Always change gloves (so no blood is carried to the rectum) and obtain a large dollop of lubricant
prior to rectovaginal examination.
Ask the patient to relax the anal sphincter. The middle finger is inserted into the rectum and the
index finger into the vagina. It is helpful to have the patient bear down as the rectal finger is
inserted slowly.
The rectovaginal septum can be felt between the index and middle finger. Palpate the posterior
aspect of the uterus, uterosacral ligaments and posterior cul-de-sac along with the anorectal area.
Note masses, nodularity and pain. A simple rectal examination is the only way to assess the
pelvis in an infant or child. Test a sample of fecal material for occult blood.
What Not To Do:
Do not be insensitive, unprofessional or humorous with the patient during the exam.
Do not perform routine pelvic exams during pregnancy. Most women will not require such exams
unless there is a strong suspicion of vaginal pathology. The exam may introduce harmful
organisms into the vagina or otherwise endanger the fetus.
Do not perform the exam in stages. Do a complete exam the first time and allow the patient to get
dressed. Do not perform an occult blood test with gloves that have been used to examine the
vagina. The test will likely be falsely positive.
Abnormal Uterine Bleeding
Introduction: Abnormal uterine bleeding (AUB) is symptom that can have a variety of etiologies,
ranging from simple to life-threatening illnesses.
The work-up of abnormal uterine bleeding is systematic and will usually lead to diagnosis.
AUB is characterized by changes in the interval and duration of menstrual flow.
48
The normal menstrual interval is 28 days with a range of 21-35 days. The normal duration of the
menstrual flow is 2-7 days with average blood loss < 80 cc. AUB can present as vaginal hemorrhage,
which is the primary focus of this section.
Symptoms
Significant change in menstrual pattern or amount of bleeding.
Acute, excessive menstrual blood loss can lead to symptomatic anemia, if so, patient will complain of
fatigue, orthostatic changes, and heart palpitations.
Excessive blood loss may be described as “gushing”; large clots may be passed; pregnant patients may
complain of associated early pregnancy symptoms such as nausea and vomiting, breast tenderness and
missing last menstrual cycle.
Signs
May have large amounts of blood issuing from the vagina; the cervix may be obscured with blood;
uterus may be misshapen by a uterine fibroid, a common cause of heavy menses; patients with acute
anemia will have heart rate and blood pressure changes based on the volume of blood loss.
Lab: Assess aneUterus
Rectum
Cervix
Pregnancy - always rule out first
Anatomic abnormalities - uterine fibroids, uterine and cervical polyps and large ovarian cysts may
secrete estrogen, which disrupts normal menstrual function. Uterine fibroids are a common cause of
AUB in women from ages 30 through menopause.
After menopause, most fibroids become asymptomatic.
A postmenopausal woman with AUB and an enlarged irregular uterus has cancer until proven
otherwise.
Infection - cervicitis and endometritis, pelvic inflammatory disease
Cancer and pre-cancerous lesions - post-coital bleeding is a presenting symptom of cervical cancer.
Postmenopausal bleeding is a primary presenting symptom of uterine carcinoma and endometrial
hyperplasia/ dysplasia. Ovarian cancer may present with bleeding due to estrogen secretion by the
tumor.
Endocrine disorders - disorders of prolactin secretion, hyper and hypothyroidism, adrenal dysfunction.
This category includes anovulation which results in irregular/heavy and occasional absent menses.
Hematologic - suspect coagulopathies in a young, newly menstruating female with abnormally heavy
flow
Treatment
Significant vaginal hemorrhage:
1. Stabilize patient (ABCs, etc.); monitor vital signs closely and transfuse if necessary
2. Maintain patient on bed rest
49
3. If evacuation delayed, give oral contraceptive pill qid (estrogen can stabilize the uterine lining) anticipate nausea and treat with oral or IV antiemetic.
4. Give antibiotics (see below) liberally for: febrile patient (start immediately), tender uterus (suspect
infection of the uterine lining), foul-smelling discharge.
Minor menstrual irregularities:
1. If HCG negative and HCT and physical examination are normal, treatment may be delayed until
appropriate consultative services are available.
2. NSAIDs (ibuprofen 800 mg po tid or Naprosyn 500 mg po bid) may reduce blood flow.
3. Oral contraceptive pills are the most effective way to control menstrual irregularities (see
Contraception section on CD-ROM).
Antibiotic regimens:
Primary: Ampicillin/sulbactam 3 gm IV q 4-6 hours
Alternate: Cefotetan 1-2 gm IV q 12 hours or piperacillin 3-4 gm IV q 4 hours, or
ticarcillin/clavulanate 3.1 gm IV q 6 hours, or gentamicin 1.5 mg/kg load then 1.0 mg/kg IV q 8 hours
and clindamycin 900 mg IV q 6 hours (if patient remains febrile after 48 hours, add ampicillin 2 gm
IV q 6 hours).
Empiric: If IV therapy is not available, treat the patient as per oral PID protocol with IM ceftriaxone
250 mg and 1 gm of oral azithromycin or 100 mg doxycycline po bid.
OB/GYN expert as needed for continued or recurrent symptoms.
Pelvic Pain, Acute
Introduction: Internal gynecologic pathology is a common cause of pelvic and abdominal pain. Acute
pain may be secondary to an ectopic pregnancy, a ruptured ovarian cyst, torsion of the ovary, pelvic
inflammatory disease or a non-GYN cause such as appendicitis.
All of these situations require close observation for possible surgical intervention or transfer to an
acute care facility.
Symptoms
Abrupt onset of abdominal/pelvic pain. Character of pain and other symptoms vary depending on
the cause.
Ruptured ovarian cyst: acute lower pelvic pain, often mid-cycle (day 12-16); occasional postcoital
onset of pain due to disruption of cyst during intercourse; should not have associated fever; may
present acutely and improve over 8-12 hours; minimal blood loss.
Torsion of the ovary: intermittent severe pelvic pain initially localized in right or left lower quadrant
then becoming more diffuse as the ovary necroses. The ovary will often torse and de-torse prior to a
final torsion so the patient will describe this same pain lasting for shorter intervals prior to the event
that brings the patient in for care. Not initially associated with fever; pain often radiates down inner
thigh on affected side; hematologically stable. Fever and elevated white blood cell count are seen if
the ovary has become necrotic (prolonged torsion - usually greater than 8 hours although no good data
is available on exact time).
Ectopic pregnancy: late, short or missed menses; suddenly worsening abdominal pain which may
radiate to a shoulder due to irritation of the diaphragm; circulatory collapse due to internal bleeding;
history of vaginal bleeding, infertility, prior PID or pelvic surgery to include infertility procedures;
increased risk if prior ectopic pregnancy.
Pelvic Infection: See PID section.
50
Signs
Ruptured ovarian cyst: tender adnexa, normal ovaries after rupture. Fullness in posterior cul-de-sac
may suggest blood in pelvis. Localized guarding but no rebound until rupture, no abnormal vaginal
discharge, normal uterine exam, afebrile, normal vitals.
Torsion of the ovary: Very tender mass in right or left lower quadrant; rebound and guarding; afebrile
early with normal WBC, but both elevated later; nausea and vomiting; rare anorexia; NO leg
numbness or weakness to accompany pain (consider disc herniation if present); hemodynamically
stable.
Ectopic pregnancy: If ruptured: acute abdomen with peritonitis; nausea and vomiting;
hemodynamically unstable with tachycardia, hypotension and anxiety; slightly enlarged, tender uterus
with severe cervical motion tenderness. If not ruptured: unilateral, palpable, tender mass without
peritonitis; early ectopic will not be palpable and may have intermittent, severe, cramping pain; mild
spotting through a closed cervical os (open os with significant vaginal bleeding is a miscarriage).
Pelvic Infection: Lower abdominal tenderness, bilateral adnexal tenderness (see PID section).
NOTE: Perform rectal examination with Hemocult for blood. Change gloves before rectal/ Hemocult
exam if the patient is having vaginal bleeding. Positive Hemocult does not occur with the above
diagnoses without co-existing GI disease.
Lab: WBC count (elevated in later torsion and in PID), urine HCG (ectopic), CBC (anemia due to
hemorrhage), stool Hemocult (guaiac), cervical cultures for gonorrhea, type blood
Differential Diagnosis (see Symptom: Abdominal Pain and GI chapter)
Appendicitis- frequently confused with gynecological acute pathology. Appendicitis begins in the
epigastrium, migrates to the periumbilical region and then settles in the right lower quadrant (RLQ)
after 6 to 8 hours, with rebound tenderness and RLQ tenderness to palpation (most common finding).
Anorexia, nausea and vomiting are common. Prodromal symptoms include indigestion and
irregularity of the bowels. The WBC count is often NOT elevated until the patient has had
symptoms for over 24 hours.
Diverticulitis- pain due to infected diverticulum is usually left lower quadrant. Past history includes
diarrhea and bloody stools, low-grade fever, elevated WBC counts and age over 40.
Severe Constipation- acute cramping pain; anorexia and nausea or vomiting; common in the second
and third trimesters; treatment with fluids and fiber will be sufficient for many pregnant women. Acute
constipation can indicate underlying disease.
Inflammatory Bowel Disease or Irritable Bowel Syndrome- abdominal pain rarely sudden in onset; will
have a past history of intermittent symptoms including diarrhea and bloody stools.
Plan
1. Stabilize patient (airway, breathing, circulation, etc).
2. Start 2 large bore IVs and initiate fluid resuscitation for unstable patients (see Shock: Fluid
Resuscitation).
3. If PID, then treat per PID section (antibiotics and bedrest).
4. Initiate transfer/evacuation if patient has: possible ovarian torsion, ectopic pregnancy or is
hemodynamically unstable.
5. If the patient’s diagnosis is consistent with ruptured ovarian cyst and she is hemodynamically
stable, she can be placed on bedrest. Repeat vital signs and physical examination q 4 hours. She
should improve and be ambulatory in 6-12 hours, NSAIDs may be given, as well as mild narcotics
(should only be necessary for the 1st 12-24 hours, if at all. If a significant narcotic need exists beyond
12 hours the patient should be evacuated).
If you are unable to evacuate the patient immediately, institute bedrest and fluid resuscitation with
lactated Ringer’s or normal saline. Blood transfusion may be life saving and should be given if patient
has failed resuscitation with crystalloid or is otherwise showing signs of inadequate tissue perfusion.
Type and crossmatched vs. type specific vs. O negative depending on urgency and availability
51
Pelvic Pain, Chronic
Defined as pelvic pain of greater than 6 months duration, chronic pelvic pain is usually multifactorial in
etiology.
Primary Dysmenorrhea - a major cause of chronic pelvic pain and the easiest to diagnose.
Dysmenorrhea (painful menstruation) is classified as primary when there is no underlying organic
cause other than prostaglandin release from the uterus itself during the time of menstruation.
Symptoms:
Once a woman’s cycles become ovulatory, anywhere from 6 months to 2 years after the start of her
periods, she can experience dysmenorrhea and most do.
Age of onset is therefore 6-24 months after the start of menstruation.
The pain ranges from very mild to quite severe. It is described as cramping in nature and is felt in the
sacral area, low pelvis and inner thigh area.
Usually starts and ends with menstruation. The patient feels well throughout the remainder of her
cycle. Some will have a day or two of premenstrual pain. Many young women will “grow out of”
their primary dysmenorrhea.
May have associated nausea, vomiting and diarrhea (due to excessive prostaglandin release from the
uterus).
Some may be severely fatigued, pale and ill appearing. Occasionally vasovagal loss of consciousness
may occur -usually with the early years of menstruation only.
Fever is not present; anorexia is rare other than with the first day of a severe menstrual cycle.
Diagnosis: Based on history.
Treatment:
Involves prostaglandin release suppression with NSAIDs and/or hormonal suppression of
ovulation with birth control pills.
Birth control pills are very effective at decreasing menstrual pain and should be prescribed to all who
fail NSAIDs.
They may have endometriosis.
Endometriosis -
Very common cause (60-70%) of chronic pelvic pain in premenopausal women.
Caused by the presence of functional ectopic endometrial glands, which may be located in the ovaries,
uterus, uterosacral ligaments or any area within the pelvis.
The usual age of onset is in between age 30 and 40.
Symptoms:
Dysmenorrhea (pain with menstruation) will occur in most women with endometriosis.
Worsening from the normal minor menstrual discomfort
Start at least a week prior to the onset of menstruation and may last a few days after blood flow stops.
Pain often radiates to the rectum and inner thighs.
Pain with intercourse (dyspareunia)
It is not uncommon for women with endometriosis to have daily pelvic pain
52
Pelvic Examination: Palpating the uterus and ovaries often reproduces the pain. The pain may be
reproduced with deep abdominal palpation but this is not a reliable finding. As endometriosis can
cause scarring in the pelvis, one can find that the uterus and ovaries are immobile due to adhesions.
Endometriosis can also cause ovarian cysts. Often the examination is unremarkable other than in the
fact that you can reproduce the patient’s pain. This is because very small areas of endometriosis can
cause great pain.
Treatment:
Many women are not diagnosed for years and so treatment is delayed.
Ibuprofen 800 mg po tid or Naprosyn 500 mg po bid should be helpful. Birth control pills suppress
ovulation, which will decrease the activity of the endometriosis implants.
Patient with any history consistent with the above review it is best to start NSAIDs, birth control
pills and refer to Gynecology as surgery (laparoscopy) gives the definitive diagnosis and often
alleviates symptoms.
Mittelschmerz - ovulatory pain.
Some women have midcycle pain due to either distension of the ovarian capsule or spillage of the
ovarian contents at the time of ovulation.
This pain usually coincides with the 12th-16th day of the menstrual cycle (count the first day of
bleeding as day #1). Women will sometimes have a small amount of vaginal bleeding during this time.
Symptoms:
Gradual or rapid onset of pelvic pain that will usually peak in 24 hours and then remit.
Occasionally the pain will be acute in onset and more painful then usual. This may be a ruptured
ovarian cyst.
The most significant piece of history is the timing of the pain- Mittelschmerz will usually be on the
12th-16th day.
Pelvic Examination:
Only significant for generalized lower pelvic discomfort that is mild to moderate in nature. The ovary
will sometimes be enlarged (a woman ovulates from only one side each month so the pain is often
lateralizing and changes sides month-to-month).
Diagnosis:
If the pain occurs only during midcycle it is Mittleschmerz. Pain that occurs frequently throughout
the month will fall into another category.
Treatment: NSAIDs such as ibuprofen 800 mg po tid will help to alleviate discomfort. Primary
treatment is ovulatory suppression with birth control pills.
Irritable Bowel Syndrome (IBS) - may be the source of 50% of cases of chronic pelvic pain or may
occur in conjunction with diseases such as endometriosis.
53
IBS is a disease of abnormal bowel motility triggered by situational stress and certain substances
(lactose). Studies show that patients with IBS have increased colonic contractions particularly in
response to meals. The discomfort that occurs is often left lower quadrant and lower abdominal causing many women to interpret their symptoms as related to the uterus and/or ovaries.
Symptoms:
Colicky abdominal pain with a sensation of rectal fullness and bloating.
Pain is often relieved with bowel movement and exacerbated by meals.
The symptoms wax and wane in a cyclic fashion, sometimes lasting for months.
The cycles often parallel physical or emotional stress.
Abdominal pain is usually accompanied by diarrhea and/or constipation but occasionally may be the
only complaint.
Physical Examination:
In patients with IBS the uterus and ovaries should be WNL unless a coexisting gynecological problem
exists.
Treatment: Involves behavior and dietary modifications.
Diagnostic Tests
1. Urine culture, cervical cultures to rule out gonorrhea and chlamydia.
2. The patient should chart the days of menstruation. She should note pain on a scale of 1-10 and
any other accompanying symptoms, including physical and psychological symptoms.
3.If available, radiographs of the pelvis and lumbo-sacral spine can identify other potential
explanations of chronic pelvic pain.
Treatment
Warm compresses, rest and warm baths can be helpful for many types of chronic pain. Relaxation
and meditation have helped many women deal with and decrease pain.
Bacterial Vaginosis
Introduction: Bacterial vaginosis is caused by a vaginal overgrowth of several indigenous bacterial
species.
Symptoms
Symptoms are localized to the vagina rather than throughout the pelvis: a gray-yellowish, thin vaginal
discharge with a foul-fishy odor made worse after intercourse; vulvar burning and irritation; pain
during and after intercourse due to vaginal irritation.
Signs
Pelvic exam: Thin, homogenous, gray or greenish-yellow discharge adherent to side walls of the
vagina; pooled fluid in the posterior vaginal cul-de-sac; normal vaginal epithelium; amine (fishy)
odor to discharge; erythema of external genitalia; normal uterus and ovaries.
Lab: Examine discharge, prepare wet mount/KOH slides (see Lab Procedures), test pH with urine
dipstick.
54
Consider STD and pregnancy evaluation.
Diagnosis based on the discharge having three of the following four characteristics: pH greater than
4.7; Thin yellow-white discharge present on vulva and vagina; Wet prep reveals clue cells
Candida Vaginitis/Vulvitis
Introduction: Candida vaginitis and vulvitis are inflammatory conditions caused by Candida yeast.
Symptoms
Vulvar and vaginal itching are the most common complaints; thick, curdy white discharge - increased
from baseline; external irritation and occasionally dysuria and pain with intercourse; no systemic
symptoms (i.e., fever or abdominal pain) unless there is another illness; no foul-smelling vaginal
discharge.
Signs
Thick, white, curdy discharge adherent to side walls of the vagina (may look like cottage cheese or be
thick and white/yellow)
Later signs include erythema and edema of the vulva/vagina (perineal rash with red, shiny
appearance); fissures of the vulva; self-inflicted scratches of the vulva; swelling and redness of the
labia; abdominal exam will be benign.
Lab: KOH (potassium hydroxide) wet-mount examination yields yeast hyphae in 50-80% of patients
Vaginal pH: will be < 4.7 in patient with candida (test with urine dipstick).
Differential Diagnosis: Bacterial vaginosis, trichomonas, gonorrhea or chlamydial infection, atrophic
vaginitis (see Vaginal Discharge Table and STD chapter).
Treatment
Various intravaginal azole agents used for 3-7 days (miconazole, clotrimazole are most common)
Alternative: Oral fluconazole 150 mg X 1
Pelvic Inflammatory Disease
Introduction: Pelvic Inflammatory Disease (PID) results from organisms spreading directly from the
cervix to the endometrium (uterine lining) and then to the Fallopian tubes.
Symptoms: Lower abdominal pain with or without signs of peritoneal irritation; severe and continuous
pain in both lower quadrants, increased by movement and intercourse (dyspareunia); abnormal vaginal
bleeding in 15-35%; fever in less than 50%; onset of symptoms likely within 7 days of onset of
menses.
Signs
Lower abdominal tenderness, bilateral adnexal tenderness, cervical motion tenderness;
also fever >101°F, mucopurulent cervicitis.
Lab: Cervical culture positive for gonorrhea (chocolate bar), WBC count > 10,500; Gram stain of
cervical discharge with gram-negative intracellular diplococci and >10 WBC/hpf.
55
Minimum criteria for clinical diagnosis of PID: Lower abdominal tenderness, bilateral adnexal
tenderness, cervical motion tenderness
Treatment
1. Ceftriaxone 250 mg IM plus doxycycline 100 mg po q 12 hours X 14 days or cefoxitin 2 gm IM
plus probenecid 1 gm po plus doxycycline 100 mg po q 12 hours X 14 days.
2. Tetracycline 500 mg po qid X 10-14 days may be substituted for doxycycline.
3. Pregnant patients or those with GI intolerance to doxy/tetracycline may use erythromycin 500 mg
po qid X 10 days.
4. Azithromycin 1 gm x 1 day may be substituted for doxy/tetracycline or erythromycin.
5. Strict rest is mandatory during the first 72 hours of therapy. Family members should facilitate
patient compliance.
6. Treat partners after patient provides identity.
7. Due to the significant consequences of PID, it is better to treat the patient at risk that has only
uterine tenderness or lower pelvic discomfort.
Bartholin’s Gland Cyst/Abscess
Introduction: The mucus-secreting Bartholin’s glands drain by way of a 2 cm duct into the vaginal
vestibule immediately outside the hymenal ring at about the 4:00 and 8:00 position. Blockage of the
duct causes secretion accumulation and cyst formation in the gland itself.
Symptoms: Pain with walking, tight clothing or intercourse; mass presents right or left outside of the
vagina.
Signs: Tender, cystic mass in the area of the Bartholin’s duct and gland; warm, red overlying
skin; purulent drainage from duct. A chronic duct obstruction will often be asymptomatic and an
incidental finding on pelvic exam (no treatment required).
Lab: Gram stain may disclose gonococci or clue cells. Culture gonorrhea from exudate.
Treatment
1. Antibiotics (per pelvic inflammatory disease protocol): ceftriaxone 250 mg IM and doxycycline
100 mg po bid x 10-14 days.
2. Incision & drainage
3. Pain control with ibuprofen 800 mg tid (or other NSAID). Occasionally patient will need a mild
narcotic for the first 24-48 hours (Tylenol #3 or Percocet).
ADVANCED
Incision and Drainage of Bartholin’s Gland Abscess
When: When the Bartholin’s cyst becomes an abscess.
What You Need: Sterile prep and drape, local anesthetic agent such as 1% lidocaine (with or without
epinephrine), 5 cc syringe, 18 gauge needle to draw up the lidocaine, 22-26-gauge needle for injection,
scalpel with 15 or 11 blade, Kelly clamp or other instrument to insert into abscess and break up any
loculations or adhesions, Foley catheter (if available), suture with needle (if available).
56
What To Do:
1. Discuss and describe procedure with the patient. Keep her informed as you move along.
2. Give dose of antibiotics as above.
3. Gather materials and set up surgical site
4. Fill 5 cc syringe with lidocaine using 18-gauge needle; replace 18 gauge with smaller gauge
needle for injection.
5. Protect yourself – abscess may spray when opened and decompressed (mask, gloves, gown if
you have one).
6. Place patient in low lithotomy position (patient lies on her back with her buttocks at the end of
the table and her feet supported in stirrups).
If table with stirrups not available then patient may lie on table or bed with feet drawn up to
buttocks and ankles together in midline.
It may help to place a pillow underneath the buttocks.
7. Apply sterile prep and drape
8. Inject anesthesia (3-5 cc of lidocaine should be sufficient) in triangular pattern around
abscess. Wait 5 minutes.
9. Test for numbness by pinching skin lightly with Adson forceps or other sharp object. Inject 2-3
cc more anesthetic if necessary.
10. Identify incision site – inside the vaginal mucosa outside the hymenal ring near the usual duct
opening
11. Make a vertical incision in the vaginal mucosa approximately 1 cm long. It must enter the
abscess cavity. If pus is not draining out you are not there yet. Gradually deepen the incision until
reaching the abscess.
12. Insert Kelly clamp into the abscess to a depth of 2-3 cm if possible, and break up any
loculations or adhesions. Allow the abscess to drain.
13. Evacuate patient to a gynecologist for definitive care. If evacuation not possible, proceed with
the following steps.
14. Cut a 15cm length of Iodoform gauze and loosely pack the cavity with it. This will keep the
incision open and allowing continuous drainage over the next few days. Have the patient return in
24 hours for reassessment.
15. If the abscess recurs, marsupialize the gland. Open the cyst again as in before, then suture the
everted edges of the gland to the vaginal mucosa. This allows for continuous drainage and a
permanent open path
Do not open abscess through normal skin. Enter via the vaginal mucosa.
Do not make too large or deep an incision.
Do not attempt marsupialization of the gland unless evacuation is not available to a trained
gynecologist.
Headache
Introduction: There are virtually hundreds of conditions that can cause headaches. Therefore a
good examination of HEENT, neck, and the nervous system is crucial.
Symptoms: Head pain, which can vary in severity, and be accompanied by virtually any symptoms;
fever, rash, neck stiffness; loss of consciousness or altered mental status.
Migraine: Pounding/throbbing pain, usually but not always unilateral, moderate to severe in
intensity, often with nausea/vomiting, often with light or noise sensitivity; routine activities make it
worse, patient wants to lie down in a quiet, dark room; builds up over minutes to hours and lasts
hours to days; some patients have an “aura”, such as ashing lights; women affected more than men.
57
Tension-type: Global, squeezing headache; less severe than migraine; can last hours to weeks; no
nausea or aversion to light and sound.
Cluster: Less common, but affect young men predominantly; severe, short-lived unilateral headaches,
usually around the eye, lasting at most a few hours; can occur many times in a day and even wake the
patient at night; may want to pace the halls (compare to migraine).
Signs
Possible tachycardia and hypertension; fever in infection or some CNS trauma; neck stiffness in
meningitis; neck tenderness in tension-type headache; abnormal neurological examination (including
mental status examination [MMSE is adequate]; see Appendix) suggests signicant CNS or PNS;
papilledema suggests intracranial swelling; neurological exam may change over time, indicating a
worsening condition.
Lab: WBC for infection.
Treatment
1. Meningitis should be treated as soon as suspected. (See Neurology: Meningitis)
2. First or worst headache needs emergent evacuation (CT, MRI and/or spinal tap may be needed).
3. Treat source of secondary headache, such as sinusitis, if recognized.
4. Treat primary headache symptomatically. Some patients need all three methods.
a. Behavioral/nonpharmacologic: Ensure patients sleep regularly, get aerobic exercise, manage stress
constructively and eat a healthy diet. Avoid caffeine or analgesic withdrawal.
b. Prophylactic medications (oral): Inderal 40 – 160 mg/d, Pamelor 25 – 75 mg q hs, Neurontin 300
mg tid, or Depakote 500 mg bid. Start at a low dose and increase every 2 weeks to effect. Ask
women about pregnancy before prescribing.
c. Abortive or acute therapy:
(1) Pain relief: 2 – 3 adult aspirin tablets, or 1000 mg Tylenol, or 800 mg Motrin with food, or 500 mg
Naprosyn with food works for most headaches. Caffeine in coffee or cola sometimes helps. Midrin (2
initially, then 1 q 1 h to max of 5 in 12 h) is a combination medication with acetaminophen. Fiorinal
and Fioricet (1-2 po q 6 h prn) each have caffeine and a mild barbiturate as well as aspirin or Tylenol
respectively. IM Toradol 60 mg is an option for nausea. The “Triptans”, such as sumatriptan
(Imitrex) 50 – 100mg po, 20 mg in a nasal spray, or 6 mg in a sq auto-injector or rizatriptan (Maxalt)
5 –10mg po are the most effective migraine medications, but nothing works
for everyone. Narcotics are rarely needed. Beware that overuse of analgesic medications can produce
rebound headaches.
(2) Nausea or vomiting: Reglan 10 mg po q 8 h prn or Compazine 5-10 mg IM q 3-4 hrs, max 40 mg/
day.
58
Cancer Screening
As recommended by the American Cancer Society, if you’re a woman over age 20, you should have a
Pap smear taken every year or two; after three normal tests, have a Pap smear every 3 years from then
on.
Practice breast self-examination monthly.
Any suspicious change should be checked out with a doctor.
Mammography is a yearly screening procedure recommended for women after age 40 (with high risk)
or age 50. After age 50, tests for colorectal cancer (digital rectal exam and occult blood test) are
advisable on an annual basis. In addition, sigmoidoscopy every 5 years or colonoscopy every 10 years
is recommended. Your skin should be examined annually for any suspicious moles or other lesions.
Breast Self-Examination
Most women will have lumps in their breasts at some time during their lives. Regular self-examination
of your breasts improves your chances of avoiding serious consequences. Self-examination should be
done monthly, just after the menstrual period, when the breasts have fewer hormone-related lumps.
Self- examination is an absolute necessity for a woman with naturally lumpy breasts. If there is a new
lump or change in an existing lump, seek immediate medical care.
To do a self-exam, examine your breasts in the mirror, first with your arms at your sides and then with
both arms over your head. The breasts should look the same. Watch for any change in shape or size, or
for dimpling of the skin. Occasionally a lump that is difficult to feel will be quite obvious just by
looking.
Next, while lying flat, examine the left breast using the inner fingertips of the right hand and pressing
the breast tissue against chest wall. Don't pinch the tissue. Your left arm should be behind your head
when you examine the inner half of the left breast and down by your side when you examine the outer
half. Don't neglect the part of the breast underneath the nipple, plus the part that extends away from the
breast toward the underarm. A small pillow under the left shoulder may help. Repeat this process on the
opposite side. Many doctors recommend repeating the self-examination in the shower, where smooth,
slightly soapy skin can make lumps easier to detect.
59
Breast self-examination is a supplement to other screening techniques for breast cancer. Mammography
is strongly recommended yearly after age 50, or after age
40 for women with a history of breast cancer in their family. An annual examination by a health care
worker is also of benefit. These guidelines are based upon current technology. It is very likely that the
diagnostic value of these and newer tests will continue to improve, while the associated cost, risk, and
discomfort will diminish.
INFORMATION ON DISEASES, SYMPTOMS AND CONDITIONS
Vaginal Discharge and/or Itching
Normal vaginal secretions are thin, clear, and painless.
Abnormal vaginal discharge is common, however, and could have many causes.
Bacteria, common viruses, and other microbes can infect the vagina and cause discharge.
Laboratory tests allowing microscopic evaluation of vaginal fluid are required for a correct diagnosis. A
variety of effective drugs are available for treating vaginal infections.
Bacterial vaginosis is the most common cause of vaginal symptoms among women of childbearing age.
The primary symptom is an abnormal vaginal discharge with a fishy odor.
Trichomoniasis is a very common vaginal infection caused by a single-celled protozoan parasite.
Symptoms in women include a heavy, yellow-greenish vaginal discharge, discomfort during
intercourse, and painful urination.
A woman and her partner both need to be treated to eliminate this infection.
Vulvovaginal candidiasis, sometimes referred to as candidal vaginitis, monilial infection, or vaginal
yeast infection, is a common cause of vaginal itching, burning and irritation.
Candidiasis is caused by an overabundance or overgrowth of yeast cells (primarily Candida albicans)
that normally colonize in the vagina.
Associated with symptomatic candidiasis in women, including pregnancy, diabetes mellitus, and the
use of oral contraceptives or antibiotics.
60
The discharge is typically described as cottage-cheese-like in nature, although it may vary from watery
to thick in consistency.
Non-infectious irritation or allergic symptoms can be caused by spermicides, vaginal hygiene
products, detergents, and fabric softeners.
Tampon Reactions
Symptoms of toxic shock syndrome can be hard to recognize because they mimic the flu.
Sudden high fever, vomiting, diarrhea, dizziness, fainting, or a rash that looks like sunburn during your
menstrual period or a few days after.
Bleeding Between Menstrual Periods
The interval between two menstrual periods is usually free of bleeding or spotting.
Women using an intrauterine birth control device are particularly likely to have occasional spotting.
Taking birth control pills may also cause spotting between periods. Such spotting is probably not a
cause for concern.
Bleeding along with abdominal pain may be a sign of a pregnancy developing outside the uterus
(ectopic pregnancy), which requires immediate surgery. It may also be a sign of a uterine miscarriage.
However, some women may have some bleeding throughout a normal pregnancy.
Difficult Menstrual Periods
Adverse mood changes with fluid retention and bloating are very common in the days just prior to a
menstrual period. Such problems are difficult to treat and are a result of normal hormonal variations
during the menstrual cycle. Salt tends to hold fluid in tissues. If you can reduce the salt in your diet
and increase your water intake (to “wash” out the salt), you may have less swelling and less fluid
retention. For menstrual cramps use ibuprofen or naproxen. Most products designed for menstrual
cramps now have ibuprofen as the main ingredient.
Menopause
During menopause, the ovarian production of female hormones decreases. Most women can tell if they
are approaching menopause because their menstrual periods start changing. Menstrual periods usually
become lighter and irregular, then stop altogether. Some menopausal symptoms mentioned below can
start long before menstrual periods become irregular. Some women report the symptoms as early as
their mid-30s.
Hot flashes, sudden feelings of intense heat lasting two or three minutes, are an annoying symptom of
menopause. They can happen anytime during the day but are most common in the evening or at night.
For most women, hot flashes gradually decrease over about two years and eventually disappear
altogether. Staying cool is the key to treating hot flashes.
Sleep is often affected by menopause, whether it is interrupted by hot flashes or there is difficulty
falling asleep.
Many women also have mood swings during menopause. Irritability may be triggered by sleep
deprivation.
Vaginal dryness and frequent urinary tract infections may occur after menopause. Urine
leakage may become a problem as muscle support for the bladder and urethra weakens. vaginal creams
help with vaginal dryness.
62
After menopause, a few women are aggravated to find they have trouble remembering things or
concentrating. These symptoms may be caused by changes in estrogen levels. Not getting enough sleep
or having sleep disrupted may also contribute to memory and concentration problems.
Hormone replacement therapy (HRT) has been prescribed for menopause- related changes and to
reduce the risk of osteoporosis that may develop in the years following menopause because of estrogen
depletion. HRT also has some risks..
There are at least two major health conditions that can develop in the years after menopause because
of the decrease in hormone production that occurs: coronary artery disease and osteoporosis.
Osteoporosis
A number of research projects involving experimental preventive measures have been reported in the
current medical literature. Some of this research may prove to be helpful in reducing the risk of
osteoporosis, or perhaps preventing it altogether: (1) in women, administering estrogen before bone
loss becomes severe to prevent the progress of the disease; (2) exercising to prevent bone loss; (3)
taking calcium supplements and vitamin D, with magnesium, in order to limit excessive bone loss; and
(4) for both men and women, giving up smoking and alcohol.
Regular exercise and adequate dietary calcium are important to prevent osteoporosis. Physical activity
will help keep bones strong. Menopausal women should take in about 1500 mg of calcium per day,
about as much as in a quart of skim milk, with 400 IU of vitamin D. You can use a calcium supplement
if you cannot get enough from dairy products.
Management of Recurrent Urinary Tract Infection
The best-known symptoms of bladder infection are pain or burning on urination, frequent and urgent
urination, and blood in the urine. Bladder infection is far more common in women than it is in men.
The female urethra, the tube leading from the bladder to the outside of the body, is only about one-half
inch long in women, a short distance that makes it easy for bacteria to travel upward to reach the
bladder. Most bacteria that cause bladder infections come from the rectal area, and sometimes bladder
infection is related to sexual activity.
Breast Problems: Mastitis
Mastitis is inflammation of the breast most commonly presenting as a cellulitis of the subcutaneous
tissues in a lactating breast (1-3% of breastfeeding women).
The causative organisms, S. Aureus, E. Coli and streptococcus (rarely), are easily treated with
antibiotics.
One of the risk factors for mastitis is plugging or obstruction of one of the milk ducts which drain to
the nipple.
Obstruction can be secondary to delayed infant feedings, which can lead to engorgement, and tight
clothing (poorly fitting brassieres and underwires that dig in).
Other risk factors include cracked nipples, maternal stress and fatigue. Do not let mastitis interrupt
breastfeeding.
The infected breast will worsen if the baby does not empty it, and the infection cannot be
transmitted to the infant through the milk.
63
Untreated or delayed and inappropriate treatment can lead to breast abscesses and stop lactation in the
affected breast, which deprives the infant of its food source.
Symptoms: Localized pain, redness, swelling, warmth in one breast; fever; chills; body aches;
fatigue; headache; occasionally nausea and vomiting.
Signs
Fever - often greater than 101°F
Pink, wedge-shaped area on the breast.
Patient appears in mild to moderate distress.
Palpation: Tender, occasionally indurated, warm area.
There SHOULD NOT be a palpable, fluctuant mass - that is a sign of abscess.
Differential Diagnosis:
Plugged Duct - Tender lump in the breast of a mother who is otherwise well. Caused by partial
obstruction of a duct. Infection is not present but MAY RESULT if the duct remains blocked. See
end of this section for treatment.
Breast Engorgement - Gradual onset in the immediate postpartum period (peak on days 2-4) of
bilateral breast swelling and warmth. Pain is generalized. Fever may occur but is rarely over
101°F. The breasts feel better after they are emptied. Caused by inadequate emptying of the breasts.
Breast Abscess - Painful, fluctuant mass. 10-15% of women who delay treatment of mastitis will
develop a breast abscess. Should be suspected if a patient on antibiotics for mastitis does not improve
after 72 hours of antibiotic therapy.
Breast Cancer - Very rare. Unilateral, unchanging lump or mass that persists despite treatment for
engorgement. Plugged duct or persistent mastitis must be evaluated by appropriate radiological and
surgical approaches, if possible.
Treatment for Mastitis
Primary:
1. Ensure infant nurses on both breasts, starting on the unaffected side. Even after feeding the
affected breast may need to be more thoroughly emptied by manual expression or pumping.
2. Put mother on bedrest. Maternal fatigue and stress are risk factors for recurrent mastitis. The
baby should be right next to the mother either in the same bed or readily available in a nearby crib to
facilitate frequent emptying of the breast.
3. Ensure mother completes full course of therapy:
a. Dicloxacillin or cephalexin 500 mg po q 6 hrs x 10 days
b. Patients allergic to penicillin: clindamycin 300 mg po q 6 hours x 10 days or erythromycin 500 mg
po q 6 hours x 10 days
c. If patient does not improve after 48 hours of rest and therapy, switch to Augmentin (amoxicillin/
clavulanate) bid if 875/125 mg or tid if 500/125 mg.
4. Apply ice packs or warm packs to the breast (whichever the mother prefers). Hot packs provide
drainage and pain relief.
5. Ensure mother drinks plenty of fluids.
6. Give ibuprofen or acetaminophen for pain relief.
7. Advise mother to wear a support bra or other supportive clothing that does not cause painful
pressure on the breast.
64
Alternate: Patients who are intolerant of oral medications may need IV therapy. You may use
nafcillin or oxacillin 2.0 gm q 4 hrs IV or cefazolin 1.0 gm IV q 8 hours. Penicillin allergic patients
can be given clindamycin 300 mg IV q 6 hrs.
Primitive: If antibiotics are not available, initiate rest, hydration and MOST IMPORTANTLY,
drainage (nursing) of the affected breast. Mastitis will recur in at least 50% of women not treated
with antibiotics, and the breast abscess rate will be high.
If the patient remains febrile after 72 hours:
1. If possible, transfer the patient immediately. If not, then see below.
2. If non-compliant, administer ceftriaxone 1 gm IM. See if the patient would also take one gram of
oral
azithromycin. Follow-up in 24 hrs and repeat the ceftriaxone.
3. If compliant add clindamycin IV as above.
4. Find an experienced person in the community who can stay with the patient and assist with
breastfeeding and manual expression.
Treatment for Plugged Duct: Massage the area, gently pressing toward the nipple. Warm
compresses help. The most important intervention is frequent feeding on the affected side.
Consecutive feedings should be started on the affected side to facilitate flow from the obstruction.
Because different lobes of the breast are drained better with different nursing positions, place the infant
with its chin pointing toward the blocked duct.
If the mother is separated from her infant for any reason the breast should be emptied by handexpression or by using an effective breast pump. Be sure to follow the mother closely as mastitis can
occur. NOTE: Plugged ducts will last only for short periods of time (a few days). Any lump that
persists for many days must be evaluated for malignancy.
Treatment for Engorgement: Frequent breastfeeding is the most effective treatment. If the nipples
are engorged it may be difficult for the baby to latch on. Relieve nipple engorgement by applying
warm compresses before the feeding, gently express some milk to soften the breast, or lean the breasts
into a
large bowl of warm water (or take a warm shower) just before the feeding to facilitate milk release and
soften the nipples. After the feeding, apply cold compresses, or cool cabbage leaves to the breast for
20 minutes leaving the nipple exposed. Use standard doses of acetaminophen and/or ibuprofen for
pain relief. Support the breasts with a good-fitting brassiere. Do not bind the breasts as this will
increase the engorgement.
Breast Abscess Incision and Drainage Procedure
When: A breast abscess is causing systemic symptoms that are unresponsive to less invasive therapy.
The abscess will be a fluctuant breast mass related to non-resolving or worsening mastitis (see Mastitis
section). The condition is rare, except when antibiotic treatment has been delayed or discontinued too
early. Needle aspiration of a recurrent abscess should be attempted twice before incision and drainage
is required.
What You Need: Sterile prep and drape, 18 and 24-26 gauge needles, 5 cc and 10cc syringes, alcohol
prep pads, local anesthetic agent such as 1% lidocaine with epinephrine, 2x2 and 4x4 dressings,
scalpel with #15 blade (but any blade will work), sterile irrigation if available, gloves, and a small
Penrose drain
What To Do:
Needle Aspiration: Anesthetize skin and subcutaneous tissues over fluctuant area using 5cc syringe
and
24-26 gauge needle. Insert 18 gauge needle attached to 10cc syringe into the abscess, aspirating as
you advance the needle. Drain as much pus as possible once the cavity is entered. Then remove
needle and cover puncture site with a small dressing.
65
Incision and Drainage of Abscess: Anesthetize the skin and subcutaneous tissues over the fluctuant
mass. If possible, choose your incision point close to but not in the areola (allow room for an infant
to nurse without contacting the incision). Make the incision parallel to the edge of the areola and
over the fluctuant area. Try not to make transverse incisions- they leave an unacceptable scar.
Circumareolar incisions will heal with a
better cosmetic result. Keep the incision small, only large enough to allow entrance of your 5th
digit. Do
not cut deeply into the breast tissue, but start superficially and advance carefully. Make your incision
deeper until the cavity is just reached and pus begins to drain. Insert your 5th digit into the wound
to break up any loculations and to ensure complete drainage. Irrigate the wound, and if possible place
a Penrose drain, pack with 2x2 dressings and cover with 4x4 dressings.
Follow-up care: Remain at bedrest, continue warm soaks and hydrate well. Continue antibiotic
therapy with Augmentin (amoxicillin/clavulanate) po bid if 875/125 mg or tid if 500/125 mg for 10
days after resolution of the abscess. Engorgement of the breast will interfere with healing. Feed
infant or empty the affected breast on a regular basis, every 2-2 1⁄2 hours. The milk is clean as long
as the abscess drains to the outside (through the skin). Nursing can continue when the abscess is
surgically drained as long as the incision and drainage tube are far enough from the areola. If the
drain is too near the areola for the infant to nurse, the breast still must be emptied by manual
expression or pumping. Milk may drain from the incision during breastfeeding. Apply pressure over
the incision while breastfeeding to minimize leakage. If the patient cannot do this herself, her spouse
or another person may hold light pressure over the incision.
What Not To Do:
Do not make incision any deeper than necessary.
Do not make the incision too close to the areola to avoid compromising breastfeeding.
Do not allow the skin to close over the incision until the abscess has healed from the inside out to the
surface.
67
CHAPTER 16
Male Genital Problems
Genital Inflammation
Balanitis: Inflammation of the glans penis and foreskin occurs primarily in the uncircumcised male
but is rare in the circumcised male. The glans will look wet, red and may have multiple small red
bumps and a whitish material on the surface consistent with yeast.
The shaft of the penis just under the skin and on the surface of the erectile bodies contains numerous
large veins that can develop clots. They will appear as dark, hard, raised bumps that follow the course
of the vein.
Lymph channels can also become hard cords, but will be more clear or lack color. These conditions
probably result from overly vigorous intercourse.
Fournier’s Gangrene: This condition is life threatening and is most likely to occur in the severely
injured patient with poor circulation or diabetes. It presents as a rapidly spreading skin inflammation
with development of necrotic/purplish tissue.
Candidal Infection: Most cases will present as balanitis. Occasionally, the patient will present
with a red scrotum with satellite red lesions. The rash will be itchy, painful and tender.
Cellulitis: Patients will have diffusely red and painful scrotal or penile skin. The skin may be
weeping, thickened and have pustules.
When the skin lacks pustules, it is important to determine if the skin changes are a reaction to
underlying inflammation such as epididymo-orchitis or torsion of the testis.
In the latter cases, the testis and epididymis are markedly tender. The patient can usually differentiate
testis pain from skin pain.
Contact Dermatitis: Contact with chemicals and even some ointment may cause a profound
inflammation of the scrotal skin. The skin may have the appearance and tenderness of cellulitis.
History of exposure is extremely important.
Signs: Swelling, tenderness and redness; purulent discharge in the case of severe phimosis;
swollen lymph nodes.
Lab: Urinalysis for presence of glucose, leukocytes, blood or nitrite; KOH prep of the weepy
material on the skin may show the presence of yeast elements such as budding yeast or strands called
hyphae.
Differential Diagnosis
Sexually transmitted disease lesions are usually much more focal than these inflammatory conditions.
Treatment
Phimosis: Keep the penis clean with soap and water several times per day. Broad-spectrum
antibiotics such as ciprofloxin 500 mg po bid or Keflex 500 mg po qid x 1 week may be used if
purulent discharge is noted from the meatus. If the phimosis is symptomatic and severe, perform a
dorsal slit (procedure below) and refer for circumcision later.
Paraphimosis: Try to reduce the foreskin by pushing the glans in and pulling the edematous skin
forward.
Balanitis: Wash the penis several times a day and apply antifungal cream such as Nystatin, Mycolog
or Lotrimin bid. If a wet prep shows no yeast elements, can give Flagyl 500 mg po bid x 1 week.
Thrombosis of Penile Vein and Sclerosing Lymphangitis: Refrain from any sexual activity. Use
NSAIDs such as ibuprofen.
68
Fournier’s Gangrene: Perform emergent aggressive surgical debridement. Broad-spectrum IV
antibiotics such as ampicillin 2 gm q 8 h, gentamicin 5 mg/kg qd and Flagyl 500 mg q 6 h are usually
warranted.
Candidal Fungal Infection: Keep skin dry and antifungal medications such as Nystatin, Mycolog or
Lotrimin bid for 1 week or single dose fluconazole 150 mg po. See ID: Candidiasis section for more
information.
Cellulitis: Treat with dicloxacillin 500 mg po q 6 h or Keflex 500 mg po q 6 h for mild cases. For
severe cases, treat with oxacillin 2 gm IV q 4 h or vancomycin 1 gm IV q 12 h.
Contact Dermatitis: For mild, treat with topical 1% hydrocortisone and oral diphenhydramine
(Benadryl). In severe cases, add prednisone 50 mg po qd and wean by 10 mg /day over 5 days. If there
is a question of infection, treat for cellulitis also.
Alternative: Yeast infections can be treated with alkaline washes to the glans penis, if no oral agent is
available. Dissolving a few sodium bicarbonate tablets in a small container of water can make an
alkaline solution, which can be directly applied to the skin.
General: If the patient has balanitis, phimosis or paraphimosis and has not been circumcised, he
should have it done electively.
Dorsal Slit Procedure
Essential: If the patient has severe phimosis where the foreskin has scarred down to a small hole and
the patient is having significant pain and discharge from the penis, the foreskin needs to be incised
(dorsal slit). Similarly, if paraphimosis is severe, excessive circumferential swelling may compromise
blood flow in the penis, which can be relieved with a dorsal slit.
ADVANCED
1. Attempt non-surgical reduction with anti-inflammatory medications, ice water and lubricants.
Evacuate patient to a trained provider for this procedure if possible. If there are signs of systemic
infection (fever, nausea, fatigue, etc.), and prompt evacuation is not available, perform a dorsal slit.
2. Assemble equipment: 1% lidocaine (w/o Epi), needle and syringe, clamp, forceps, scalpel or
surgical scissors, needle driver, 4-0 suture, prep solution, alcohol.
3. Prep the penis as with any surgical procedure (sterile scrub, Betadine, drape), and attempt to clean
between the head and the foreskin, especially on the dorsal side.
4. Use 1% lidocaine and a small needle (25-26 gauge) infiltrate the skin about mid-shaft and extend
the wheal at least halfway around the shaft of the penis.
5. Confirm the top of the penis (dorsal side) is numb with forceps or needle.
6. Use a straight clamp to crush the skin from the phimotic area back to the glans (head). Make sure
the jaw stays between the glans and the foreskin. Do NOT pass the jaw into the meatus. The glans
will still have sensation and the patient should be able to tell you if the meatus is being cannulated.
7. Leave the clamp on for 5 minutes to compromise blood flow in the area to be incised.
8. Remove the clamp and use a scissors to cut the crushed skin where the clamp had been. Do not
incise the glans.
9. This should expose the glans. Control bleeding with figure 8 stitches using 4-0 non-absorbable
sutures.
10. Clean the penis with sterile prep solution between the head and foreskin, then wipe prep solution
away with alcohol. Allow to air dry and apply a sterile dressing leaving the meatus clear.
11. Monitor the patient, as this maneuver is only temporary and the slit can contract. He should have
elective circumcision later.
69
Testis/Scrotal Mass
Testis masses are alarming to the patient since they may represent cancer. Testis cancer is quite
curable in its early stages. However, the cancer can grow rapidly so early detection and referral is
necessary to avoid treatment delays.
Symptoms: Testicular pain, enlarged scrotum or testis. Increased risk of benign tumors with history
of trauma and
vasectomy.
Signs
Tender testis; palpable mass in testis, spermatic cord or epididymis; mass may appear
smooth and spherical, be located on the surface or deep in the testis, enlarge with standing,
transilluminate with a bright flashlight.
Lab: Urinalysis: Nitrite and leukoesterase positive urine suggest infection.
Differential Diagnosis
Solid, non-transilluminating mass that is >4 millimeter size, located below the testicular surface and
inseparable from the testis must be considered to be cancer until proven otherwise.
Transilluminating smooth spherical masses are benign and are hydrocele (around the testis),
spermatocele or loculated hydrocele (above the testis).
Rarely it can be a cyst adenoma. Small 1-4 mm size nodules on the surface of the testis are benign.
“Wormy” mass above the left testis that gets smaller when patient shifts from the standing to the
supine position are varicoceles. Right-sided varicoceles need elective referrals.
Other masses in the scrotum, either on the cord, in the scrotal skin or in the midline area near the
penis are almost always benign.
Painful area behind the testis is usually an indication of epididymitis (see Epididymitis section).
If the pain in the scrotum is severe, refer to sections on epididymitis and torsion.
Treatment
Give 2-week course of NSAIDs (e.g., Naprosyn 375 mg po bid or ibuprofen 800 mg po tid with
food). If epididymitis is suspected or cannot be eliminated, add doxycycline 100 mg po bid x 14
days. Elevate scrotum with comfortable athletic supporter and decrease activity.
Avoid sun exposure if on doxycycline.
Prostatitis
Introduction: Prostatitis is used liberally to describe voiding problems and pain associated with the
prostate.
Symptoms: Obstructive symptoms include slow start, low flow and dribbling; irritative symptoms
include frequency (> q 2 hours) and/or urgency; pain in the head of the penis or under the scrotum;
low back pain; fever.
Signs: Tender prostate with/without tender pelvic floor or coccyx (palpate 360° on rectal exam);
distended bladder
Lab: Urinalysis: heme and leukoesterase positive urine (infection).
70
Differential Diagnosis
Irritative voiding symptoms with or without fever - urinary tract infection until proven otherwise, distal
ureteral stone, urethral stricture, bladder neck dysfunction, bladder or prostate cancer, foreign body in
bladder, overflow incontinence.
Obstructive voiding - enlarged prostate, urethral stricture, and neurologic disease of the spine or
peripheral nerves.
Painful prostate - urinary tract infection, bladder neck dysfunction/prostatodynia/pelvic floor
dysfunction, musculoskeletal pain, coccydynia, seminal vesiculitis
Treatment: Infection
1. If the patient is lethargic and febrile, begin high dose IV ampicillin 1-2 gm IV q 6-8h and
gentamicin 5 mg/ kg IV qd. If penicillin allergic, use IV fluoroquinolones (Levaquin 250 mg IV q day
or Cipro 400 mg IV bid) or vancomycin 1 gm IV bid and gentamicin 5 mg per kg IV qd. Hydrate
aggressively. When the patient is afebrile, switch to oral fluoroquinolone (see UTI section) for a total
of 30 days.
2. If the patient is alert and manifesting either low-grade fever or no fever, treat with
fluoroquinolones (see UTI section).
3. Treat any male suspected of having an infection for 30 days regardless of the location of
symptoms (kidney, prostate or scrotum). Infected urine can easily reflux into prostatic ducts, therefore
assume the prostate is infected.
4. If symptoms persist and urinalysis continues to be abnormal without improvement after 3-5 days,
suspect bacterial resistance and change antibiotics.
5. If a bladder is palpated, attempt to pass a Foley catheter. Inability to pass catheter suggests a
stricture. If patient’s symptoms worsen, consider suprapubic aspiration .
6. If the entire pelvic floor is tender, pain is not from prostate alone. Treat for musculoskeletal pain
with NSAIDs.
Alternative Antibiotics:
Septra DS po tid until fever resolves, followed by Septra DS po bid x 30 days, Augmentin 500 mg po
bid x 30 days, or Keflex 500 mg po qid x 30 days.
Doxycycline or Vibramycin are not as effective since they are bacterio-static, and should only be used
(100 mg po bid) if there is no other alternative.
Nitrofurantoin has minimal tissue penetration and should not be used in prostatitis.
Treatment: No Infection
Primary:
1. Treat initially with a course of antibiotics, with or without alpha-blockers.
Levaquin 500 mg po qd has broad coverage for both C. trachomatis and urinary pathogens. Treat for
30 days.
Alpha blockers include the following:
Hytrin (terazosin) 1-5 mg po q hs (start at low dose and titrate up over several weeks) Cardura
(doxazosin) 1-4 mg po q hs (start at low dose and titrate up over several weeks) Flomax (tamsulosin) 1
po q d (No titration necessary) Minipress 1-5 mg PO q hs
71
2. Patients who complain of frequency should be given bladder antispasmodics with caution since they
can cause urinary retention. Hyoscyamine 1 po bid prn, Ditropan 5 mg po TID prn, Elavil 10-25 mg po
qd, or Flavoxate 1 po bid can all be used.
72
Testis Torsion
Introduction: Rapid identification and treatment of torsion is necessary to preserve testis function.
Such patients require tacking or fixation of the opposite testis to the scrotal skin since it is also at risk.
Loss of both testes not only results in sterility but loss of testosterone, which requires lifelong
supplementation for normal body function. Salvage of the affected testis can be achieved if reduced in
4 hours.
Symptoms
Acute (< 2 hr): Severe scrotal pain, onset can be at night while asleep, may have prior history of
scrotal pain lasting less than 1 day, may have nausea/vomiting, testis is extremely painful, spermatic
cord may be tender
Sub-acute (2-48 hr): Scrotal pain increases over several hours. After 24 hours, some of the pain may
start to subside Chronic (>48 hr): History of acute onset of pain. Testis pain is improved but not gone.
Signs : Extreme, diffuse tenderness of the entire testis; edema; vomiting.
Lab: Urinalysis: Strongly heme or leukoesterase positive sample suggests kidney stone or infection.
Differential Diagnosis
Orchitis - fatigue, muscle aches, sore throat or other flu-like symptoms with gradual onset and normal
spermatic cord. Mumps orchitis is extremely rare with modern vaccinations.
Severe epididymo-orchitis - voiding symptoms with leukoesterase and nitrite positive urine. Testis
tumor - considered when there is a mass with mild to moderate pain
73
Torsion of the appendix testis/epididymis - point tenderness on the superior portion of the
testis/epididymis with the remaining testis being non-tender.
Ruptured testis - history of trauma
Spermatic cord torsion - tender testis with a non-palpable vas deferens.
Kidney stone - especially if lodged just below the kidney will present with scrotal pain, but a nontender, normal scrotal exam. Severe flank pain
Incarcerated hernia - most of the discomfort will be above the testis. A hydrocele may be present,
making it difficult to examine the testis. If omentum is in the hernia, there may not be any bowel
symptoms.
Treatment
Manual detorsion, with or without injection of the spermatic cord with local anesthesia. Torsion
may be 180-720° (2 full twists).
Attempt to detorse the testis first by rotating the testis outward (like opening a book). If the pain
worsens or does not improve, rotate the other direction. The torsion may be 2 full twists. If the testis
hangs lower but pain persists, continue untwisting the cord.
If lidocaine is available, inject into the cord using a long needle or spinal needle in the
spermatic cord.
TECHNIQUE
This can be accomplished by straddling the cord on the affected side between two fingers just as the
cord crosses over the pubic bone lateral and superior to the penis. Make multiple passes through the
cord and down to the pubic bone injecting a total of 10 cc of 1% lidocaine local anesthetic. This
should numb the testis. This may relieve the pain, causing the cremasteric muscles to relax and may
result in spontaneous de-torsion. If the pain is gone, check the testis for descent to the normal
position and if the testis has become less tense. Also try to palpate the vas deferens posteriorly. This
tube is about the consistency and size of uncooked spaghetti and is located behind and is easily
separable from the bulk of the spermatic cord. If the tube is in its normal location, spermatic cord
torsion is unlikely. You can use the vas deferens as a guide to untwist the cord. The vas deferens
should lie posteriorly to the cord. Palpate the vas high in the scrotum and try to follow it down.
If unable to detorse the testis, treat with narcotics and empirically with antibiotics (Cipro 500 mg po
bid or Keflex 500 mg po qid or Septra DS 1 po bid) until pain has resolved. Most pain from a dead
testis will improve after 48 hours. Increasing pain would suggest the presence of infection or testis
tumor or rupture of testis (suspect if there is a history of blunt trauma).
Epididymitis
Introduction: It can become painful from either mechanical or infectious irritation.
Symptoms: Pain in the scrotum behind the testis with tenderness of the epididymis, and without pain
In the testis.
Signs
Marked swelling of the hemi-scrotum, urethral discharge, frequent and urgent urination,
fever. Use penlight or otoscope to transilluminate the scrotum to differentiate swelling due to a mass
vs. fluid (bright, diffuse glow; seen with spermatocele or hydrocele).
74
Lab: Urinalysis: nitrite and leukoesterase positive urine (infection). Do urine culture if available and
dipstick is positive. Gram stain urethral discharge to screen for gonorrhea and chlamydia.
Differential Diagnosis
Pain and tenderness in other areas of the scrotum, such as the cord or groin, of equal or greater
severity would suggest other causes of the pain such as hernia, varicocele, musculoskeletal pain or
entrapped nerve.
An abnormal testis on physical exam may suggest tumor, appendix testis, viral orchitis, testis trauma
or testis torsion. Recurrent symptoms lasting less than 1 day are much more suggestive of intermittent
testicular torsion.
Treatment :
1. Scrotal support/elevation, bedrest.
2. NSAIDs such as ibuprofen 800 mg po tid with food.
3. If the urine is nitrite and leukoesterase positive, treat with antibiotics. a. If a fever is present and
there is no urethral discharge, give:
Levaquin 500 mg po bid x 10 days or Septra DS 1 po bid x 30 days.
In severe cases ampicillin 1 gm IV q6h plus gentamicin (loading dose of 1.5 mg/kg followed by 1 mg/
kg IV q8h) or Rocephin 5 mg/kg IV qd (ceftriaxone 500 mg to 1gm IV bid) should be given until
fever resolves, then convert to oral antibiotics (above).
If there is a urethral discharge and no fever, give ceftriaxone 250 mg IM (or Cipro 500 mg po or
Floxin 400 mg po) single dose to treat gonorrhea, and follow with 7-10 days of doxycycline 100 mg
po bid (or Floxin 400 mg po qd or Levaquin 500 mg po qd).
If both fever and urethral discharge are present, treat for disseminated gonorrhea: ceftriaxone 1 gm IV
qd (or spectinomycin 2 gm IV q 12 hours) until symptoms improve, followed by Cipro 500 mg po
bid (or Levaquin 500 mg po qd) for 7 more days.
If neither fever nor discharge are present, empirically treat for chlamydia: doxycycline 100 mg po bid
for 7-10 days (or Floxin 400 mg po qd for 7-10 days or Levaquin 500 mg po qd for 775
CHAPTER 17
Bacterial Infections
Anthrax
Introduction: Anthrax is an acute bacterial (spore-forming Bacillus anthracis) infection transmitted
through broken skin or mucous membranes, inhalation, or ingestion (rare). Fatally infects herbivores
(sheep, cattle, horses, pigs, goats, water buffalo, elephants, zebras or antelopes) that shed the bacilli
into the environment. Spores remain viable in contaminated soil for years. Dried skins, hides, wool,
bone or bone products can transmit infection. Veterinarians, farmers, tannery, wool workers are
occupationally exposed. There are three forms of disease, dictated by entry site; 95% of cases are
cutaneous. Less common gastrointestinal and pulmonary anthrax infections are generally fatal within
days.
Symptoms
Cutaneous anthrax: Acute (< 1 week): Local pruritus, papule with vesicles Sub-acute (1-2 weeks):
Ulcer that dries to a black painless eschar, brawny edema, regional adenopathy Chronic (> 2 weeks):
Without treatment, 80% resolve over 6 weeks.
Pulmonary anthrax (acute symptoms only): Fever; URI-like cough and chest discomfort; 36-48 hours
after infection may observe stridor; respiratory distress; shock and death.
Gastrointestinal anthrax (acute symptoms only): Neck swelling, fever, painful swallowing, nausea,
vomiting, severe abdominal pain, gastrointestinal hemorrhage and death.
Objective:
Cutaneous anthrax: Acute(< 1 week): Papule with vesicles forms an ulcer Sub acute (1-2 weeks):
Non-tender ulcer with black eschar, edema (can persist) Chronic (>2 weeks): Eschar loosens and
separates
Pulmonary anthrax: Rapid respiratory rate; neck and chest edema
Gastrointestinal anthrax: Acute(< 1 week): Edema of oropharyngeal tissues Sub acute (1-2 weeks):
Oropharyngeal/tonsillar ulcers; may see bloody ascites Auscultation: Pulmonary anthrax: Rhonchi or
rales; hypotension Palpation: Cutaneous anthrax: Acute(< 1 week): Regional adenopathy
Pulmonary anthrax: Neck and chest edema
Gastrointestinal anthrax: Tender abdomen
Pulmonary: Percussion: localized dullness
Lab: Boxcar-shaped, gram-positive rods on Gram stain of skin lesion fluid, or blood/sputum (late in
course) (see Color Plates Picture 13).
Differential Diagnosis:
Cutaneous anthrax:
Staphylococcal boil - does not ulcerate or turn blackish; usually pus-filled and painful.
Scrub typhus - “tache noire” lesion is blackish; usually patient is febrile, often with a generalized
petechial rash.
Spider bite - brown recluse spider bite turns blackish with necrotic changes; usually painful lesion.
Cutaneous plague and tularemia - usually more vivid, painful skin lesions.
Pulmonary anthrax:
Influenza - initial symptoms are similar, but no hemorrhagic mediastinitis or death within 24 hours of
onset. Mediastinitis - usually seen post-operatively (thoracic surgery), with histoplasmosis or after
esophageal perforation.
76
Gastrointestinal anthrax:
Severe gastroenteritis - early similar symptoms, but no progression to hematemesis, bloody stools,
occasionally bloody ascites, shock and frequent death in 2-5 days.
Treatment: Even if left untreated, 80% of cutaneous anthrax remains localized. However, 20% of
skin cases and all other forms of anthrax may die from untreated infection.
Primary:
Cutaneous: Penicillin V 30 mg/kg in four doses/day x 5-7 days and Cipro 750 mg bid for 60 days
Pulmonary: Ciprofloxacin IV 400 mg q12hours x 7-10 days Gastrointestinal: Ciprofloxacin 750 mg
po bid x 60 days Alternative:
Cutaneous: Levofloxacin 500 mg po q d x 60 days
Pulmonary/Gastrointestinal: Doxycycline 100 mg q12hour or penicillin G 4 MU q4hours IV for 710 days
Empiric (presumed exposure):
Pulmonary: Ciprofloxacin 500 mg po bid for 6 weeks, and vaccination
DO NOT NECROPSY any animal showing this sign. The chronic form is characterized by
localized, subcutaneous, edematous swelling of the ventral neck, thorax and shoulders. In horses the
disease is acute, with signs of fever, chills, colic, anorexia, and swelling of the animal’s ventrum, with
death in 2-3 days. Swine may die acutely without showing signs, or having a rapid swelling of the
throat.
Bartonellosis (Cat Scratch Disease, Trench Fever, Oroya Fever)
Introduction: There are several Bartonella bacterial species that cause different illnesses.
Bartonella bacil- liformis causes Oroya fever, a febrile anemia and chronic skin eruption (verruga
peruana) in a limited area of mountain communities in Peru, Ecuador and Colombia. It is thought to
be transmitted by the bite of a sand fly.
Bartonella quintana, transmitted by body lice, causes trench fever, a febrile illness that which can recur
years later.
Bartonella henselae is inoculated by cat scratch or bite and causes lymphadenitis and variable fever 310 days after cat exposure.
Symptoms
S. American Bartonella (Oroya fever): Fever, which can persist up to 6 weeks; pallor; weakness;
chills; muscle/joint aches. After 2-20 weeks, crops of painless, red, 2-4 mm skin lesions can be seen,
mainly on head and extremities.
Trench fever: Headache; fever (episodic fever of 3-5 days duration - can have fever relapses up to 10
years later); back/leg ache; shin pain; transient rash (maculopapular).
Cat scratch disease: Papule at inoculation site; regional adenopathy that can suppurate; nodes
subside in 2-5 months without treatment.
Signs
Oroya fever: Fever (up to 105°F) begins early and may persist for weeks, skin pallor and slight
jaundice. After several weeks, crops of persistent, 2-4 mm, red to purple skin nodules appear on the
exposed parts of the body.
Trench fever: Fever (up to 105°F) lasting 4-5 days, recurs in paroxysms for 3-6 weeks. In the
immunocompromised, crops of crusted red-purple papules appear.
77
Cat scratch disease: Variable fever >101°F is accompanied by crusted papule or pustule at
inoculation site. Later: tender, fluctuant, regional adenopathy develops, which may last about 3
months
Lab: The Oroya fever organism can be seen on a peripheral blood smear inside red blood cells.
Differential Diagnosis:
Kaposi’s sarcoma (KS) - trench fever skin lesions (immunocompromised patients) and Verruga
peruana may resemble disseminated KS, a malignancy seen in immunocompromised hosts with HIV
and in elderly men who live in the Mediterranean area.
Chronic febrile illnesses of the tropics, including Salmonella, malaria, tuberculosis, or brucellosis,
may co-exist with Oroya fever or mimic it. Oroya fever is differentiated by severe anemia and the
presence of bacteria in the red blood cells on blood smear.
The suppurative adenopathy associated with a skin lesion of cat scratch can mimic cutaneous plague,
tularemia, toxoplasmosis, and sporotrichosis infection. Exposure to cat injury helps differentiate.
Treatment Primary:
Oroya fever: Chloramphenicol 2-4 g/d po in divided doses x 7 days
Verruga Peruana: Rifampin 10 mg/kg/day po x 14-21 days Salmonella is a frequent life-threatening
secondary infection, and is often suggested by splenomegaly. Infection during pregnancy can result in
fetal death or abortion.
Trench fever: Aspirin prn, doxycycline 100 mg po qd x 15 days
Cat scratch disease: Azithromycin 500 mg po day 1, then 250 mg po qd x 4 days; analgesics
Brucellosis
A bacterial infection acquired by ingesting raw milk, unpasteurized cheese or by direct contact with
secretions or birth products of infected animals (cattle, goats, buffalo, camels, reindeer, caribou, yaks,
coyotes, deer or swine). Average incubation period is 2 weeks, but can take up to several months.
Symptoms
Acute (1-7days): PM fever > 100°F; profuse, malodorous sweating; flu-like symptoms and a peculiar
taste in mouth
Sub-acute (1-2 weeks): Fever, weight loss, arthralgias and myalgias
Chronic (weeks to months): Recurrent undulant fever if not treated, arthralgias or arthritis,
constipation, depression and back pain. Focused History: Exposure– Have you had any raw
milk or cheese? Have you come in contact with cattle, goats, buffalo, camels, reindeer,
caribou, yaks, coyotes, deer or swine? Fever– Do you have a fever? (up to 104°F).
Signs
Inspection: Temperatures to 104°F
Palpation: Acute (1-7 days): Generalized adenopathy Sub-acute (1-2 weeks): Hepatomegaly
(>50%), splenomegaly (30%)
Differential Diagnosis: Enteric fever, nonpulmonary tuberculosis, or non-falciparum malaria (with
chronic relapses of fever), may have similar symptoms.
Treatment
Primary: Doxycycline 100mg po bid x 6 weeks with gentamicin 5mg/kg q 24 hours IV x 14 days
(danger of renal insufficiency)
78
Alternate: Doxycycline 100 mg po bid and rifampin 900 mg qd, but twice as high relapse rate
Ehrlichiosis: Ehrlichiosis is a tick-borne bacterial illness.
Symptoms Headache, fever, rash, myalgias.
Signs Temperature over 101°F; rash in 30% (most commonly involving the trunk; not
associated with site of tick bite).
Differential Diagnosis: Many infections present similarly, but fever and headache (especially in a
patient with exposure to ticks) should prompt the consideration of ehrlichiosis. Rocky Mountain
Spotted Fever and meningitis have substantial clinical overlap.
NOTE: Serology testing of blood is available at many hospitals.
Treatment: Doxycycline 100 mg bid for x 7-10 days. Treatment often results in rapid clinical
improvement
Plague: a highly fatal illness, is usually transmitted by a bite from a rodent flea or by contact with
infected wild rodents (rats, squirrels, chipmunks, prairie dogs), rabbits, or domestic cats. The current
plague vaccine does not protect against pneumonic plague, which can spread by droplet inhalation.
The incubation period is 1-7 days. This rare disease has foci in the western USA, South
America, Asia and Africa. The bubonic form (90-95% of cases) has a very rapid onset associated with
a toxic state characterized by enlarged and very tender lymph nodes (buboes). The other forms of
plague, pneumonic (progression of 5% of bubonic cases) and septicemic (5-10% of cases) are rapidly
toxic and nearly always fatal if untreated.
Symptoms
Constitutional: Acute (< 2 hr): Sudden onset fever, chills, headache, myalgias, lethargy
Specific:
Sub-acute (24-48 hr): Cough, if pneumonic form; buboes* (85% cases), diarrhea (septicemic plague),
abdominal pain Chronic (>48 hr): Bloody, frothy sputum; buboes suppurate *Tender, swollen lymph
nodes with red, edematous overlying skin, often in inguinal and axillary regions.
Signs
Inspection:
Acute (< 48 hrs): Fever to 104°F; a skin lesion at site of flea bite (25%); lethargy; tachycardia
110-140; hypotension; toxic appearance; Pneumonic: respiratory distress, tachypnea
Chronic (>2 weeks): Can see meningeal signs: Plague meningitis is particularly associated with
axillary buboes. Auscultation: Sub-acute (up to one week): Rales if pneumonic
Palpation: Acute (< 48 hrs): Buboes Sub-acute (up to one week): Buboes may start to recede, also
could suppurate.
Lab: Gram's stain of bubo needle aspirate (usually need to inject and withdraw some saline to get
sample) or sputum may show gram-negative coccobacillus with a bipolar (safety pin) staining
appearance. In severely septicemic patients this may even be seen with a Gram's stain of blood.
CXR: Can be normal but rapidly progress to diffuse pneumonitis (increased markings throughout
lung fields).
79
Differential Diagnosis: Tularemia, enteric fever, rickettsial infection, acute lymphadenitis, dengue,
typhus and Hantavirus.
Treatment
Primary: Gentamicin 2 mg/kg load then 1.7 mg/kg q 8 hours IV (adjust lower if kidney dysfunction
as noted on urinalysis)
Alternative: Doxycycline 200 mg first day then 100 mg bid x 10-14 days
NOTE: If meningitis develops, use ciprofloxacin 750 mg po bid or chloramphenicol 50 mg/kg/day
x10-14 days.
Rat Bite Fever: Caused by infection with Streptobacillus moniliformis or Spirillum minor, rat-bite
fever is transmitted by the bite of a rodent and has worldwide distribution.
Symptoms Fever, chills, headache, myalgias, arthralgias and rash [incubation period is 3-10 days[
Signs: The rash can be maculopapular, morbilliform or petechial, and erupts over the palms,
soles and extremities.
Lab: Culture of blood, joint fluid or pus may demonstrate organism.
Differential Diagnosis: Other potential causes of fever/rash are varied, and include measles,
meningococcemia, Rocky Mountain Spotted Fever and secondary syphilis.
Treatment:
For moderately to severely ill patients, use procaine penicillin G 600,000 units IM or IV penicillin
every 12 hours.
For mildly ill patients, amoxicillin 500 mg po tid x 14 days is probably adequate.
For penicillin-allergic patients, tetracycline 500 mg po every 6 hours or doxycycline 100 mg po every
12 hours may be given.
Acute Rheumatic Fever: (ARF) typically occurs approximately 19 days after untreated
streptococcal pharyngitis in 1-3% persons.
Symptoms: Fever; migratory polyarthralgias in knees, ankles, elbows or wrists; rash which can wax
and wane over months; subcutaneous nodules and chorea.
Signs
Inspection:
Fever to 102°F (up to 21 days); rapid respiratory rate (if carditis); E. marginatum rash (irregularly
edged, transient, lacy, macular rash [pink rimmed with internal blanching] found on the trunk and
extremities) which waxes and wanes for months; chorea (short, abrupt, non-purposeful movements,
which often disappear during sleep and grimacing).
Palpation:
Migratory large joint inflammation (arthritis); 10% have subcutaneous nodules on extensor elbows and
forearms which last up to 4 weeks. Auscultation: In carditis: bibasilar rales, aortic insufficiency or
mitral regurgitation murmurs, pericardial friction rub, S3 gallop.
In carditis, CXR may show cardiomegaly. EKG may have prolonged PR interval.
80
Diagnosis
Based on clinical observation and application of the Jones criteria for diagnosis: 2 major criteria,
OR
1 major and 2 minor criteria AND evidence for prior streptococcal infections (prior scarlet fever, +
throat culture)
Major Criteria: Carditis, polyarthritis, subcutaneous nodules, and chorea, E. marginatum rash
Minor Criteria: Fever, arthralgias prior rheumatic fever, heart block seen on EKG
Differential Diagnosis
Polyarthritis is often the main presenting symptom. The differential diagnosis should include:
Gonococcal arthritis - sexual exposure; dysuria; urethral discharge; characteristic gun metal blue skin
lesion Subacute bacterial endocarditis - diagnose with blood cultures (if available); usually few joints
involved; may see embolic skin lesions
Lyme disease - fever less frequent; fewer joints involved; history of tick bite
Reiter’s syndrome - fever is unusual; prior history of sexually transmitted disease or acute diarrheal
illness; characteristic skin lesions (painless, superficial erosions) in genital area/soles of feet
Carditis:
Viral myocarditis - unlikely to see joint symptoms or the E. marginatum rash
Pericarditis - may see diffuse ST segment elevations
Treatment
Primary:
Benzathine penicillin 1.2 MU IM (600,000 U in children) or oral penicillin 250 mg po qid x 10 days
Salicylates: 4-8 grams aspirin per day x 3-4 weeks
Alternative: Erythromycin x 10 days or azithromycin x 5 days can be used in patients allergic to
penicillin. Other NSAIDs may be used in place of aspirin
Streptococcal Infections
Streptococcal Pharyngitis and Scarlet fever:
Introduction: Streptococci are gram positive bacteria. Some species are pathogenic in humans,
responsible for illnesses ranging in severity from mild upper respiratory infections to life-threatening
necrotizing fasciitis. Fulminant necrotizing fasciitis due to group A streptococcus may begin at a site of
trivial trauma (for example a paper cut, abrasion on a cinder block), with rapid progression over 2472 hours and 20-70% mortality even with ICU care. This is a deep-seated, fast moving infection that
destroys fascia, fat, muscle and other tissue but may spare the skin. It often involves the extremities.
Streptococcal infection of muscle (myositis) often is from blood infection, not associated with trauma.
It may involve a single muscle group and be associated with compartment syndrome
Symptoms
Initial flu-like symptoms with fever to 104°F, extreme pain and erythema at infection site.
Signs
Inspection:
Acute (< 24 hr): Ill-appearing, fever as high as 105oF, SBP <110, increased heart rate,
abrupt onset red/swollen affected area, confusion/mental status changes common.
81
red/swollen area spreads locally, color turns to blue/purple with bullae, may see gangrene by day 4-5.
Lab: Gram stain of fluid or tissue (blood, throat, wound and debrided tissue) for gram-positive cocci
in chains (see Color Plates Picture 26). CXR to assess for early ARDS development.
Chronic (>7 days): Earlier signs continue, clear demarcation at site of involvement
Palpation:
Acute (< 24 hr): Tenderness >inflammatory change, area warm to touch; may see capillary leak
syndrome with generalized edema (the “Michelin man” look), in myositis find changes c/w
compartment syndrome of affected area.
Sub-acute/Chronic: Continuation of earlier signs, other physical findings related to multi-organ system
failure in severe cases
Differential Diagnosis:
Necrotizing fasciitis - due to Clostridia; crepitus on physical exam or gas on X-ray.
Cellulitis or lymphangitis - deep streptococcal infection is much more painful and purpuric.
Treatment
1. Immediately for surgical and intensive care support.
2. If medical help is delayed or not possible, give antibiotics. IV Penicillin 24 MU/day (4 MU q 4
hrs) and Clindamycin 900 mg q 8 hrs for 10-14 days. Clindamycin decreases streptococcal toxin
production. Intravenous immunoglobulin (IVIG) 150 mg/kg/day for 5 days given early may decrease
mortality.
3. Aggressively debride deep-seated infection. External findings are often the “tip of the iceberg”
regarding tissue involvement. (see Procedure: Wound Debridement)
4. Oxygen, IV fluids (LR or NS) and other treatment as in ARDS section. Consider adding
ceftriaxone or ciprofloxacin.
Tetanus
Introduction: Clostridium tetani bacteria are introduced into the body through contaminated open
wounds, burns, frostbite, needles, or unclean cutting/dressing of the umbilical cord. The tetanus toxin
(tetanospasmin) causes acute central nervous system intoxication. Case fatality rate is 10-90%. The
incubation period is 3-30 days There are four subtypes described for tetanus: generalized, localized,
cephalic and neonatal.
Symptoms
Neonatal cases: Weakness, irritability, trouble nursing, unable to suck
Specific: Acute (1-7days): Pain at wound site, local muscle spasticity Sub-acute (7-14 days):
Trismus (lockjaw), painful tetanic spasm, glottic or respiratory muscle spasm, urinary retention,
constipation, rigid abdominal wall muscles, trouble swallowing
Chronic (>2 weeks): Slow recovery phase (4 weeks)
Signs
Inspection: Acute (1-7 days): Afebrile; localized muscle spasticity, localized pain at inoculation site,
neonatal cases: unable to nurse, with stiff muscles or spasming Sub-acute (7-14 days): Afebrile, tetanic
spasm (stimulus induced) trismus (lockjaw), opisthotonos (arched back spasm), glottic/respiratory
muscle spasm, cyanosis/asphyxia, profuse sweating
Palpation: Sub-acute (7-14 days): Abdominal muscle wall rigidity
Percussion: Acute (1-7 days): Brisk local deep tendon reflexes
82
Differential Diagnosis
Meningoencephalitis - usually associated with fever; true seizures and mental status changes not seen
in tetanus.
Strychnine poisoning - mimics tetanus; abdominal wall muscle rigidity more often seen in tetanus;
ask about an ingestion history
Hypocalcemic tetany - involves extremities; rare to see lockjaw; tapping on facial nerve (over parotid)
can induce facial muscle spasm in low calcium states (Chvostek’s sign)
Generalized seizures - associated with loss of consciousness, no trismus
Phenothiazine toxicity - drug history; can see torticollis (not in tetanus); relieved with Benadryl (not
in tetanus)
Treatment
1. Maintain airway (ET tube can stimulate spasm so may need early tracheostomy for respiratory
difficulty)
2. Medications:
a. Tetanus (human) immune globulin (HTIG, Hyper-tet) 500 IU intramuscularly or injected directly
into wound
b. Tetanus immunization 0.5 ml IM at site away from HTIG administration.
d. Diazepam titrated for effect 5-10 mg q 2-4 hours to control muscle spasms (lorazepam or midazolam
are also effective)
e. Metronidazole 30 mg/kg/day divided in q 6 hour dosing for 7-10 days (average about 500 mg q 6 hrs
IV); can also be given 1 gm per rectum q 8 hrs
3. Nursing: Keep patient in a quiet, darkened room; avoid unnecessary touching; use Foley catheter
for urinary retention.
Alternate Antibiotics: Penicillin G 4 million units IV q 6 hrs for 10 days or doxycycline 100 mg q 12
hrs IV
Tularemia
Introduction: Francisella tularensis is a small gram-negative bacillus that can enter the body by
ingestion (eating undercooked meat, drinking contaminated water), inoculation (bites, skinning/
trapping animals), inhalation or contamination. This organism can penetrate unbroken skin.
It is common in rabbits, opossums, beavers, water rats, raccoons, muskrats and feral cats. It is
transmitted by ticks, and less commonly by deer flies.
Symptoms
Constitutional: Acute (< 2 hr): Fever 101-104°F, chills, malaise, anorexia, fatigue Sub-acute (2-48
hr):
Fever Chronic (>48 hr): Fever, if untreated, can last up to 30 days; chronic debilitation for months.
Specific: Acute (< 2 hr): Tender adenopathy; oculoglandular: tearing, photophobia; pharyngeal:
severe sore throat; typhoidal: dry cough; pneumonic: Dry cough Sub-acute (2-48 hr): All: rash
(35%); ulcer (skin); typhoidal: abdominal pain, diarrhea; pneumonic: pleurisy, rare hemoptysis;
Chronic (>48 hr): Suppuration of lymph nodes
Signs
Inspection: Acute (< 2 hr): Fever to 104°F; relative bradycardia. Ulceroglandular form: papule;
pharyngeal form: exudative pharyngitis; oculoglandular form: purulent conjunctivitis, eyelid edema
Sub-acute (2-48 hr): sometimes develops membrane or oral ulcer; rash (35%): acneiform, E.
Nodosum, E. multiforme, urticaria, Diffuse maculopapular Chronic (>48 hr): Ulcer (skin)
84
Auscultation: Sub-acute (2-48 hr): Pneumonic form: rales
Palpation: Acute (< 2 hr): Swollen localized lymphadenopathy Sub acute (2-48 hr): Fluctuant
regional lymph nodes, typhoidal form: hepatosplenomegaly
Percussion: Acute (< 2 hr); Sub acute (2-48 hr) Typhoidal form: Enlarged liver and spleen;
pneumonic form: Signs of consolidation (dullness to percussion), egophony.
Differential Diagnosis:
Meningococcal infection - rapidly progressive; petechial to purpuric rash; often with meningeal signs;
no tick or animal exposure
Rickettsial infection - febrile illness with rash after tick bite; not likely to have suppurative
lymphadenopathy or skin ulcers
Cat scratch disease - can be confused with ulceroglandular tularemia, history of cat scratch and lack of
risk factors for tularemia
Sporotrichosis - history of thorn/cactus/plant related injury to body; lymphangitis seen commonly with
sporotrichosis while it is less common with oculoglandular tularemia
Syphilis - sexual contact; genital ulcer, which is painless; patient often afebrile
Lymphogranuloma venereum - sexually transmitted infection; can cause regional and generalized
adenopathy with genital ulcer; less likely to have ulcer elsewhere on body
Other less likely possibilities are cutaneous tuberculosis, plague and anthrax.
Treatment
Gentamicin 5 mg/kg/day divided q 8 hrs IV or IM for 7-10 days. Due to risk of renal toxicity, ensure
adequate hydration and urine output. If in doubt, use alternate drug.
Alternative: Tetracycline 500 mg q 6 hrs until fever breaks, then 250 mg qid for 5-7 days (higher
relapse than gentamicin)
Typhoid Fever: caused by Salmonella typhi. The incubation period is 1-3 weeks after exposure.
Symptoms
Acute (3-7days): Fever, flu-like symptoms, chills, weakness, anorexia, myalgias, Sore throat, nonproductive cough, constipation, diarrhea (5-10%), abdominal discomfort
Chronic (>3 weeks): If fever> 4 weeks, consider metastatic focus. Abdominal pain, abdominal
perforation, lower GI bleed
Signs
Acute (3-7 days) Inspection: Stepladder temperatures to 104°F (usually in afternoon/night), relative
bradycardia in 25%; moderately ill appearing; rose spots (2-3 mm pink to red papules on
chest/abdomen that fade with pressure) in fair skinned persons, furry tongue; (thick white to brown
coating that spares edges)
Palpation: Abdominal distension; mild, diffuse abdominal tenderness.
Sub-acute (1-3 weeks): Palpation: splenomegaly (50%), Percussion: liver can be slightly enlarged 2-3
cm below costal margin.
Lab: Urine culture is positive after one week, blood culture may be positive for first 2 weeks, and stool
culture is positive for weeks 3-5. Other clues from stool include fecal leukocytes (may suggest an
invasive gastroenteritis). Blood smear may demonstrate low white blood count and anemia.
85
Differential Diagnosis
Nontyphoidal Salmonella - infections are generally milder, without rose spots.
Tuberculosis - generally chronic, lower grade fever; night sweats; cough; hemoptysis; abnormal CXR.
Hepatitis - more often see jaundice, dark urine, gastrointestinal symptoms, malaise and fatigue
Leptospirosis - remarkable conjunctival injection; has similar fever pattern; history of exposure to
contaminated fresh water
Malaria - nocturnal fever pattern typical; thick and thin blood smears will help detect the malaria
parasite
Amebic liver abscess - may see more tenderness in hepatic region
Brucellosis - chronic febrile illness with relative bradycardia, splenomegaly; animal exposure,
occupation may help differentiate
Treatment: Antibiotics prolong Salmonella excretion in the stool and should not be given unless
patient is febrile.
Ceftriaxone 1 gm q 12 hrs IV or IM x 14 days (recent study suggests that a 5 day course may be as
effective), azithromycin 1 gm load on day 1 then 500 mg po days 2-6
86
CHAPTER 18
Mycobacterial Infections
Tuberculosis
Mycobacterium tuberculosis, M. Bovis and others cause tuberculosis (TB), a chronic pulmonary
infection that is seen worldwide.
Infection is spread by airborne particles.
Clinical disease (TB) develops in only about 10% of those infected. Others have latent tuberculosis
infection (LTBI), since they do not have evidence of active disease.
Symptoms: Chronic productive cough (bloody), chest pain, fever, chills, night sweats, anorexia,
weight loss, fatigue.
Signs
Vital Signs: Normal to low-grade fever, weight loss
Percussion: Unilateral, localized dullness over the upper lung fields
Auscultation: Decreased breath sounds or rales corresponding to percussed dullness (upper lung
fields)
CXR: consolidation or cavitary lesion in upper lung fields; purified protein derivative (PPD) skin
testing to document tuberculosis infection.
NOTE: PPD may be negative in persons with active infections.
Differential Diagnosis
Chronic cough - chronic bronchitis or COPD not associated with progressive weight loss or night
sweats
Lung cancer - usually seen in patient with smoking history
Fungal pneumonias (histoplasmosis, blastomycosis, paracoccidioidomycosis) - chronic pulmonary
symptoms are rare and usually seen in smokers in endemic areas.
Treatment
Primary: Base the selection of antimycobacterial drugs on knowledge of local resistance patterns.
Usually, 3-4 drugs are initiated. The most common regimen is isoniazid (INH), rifampin (RIF),
pyrazinamide (PZA), and either ethambutol (EMB) or streptomycin (SM). In cases of sensitive
tuberculosis, these drugs are given for 8 weeks, followed by a 6-month course of INH and RIF only.
Medicines may be given 2, 3 or 7 times each week. Use directly observed therapy (DOT) to assure
compliance. Treat PPD positive contacts without active disease (LTBI) with isoniazid, 300 mg/day
for 9-12 months. Children under 5 years of age who are contacts of an active pulmonary case should
receive isoniazid, 10-20 mg/kg (300 mg maximum) even if initial PPD is negative. If the PPD
remains negative on retesting after three months, INH may be stopped.
Alternative: Alternate regimens are usually based on results of susceptibility testing.
NOTE: Multidrug resistant tuberculosis (MDR-TB) is defined as any M. tuberculosis that is resistant
to both INH and RIF.
87
PPD skin testing is done as follows:
1. Placement of PPD: inject 5 IU (0.1 mL) intradermally into flexor surface of LEFT forearm (so you
will remember where to look for reaction).
2. Interpretation of PPD reaction:
a. Measure diameter (in mm) of INDURATION or swelling (not redness) of reaction, when viewed in
cross-section at 48-72 hours.
b. >5mm is positive in HIV patients, and in close or household contacts of a patient with an active TB
infection.
c. >10mm is positive for those personnel exposed to people at high-risk for having TB. This standard
applies to medical personnel and team members.
d. >15mm is positive for personnel with no risk factors for exposure. This standard applies to most
Americans.
Nontuberculous mycobacterial (NTM)
Nontuberculous mycobacterial (NTM) or mycobacteria other than tuberculosis (MOTT) infectious
diseases include lymphadenitis caused by Mycobacterium avium complex (MAC) and M.
scrofulaceum; skin and soft tissue infection secondary to M. fortuitum, M. abscessus, M. marinum,
and M. ulcerans; and pulmonary disease, most commonly secondary to MAC or M. kansasii.
Lymphadenitis in children age 1-5 years is most commonly caused by M. avium complex.
Pulmonary syndromes are usually chronic, often occurring in persons with other underlying
pulmonary disease.
Symptoms
Lymphadenitis (painless enlargement of the lymph nodes of the neck), usually unilaterally; skin and
soft tissue infections - edema, erythema; pulmonary infection - chronic, productive cough with fever
and weight loss; accompanied by malaise, night sweats and hemoptysis.
Signs
Lymphadenitis: Enlarged, unilateral nodes of the neck (usually anterior cervical chain) that may
spontaneously form sinus tracts and drain. No overlying erythema. Individual nodes are difficult to
identify.
Normal vitals.
“Swimming pool or fish tank granuloma” caused by M. marinum starts as a papule (usually on
extremity) that slowly enlarges and ulcerates. These lesions are associated with water or fish exposure.
Introduction of the organism is likely via an abrasion or puncture.
Pulmonary disease: Presents similar to tuberculosis (see ID: TB). Perform PPD testing to rule out
tuberculosis.
CXR may reveal thin-walled cavities and more pleural thickening than tuberculosis.
Differential Diagnosis
Lymphadenitis - cat scratch disease (kitten exposure, pain), lymphoma, tuberculous lymphadenitis (also
called scrofula; positive PPD or TB exposure)
Skin and soft tissue infection - nocardiosis (no water exposure), sporotrichosis (exposure to soil,
organic gardening materials), leishmaniasis (endemic area, sandfly exposure)
Pulmonary disease - TB; see Respiratory: Pneumonia, COPD
88
Treatment
Primary: Lymphadenitis (due to MAC or M. scrofulaceum) - excisional surgery without antimicrobial
drugs.
Cutaneous lesions (due to M. marinum) - doxycycline 100 mg bid or trimethoprim/sulfamethoxazole,
160/800 mg bid for 3 months. Excisional therapy is also an option.
NOTES: Disseminated M. avium complex (DMAC) is another NTM disease that is virtually restricted
to persons with late stage AIDS. This infection presents as a chronic febrile wasting syndrome with
associated anemia and MAC bacteremia.
89
CHAPTER 19
Fungal Infections
Candidiasis (Thrush)
Candida albicans is a yeast normally found in the mouth, intestines, and vagina.
Overgrowth of this yeast can cause skin or mucosal diseases including oropharyngeal candidiasis
(thrush), intertrigo (disease limited to moist skin folds), esophagitis, and vaginitis (see GYN section).
In adults, disease commonly occurs in diabetics, the immunocompromised, and after antibiotic
treatment for other disorders.
Inhaled and oral corticosteroid preparations also increase risk. Disseminated, life-threatening infection
can also occur in severely immunocompromised persons.
Symptoms
Oral thrush: Usually asymptomatic; may cause mouth discomfort or difficulty swallowing.
Esophageal thrush: Painful or difficult swallowing.
Intertrigo: Local burning-like pain, often with pruritus.
Vaginal thrush: Itching, dyspareunia (pain with intercourse) and change in the odor or consistency of
vaginal discharge.
Signs
Inspection:
Oral/esophageal: white plaques, which are scraped to reveal an erythematous base and are seen on any
oral mucosal surface except the tongue.
Cutaneous (intertrigo or vulvar): erythematous, shiny rash with small “satellite” lesions at its
periphery.
Candidal vaginitis is associated with a curd-like vaginal discharge Candidal vaginitis).
Lab: Potassium hydroxide (KOH) wet mount of scrapings or discharge reveals typical yeast, usually
with pseudohyphae and/or hyphae.
Differential Diagnosis
Oropharyngeal candidiasis - particulate debris secondary to poor oral hygiene (debris is usually easily
removed)
Esophageal candidiasis - esophagitis due to herpes simplex, cytomegalovirus, aphthous ulcers, and
toxins
Candidal vaginitis - trichomoniasis, bacterial vaginosis (can be differentiated with wet mount)
Treatment
Oropharyngeal candidiasis - nystatin solution, 400,000-600,000 units qid po as a swish and
swallow x 7 - 14 days. Esophageal candidiasis - fluconazole, 200 mg/day po or IV x 14 days.
Intertrigo - nystatin powder or clotrimazole or miconazole cream twice daily until resolved.
Candidal vaginitis – see GYN Problems section.
Alternative:
Oropharyngeal candidiasis - clotrimazole troches (lozenges), 10 mg 5/day, oral fluconazole,
50-200 mg/day, itraconazole, 100-200 mg/day, or ketoconazole, 200 mg/day. Esophageal candidiasis itraconazole 100-200 mg/day, or intravenous amphotericin B, 0.3-0.5 mg/kg/day, in refractory cases.
90
NOTE: Oral candidiasis (thrush) in a young adult should always raise the suspicion of
immunocompromise, especially undiagnosed HIV infection.
Blastomycosis
(North American Blastomycosis, Gilchrist Disease)
Blastomyces dermatitidis is a yeast-like fungus that causes a spectrum of disease including
asymptomatic infection, acute and chronic pulmonary infection and disseminated infection of the skin,
bone, GU tract, and rarely, the CNS.
This infection is seen most often in central and southeast US in areas near rivers or streams.
Approximately 1/2 of exposed persons will develop symptomatic disease. The incubation period is 3045 days. Most individuals seeking care for this infection have progressive pulmonary disease or
cutaneous lesions.
Symptoms
Acute pulmonary infection: fever, cough, and pleuritic chest pain
Chronic pulmonary disease : presents with similar symptoms over a longer course.
Skin lesions are typically painless or slightly tender. )
Signs
Pulmonary infection: associated with diffuse auscultatory findings and fever. Chronic pulmonary
disease can also include hemoptysis, weight loss, and skin lesions.
Skin lesions are most often located on the face, scalp, neck, and extremities. These begin as red papules
or nodules that enlarge and then ulcerate or become verrucous. Associated adenopathy is uncommon.
Lab: Large (8-15 mm), thick-walled, broad-based, budding yeast cells may be visible on Gram stain
of sputum or lesion.
Differential Diagnosis
Acute pulmonary infection - influenza, bacterial pneumonia
Chronic pulmonary infection - tuberculosis, lung cancer, other fungal pneumonias
Skin lesions - squamous cell carcinoma, mycosis fungoides
Treatment
IV amphotericin B is required in life-threatening infections, all central nervous system infections,
infections in immunocompromised patients and in pregnant patients. Itraconazole can be used in all
other infections at a dose of 200-400 mg/day po, usually for 6-12 months.
Alternative: Ketoconazole 400-800 mg/ day or fluconazole 400-800 mg/ po day
Coccidioidomycosis (Valley Fever, Desert Rheumatism)
Coccidioides immitis is a dimorphic fungus that causes disease ranging from self-limited pulmonary
infection to chronic meningitis. Incubation period is 7-21 days. More than 60% of all infections are
asymptomatic.
Most symptomatic infections take the form of acute pulmonary disease. Untreated, acute infection
resolves in 95% of patients. About 1% of those infected develop chronic pulmonary disease or
disseminated infection to the meninges, skin, bone, or soft tissue.
91
It occurs in the southwest deserts of the US and northern Mexico, and a few pockets of in Central and
South America. It has frequently been reported in service members training at Fort Irwin, California.
Symptoms
Cough (usually dry), fever, pleuritic chest pain, malaise, headache, anorexia, myalgia and often rash;
severe disease may present with a sepsis-like syndrome.
Large joint pain may occur after asymptomatic infection (desert rheumatism).
Meningitis presents with chronic headache, memory loss, lethargy, or confusion.
Signs
Vital signs: Fever and tachypnea
Inspection: Various rashes: Diffuse, faint erythematous rash lasting less than one week; or erythema
multiforme (painless, diffuse rash consisting of rings and disks); or erythema nodosum (painful red
nodules usually occurring on the shins).
Auscultation: Diffuse ausculatory findings (abnormal breath sounds).
Ophthalmoscope: Patients with meningitis may have papilledema on funduscopy.
Lab: Eosinophils may be seen on blood smear. Gram stain or KOH of sputum for spherules (10-80
µm round structures with 2-5 µm round endospores inside)
Differential Diagnosis
Acute pulmonary disease - influenza, “atypical” pneumonia, histoplasmosis, blastomycosis
Meningitis - tuberculosis, syphilis, cryptococcosis (see respective topics); and CNS tumors (see
Neurology: Seizure Disorders and Epilepsy)
Treatment
Primary: Amphotericin B 0.5-1 mg/kg IV daily should be used in acute life-threatening infection.
This can be followed with fluconazole 400-800 mg/day to complete 3-6 months of therapy. Meningeal
infection is treated with fluconazole, 400-800 mg daily for life. All other forms of coccidioidomycosis
are treated with long-term fluconazole.
Alternative: Itraconazole (400-600 mg/day) may be used in non-meningeal infections. Some
authorities add intrathecal amphotericin B in the initial therapy of meningeal disease.
Histoplasmosis (Darling’s Disease)
Histoplasma capsulatum is a dimorphic fungus that can cause disease ranging from asymptom- atic
pulmonary infection to life-threatening disseminated infection.
Acute infection occurs 3-21 days after exposure. Most infection is asymptomatic or self-limiting
pulmonary disease. Severity is dependent on patient’s immunity and intensity of exposure.
Chronic pulmonary disease, mediastinitis and disseminated disease are rare.
Found worldwide, this infection is most common in the central US (Mississippi and Ohio River
basins).
Risk Factors: Outbreaks may occur with the removal of debris containing contaminated bird or bat
droppings.
92
Symptoms
Acute (days): Malaise, fever, chills, anorexia, myalgias, cough, pleuritic chest pain.
Chronic (months): cough
Signs
Inspection: Fever, weight loss; hypotension and shock in immunocompromised patient (sepsis)
Auscultation: coarse breath sounds, pleural friction rub
Palpation: hepatomegaly and/or splenomegaly may be seen in disseminated infection
CXR: Hilar or mediastinal lymphadenopathy with or without patchy infiltrates.
Treatment
Primary: Itraconazole 200 mg daily for 6-12 weeks, can be given in those cases that do not
spontaneously improve/resolve.
For severe infection, including acute or chronic pulmonary disease, disseminated disease or meningitis,
give amphotericin B 0.7-1 mg/kg IV daily. This therapy can be changed to intraconazole 200 mg once
or twice daily, for 6-24 months when clinically stable or continued for 3-4 months (35 mg/kg total
amphotericin B).
Alternative: Ketoconazole 200-800 mg/day can be used as an alternative to itraconazole.
NOTES: Lung granulomas, and hilar and splenic calcifications are commonly seen on CXR of
persons who have had acute pulmonary histoplasmosis in the past. Outside the endemic area
however, lung granulomas and hilar calcifications more commonly represent inactive tuberculosis.
Paracoccidioidomycosis
(South American Blastomycosis)
Paracoccidioides brasiliensis is a dimorphic fungus that typically causes chronic, progressive,
pulmonary disease in rural male workers.
Incubation may be prolonged up to 15 years.
Symptoms: Chronic, productive cough, +/- bloody sputum; shortness of breath; weight loss; painful
mouth or nose ulcers; hoarseness.
Signs
Vital signs: Normal
Inspection: Ulcerative lesions of the face, mouth, larynx, or pharynx
Auscultation: Rales or decreased breath sounds in the middle or lower lung fields
Treatment
Primary: Itraconazole 100-400 mg/day x 3-6 months.
Alternative: Sulfadiazine 4 gm/day for weeks to months, based on clinical response, then 2 gm/day
for 3-5 years. Other sulfa-based antibiotics can be used. Amphotericin B can be used in life-threatening
and unresponsive infections. Ketoconazole 200-400 mg/day and fluconazole 600 mg/day have also
been used.
NOTE: Paracoccidioidomycosis has a less common juvenile form which causes acute, progressive,
disseminated infection similar to acute disseminated histoplasmosis seen with AIDS and in younger
individuals.
93
CHAPTER 20
INFECTIOUS DISEASES REVIEW
Since the epidemiology and treatment recommendations change over time, as new antibiotics are
developed and resistance to older ones evolves, more current information is available at the Centers for
Disease Control and Prevention website at: http://www.cdc.gov/.
SEXUALLY TRANSMITTED DISEASES
Over 30 microorganisms can be sexually transmitted with many having similar symptoms. Despite
this complexity, initial management (with subsequent referral) can be accomplished in many settings
with a minimum of resources. The following clinical syndromes associated with sexually transmitted
diseases will be discussed in this section:
f Urethral discharge (urethritis)
f Painful testicle (epididymitis)
L Genital ulcer
L Genital warts
f Lymphogranuloma venereum (LGV)
m Pruritis (itching)
M Vaginal discharge
ˆ Lower abdominal pain
In evaluating patients at risk for STDs, remember that many of these diseases can be asymptomatic and
the patient may not suspect he/she has infection. However, asymptomatic patients can also transmit
disease to others.
Urethral Discharge (Urethritis)
Urethritis is characterized by a discharge from the urethra and burning with urination.
It is usually caused by one of two bacteria: Neisseria gonorrhoeae (which causes gonorrhea) and
Chlamydia trachomatis (which causes chlamydia), both of which infect and irritate the urethra.
The usual incubation period for gonorrhea is 3-5 days and the discharge is yellow or green.
The incubation period for chlamydia is longer, 1-5 weeks (usually 10-16 days), and the discharge is
less profuse, less purulent (often white or watery) and less painful.
About 20% of men with gonorrhea also contract chlamydia at the same time.
Examination of a Gram-stain of the discharge may disclose gram-negative diplococci inside of white
blood cells, diagnostic of gonorrhea and the patient should be treated for both gonorrhea and
chlamydia.
If the Gram stain of the exudate does not disclose white cells with gram-negative intracellular
diplococci, the patient should be treated for chlamydia. If no microscope is available, it is difficult to
distinguish gonococcal urethritis from chlamydial urethritis with surety and the patient should be
treated for both.
Younger women may occasionally develop urethritis caused by C. trachomatis.
These women do not have a urethral discharge, but have pain with urination due to the urethral
inflammation. However, a urinary tract infection is more common cause of painful urination.
Painful Testicle (Epididymitis)
The epididymis, which stores sperm and is located on the posterior side of the testicle, may become
infected by C. trachomatis (most commonly) or N. gonorrhoeae.
94
Epididymitis must be differentiated from acute testicular torsion (twisting of the testicle inside the
scrotal skin, which can lead to loss of blood supply to the testicle.)
Examination of a patient with epididymitis shows tenderness of the epididymis and possible swelling.
In men with sexually transmitted epididymitis, there will usually be symptoms or signs of urethritis,
but this may not be prominent (particularly in men with chlamydia).
Genital Ulcer
Erosions of the skin (ulcers) may be caused by Herpes simplex virus (genital herpes), Treponema
pallidum (syphilis) and Haemophilus ducreyi (chancroid). Erosions may be caused by trauma (during
sex or in zippers) or less commonly by reactions to medications (particularly tetracyclines).
The most common disease is genital herpes, whose incubation period is five to10 days. Initially, small,
painful, grouped blisters occur which, over several days, break open into shallow ulcerations. Painful,
swollen, lymph nodes in the groin may accompany the blisters and ulcers.
Over ensuing days, the ulcers crust and heal; the entire process takes about 21 days for initial attacks.
Subsequent attacks may occur and last seven to 10 days.
Women with initial attacks may have accompanying erosions of the cervix.
The primary stage of syphilis is characterized by one to four painless smooth ulcers which appear about
21 days following infection.
Small, minimally tender lymph nodes in the groin may occur. Without treatment, the ulcers heal after
two to six weeks
As the ulcers are healing, or several weeks afterward, the secondary stage of syphilis occurs and is
characterized by a skin rash consisting of small flat patches, often most noticeable on the palms and
soles; patients may have a low-grade fever.
Without treatment, the rash will resolve after about two to six weeks, but may return. Without
treatment at this stage, patients may develop tertiary syphilis in one to 30 years, characterized by
neurologic (stroke, dementia) or cardiac (heart valve disease) abnormalities.
Chancroid is characterized by one to four very painful ulcers which often appear quite ragged. Painful
enlargement of the lymph nodes in the groin occurs in half of patients.
Genital Warts
Genital warts occur several weeks following infection with human papilloma virus (HPV).
HPV warts look like warts elsewhere on the body, but differentiation from other causes of skin
growths is not always easy.
Lymphogranuloma Venereum (LGV)
LGV is a systemic disease of venereal origin caused by a virus-like organism.
The infectious agent is a Bedsonia organism closely related to that of psittacosis.
After an incubation period averaging one to four weeks, a small painless genital lesion occurs in about
one fourth of patients.
The lesion is an inconspicuous bump, blister, or shallow ulcer that heals within a few days and typically
goes unnoticed by the patient.
The earliest clinical signs are fever up to 1030F (39.40C), chills, headache, malaise, coughing, and
muscle and joint pain.
95
Shortly after the onset of these symptoms, the patient becomes aware of a painful swelling in one or
both groin areas.
The inguinal bubo is common in males.
Early in the course of regional node involvement, one can feel one or more enlarged discrete movable
tender nodes. These eventually become matted together into an oval-shaped mass.
As the disease progresses, some of these matted nodes undergo softening. Because there are nodes in
different stages of evolution, the mass becomes large and lobulated with alternating areas of softening
and hardness. The overlying skin becomes swollen, sometimes bluish-red in color, and fixed to the
underlying mass. When pus forms and breakdown occurs, multiple fistulous tracts may open to the skin
surface.
Pruritus (Itching)
Pruritus may be caused by pubic lice (crabs) and scabies; both are parasites and in both cases, pruritus
is caused by sensitization to the organism.
The pruritus caused by lice is limited to the genital area while that due to scabies often occurs
elsewhere on the body where the mite
Adult lice and their eggs (nits) in egg casings may be seen with the naked eye clinging to pubic hairs,
or adult lice may be in the crusts of skin scabs formed from scratching; a magnifying lens helps
visualize adults and eggs.
Sarcoptes mites burrow under the skin, forming linear tracks and nodules (which house the mite);
common locations are the groin, finger webs and axilla.
Diagnosis of lice depends upon seeing the lice or their eggs; diagnosis of scabies depends upon seeing
typical nodules.
Pubic lice are treated by: lindane shampoo (1%), (not recommended for pregnant or nursing
women, or children <2 years of age);or, permethrin creme rinse (1%) or pyrethrins with
piperonylbutoxide.
Scabies is treated by: permethrin cream (5%); or, lindane (1%), applied to the body from the neck
down and washed off after 8 hours.
Carefully read and follow directions when using any of these preparations. They are toxic substances
and are dangerous if misused.
For both diseases, bedding and clothing should be machine washed and machine dried using a hot
cycle. Ironing clothes also kills the parasites.
Vaginal Discharge
Vaginal discharge is a common symptom that can be normal or a symptom of various infections.
Normal vaginal secretions vary with hormonal balance and the menses cycle. Normal secretions are
painless, clear, and thin, but can be quite profuse at some times of the month.
Some infections present with a vaginal discharge.
Trichomonas causes a white, frothy discharge with itching.
Monilia, or a yeast infection, is characterized by a white, cheesy discharge resembling cottage cheese.
Nonspecific vaginitis is due to a range of bacteria, and can have differing presentations. Some
infections, such as chlamydia and gonorhhea in women, may have no symptoms.
96
Lower Abdominal Pain
Lower abdominal pain is characteristic of pelvic inflammatory disease (PID), in which microorganisms
ascend through the cervix into the uterus and fallopian tubes.
The most common organisms involved are N. gonorrhoeae and C. trachomatis.
Other causes of lower abdominal pain, i.e. appendicitis, should always be considered before making a
diagnosis of PID. Appendicitis is a medical emergency that is life threatening if untreated.
PID is characterized by acute or gradual onset of pain in the lower abdomen.
HUMAN IMMUNODEFICIENCY VIRUS INFECTION/ ACQUIRED
IMMUNODEFICIENCY SYNDROME (HIV/AIDS)
Incubation Period:
The time from HIV infection to seroconversion (a positive result on an HIV antibody laboratory test on
blood or oral fluid) is a few weeks to a few months.
The interval between HIV infection and diagnosis of AIDS varies greatly with today’s treatment; the
range in adults is from about two to 15 years.
AIDS is caused by a retrovirus, known as human immunodeficiency virus (HIV). Tests for HIV
antibodies are in widespread use and confirmed positive test results indicate infection by the virus.
HIV is transmitted sexually and through contact with blood such as when injecting illicit drugs or in
tattooing. HIV also may be transmitted through transfusions of blood or blood components, medical
contact with blood (as in surgery or in treating open wounds), and prenatally from HIV infected
mothers to their infants.
Tthe more common manifestations include severe immunosuppression (as measured by a decline in the
T-helper lymphocyte count to below 200 cells per ml of blood), wasting syndrome (loss of more than
10% of body weight), Pneumocystis carinii pneumonia (PCP), tuberculosis (TB), bacterial pneumonias,
cytomegalovirus retinitis, Kaposi's sarcoma, cryptococcal meningitis, candidiasis of the esophagus,
toxoplasmosis of the central nervous
Adenoviruses
Many adenoviruses cause febrile syndromes commonly associated with upper and lower airway
diseases such as pharyngitis, bronchitis, and pneumonia .
Over 49 adenoviruses have been described as etiologic agents of acute respiratory distress syndrome
(ARDS) but only a few are major respiratory pathogens. These agents are extremely contagious,
resulting in epidemic outbreaks worldwide in crowded quarters such as recruit training sites.
Symptoms
Fever, headache, prostration, coryza (nasal mucous membrane inflammation and discharge), sore
throat and cough after short (1-5 days) incubation period; usually occurs with constitutional
symptoms of malaise, chills, anorexia; persists for 2-5 days then spontaneously resolves.
Signs
Vitals: fever up to 102°F
Inspection: Follicular, erythematous, or exudative pharynx/tonsils; swollen, tender cervical lymph
nodes; conjunctivitis.
Auscultation: Possible rales
97
Lab: Monospot to rule out mononucleosis
Differential Diagnosis
Pneumonia - may be indistinguishable from viral ARD or ARDS (see Respiratory: Pneumonia).
Pharyngitis - ulcerative pharyngitis is associated with the enteroviruses; palatal petechiae, red
beefy uvula, and scarlatiniform rashes are often associated with Group A streptococcal pharyngitis.
Influenza - typically results in more systemic disease, including sustained fever, malaise, and
myalgia accompanying respiratory manifestations in adults
Infectious Mononucleosis - persistent illness for several weeks suggests Infectious Mononucleosis
Treatment: There is no specific therapy.
Arboviral Encephalitis
Arthropod-borne viruses (arboviruses), including Japanese encephalitis (JE), West Nile (WN), tickborne encephalitis (TBE), St. Louis encephalitis (SLE), Kunjin, and Murray Valley encephalitis
(MVE) flaviviruses have been associated with sporadic fatal meningoencephalitis in humans.
Japanese encephalitis is the most common and one of the most dangerous arboviral encephalitides
(inflammation of the brain tissue), with over 50,000 cases reported annually. 25% of individuals
with JE die from the disease and 50% are left with permanent neurologic or psychiatric sequelae.
Symptoms
Sudden fever, headache, vomiting, and dizziness; rapid progression of mental status changes—
disorientation, focal neurologic signs, seizures, stupor and coma; followed usually by recovery, or
death (1-60% mortality) or severe sequelae.
Signs
Neurological: Use Glasgow coma scale (GCS) to track progression of mental status changesVitals:
Fever and respiratory insufficiency.
Inspection: Transient weakness, diminished sensorium, hyperactive deep tendon reflexes, sensory
disturbances; limb paralysis (JE, TBE), paresis of the shoulder girdle or arms (TBE); tremors,
abnormal move- ments, and cranial nerve abnormalities (gaze paralysis, speech disorders) (JE).
Palpation: Nuchal (neck) rigidity may be present
Definitive diagnosis may require lumbar puncture, CT, EEG and other advanced testing.
Differential Diagnosis
Herpes simplex encephalitis - focal, non-motor changes (personality, speech, temporal seizures)
Other Herpesviruses or HIV - Infectious Mononucleosis and HIV sections
Rabies, TB, meningitis
Subdural hematoma and other trauma Treatment: There is no drug treatment for arboviruses.
ANTHRAX (CUTANEOUS)
Incubation Period: Within 7 days (usually 2 to 5 days).
98
Cover skin lesion until lesion is free of anthrax bacilli. Anthrax is an acute, infectious bacterial disease
that is caused by Bacillus anthracis.
When anthrax appears as a skin disease, it may look like an ordinary vesicle, boil, or carbuncle.
However, the surrounding skin may become swollen.
If the skin lesion ruptures, serous (straw-colored) fluid escapes, revealing a black eschar or scab at the
base of the ulcer. There may be severe systemic symptoms such as fever or prostration.
It is difficult to distinguish anthrax from an ordinary boil. Someone with a severe skin reaction
surrounding a boil plus other bodily symptoms should be treated with antibiotics.
CHICKENPOX (VARICELLA)
Incubation period: 14 to 21 days.
Isolation period: For 1 week after rash appears or until all lesions become crusted.
Chicken pox is a highly contagious viral disease that produces a typical rash.
It is usually a disease of children and typically occurs in the late winter and early spring.
The virus is spread by airborne respiratory secretions as well as by direct contact. It is communicable
from a few days before the rash appears until all vesicles have crusted.
Individuals normally have it one time and will not be infected again as adults. However, if one did not
have it as a child, one can get it as an adult.
The disease begins with a running nose, tearing eyes, slight fever to about 101oF (38.3oC), occasional
sore throat, loss of appetite, decreased energy, and restlessness.
Within 24 hours an eruption appears, mostly on the trunk and face, and occasionally on the arms and
legs.
The skin lesions arise in crops of vesicles (clear fluid-filled blisters on a slightly raised red base), may
become pus-filled, and crust in a few days. As healing occurs, the crusts or scabs fall off.
CHOLERA
Incubation Period: 12 hours to 5 days (usually 1 to 3 days).
Cholera is an acute disease characterized by profuse watery diarrhea, often with vomiting and
prostration.
It is caused by intestinal infection with certain strains of the bacterium Vibrio cholerae. In severe
cases, it causes profound and sometimes fatal dehydration.
Cholera is usually acquired by exposure to unclean water sources or by eating seafood exposed to such
water sources.
Cholera is not transmitted through direct contact with an infected person, though it is readily
transmitted through any fecal contamination from an infected person.
The symptoms of cholera usually begin within one to three days after exposure. Diarrhea may be the
only symptom in mild cases.
In more severe cases, patients have profuse watery diarrhea, vomiting, and prostration or collapse.
Typical stools are almost clear water with shreds of mucus, and are described as rice-water stools.
The diarrhea may be continuous, leading to tremendous loss of body fluids and dehydration.
Cholera is an officially notifiable disease.
99
DENGUE FEVER (BREAKBONE FEVER)
Incubation Period: 3 to 15 days (usually 4 to 6 days).
Isolation Period: 5 days after onset or until fever abates, in a screened room or under a bednet.
Dengue fever is an acute viral disease that is transmitted by the bite of an infective Aedes mosquito.
Aedes aegypti, a highly domesticated urban mosquito, is the principal vector.
For the virus to be transmitted, the following sequence of events must take place:
Ð female mosquitoes feed on the blood of an infected person from 1 to 2 days before the person's
illness began to 5 days after onset of illness
P the virus develops in the mosquito tissues for 8 to 12 days
\ the female mosquito transfers the virus to susceptible persons when it feeds
Dengue fever is characterized by a sudden onset of fever, which may rise to 102o to
105oF (38.8-40.5oC), headache, eye pain, backache, bone and joint pain, weakness, and malaise.
Nausea and vomiting are common.
Some patients have a blotchy rash, flushing, conjunctivitis, taste aberrations, loss of appetite, and
abdominal pain.
Fever and associated symptoms may last for 3 to 5 days, followed by complete recovery.
The decline in fever may be followed 1 to 3 days later by another rise in temperature and associated
symptoms (saddleback fever).
A second rash, varying in form, may appear with the first decline in temperature.
Mild to severe bleeding may occur from the nose, gums, gastrointestinal tract, and skin.
DIPHTHERIA
Incubation Period: 2 to 5 days.
Isolation Period: 14 days after onset.
Diphtheria is a serious acute infectious disease that is caused by the Corynebacterium diphtheriae
bacillus.
The bacteria grow in the throat, nose, or windpipe and give off a toxin (poison) that causes an illness
of the entire body.
Prevented by diphtheria toxoid injection with booster doses every ten years.
Early symptoms of diphtheria include: overall body discomfort, restlessness, weakness, loss of appetite,
headache, and chills.
Sore throat with fever to 103oF (39.4oC), prostration, vomiting, and convulsions may develop in some
cases.
Dirty gray patches of an adherent membrane form in the back of the throat and in the windpipe itself.
These patches resemble dead skin and when brushed, come away with difficulty leaving tiny bleeding
points in the uncovered mucous membrane. There may be a bloody nasal discharge and a “croupy”
cough.
GASTROENTERITIS/DIARRHEAL ILLNESSES
Diarrheal disease is often due to inflammation of the intestines and may be referred to as
gastroenteritis, colitis or dysentery.
100
Gastroenteritis is inflammation of the stomach and intestines. Inflammation of the large bowel is
referred to as colitis.
Dysentery usually presents with bloody diarrhea and is often of bacterial origin. These terms are often
used interchangeably.
Specific causes of diarrhea and some special treatments are outlined below:
Viruses - Many viruses present as intestinal illness. Usually, there is little or no fever. The onset of
illness lasts several hours and is usually over within two or three days. The vomitus and stools are
typically watery without blood or mucus. The patient often feels reasonably well in between bouts of
diarrhea and vomiting.
Bacteria - Salmonella, shigella, campylobacter, yersinia, and cholera are some of the bacterial causes of
dysentery. Clinically these infections can resemble viral gastrointestinal illness, although blood or
mucus in the stool is more typical. Shigella may present with seizures. Salmonella may be carried in
undercooked poultry, powdered eggs, powdered milk, or other food, as well as by livestock and pets.
Pets may also be a source for campylobacter and yersinia. Diagnosis requires stool examination and
culture.
Toxin induced food poisoning - Although staphylococcal organisms are bacteria, it is the toxin they
produce that is responsible for the symptoms of food poisoning. Undercooked poultry and poorly
refrigerated foods such as pastries, custards, and mayonnaise are typical sources. Symptoms usually
begin rapidly and violently within one to six hours after eating contaminated food. Profuse vomiting,
diarrhea, abdominal cramps, and prostration occur.
Campyolobacter difficille colitis - Referred to as C. diff. colitis, is another form of toxin producing
colitis, and commonly follows antibiotic therapy. Antibiotics destroy normal gut flora which allows
this organism to take over and multiply, producing bloody or non-bloody diarrhea. History of antibiotic
use, severity of symptoms, and prolonged illness can be clues to diagnosis. Stool cultures are required
to detect the toxin, and medical advice and referral are necessary.
Amebic dysentery - The only known human infectious cause of amebic dysentery is via the parasite
Entamaeba histolytica. Amoebiasis tends to be a chronic diarrheal illness that may produce an acute
colitis which is indistinguishable from bacterial dysentery. Diagnosis requires laboratory identification
of the amoeba in the feces. Fever is usual. Abcesses may form in the liver or elsewhere, which may
prove fatal in exceptional cases.
Other - Chronic forms of diarrheal illness can be non-ifectious such as ulcerative colitis, regional
enteritis, functional/spastic colon, and malabsorption syndromes.
Hantavirus
Hantaviruses infect rodents worldwide and aerosolization of rodent excreta (especially urine) is
responsible for transmitting infection. There are many hantaviruses, Sin Nombre virus, mainly found
in the western U.S. and Canada, causes Hantavirus Pulmonary syndrome (HPS). The incubation
period is generally 1 to 4 weeks.
Symptoms
Constitutional: Acute (1-4 days): High fever, chills, myalgias, headache; Sub-acute (5-14 days):
Low grade fever, apprehension; Chronic (> 2 weeks): Fatigue and lethargy
Specific: Acute (1-4 days): Abdominal pain, flushed face; Sub acute (5-14 days): Low urine output,
back pain; Chronic (> 2 weeks): Diuresis, renal concentrating defect
Signs
Acute (1-4 days): Toxic appearance, fever to 104°F, conjunctival injection, flushed face/neck/ upper
torso (blanches with pressure), dermatographism (drawing on skin leaves an exaggerated mark);
101
Sub-acute (5-14 days): Temperature up to 101°F, truncal and axillary fold petechiae, lowered blood
pressure, low urine output up to day 7, profound diuresis thereafter(up to liters/day)
Inspection: Acute (1-4 days): Increased respiratory rate, accessory muscle use for breathing, Fever to
104° F
Auscultation: Acute (1-4 days): Lungs often normal, tachycardia, mild hypotension;
Sub acute (5-14 days): Diffuse “Velcro” rales
LAB: Urine is dilute (specific gravity 1.010) with proteinuria, hematuria, occasional red and white
blood cell casts; may see elevated white blood count, thrombocytopenia, increased hematocrit (up to
55-65% in severe infection).
Pulse oximetry may demonstrate hypoxia even if CXR is normal in HPS. CXR may show bilateral
whiteout, pleural effusion, increased vascular markings; may see elevated white blood count,
thrombocytopenia, increased hematocrit (up to 55-65% in severe infection).
Differential Diagnosis
Leptospirosis - pulmonary hemorrhage presentation of leptospirosis (as seen in Hawaii) may present
similarly to HPS. Travel history, conjunctival redness and skin contact with standing fresh water all
suggest leptospirosis.
Hemorrhagic fever virus - more prominent bleeding (HFRS can have bleeding, but late in course) and
rash seen with some types.
Typhus - responds to doxycycline, presents with a rash, lowered white blood cell count, and tache
noire for some types. Also consider plague, tularemia.
Treatment
Avoid excess fluids; consider blood transfusion and Trendelenburg position for shock; give O2. For
HFRS, ribavirin IV 2 gram loading dose, then 1 gram q 6 hours for 4 days, then 500mg q 8 hours for 6
days.
General: This infection has high mortality. Most deaths occur within the first 48 hrs.
HEPATITIS, VIRAL
Hepatitis is an inflammation of the liver that results in acute and chronic forms of disease. Many agents
cause hepatitis including viruses, drugs, alcohol, and other non-viral infectious diseases.
It is important to exclude non-viral causes of hepatitis since their treatment differs.
Hepatitis A and E virus transmission mainly occurs by a fecal-oral route via person-to-person
transmission and foodborne outbreaks.
Hepatitis B, hepatitis C, and the hepatitis delta agents are transmitted by percutaneous and mucous
membrane exposures to infectious blood and other body fluids.
The most frequent symptoms of acute viral hepatitis are fatigue, muscle pains, nausea, and absence of
appetite, which typically develop 1 to 2 weeks before the onset of jaundice. [ yellowing of the skin or
eyes, dark brown urine and/or clay-colored stools.]
Headaches, joint pains, vomiting, and right-upper-quadrant tenderness are also common.
Chronic hepatitis is defined as an inflammation of the liver lasting longer than 6 months. It may be
asymptomatic for years. Over time it can develop into serious liver disease or liver cancer. Patients
who are chronic carriers can spread the disease to others. Hepatitis A and E are not known to cause
chronic hepatitis. Hepatitis B plus or minus the hepatitis delta agent, and hepatitis C typically cause
chronic hepatitis.
HEPATITIS A (HAV) (Infectious hepatitis, epidemic jaundice)
Incubation Period: 15 to 50 days, depending on dose; average 28.
102
Hepatitis A virus (HAV) is transmitted mainly by the fecal-oral route, most commonly by direct personto-person contact.
Acute hepatitis A may be symptomatic or asymptomatic. Severity of illness varies and most
commonly presents as a mild flu-like illness lasting 1 to 2 weeks.
Because clinical signs and symptoms are similar to those of other types of viral hepatitis, serologic
detection of specific antibody responses to HAV is necessary to confirm the diagnosis.
HEPATITIS B (HBV) (Serum hepatitis, Australia antigen hepatitis)
Incubation Period: 45 to 160 days, average 120 days.
Hepatitis B virus (HBV) is transmitted primarily by percutaneous and mucous membrane exposures to
blood and other infectious body fluids.
The course of acute hepatitis B is usually divided into an incubation period, pre-icteric, icteric, and
convalescent phases.
The preicteric phase, typically lasting less than a 1 week, is characterized by the gradual onset of
malaise, nausea, right-upper-quadrant pain, and lack of appetite. Fever may be absent or mild.
With the onset of the icteric phase, symptoms worsen and dark urine and jaundice appear. This phase
may last a few days to several months. Itching and pale stools usually occur after the onset of jaundice.
Weight loss of 2 to 10 kilograms is typical.
No specific therapy exists for acute hepatitis B.
DELTA HEPATITIS (HDV) (Viral hepatitis D, Hepatitis delta virus, Delta agent hepatitis, Deltaassociated hepatitis)
Incubation Period: About 2 to 8 weeks as a superinfection; requires HBV as a coinfection.
Isolation Period: Same as that for HBV. (See above).
Hepatitis delta agent (HDA) is an incomplete virus requiring the helper function of HBV to replicate.
Therefore, HDA causes hepatitis but only in conjunction with HBV. HDA can be acquired mainly via
sexual transmission as a coinfection with HBV or as a superinfection of chronic HBV carriers.
No specific therapy exists for acute Hepatitis D.
HEPATITIS C (HCV) (Formerly called post transfusion non-A non-B hepatitis)
Incubation Period: 2 weeks to 26 weeks, average 6 to 7 weeks.
Isolation Period: None.
Groups at high risk include injection-drug users, hemophiliacs, hemodialysis patients, persons with
high-risk sexual behaviors, or those with sexual or household exposure to HCV carriers, and health
care workers.
HCV may present asymptomatically.
Because clinical signs and symptoms are similar to those of other types of viral hepatitis, specific
serologic tests for antibodies to HCV are required to establish a diagnosis of hepatitis C.
HEPATITIS E (HEV) (Enterically transmitted or epidemic non-A non-B hepatitis, fecal-oral non-A
non- B hepatitis)
Incubation Period: 15 to 64 days; mean incubation ranges of 26 to 42 days have been reported.
Isolation Period:
103
Hepatitis E is a self-limited, acute disease similar to hepatitis A in that it only presents acutely (no
chronic state exists) and it is transmitted via the fecal oral route.
INFLUENZA (FLU)
Incubation period: 1 to 3 days.
Isolation period: None.
Influenza is an acute respiratory illness caused by influenza type A or B viruses.
Typical manifestations include fever, cough, sore throat and coryza, accompanied by headache, muscle
and joint aches and extreme fatigue.
Influenza is easily transmitted by airborne spread.
The most severe symptoms typically occur over 2 - 4 days and frequently require bedrest.
Immunization with influenza vaccine is the primary method of prevention.
Persons at highest risk who should be immunized include:
N persons age 65 yrs or older and those any age who have certain chronic health conditions
à health care providers and household contacts of persons at high risk
Q military personnel to prevent disruption of activities during epidemics
à students living in dormitories because of close living conditions
LEGIONNAIRES’ DISEASE (LEGIONELLOSIS)
Incubation period: 2-14 days
Isolation period: None..
Legionnaires' disease is a common type of pneumonia caused by Legionella bacteria.
Symptoms often include fever, shortness of breath, cough, chest discomfort, weakness, headache,
confusion, and diarrhea.
Illness can range from gradual malaise, muscle aches, loss of appetite, and low grade fever to
explosive high fever and respiratory failure developing within 24 hrs. The illness can be quite serious
and up to 15% of cases end in death.
Legionnaires' disease is not spread from person-to-person.
Most illnesses occur as a result of inhalation of aerosols or mists containing Legionella within water
droplets. such as from air handling systems Only a small proportion of those exposed to contaminated
aerosols during outbreaks develop illness.
Antimicrobial treatment, given early in the course of illness, can substantially reduce the risk of serious
complications. Antibiotics such as fluoroquinolones (ciprofloxacin), erythromycin, or azithromycin are
used for treatment.
MALARIA
Incubation period: 7-28 days.
Malaria transmission occurs on every continent in subtropical and tropical regions.
Disease in humans is caused by one of four parasites called Plasmodium (falciparum, vivax, ovale and
malariae). Plasmodium falciparum causes the most severe infections, and greatest number of deaths.
P. falciparum has developed resistance to chloroquine, a drug widely used to both prevent and treat
malaria in many areas.
P. vivax has developed resistance to chloroquine on the island of Papua New Guinea.
104
Infection results from a bite from an infected female Anopheles mosquito which injects parasites when
it takes a blood meal; these enter human liver cells.
After one to two weeks of development, blood stage parasites burst from liver cells, enter the blood,
and invade red blood cells.
Asexual reproduction occurs in red blood cells, forming many more parasites.
The red blood cells rupture releasing more parasites, which then infect more red blood cells. This
continuous cycle causes symptoms of malaria illness and destruction of red blood cells.
MEASLES (RUBEOLA)
Incubation Period: 8 to 13 days, sometimes more.
Isolation Period: From diagnosis until 7 days after the rash appears. In the U.S. measles is largely
prevented by vaccination
Measles, an acute viral disease, is among the most contagious of all communicable diseases.
The virus is found in secretions of the nose, mouth, throat, and lungs of infected persons.
Many adults have had the disease in childhood, and one attack provides lifelong immunity.
Complications include diarrhea, pneumonia, ear infection, and inflammation of the brain
(encephalitis). In unvaccinated populations in developing countries measles is a leading cause of
pediatric deaths.
Symptoms begin within 2 wks of exposure.
Onset is sudden with a general overall feeling of illness, sneezing, runny nose, headache, sore throat,
cough, soreness of the eyes, dislike of bright light, and a rise in temperature to about 102oF (38.8oC).
Copious tears, swollen lids, and bloodshot eyes may be present.
During this early stage the disease is most contagious. On the second and third day symptoms
become more marked and the face gets a puffy look.
On the inner side of the cheeks, where the back teeth meet, tiny whitish spots (Koplik’s spots) may be
seen. The patient now should be isolated, if not already done. After 3 - 5 days of the disease, the
typical measles rash appears. The rash of a reddish hue with slightly raised irregular blotch patches
starts on the forehead and behind the ears, and gradually spreads to the face, body, and limbs.
The rash remains about 4 - 5 days, then fades in the same sequence that it appeared. This is followed
by a fine peeling of the skin.
As the rash disappears, the patient becomes non-infectious and the temperature drops to normal.
MEASLES, GERMAN (RUBELLA)
Incubation Period: 12 to 23 days (rash 14 to 17 days after exposure).
Isolation Period: 7 days after onset of rash.
German Measles usually called three-day measles
In the week preceding rash, older children and adults may have low-grade fever, malaise, symptoms of
upper respiratory infection, and swelling and tenderness of lymph nodes in the neck, especially behind
the ears.
A pink rash, which begins on the face and moves to the trunk, lasts about 3 days.
There may be a general feeling of bodily discomfort, headache, symptoms of a common cold, eye
soreness, stiffness of joints, and a slight fever, about 102oF (38.8o C).
Rubella vaccine is a live attenuated vaccine commonly given in combination with the measles and
mumps vaccines (MMR).
105
MENINGOCOCCAL DISEASE
Incubation Period: 1 to 10 days, most commonly less than 4 days.
Isolation Period: Routine isolation for the first 24 hrs of therapy and prophylaxis of household contacts
as described below.
Infections caused by the gram-negative bacterial pathogen Neisseria meningitidis.
Fever, headache, and stiff neck are the most common symptoms
Alteration in mental status may also occur, and patients may have a rash.
Onset of rash may be quite abrupt and the patient appear quite toxic.
The rash itself may be petechial (pink dots), purpuric (look like diffuse bruises or blueberry muffin), or
macular (larger pink rash difficult to distinguish from other viral rashes). Meningeal inflammation
may be manifested by Kernig's sign and/or Brudzinski's sign. Kernig's sign is resistance to passive
extension of the leg when the hip is flexed while supine. Brudzinski's sign is spontaneous flexion of
hips and knees with passive flexion of the neck.
MONONUCLEOSIS, INFECTIOUS
Incubation period: 21 to 42 days.
Isolation period: None.
Infectious mononucleosis is an acute viral disease, caused by Epstein-Barr virus (EBV), and
characterized by fever, sore throat (often with exudative pharyngitis), and lymphadenopathy.
The first symptoms are similar to any upper respiratory infection: with fever, chills, headache, cough,
and general malaise.
After two to three days, swollen lymph glands may appear on the sides and back of the neck, in the
armpits, and the groin.
Enlargement of the spleen is noted in 50% of young adults, and jaundice (yellow color) of the skin and
eyes in about 4%.
The diagnosis is aided by finding lymphocytosis of greater than 50% with 10% or more atypical
lymphocytes on a peripheral blood smear. It is serologically confirmed by heterophile and EpsteinBarr virus blood tests.
Treatment:
There is no specific treatment for infectious mononucleosis except bed rest during the acute phase.
Bed rest should be extended in cases with prolonged fever.
Robust exercise should be avoided by any cases with abdominal pain or tenderness, which may be
associated with enlargement of the spleen, to reduce the possibilities of rupture.
MUMPS (EPIDEMIC PAROTITIS)
Incubation Period: 12 to 26 days.
Isolation Period: 9 days from onset of parotitis (swelling of salivary glands).
Acute, contagious, viral disease identified by tenderness and swelling of one or more of the salivary
glands. Usually the parotid glands are affected.
The virus may be spread by direct or indirect contact with nose and throat discharges from an infected
person.
106
One attack usually gives immunity for life.
The disease begins with malaise, headache, a slight rise in temperature, and possibly nausea.
In severe cases the temperature may reach 104oF (40oC) and last as long as a week.
On the second day the swelling usually begins on one side of the jaw or cheek and increases greatly.
In a couple of days, there is considerable enlargement at the side of the neck, posterior part of the
cheek, and underneath the side of the jawbone.
The patient complains of pain and stiffness on moving the lower jaw. The opposite side of the face
usually becomes affected in a few days, though infection may occur unilaterally. The swelling lasts
about 10 days.
In young adult males, the infection may spread to one or both testicles to produce a painful
inflammation and swelling called orchitis. Some degree of testicular atrophy is common, but sterility
is rare.
Treatment
Bed rest with strict isolation nursing technique.
Analgesics-antipyretics such as acetaminophen relieve pain caused by salivary gland inflammation and
reduce fever.
Warm or cold packs applied to the inflamed areas may relieve discomfort. Fluids should be encouraged
with a soft diet.
PLAGUE
Incubation Period: 2 to 6 days.
Isolation period: Until declared free from infection by a physician.
An acute, sometimes fulminating disease caused by the Gram-negative bacillus, Yersinia pestis. Plague
is primarily a disease of rodents and is most often transmitted to humans by the bite of
BUBONIC PLAGUE
Most common form, is usually acquired by the bite of an infected rodent flea.
The disease may also be transmitted by direct contact with tissues or body fluids of an infected animal.
The onset of illness is usually heralded by fever, intense headache, fatigue, and profound weakness.
The fever often rises to 102o F (38.9o C) or higher on the first day of illness, then fluctuates. The pulse
is rapid, sweating and chills may occur, and the patient may experience extreme thirst.
The patient often becomes anxious or agitated, and delirium and convulsions may develop. The
characteristic buboes (swollen, extremely tender lymph nodes) usually develop on the second or third
day of illness, most often in the inguinal (groin) area, in the axillary (armpit) area and in the cervical
(neck) region.
The affected glands often swell to a size of 2 or more inches (5 cm) in diameter and are surrounded by
edema of the soft tissues. The overlying skin is usually reddened, warm, and extremely painful.
PNEUMONIC PLAGUE
Primary pneumonic plague, spread by respiratory droplets exhaled by coughing, talking, or sneezing, is
the least common, but most serious form of the disease.
107
Fatal, unless the patient is treated early with the appropriate antibiotic regimen (within 18-24 hours
after onset of symptoms).
Symptoms are as described above with the additional problems of cough, rapid respirations, difficulty
in breathing, and cyanosis that may occur as the pneumonia advances. The sputum may be scant and
blood-tinged, or may be profuse, watery, and bloody.
SEPTICEMIC PLAGUE
Primary septicemic plague (infection of the bloodstream) occurs in 10% or less of all cases.
It usually arises from direct handling of infected tissue and fluids of infected animals.
Septicemia secondary to bubonic or pneumonic plague is not uncommon
The patient is rapidly prostrated and may develop irreversible septic shock. Clotting problems as
evidenced by bleeding are common. If not treated promptly, death often occurs in 2 to 4 days,
frequently preceded by delirium, stupor, and coma.
POLIOMYELITIS
Incubation Period: Commonly 7 to 14 days, with a range from 3 to 35 days.
Poliomyelitis is an acute viral disease that occurs chiefly in children.
It is spread by respiratory and fecal routes.
Today polio is wholly preventable with two types of vaccine available: the injectable Salk vaccine
(IPV) and the oral Sabin vaccine (OPV).
RABIES (HYDROPHOBIA)
Incubation Period: 10 days to more than 12 months (usually under 4 months).
Patients bitten about the head and those with extensive bites may have shorter incubation periods.
Isolation Period: Duration of the illness.
Rabies is an acute infectious viral disease that is almost always fatal.
When a rabid mammal bites a human or other animals, its saliva transmits the infection into the wound
where it spreads to the central nervous system.
Human rabies may begin with fever, nausea, headache, loss of appetite, and sore throat.
The body temperature may rise to 1030F (39.40C).
At the bite wound, there may be a tingling or burning feeling. As the infection progresses, extensive
portions of the brain and central nervous system become involved.
Paralysis and muscle spasms occur, with spasms of muscles in the mouth and throat that control
swallowing.
The term hydrophobia (fear of water) derives from the patient’s inability to drink, regardless of thirst.
Patients become very weak and their mental outlook changes.
They become apprehensive, irrational, even maniacal. They may suffer from widespread muscular
twitching and convulsive seizures provoked by any stimulus, especially by attempts to drink or
even air currents.
Thick ropy saliva may drip from the lips. Eventually there are breathing difficulties, coma, and general
paralysis.
Tetanus toxoid or prophylactic antibiotics may be indicated depending upon the patient’s vaccine
history and the extent of the bite.
108
RHEUMATIC FEVER
Incubation Period: 7-14 days.
Isolation Period: None.
Evidence of a recent strep throat infection is of course supportive.
A positive throat culture, a rapid antigen detection test and/or elevated or rising ASO (strep antibody)
titers would be tests which would be supportive, were one to have access to such studies.
symptoms:
b migratory joint pains or
heart problems such as chest discomfort that suggest swelling,
0 a new murmur, rapid heart rate, skin nodules
migratory rash
fever
RELAPSING FEVER (TICK-AND LOUSE-BORNE RELAPSING FEVER)
Incubation Period: 5 to 15 days (usually 8 days).
Isolation Period: None.
Relapsing fever is an acute infectious disease caused by spirochetes of the genus Borrelia.
It is transmitted by lice and ticks.
The disease is characterized by rapid onset of fever, chills, dizziness, headache, muscle and joint pains,
vomiting, and at times delirium.
The fever remains high for two to nine days, then ends suddenly by crisis, in which there is a further
rise in fever accompanied by rigors, followed by a rapid fall in body temperature and drenching sweats.
This is followed by several days of fair health without symptoms, after which a relapse usually occurs,
plus jaundice in some cases. There may be three, four, or more recurrent attacks, each decreasing in
severity, as immunity develops.
SCARLET FEVER
Incubation period: 1-4 days.
Isolation period: None.
Scarlet fever consists of a streptococcal infection, usually a strep throat, accompanied by a
characteristic rash.
The symptoms of scarlet fever include those of a strep throat: mild to severe sore throat (sometimes
asymptomatic), fever, chills, malaise, abdominal complaints/vomiting.
The throat may look normal or erythematous with a purulent exudate over the tonsils.
Enlarged, tender anterior cervical lymph nodes may be palpable accompanying the infection.
The scarlet fever rash typically has a sandpaper-like quality and begins on the first or second day of
illness.
It spreads over the trunk to the extremities but spares the palms and soles. The rash may also be
accentuated in areas of the skin folds (Pastia’s lines).
The tongue may have a strawberry-like appearance (strawberry tongue). The rash usually subsides
within a week and is often followed within several days by desquamation of the palms and soles. It is
one of few rashes affecting the palms of the hands and soles of the feet.
109
Treatment: intramuscular benzathine penicillin G or a complete 10 day course of oral penicillin V, or
erythromycin for those with penicillin allergy.
SHINGLES
Herpes Zoster
Same virus that causes chicken pox.
The rash of shingles follows a dermatome pattern and is typically quite painful.
TETANUS (LOCKJAW)
Incubation Period: 3 - 21 days or more (depending on character, location, and extent of wound).
Isolation Period: None.
Tetanus can be prevented with vaccine – current vaccination is critical.
Tetanus is caused by a toxin produced by the bacillus Clostridium tetani, a bacterium that grows in the
absence of air at the site of an injury.
Tetanus bacteria commonly enter the body through wounds contaminated by debris or foreign bodies.
Early symptoms are aches and pains in the muscles, general fatigue, and headache.
Soon the characteristic signs appear - stiffness of the neck and jaw that gradually extends to the
muscles of the back and the extremities.
The jaw may become clenched tightly (lockjaw).
The body is held rigidly straight or arched so that the patient’s back may touch the bed only with his
head and heels.
TUBERCULOSIS
Incubation Period: Variable, from 10 weeks to years.
Isolation period: Isolation should be discontinued only after the patient has been evaluated, treated,
and declared noninfectious by a physician.
Tuberculosis (TB) is an infectious disease caused by bacteria called Mycobacterium tuberculosis.
TB can attack any part of the body, but most commonly causes lung disease.
Bacteria are expelled into the air by a person with active TB and patients are most infectious when they
have a cough.
Persons with human immunodeficiency virus (HIV) infection or other immune suppressing
conditions(transplant recipients); persons with other medical conditions such as diabetes, silicosis, and
malnutrition; or those in the extremes of ages (infants and elderly).
General symptoms include a persistent cough, weight loss, fever, night sweats, chills, loss of appetite,
and fatigue.
The most reliable signs of TB are a cough that persists for more than 2 weeks, often with blood tinged
sputum, and chest pain.
TB therapy consists of several drugs, which must be taken for an extended period, usually for at least 6
months. Some of the drugs used include isoniazid, pyridoxine and rifampin. Susceptibility to TB
drugs should be tested.
110
TYPHOID FEVER (ENTERIC FEVER)
Incubation Period: Usually 1-3 wks, depending upon size of infectious dose and vaccine status.
Isolation Period: Isolation not required.
Typhoid fever is caused by the bacterium Salmonella typhi.
A high fever with a slow pulse rate, lasting more than a week, plus headache and abdominal pain, may
be presenting signs.
Onset of fever is gradual and may rise in a stepwise fashion over 2 - 3 days, peaking at 103-104oF
(38.8 - 40oC).
Chills, mental cloudiness, malaise, constipation, abdominal pain, nausea, and loss of appetite may
present early on. Diarrhea and vomiting are less common. One-third will have a dry cough.
Within the first week, a sparse rash may appear on the chest and/or abdomen which typically consists
of a few red, flat, nontender lesions ("rose spots"), 1-2 mm in diameter. The abdomen may be slightly
distended with a varying degree of tenderness.
Bleeding and perforation of the bowels are two of the most common complications of typhoid fever;
typically occurring 2-3 weeks after the onset of the illness.
TYPHUS FEVER
Incubation period: 10 to 20 days.
Isolation period: Until declared free from infection by a physician.
Typhus fever is a term applied to several worldwide forms of disease that are caused by obligate
intracellular bacteria of the family Rickettsiaceae.
Each form of this disease is characterized by sudden onset of nonspecific symptoms that often include
fever, headache, chills, muscle aches, joint pains, and rash.
Malaise may progress to prostration. Anorexia, cough, and photophobia (pain from bright lights) may
also occur. Each species of rickettsia is transmitted via a particular arthropod vector, including ticks,
lice, fleas, and mites. Humans who engage in activities that bring them in close contact with vectors,
reservoirs, or both, are at increased risk for these zoonotic diseases.
The most serious of the typhus fevers is Rocky Mountain spotted fever (RMSF). This disease is carried
by a tickborne vector and is the most commonly encountered rickettsia in the United States. Persons
who have frequent outdoor exposures to ticks, including campers, hikers, fisherman, and hunters, are at
increased risk for infection. Other tickborne typhus fevers are named for the geographic region where
they are found.
Louse-borne typhus is transmitted within populations living at high altitudes or cold climates where
pediculosis is common and bathing and laundering of clothing are infrequent. The disruption of
community services, such as electricity and water supplies, that often accompanies armed conflict and
natural disasters, provides a potential setting for epidemics.
Brill-Zinsser disease occurs as a milder recurrence (recrudescence) among persons who have been
inadequately treated in the past for their louse-borne typhus (or among those who have recovered from
louse-borne typhus whose immune status has diminished).
Fleaborne typhus has a worldwide distribution but is uncommonly reported in the U.S. It is prevalent
among populations that live in close association with rodents and their fleas. Persons who have
occupational exposure to rodents (e.g., agricultural workers) are at risk.
111
Miteborne typhus (scrub typhus) is widespread throughout Asia and the Pacific Islands. Edge or scrub
vegetation provides habitat for rodent hosts of vector mites, and human populations that frequent these
areas, including military personnel and agricultural workers, have increased risk.
UNDULENT FEVER (BRUCELLOSIS, MALTA FEVER OR MEDITERRANEAN
FEVER)
Incubation period: Less than 5 days to several months, most cases occur 2 - 8 wks after exposure.
Isolation period: Unless the patient has a draining wound, no special precautions are required.
Brucellosis is acquired by direct contact with secretions and excretions of infected animals and by
ingestion of the milk of cows, sheep, or goats or the products of their milk (butter and cheese)
containing the Brucella organisms.
The disease is characterized by an acute febrile stage and by a chronic stage with relapses of fever,
weakness, sweats, and general aches and pains.
WHOOPING COUGH (PERTUSSIS)
Incubation Period: 7 to 14 days.
Isolation Period: For 4 weeks (after the cough begins.)
Whooping cough is a highly communicable bacterial disease that is caused by the bacillus Bordetella
pertussis. The coughing spasms often result in vomiting and are associated with the typical “whoop.”
The disease is spread by the patient’s respiratory secretions through coughing, sneezing, and close
contact.
The characteristic whooping type of cough reaches its worst stage about two or three weeks after
symptoms begin.
YAWS
Incubation Period: 9 to 90 days; generally 21 to 42 days.
Isolation Period: None. Avoid intimate contact and contamination of the environment prior to
treatment and until 48 to 72 hrs after penicillin treatment.
Yaws is a highly infectious, nonvenereal, bacterial tropical disease caused by Treponema pallidum,
subspecies pertenue, a species of spirochete similar to that of syphilis.
Yaws is limited to tropical and remote regions of Africa, South America, the Caribbean, Southeast Asia
and Indonesia. I
About a month after a person becomes infected, the first symptom appears as a painless inflamed
raspberry-red elevation of the skin. This is called the "mother yaw" that enlarges and forms an ulcer in
its center. The primary lesion may heal in a few weeks or persist for months if left untreated.
Two to eight weeks after the appearance of the "mother yaw," open oozing sores occur on the face,
scalp, trunk, hands, or feet.
The patient may show a slight rise in temperature, general malaise, headache, and pains in bones and
joints.
113
CHAPTER 21
Neurologic Disorders
Seizure Disorders and Epilepsy
A seizure is an uncommon event that can be caused by many different ailments and processes.
Not all convulsions become an epileptic condition, and most are brief and self-limited.
Once a “diagnosis” of epilepsy is documented, it will follow the patient for the rest of their life and
greatly impact their employability, insurability, driving status and many other areas.
Symptoms: Abrupt onset of abnormal muscle activity, or prodrome of confusion, déjà vu, peculiar
behavior, automatisms, or other psychic phenomena preceding onset.
Signs
Sudden onset of loss of consciousness, followed by abnormal motor activity such as tonicrigidity,
clonic rhythmic movements of the limbs, urinary incontinence, frothing at the mouth, and biting the
tongue and mouth; may last seconds to minutes, and is usually followed by a period of weakness,
somnolence and confusion (postictal state); will spontaneously stop without any intervention after a
few minutes.
Differential Diagnosis - the differential diagnosis of a convulsive event is extensive: idiopathic
epilepsy, alcohol or drug associated seizures, post concussive syndrome, convulsive syncope, heat
stroke, infectious (meningitis), brain mass lesions, nerve gas exposure and metabolic abnormalities.
Treatment:
Symptomatic treatment initially.
1. Remove the patient from an area where he could injure himself or others. Keep sharp and
breakable objects away from the patient. Pad objects if possible to avoid injury.
2. Do not put anything in the patient’s mouth. Never put your figers in the patient’s mouth.
3. MEDICATIONS ARE RARELY INDICATED FOR A FIRST TIME SEIZURE.
4. After the seizure, evacuate the patient to an appropriate treatment facility for a neurological
examination and further evaluation.
For recurrent seizures:
1. If the seizure lasts more than 10 minutes, immediate medical intervention is indicated.
2. Begin an IV access line.
3. EEG monitoring if available.
4. Give 5 to 10 mg IV Valium.
5. If this does not stop the seizure, consider Dilantin 1000 mg IV as an infusion over 30 minutes, not
to exceed 50 mg/min. When giving Dilantin as an infusion, do not mix it with D5W because it will
precipitate. Clear the IV tubing with normal saline first.
6. If this does not stop the seizure, consider Phenobarbital 10 mg/kg IV over 10 minutes. May be
repeated one time. Must have a secure airway and closely monitor breathing.
7. If this does not stop the seizure, general anesthesia or barbiturate coma may be required.
Advanced care will be required.
8. Transport to the nearest MTF for further evaluation and disposition.
Use Dilantin 300 mg po or IV qd y as these drugs may cause respiratory suppression.
114
If IV unavailable, Phenobarbital may be given IM. Do not give Dilantin or Valium IM.
NOTES: If seizure lasts more than ten minutes, there is the possibility of Status Epilepticus. These
seizures must be stopped ASAP. This is a life-threatening event and may produce significant brain
injury if the patient survives. Emergency medical assistance and intervention must be rapidly sought
Meningitis
Meningitis is an acute, life-threatening infection of the lining of the brain and spinal cord.
It can be caused by a virus, bacteria, fungus, parasite, or more complex organism.
Bacterial meningitis is rapidly progressive and should be considered an emergency.
Aseptic meningitis (normally caused by viruses) has a slower course. .
Symptoms: Fever, stiff neck, headache, photophobia, malaise; later: delirium, coma, seizures, nausea,
vomiting, dizziness
Signs
Fever to 104°F; cervical meningismus (stiff neck, painful to move); prostration; toxic appearance;
positive Kernig’s sign (inability to completely extend the knees straight – stretches spinal cord);
positive Brudzinski sign (forward flexion of the head produces flexion at hip and knee – stretches
spinal cord); rash (may indicate activation of the clotting cascade—hemorrhagic fevers; or petechial
with meningococcus).
Chronic infection: deafness.
NOTE: Do complete neurological examination, including Glasgow Coma Scale, looking for alterations
of mental status or ambulation, and focal neurological deficits. Perform a thorough examination for
possible sources of infection, such as middle ear, sinus, lungs, urinary tract, and wounds.
Lab: WBC count or blood smear (may show leukocytosis in bacterial meningitis), urinalysis; RPR,
blood cultures; chest X-ray
Differential Diagnosis:
If in doubt, treat for bacterial meningitis.
Meningitis comes in many forms that are infectious, the most common including bacterial and viral.
Fungal forms also may occur in immuno-compromised patients.
Other more rare forms include tuberculous, parasitic, spirochetal.
Rickettsial infection - usually no leukocytosis; no meningeal signs; “tache noire” lesion (ulcer covered
with black, adherent crust).
Leptospirosis - look for conjunctival discharge; history of exposure to water which might be
contaminated with animal urine
Cerebral malaria - no meningeal signs; positive blood smear; thrombocytopenia
Malignancy - variable symptoms based on lesion location.
Severe viral or bacterial sepsis with headache, high fever, but without meningeal seeding.
Brain abscess - focal neurologic ndings; low-grade temperatures; no neck stiffness or tenderness
Subdural/Epidural hematoma - history of trauma with rapid or progressive development of symptoms.
Subarachnoid hemorrhage - often low-grade temperature; acute onset preceded by severe head aches;
focal neurologic findings.
Stroke - variable symptoms based on lesion location.
115
Treatment:
1. Begin antibiotics as soon as possible if bacterial meningitis is suspected (time to antibiotic
administration is correlated with outcome). Empiric Choices: Penicillin: 24 million units/day in 6
divided doses, ampicillin: 12 gm/day in 6 divided doses, vancomycin: 2 gm/day in 2 divided doses,
ceftriaxone: 6 gm/day in 3 divided doses.
2. Evacuate immediately.
3. Airway support and oxygen. Intubate as needed.
4. Fluid hydration with IV NS or LR.
5. Control fever with Tylenol.
6. If viral meningitis is suspected (slower onset, less severe symptoms), give acyclovir 12.5
mg/kg/day IV divided tid x 10 days.
7. Consider steroids (Decadron 0.4 mg/kg q 12 hour for 4 doses), with first dose prior to starting
antibiotics, if bacterial meningitis is likely present (based on an acute presentation).
Bell’s Palsy (Idiopathic Facial Nerve Palsy)
Bell’s palsy is a common peripheral mononeuropathy involving the seventh cranial nerve. It usually
follows a benign course, has no obvious underlying cause and is a condition from which nearly all
patients recover fully.
Symptoms: Abrupt onset of ear pain followed by weakness in muscles of facial expression, slurred
speech and drooling when drinking; diminished or altered taste, increased sensitivity to sound on
the involved side; evolves over 1-2 days; bilateral involvement and numbness are rare.
Signs: Unilateral weakness (paresis) of the entire face, slurred speech and drooling
Differential Diagnosis:
Bilateral involvement can occur, but is rare and suggests more serious disease such as sarcoidosis,
Lyme disease or Guillain-Barre syndrome.
Idiopathic neuropathy
Herpes zoster - simultaneous characteristic vesicular eruptions in the ear canal or on the face.
Lyme disease - a history of tick bite and characteristic rash (erythema migrans).
Sarcoidosis - paralysis of additional parts of the nervous system. Guillain-Barre - absence of reflexes
are typical of Guillain-Barre.
Myasthenia gravis - weakness of additional muscles (especially the eye muscles, causing double
vision).
Peripheral Nerve System (PNS) Lesion - weakness of the forehead corrugator muscles and absence of
involve- ment in other parts of the nervous system suggest a more serious disorder such as a peripheral
nerve problem from a central lesion in the cerebrum or brainstem.
Treatment:
1. Protect the eye from exposure keratitis (dryness, erythema, poor vision) and foreign bodies by
wearing eyeglasses when outdoors and taping or patching the eye during sleep.
2. Instill artificial tears several times throughout the day and viscous artificial tears (if available)
at bedtime will help keep the eye surface lubricated and free of debris.
3. Prednisone 60mg/day po with taper over 10 – 14 days for severe cases. Most young adults will
make a full recovery with no treatments.
4. For herpes zoster, give Acyclovir 800 mg po five times a day x 5 days.
116
Examining the peripheral nerves
Whenever a patient has injured a limb, especially if he has a penetrating wound, test the function of its
nerves and tendons before you anaesthetize him.
Test the most distal point supplied by each nerve.
The following tests are so quick that you can do them all in a few seconds.
Always record your results. It will then be certain that paralysis is not the result of treatment.
QUICK TESTS FOR PERIPHERAL NERVES
Record both power and sensation when you first see a patient, and after each subsequent examination.
AXILLARY (CIRCUMFLEX) NERVE
This arises from the posterior cord of the bachial plexus, and winds round the neck of a patient’s
humerus to supply his deltoid and the skin over the lower part of this muscle. It is injured in
dislocations of the shoulder.
Ask the patient to abduct his arm. Put the palm of your hand over his deltoid. Even a flicker of
contraction shows that his deltoid is working.
Test sensation with a pin on the outer part of his shoulder, over the insertion of his deltoid. If his
axillary nerve has been injured, there will be a small patch of anaesthesia.
MUSCULOCUTANEOUS NERVE
If this nerve has been injured there will be anaesthesia along the outer side of his forearm, and he will
be almost unable to flex his arm.
SCIATIC NERVE
This is sometimes injured by pelvic fractures. Test its peroneal and tibial branches as described below.
Test the sensation of the dorsum of his foot.
SOME QUICK TESTS FOR PERIPHERAL NERVES.
Test the function of an injured patient’s nerves and tendons before you anaesthetize or refer him.
COMMON PERONEAL BRANCH OF SCIATIC NERVE
Paralysis causes foot drop. Can he walk on his heels with his forefoot raised? Test for anaesthesia in the
distribution of his deep peroneal nerve in the web between his big and second toe. His common
peroneal nerve can be injured by Thomas splints, badly applied skin traction, or blows to the neck of
his fibula.
TIBIAL BRANCH OF SCIATIC NERVE Ask him to plantar flex his ankle, or stand on tip toe.
118
CHAPTER 23
Toxicology
Poisoning: General
Almost anything in sufficient quantity can be toxic, even substances that are essential to life such as
water and oxygen.
A poison is any substance that even in small quantities produces harmful physiologic or psychological
effects.
Poisonings are responsible for 10% of all emergency department visits, 9% of all ambulance patient
transports, and 5%-10% of all medical admissions to hospitals.
Poisons enter the body through a variety of different routes - ingestion, inhalation, injection, and
surface or dermal absorption.
The toxic effects of ingested poisons may be immediate when inhaled or injected, or delayed when
absorbed through the skin or ingested.
Because most substances are absorbed through the small intestine, it may take several hours for
the poison to enter the bloodstream. Alcohol, which is absorbed in the stomach, is a notable
exception.
Use the mnemonic:
AEIOUTIPS to recall other causes of altered mental status:
A - Alcohol and other toxins/drugs,
E - Endocrine (hypothyroidism);
I - Insulin, too much (hypoglycemia), or Insulin, too little (hyperglycemia);
O - Opiates (heroin, morphine, etc.) and Oxygen, too little (hypoxia);
U - Uremia (kidney failure);
T - Trauma (head injury, shock)/Temperature (hyper/hypothermia);
I - Infection (meningitis, encephalitis);
P - Psychiatric (pseudocoma);
S - Space-occupying lesion (epidural/subdural hematoma), Stroke, Subarachnoid hemorrhage,
Shock.
When treating a poisoned/intoxicated patient, the medical practitioner should protect himself. If the
patient has been poisoned by a hazardous material, this substance may also pose a risk to the
practitioner .
Patients who are intoxicated may behave irrationally or violently.
Symptoms
An accurate history is the most important component of the workup.
If poisoning was suicidal in nature or involved the use of illicit drugs, history from patient is often
inaccurate or intentionally misleading.
Obtain history from family members and obtain description of the scene from persons who initially
found the patient. Determine which drugs (legal and illicit) or toxins to which the patient may have
had access. In the event of ingestion, determine what was ingested, when it was ingested, and
whether the patient vomited. In cases of possible occupational exposure, identify the patient’s job and
the types of toxins to which he/she may have been exposed.
119
Symptoms:
hr) Constitutional
recovery
Acute (< 2 hr)
Nausea/vomiting
Sub-acute (2-48 hr)
Signs/symptoms of
Chronic (>48
Death or
organ failure +/symptoms are
of
common
chronic organ
system
damage
Location: Three organ systems are most likely to produce immediate morbidity and mortality.
Respiratory
Difficulty breathing,
Shortness of
Recovery or
chronic
shortness of breath
breath on exertion
shortness of
breath,
chronic cough, etc…
Cardiovascular
Fainting/near fainting,
Postural hypotension,
Recovery or
symptoms
of
palpitations, chest pain
shortness of
breath on
exertion CHF
CNS
Hallucinations,
difficulty concentratingNumbness/tingling/
Recovery or
symptoms of,
visual disturbances
pain, long term visual
visual disturbances
painful sensations,
disturbances
learning disabilities,
chronic headaches
Signs
Focus of the initial physical examination should be on ruling out life/limb/sight threatening
conditions. In poisonings these involve the respiratory, cardiovascular, and central nervous systems.
Inspection: Should reveal spontaneous conversation, gait, posture, general appearance, affect
(depressed, agitated, happy) and appearance of the skin (needle track marks or other evidence of drug
use, evidence of trauma, discoloration).
Vital signs can indicate type and severity of systemic effects. Monitor cardiac function. Perform a basic
neuro examination with a focus on mental status (assess for agitation, mania, depression, etc., as well
as basic orientation) and eyes (pupil size, equality, and reactivity, nystagmus, visual acuity, and
extraocular muscles). Observe gait if possible and perform tests of cerebellar function (i.e.,finger-tonose, rapidly alternating hand movements, heel-to-shin, Romberg).
Signs
hr) Respiratory
Acute(< 2 hr)
Dyspnea, wheezing,
Sub acute (2-48 hr)
Shortness of
Chronic (>48
Recovery
or COPD,
stridor, apnea,
breath on exertion
restrictive
lung
disease,
hypo/hyperventilation,
emphysema, etc…
Cardiovascular
Hypo/hypertension,
Signs of ischemia/
Recovery or
signs of
infarction, postural recurrent
tachy/bradyarrhythmias
chronic CV disease,
hypotension, early CHF
tachy/bradyarrhytmia
CNS
Stroke, seizures, altered
Paralysis, seizures
Recovery or
persisting
mental status to include
persistent altered mental
persistent
mental
somnolence/depression
status
retardation,
paralysis, recurrent
seizures, coma, agitation/
vegetative
state
120
Pulse oximetry
(WARNING: Pulse oximetry may be normal in carbon monoxide poisoning, cyanide poisoning
initially, methemoglobinemia, and other conditions causing inadequate oxygenation of the tissues).
The presence of a normal pulse oximetry reading does not always indicate adequate oxygenation. EKG
(arrhythmias).
Lab: urinalysis, blood glucose. Drug testing
Differential Diagnosis: See AEIOU-TIPS discussion in Introduction.
Treatment
1. Secure airway. If patient is hypoxic and/or hypoventilating apply oxygen and assist respirations.
2. Start an IV in all presumed poisoned patients for drug access. Fluid resuscitate as needed to
support blood pressure.
3. Treat arrhythmias per ACLS.
4. Decontamination procedures: Decontaminate skin and mucous membranes as required with mild
soap and water. Remove patient from any further exposure to toxic vapors/fumes. Give syrup of
Ipecac (if within 20 minutes of ingestion), gastric lavage, and/or activated charcoal to minimize toxins
in the GI tract (see below).
NOTE: Inducing diarrhea is NOT effective and is likely to make the patient worse (dehydration,
electrolyte imbalance).
Syrup of ipecac - effective in some cases if administered within 20 minutes of ingestion.
1. Administration: a. In patients 1-12 years old, give 15 ml followed by 2-3 glasses of water. b. In
patients over 12 years, give 30 ml followed by 2-3 glasses of water. b. May be repeated in 20
minutes if vomiting does not occur.
2. Complications: Mallory-Weiss tear of the esophagus, causing bleeding; pneumomediastinum
(air trapped in chest cavity outside the lungs); diaphragmatic or gastric rupture; and/or aspiration
pneumonitis
3. Contraindications: Patient < 1 year old, altered level of consciousness (aspiration), ingestion of
caustic substances, loss of gag reflex, seizures, pregnancy, acute myocardial infarction, ingestion
of: acids, alkalis, ammonia, petroleum distillates, non-toxic agents, rapidly acting central nervous
system agents, or hydrocarbons.
Gastric lavage - may provide opportunity for immediate recovery of a portion of gastric contents.
1. Administration:
A. Use large-bore orogastric tube rather than a smaller nasogastric tube (Size 36-40 French for
adults, size 24-28 French for children).
B. Never insert large orogastric tubes nasally (may fracture/amputate nasal turbinate and/or
cause serious bleeding).
2. Complications: Agitation, tracheal intubation, esophageal perforation, aspiration pneumonitis,
pediatric fluid and electrolyte imbalances.
3. Contraindications: Altered levels of consciousness (relative contraindication if the airway is
protected), low-viscosity hydrocarbons or caustic agent ingestion.
Activated charcoal
1. Administration
a. Administering 20-30 minutes before gastric lavage may double the effectiveness of lavage. b.
Do not administer until after vomiting if ipecac has already been given.
c. Form slurry of 1-2 g/kg body weight (30-100 g for adults, 15-30 g for children), and administered
orally or by gastric tube.
2. INDICATIONS/ CONTRAINDICATIONS:
a. Safe and effective treatment in most toxic ingestions. b. Do not use for strong acid, strong alkali.
c. Not effective for cyanide, iron or alcohol
121
Venomous Snake Bite
Venomous snakes cause injuries and deaths worldwide in all temperate and tropical climates, but
they are a particular problem in Australia, which has 40% of the world’s neurotoxic snakes and
about 23% of all venomous snakes.
In North America, poisonous snakes cause only 14-20 deaths per year. The risk of death is greatest
in the very young, the very old, those with medical problems involving the cardiovascular and
respiratory systems and those who sustain multiple bites.
Only about 1/5 of snake bites in the U.S. are inflicted by venomous snakes and not all bites by
poisonous snakes result in envenomation.
Rattlesnakes fail to inject venom in up to 20% of bites.
Because snakes either hibernate or are inactive during winter, the peak snakebite season in
temperate climates is April-October.
In the United States the great majority of poisonous snakebites are caused by pit vipers
(Crotalidae), specifically rattlesnakes, copperheads and cottonmouth snakes.
Eastern and western diamondback rattlesnakes, although causing only about 10% of all snakebites
in the U.S., are responsible for 95% of all snakebite deaths in the U.S.
The other poisonous species of snakes in North America (not pit vipers) are the Eastern and Texas
coral snakes. They are members of the Elapidae family, along with cobras, kraits, and mambas.
Sea snakes belong to the Hydrophidae family.
Symptoms
Variable depending on type of snake, amount of venom injected, age of victim and other factors.
Crotalidae:
Acute (2 hr)
Sub-acute (2-48 hr)
Chronic (>48 hr)
Rapid onset
Persistent severe
Either improving or organ
of severe pain at bite site, pain, HA, thirst, dizziness,
system failure (renal,
severe HA, marked thirst.
chills, nausea.
Excessive perspiration
disseminated hemorrhage,
Little/no immediate pain
Hydrophidae:
Muscle aches/
Pruritus, fever, myalgia,at bite site
pains/stiffness and pain
on
arthritis
suggests serum passive movement of arm,
sickness secondary
to thigh,
neck, trunk muscles
antivenin admin.
Respiratory
Onset of anaphylaxis may be Elapidae/Hydrophidae: breathing, shortness of delayed > 2 hr.
Respiratory paralysis may be breath.
Elapidae/
SOB/ bronchospasm occur. prolonged (up to 7 days) Hydrophidae:
Severe Elapidae/Hydrophidae:
envenomation may cause respiratory paralysis/arrest respiratory paralysis/arrest possible
Cardiovascular
If anaphylaxis: Fainting/ Palpitations, shock symptoms Usually no long term
effects near fainting, shock symptoms, severe envenomation may cause arrest
GI
Nausea/Vomiting
Nausea/Vomiting
Usually
no long
Neuro
term effects
Elapidae/Hydrophidae:
Blurred vision
Elapidae/Hydrophidae:
Elapidae/Hydrophidae:
Paresthesias (numbness of
Recovery or possible
lips/soles of feet)
long-term numbness,
burning/
tingling sensation
122
Soft Tissue
Crotalidae: Usually two
Crotalidae: Significant
Crotalidae: Usually no long fang
punctures at site of swelling, tissue necrosis, term morbidity, rapid onset of petechiae, ecchymosis,
compartment syndrome, tissue swelling bullae– local & poss. diffuse
necrosis, ↓ROM may
occur
Lab: Hematocrit, urinalysis and 12-lead EKG to assess renal and cardiac complica- tions. Blood
transfusion: type and crossmatch as required.
Non-venomous snakebite; venomous bite from animal other than a snake; other sources of intoxication.
Treatment Goals: rapid transport to hospital-level care, delay progress of envenomation and
alleviate early symptoms.
Primary
1. Ensure airway is patent and adequate -- if not, secure airway. If hypoxic and/or
hypoventilating, apply O2 and assist respirations, prevent aspiration (lay the patient on their side),
intubate as required.
2. Start an IV in all snakebitten patients (in an unbitten extremity). Fluid resuscitation to support
blood pressure and maintain urine output (see below). Drink water as tolerated but otherwise
NPO. NO ALCOHOL! Be prepared for shock.
3. Monitor vital signs with pulse oximetry and cardiac monitoring if available. Treat arrhythmias
per ACLS guidelines – NOTE: Muscle breakdown may release significant potassium, so consider
hyperkalemia if arrhythmias occur.
4. Limit the systemic spread of the venom thru methods described below:
a. Keep the patient as calm and inactive as possible. Reassure. Give benzodiazepam (e.g., Valium 5
mg)
po as needed.
b. Gently clean around the bite site to remove any venom from the skin.
c. Immobilize the bitten limb in a dependant position.
d. Suctioning the bite site (NOT with mouth) within minutes after bite is reasonable if remote
from hospital care. Do not incise over the puncture site. The use of suction is controversial but all
agree: never use the mouth to apply suction. A syringe is a good alternative to other suction devices.
e. Do not apply tourniquets, ligatures, or constricting bands unless the snake is primarily
neurotoxic (Australian elapid, sea snake, krait, cobra or other neurotoxic species). Neurotoxic
bites only: apply a constricting band approximately 1 in. wide 2-4 inches above the bite and
loose enough to admit
a finger. Alternatively, wrap the bitten extremity with an elastic bandage or place it in an air splint.
Another method: Place a thick pad over the area of the bite and hold it in place with a tight wrap,
wrapping from distal to proximal. If more than 30 minutes after the bite, do not apply a constricting
band. Do NOT treat pit viper bites with these methods. Always check for a pulse after applying – this
is not a tourniquet!
f. Measure the circumference of a bitten extremity 10 cm proximal to the bite. Track this
measurement and pulses over time.
5. Remove all jewelry from bitten extremity.
6. Insert Foley catheter, record urine output and monitor fluid balance. Check urine for myoglobin
(positive for blood on urine dipstick but no RBCs on microscopic exam) and blood. Avoid
overhydration (rales, wheezing, orthopnea, respiratory distress, and distended jugular veins).
Cautiously hydrate to maintain
urine output > 30-50 cc/hr (adults). Administer furosemide (Lasix) up to 100 mg to promote urine
output as needed. Give low dose dopamine (2.5 kg/minute) by continuous infusion if necessary to
maintain urine output. Give adult victims with myoglobinuria and decreased urine output 25 grams of
Mannitol and 100 mEq (generally two ampules) sodium bicarbonate added to 1 liter 5% dextrose and
infused over 4 hours to prevent myoglobinuric nephropathy.
7. Treat pain with acetaminophen and opiates as required. Avoid NSAIDs, which interfere with
platelet function
123
8, Treat nausea/vomiting with Compazine (give slowly if administering by IV - this can cause/worsen
hypotension).
9. Give tetanus toxoid as required. Arguably this may overload the system and an alternative would be
tetanus antitoxin
10. DO NOT cauterize, incise, or amputate the bite site. DO NOT apply electric shock or pack
bitten limb in ice. These methods have been proven undocumented and unreliable. Anecdotal stories
were probably dry bites.
11. If the snake can be SAFELY killed, bring in for identification. Avoid handling the snake. Be sure
it is dead. WARNING – dead snakes can still reflexively bite!
12. Give antivenin, which is the only proven therapy for snakebite, only if it is specific for the snake
involved (monovalent), or if the envenomation is severe (polyvalent). See (and follow) package
insert for antivenin-specific instructions. The administration of any type of antivenin has a risk of
allergic reaction and serum sickness that can be life-threatening. DO NOT administer antivenin unless
the specific criteria for administration are met. Remember: death from snakebite is rare and snakebite
without envenomation is common. Inappropriate administration of antivenin can kill a patient who
would otherwise have survived without permanent sequelae. In the U.S. even when the offending
snake is venomous, and envenomation has occurred (e.g., copperhead), antivenin administration is
often not necessary.
13. Be prepared to treat anaphylaxis after giving antivenin with epinephrine 0.3 cc 1:1000 IM and
diphen- hydramine 50 mg IM. If patient rapidly becomes hypotensive and/or develops acute severe
respiratory distress it may necessary to give 1mg (10cc) 1:10000 epinephrine slowly by IV.
NOTES: 1. Snakebites on the extremities can produce extensive swelling that may (but rarely does)
lead to the development of a compartment syndrome (pain on passive stretching and active flexing of
the involved muscle groups, distal paresthesias, pulselessness, tense overlying tissues). Doing a
fasciotomy in a patient with a venom-induced bleeding disorder and local tissue necrosis may cause
significant, even life-threatening,
bleeding and/or infection. An aggressive surgical approach is more likely to cause harm than good, so
delay fasciotomy (see Procedures: Compartment Syndrome Management) as long as feasible.
2. Early, prophylactic, broad-spectrum antibiotic therapy (second-generation cephalosporin –
Keflex/Ancef) is reasonable but not generally recommended. If suction by mouth has been done,
prophylax with erythromycin. Treat infection, if it develops as appropriate. NOTE: Redness,
swelling, pain, and increased warmth in the surrounding tissue occur in both envenomation and
infection.
Alternate: Support the airway, maintain adequate oxygenation, ventilation, urine output and blood
pressure until specific, neutralizing, antivenin can be administered. There is no good evidence
supporting that any first aid measures aside from those describe herein.
3. Maintaining airway and urine output will save most patients. An overly aggressive surgical
approach and resorting to various unproven therapies will cause more harm than good.
4. In the proper circumstances, assume snakebite with envenomation and observe patient for 4-6 hours
for development of signs/symptoms. If no signs/symptoms after 6 hours, consider bite w/o
envenomation.
NOTES: Snake identification–Pit vipers: “pit” located below each nostril; triangular-shaped head;
elliptical, not round, pupils; hollow fangs; single, not double row of scales on the ventral (belly) side
distal to the anal plate; rattlesnakes usually have a rattle. Coral snakes in U.S. - encircling colored
bands of black, red and yellow/white, with the latter bands touching “red on yellow, kill a fellow;
red on black, venom lack”); no long fangs; small mouth makes it difficult for them to bite
anything larger than finger.
125
127
128
CHAPTER 28
VENAMOUS REPTILES
GUIDELINES AND CONSIDERATIONS:
• There are five venomous snake families:
1) Crotalidae. Uses hemotoxic venom. Includes all pit vipers (rattlesnake, copperhead,
cottonmouth, etc.)
2) Colubridae. Uses hemotoxic venom. Back fanged snakes. Limits ability to envenomate humans.
3) Elipidae. Uses neurotoxic venom. Includes cobras, mambas, kraits and coral snakes.
4) Viperdae. Uses hemotoxic venom. True vipers. Includes puff adders, vipers and desert adders.
5) Hydrophidae. Uses neurotoxic venom. Sea snakes.
• The majority of snakebite victims survive.
• Not all bites from poisonous snakes involve injection of venom: Up to 50% of cobra bites and 30%
of rattlesnake bites are ‘dry strikes’, meaning no venom is injected.
• Operators should be familiar with the types of venomous snakes found in their area of operation, and
the recommended field treatment of bites.
NOTE 1: All snake venoms (and some large breed lizards) contain components that are neurotoxic and
hemotoxic. You will see neurotoxic reactions to primary hemotoxic venoms and hemotoxic reactions to
primary neurotoxic venoms.
NOTE 2: Bites from large breed lizards (Gila Monster, Komodo Dragon, Monitor, etc) carry a high
incidence of infection. Debride aggressively and administer antibiotics.
WARNING: Snakebite is a true emergency, requiring fast action and emergency evacuation of the
victim.
HEMOTOXIC ENVENOMATIONS: Most common with pit vipers (rattlesnakes, copperheads,
cottonmouth moccasins, Fer-de-Lance and Bushmaster) and old world vipers.
Signs & Symptoms: Swelling and blistering at bite site; muscle fasciculation, weakness and syncope;
nausea & vomiting; chills, hypotension, lymphangitis, and respiratory distress may occur; GI and GU
bleeding may occur; Bite site tends to ooze blood constantly. Moderate to severe pain at the bite site,
starting within a few seconds of the bite; perioral numbness and tingling; metallic taste in the mouth
may occur.
NEUROTOXIC ENVENOMATIONS: Most common in bites from Elapids (cobras, coral snakes,
kraits), sea snakes, and most snakes found in Australia.
Signs & Symptoms: Mild pain or painless bite site; Numbness or tingling of bite site; perioral
numbness and metallic taste in mouth may occur. Muscle weakness, uncoordination, fasciculation’s;
difficulty in swallowing and speaking may occur; Visual disturbances, ptosis, respiratory distress,
hypotension and convulsions may occur. Respiratory paralysis may occur. NOTE: Neurotoxic
symptoms may take hours to appear and then progress rapidly.
Treatment:
1. Extractor Pump: The extractor pump (NSN 6545-01-281-1237) is known to be effective in pit viper
envenomations and is likely to be effective in elapid envenomations, removing up to 30% of the
injected venom load. It should be applied to the bite site as soon as possible after the bite (Pump is
most effective if applied within 3 minutes). Empty the bell of the pump as it fills with fluid, and reapply. Continue for 30-60 minutes. If a suction device is not available, a syringe with an enlarged tip
can be used.
NOTE 1: No incisions should be made.
NOTE 2: Mouth or rubber bulb suction is NOT a substitute for an extractor pump.
Compression/Immobilization (Used for neurotoxic-predominant bites): Apply an ace wrap and splint to
the bitten extremity. Wrap proximal to distal and slightly tight. Wrap so the extractor pump/bite site is
accessible. Do not remove wrap until at a medical facility.
129
NOTE 3. Proximal Constriction Band (Used for hemotoxic-predominant bites): Use a 1” wide penrose
drain or similar wide band. Place above the bite site, just tight enough to indent the skin (should be
loose enough to slip one finger between the band and skin). Check proximal pulses frequently. If the
band becomes too tight as a result of swelling, place a second band above the first before releasing the
first band. Once a constriction band has been placed, do not remove until at a medical facility. NOTE:
This is not a tourniquet!
•
Venomous snakes found in the United States include rattlesnakes, copperheads,
cottonmouths/water moccasins, and coral snakes.
•
It has been estimated that 7,000–8,000 people per year receive venomous bites in the United
States, and about 5 of those people die.
•
Rattlesnakes are the largest of the venomous snakes in the United States.
•
They can accurately strike at up to one-third their body length. Rattlesnakes use their rattles or
tails as a warning when they feel threatened.
Rattlesnake
Timber Rattlesnake
Western Diamond Back
Range and habitat
•
Western diamondback rattlesnake (Crotalus atrox), responsible for the majority of venomous
snakebites in North America, coiled in defensive posture with rattle erect
•
Most species live near open, rocky areas. Rocks offer them cover from predators, plentiful
prey (e.g. rodents, lizards, insects, etc. that live amidst the rocks), and open basking areas.
•
Snakes prefer a temperature range between 80 and 90°F (26-32°C), but can survive from brief
exposure to temperatures as low as 4°F (-16°C), and surviving for several days in temperatures as low
as 37°F (3°C).
130
Effects of a rattlesnake bite
•
Rattlesnakes are a group of venomous snakes of the genera Crotalus and Sistrurus of the
subfamily Crotalinae ("pit vipers").
•
There are 32 known species of rattlesnake, with between 65-70 subspecies, all native to the
Americas, ranging from southern Alberta and southern British Columbia in Canada to Central
Argentina.
•
All rattlesnakes possess a set of fangs with which they inject large quantities of hemotoxic
venom.
•
The venom travels through the bloodstream, destroying tissue and causing swelling, internal
bleeding, and intense pain.
•
Some species, such as the and the Mojave Rattlesnake, additionally possess a neurotoxic
component in their venom that causes paralysis and other nervous symptoms.
•
Rattlesnakes are the leading cause of snakebite injuries in North America. However,
rattlesnakes rarely bite unless provoked or threatened; and if treated promptly, the bites are rarely fatal.
Venom
•
Most species of rattlesnakes can control how much venom to inject and have hemotoxic venom,
destroying tissue, causing necrosis and coagulopathy (disrupted blood clotting).
•
In the U.S., the Tiger rattlesnake (C. tigris) and some varieties of the Mojave rattlesnake (C.
scutulatus) also have a presynaptic neurotoxic venom component known as Mojave Type A toxin,
which can cause severe paralysis.
•
Although it has a comparatively low venom yield, the venom toxicity of C. tigris is considered
to be the highest of all rattlesnake venoms, and the highest of all snakes in the Western Hemisphere. C.
scutulatus is also widely regarded as producing one of the most toxic snake venoms in the Americas.
•
Rattlesnake venom is a mixture of 5-15 enzymes, various metal ions, biogenic amines, lipids,
free amino acids, proteins, and polypeptides.
•
It contains components designed to immobilize and disable the prey, as well as digestive
enzymes which break down tissue to prepare for later ingestion. The venom is very stable, and retains
its toxicity for many years in storage.
Hibernation
•
•
Some rattlesnake species hibernate in the colder winter months.
They often gather together for hibernation in very large numbers (sometimes over 1,000
snakes), huddling together inside underground "rattlesnake dens" or hibernacula.
•
Rattlesnakes often return to the same den, year after year, sometimes traveling several miles to
get there.
131
Rattlesnake bites are painful when they occur. Symptoms usually begin right away and may include:
Bleeding
Breathing difficulty
Weakness
Blurred vision
Eyelid drooping
Weak pulse
Low blood pressure
Nausea and vomiting
Tiredness
Numbness
Pain at site of bite
Thirst
Paralysis
Rapid pulse
Tissue damage
Skin color changes
Swelling
132
Copperheads
•
Copperheads vary in color from reddish to golden tan.
•
The colored bands on their body are typically hourglass-shaped. Most adults are 18–36 inches
long. Rattlesnakes may be found sunning themselves near logs, boulders, or open areas. These snakes
may be found in most work habitats including the mountains, prairies, deserts, and beaches.
•
They are not usually aggressive, but will often freeze when frightened.
•
Copperheads are often found in forests, rocky areas, swamps, or near sources of water like
rivers.
Cottonmouths/Water Moccasins
Results of a cottonmouth strike
133
•
Cottonmouth snakes average 50–55 inches long.
•
The adult snake’s skin is dark tan, brown, or nearly black, with vague black or dark brown
crossbands.
•
Juveniles have a bold crossbanded pattern of brown or orange with a yellow tail.
•
Cottonmouths are frequently found in or around water. They do not scare easily and will
defend themselves when threatened.
U.S. Geographic Region: Wetland areas, rivers, lakes, etc., in the southeastern states.
Cottonmouth and copperhead bites are painful right when they occur. Symptoms, which usually begin
right away, may include:
•
•
•
•
•
•
Bleeding
Breathing difficulty
Low blood pressure
Nausea and vomiting
Numbness and tingling
Pain at site of bite
•
•
•
•
•
•
•
•
Shock
Skin color changes
Swelling
Thirst
Tiredness
Tissue damage
Weakness
Weak pulse
Scarlet King Snake
Note that the head does NOT have a blake nose
134
Western Coral Snake
Micrurus fulvius
Months after a coral snake bite
Venomous; 20-35 inches (508 to 890 mm)

Sandhills, wooded & wiregrass areas in sandy soil are home to this rare, small, secretive snake,
which spends most of its life underground.

It burrows in sand, leaf litter, and under loose boards, tin, or logs.

Coral Snake always has a bulbous black and yellow head, and the red bands are bordered with
yellow. The more common nonvenomous look-alikes have red on their heads, and the red bands are
bordered with black.
Coral snakes are related to cobras and sea snakes. Coral snakes are not pit vipers, and do not have
triangular shaped heads or cat's eye pupils. Although the venom is extremely toxic, this snake is quite
docile and is unlikely to bite unless handled or stepped on.
U.S. Geographic Region: Wooded, sandy, or marshy areas of the Southern United States.
Symptoms
Signs or symptoms associated with a snake bite may vary depending on the type of snake, but may
include:
•
A pair of puncture marks at the wound
•
Redness and swelling around the bite
•
Severe pain at the site of the bite
•
Nausea and vomiting
•
Labored breathing (in extreme cases, breathing may stop altogether)
•
Disturbed vision
•
Increased salivation and sweating
•
Numbness or tingling around your face and/or limbs
Preventing Snake Bites
•
Do not try to handle any snake.
•
Stay away from tall grass and piles of leaves when possible.
•
Avoid climbing on rocks or piles of wood where a snake may be hiding.
•
Be aware that snakes tend to be active at night and in warm weather.
•
Wear boots and long pants when working outdoors.
•
Wear leather gloves when handling brush and debris.
135
First Aid
•
Seek medical attention as soon as possible (dial 911 or call local Emergency Medical Services.)
•
Try to remember the color and shape of the snake, which can help with treatment of the snake
bite.
•
Keep still and calm. This can slow down the spread of venom.
•
Inform your supervisor.
•
Apply first aid if you cannot get to the hospital right away.
•
Lay or sit down with the bite below the level of the heart.
•
Wash the bite with soap and water.
•
Cover the bite with a clean, dry dressing.
Do NOT do any of the following:
•
•
•
•
•
•
•
•
Do not pick up the snake or try to trap it.
Do not wait for symptoms to appear if bitten, seek immediate medical attention.
Do not apply a tourniquet.
Do not slash the wound with a knife.
Do not suck out the venom.
Do not apply ice or immerse the wound in water.
Do not drink alcohol as a painkiller.
Do not drink caffeinated beverages.
Antivenin
•
Antivenin, often referred to as antivenom, is commonly used to treat the effects of local and
systemic pit viper envenomations
•
Because antivenin is derived from animal antibodies, people generally display an allergic
response during infusion, known as serum sickness.
•
When a bite occurs the amount of venom injected is under voluntary control by the snake.
•
Approximately 20% of bites result in no envenomation at all. A lack of burning pain and edema
3⁄8 in (1 cm) away from the fang marks after 1 hour suggests that either no or minimal envenomation
occurred. A lack of edema or erythema in the area of the bite after 8 hours indicates a lack of
envenomation for most rattlesnake bites.
Gila Monster or Mexican Beaded Lizard
Report on envenomation by a Gila monster (Heloderma suspectum) with a discussion of venom
apparatus, clinical findings, and treatment.
Source
137
Reptile Research and Breeding Facility, Cincinnati, OH 45238, USA.
Abstract
•
Human envenomations by Heloderma species are a rare but clinically important medical
problem. We report a case of an adult male bitten on the left hand by a 50-cm male, captive specimen
of Heloderma suspectum (Gila monster).
•
Immediate signs and symptoms included pain at the bite site radiating into the arm and axilla
and swelling of the hand and forearm.
•
Systemic complaints of nausea, diaphoresis, and dizziness (without a decrease in blood
pressure) lasted approximately 1 hour, and laboratory studies were normal.
•
The patient's course was uneventful except for persistent hyperesthesia, which eventually
abated.
•
Two types of helodermatid bites produce distinct clinical pictures.
•
The chewing bite potentially causes more envenomation than the slashing bite.
•
The venom contains a number of protein and nonprotein components including serotonin, a
bradykinin-releasing substance, protease, hyaluronidase, helodermin, and gilatoxin.
•
The clinical presentation of a helodermatid bite can include pain, edema, hypotension, nausea,
vomiting, weakness, and diaphoresis.
•
No antivenin is commercially available. Treatment is supportive.
138
CHAPTER 29
ARACHNID AND ARTHROPOD BITES AND STINGS
NOTE: This list is not inclusive. Investigate those types that are specific to your operation location and
consult with a qualified medical officer for specific treatment.
BLACK WIDOW SPIDER ENVENOMATION
Signs & Symptoms:
•
Pinprick sensation followed by minimal swelling and erythema;
•
Fang marks may be noted; Sometimes the bite is not felt.
•
Dull crampy pain may develop at sign of bite and later spread to entire body.
•
Generally, the pain is spread to the chest from upper extremity bites and to the abdomen from
lower extremity bites.
•
Abdominal cramping may be severe and mimic appendicitis.
•
Other symptoms include dizziness, restlessness, nausea, vomiting, diaphoresis, and cramping in
all muscle groups.
•
The patient may become hypertensive.
Treatment:
1.
2.
3.
4.
5.
Ice application to the area.
IV access in unaffected extremity.
Monitor airway, breathing and circulation.
If significant symptoms, consider immediate evacuation.
IV Diazepam can be given to control muscle cramping.
139
BROWN RECLUSE SPIDER BITE
Signs & Symptoms: Initial burning at site of bite, most notably within 3-4 hrs. White area then forms
from local vasoconstriction followed a central blister with surrounding erythema. The blister then
darkens as necrosis appears. Patient may exhibit or complain of fever, rash, chills, nausea, vomiting,
malaise and weakness.
Treatment:
•
Clean area with soap and water.
•
Transport as needed.
Chagas disease or American trypanosomiasis
A tropical parasitic disease caused by the flagellate protozoan Trypanosoma cruzi
T. cruzi is commonly transmitted to humans and other mammals by an insect vector, the blood-sucking
"kissing bugs"
Symptom:
Acute stage: mild and usually produce no more than local swelling at the site of infection.
The initial acute phase is responsive to antiparasitic treatments, with 60–90% cure rates.
140
After 4–8 weeks, individuals with active infections enter the chronic phase of Chagas disease, which is
asymptomatic for 60–80% of chronically infected individuals through their lifetime.
Treatment:
The currently available antiparasitic treatments for Chagas disease are benznidazole and nifurtimox,
which can cause temporary side effects in many patients including skin disorders, brain toxicity, and
digestive system irritation.
End stage Chagas disease is achieved by a devastating invasion of the Autonomic Nervous System,
especially the Parasympathetic influence of the Vagus Nerve.
The acute phase lasts for the first few weeks or months of infection. It usually occurs unnoticed
because it is symptom-free or exhibits only mild symptoms that are not unique to Chagas disease.
These can include fever, fatigue, body aches, headache, rash, loss of appetite, diarrhea, and vomiting.
The signs on physical examination can include mild enlargement of the liver or spleen, swollen glands,
and local swelling (a chagoma) where the parasite entered the body.
The primary wildlife reservoirs for Trypanosoma cruzi in the United States include opossums,
raccoons, armadillos, squirrels, woodrats, and mice
The most recognized marker of acute Chagas disease is called Romaña's sign, which includes swelling
of the eyelids on the side of the face near the bite wound or where the bug feces were deposited or
accidentally rubbed into the eye.
Of individuals with chronic Chagas disease, 60–80% will never develop symptoms (called
indeterminate chronic Chagas disease), while the remaining 20–40% will develop life-threatening heart
and/or digestive disorders during their lifetime (called determinate chronic Chagas disease). In 10% of
individuals, the disease progresses directly from the acute form to a symptomatic clinical form of
chronic Chagas disease
There are two approaches to treating Chagas disease, antiparasitic treatment, to kill the parasite; and
symptomatic treatment, to manage the symptoms and signs of the infection.
Antiparasitic treatment is most effective .
Drugs of choice include azole or nitro derivatives, such as benznidazole or nifurtimox.
Both agents are limited in their capacity to effect parasitologic cure (a complete elimination of T. cruzi
from the body), especially in chronically infected patients, and resistance to these drugs has been
reported
Chronic stage:
The disease cannot be cured in this phase
Chronic heart disease caused by Chagas disease is now a common reason for heart transplantation
surgery.
Until recently, however, Chagas disease was considered a contraindication for the procedure.
, since the heart damage could recur as the parasite was expected to seize the opportunity provided by
the immunosuppression that follows surgery.
142
SCORPION ENVENOMATION
Scorpions have two eyes on top of the head
Two to five pairs of eyes along the front corner of the head
Scorpions don’t see well and must rely on their pectines for sense of touch to find prey and for
navigation.
They have a well developed sense of hearing
Scorpions range in size from ½ inch to 7 ½ in length
Usually tan with flat bodies that enable them to hide in small cracks, under rocks and in bark
Average litter is 13 to 47
Scorpions fluoresce under an ultraviolet light
Scorpions have adapted to desert living with extra layers of fats on their exoskeleton that minimizes
water loss.
Scorpions do drink water but they derive most of their water from food
Scorpions have been known to survive 4 to 5 months without food
Scorpions are most active at nighttime temperatures are above 70 degrees.
Less active during winter and the hottest part of the summer during daylight hours
Signs & Symptoms: Local erythema and swelling may or may not be present. There can be increased
sensitivity to the area, along with numbness and weakness. Multiple symptoms may develop to include
anxiety, restlessness, muscle spasm, nausea, vomiting, excessive salivation, sweating, itching of the
nose and throat, hyperthermia, blurred vision, pseudoseizures, hypertension, hemiplegia, syncope,
cardiac arrhythmias, or respiratory distress. Symptoms can occur over 24 hrs, or respiratory arrest can
occur within 30 min.
NOTE: The less dangerous the species, the more local the reaction will be. The more dangerous the
species, the less the local reaction will be.
Treatment:
1. Ice application to the area.
2. IV access in unaffected extremity.
3. Monitor airway, breathing and circulation.
4. Arrange for immediate evacuation if possible.
5. IV Diazepam can be given to control seizures and muscle spasm.
143
Whipscorpions
Live under logs, rocks, bark
Active at night
Mastigoproctus giganteus (Vinegaroon)
Can pinch
Sprays vinegar when surprised
84% acetic acid
Can blister human skin
Tarantulas
Large, wandering predatory spiders
About 30 U.S.species
Relatively docile
Rarely bite
Bite produces local pain, edema, lymph node swelling
Flick irritating abdominal hairs if bothered
144
Hobo Spider (Tegenaria agrestis)
Found in the Pacific northwest of the US
They are aggressive because it bite with minor provocation.
Live in moist dark areas (woodpiles/basements).
They are brown with grey markings, have 7 – 14mm body length and 27 – 45mm leg span
•
•
•
•
Present similar to that of brown recluse spider.
Initial bite is painless ! delay presentation
Induration may occur with surrounding erythema, followed by blistering, rupture, and necrosis.
HA is the most common systemic symptom, but N/V and fatigue can occur.
•
Aplastic anemia and death are rare complications.
146
CHAPTER 30
BEES, WASPS, HORNETS AND ANTS
50% of 2006 sting patients experiencing allergic reaction had NO previous warning symptoms!
Hymenoptera:
Most important venomous insect known to humans
More fatalities result from stings by these insects.
Three major subgroups:
Apidae
includes honeybee and bumblebee
Vespidae & includes yellow jackets, hornets and wasps
Formicidae
ants
Most of all allergic reaction reported yearly occur from vespid stings.
Female bee is capable of stinging only once. (Male bees have no stinger).
Vespid have ability to perform multiple sting
Hymenoptera Venom
Contain several components.
Histamine is only a minor component within the venom.
50% of the venom consist of Melittin.
Melittin is a known membrane-active polpeptide that can cause degranulation of basophils and mast
cells.
Yellow jackets venom is perhaps the most potent sensitizer.
Venom:
Local Reaction
Urticarial lesion contiguous with the sting site.
Severe local reaction may involve one or more neighboring joints.
If the sting involve the mouth or throat, it can produce airway obstruction.
Toxic Reaction
Multiple stings (Africanized bees) can lead to systemic toxic reaction.
Symptoms may resemble anaphylaxis, but these pts can also develop N/V/D.
They may also have HA, fever, drowsiness, involuntary muscle spasms, edema without urticaria, and
convulsions.
Signs & Symptoms:
Initially will experience burning pain later followed with itching.
If allergic, symptoms of anaphylactic reaction may develop.
147
Locally reaction includes redness and swelling at site of bite.
Systemic reaction occurs due to an allergic response: wheezing, urticaria, abdominal cramps,
generalized edema, nausea, vomiting, dizziness, hypotension, confusion, and anaphylactic type
reaction.
Treatment:
1. Local Reaction:
a. If stinger is present: remove by scraping. b. Wash site with soap and water.
c. Apply cold compress.
δ.
Antihistamines may be useful if not contraindicated
Ants (Formicidae)
5 known species of fire ants (Solenopsis) (S. aurea, S. geminata, S. xyloni, S. invicta, and S. richteri)
•
Fire ants swarm when provoked and they may attack in numbers.
•
Fire ants sting simultaneously in response to an alarm pheromone released
•
Fire ants sting result in a papule that becomes a sterile pustule in 6 to 24 hrs.
•
Pustule can lead to localized necrosis
scarring
secondary infection.
•
Systemic reaction (urticaria / angioedema) can also occur.
•
Treatment includes:
•
•
local wound care.
Usual treatment for anaphylaxis should be initiated if there is evidence of systemic reaction.
148
CHAPTER 31
POISONOUS PLANTS
Many native and exotic plants are poisonous to humans when ingested or if there is skin contact with
plant chemicals. However, the most common problems with poisonous plants arise from contact with
the sap oil of several ever-present native plants that cause an allergic skin reaction—poison ivy, poison
oak, and poison sumac.
Poison ivy, poison oak, and poison sumac release an oil, urushiol, when the leaf or other plant parts are
bruised, damaged, or burned. When the oil gets on the skin an allergic reaction, referred to as contact
dermatitis, occurs in most exposed people as an itchy red rash with bumps or blisters. When exposed to
50 micrograms of urushiol, an amount that is less than one grain of table salt, 80 to 90 percent of adults
will develop a rash. The rash, depending upon where it occurs and how broadly it is spread, may
significantly impede or prevent a person from working. Although over-the-counter topical medications
may relieve symptoms for most people, immediate medical attention may be required for severe
reactions, particularly when exposed to the smoke from burning these poisonous plants. Burning these
poisonous plants can be very dangerous because the allergens can be inhaled, causing lung irritation.
Outdoor workers may be exposed to poisonous plants. Outdoor workers at risk include farmers,
foresters, landscapers, groundskeepers, gardeners, painters, roofers, pavers, construction workers,
laborers, mechanics, and any other workers who spend time outside. Forestry workers and firefighters
who battle forest fires are at additional risk because they could potentially develop rashes and lung
irritation from contact with damaged or burning poisonous plants. It is important for employers to train
their workers about their risk of exposure to poisonous plants, how they can prevent exposures and
protect themselves, and what they should do if they come in contact with these plants.
149
Plant Identification
The old saying "Leaves of three, Let it be!" is a helpful reminder for identifying poison ivy and oak,
but not poison sumac which usually has clusters of 7-13 leaves. Even poison ivy and poison oak may
have more than three leaves and their form may vary greatly depending upon the exact species
encountered, the local environment, and the season. Being able to identify local varieties of these
poisonous plants throughout the seasons and differentiating them from common nonpoisonous look-alikes are the major keys to avoiding exposure.
Poison Ivy
Eastern poison ivy is typically a hairy, ropelike vine with three shiny green (or red in the fall) leaves
budding from one small stem
Western poison ivy is typically a low shrub with three leaves that does not form a climbing vine
•
May have yellow or green flowers and white to green-yellow or amber berries
Poison Oak
Typically a shrub with leaves of three, similar to poison ivy
•
•
Pacific poison oak may be vine-like
May have yellow or green flowers and clusters of green-yellow or white berries
Poison Sumac
•
Woody shrub that has stems that contain 7-13 leaves arranged in pairs
•
May have glossy, pale yellow, or cream-colored berries
Exposure
Workers may become exposed to urushiol through:
•
Direct contact with the plant
•
Indirect contact, such as touching tools, livestock, or clothing that have urushiol on them
•
Inhalation of particles containing urushiol from burning plants
Symptoms
Signs or symptoms associated with dermal contact with poisonous plants may include:
•
Red rash within a few days of contact
•
Possible bumps, patches, streaking, or weeping blisters (blister fluids are not contagious)
•
Swelling
•
Itching
First Aid
Anyone who has come in contact with poisonous plants should:
•
Immediately rinse skin with rubbing alcohol, specialized poison plant washes, degreasing soap
(such as dishwashing soap) or detergent, and lots of water.
•
Rinse frequently so that wash solutions do not dry on the skin and further spread the
urushiol.
•
Apply wet compresses, calamine lotion, or hydrocortisone cream to the skin to reduce itching
and blistering.
•
Follow the directions on any creams and lotions. Do not apply to broken skin, such as
open blisters.
•
Oatmeal baths may relieve itching.
•
An antihistamine such as diphenhydramine (Benadryl) can be taken to help relieve itching.
•
Follow directions on the package.
•
Drowsiness may occur.
150
•
If children come in contact with work clothing contaminated with urushiol, a
pediatrician should be contacted to determine appropriate dosage.
•
In severe cases or if the rash is on the face or genitals, seek professional medical attention.
•
Call 911 or go to a hospital emergency room if the worker is suffering a severe allergic reaction,
such as swelling or difficulty breathing, or has had a severe reaction in the past.
Common Poisonous Plants and Plant Parts
Vegetation helps sustain life. We eat many plants, herbs and so forth in our daily diet. But, we must
remember to be choosy. Some plants, trees or shrubs are potential killers of man. Some part of the
ornamental plants or flowers in your yard may contain deadly poison. Many poisonous plants are so
common and seemingly innocuous you do not suspect their toxic qualities.
For example, who would expect that the beautiful oleander bush-grown indoors and outdoors all over
the country-contains a deadly heart stimulant, similar to the drug digitalis?
It is easy to be deceived by plants…one part may be edible while another is poisonous. The following
chart lists some of the more common poisonous plants.
PLANT
Hyacinth, Narcissus,
Daffodil
Oleander
PART
Bulbs
Nausea, vomiting, diarrhea. May be fatal.
Leaves, branches
Extremely poisonous. Affects the heart, produces
severe digestive upset and has caused death.
Dieffenbachia (Dumb Cane),
All parts
Elephant Ear
Rosary Pea, Castor
Bean
SYMPTOMS
Seeds
Intense burning and irritation of the mouth and
tongue. Death can occur if base of the tongue swells
enough to block the air passage of the throat.
Fatal. A single Rosary Pea seed has caused death.
One or two Castor Bean seeds are near the lethal
dose for adults.
FLOWER GARDEN PLANTS
Larkspur
Young plant,
seeds
Digestive upset, nervous excitement, depression.
May be fatal.
Monkshood
Fleshy roots
Digestive upset and nervous excitement.
Autumn Crocus, Star of
Bethlehem
Lily-of-the-Valley
Iris
Foxglove
Bleeding Heart
Bulbs
Leaves, flowers
Underground
stems
151
Vomiting and nervous excitement.
Irregular heart beat and pulse, usually accompanied
by digestive upset and mental confusion.
Severe-but not usually serious-digestive upset
.
Leaves
Large amounts cause dangerously irregular heartbeat
and pulse, usually digestive upset and mental
confusion. May be fatal.
Foliage, roots
May be poisonous in large amounts. Has proved fatal
to cattle.
VEGETABLE GARDEN PLANTS
Rhubarb
Leaf blade
Fatal. Large amounts of raw or cooked leaves can
cause convulsions, coma, followed rapidly by death.
ORNAMENTAL PLANTS
Daphne
Berries
Fatal. A few berries can kill a child.
Wisteria
Seeds, pods
Mild to severe digestive upset. Many children are
poisoned by this plant.
Golden Chain
Jasmine
Bean-like
capsules in
which the seeds
Severe poisoning. Excitement, staggering,
are suspended
convulsions and coma. May be fatal
Berries
Lantana Camara (Red Sage) Green berries
Yew
Berries, foliage
Fatal. Digestive disturbance and nervous symptoms.
Fatal. Affects lungs, kidneys, heart and nervous
system. Grows in the southern U.S. And in moderate
climates.
Fatal. Foliage more toxic than berries. Death is
usually sudden without warning symptoms.
TREES AND SHRUBS
Wild and cultivated cherries Twigs, foliage
Oaks
Elderberry
Black Locust
Foliage, acorns
Fatal. Contains a compound that releases cyanide
when eaten. Gasping, excitement and prostration are
common symptoms.
Affects kidneys gradually. Symptoms appear only
after several days or weeks. Takes a large amount for
poisoning.
Children have been poisoned by using pieces of the
All parts,
pithy stems for blowguns. Nausea and digestive
especially roots
upset.
Bark, sprouts,
foliage
Children have suffered nausea, weakness and
depression after chewing the bark and seeds.
152
PLANTS IN WOODED AREAS
Jack-in-the-Pulpit
Like Dumb Cane, contains small needle-like crystals
All parts,
of calcium oxalate that cause intense irritation and
especially roots
burning of the mouth and tongue.
Moonseed
Berries
Blue, purple color, resembling wild grapes. May be
fatal.
Mayapple
Apple, foliage,
roots
Contains at least 16 active toxic principles, primarily
in the roots. Children often eat the apple with no ill
effects, but several apples may cause diarrhea.
Mistletoe
Berries
Fatal. Both children and adults have died from eating
the berries.
PLANTS IN SWAMP OR MOIST AREAS
Water Hemlock
All parts
Fatal. Violent and painful convulsions. A number of
people have died from hemlock.
PLANTS IN FIELDS
Buttercups
All parts
Irritant juices may severely injure the digestive
system.
Nightshade
Poison Hemlock
All parts,
Fatal. Intense digestive disturbance and nervous
especially the
symptoms.
unripened berry
All parts
Jimson Weed (Thorn Apple) All parts
Fatal. Resembles a large wild carrot.
Abnormal thirst, distorted sight, delirium,
incoherence and coma. Common cause of poisoning.
Has proved fatal.
154
CHAPTER 32
Poisonous Marine Animals
NOTE: This section does not address all the many creatures that can envenomate humans, but does
include the noteworthy ones.
Jelly Fish Stings
Photo courtesy of Wikimedia
Jellyfish
Most jellyfish stings are mild and don’t require treatment or can be treated yourself.
However, seek medical assistance (dial 999) if there are severe symptoms, such as difficulty breathing,
chest pain, or if a large or sensitive area of the body, such as the face or genitals, has been stung.
Get the Person Out of the Water
Applying shaving cream to the affected area will help prevent the spread of toxins. Use a razor blade,
credit card or shell to remove any nematocysts (small poisonous sacs) that are stuck to the skin
Stop Stinging [don't use vinegar or alcohol to wash the affected area because it can make the pain
worse.The use of other substances, such as alcohol and baking soda, should also be avoided.]
For a jellyfish sting in non-tropical waters:
• Wash the area with seawater to deactivate stinging cells.
For a sting in tropical waters -- especially from box jellyfish:
• Rinse immediately with vinegar. Do not use fresh or tap water, which can reactivate stinging cells.
• Continue until you can get medical help.
For a jellyfish sting in non-tropical waters:
• Wash the area with seawater to deactivate stinging cells.
For a sting in tropical waters -- especially from box jellyfish:
• Rinse immediately with vinegar. Do not use fresh or tap water, which can reactivate stinging cells.
155
The American Heart Association and the American Red Cross have recommended the following:
Rinse the area with vinegar for at least 30 seconds. If vinegar is not available, a solution of baking soda
can be used. This will deactivate the stinging cells.
• Next, soak the area in hot water for at least 20 minutes if possible. Cold packs can be used instead if
the area can’t be soaked in hot water
• Use mild hydrocortisone cream or oral antihistamine to relieve itching and swelling.
NOTE:
Rinse the area with vinegar for at least 30 seconds. These treatments are based on research done in the
Indo-Pacific areas, however, and may not be effective in the oceans of the North Atlantic . Some
experts therefore recommend a hot water rinse and lidocaine applied to the area if available. If this is
not possible, then removing the stinging cells and rinsing in seawater would also be an option.
Aftercare
•
After a jellyfish sting, any pain and swelling can be treated with painkillers, such as
paracetamol and ibuprofen.
For less severe sting:
• Use ice packs or over-the-counter pain relievers for welts.
• Clean open sores 3 times a day and apply antibiotic ointment. Bandage if needed.
For a severe reaction:
• The person may be hospitalized for several days.
• Anti-venom will be administered for box jellyfish stings.
SEA URCHIN
•
If there are signs that you or someone you're with has had a severe allergic reaction
(anaphylaxis), dial 999 to request an ambulance.
•
The small, venomous organs (pedicellariae) can be removed by applying a small amount of
shaving cream to the affected area and using a razor blade to gently scrape them out.
•
•
Any large spines should be carefully removed from the wound using tweezers.
Scrub the wound using soap and water and then rinse it with fresh water. Do not close the
wound with tape.
157
Aftercare
•
Pain and swelling can be treated with painkillers, such as ibuprofen.
•
If the skin is red and badly inflamed, a topical antibiotic cream or ointment should be applied
three times a day.
Stingrays
Stingrays are common in tropical and temperate areas. They hide in the ocean floor sand with eyes
and tail exposed. Most attacks from stingrays occur from swimmers or divers stepping on them. The
tail will whip up in self-defense and impale the diver/swimmer’s leg with a barbed spine.
•
The wound area has a blue rim and is typically swollen, painful, and pale.
Generalized reactions can include:
1.
2.
3.
4.
fainting
nausea, vomiting
Frequent urination
sweating
5.
6.
7.
respiratory difficulty
cardiovascular collapse
No antivenin is available.
158
•
•
•
•
•
Alert a lifeguard and dial 999 to request an ambulance if you're stung by a stingray.
There's no antidote to stingray venom
immersing the affected area in hot water (as hot as can be tolerated) for 30-90 minutes
use pain-numbing medication (Lidocaine)
you'll usually be given antibiotics because there's a high risk of the wound being contaminated
by bacteria in the sting and the seawater, which could lead to an infection.
•
The wound will initially be left open before being closed with stitches after about 48 hours if it
hasn't become infected.
Coral
This porous, rock-like formation found in water often has sharp edges. Usually cuts from coral are
self-limiting and have only a mild skin reaction. Unfortunately, they usually take a long while to heal.
Some coral can sting (coelenterate family). One of the deadliest poisons known was found recently in
coral (genus Palythoa).
159
If it is introduced into a deep cut in the body, it may be fatal. No antidote is known. Divers
should wear dive suits to protect them from coral cuts, especially in surging waves.
Coral treatment
1. Control bleeding.
2. Promptly clean with hydrogen peroxide or 10% povidone-iodine solution and debride the
wound.Remove all foreign particles.
3. Cover with a clean dressing.
4. Administer tetanus prophylaxis.
5. Topical antibiotic ointment.
6. Manage pain Do NOT use narcotics in cases of RESPIRTORY DISTRESS or FAILURE.
7. Evacuate to medical treatment facility if symptoms are severe.
Octopi
•
The octopus is an underwater chameleon, changing colors often in the water trying to conceal
itself from its enemies.
•
Most species of octopi found in the U.S. are harmless to humans. Octopi can envenomate by
biting and injecting venom from salivary glands.
•
An octopus bite consists of two small punctures, surrounded by swollen, red and painful tissue.
•
Bleeding may be severe due to anticoagulant effects of the venom.
•
The blue ringed octopus found in Australian and Indo-Pacific waters is often deadly. It injects
a neuromuscular blocker called maculotoxin that may cause paralysis, vomiting, respiratory difficulty,
visual disturbances and cardiovascular collapse. No antivenin is available. Paralysis may last 4-12
hours (with mechanical ventilation).
160
Octopi Treatment
1.
2.
3.
4.
Control local bleeding with pressure
Clean and debride wound.
Cover with clean dressing.
If blue-ringed octopus is suspected:
a. Apply pressure bandage and immobilize the bitten extremity. Place extremity lower than
the heart.
b. Be prepared to administer CPR and ventilate patient
c. Immediately evacuate patient to medical treatment facility for intensive care.
5. Administer tetanus prophylaxis.
Cone Shells
•
The cone shell is widely distributed throughout the world.
•
Venom is contained in darts inside the proboscis, which extrudes out of the narrow end but
can reach most of the shell.
•
A stinging or burning sensation begins at the site of the sting; followed by numbness and
tingling that spread from the wound to the rest of the body. Involvement of the mouth and lips is
severe.
•
Generalized symptoms include:
1.
muscular paralysis
2.
difficulty swallowing or talking
3.
visual disturbances and respiratory distress.
4.
A cone shell sting should be viewed as severe as snakebite
5.
Cone shell victims will probably experience paralysis or paresis of skeletal muscle with our
without myalgia.
6.
Symptoms develop within minutes and can last up to 24 hours.
7.
No antivenin is available and mortality reaches 25%.
Cone Shell Treatment
1. Place patient supine.
2. Apply pressure bandage to wound and place injury site at a level below the heart. Keep the
patient from moving.
3. Immediately transport patient to medical treatment facility for intensive care. Be prepared to
ventilate patient and administer CPR. Treat symptoms with supportive care as they present.
4. Avoid any analgesics that cause respiratory depression (narcotics).
5. Administer tetanus prophylaxis
161
SEA SNAKES
•
Sea snakes are air-breathing reptiles that swim underwater for great distances (over 100 miles
from land).
•
•
•
•
They inhabit the Pacific and Indian Oceans and the Red Sea.
The neurotoxin venom of a sea snake is 2-10 times more potent than that of a cobra.
Bites are usually not painful, and only about 25% cause envenomization.
There is a latent period of 10 minutes to several hours after the bite before generalized
symptoms develop:
1.
muscle aches and stiffness
2.
thick tongue sensation
3.
progressive paralysis
4.
nausea and vomiting
5.
difficulty with speech and swallowing
6.
respiratory distress and failure
7.
and smoky colored urine from myoglobinuria (which may progress to kidney failure).
8.
antivenin is available
TREATMENT
•
Lidocaine may be used in the wound for pain relief, but NEVER use epinephrine.
•
Explore the wound and clean out any remaining spines or barbs.
•
Immobilize the affected extremity.
•
Administer tetanus and antibiotic prophylaxis (tetracycline 250 mg po qid, and neomycin or
bacitracin topically).
•
Keep victim still.
•
Apply pressure dressing to bite site and place bite in a position below the heart.
•
Transport patient immediately to medical treatment facility for antivenin treatment and
intensive care.
•
Be prepared to ventilate patient and perform CPR.
NOTE: Antivenins are available from Commonwealth Serum Lab; 45 Poplar Rd, Parkville; Melbourne,
Victoria, Australia. Telephone: 011-61-3-389-1911. Telex: AA-32789.
162
Poisonous Spiney Fish
If you're stung it's important to get first aid and medical attention immediately.
To control the pain, the affected area should be immersed in hot water (as hot as can be tolerated) for
30-90 minutes.
You can use simple painkillers, such as acetaminophen, to relieve remaining pain
Any large spines should be carefully removed from the wound using tweezers (avoid touching the
spines with your bare hands).
Clean the wound using soap and water and then rinse it with fresh water. Do not cover the wound.
A severe allergic reaction (anaphylaxis) will need to be treated in hospital immediately.
Aftercare
•
If there is itching, hydrocortisone cream can be applied 2-3 times a day.
•
However, this should be stopped immediately if there are any signs of infection (severe
inflammation and redness).
•
Pain and inflammation can also be treated with painkillers, such as acetaminophen and
ibuprofen.
•
If an infection develops, a course of antibiotics may be prescribed. They should be taken for a
minimum of five days after the signs of infection have disappeared.
GENERAL INFORMATION FOR FIRST RESPONDERS
1. Remove the victim from the water.
2. Spray the sting area with vinegar; remain on the skin for 5 minutes
3. Wash the area with seawater. (Avoid fresh water or alcohol, which cause stinging cells to discharge)
4. Remove tentacles with a gloved hand or forceps.
5. Area should not be rubbed with sand.
6. Spray the sting area with vinegar again.
7. Dust the area with talcum powder or cover with shaving cream, and then gently scrape off with a
knife or safety razor.
8. Wash with sea water and apply a steroid cream.
STINGS (Sea Urchins, Cone Shells, Stingray, Bony Fish) Sea Urchins
Signs &Symptoms: Pain. Small, possibly discolored puncture wounds in area of contact. The spines
generally break off in the wound causing more problems with infection that with a toxic reaction.
Burning pain and discoloration. Usually no systemic symptoms.
164
CHAPTER 33
WEAPONS OF MASS DESTRUCTION
CHEMICAL WARFARE AGENTS:
Divided into two categories:
1.
Casualty Agents and Incapacitating Agents. Casualty Agents (Choking, Nerve, Blood, and
Blister) have the ability to cause severe and permanent injury, or even death.
2.
Incapacitating Agents (vomiting and tearing agents) are usually not lethal, produce no
CHOKING AGENTS
Phosgene (CG):
•
A colorless fog-like gas that characterized by the smell of new-mown hay or green corn.
Protective Measures: Protective mask.
Persistency: Will dissipate within 20 min in open terrain, but may persist for up to 10 hrs in shaded
areas, low terrain and in temperatures below 68° F.
Signs & Symptoms:
•
Eye irritation, throat, lung irritation, cough and dyspnea.
•
Most deaths will occur within 24 hrs.
NERVE AGENTS
Signs & Symptoms:
•
Difficulty breathing, drooling, nausea, vomiting, cramps, involuntary defecation and urination,
twitching, seizures, staggering, headache, drowsiness, coma, constricted pupils.
•
Very small skin dosages sometimes causes local sweating and tremor with little other effects.
Treatment: See Nerve Agent Exposure Treatment.
Tabun (GA): A colorless to brownish liquid that emits a colorless vapor. Tabun is odorless in pure
concentration, but emits a fruity odor in impure concentrations.
Persistency: Persists 1-2 days under average conditions
Sarin (GB):
A colorless liquid, which emits a colorless vapor.
Sarin is odorless in pure concentrations and has a slightly fruity odor in impure concentrations.
Soman (GD):
A colorless liquid that emits a colorless vapor.
Soman has a fruity odor in pure concentrations and a camphor (Vicks Vapor Rub®, mothballs, or
strong pine pitch) odor in impure concentrations.
NOTE: This agent ‘ages’ rapidly, resulting in an irreversible agent-AChE (acetylcholinsterase) bond.
Use of pyridostigmine bromide (PB) tabs prior to exposure to this agent can ‘preserve’ functional.
Persistency: Persists for 1-2 days under average conditions.
Treatment: See Nerve Agent Exposure Treatment.
V-Agents:
A colorless to amber liquid, which emits a colorless vapor.
V-Agents are odorless when in pure concentration.
Persists for long periods of time under average weather conditions.
165
Treatment:
•
(MARK 1) 2 mg of atropine and 600 mg of 2-PAM chloride.
WARNING: Seizures associated with exposure to nerve agents indicate serious and possible lethal
exposure. Seizures due to nerve agent exposure must be treated aggressively and prevented if possible.
LIQUID EXPOSURE (Liquid on Skin):
LONG TERM CARE OF THE NERVE AGENT CASUALTY:
1. Continue giving atropine injectors every 5 minutes as long as symptoms are present or until IV
atropine is available.
2. Suction and ventilate the patient as needed.
3. When possible, safely remove chemical protective gear and perform complete evaluation of the
patient.
4. If hypoxia is NOT present, give 1-2 mg (0.02-0.05 mg/Kg) of atropine IV every 10-15 minutes until
signs of atropinization occur (secretions stop, muscle fasciculation’s stop, and patient become easy to
ventilate)
CAUTION: DO NOT use pupil dilation as a sign of endpoint of atropine therapy: It is unreliable in
nerve-agent poisoning.
5. If hypoxia is present or cannot be ruled out, continue giving atropine 2 mg (0.02-0.05 mg/Kg) IM
every 10-15 minutes until signs of atropinization occur.
6. Administer pralidoxime:
a) If 3 Mark 1’s have been given (600 mg of pralidoxime each, total of 1800 mg), then begin an IV drip
of 10-20 mg/Kg per hour of pralidoxime, to a max dose of 500 mg/hour.
b) If no Mark 1’s have been given or the 2-PAM injectors were not used: Administer an initial IV bolus
of 1-2 grams of pralidoxime (25-50 Mg/Kg, max of 2 grams) IVPB over 15-20 minutes, then begin an
IV drip at 10-20 mg/Kg per hour as above.
χ)
Continue the pralidoxime drip for 12 hours, or as directed by medical control.
7. If signs of nerve agent poisoning reoccur, treat with atropine and pralidoxime as above.
8. Symptoms may reoccur up to 24 hours after exposure/treatment.
DECONTAMINATION:
1. Bleach slurry or dilute alkali solutions (equipment).
2. In confined areas use steam and ammonia or hot, soapy water (equipment).
3. Warm soapy water for skin decontamination if the above are not available.
BLOOD AGENTS
Hydrogen Cyanide (AC):
A colorless gas that emits an odor of bitter almonds.
Persistency: Quickly dissipates into the air.
Signs & Symptoms: Irritation to the eyes and skin, low levels cause weakness, headache,
disorientation, nausea and vomiting. Increased dosages result in loss of consciousness.
Treatment: Complex, multi-step process. Requires specialized medications, advanced level of care. If
patient is still alive after exposure
Decontamination: Aeration under confined conditions. For complete decontamination, use caustic soda
with steam.
Cyanogen Chloride: A colorless gas with a sharp and peppery odor.
Persistency: Rapidly disperses, vapor may linger in jungle and forest for some time under suitable
weather conditions.
166
Signs & Symptoms: Highly irritating to the eyes and upper respiratory tract. Low levels cause
weakness, headache, disorientation, nausea and vomiting. Increased levels causes loss of
consciousness.
Treatment: Treat ABC’s, oxygen and evacuate.
Decontamination: Same as AC.
BLISTER AGENTS
Distilled Mustard (HD): An amber-brownish liquid that produces low-lying colorless vapor with a
garlic-like odor.
Persistency: 1-2 days under average weather conditions. A week to several months under cold
conditions
Signs & Symptoms: Conjunctivitis or inflammation of the eyes, redness of the skin followed by
blistering or ulceration, inflammation of the nose, throat, trachea, bronchia and lung tissue. Vapors will
cause temporary blindness. Symptoms may be delayed 4-6 hrs after exposure.Treatment: Strong bleach
solutions and caustic soda.
Decontamination: Strong bleach solutions and caustic soda for terrain. Live steam for buildings and
substructures.
Levinstein Mustard (H): An amber- brownish liquid, which produces a low-lying colorless vapor
with a sulfur odor.
Persistency: 1-2 days under average weather conditions. A week to several months under cold
conditions.
Signs & Symptoms: Symptoms may be delayed up to 12 hrs after exposure. Skin lesions. Irritation to
the nose and throat, hoarseness, loss of voice and persistent cough. Ingestion may cause diarrhea,
nausea and vomiting.
Treatment: Same as HD.
Nitrogen Mustard (HN-1, HN-2, HN-3): A pale-to-amber liquid, which produces a colorless
vapor.
HN-1 emits a fishy or musty odor. In low concentrations,
H-2 emits a soft soap odor and in high concentrations a fruity odor.
HN-3 is odorless.
Persistency: HN-1 and HN-2 persists up to a day or two in moderate climate and less in dry arid
conditions. HN-3 persists considerably longer than HN-1 and HN-2. May last for up to a week under
cold conditions.
Signs & Symptoms: Irritation to the eyes, nose and throat. Hoarseness, loss of voice and persistent
cough. Ingestion may cause diarrhea, nausea and vomiting. Cumulative poison with symptoms delayed
up to 12 hrs after exposure.
Treatment: Same as HD.
Decontamination: Same as HD.
Phosgene Oxime (CX):
May be crystalline solid or clear liquid. The crystalline solid is colorless, while the clear liquid has a
sharp penetrating and disagreeable odor or pepperish smell.
Persistency: Liquid form 1-2 days under average weather conditions. A week to several months under
cold conditions. Crystalline form may lasts for several months in dry, arid and cold conditions.
Signs & Symptoms: Symptoms: Red circle from area of contact. Causes immediate pain from prickly
sensation to severe bee sting. Irritates the mucus membranes of the eyes and nose. Effects are
instantaneous.
Treatment: No treatment available.
Decontamination: Flush with warm water to dissolve the agent. Bleaches and strong oxidizers will
break down the compound. Use strong alkali solutions (sodium hydroxide) with live steam to
decontaminate large ground and structural areas.
167
BIOLOGICAL AGENTS
GUIDELINES AND CONSIDERATIONS
• Biological warfare agents are difficult to detect, but relatively easy to protect against. Most biological
agents capable of being weaponized require inhalation of the agent for infection
• Immunizations against specific biowarfare agents may be required. Keep immunizations current.
• Avoid water that hasn’t been properly purified and food from the local area if possible.
• Decontamination for most biowarfare agents is done with 5% sodium hypochlorite solution (Clorox
bleach out of the bottle is 5% hypochlorite) for equipment, and 0.5% hypochlorite solution for skin
(dilute the Clorox solution 1:10 with water). Allow the solution to dry on the equipment and skin.
NOTE: For most biological agents, washing with warm soapy water is just as effective for skin
decontamination as a bleach solution is.
NUCLEAR CONTAMINATION
:Nuclear/radiation exposure can be divided into several different categories.
The patient themselves DO NOT become radioactive from exposure to radiation
NOTE: In some cases, patients can become contaminated with dust or other material that has
radioactive material in it. Once this is removed, the patient is cared for in the normal manner.
GUIDELINES AND CONSIDERATIONS
Prevention of exposure depends on the type of threat in the area.
In all cases, remember that radiation protection is dependent on:
1) TIME OF EXPOSURE, 2) DISTANCE FROM THE SOURCE, and 3) SHIELDING.
• For a fixed radiation source that is not in particulate form: It is best to limit exposure during rescue.
Move the patient as rapidly as possible, keeping as far away from the radiation source as possible.
• For a particulate radiation source with external contamination (dust/debris containing radioactive
material is on the patient): Wear a chemical protective mask with war filters in place to prevent
inhalation of dust. Wear an overgarment that can be discarded after leaving the contaminated area.
Decontaminate the patient by removing all clothing and washing off any dust.
• For a patient with internal contamination (radioactive material either ingested or driven into wounds):
Wear protective clothing as noted above. Once out of the contaminated area, Decontaminate the patient
as above. Debride the wounds to remove any particulate matter, if possible. Cover the wounds and
Evac the patient, making sure the next echelon of medical care knows that an internally contaminated
patient is on the way. Patients who have inhaled, or ingested radioactive material should be evacuated
to the next echelon of care.
168
CHAPTER 34
MEDICAL EMERGENCIES
CHEST PAIN: All non-traumatic chest pain must be evaluated to rule out cardiac ischemia. A
thorough history of events is needed, including onset of pain, severity, and duration of pain. Other
history includes association with activity, previous history of cardiac problems, hypertension, diabetes,
hypercholesterolemia, smoking and family history of cardiac disease.
GUIDELINES AND CONSIDERATIONS
CHEST PAIN OF CARDIAC ORIGIN: Determining if chest pain is due to cardiac ischemia or not is a
difficult process, often requiring considerable clinical skill and experience. Classically, chest pain of
cardiac origin has the following characteristics:
• Dull and diffuse pain, often described as a ‘weight’ on the chest, a heavy sensation or a squeezing
sensation. The pain can radiate to the left arm (or less commonly, right arm), neck or jaw.
NOTE: A sharp, well-localized chest pain is less likely to be cardiac in origin if the pain is reproduced
by palpation at the painful area; by taking a deep breath; or twisting the torso.
• Chest pain of cardiac origin is frequently accompanied by associated symptoms, such as shortness of
breath, diaphoresis, nausea, dizziness, feelings of dread, and verbal denial.
• Patients with a history of cardiac chest pain (angina) can be asked if this pain is similar to their
previous episodes of angina. Angina usually lasts less than 5 minutes. Any angina- like pain that has
lasted longer than 5-10 minutes must be treated as a possible heart attack.
• Asking the patient to rate their pain on a scale of 1-10 (1= no pain, 10= worst pain they have ever had)
is a simple method of following the success of any treatments.
• Don’t be overconfident: Cardiac chest pain can be a subtle, difficult diagnosis, even under ideal
conditions. Patients with diabetes are especially prone to having unusual presentations of cardiac pain.
When in doubt, treat for a cardiac event, and evacuate the patient as soon as possible.
MANAGEMENT OF SUSPECTED ISCHEMIC CHEST PAIN
1. Place patient at rest to reduce anxiety
2. Administer 100% Oxygen, place on cardiac monitor, if available.
3. Initiate IV with normal saline
4. Obtain vital signs
5. Give 325 mg of aspirin PO if patient is not allergic, and no recent GI bleeding or stroke.
6. Nitroglycerin 0.4 mg sublingually every 5 minutes X3. Do not give if systolic BP below 100.
Check BP after every dose, and just before giving next dose. Record any changes in intensity of pain
associated with administration of nitroglycerin.
7. Morphine Sulfate, 4mg bolus then titrate every 2-4 minutes by 2mg until pain relief.
NOTE: If resuscitative equipment is available and individual is ACLS qualified, refer to specific
cardiac algorithms for further direction. See pages 94-112.
169
PULSELESS ELECTRICAL ACTIVITY (PEA): PEA may be a result of trauma necessitating a
thorough evaluation of potential causes and rapid correction. Consider the following:
CONDITION
1. HYPOVOLEMIA
2. HYPOXIA
Ventilation with 100% O2
CLUES
History, flat neck veins
Cyanosis, pulse oximetry
MANAGEMENT
Volume expansion
Airway establishment
3. CARDIAC
History of MOI; No pulse with CPR
Pericardiocentesis
TAMPONADE
Neck vein distention, hypotension, Low pulse pressure;, change from
tachycardia to bradycardia as a terminal event.
4. TENSION
PEUMOTHORAX
5. HYPOTHERMIA
Algorithm
No pulse with CPR, neck vein
distention, tracheal deviation.
History of cold exposure
Needle decompression
See hypothermia
DIABETES: There are two life threatening diabetic conditions that the pararescueman needs to be
aware of: Hypoglycemia and Hyperglycemia. Diagnosis and treatment is extremely limited in the field
environment.
HYPOGLYCEMIA (INSULIN SHOCK): Extremely low levels of circulating glucose. Often a
result of excess insulin or inadequate glucose intake to meet metabolic needs.
Signs & Symptoms: Weak rapid pulse, cold clammy skin, weakness/uncoordination, headache,
irritability, may appear intoxicated, decreased level of consciousness.
Treatment:
1. Maintain ABCs
2. Establish IV with normal saline
3. If patient is unconscious, administer 50 cc’s of 50% Dextrose solution IV, if available (consult
medical control if possible)
4. If patient is conscious, administer PO sugar solution or dextrose paste if available.
5. If patient is unconscious and IV Dextrose is unavailable, insert NG tube and administer sugar slurry
via the NG tube.
HYPERGLYCEMIA (DIABETIC COMA / DIABETIC KETOACIDOSIS): Elevated
levels of circulating glucose often the result of concurrent disease; excessive intake of glucose;
decreased effective insulin or excessive alcohol consumption.
Signs & Symptoms: Polyuria, polydypsia, nausea and vomiting, tachycardia, deep, rapid respirations,
warm, dry skin, fruity odor on breath, decreased level of consciousness, hypotension. Dry mouth,
intense thirst, and abdominal pain.
Treatment:
1. Maintain ABCs
2. Establish IV with normal saline (Note: If medical control is not available, infuse normal saline 1
liter bolus, followed by infusion of 500 cc/hr not to exceed a total of 2 liters.
3. Administer 100& oxygen.
4. If patient is a known diabetic, and unconscious, 50% Dextrose may be given under physician
direction.
5. If patient is unconscious, administer naloxone 2mg IV (may repeat X1 in 5 minutes if no result)
6. Insulin, if available, is only to be given under direct medical control
170
COMA: In general only two mechanisms produce coma: 1) structural lesions that depress
consciousness by destroying or encroaching on the ascending reticular activating system (RAS) in the
brain stem and 2) toxic metabolic states that involve the presence of circulating toxins or metabolites or
the lack of metabolic substrate (i.e., glucose or oxygen). Preserved pupillary response suggest that the
origin is toxic, whereas unresponsive or asymmetrical pupillary responses point to a structural cause.
Treatment: In general, treatment is directed at support of patient’s vital functions, prevention of further
deterioration and treatment of reversible causes.
1. If respirations are slow or shallow or if cerebral edema is suspected, hyperventilate at 24-30 breaths/
minute with 100% oxygen.
2. If no gag reflex, intubate.
3. Establish IV with normal saline or start saline lock.
4. If hypoglycemia is suspected, refer to hypoglycemia treatment (above).
5. Naloxone 2mg IV, repeat X1 in 5 minutes if no response
6. If medical control is available, thiamine 50-100 mg IV may be considered. This should be given
prior to any dextrose.
SEIZURES: A temporary alteration in behavior or consciousness caused by abnormal electrical
activity in the brain. May result from multiple factors: stroke, head trauma, hypoxia, infection,
hypoglycemia and drug overdose. Aim of treatment is to address correctable causes and reduce or
eliminate additional seizure activity. MOST SEIZURES ARE SELF-LIMITING and will stop once
underlying causes are corrected. If seizure activity persists for greater than 3-5 minutes, intervention
may be required. NOTE 1: If a patient has multiple seizures without fully recovering between episodes,
intervention is required. After a seizure has stopped, it is normal for the patient to be drowsy,
incoherent and/or disoriented. This is referred to as the postictal period. The patient will usually recover
from this within 15-20 minutes. NOTE 2: If the patient has another seizure before the end of the
postictal period, then treatment for the seizure is needed.
Treatment:
1. Prevent patient from sustaining physical injury. NOTE: Do not restrain patient nor should objects be
forced between the patient’s teeth to maintain an airway.
2. Place in a lateral recumbent position to allow drainage of oral secretions and facilitate suctioning if
needed.
3. Supplemental oxygen should be administered with a non-rebreather mask.
4. Consider intubation during flaccid period if there is no gag reflex. Provide 100% oxygen and
ventilation support.
5. Establish IV access with normal saline and secure with tape and elastic bandage.
6. If hypoglycemia is suspected, administer 50% Dextrose, if available (only under physician
direction.).
7. If prolonged seizure activity or repeated episodes, give Diazepam 5mg IV and repeat every 5-10
minutes until seizure stops. Do not exceed 20 mg of diazepam.
ASTHMA: A reversible obstruction to airflow caused by bronchial smooth muscle contraction,
hypersecretion of mucus resulting in bronchial plugging and inflammatory changes in the bronchial
walls.
Signs & Symptoms: Obvious respiratory distress with rapid and loud respirations, audible
wheezing may be present. In severe cases hypoxic signs may be present (i.e., lethargy, exhaustion,
agitation, and confusion). Other severe signs include: diaphoresis and pallor, abdominal and intercostal
retractions, inability to speak, tachycardia greater than 120, tachypnea greater than 30, pulseless
paradoxus greater than 20 mm Hg and altered mental status.
Treatment:
1. Assure ABCs
2. Administer 100% oxygen via non-rebreather mask.
3. Establish an IV with normal saline, run at 250 cc/hr and monitor closely for S&S of pulmonary
edema.
4.
Epinephrine 1:1000 administer .01cc/lb subcutaneuosly and repeat every 5 minutes for 3 doses.
171
5. Do not exceed 0.3cc per dose (by physician direction only).
6. Administer Albuterol via nebulizer, 0.5ml in normal saline for a total volume of 3cc, repeat
treatment every 15-10 minutes X3, under the direction of a physician.
7. Albuterol metered-dose inhaler (MDI) can be used instead of the nebulizer as noted in #5 above.
8. Dose is 2 puffs every 10-15 minutes x 3.
NOTE: If available, albuterol is the preferred treatment for asthma, as versus giving epinephrine. Use
epinephrine if albuterol is not available. Solu-Medrol or Decadron may be given for severe asthma
attacks, however this should only be done under direct medical control.
INFECTIOUS DIARRHEA: Defined as watery stool, associated with bloody stool, mucus, and/or
fever.
Treatment:
1. Encourage oral clear fluids, electrolyte replacement if available.
2. If tilt positive, Establish an IV with normal saline, and give 2 liter bolus of saline, then run 250
cc/hr.
Do not exceed 3 liters.
3. Phenergan 12.5 mg IV if significant abdominal cramping or nausea and vomiting.
4. Imodium 2mg caps initially, then 2mg after each lose stool, not exceed 10 mg/24hrs.
NOTE: Do not give Imodium unless ciprofloxin is given first.
5. Ciprofloxin 500 mg bid X 5 days.
STOOL GUIAC TESTING: The presence of obvious blood in the stool (bloody diarrhea) is usually
indicative of infectious diarrhea. In some cases, blood in the stool may not be obvious. In cases of
diarrhea, testing the stool with a guiac card may show the presence of occult (hidden) blood. In cases of
diarrhea with a positive stool guiac, treat as infectious diarrhea. This test can also be used to detect
small amounts of blood in the stool of trauma victims.
Procedure:
1. Place a small sample of stool on the front of the guiac card. Close the cover.
2. Open the back side of the card and put 1-2 drops of guiac developer on the card.
3. Place a drop of the developer on the ‘control’ section of the card.
4. Any blue color, or a color that resembles the color of the ‘control positive’ part of the card is a
positive stool guiac, indicating the presence of occult blood.
173
CHAPTER 35
PHARMACOLOGY
What went wrong with Antibiotic Usage?
Treating trivial infections / viral Infections with Antibiotics has become routine affair.
Many use Antibiotics without knowing the Basic principles of Antibiotic therapy.
Many Medical practioners are under pressure for short term solutions.
Commercial interests of Pharmaceutical industry pushing the Antibiotics, more so Broad spectrum and
Newer Generation antibiotics. as every Industry has become profit oriented.
Poverty encourages drug resitance due to under utilization of appropriate Antibiotics.
Why we Need Antibiotic Policy
•
Reduce the Antimicrobial resistance
•
Initiate best efforts in the hospital area as many resistance Bacteria are generated in Hospital
areas and in particular critical care areas.
•
Initiate good hygienic practices so these bacteria do not spread to others
•
Practice best efforts, these resistance strains do not spill into critically ill patients in the
Hospital
•
To prevent spill into Society, as they present as community associated infections..
•
Antibiotics should not be used casually
•
Policy emphasizes, avoiding the use of powerful Antibiotics in the Initial treatments.
•
We should create awareness that we are sparing the powerful Broad spectrum Drugs for later
treatment
•
To many drugs creates complex problems in drug resitance.
•
The clinicians should optimize the duration of empherical treatment.
GUIDELINES AND CONSIDERATIONS: The key to drug use is using caution. Familiarity with
adverse drug effects and preparedness to deal with those effects are also paramount to safe use. The
following factors can influence the therapeutic effects of medications:
• Age
• Body Weight
•Time of administration
• Pathological state
• Sex
• Route of administration
• Rate of inactivation and excretion
• Genetic factors
• Tolerance
• Drug interaction
Allergy and Hypersensitivity: Hypersensitivity reactions can vary in their presentation.
Antibiotics are the most common cause, however, any medication may be at fault. Allergic reaction to
any antigen, e.g. snake envenomation, insect stings, pollens, etc., can cause similar symptoms.
Reactions may include, but are not limited to:
• Allergic rhinitis, urticaria (hives), reactive airway/asthma or profound hypotension.
• Local reactions may include GI distress and/or dermal presentation, e.g. nausea, vomiting,
cramps, diarrhea, pruritic skin, hives, local rash.
• Life threatening reactions (such as anaphylaxis) can occur in seconds to minutes and may include:
•• Tightness in the chest and wheezing
•• Skin changes: diffuse redness, hives and flushing
174
•• Angioedema or swelling of the periorbital and perioral area
•• Rapidly progressive respiratory distress due to laryngeal edema, bronchospasm and
fluid accumulation in the lungs.
•• Hypotension/overt signs of shock
OBSERVE THE FOLLOWING:
1. Medications are not always indicated. You must weigh the benefits against the potential adverse
patient and mission effects.
2. All medications have potential adverse effects and many patients have a history of adverse reactions
to various medications. In a conscious patient obtain a drug history. In an unconscious patient search
for identification/warning tags denoting medication sensitivities.
3. Recommended doses will be followed.
4. When using IV medication, have a reliable IV fluid line running and inject the medication into the
rubber fitting in the IV line.
5. When injecting through a saline lock, flush the lock with 10 cc of normal saline after administering
the medication.
6. In addition to medication, your patient will require maintenance fluids, electrolytes, and nutritional
balance.
7. CAUTION: Be prepared for anaphylactic reactions at all times.
GENERAL RULES:
• Sterile technique: Alcohol cleaning of injection port or skin.
• Always aspirate before injecting medication to make sure you are not in a vessel or to insure proper
placement in a vein for IV medication.
• For IVs: Mark on tape the date, time, and needle size.
• CAUTION: Be prepared for immediate hypersensitivity reactions and anaphylactic shock
reactions at all times.
ROUTES OF ADMINISTRATION:
• Oral: Give adequate fluids
175
• Subcutaneous (SQ or SubQ) injection: Gently grasp skin over injection site and pull skin away from
underlying muscle, forming a mound. Insert the needle at a 450 angle. Aspirate before
injection.
• Intramuscular (IM) injection: Hold needle at 90 degrees to the skin, insert deep into the muscle,
aspirate to make sure you are not in the vein or artery, and inject.
• Intravenous (IV) injection: Inject slowly into the tubing of an actively running, reliable IV. You may
"piggy back" (run one IV into the tubing of another) a medication. IV injection through the port of a
saline lock should be followed by at saline flush of 5-10 cc’s.
176
MEASUREMENT OF DOSAGES:
• Grain (gr): Measure of weight (apothecary system).
• Gram (gm): Measure of weight (metric system) equals to 1,000 milligrams (mg).
• Liter (l) and Cubic Centimeter (cc): Measures of volume.
• Milligrams per milliliter (mg/ml) and milligrams per cubic centimeter (mg/cc): Units of
concentration.
• Milligrams per Kilogram (mg/Kg): Most commonly used with pediatric medications
• Units (u): An arbitrary measure of an active ingredient, e.g., penicillin, established to determine the
effective dosage of medication.
ANAPHYLAXIS PROTOCOL
Signs/Symptoms of Anaphylaxis Present?
• 100% Oxygen by mask
• Support Ventilation as needed
• Start IV NS
• Evaluate severity of
symptoms:
• Urticaria
• Rhinitis
• Mild Angioedema
• Bronchospasm
• Early Laryngeal
• Edema
• BP less than 100
• Laryngeal Edema
• Respiratory Failure
• Shock
• Cardiovascular Collapse
177
Epinephrine, 1:1,000 0.3 SC
Repeat in 5 min
•
if no improvement
Epinephrine,,1:1,000 0.3-0.5 cc SC
Repeat in 5 min
•
if no improvement
Epinephrine
1:10,000 0.5-1.5 cc IV*
Repeat in 5 min if
•
no improvement
Benadryl, 25-50 mg PO or IM
Zantac,
50 mg IM or 150 mg PO
Zantac, 50 mg IV or IM
Observe for 24 hours
SoluMedrol, 125 mg IM or IV
Benadryl, 50 mg PO or IM
Benadryl, 50-75 mg IV**
Zantac, 50 mg IV
SoluMedrol, 125 mg IM or IV
NOTE 1: *If unable to obtain IV access consider sublingual injection (injection into the plexus of veins
under the tongue) of epinephrine as a temporary measure while establishing an IV. May also be given
by ET Tube (dilute to 1:10,000 and follow with 5-10cc of saline to flush).
NOTE 2: **May give IM if no IV access.
CAUTION: SxS of anaphylaxis may reoccur 12-24 hours after the original reaction. Keep the patient
under close observation at all times for the first 24 hours following initial reaction. If symptoms
reoccur, treat via the above protocol. Patients with moderate or severe reactions should be evacuated as
soon as possible, with close observation while awaiting evacuation.
Caution: In the treatment of anaphylactic shock, IV epinephrine must be given very slowly, preferably
at least 5 minutes per dose. Rapid bolus IV injection can cause myocardial ischemia and potentially
fatal cardiac arrythmias.
Caution: IV epinephrine must be injected SLOWLY: Give dose over at least 5 minutes.
179
VITAMINS
VITAMINS AND MINERALS
•
Organic substances required for normal cell function, growth, and development. There are 13
essential vitamins.
1.
Fat-Soluble Vitamins: Fat-soluble vitamins are those that bind to fat in the stomach and are then
stored in the body for later use. We are less likely to become deficient in these vitamins (A, D, E, and
K), but more likely to build up to toxic levels, usually due to extreme overconsumption or overzealous
supplement use.
2.
Water-Soluble Vitamins: The rest of the vitamins are water-soluble, meaning they can be
absorbed directly by cells. When in excess, these vitamins are flushed out of our system with each
bathroom break. The water-soluble vitamins — biotin, vitamin C, niacin, folic acid, pantothenic acid,
and the four B complex vitamins — need to be restored more frequently, but the body can tolerate
higher doses.
3.
Minerals: Minerals are inorganic substances. They’re also necessary for normal body function
and development. There are two groups of minerals: macrominerals (which the body needs in large
doses) and trace minerals (only a pinch required).
RDA: Recommended Dietary Allowances, or RDAs, represent the average daily dietary intake of each
vitamin and mineral a person needs to stay healthy and steer clear of deficiencies. The values, which
are all backed by scientific data, are broken down by age and gender.
AI: For those vitamins for which an RDA has not yet been set (usually due to lack of scientific data),
or adequate intake level, is used in place.
UL: The tolerable upper intake level (UL) is the maximum amount of daily vitamin or mineral dosage
that is likely to be safe for the average person. Stay under the UL radar (especially when using
supplements) to prevent toxicities.
•
•
Vitamins or minerals that are needed in larger doses are expressed in units of milligrams (mg).
Trace minerals and vitamins are expressed in micrograms (mcg).
Biotin (a.k.a. Vitamin B7 or Vitamin H):
•
Like the rest of the water-soluble B-complex vitamins, biotin plays a huge role in cell growth
and food metabolism.
•
Deficiency of this vitamin is extremely rare, but overdoing it on raw egg whites has been
known to prevent biotin absorption
RDA: 30 mcg
Sources: Cooked salmon (4-5 mcg per 3 ounces) whole grains (0.02-6 mcg per slice of bread), eggs
(13-25 mcg per large egg), or avocados (2-6 mcg per avocado)
Calcium:
•
•
A macromineral crucial for the healthy development of bones and teeth.
Calcium also offers a helping hand in muscle function, blood clotting, nerve signaling, hormone
secretion, and blood pressure .
•
Requires:Vitamin D and Magnesium for assimilation.
RDA: 1,000 mg
180
Sources: Milk (300 mg per cup), yogurt (300 mg per cup), cheddar cheese (303 mg per 1.5 ounces),
tofu (258 mg per ½ cup), bok choy (79 mg per ½ cup), spinach (115 mg per ½ cup), and rhubarb (174
mg per ½ cup).
Threshold: 2,500mg
Choline:
•
Choline, another water-soluble B vitamin, is a building block of the neurotransmitter
acetylcholine, which is essential for the nerve and brain activities that control memory and muscle
movement. Choline also helps turn the food we eat and our stored energy into fuel .
•
Vegetarians, vegans, pregnant women, and endurance athletes are at greater risk for choline
deficiency, which is linked to fatty liver disease, atherosclerosis, neurological disorders, and impaired
fetal development .
•
Extremely high doses, more than 10 grams per day, can cause vomiting, increased sweating and
salivation, and a fishy body order .
RDA: Men = 550 mg; Women = 425mg
Sources: Eggs (126 mg per egg), milk (38 mg per cup), cooked broccoli and Brussels sprouts (both 62
mg per cup), beef (67 mg per 3 ounces), and milk chocolate (20 mg per 1.5 ounce bar).
Threshold: 3,500 mg
Chromium:
•
Though this trace mineral is thought to enhance insulin activity and the breakdown of the sugars
that we eat, it’s only needed in small amounts and is not considered “essential”
•
Overconsumption of chromium supplements could cause kidney damage.
RDA: 35 mcg; Women = 25 mcg
Sources: broccoli (22 mcg per cup), grape juice (7.5 mcg per cup), and whole-wheat products like
whole-wheat frozen waffles (6.7 mcg per waffle) or whole-wheat English muffins (3.6 mcg per
muffin).
Threshold: Not determined
Copper:
•
Essential trace element and antioxidant.
•
Frontline in the creation of red blood cells, copper is also important for proper energy
metabolism, immunity, and nervous system function .
•
Copper deficiencies may manifest as anemia, a low white blood cell count, and bone
deterioration .
RDA: 900 mcg
Sources: liver (4,049 mcg per ounce), oysters (670 mcg per medium oyster), crabmeat (634 per 3
ounces), nuts (cashews, for example, offer 629 mcg per ounce), raw mushrooms (344 mcg per cup),
and semisweet chocolate (198 mcg per ounce).
Threshold: 10,000 mcg
Fluoride:
•
This non-essential trace mineral helps keep teeth cavity-free and bones less breakable .
RDA: Men = 4 mg; Women = 3 mg
Sources: Food sources include grape juice (0.05-0.64 mg per cup), canned sardines (0.2-0.4 mg per 3.5
ounces), and chicken (0.06-0.10 mg per 3.5 ounces).
Threshold: 10 mg
181
Folic Acid (a.k.a. folate or folacin):
•
Folic acid is such a key part of our diet that the U.S. government decided to fortify most
commercial flour with this water-soluble vitamin.
•
Vital for pregnant women to ensure the baby’s proper development, helping prevent birth
defects in the brain and spine .
•
Folic acid also helps create most all cells in the body and may reduce the risk of heart disease
and colon cancer.
RDA: 400 mcg
Sources: fortified grains and cereals (200-400 mcg per cup), asparagus (134 mcg per 6 spears), spinach
(132 mcg per half cup), orange juice (83 mcg per cup), and lentils (179 per half cup).
Threshold: 1,000 mcg
Iodine:
•
This essential trace mineral is a crucial component of thyroid hormones, which maintain our
basal metabolic rate (BMR).
•
Iodine also helps to regulate body temperature, nerve and muscle function, and plays a role in
the body’s growth and development .
•
Too little iodine can lead to thyroid dysfunction, developmental abnormalities, and even
goiters, a swelling of the thyroid gland .
•
Iodine is found in most table salt
•
Excess of iodine can cause hyperthyroidism, goiters, and in severe cases, GI discomfort and
burning of the mouth, throat, and stomach, though rare.
RDA: 150 mcg
Sources: cod (99 mcg per 3 ounces), shrimp (35 mcg per 3 ounces), canned tuna (17 mcg per half can),
milk (56 mcg per cup), baked potatoes (60 mcg per medium potato), and (small amounts of) seaweed
(more than than 4,500 mcg per ¼ ounce!).
Threshold: 1,100 mcg
Iron:
•
A large componenet of hemoglobin, a component of red blood cells, and myoglobin
(hemoglobin’s counterpart in muscles) bring oxygen to all the cells that need it.
•
Iron is also important in the production of amino acids, collagen, neurotransmitters, and
hormones .
•
Since this mineral is more easily absorbed from red meat and poultry, vegetarians and vegans
may want to consider iron supplements, or at least consume more iron-rich fruits and leafy green
vegetables.
•
Acute overdose of iron can be lethal, and general excess can cause GI irritation, nausea,
vomiting, diarrhea, and constipation .
RDA: Men = 8 mg; Women = 18 mg
Sources: Consider beef (2.32 mg per 3 cooked ounces), oysters (5.04 mg per 6 medium oysters), raisins
(0.81 mg per small box), prune juice (2.28 mg per 6 fluid ounces), potatoes (1.87 mg per medium
potato), cooked lentils (3.30 mg per half cup), tofu (2.15 mg per ¼ block), and cashews (1.89 per
ounce).
Threshold45 mg
Magnesium:
•
Ionically drawn to calcium, magnesium is a macromineral that partners with calcium to assist
with proper muscle contraction, blood clotting, cell signaling, energy metabolism, blood pressure
regulation, and building healthy bones and teeth.
•
Magnesium deficiency is rare and so are toxicities
182
•
•
Excess leads diarrhea, lethargy, heart rate disturbances, and muscle weakness.
May play a role in fibromyalgia, if deficient
RDA: Men = 400 mg; Women = 310 mg
Sources: oat bran (96 mg per half cup), almonds (78 mg per ounce), brown rice (86 mg per cup),
cooked spinach (78 mg per half cup), bananas (32 mg per banana), and molasses (48 mg per
tablespoon).
Threshold: There is no upper limit for dietary magnesium, but supplemental magnesium should not
exceed 350 mg/day.
Manganese:
•
•
Though an essential trace mineral and antioxidant, it is also potentially toxic in excess .
Important for energy, bone development, and wound healing, overindulgence of this magic
mineral — usually a result of water contamination — may cause a dip in intellectual function .
RDA: Men = 2.3 mg; Women = 1.8 mg
Sources: pineapples (0.77 mg per half cup), pecans (1.28 mg per ounce), oatmeal (0.99 mg per instant
oatmeal packet), brown rice (1.07 mg per half cup), and green tea (0.41-1.58 mg per cup).
Threshold: 11 mg
Molybdenum:
•
A necessary factor of many enzymes, which speed up the body’s biochemical reactions that
break down dietary and stored nutrients into energy.
•
Molybdenum deficiency has never been documented in healthy people, and toxicity is similarly
rare.
RDA: 45 mcg
Sources: rich in molybdenum includes legumes like black beans (130 mcg per cup) and split peas (148
mcg per cup), and nuts like almonds, chestnuts, and peanuts (all about 42 mcg per cup).
Threshold: 2,000 mcg
Niacin ( a.k.a. Vitamin B3 or Nicotinic Acid):
•
Like other water-soluble B vitamins, niacin is essential for converting food into energy.
•
It’s also central for the health of skin, hair, eyes, liver, and the nervous system, and is believed
to lower risks of high cholesterol and heart disease .
•
Extreme deficiencies in niacin may lead to pellagra, which is associated with the “the four D’s”:
dermatitis (skin irritation), diarrhea, dementia, and death .
RDA Men = 16 mg; Women = 14 mg
Sources: peanuts (3.8 mg per ounce), chicken (7.3 mg per 3 ounces), salmon (8.5 mg per 3 ounces),
fortified cereals (20-27 mg per cup), and coffee (0.5 mg per cup).
Threshold: 35 mg “niacin flush” — if doses exceed 50 mg per day .
Pantothenic Acid (a.k.a. Vitamin B5):
•
Important in food metabolism and helps synthesize neurotransmitters, steroid hormones, red
blood cells, and more.
•
Toxicity is virtually nonexistent, and while B5 deficiency is fairly rare (it tends to accompany
severe malnutrition) neurologic symptoms such as burning feet may crop up.
RDA: 5 mg (AI)
Sources: chicken (0.98 mg per 3 ounces), eggs (0.61 mg per large egg), whole grains (0.19 mg per slice
of whole wheat bread), mushrooms (0.52 mg per half cup), sweet potato (0.88 mg per medium potato),
avocados (1.99 mg per whole avocado), and yogurt (1.35 mg per cup).
Threshold: Not determined
183
Phosphorus:
•
A macromineral that primarily builds and protects teeth and your skeleton.
•
Phosphorus is also a component of DNA and RNA, helps convert food into energy, and aids in
shuttling nutrients to the organs that need them .
•
Rare cases of phosphorus deficiency can lead to anemia, muscle weakness, loss of appetite,
rickets (in children), and numbness and tingling in the legs .
RDA: 700 mg
Sources: milk (257 mg per cup), yogurt (385 mg per cup) and cheese (131 mg per ounce). Salmon
(252 mg per 3 ounces), eggs (104 mg per large egg), beer (173 mg per 3 ounces), chicken (155 mg per
3 ounces), and carbonated cola drinks (40 mg per 12 ounces).
Threshol 4,000 mg
Potassium:
•
A macromineral and electrolyte that’s essential for a steady heartbeat, the transmission of
nervous system signals, and muscle function.
•
Alongside sodium, potassium is also utilized in balancing fluids by helping the kidney save
fluids when we are dehydrated or excrete fluids that are in excess.
•
Potassium is thought to lower blood pressure and benefit bones
•
Short-term potassium deficiencies (often from prolonged vomiting or diarrhea) may cause
fatigue, muscle weakness and cramps, bloating, abdominal pain, and constipation.
•
Consuming high doses (typically from supplements) can lead to muscle weakness, tingling in
hands and feet, GI symptoms, and abnormal heart rhythms.
RDA: 2,000 mg
Sources: baked potatoes (926 mg per medium potato), artichokes (343 mg per medium artichoke),
plums (637 mg per ½ cup), raisins (598 mg per ½ cup), and bananas (422 per medium banana).
Threshold: Not determined
Riboflavin (Vitamin B2):
•
This water-soluble B vitamin helps convert food to fuel, encourages iron absorption in the
intestines, and also enhances the health of hair, skin, muscles, eyes, and the brain.
•
Riboflavin deficiency is uncommon, but is associated with a sore throat, cracks and sores
around the lips, an inflamed “magenta tongue” , and scaly skin.
•
Administration of niacin will reverse the neurologic symptoms and signs. 10-20 mg per day in
the presence of adequate amounts of dietary protein is sufficient.
•
While enormous intake of riboflavin may turn your urine bright yellow (a phenomenon called
flavinuria), this side effect is harmless.
RDA: Men = 1.3mg; Women = 1.1mg
Sources: milk (0.34 mg per cup), almonds (0.23 mg per ounce), cheddar cheese (0.11 mg per ounce),
eggs (0.27 mg per large egg), and enriched grains and cereals (0.59-2.27 mg per cup).
Threshold: Not determined
Selenium:
•
Thyroid hormone regulation, and also acts as an antioxidant .
•
Antioxidants
•
Chronic excess of this trace mineral is known to cause nausea, GI discomfort, and hair and nail
brittleness, and can be fatal
RDA: 55 mcg
184
Threshold: Brazil nuts (544 mcg per six kernels) are sky-high in selenium, and shrimp (34 mcg per 1012 shrimp), crabmeat (41 mcg per 3 ounces), salmon (40 mcg per 3 ounces), enriched noodles (38 mcg
per cup), beef (16 mcg per 3 ounces), and pork (35 mcg per 3 ounces)
Threshold: 400 mcg
Sodium Chloride (a.k.a. salt):
•
NaCl orsalt.
•
While it is essential for fluid balance, nerve signal transmission, muscle contractions, digestion,
and blood pressure, excess sodium intake can raise blood pressure above normal limits, increasing the
risk for hypertension and cardiovascular disease down the road .
•
Since the average daily diet already includes salt waaaay in excess, consider low-salt
alternatives like olive oil (instead of butter), unsalted nuts in favor of salted ones, and fresh fruit.
•
Salt toxicity has been noted where salt water has been used.
RDA: 500 mg of sodium; 750 mg of chloride
Sources: white bread (850 mg per two slices), pickles (800 mg per 1 spear), hot dogs (1,300 mg per
hot dog), and canned goods such as chicken noodle soup ( 3,400 mg of NaCl per cup).
Threshold: 2,300 mg of sodium (the equivalent of 5.8 g of salt per day)
Thiamin (a.k.a. Vitamin B1):
•
Another member of the water-soluble B pack, thiamin helps with food metabolism and boosts
the health of hair, skin, muscles, and the brain .
•
Toxicity has never been observed, and though thiamin deficiency (also known as beriberi) is
rare in the U.S., it’s not nonexistent.
•
Whole and enriched grains, dried beans, peas, sunflower seeds, pork
•
Dry beriberi-peripheral neuropathy in legs Cerebral beriberi-dementia, Wernicke- Korsakoff
syndrome Wet beriberi-heart failure
•
The usual treatment daily dose for adults is 50 to 100 mg IV or IM x 7 -14 days. Subsequently,
a dose of 10 mg per day po until the patient is fully recovered. Adjust dosage for children.
Improvement should be apparent within 6- 24 hours by reduced restlessness; the disappearance of
cyanosis, reduction in heart rate, respiratory rate, and cardiac size, and clearing of pulmonary
congestion.
•
Symptoms affect the cardiovascular, nervous, muscular, and gastrointestinal systems in a
variety of ways .
RDA: Men = 1.2 mg; Women = 1.1 mg
Sources: milk (0.10 mg per cup), lentils (0.17 mg per ½ cup), cantaloupe (0.11 mg per ½ fruit),
enriched long grain white rice (0.26 mg per cup), and pecans (0.19 mg per ounce).
Threshold: Not determined
Vitamin A (a.k.a. retinol, retinal, retinoic acid):
•
Though known as being good for vision, vitamin A has many other vital tasks:
•
It encourages red and white blood cell production and activity, keeps the immune system fit and
blood vessels healthy, helps rebuild bone, regulates cell growth and division, and may reduce the risk
for some cancers .
•
Retinoids, variations of Vitamin A, are also used in medications to treat various skin diseases
and acne .
•
Vitamin A deficiency can cause night blindness and, in extreme instances, complete blindness.
Vitamin A deficiency also plays a role in diarrhea and increased susceptibility to infectious diseases in
developing countries .
•
The only case of toxicity was when explorers were ingesting raw polar bear liver.
•
You can NOT overdose on carotene, but will turn a orangish yellow
185
RDA: Men = 900 mcg; Women = 700 mcg
Sources: Consider kale (443 mcg per ½ cup), eggs (91 mcg per large egg), carrots (538 mcg per ½ cup)
baked sweet potatoes (961 mcg per ½ cup), canned pumpkin (953 mcg per ½ cup), cantaloupe (467
mcg per ½ a melon), mango (79 mcg per fruit), and butternut squash (572 mcg per ½ cup).
Threshold: 3,000 mcg
Vitamin B6 (a.k.a. pyridoxal, pyridoxine, pyridoxamine):
•
This essential, water-soluble vitamin flies high above the others.
•
Vitamin B6 helps out with the production of serotonin, a hormone that plays a hand in sleep,
appetite, and mood.
•
It also assists with manufacturing red blood cells and steroid hormones, influences cognitive
and immune function, and is linked to reducing the risk of heart disease .
•
Diets lacking B6 show evidence of seizures and other neurologic systems are observed in
extreme deficiency.
•
Adverse effects from high doses are primarily seen in people taking supplements, and include
pain and numbness in the limbs .
RDA: 1.3 mg
Sources: salmon (0.48 mg per 3 ounces), chicken (0.51 mg per 3 ounces), bananas (0.43 mg per
medium banana), baked russet potatoes with the skin (0.70 mg per medium potato), hazelnuts (0.18 mg
per ounce), and cooked spinach (0.44 mg per cup).
Threshold: 100 mg
Vitamin B12:
•
Another water-soluble B vitamin, vitamin B12 offers a helping hand in the metabolism of fatty
acids and amino acids, cell creation, and the protection of nerve cells , and also may reduce the risk of
Alzheimer’s .
•
Deficiencies are common in the elderly and may cause memory loss, dementia, and anemia .
•
Toxicities are not observed, and vegetarians and vegans may even need supplements.
•
Requires an acidic stomach for ingestion. Elder should take this sublinquinally
RDA: 2.4 mcg
Sources: clams (84 mcg per 3 ounces) and mussels (20.4 mcg per 3 ounces). Beef (2.1 mcg per 3
ounces), salmon (2.4 mcg per 3 ounces), poached eggs (0.6 mcg per large egg), skim milk (0.9 mcg per
cup), and brie chees (0.5 mcg per ounce).
Treshold: Not determined
Vitamin C (a.k.a. asorbic acid):
•
Vitamin C is thought to lower the risk for some cancers, including cancers of the mouth,
esophagus, stomach, and breast .
•
It also helps make collagen,t its antioxidant properties and immune-boosting effects
•
A review of 30 research trials that included over 11,000 people showed that the incidence of
the common cold is not decreased with high Vitamin C intake .
•
Scurvy — the severe vitamin C deficiency linked to bleeding, bruising, join pain, and hair and
tooth loss .
RDA: Men = 90 mg; Women = 75mg (Smokers should add 35 mg)
Sources: Choose citrus, like OJ (100+ mg per cup) and grapefruits (76 mg per medium fruit),
strawberries (85 mg per cup), tomatoes (16 mgg per medium tomato), red peppers (95 mg per ½ cup),
and broccoli (51 mg per ½ cup).
Threshold: 2,000 mg
186
Vitamin D:
•
This essential fat-soluble vitamin is vital for normal calcium metabolism, immunity, nervous
system function, and bone density .
•
Before vitamin D can live up to its expectations, it must be activated by a burst of UV rays.
•
consider supplements or cereals, milk, and juices that are fortified with the active form, which
is equally effective.
•
Chronic deficiency puts you at risk for osteoporosis later in life.
RDA: 15 mcg
Sources: fortified cereals (1.0-1.3 mcg per cup), fortified milk (2.4 mcg per cup), canned salmon (13.3
mcg per 3 ounces), and egg yolks (0.53 mcg per large egg.
Threshold: 50 mcg
Vitamin E:
•
There are eight antioxidants, vitamin E protects essential lipids from damage, battles free
radicals, and maintains the integrity of cell membranes .
•
Deficiencys: impaired balance and coordination, muscle weakness, and pain and numbness in
the limbs, all signs of extreme deficiency .
•
More than 90 percent of Americans do not meet the recommendations for this vitamin’s daily
intake, due to the lack of being in the sun.
RDA: 15 mg
Sources: vegetable oils like olive oil (1.9 mg per tablespoon), canola oil (2.4 mg per tablespoon),
almonds (7.4 mg per ounce), avocados (2.7 mg per avocado), and hazelnuts (4.3 mg per ounce).
Threshold: 1,000 mg
Vitamin K:
•
This essential fat-soluble vitamin is a must for normal wound healing and bone development .
•
K is for “koagulation,” the German word for coagulation, or clotting.
•
While blood clots sound menacing, consider the importance of scabs, which are simply patches
of clotted blood to protect cuts and scrapes.
•
Ladies taking birth control pills should be careful with overconsumption of vitamin K, as a
combination of the birth control pill and excess Vitamin K could put you at risk for unwanted clots
deficiencies in vitamin K include easy bruisability, bleeding, nosebleeds, and heavy menstrual periods.
RDA: Men = 120 mcg; Women = 90 mcg (AI)
Sources: cooked broccoli (220 mcg per cup), kale (547 mcg per cup), parsley (246 mcg per ¼ cup), and
Swiss chard (299 mcg per cup).
Threshold: Not determined
Zinc:
•
A trace element that is a building block for enzymes, proteins, and cells.
•
It is also responsible for freeing Vitamin A from the liver, through its enzymatic activity .
•
Zinc also plays a role in boosting the immune system, mediating senses such as taste and smell,
( a lack of taste in the elderly is an indication of a deficiency) and wound healing .
•
Zinc toxicity is rare,
•
zinc deficiency (most commonly occurring in the developing world) may lead to delays in
growth and development, rough skin, cognitive impairment, a weakened immune system (leading in
increased susceptibility of infectious diseases, particularly in kids
•
Topically used as an antimicrobial.
RDA: Men = 11 mg; Women = 8 m
187
Sources:oysters (76.3 mg per 6 oysters), beef (6 mg per 3 ounces), turkey (3.8 mg per 3 ounces), milk
(1.8 mg per cup), and cashews (1.6 mg per ounce). Vegetarians and vegans take note: zinc is less easily
absorbed from vegetables so consider supplements or munching on more zinc rich foods.
Threshold: 40 mg
188
STANDARD MEDICATIONS
PHARMACOLOGY
GUIDELINES AND CONSIDERATIONS: The key to drug use is using caution. Familiarity with
adverse drug effects and preparedness to deal with those effects are also paramount to safe use. The
following factors can influence the therapeutic effects of medications:
• Age
• Body Weight
• Sex
• Route of administration
•Time of administration
• Rate of inactivation and excretion
• Pathological state
• Genetic factors • Drug interaction
• Tolerance
Pharmaceuticals are expiration dated and should be rotated to avoid waste.
Allergy and Hypersensitivity:
Hypersensitivity reactions can vary in their presentation.
Antibiotics are the most common cause, however, any medication may be at fault.
Allergic reaction to any antigen, e.g. snake envenomation, insect stings, pollens, etc., can cause
similar symptoms.
Reactions may include, but are not limited to:
• Allergic rhinitis, urticaria (hives), reactive airway/asthma or profound hypotension.
• Local reactions may include GI distress and/or dermal presentation, e.g. nausea, vomiting,
cramps, diarrhea, pruritic skin, hives, local rash.
• Life threatening reactions (such as anaphylaxis) can occur in seconds to minutes and may include:
•• Tightness in the chest and wheezing
•• Skin changes: diffuse redness, hives and flushing
•• Angioedema or swelling of the periorbital and perioral area
•• Rapidly progressive respiratory distress due to laryngeal edema, bronchospasm and
fluid accumulation in the lungs.
•• Hypotension/overt signs of shock
OBSERVE THE FOLLOWING:
1. Medications are not always indicated. You must weigh the benefits against the potential adverse
patient and mission effects.
2. All medications have potential adverse effects and many patients have a history of adverse reactions
to various medications. In a conscious patient obtain a drug history. In an unconscious patient search
for identification/warning tags denoting medication sensitivities.
3. Recommended doses will be followed.
4. When using IV medication, have a reliable IV fluid line running and inject the medication into the
rubber fitting in the IV line.
5. When injecting through a saline lock, flush the lock with 10 cc of normal saline after administering
the medication.
6. In addition to medication, your patient will require maintenance fluids, electrolytes, and nutritional
balance.
7. CAUTION: Be prepared for anaphylactic reactions at all times.
189
CHAPTER 36
MEDICINES OF CHOICE
AEROBIC BACTERIA
Infecting Organism
Medication of Choice
Alternatives
A. Gram-positive Cocci
1. Staphylococi
a. S. aureus (methicillin-sensitive)
PRP, Cephalosporin
b. S. aureus (methicillin-resistant)
Vancomycin
c. S. epidermidis
Quinupristin-dalfopristin
Vancomycin
Linezolid, Quinupristindalfopristin
2. Streptococci
a. Streptoccocus, Group A, B, C, G,
S. viridans and penicillin-sensitive
pneumoniae
pneumoniae with high level
penicillin-resistance
c. Enterococci
Penicillin G or V
Vancomycin
Vanocomycin, Clindamycin,
(1st generation)
Sulfatrimethaprim
Clindamycin, Sulfatrimethoprim, Linezolid,
Cephalosporin (1st
generation),
Vancomycin, Clindamycin, S.
Erythromycin, Azithromycin b. S.
Levofloxacin
Ampicillin and Gentamicin
Vancomycin and
Gentamicin
B. Gram-positive Bacilli
1. Bacillus anthracis
2. Corynebacterium diphtheriae
3. Listeria monocytogenes
Penicillin or Ciprofloxacin
Erythromycin and Antitoxin
Ampicillin or Penicillin
Doxycycline
Clindamycin, Penicillin G
Sulfa-trimethoprim
C. Gram-negative Cocci
1. Neisseria gonorrhoeae
Ceftriaxone or
2. Neisseria meningitidis
3. Moraxella catarrhalis
Penicillin G or V
Sulfa-trimethoprim,
D. Gram-negative Bacilli
1. Escherichia coli
Sulfa-trimethoprim
(if sensitive)
Cefixime
Fluoroquinolone
Ceftriaxone
Azithromycin,
doxycycline
Amoxicillin-clavulanate
Cephalosporin (3rd
generation),
fluoroquinolone
190
2. Enterobacter species
Imipenem
3. Klebsiella species
Imipenem
4. Pseudomonas aeruginosa
5. Proteus species
APP
APP
6. Serratia marcescens
Cephalosporin (3rd
generation)
7. Salmonella typhi
Fluoroquinolone, Cephalosporin
(3rd generation)
Fluoroquinolone, Cephalosporin
(3rd generation)
Ceftazidime
Cephalosporin (3rd generation),
fluoroquinolone
Imipenem, Fluoroquinolone
10. Brucella species
Sulfa-trimethoprim
fluoroquinolone
Ceftriaxone or
Azithromycin, doxycycline,
fluoroquinolone
Amoxacillin-clavulanic acid
Ceftriaxone or
Amoxicillin-clavulanic acid,
Azithromycin, fluoroquinolone
Erythromycin
Doxycycline and rifampin
Doxycycline and Gentamicin
11. Francisella tularensis
Streptomycin or gentamicin
12. Yersinia pestis
Streptomycin
8. Haemophilus influenzae
9. Haemophilus ducreyi
Ceftriaxone or
Doxycycline
Gentamicin
ANAEROBIC BACTERIA
1. Clostridium tetani
2. Bacteroides species
ACID FAST BACILLI
1. Mycobacterium tuberculosis
2. M. kansasii
3. M. avium intracellulare complex
4. M. leprae
Penicillin and tetanus toxoid
Metronidazole
Isoniazid + Rifampin+Pyrazinamide + Ethambutol
Isoniazid + Rifampin+ Ethambutol
Clarithromycin + Ethambutol
Azithromycin + Ethambutol +
+ Rifabutin
Rifabutin
Rifampin + Dapsone
(paucibacillary disease)
ACTINOMYCETES
Imipenem, Clindamycin,
Metronidazole
and tetanus immune globulin
Imipenem, Clindamycin,
Betalactam- betalactamase
inhibitor
Rifampin + Dapsone +
Clofazamine
(multibacillary disease)
1. Nocardia species
2. Actinomyces species
Sulfa-trimethoprim
Penicillin
Minocycline + sulfonamide
Clindamycin
191
MISCELLANEOUS
1. Chlamydia species
2. Rickettsia species
3. Treponema pallidum (syphilis)
4. Mycoplasma pneumoniae
5. Pneumocystis carinii
Doxycycline
Doxycycline
Penicillin
Azithromycin
Sulfa-trimethoprim
Erythromycin
Chloramphenicol
Ceftriaxone
Doxycycline
Pentamidine
1. Aspergillus species
2. Blastomyces dermatitidis
3. Coccidioides immitis
4. Cryptococcus neoformans
Amphotericin
Amphotericin
Fluconazole
Amphotericin
Itraconazole
Itraconazole
Amphotericin
Fluconazole
5. Histoplasma capsulatum
6. Candida species
7. Sporothrix schenckii
iodide
8. Tinea versicolor
Amphotericin
Amphotericin
Itraconazole
Itraconazole
Fluconazole
Saturated solution of potassium
Topical selenium sulfide
Ketoconazole
FUNGAL
VIRUSES
1. Herpes simplex
2. Herpes zoster
3. Influenza
Acyclovir
Valacyclovir, Famciclovir
Acyclovir
Valacyclovir, Famciclovir
Amantadine or rimantadine or zanamivir or oseltamivir
ANALGESIC’S & ANESTHETICS
Lidocaine HCL 2% (Xylocaine): Local anesthetic
• See ACLS drugs for cardiac therapy.
• CAUTION: Some lidocaine solutions contain 1:10,000 epinephrine. This causes
intense vasoconstriction, and prolongs the duration of the anesthesia. These solutions
are identified by a red label or red lettering on the label. DO NOT use solutions containing epinephrine
on or near the fingers, toes, nose, ears or penis.
Rx: (As a local anesthetic): Suturing, debridement, nerve blocks, thoracostomy or other similar
procedures. Duration of anesthesia is 30-60 minutes.
Dose: To desired effect.
• Maximum single adult dose is 4.5 mg/Kg or 300 mg (15 cc’s of the 2% solution contains 300 mg
lidocaine).
• NOTE 1: This is different max dose than with IV lidocaine for ACLS use.
• NOTE 2: 2% lidocaine contains 20 mg of lidocaine per cc. Diluting 2% lidocaine 1:1 with
normal saline gives a 1% solution (10 mg per cc) that is just as effective as the 2% solution.
Contra: 2nd degree, 3rd degree, hypotension, Stokes-Adams Syndrome
SE: slurred speech, altered mental status, tinnitus, edema
AR: Skin: dermatologic reactions, status asthmaticus, anaphylaxis, and seizures
192
Morphine Sulfate: Narcotic analgesic (opiod). Alters perception of pain and emotional response to pain.
Have Narcan available when using Morphine.
Rx: Severe Pain, pain from cardiac ischemia, CHF
• Alters perception & emotional response to pain
Contra: Respiratory depression, hypotension, head injury
Dose: 4-15 mg IV slow push (Dilute in 5 cc saline & inject slowly over 4-5 min)
Peds: 0.1-0.2 mg/Kg SC. Do not exceed 15 mg.SE: ↓ RR, hypotension, bradycardia, N & V, dizziness,
pruritus and skin flushing
AR: Seizures with large doses, constipation, ileus, urinary retention
Narcan (Naloxone HCL): Narcotic antagonist.
Rx: Known or suspected narcotic-induced respiratory depression.
• NOTE: Have available when using morphine.
• WARNING: The duration of action of Narcan is 20-40 minutes, much less than the
duration of action of morphine. After use of Narcan, observe patient closely, repeat
doses of Narcan may be necessary after 20-30 minutes.
Dose: 0.4-2 mg IV. Repeat q. 2-3 min/prn.
• Duration is 20-40 minutes (< duration of action of morphine). Repeat doses of may be necessary after
20-30 minutes.
• Peds: 0.01 mg/Kg dose IM, IV or SC q. 2-3 min.
116
•• If initial dose does not result in clinical response, increase dose up to 0.1 mg/Kg
•• If no response after 10mg has been administered, diagnosis of narcotic-induced
toxicity should be questioned.
SE: In narcotic dependent patient, withdrawal symptoms may be precipitated.
ANTIBIOTICS
Cefotetan (cefotan): Broad-spectrum bactericidal antibiotic for IV/IM use (cephalosporin)
Rx: For serious infections of: Lower respiratory tract (i.e. pneumonia); urinary tract; skin
infections; intra-abdominal infections (especially penetrating abdominal trauma); & penetrating trauma
to the extremities.
• NOTE: NOT effective in CNS infections (see Rocephin)
Contra: Use caution in pts w/ hx of penicillin allergy, hepatic and/or liver dysfunction
• Not recommended for children
Dose: 1-2 Gm IV/IM q. 12 hours
SE: headaches, dizziness, nausea, vomiting, diarrhea, abdominal cramps, urticaria, elevated
temperature
AR: eosinophilia, thrombocytosis, leukopenia; pain at injection site; induration, sterile abscess, tissue
sloughing, phlebitis; thrombophlebitis with IV use.
Cipro (Ciprofloxacin): Broad-spectrum oral antibiotic (quinolone).
Rx: Infectious diarrhea, Typhoid, acute sinusitis, wounds contaminated by seawater or freshwater,
some biological warfare bacteria
Contra: Not be used by pregnant women. Not recommended for children < 18 y.o. Dose: 500 mg q.
12hrs (take w/ meals). Continue for two days after symptoms resolve. SE: syncope, irritability, lethargy,
drowsiness, urticaria, edema, dyspnea,
AR: GI bleed, insomnia, nightmares, manic reaction, ataxia, seizures, depression, parethesias,
blurred vision, diplopia, tinnitus, joint or back pain, gout, acidosis, HTN, angina, AMI, bronchospasm
193
Garamycin (Gentamycin) Ophthalmic Ointment: Ophthalmic antibiotic ointment.
• Erythromycin Opthalmic Ointment can be substituted. Use/dose are the same.
• No corneal toxicity noted w/ erythromycin.
Rx: conjunctivitis, prophylaxis for ocular infection.
Dose: Instill 1/2 to 1 inch of ointment into conjunctival sac q.i.d. and at bedtime. Contra: Known
allergy
SE: Hypersensentivity, photophobia, slowed corneal wound healing
AR: corneal toxicity w/ prolonged use (> 5 days), overgrowth of nonsusceptible organisms.
Keflex (Cephlexin): Broad-spectrum bactericidal oral antibiotic (cephalosporin)
Rx: Respiratory, genito-urinary tract infections, skin and soft tissue infection, bone and joint infection.
Contra: Use caution in pts w/ hx of penicillin allergy, hepatic and/or liver dysfunction
Dose: 250 mg to 1 gm PO q. 6hrs. Peds: 6 - 12 mg/Kg PO q6h.
SE: dizziness, headache, malaise, N & V, diarrhea, urticaria
AR: neutropenia, eosinophilia, anemia, parethesias, abdominal cramps, skin disorders
Mefoxin (Cefoxitin sodium): Broad-spectrum antibiotic for IV/IM use. (cephalosporin)
• Similar to Rocephin, but covers GI organisms better. Does not cover CNS infections or penetrating
trauma to CNS. Similar in coverage to Cefotan.
Rx: As an alternative to Rocephin. Infections of GI, lower respiratory, and urinary tracts. Contra: Use
caution in pts w/ hx of penicillin allergy, hepatic and/or liver dysfunction Dose: 1-2 grams IV/IM q. 6–
8/hrs.
Peds: 80-160 mg/Kg per 24 hours, divided into 3-4 doses 6-8 hours apart.
SE: headaches, dizziness, nausea, vomiting, diarrhea, abdominal cramps, urticaria,
↑ temperature
AR: eosinophilia, thrombocytosis, leukopenia; pain at injection site; induration, sterile
abscess, tissue sloughing, phlebitis; thrombophlebitis with IV use.
Rocephin (ceftriaxone sodium): Broad-spectrum bactericidal antibiotic for IV/IM use. (cephalosporin)
Rx (Serious infections of): Lower respiratory tract (i.e. pneumonia); urinary tract; skin infections;
intra-abdominal infections (especially penetrating abdominal trauma); penetrating trauma to the
extremities; & CNS infections
Contra: Use caution in pts w/ hx of penicillin allergy, hepatic and/or liver dysfunction
Dosage: 1-2 gm IM/IV daily or in divided doses bid; Max dose 4 gm/day
Peds: 50-75 mg/Kg given in divided doses q12 hours, max dose 2 gm/day.
Preparation procedure:
1. W/draw 10cc NaCl from a 100cc bag. Inject 10cc NaCl into 1 gm Rocephin vial. Mix.
2. W/draw entire contents of vial and inject into original 100cc NaCl IV bag. Mix.
3. Piggyback with running IV.
NOTE: If giving IM, reconstitute with 1% lidocaine WITHOUT epinephrine.
SE: headaches, dizziness, N & V, diarrhea, abdominal cramps, urticaria, ↑ temperature
AR: eosinophilia, thrombocytosis, leukopenia; pain at injection site; induration, sterile
abscess, tissue sloughing, phlebitis; thrombophlebitis with IV use.
Silvadene Cream (Silver sulfadiazine) Topical microbial
Rx: Treatment and prevention of sepsis in 2nd and 3rd degree burns.
Dosage: Using sterile technique, apply thick layer to burn area, cover w/ saran wrap (if available), then
bulky dressing. Change dressing q. 12-24 hours.
• It is normal for silvadine will turn gray/black color on exposure to light.
Contra: G6PD deficiency. Do not use on face. Use extreme caution in sulfa sensitivity.
SE: burning sensation, rash
AR: transient leukopenia, systemic sulfa reaction
194
ANTIHISTAMINES
Benadryl (Diphenhydramine HCL): Antihistamine.
• Prevents (but does not reverse) histamine-mediated responses.
Rx: Mild to moderate allergic symptoms and/or allergic reactions, dystonic reaction
Dose: 25-50mg IM/IV or 25-50mg/PO/t.i.d.
• Max dose 400mg/day • May be given PO, IM or IV
Peds: (Children < 12 years): 5 mg/Kg/day in divided doses q.i.d. • May be given PO, IM or IV
Contra: asthma, pregnant or lactating females
SE: sedation, blurred vision, N & V, vomiting, diarrhea, headache
AR: insomnia, vertigo, palpitations, dry mouth, constipation, dysuria, urine retention
Phenergan (Promethazine Hydrochloride): Antihistamine
• Prevents but does not reverse histamine mediated response.
• Phenergan can induce an acute dystonic reaction (symptoms may resemble a
stroke). Rx w/ 25-50 mg of Benadryl IV or IM. Symptoms normally resolve within 15-20
minutes.
Rx: Motion sickness, nausea and vomiting, sedation. Dose: 25-50 mg IM q. 4-6h prn. (IM Injection is
painful).
Peds: 0.5-1mg/Kg IM q6-8h prn not to exceed 25 mg.
IV administration:
• Administer over a prolonged time > 5 min and through a free flowing IV line, rather than a saline
lock.
• The 50-mg/ml formulation must be diluted to 25 mg/ml (50/50 dilution) or less before being
administered IV.
• Dosage is 12.5-25 mg every 6-8 hours.
• Peds: 0.5-1mg/Kg IM q6-8h prn not to exceed 25 mg.
Contra: Additive effect w/ ALL other sedation medication. May cause excessive drowsiness or
apnea. Monitor patient closely.
SE: hypotension, dry mouth, constipation, restlessness, N & V
AR: confusion, acute dystonic reaction, anorexia, photosensitivity, urine retention
ANTI-INFLAMMATORY’S
Decadron (Dexamethasone): Parenteral steroid. (glucocorticoid)
Rx: Emergency treatment of AMS, HACE, HAPE, when tactical conditions preclude descent or
acclimatization
• Use of Decadron ↓symptoms of AMS, but does not speed acclimatization.
• Use of Decadron does not preclude the need for an emergency descent. (Administer
Decadron every 6 hours until descent is accomplished)
Dosage: 4mg IV/IM or PO every 6 hours
Contra: Use caution in pts w/ hx of diabetes, hypertension, and ulcers
SE: delayed wound healing, acne, various skin eruptions, edema
AR: Usually dose related. Psychotic behavior, CHF, HTN, cataracts, glaucoma, hypokalemia,
hyperglycemia, and carbohydrate intolerance
Motrin (Ibuprofen): Analgesic, antipyretic (NSAID) Rx: mild to moderate pain, arthritis
Dose: 200-800 mg PO t.i.d. or q.i.d. Not to exceed 2400 mg/day (800 mg TID) Contra: Penetrating
trauma, suspected internal bleeding, or suspected intracranial bleeding, pregnancy, nursing mothers.
• NOTE: Should not be given to pts w/ hx of aspirin sensitivity or severe asthma.
SE: N & V, headache, dizziness, drowsiness
AR: Prolonged bleeding time, tinnitus, edema, peptic ulcer
196
Solumedrol (Methylprednisolone): Parenteral steroid. Decreases inflammation, reduces immune
response in allergic conditions. (glucocorticoid)
Rx: Severe inflammation, severe asthma, severe allergic reaction, anaphylaxis.
• For blunt, Non-Penetrating, spinal chord trauma w/ SxS of spinal chord injury.
• Most effective when started as soon as possible after the injury occurs.
Dose: 125 mg IM or IV q. 6hrs. Peds: 1-2 mg/Kg IV or IM q. 6hrs
Anaphylaxis: 125 mg IV or IM (see protocol)
Spinal trauma: Initial bolus = 30mg/kg IV slow push followed by IV drip of
5.4 mg/kg/hr for subsequent 23 hours (see protocol)
• If started > 6 hrs after the original injury, continue the IV drip for 48 hours.
• All persons started on the Solu-Medrol protocol should also receive ulcer prophylaxis
of Zantac 50 Mg IV or IM every 6-8 hours, or 150 Mg orally every 12 hours.
Contra: Use caution in pts w/ hx of diabetes, hypertension, ulcers
SE: delayed wound healing, acne, various skin eruptions, edema
AR: Usually dose related. Psychotic behavior, CHF, HTN, cataracts, glaucoma, hypokalemia,
hyperglycemia, and carbohydrate intolerance
Toradol (Ketorlac Tromethamine): Analgesic (NSAID)
Rx: Short term pain relief (especially musculoskeletal pain).
• May be used as single or multiple dose, for the management of moderately severe, acute pain
requiring analgesia at the opiate level
• Analgesic effect starts w/in 30 minutes of administration, peaks at 2 hours.
• Increasing dosage does not increase analgesic effect. If additional analgesia is
needed, consider using small doses of morphine.
Dose: 30 mg IM or IV. May be repeated every 6 hours prn; not to exceed 120 mg per day;
total duration of therapy not to exceed 5 days
• Rapid IM injection is painful. Administer slowly into deep muscle
• IV bolus must be given over no less than 15 seconds
Contra: Penetrating trauma; Suspected internal bleeding; Suspected intracranial bleeding;
Pts currently receiving aspirin, NSAIDs, or anticoagulant therapy; active peptic ulcers or recent GI
bleed
• Use w/ extreme caution in pts w/ hx of: renal & liver disease, COPD, asthma, ulcers, bleeding
disorders, elderly, diabetes
SE: Nausea, GI bleed, edema.
• Does not usually cause drowsiness or altered mental status. Check for other causes of altered mental
status.
AR: GI bleeding and/or perforation; renal impairment and/or failure; inhibits platelet function
MISCELLANEOUS
Activated Charcoal
Class: Adsorbent
Actions: Adsorbs toxins by chemical binding and prevents gastrointestinal adsorption.
Indications: Poisoning following emesis or when emesis is contraindicated.
Contraindications: None in severe poisoning.
Precautions: Should only be administered following emesis, in cases in which it is so indicated. Use
with caution in patients with altered mental status. May adsorb Ipecac before emesis; If Ipecac is
administered, wait at least 10 minutes to administer activated charcoal.
Side Effects: Nausea, vomiting, and constipation.
Dosage: 1 g/kg (typically 50-75 grams) mixed with a glass of water to form a slurry.
Routes: Oral
Pediatric Dosage: 1 g/kg mixed with a glass of water to form a slurry
197
Alcohol, Ethyl (Ethanol) (EtOH)
Class: Solvent, depressant
Description:A colorless, volatile, flammable liquid of the formula C2H5OH. Acts as a depressant on
the CNS when taken in excessive amounts. Used IV to stop premature labor.
The other to "common" Alcohols are Isopropyl (C3H7OH, Isopropanol, IPA), and Methyl (CH3OH,
Methanol, MeOH).
Afrin Nasal Spray (Oxymetazoline HCL): Vasoconstrictor (decongestant)
Rx: Use as an adjunct to clear ears and sinuses during compression and decompression. Dose: Spray
into each nostril 2 times, twice daily. Not to exceed three consecutive days.
• NOTE: Do not tilt head backwards while spraying.
Contra: Severe damage to tympanic membrane/sinuses from barotrauma (see Barotrauma)
SE: Burning, sneezing and stinging of nasal mucosa
AR: Rhinitus
Atropine sulfate: Vagolytic
Rx: Organophosphate or chemical poisoning, asthma, symptomatic bradycardia (see ACLS
medications)
• NOTE: Successful treatment of organophosphate or chemical exposure may require mass quantities
and repeated administration of atropine.
Dosage: 0.5-1.0 mg q. 5 minutes up to max dosage is 3 mg (0.04 Mg/Kg).
• Organophosphate poisoning: 2-5 mg IV q. 15-30 minutes
• Pediatric: 0.015 mg/Kg up to a maximum dose of 0.04 mg/Kg.
Contra: Atrial fibrillation, atrial flutter, glaucoma
• Use extreme caution in patients w/ hx of Type ll AV block and in 3rd degree block.
SE: Dilated pupils, ↑HR, VT, VF, dry mouth
AR: Delirium
Diamox (acetazolamide): Non-diuretic antihypertensive(carbonic anhydrase inhibitor)
Rx: Prevention and/or amelioration of symptoms associated with acute mountain sickness in climbers
attempting rapid ascent and/or in those who are very susceptible to acute mountain sickness despite
gradual ascent.
• For maximum benefit begin regimen 7 days prior to ascent
• Of minimal benefit in Rx of AMS, HACE, or HAPE
Dose: 125-250 mg b.i.d., 24 hours prior to ascent, continuing for 48 hours after ascent.
• Prevention and/or amelioration benefits is nominal once ascent has commenced
• If the 500 mg sustained release tablet is used, dose is 500 mg every 24 hours.
Contra: Sulfa allergy.
SE: Paresthesia in extremities, hearing dysfunction/tinnitus, loss of appetite, taste alterations, N & V,
diarrhea, polyuria, drowsiness and confusion.
NOTE: Use of Diamox results in a significant alteration in taste. Carbonated beverages will have
seriously altered taste, and may be undrinkable.
• Increased fluid intake is required with use of Diamox: It is a diuretic, and can result in serious
dehydration unless great care is taken to maintain proper hydration.
AR: Transient myopia (usually resolves w/ DC of drug). Uticaria, melena, hematuria, flaccid paralysis,
photosensitivity, convulsions.
198
Epinephrine (Adrenaline): Alpha and beta adrenergic sympathomimetic. First-line drug for anaphylaxis
(See ACLS drugs for cardiac therapy)
• Causes bronchodilitation, vasoconstriction, increases blood pressure.
• Decreases edema/swelling due to allergic reactions.
• NOTE: 1:1,000 dilution epinephrine (1mg in 1 cc) is standard pararescue issue. 1:10,000
dilution (1 mg in 10cc) is the standard ‘Cardiac’ dosage form, the only dilution that can be
used IV. 1:1,000 epinephrine can be diluted to the 1:10,000 form by putting 1 cc of 1:1,000
epinephrine (1 mg epinephrine) in 9 cc’s of normal saline.
Rx: Anaphylaxis, Allergic reactions (mild/moderate/severe), & Asthma
Dose: Anaphylaxis: 0.3-0.5 mg (3-5 cc of 1:10,000 dilution) IV or
0.3-0.5 mg (0.3-0.5 cc of 1:1,000 dilution) IM
Allergic reaction: 0.2-0.5 mg (0.3-0.5 cc of 1:1,000 dilution) SubQ or IM Asthma: 0.3-0.5 mg (0.3-0.5
cc of 1:1,000 dilution) SubQ
Pediatric: 0.01 mg/Kg SubQ or IM. Not to exceed 0.5 mg
Contra: 1:1,000 Epi is NOT given IV.
• Use caution in pts with a hx of heart disease, or over the age of 40.
• Do not inject Epi (or solutions containing Epi) into/near the fingers, toes, nose,
ears or penis. Intense vasoconstriction may cause necrosis.
SE: Cardiac arrhythmias, VT, VF, angina, HTN, ↑BP, nausea and vomiting, vasoconstriction
AR: Uncontrolled effects on myocardium & arterial system
Imodium (loperamide HCL) Anti-Diarrheal (opiod) Rx: Treatment of acute diarrhea.
• For use in acute, non-invasive diarrhea only.
• Refer to medical emergencies if blood and/or mucus are present in stool, or diarrhea is
associated with fever (infectious diarrhea).
• NOTE: The best course of action for acute diarrhea is to allow it to “run its course”. Ensure copious
hydration.
Dose: 2 capsules (4 mg) first dose, then 1 capsule (2 mg) after every unformed stool, not to exceed 10
mg (5 capsules) in 24 hours.
• Use only if control of diarrhea is critical for continued operations.
Contra: Acute dysentery. Not for use in children < 12 y.o.
SE: Abdominal pain/distention, N & V, severe constipation, drowsiness, dizziness. AR:
Hypersensitivity
Lasix (Furosemide): Diuretic
Rx: CHF w/ pulmonary edema, acute pulmonary edema, hypertensive crisis
• Use in HAPE is controversial, not currently recommended without direct physician control.
• Should have a urinary catheter in place to monitor urine output.
Dosage: 20-40 mg slow IV push.
Peds: 1mg/kg IV or IO slow push.
Contra: Dehydration, hypotension, hypokalemia, hepatic coma
SE: Hypokalemia, hypotension, dehydration
AR: Agranulocytosis, leukopenia, thrombocytopenia; transient deafness w/ rapid IV
Mannitol: Osmotic diuretic
Rx: ICP; Myoglobinuria secondary to crush syndrome and rhabdomyolysis
Dose: 0.25-1.0 grams/Kg IV (Takes effect w/in minutes of administration and can last 6-8 hours)
• Increases urine flow, making this an unreliable indicator of resuscitation.
• Use mannitol ONLY if there is evidence of ICP.
199
Contra: suspected/actual renal failure, suspected/actual intracranial hemorrhage
SE: headache, nausea/vomiting, blurred vision, dizziness, rash, dehydration
AR: seizures, pulmonary edema, cardiovascular collapse.
Valium (Diazepam): General CNS depressant (Anticonvulsant/sedative).
Rx: Acute anxiety, seizures, status epilepticus, relaxation of skeletal muscle
• Drug of choice for treatment of convulsions associated with chemical agents or organophosphates.
NOTE: Successful treatment of convulsions from organophosphate or chemical exposure may require
mass quantities and repeated administration Valium.
•Overdose may be reversed w/ Flumazenil
Dose: • Status Epilepticus: 5-10 mg IV slow push
• Acute anxiety: 5-15 mg IV slow push
• Relaxation of skeletal muscle: 5-15 mg IV slow push
• Chemical Warfare∗: 10-15 mg IV slow push
∗Auto injection Diazepam should be used for seizures induced by chemicals
Contra: head injury, ↓BP, acute narrow angle glaucoma
• Has additive effect with other respiratory depressants (morphine, phenergan and alcohol). Be
prepared to perform BLS.
SE: ↓BP, ↓Respirations, drowsiness, venous irritation, pain at injection site, N & V AR: bradycardia,
CV collapse, amnesia, abdominal discomfort
Zantac (ranitidine): H-2 blocker; ↓ secretion of stomach acid
• NOTE: Drug Interactions: ↓absorption of oral diazepam.
Rx: Gastric and/or peptic ulcers, upper GI bleeds, prevention of stress ulcers in burn
victims or patients on steroid treatment.
• Drug of choice for treatment of gastric or peptic ulcers.
• Adjunct in treatment of urticaria and anaphylaxis.
Dosage: 50 mg IV or IM q. 6-8 hours for ulcers, burns, steroid use, upper GI bleeds, urticaria
or anaphylaxis.
• Oral dose: 150 mg b.i.d. for ulcer, urticaria.
• Peds: 1.5 mg/Kg IV x 1, then 0.75 mg/Kg IV every 12 hours
Contra: Known/suspected liver disease
SE: Headache, diarrhea/constipation, muscle aches, vertigo, malaise, dry mouth, N & V AR:
Thrombocytopenia, liver toxicity.
ALAPHABETICAL RX
Adenosine (Adenocard)
Class: Antiarrhythmic
Indications: symptomatic PSVT
Contraindications: second- or third-degree heart block, sick-sinus syndrome
Precautions: Arrhythmias, including blocks, are common at the time of cardioversion. Use with caution
in patients with asthma.
Side Effects: Facial flushing, headache, shortness of breath, dizziness, and nausea.
Dosage: 6 mg given as a rapid IV bolus over a 1-2 second period; if, after 1-2 minutes, cardioversion
does not occur, administer a 12-mg dose over 1-2 seconds.
Routes: IV; should be administered directly into a vein or into the medication administration port
closest to the patient and followed by flushing of the line with IV fluid.
200
Albuterol (Proventil) (Ventolin)
Class: Sympathomimetic (ß2 selective)
Actions: Bronchodilation
Indications: Asthma reversible bronchospasm associated with COPD
Contraindications: symptomatic tachycardia
Precautions: Blood pressure, pulse, and EKG should be monitored use caution in patients with known
heart disease
Side Effects: Palpitations, anxiety, headache, dizziness, and sweating
Dosage: Metered Dose Inhaler: 1-2 sprays (90 micrograms per spray)
Small-Volume Nebulizer: 0.5 ml (2.5 mg) in 2.5 ml normal saline over 5-15 minutes
Rotohaler: one 200-microgram rotocap should be placed in the inhaler and breathed by the patient
Routes: Inhalation
Aminophylline
Class: Xanthine bronchodilator
Actions: Smooth muscle relaxant, causes bronchodilation, has mild diuretic properties, increases heart
rate.
Indications: Bronchial asthma, reversible bronchospasm associated with chronic, bronchitis and
emphysema, congestive heart failure, pulmonary edema.
Contraindications: hypotension, patients with peptic ulcer disease.
Precautions: Monitor for arrhythmias. Monitor blood pressure. Do not administer to patients on chronic
theophylline. Preparations until the theophylline blood level has been determined.
Side Effects: Convulsions, tremor, anxiety, and dizziness vomiting palpitations, PVCs, and tachycardia.
Dosages: Method 1: 250 - 500 mg in 90 or 80 ml of d5w, respectively, infused over 20-30 minutes
(approximately 5-10 mg/kg/hr)
Method 2: 250 - 500 mg (5-7 mg/kg) in 20 ml of D5W infused over 20-30 minutes
Routes: Slow IV infusion.
Pediatric Dosage: 6 mg/kg loading dose to be infused over 20-30 minutes; maximum dose not to
exceed 12 mg/kg per 24 hours.
Amrinone (Inocor)
Class: Cardiac inotrope.
Actions: Increases cardiac contractility, vasodilator.
Indications: Short-term management of severe CHF.
Contraindications: Patients with history of hypersensitivity to the drug.
Precautions: May increase myocardial ischemia. Blood pressure, pulse, and EKG should be constantly
monitored. Amrinone should only be diluted with normal saline or 1/2 normal saline; no dextrose
solutions should be used. Furosemide (Lasix) should not be administered into an IV line delivering
Amrinone.
Side Effects: Reduction in platelets, nausea and vomiting cardiac arrhythmias.
Dosage: 0.75 mg/kg bolus given slowly over 2-3 minute interval followed by maintenance infusion of
2-15 µg/kg/minute.
Routes: IV bolus and infusion as described earlier.
Pediatric Dosage: Safety in children has not been established.
Aspirin (Bufferin)
Class: Platelet inhibitor/anti-inflammatory.
Actions: Blocks platelet aggregation.
Indications: New-onset chest pain suggestive of MI signs and symptoms suggestive or recent CVA.
Contraindications: Patients with history of hypersensitivity to the drug.
201
Precautions: GI bleeding and upset.
Side Effects: Heartburn, nausea and vomiting, wheezing.
Dosage: 150-325 mg PO or chewed.
Routes: PO.
Pediatric Dosage: not recommended.
Atropine
Class: Parasympatholytic (anticholinergic).
Actions: Blocks acetylcholine receptors, increases heart rate, decreases gastrointestinal secretions.
Indications: Hemodynamically-significant bradycardia, hypotension secondary to bradycardia, asystole,
organophosphate poisoning.
Contraindications: None when used in emergency situations.
Precautions: Dose of 0.04 mg/kg should not be exceeded except in cases of organophosphate
poisonings, tachycardia, hypertension.
Side Effects: Palpitations and tachycardia, headache, dizziness, and anxiety, dry mouth, pupillary
dilation, and blurred vision, urinary retention (especially older males).
Dosage: Bradycardia: 0.5 mg every 5 minutes to maximum of 0.04 mg/kg.
Asystole: 1 mg.
Organophosphate poisoning: 2-5 mg.
Routes: IV, ET (ET dose is 2 - 2.5 times IV dose).
Pediatric Dosage: Bradycardia: 0.02 mg/kg
Maximum single dose (child 0.5 mg) (adolescent 1.0 mg)
Maximum total dose (child 1.0 mg) (adolescent 2.0 mg)
Bretylium (bretylol)
Class: Antiarrhythmic.
Actions: Increases ventricular fibrillation threshold, blocks the release of Norepinephrine from
peripheral, sympathetic nerves.
Indications: Ventricular fibrillation refractory to Lidocaine, ventricular tachycardia refractory to
Lidocaine, PCVs refractory to first-line medications.
Contraindications: None when used in the management of life-threatening arrhythmias.
Precautions: Postural hypotension occurs in almost 50% of patients receiving Bretylium. Patient must
be kept supine decrease dosage in patients being treated with catecholamine sympathomimetics.
Side Effects: Hypotension, syncope, and bradycardia, Increased frequency of arrhythmias, dizziness
and vertigo.
Dosage: 5 mg/kg. may be repeated at dose of 10 mg/kg up to a total dose of 30 mg/kg.
Routes: Rapid IV bolus.
Pediatric Dosage: 5 mg/kg
Calcium Chloride (CaCl)
Class: Electrolyte.
Actions: Increases cardiac contractility.
Indications: Acute hyperkalemia (elevated potassium), acute hypocalcemia (decreased calcium),
calcium channel blocker (Nifedipine, Verapamil, etc.), overdose, abdominal muscle spasm associated
with spider bite and portuguese man-o-war stings, antidote for magnesium sulfate.
Contraindications: Patients receiving digitalis.
Precautions: IV line should be flushed between calcium chloride and sodium bicarbonate
administration. Extravasation may cause tissue necrosis.
Side Effects: Arrhythmias (bradycardia and asystole), hypotension.
Dosage: 2-4 mg/kg of a 10% solution; may be repeated at 10-minute intervals.
202
Routes: IV.
Pediatric Dosage: 5-7 mg/kg of a 10% solution.
Dexamethasone (Decadron, Hexadrol)
Class: Steroid.
Actions: Possibly decreases cerebral edema, anti-inflammatory, suppresses immune response
(especially in allergic reactions).
Indications: Cerebral edema, anaphylaxis (after Epinephrine and diphenhydramine), asthma, COPD.
Contraindications: None in the emergency setting.
Precautions: Should be protected from heat, onset of action may be 2-6 hours and thus should not be
considered to be of use in the critical first hour following an anaphylactic reaction.
Side Effects: Gastrointestinal bleeding, prolonged wound healing.
Dosage: 4-24 mg.
Routes: IV.
Pediatric Dosage: 0.2-0.5 mg/kg
Dextrose 50%
Class: Carbohydrate.
Actions: Elevates blood glucose level rapidly.
Indications: Hypoglycemia.
Contraindications: None in the emergency setting.
Precautions: A blood sample should be drawn before administering 50% dextrose.
Side Effects: Local venous irritation.
Dosage: 25 grams (50 ml).
Routes: IV.
Pediatric Dosage: 0.5 g/kg slow IV; should be diluted 1:1 with sterile water to form a 25% solution.
Diazepam (Valium)
Class: Tranquilizer (Benzodiazepine).
Actions: Anticonvulsant, skeletal muscle relaxant, sedative.
Indications: Generalized seizures, status epilepticus, premedication before cardioversion, skeletal
muscle relaxant, acute anxiety states.
Contraindications: Patients with a history of hypersensitivity to the drug.
Precautions: Can cause local venous irritation. Has short duration of effect. Do not mix with other
drugs because of possible precipitation problems.
Side Effects: Drowsiness, hypotension, respiratory depression, apnea.
Dosage: Status epilepticus: 5-10 mg IV.
Acute anxiety: 2-5 mg IM or IV.
Premedication before cardioversion: 5-15 mg IV.
Routes: IV (care must be taken not to administer faster than 1 ml/min)
IM rectal.
Pediatric Dosage: Status epilepticus: 0.1 - 0.2 mg/kg.
Digoxin (Lanoxin)
Class: Cardiac glycoside.
Actions: Increases cardiac contractile force, increases cardiac output, reduces edema associated with
congestive heart failure, slows AV conduction.
Indications: Congestive heart failure, rapid atrial arrhythmias, especially atrial flutter and atrial
fibrillation.
203
Contraindications: Any patient with signs or symptoms of digitalis, toxicity, ventricular fibrillation.
Precautions: Monitor for signs of digitalis toxicity. Patients who have recently suffered a myocardial
infarction have greater sensitivity to the effects of digitalis. Calcium should not be administered to
patients receiving digitalis.
Side Effects: Nausea, vomiting, arrhythmias, yellow vision.
Dosage: 0.25-0.50 mg.
Routes: IV.
Pediatric Dosage: 25-40 µg/kg.
Diltiazem (Cardizem)
Class: Calcium channel blocker.
Actions: Slows conduction through the AV node, causes vasodilation, decreases rate of ventricular
response, decreases myocardial oxygen demand.
Indications: To control rapid ventricular response associated with atrial fibrillation and flutter.
Contraindications: Hypotension, wide complex tachycardia, conduction system disturbances.
Precautions: Should not be used in patients receiving intravenous ß blockers. Hypotension. Must be
kept refrigerated or discarded one month after removal from refrigeration.
Side Effects: Nausea, vomiting, hypotension, and dizziness.
Dosage: 0.25 mg/kg bolus (typically 20 mg) IV over 2 minutes. This should be followed by a
maintenance infusion of 5-15 mg/hour.
Routes: IV, IV drip.
Pediatric Dosage: Rarely used.
Dimenhydrinate (Dramamine)
Class: Antihistamine.
Actions: Blocks histamine receptors, antiemetic.
Indications: Nausea and vomiting, motion sickness, to potentiate the effects of analgesics.
Contraindications: Comatose states, patients who have received large amounts of depressants
(including alcohol).
Precautions: Use with caution in patients with seizure disorders, asthma.
Side Effects: May impair mental and physical ability, drowsiness, bronchial secretions.
Dosage: 25-50 mg slow IVP (over 2 minutes) 50 - 100 mg IM.
Routes: IV, IM.
Pediatric Dosage: Not recommended.
Diphenhydramine (Benadryl)
Class: Antihistamine.
Actions: Blocks histamine receptors, has some sedative effects.
Indications: Anaphylaxis, allergic reactions, dystonic reactions due to phenothiazines.
Contraindications: Asthma, nursing mothers.
Precautions: Hypotension.
Side Effects: Sedation, dries bronchial secretions, blurred vision, headache, palpitations.
Dosage: 25-50 mg.
Routes: Slow IV push deep IM.
Pediatric Dosage: 2-5 mg/kg.
Dobutamine (Dobutrex)
Class: Sympathomimetic.
Actions: Increases cardiac contractility, little chronotropic activity.
Indications: Short-term management of congestive heart failure.
204
Contraindications: Should only be used in patients with an adequate heart rate.
Precautions: Ventricular irritability. Use with caution following myocardial infarction. Can be
deactivated by alkaline solutions.
Side Effects: Increased heart rate, palpitations.
Dosage: 2.5-20 µg/kg/minute.
Method: 250 mg should be placed in 500 ml of d5w, which gives a concentration of 0.5 mg/ml.
Routes: IV drip.
Pediatric Dosage: 2 - 20 µg/kg/min.
Dopamine (Intropin)
Class: Sympathomimetic.
Actions: Increases cardiac contractility, causes peripheral vasoconstriction.
Indications: Hemodynamically significant hypotension (systolic BP of 70-100 mmhg) not resulting
from hypovolemia, cardiogenic shock.
Contraindications: Hypovolemic shock where complete fluid resuscitation has not occurred.
Precautions: Should not be administered in the presence of severe tachyarrhythmias. Should not be
administered in the presence of ventricular fibrillation, ventricular irritability. Beneficial effects lost
when dose exceeds 20 µg/kg/min.
Side Effects: Ventricular tachyarrhythmias, hypertension, palpitations.
Dosage: 2-20 µg/kg/minute. Start low and increase as needed.
Method: 800 mg should be placed in 500 ml of D5W giving a concentration of 1600 µg/ml.
Routes: IV drip only.
Pediatric Dosage: 2-20 µg/kg/minute.
Epinephrine (Adrenalin):
Description: A hormone produced by the adrenal gland (attached to the kidneys) and synthesized
commercially. It is employed therapeutically as a vassoconstrictor, as a cardiac stimulant, and to relax
bronchioles. It is also used to treat asthmatic attacks and treat anaphylactic shock.
Epinephrine 1:1,000
Class: Sympathomimetic.
Actions: Bronchodilation.
Indications: Bronchial asthma, exacerbation of COPD, allergic reactions.
Contraindications: Patients with underlying cardiovascular disease, hypertension, pregnancy, patients
with tachyarrhythmias.
Precautions: Should be protected from light. Blood pressure, pulse, and EKG must be constantly
monitored.
Side Effects: Palpitations and tachycardia, anxiousness, headache, tremor.
Dosage: 0.3-0.5 mg.
Routes: Subcutaneous (IV and ET for pediatric cardiac arrest).
Pediatric Dosage: 0.01 mg/kg up to 0.3 mg.
Epinephrine 1:10,000
Class: Sympathomimetic.
Actions: Increases heart rate and automaticity.
Increases cardiac contractile force.
Increases myocardial electrical activity.
Increases systemic vascular resistance.
Increases blood pressure.
Causes bronchodilation.
Indications: Cardiac arrest, anaphylactic shock severe reactive airway disease.
205
Contraindications: Epinephrine 1:10,000 is for intravenous or endotracheal use; it should not be used in
patients who do not require extensive resuscitative efforts.
Precautions: Should be protected from light. Can be deactivated by alkaline solutions.
Side Effects:Palpitations, anxiety, tremulousness, nausea and vomiting.
Dosage: cardiac arrest: 0.5-1.0 mg repeated every 3-5 minutes.
severe anaphylaxis: 0.3-0.5 mg (3-5 ml); occasionally and Epinephrine drip is required.
Routes: IV, IV drip, ET.
Pediatric Dosage: 0.01 mg/kg initially. with subsequent doses, Epinephrine 1:1,000 should be used at a
dose of 0.1 mg/kg.
Flumazenil (Romazicon)
Class: Benzodiazepine antagonist.
Actions: Reverses effects of benzodiazepines.
Indications: To reverse CNS, respiratory depression associated with Benzodiazepines.
Contraindications: Flumazenil should not be used as a diagnostic agent for Benzodiazepine overdose in
the same manner Naloxone is used for narcotic overdose. Known hypersensitivity to the drug.
Precautions: Administer with caution to patients dependent upon Benzodiazepines as it may induce
life-threatening Benzodiazepine withdrawal.
Side Effects: Fatigue, headache, nervousness, dizziness.
Dosage: 0.2-0.3 mg IV over 30 seconds; repeated as needed to a maximum dose of 1.0 mg.
Routes: IV.
Pediatric Dosage: Pediatric data unavailable.
Furosemide (Lasix)
Class: Potent diuretic.
Actions: Inhibits reabsorption of sodium chloride, promotes prompt diuresis, vasodilation.
Indications: Congestive heart failure, pulmonary edema.
Contraindications: Pregnancy, dehydration.
Precautions: Should be protected from light, dehydration.
Side Effects: Few in emergency usage.
Dosage: 40-80 mg.
Routes: IV.
Pediatric Dosage: 1 mg/kg.
Glucagon
Class: Hormone (antihypoglycemic agent).
Actions: Causes breakdown of glycogen to glucose.
Inhibits glycogen synthesis.
Elevates blood glucose level.
Increases cardiac contractile force.
Increases heart rate.
Indications: Hypoglycemia.
Contraindications: Hypersensitivity to the drug.
Precautions: Only effective if there are sufficient stores of Glycogen within the liver. Use with caution
in patients with cardiovascular or renal disease. Draw blood glucose before administration.
Side Effects: Few in emergency situations.
Dosage: 0.25-0,50 mg (unit) IV 1.0 mg, IM.
Routes: IV, IM.
Pediatric Dosage: 0.03 mg/kg.
206
Haloperidol (Haldol)
Class: Major tranquilizer.
Actions: Blocks dopamine receptors in brain responsible for mood and behavior has antiemetic
properties.
Indications: Acute psychotic episodes.
Contraindications: Should not be administered in the presence of other sedatives. Should not be used in
the management of dysphoria caused by Talwin.
Precautions: Orthostatic hypotension.
Side Effects: Physical and mental impairment, Parkinson-like reactions have been known to occur,
especially in children.
Dosage: 2-5 mg.
Routes: IM.
Pediatric Dosage: Rarely used.
Heparin
Class: Anticoagulant.
Actions: Functions as an anticoagulant by accelerating neutralization of activated clotting factors.
Indications: Situations where a hypocoaguable state is required (i.e. post MI, post-CVA, pulmonary
embolism).
Contraindications: Should not be used unless there is a medical reason to anticoagulate the patient.
Precautions: Sever, urticaria, and anaphylaxis have been reported following heparin administration skin
necrosis can develop at site of subQ injections.
Side Effects: Fever, bruising, oozing of blood.
Dosage: Loading dose: 5,000 iu IV is a typical loading dose although large patients and patients with
heparin resistance may receive larger doses.
Maintenance dose: Infusion therapy is typically started at 800 - 1,000 iu/hour. the dosage is modified
based upon the patient's prothrombin (pt) time.
Routes: IV subQ (for prophylaxis).
Pediatric Dosage: Rarely used.
Hydrocodone (Vicodin, Lortab)
Class: Narcotic analgesic.
Actions: CNS depressant, decreases sensitivity to pain.
Indications: Relief of cough and moderate to severe pain.
Contraindications: Patients with a history of hypersensitivity to the drug or acetaminophen (Tylenol).
Precautions: May exaggerate the effects of other CNS depressants. May cause repiratory depression at
high dosages. May elevate intracranial and cerebrospinal fluid pressure in the presence of a head injury
or a pre-existing increase in intracranial pressure.
Side Effects: Lightheadedness, dizziness, drowsiness, nausea, and vomiting.
Dosage: 2.5/5.0/7.5 mg tablets; 1-2 every 4-6 hours.
Routes: Oral.
Pediatric Dosage: Not recommended.
Hydroxyzine (Vistaril)
Class: Antihistamine.
Actions: Antiemetic, antihistamine, antianxiety, potentiates analgesic effects of narcotics and related
agents.
Indications: To potentiate the effects of narcotics and synthetic narcotics, nausea and vomiting, anxiety
reactions.
Contraindications: Patients with a history of hypersensitivity to the drug.
Precautions: Orthostatic hypotension, analgesic dosages should be reduced when used with
Hydroxyzine, urinary retention.
Side Effects: Drowsiness.
207
Dosage: 50-100 mg.
Routes: Deep IM.
Pediatric Dosage: 1 mg/kg.
Insulin (Humulin)
Class: Hormone (hypoglycemic agent).
Actions: Causes uptake of glucose by the cells, decreases blood glucose level, promotes glucose
storage.
Indications: Elevated blood glucose, diabetic ketoacidosis.
Contraindications: Avoid overcompensation of blood glucose level; if possible, administration should
wait until the patient is in the emergency department.
Precautions: Administration of excessive dose may induce hypoglycemia. Glucose should be available.
Side Effects: Few in emergency situations.
Dosage: 10-25 units regular insulin IV followed by an infusion at 0.1 units/kg/hr.
Routes: IV subQ.
Pediatric Dosage: Dosage is based on blood glucose level.
Ipatropium (Atrovent)
Class: Anticholinergic.
Actions: Causes bronchodilation, dries respiratory tract secretions.
Indications: Bronchial asthma, reversible bronchospasm associated with chronic bronchitis and
emphysema.
Contraindications: Patients with history of hypersensitivity to the drug, should not be used as primary
agent in acute treatment of bronchospasm.
Precautions: Blood pressure, pulse, and EKG must be constantly monitored.
Side Effects: Palpitations, dizziness, anxiety, tremors, headache, nervousness, dry mouth.
Dosage: Small-volume nebulizer: 500 µg should be placed in small volume nebulizer (typically
administered with a ß agonist).
Routes: Inhalation only.
Pediatric Dosage: Safety in children has not been established.
Isoetharine (Bronkosol)
Class: Sympathomimetic (ß2 selective).
Actions: Bronchodilation, increases heart rate.
Indications: Asthma, reversible bronchospasm associated with chronic bronchitis and emphysema.
Contraindications: Patients with history of hypersensitivity to the drug.
Precautions: Blood pressure, pulse, and EKG must be constantly monitored.
Side Effects: Palpitations, tachycardia, anxiety and tremors, headache.
Dosage: Hand nebulizer: four inhalations.
Small-volume nebulizer: 0.5 ml (1:3 with saline).
Routes: Inhalation only.
Pediatric Dosage: 0.25-0.5 ml diluted with 4 ml normal saline.
Ketorolac (Toradol)
Class: Non-steroidal anti-inflammatory agent.
Actions: Anti-inflammatory, analgesic (peripherally-acting).
Indications: Mild to moderate pain.
Contraindications: Patients with a history of hypersensitivity to the drug, patients allergic to Aspirin.
Precautions: GI irritation or hemorrhage can occur.
Side Effects: Edema, rash, heartburn.
Dosage: IV 15-30 mg, IM 30-60 mg.
209
Routes: IV, IM.
Pediatric Dosage: Safety in children has not been established.
Labetalol (Trandate) (Normodyne)
Class: Sympathetic blocker.
Actions: Selectively blocks ÿ1 receptors and nonselectively blocks ß receptors.
Indications: Sypertensive crisis.
Contraindications: Sronchial asthma, congestive heart failure, heart block, bradycardia, cardiogenic
shock.
Precautions: Blood pressure, pulse, and EKG must be constantly monitored. Atropine and
transcutaneous pacing should be available.
Side Effects: Bradycardia, heart block, congestive heart failure, bronchospasm, postural hypotension.
Dosage: Method 1: 20 mg by slow IV infusion over 2 minutes; doses of 40 mg can be repeated in 10
minutes until desired supine blood pressure is obtained or until 300 mg of the drug has been given.
Method 2: 200 mg placed in 500 ml d5w to deliver 2 mg/minute.
Routes: IV infusion or slow IV bolus as described earlier.
Pediatric Dosage: Safety in children has not been established.
Lidocaine (Xylocaine)
Class: Antiarrhythmic.
Actions: Suppresses ventricular ectopic activity, increases ventricular fibrillation threshold, reduces
velocity of electrical impulse through conductive system.
Indications: Malignant PVCs, ventricular tachycardia, ventricular fibrillation, prophylaxis of
arrhythmias associated with acute myocardial infarction and thrombolytic therapy, premedication prior
to rapid sequence induction.
Contraindications: High-degree heart blocks, PVCs in conjunction with bradycardia.
Precautions: Dosage should not exceed 300 mg/hr. Monitor for CNS toxicity. Dosage should be
reduced by 50% in patients older than 70 years of age or who have liver disease in cardiac arrest, use
only bolus therapy.
Side Effects: Anxiety, drowsiness, dizziness, and confusion, nausea and vomiting, convulsions,
widening of QRS.
Dosage: Bolus: Initial bolus of 1.5 mg/kg; additional boluses of 0.5 - 0.75 mg/kg can be repeated at 810-minute intervals until the arrhythmia has been suppressed or until 3 mg/kg of the drug has been
administered; reduce dosage by 50% in patients older than 70 years of age.
Drip: after the arrhythmia has been suppressed a 2-4 mg/minute infusion may be started to maintain
adequate blood levels.
Routes: IV bolus, IV infusion.
Pediatric Dosage: 1 mg/kg.
Magnesium Sulfate
Class: Anticonvulsant/Antiarrhythmic.
Actions: CNS depressant, anticonvulsant, antiarrhyhmic.
Indications: Obstetrical eclampsia (toxemia of pregnancy), pre-eclampsia/PIH, cardiovascular severe
refractory ventricular fibrillation, pulseless ventricular tachycardia, post-MI as prophylaxis for
arrhythmias, torsades de pointes (multi-axial ventricular tachycardia).
Contraindications: Shock, heart block.
Precautions: Caution should be used in patients receiving digitalis. Hypotension. Calcium Chloride
should be readily available as an antidote if respiratory depression ensues. Use with caution in patients
in renal failure.
Side Effects: Respiratory depression, drowsiness.
Dosage: 1-4 g.
Routes: IV, IM.
Pediatric Dosage: Not indicated.
210
Mannitol (Osmotrol)
Class: Osmotic diuretic.
Actions: Decreases cellular edema, increases urinary output.
Indications: Acute cerebral edema, blood transfusion reactions.
Contraindications: Pulmonary edema, patients who are dehydrated, hypersensitivity to the drug.
Precautions: Rapid administration can cause circulatory overload crystallization of the drug can occur
at lower temperatures. An in-line filter should be used.
Side Effects: Pulmonary congestion, sodium depletion, transient volume overload.
Dosage: 1.5-2.0 g/kg.
Routes: IV.
Pediatric Dosage: 0.25-0.5 g/kg IV over 60 minutes.
Methylprednisolone (Solu-Medrol)
Class: Steroid.
Actions: Anti-inflammatory, suppresses immune response (especially in allergic reactions).
Indications: Severe anaphylaxis, asthma/COPD, possibly effective as an adjunctive agent in the
management of spinal cord injury.
Contraindications: None in the emergency setting.
Precautions: Must be reconstituted and used promptly. Onset of action may be 2-6 hours and thus
should not be expected to be of use in the critical first hour following an anaphylactic reaction.
Side Effects: GI bleeding, prolonged wound healing, suppression of natural steroids.
Dosage: General usage: 125-250 mg.
Spinal cord injury: Initial bolus of 30 mg/kg administered over 15 minutes, followed by a maintenance
infusion of 5.4 mg/kg/hr.
Routes: IV, IM.
Pediatric Dosage: 30 µg/kg.
Midazolam (Versed)
Class: Benzodiazepine tranquilizer.
Actions: Hypnotic, sedative.
Indications: Premedication prior to cardioversion/RSI, acute anxiety states.
Contraindications: Patients with known hypersensitivity to the drug, narrow-angle glaucoma, shock.
Precautions: Emergency resuscitation equipment should be available. Flumazenil (Romazicon) should
be available. Dilute with normal saline or D5W prior to intravenous administration. Respiratory
depression more common with Midazolam than with other Benzodiazepines.
Side Effects: Drowsiness, hypotension, amnesia, respiratory depression, apnea.
Dosage: 1.0- 2.5 mg IV.
Routes: IV, IM, intranasal.
Pediatric Dosage: 0.03 mg/kg.
Morphine
Class: Narcotic.
Actions: CNS depressant, causes peripheral vasodilation, decreases sensitivity to pain.
Indications: Severe pain, pulmonary edema.
Contraindications: Head injury, volume depletion undiagnosed abdominal pain, patients with history of
hypersensitivity to the drug.
Precautions: Respiratory depression (narcan should be available), hypotension, nausea.
Side Effects: Dizziness, altered level of consciousness.
211
Dosage: IV: 2-5 mg followed by 2 mg every few minutes until the pain is relieved or until respiratory
depression ensues.
IM: 5-15 mg based on patient weight.
Routes: IV, IM.
Pediatric Dosage: 0.1-0.2 mg/kg IV.
Nalbuphine (Nubain)
Class: Synthetic analgesic.
Actions: CNS depressant, decreases sensitivity to pain.
Indications: Moderate to severe pain.
Contraindications: Patients with a history of hypersensitivity to the drug.
Precautions: Use with caution in patients with impaired respiratory function, respiratory depression
(Naloxone should be available). Patients dependent on narcotics may experience, symptoms of
withdrawal, nausea.
Side Effects: Dizziness, altered level of consciousness.
Dosage: 5-10 mg.
Routes: IV, IM.
Pediatric Dosage: Rarely used.
Naloxone (Narcan)
Class: Narcotic antagonist.
Actions: Reverses effects of narcotics.
Indications:
•
Narcotic overdoses including the following: Codeine, Demerol, Dilaudid, Fentanyl, Heroin,
Lortabs, Methadone, Morphine, Paregoric, Percodan, Tylox, Vicodin, synthetic analgesics,
•
Overdoses including the following: Darvon, Nubain, Stadol, Talwin, alcoholic coma,
•
To rule out narcotics in coma of unknown origin.
Contraindications: Patients with a history of hypersensitivity to the drug.
Precautions: Should be administered with caution to patients dependent on narcotics as it may cause
withdrawal effects. Short-acting, should be augmented every 5 minutes.
Side Effects: none.
Dosage: 1-2 mg.
Routes: IV, IM.
ET (ET dose is 2.0-2.5 times IV dose).
Pediatric Dosage: < 5 years old > 5 years old 0.1 mg/kg 2.0 mg.
Nifedipine (Procardia)
Class: Calcium channel blocker.
Actions: Relaxes smooth muscle causing arteriolar vasodilation decreases peripheral vascular
resistance.
Indications: Severe hypertension, angina pectoris.
Contraindications: Known hypersensitivity to the drug, hypotension.
Precautions: Blood pressure should be constantly monitored. May worsen congestive heart failure.
Nifedipine should not be administered to patients receiving intravenous beta blockers.
Side Effects: Dizziness, flushing, nausea, headache, and weakness.
Dosage: 10 mg sublingually; puncture the capsule several times with a needle and place it under the
patient's tongue and have them withdraw the liquid medication.
Routes: Oral, sublingual.
Pediatric Dosage: 0.25-0.5 mg/kg.
212
Nitroglycerin Spray (Nitrolingual Spray)
Class: Antianginal.
Actions: Smooth-muscle relaxant, decreases cardiac work, dilates coronary arteries, dilates systemic
arteries.
Indications: Angina pectoris, chest pain associated with myocardial infarction.
Contraindications: Hypotension.
Precautions: Constantly monitor vital signs. Syncope can occur.
Side Effects: Dizziness, hypotension, headache.
Dosage: One spray administered under the tongue; may be repeated in 10-15 minutes; no more than
three sprays in a 15-minute period; spray should not be inhaled.
Routes: Sprayed under tongue on mucous membrane.
Pediatric Dosage: Not indicated.
Nitropaste (Nitro-Bid)
Class: Antianginal.
Actions: Smooth-muscle relaxant, decreases cardiac work, dilates coronary arteries, dilates systemic
arteries.
Indications: Angina pectoris, chest pain associated with myocardial infarction.
Contraindications: Children younger than 12 years of age, hypotension.
Precautions: Constantly monitor blood pressure, syncope, drug must be protected from light, expires
quickly once bottle is opened.
Side Effects: Dizziness, hypotension.
Dosage: 1/2 to 3/4 inches.
Routes: Topical.
Pediatric Dosage: Not indicated.
Norepinephrine (Levophed)
Class: Sympathomimetic.
Actions: Causes peripheral vasoconstriction.
Indications: Hypotension refractory to other sympathomimetics, neurogenic shock.
Contraindications: Hypotensive states due to hypovolemia.
Precautions: Can be deactivated by alkaline solutions. Constant monitoring of blood pressure is
essential. Extravasation can cause tissue necrosis.
Side Effects: Anxiety, palpitations, hypertension.
Dosages: 0.5-30 µg/minute. Method: 8 mg should be placed in 500 ml of D5W, giving a concentration
of 16 µg/ml.
Routes: IV drip only.
Pediatric Dosage: 0.01-0.5 µg/kg/minute (rarely used).
Oxygen (O2)
Class: gas.
Actions: Necessary for cellular metabolism.
Indications: Hypoxia.
Contraindications: None.
Precautions: Use cautiously in patients with COPD, humidify when providing high-flow rates.
NOTE: O2 FEEDS FIRE AND CAN BE EXPLOSIVE
Side Effects: Drying of mucous membranes.
Dosage: Cardiac arrest: 100%.
Other critical patients: 100%.
COPD: 35%.
Routes: Inhalation.
Pediatric Dosage: 24-100% as required.
213
Phenytoin (Dilantin)
Class: Anticonvulsant/antiarrhythmic.
Actions: Inhibits spread of seizure activity through motor cortex, antiarrhythmic.
Indications: Status epilepticus, arrhythmias due to digitalis toxicity.
Contraindications: Any arrhythmia except those due to digitalis toxicity, patients with history of
hypersensitivity to the drug.
Precautions: Should not be administered with glucose solutions. Hypotension. EKG monitoring during
administration is essential.
Side Effects: Local venous irritation, central nervous system depression.
Dosages: Status epilepticus: 150-250 mg (10-15 mg/kg) not to exceed 50 mg/minute.
Digitalis toxicity: 100 mg over 5 minutes until the arrhythmia is suppressed or until symptoms of
central nervous system depression occur.
Routes: IV (dilute with saline).
Pediatric Dosage: Status epilepticus: 8-10 mg/kg IV.
Digitalis toxicity: 3-5 mg/kg IV over 10 minutes.
Procainamide (Pronestyl)
Class: Antiarrhythmic.
Actions: Slows conduction through myocardium, elevates ventricular fibrillation threshold, suppresses
ventricular ectopic activity.
Indications: Persistent cardiac arrest due to ventricular fibrillation and refractory to Lidocaine, PVCs
refractory to Lidocaine, ventricular tachycardia refractory to Lidocaine.
Contraindications: High-degree heart blocks, PVCs in conjunction with bradycardia.
Precautions: Dosage should not exceed 17 mg/kg. Monitor for central nervous system toxicity.
Side Effects: Anxiety, nausea, convulsions, widening of QRS.
Dosage: Initial: 20 mg/minute until arrhythmia abolished, hypotension ensues, QRS widened by 50%
of original width total of 17 mg/kg has been given.
maintenance: 1-4 mg/minute.
Routes: slow IV bolus, IV drip.
Pediatric Dosage: Rarely used.
Prochlorperazine (Compazine)
Class: Phenothiazine antiemetic.
Actions: Antiemetic.
Indications: Nausea and vomiting, acute psychosis.
Contraindications: Comatose states, patients who have received a large amount of depressants
(including alcohol), patients with a history of hypersensitivity to the drug.
Precaution: EPS (extra-pyramidal seizure) (dystonic) reactions have been reported.
Side Effects: May impair mental and physical ability, drowsiness.
Dosage: 5-10 mg slow IV or IM.
Routes: IV, IM.
Pediatric Dosage: Not recommended.
Promethazine (Phenergan)
Class: Antihistamine (h1 antagonist).
Actions: Mild anticholinergic activity, antiemetic, potentiates actions of analgesics.
Indications: Nausea and vomiting, motion sickness, to potentiate the effects of analgesics, sedation.
Contraindications: Comatose states, patients who have received a large amount of depressants
(including alcohol).
Precautions: Avoid accidental intra-arterial injection.
214
Side Effects: May impair mental and physical ability, drowsiness.
Dosage: 25 mg.
Routes: IV.
Pediatric Dosage: 0.5 mg/kg.
Return to top of page
Racemic Epinephrine (Micronefrin) (VapoNefrin)
Class: Sympathomimetic.
Actions: Bronchodilation, increases heart rate, increases cardiac contractile force.
Indications: Croup (laryngotracheobronchitis).
Contraindications: Epiglottitis, hypersensitivity to the drug.
Precautions: Vital signs should be constantly monitored. Should be used only once in the prehospital
setting.
Side Effects: Palpitations, anxiety, headache.
Dosage: 0.5-0.75 ml of a 2.25% solution in 2.0 ml normal saline.
Routes: Inhalation only (small-volume nebulizer).
Pediatric Dosage: 0.25-0.75 ml of a 2.25% solution in 2.0 ml normal saline.
Rifabutin:
Description: A drug used to help prevent mycobacterium avium complex disease in patients with HIV
infections.
Ringer's Solution (lactated):
Description: A sterile solution of specified amounts of calcium, potassium chloride, sodium chloride,
and sodium lactate in water for injection. It is used intravenously to treat dehydration and replace
electrolytes.
Sodium Bicarbonate
Class: Alkalinizing agent.
Actions: Combines with excessive acids to form a weak volatile acid, increases ph.
Indications: Late in the management of cardiac arrest, if at all, tricyclic antidepressant overdose, severe
acidosis refractory to hyperventilation.
Contraindication: Alkalotic states.
Precautions: Correct dosage is essential to avoid overcompensation of ph. Can deactivate
catecholamines. Can precipitate with calcium preparations. Delivers large sodium load.
Side Effects: Alkalosis.
Dosage: 1 mEq/kg initially followed by 0.5 mEq/kg every 10 minutes as indicated by blood gas studies.
Routes: IV.
Pediatric Dosage: 1 mEq/kg initially followed by 0.5 mEq/kg every 10 minutes.
Succinylcholine (Anectine)
Class: Neuromuscular blocking agent (depolarizing).
Actions: Skeletal muscle relaxant, paralyzes skeletal muscles including respiratory muscles.
Indications: To achieve paralysis to facilitate endotracheal intubation.
Contraindications: Patients with known hypersensitivity to the drug.
Precautions: Should not be administered unless persons skilled in endotracheal intubation are present.
Endotracheal intubation equipment must be available. Oxygen equipment and emergency resuscitative
drugs must be available. Paralysis occurs within 1 minute and lasts for approximately 8 minutes.
Side Effects: Prolonged paralysis, hypotension, bradycardia.
Dosage: 1-1.5 mg/kg (40-100 mg in an adult).
Routes: IV.
Pediatric Dosage: 1 mg/kg.
215
Terbutaline (Brethine)
Class: Sympathomimetic.
Actions: Bronchodilator, increases heart rate.
Indications: Bronchial asthma, reversible bronchospasm associated with COPD, preterm labor.
Contraindications: Batients with known hypersensitivity to the drug.
Precautions: Blood pressure, pulse, and EKG must be constantly monitored.
Side Effects: Palpitations, tachycardia, and PVCs, anxiety, tremor, and headache.
Dosage: Metered-dose inhaler: two inhalations, 1 minute apart.
Subcutaneous injection: 0.25 mg; may be repeated in 15-30 minutes.
Preterm labor: 0.25 mg IM or IV. may be repeated in 15-30 minutes as needed.
Routes: Inhalation, subcutaneous injection, IV (preterm labor only).
Pediatric Dosage: 0.01 mg/kg subcutaneously.
Torsemide (Demadex)
Class: Potent diuretic.
Actions: Inhibits reabsorption of sodium chloride, promotes prompt diuresis.
Indications: Congestive heart failure, pulmonary edema.
Contraindications: Patients with known hypersensitivity to the drug, anuria.
Precautions: Should be used with caution in patients taking NSAIDs, dehydration.
Side Effects: Dizziness, headache, nausea.
Dosage: 10-20 mg.
Routes: IV.
Vecuronium (Norcuron)
Class: Neuromuscular blocking agent (non-depolarizing).
Actions: Skeletal muscle relaxant, paralyzes skeletal muscles including respiratory muscles.
Indications: To achieve paralysis to facilitate endotracheal intubation.
Contraindications: Patients with known hypersensitivity to the drug.
Precautions: Should not be administered unless persons skilled in endotracheal intubation are present.
Endotracheal intubation equipment must be available. Oxygen equipment and emergency resuscitative
drugs must be available. Paralysis occurs within 1 minute and lasts for approximately 30 minutes.
Side Effects: Prolonged paralysis, hypotension, bradycardia.
Dosage: 0.08-0.10 mg/kg.
Routes: IV.
Pediatric Dosage: 0.1 mg/kg.
Verapamil (Isoptin) (Calan)
Class: Calcium channel blocker.
Actions: Slows conduction through the AV node, inhibits reentry during PSVT, decreases rate of
ventricular response, decreases myocardial oxygen demand.
Indications: PSVT.
Contraindications: Heart block, conduction system disturbances.
Precautions: should not be used in patients receiving intravenous ß blockers, hypotension.
Side Effects: Nausea, vomiting, hypotension, and dizziness.
Dosage: 2.5 - 5.0 mg. a repeat dose of 5 - 10 mg can be administered after 15-30 minutes if PSVT does
not convert. maximum dose is 30 mg in 30 minutes.
Routes: IV.
Pediatric Dosage: 0-1 year: 0.1-0.2 mg/kg (maximum of 2.0 mg) administered slowly.
1-15 years: 0.1-0.3 mg/kg (maximum of 5.0 mg) administered slowly.
216
GLOSSARY
MEDICAL TERMS
@ -at
b.i.d. -twice a day
BM -Bowel Movement
BPM -Beats/Breaths per Minute
B/P -Blood Pressure BS -Bowel Sounds BVM -Bag-Valve-Mask CC -Chief Complaint
cc -cubic centimeter
CVA -Cerebrovascular Accident d/c -discontinue
Dx -diagnosis
ET -Endotracheal Tube
ETOH -ethyl alcohol
FB -Foreign Body
FROM -Full Range of Motion
Fx -Fracture gtts -drops
GSW -Gun Shot Wound hr -hour
HTN -Hypertension KVO -Keep Vein Open kg -kilogram
LMP -Last Menstrual Period
LR – Lactated Ringers
mmHg -millimeters of mercury
NaCl -sodium chloride
NG -Nasogastric
NPO -Nothing by mouth
NS -Normal Saline
N&V -Nausea and Vomiting OCP -Oral Contraceptive Pills PE -Physical Exam
PERLA -Pupils Equal and Reactive to Light and Accommodation
PO -by mouth PRN -as needed q -every
q.i.d. -four times daily ROM -Range of Motion SaO2 -oxygen saturation SC/SubQ - Subcutaneous SL Sublingual
SOB -Short of Breath
TKO -To Keep Open
VA -Visual Acuity
y/o -year old
Pos -positive NEG -negative
ANATOMIC LOCATIONS
abd -abdomen AD -right ear AS -left ear
AU -both ears
CNS -Central Nervous System
C1-C7 -Cervical Spine
DIP -Distal Interphalangeal
GI -Gastrointestinal GU -Genitourinary GYN -Gynecological LLL -Left Lower Lobe
LUQ -Left Upper Quadrant LLQ -Left Lower Quadrant L1-L5 -Lumbar Spine
OD -right eye OS -left eye OU -both eyes
PIP -Proximal Interphalangeal
RLL -Right Lower Lobe
RUL -Right Upper Lobe
RLQ -Right Lower Quadrant RUQ -Right Upper Quadrant TM -Tympanic Membrane TMJ
-Tempomandibular Joint T1-T12 -Thoracic Spine
218
APGAR
(ACCOMPLISHED 1 MIN AFTER BIRTH AND 5MIN AFTER BIRTH)
APPEARANCE
Blue or pale
Body pink, extremities blue
Completely pink
PULSE RATE
Below 100
Above 100
GRIMACE
Grimaces
Cries
ACTIVITY
Some flexion of extremities
Active motion
RESPIRATORY
Slow, irregular
Good, strong cry
0
1
2
Absent
0
1
2
No response
0
1
2
Limp
0
1
2
Absent
0
1
2
APGAR < 4 = SERIOUS CONDITION REQUIRING SOME DEGREE OF RESUSCITATION
APGAR 4-6 = CONDITION IS GUARDED
APGAR 7-10 = NORMAL STABLE INFANT
MNEMONICS CAUSES OF COMA:
A - Alcohol, acidosis (hyperglycemic coma)
E - Epilepsy, Electrolyte abnormality, Endocrine problem
I - Insulin (hypoglycemic shock)
O - Overdose (or poisoning)
U - Uremia and other renal problems
T - Trauma; temperature (hypothermia, heat stroke)
I - Infection (e.g., meningitis)
P - Psychogenic ("hysterical coma")
S - Stroke or space-occupying lesions in the cranium
COMA ASSESSMENT:
D - Depth of coma (verbal or painful stimuli)
E - Eyes (PERLA)
R - Respiration (rate and rhythm)
M - Motor (loss of movement/sensation)
LEVEL OF CONSCIOUSNESS: A - Alert
V - Responds to Verbal stimuli P - Responds to Painful stimuli U - Unresponsive
PATIENT HISTORY:
A – Allergies
M – Medications
Weight
1 gr = 65 mg
15 gr = 1 gm
219
P - Past medical history (illness, injury)
P – Pain (PQRST)
L - Last intake (food, fluid)
E - Ever happen before?
1000 mg = 1 gm
1 oz. = 28 gm
454 gm = 1 lb
1000 gm = 1 kg 1 metric ton = 2,000 lbs
P – Pain (sharp or dull)
Q – Quality (diffuse or pinpoint)
R - Radiating
S -Severity (scale of 1-10)
T – Time of onset
To convert °F to °C
(°F – 32) divide by1.8
To convert °C to °F
(°C x 1.8) + 32
PUPIL REACTION
P - Pupils
E - Equal
R – Reactive
L - Light
A - Accommodation
USEFUL CONVERSIONS
TEMPERATURE
°F
106
105
104
103
102
101
100
99
98.6
98
97
96
95
94
93
92
°C
41.1
40.6
40
39.4
38.9
38.3
37.8
37.2
37
36.7
36.1
35.6
35
34.4
33.9
33.3
WEIGHT
POUNDS
396
374
352
330
308
286
264
242
220
209
198
187
176
165
154
143
KILOGRAM S
180
170
160
150
140
130
120
110
100
95
90
85
80
75
70
65
OTHER
Volume
1 cc = 1ml
1 tsp = 5 cc
1 tbsp = 15 cc
1 fl. oz. = 30 cc
1 jigger = 45 cc
1 pt = 473 cc
2 pt = 1 qt
1 qt = 946 cc
4 qt = 1 gal
1 gal = 8 lbs
Length
1 cm = .39 in
1 in = 2.54 cm
1 yard = 3 ft
1 ft = .31 m
91
90
85
80
75
70
32.8
32.2
29.4
26.7
23.8
21.1
132
121
110
99
88
77
60
55
50
45
40
35
1 m = 3.3 ft
1 km = .62 miles
1 mi = 1.61 km
1 mi = 5280 ft
220
References
Katzberg, R., Anderson, Q., Manzione, J., Helms, C.A., Tallents, R., & Hayakawa, K.(1984).
Dislocation of Jaws. Skeletal Radiology.
Schwartz, A.J. (2000). Dislocation of the mandible: a case report. American Association Of Nurse
Anesthetists Journal. 68 (6)
Blake, J. (1918). Recurrent Dislocation Of The Lower Jaw. Annuals of Surgery.
Parida S, Allampalli VD, Krishnappa S. Catatonia. (2011) Jaw dislocation in the Postoperative period
with epidural morphine. Indian Journal of Anaesthesia. 55:
Huang, IY, Chen, CM, Kao, YH, Chen, CM, & Wu, CW. (2011). Management of long-standing
mandibular dislocation. International Journal of oral and maxillofacial surgery.
Mayer, L. (1933). Recurrent Dislocation of the Jaw. The Journal of Bone & Joint Surgery.
How To Treat a Stingray Sting By Rod Brouhard Wilderness Environ Med. 1997 May;8(2):111-6.
Report on envenomation by a Gila monster (Heloderma suspectum) with a discussion of venom
apparatus, clinical findings, and treatment.Strimple PD, Tomassoni AJ, Otten EJ, Bahner D. Price,
Andrew H. (2009).
Venomous Snakes of Texas: A Field Guide University of Texas Press
Barceloux, 2008:Willis Lamm. RATTLESNAKE!
Kini, R. Manjunatha et al., ed. (2011). Toxins and Hemostasis Springer 2011.
Fox, William Sherwood (1988). The Bruce beckons: the story of Lake Huron University of Toronto
Press.
Place, Arron J; Abramson, Charles I. (2004). "A Quantitative Analysis of the Ancestral Area of
Rattlesnakes". Journal of Herpetology 38 .
Parker, M. Rockwell & Kardong, Kenneth V. (2005).
In Mason, Robert T. et al. Chemical signals in vertebrates 10. Springer.
Rubio, 1998: -- Knowledge that rattlesnakes are so afraid of kingsnakes' odor led to the development
of effective synthetic rattlesnake repellents.
Cetaruk, Edward W. (2005). Rattlesnakes and Other Crotalids
In Brent, Jeffrey. Critical care toxicology: diagnosis and management of the critically poisoned patient.
Elsevier Health Sciences.\
Vitts, Laurie J. (1999). In Mares, Michael A. et al. Encyclopedia of deserts. University of Oklahoma
Press.
221
Schoenherr, Allan A. (1995). A Natural History of California . University of California Press.
Lessenger, James E., ed. (2006). Agricultural medicine: a practical guide
Luch, Andreas, ed. (2010). Molecular, Clinical and Environmental Toxicology
Weinstein and Smith (1990)
Glenn, J.L., R.C.Straight. 1982. The rattlesnakes and their venom yield and lethal toxicity. In: Tu, A.
(ed) Rattlesnake Venoms, Their Actions and Treatment. New York: Marcel Dekker, Inc.
Gupta, Ramesh Chandra, ed. (2007). Veterinary toxicology: basic and clinical principles Academic
Press.
Burton, Maurice & Burton, Robert, ed. (1970). The international wildlife encyclopedia, Volume 1.
Marshall Cavendish.
Fergus, Charles (2003). Wildlife of Virginia and Maryland and Washington, Part 3 Stackpole Books.
Graham, Karen S. (2001Rattlesnake
In Bell, Catharine E. Encyclopedia of the world's zoos, Volume 3. Taylor & Francis.
Adams, Clark E. & Thomas, John K. (2008). Texas Rattlesnake Roundups Texas A&M University
Press.
Amerello, Melissa; Smith, Jeffrey; and Slone, John. 2011. Family values: Maternal care in
Rattlesnakes is more than mere attendance. Nature Precedings.
Hammerson, Geoffrey A. (2004). Connecticut wildlife: biodiversity, natural history, and conservation
UPNE.
Rubio, 1998: _1_rattle-snakes-venomous>Rattlesnake danger grows as more serpents strike without
warning The San Francisco Chronicle. June 24, 2011.
Mackessy, Stephen P., ed. (2009). Handbook of venoms and toxins of reptiles CRC Press.
Phillips, Steven J. et al., ed. (2009). A natural history of the Sonoran Desert University of California
Press.
O'Neil ME, Mack KA, Gilchrist J, Wozniak EJ (2007). "Snakebite injuries treated in United States
emergency departments, 2001-2004". Wilderness Environ Med 18
Werler, John E. & Dixon, James Ray, ed. (2000). Texas snakes: identification, distribution, and natural
historyUniversity of Texas Press.
Henkel, John. For Goodness Snakes! Treating and Preventing Venomous Bites Reptiles. USDA /
emergency response.
Fleisher, Gary R. & Ludwig, Stephen, ed. (2010). Textbook of Pediatric Emergency Medicine (6th
ed.). Lippincott Williams & Wilkins.
Tibballs, James et al. (2010). Envenomations
222
In Wheeler, David S. et al. Pediatric Critical Care Medicine: Basic Science and Clinical Evidence (6th
ed.). Springer.
Taylor, Robert B., ed. (2002). Manual of family practice (2nd ed.). Lippincott Williams & Wilkins.
Goldfrank, Lewis R., ed. (2006). s toxicologic emergencies (8th ed.). McGraw-Hill Professional.
Adams, Clark E. & Thomas, John K. (2008). Texas Rattlesnake Roundups Texas A&M University
Press.
Meier, Jürg & White, Julian, ed. (1995). Handbook of clinical toxicology of animal venoms and
poisons, Volume 236. CRC Press
Slatter, Douglas H. (2002). Textbook of small animal surgery Elsevier Health Sciences.
Kimbrough, David L. (2002). Taking up serpents: snake handlers of eastern Kentucky Mercer
University Press.
Tintinalli JE, Kelen GD, Stapczynski JS, Ma OJ, Cline DM. Reptile bites. In: Tintinalli JE, Kelen GD,
Stapczynski JS, Ma OJ, Cline DM, eds. Emergency Medicine: A Comprehensive Study Guide. 6th ed.
New York, NY: McGraw-Hill; 2004
Chin J., editor. Control of Communicable Diseases Manual. Seventeenth edition. Washington, DC:
American Public Health Association, most recent edition.
Osterholm MT, Hedberg CW, Moore KA, Chapter 11, Epidemiologic Principles, in: Mandell GL,
Bennett JE, and Dolin R, editors. Principles and Practice of Infectious Diseases, fifth edition. New
York: Churchill Livingstone, 2000
Wenzel RP, editor. Section 2, Control of Communicable Diseases, in: Wallace RB, Last JM,
Doebbeling BN, editors, Maxcy-Rosenau-Last
Public Health and Preventive Medicine, 14th edition. Norwalk CT: Appleton and Lange, most recent
edition.
U.S. Department of Health and Human Services, Public Health Service.
Food Code 2001. Washington, DC: Food and Drug Administration, 2001 or most recent edition.
Isbister GK. Marine envenomation and poisoning. In: Dart RC, editor. Medical toxicology. 3rd ed.
Philadelphia: Lippincott, Williams & Wilkins; 2004.
Williamson JA, Fenner PJ, Burnett JW, Rifkin JF. Venomous and poisonous marine animals: a medical
and biological handbook. 1st ed. Sydney: University of New South Wales Press; 1996.
Loten C, Stokes B, Worsley D, Seymour JE, Jiang S, Isbister GK. A randomised controlled trial of hot
water (45 degrees C) immersion versus ice packs for pain relief in bluebottle stings. Med J Aust 2006
Currie BJ, Jacups SP. Prospective study of Chironex fleckeri and other box jellyfish stings in the 'Top
End' of Australia's Northern Territory. Med J Aust 2005
O'Reilly GM, Isbister GK, Lawrie PM, Treston GT, Currie BJ. Prospective study of jellyfish stings
from tropical Australia, including the major box jellyfish Chironex fleckeri. Med J Aust 2001;175:6525.
223
Currie BJ. Marine antivenoms. J Toxicol Clin Toxicol 2003
Huynh TT, Seymour J, Pereira P, Mulcahy R, Cullen P, C arrette T, et al. Severity of Irukandji
syndrome and nematocyst identification from skin scrapings. Med J Aust 2003
Corkeron M, Pereira P, Makrocanis C. Early experience with magnesium administration in Irukandji
syndrome. Anaesth Intensive Care 2004
Little M, Pereira P, Carrette T, Seymour J. Jellyfish responsible for Irukandji syndrome. QJM 2006
Isbister GK. Venomous fish stings in tropical northern Australia. Am J Emerg Med 2001
Isbister GK, Hooper JN. Clinical effects of stings by sponges of the genus Tedania and a review of
sponge stings worldwide. Toxicon 2005
Thomas C, Scott S. All stings considered: first aid and medical treatment of Hawai'i's Marine Injuries.
United States of America: University of Hawai'í's Press, 1997
Millington JT, Wihelm P. Marine microbiology of Roca Alijos. J Wild Med 1983
Haddad Jr V, Miot HA, Camargo RMP, Chiaro A. Cutaneous sporotrichosis associated with a puncture
in dorsal fin of a fish (Tilapia sp): report of a case. Medical Micology 2002
Schiera A, Battifoglio ML, Scarabelli G, Crippa D. Stingray injury in a domestic aquarium. Int J
Dermatol 2002
Desert USA internet Southwest Adventure, Living & Travel
World Health Organization Cagas Disease
Centers for Disease Control and Prevention
American Mosquito Control Association®15000 Commerce Parkway, Suite C
Mount Laurel, NJ 08054
Susannah F Locke (1 December 2008). "Bug vs Bug: How do mosquitoes survive deadly viruses
unscathed?".
Koella, J.C.; Sorensen, Anderson (7). "The malaria parasite, Plasmodium falciparum, increases the
frequency of multiple feeding of its mosquito vector, Anopheles gambiae". Proceedings of the Royal
Society B 265 (1398)
"Mosquitoes and Mosquito Repellents: A Clinician's Guide"; by Mark S. Fradin: Annals of Internal
Medicine, 1 June 1998. Retrieved 10 July 2006.
The American Plague, by Molly Caldwell Crosby,, Berkley Books, New York, 2005
The Path Between the Seas: The Creation of the Panama Canal 1870-1914, by David McCullough,
1977, Simon and Schuster
The American Plague, by Molly Caldwell Crosby, , Berkley Books, New York, 2005
224
Mosquito-borne diseases, infectious disease information, NCID, CDC
Naides SJ. Arthropod-borne viruses causing fever and rash syndromes. In: Goldman L, Ausiello D, eds.
Cecil Medicine . 23rd ed. Philadelphia, Pa: Saunders Elsevier; 2007
Bleck TP. Arthropod-borne viruses affecting the central nervous system. In: Goldman L, Ausiello D,
eds. Cecil Medicine . 23rd ed. Philadelphia, Pa: Saunders Elsevier; 2007
Bausch DG. Viral hemorrhagic fevers.In: Goldman L, Schafer AI, eds. Cecil Medicine . 24th ed.
Philadelphia, PA: Saunders Elsevier; 2011
Skarbinski,J, James,EM, Causer,LM. ,et al.,Malaria surveillance–United States, 2004., MMWR
Surveill Summ.,2006
Newman,RD, Parise,ME, Barber,AM, Steketee,RW.,Malaria-related deaths among U.S. Travelers,
1963-2001. Ann Intern Med.,2004
Mendis,K, Sina,BJ, Marchesini,P, Carter,R. The neglected burden of Plasmodium vivax malaria. Am J
Trop Med Hyg. 2001;64:(1-2 suppl)
Health Information for International Travel 2005-2006. Atlanta, Ga: Elsevier Inc; 2005
Baird,JK, Hoffman,SL. Primaquine therapy for malaria. Clin Infect Dis. 2004
Marlar,T, Myat Phone,K, Aye Yu,S, Khaing Khaing,G, Ma,S, MyintO. Development of resistance to
chloroquine by Plasmodium vivax in Myanmar. Trans R Soc Trop Med Hyg. 1995
Jamaiah,I, Anuar,AK, Najib,NA, Zurainee,MN. Imported malaria: a retrospective study in University
Hospital, Kuala Lumpur, a ten-year experience. Med J Malaysia. 1998
Phan,GT, De Vries,PJ, Tran,BQ. et al. Artemisinin or chloroquine for blood stage Plasmodium vivax
malaria in Vietnam. Trop Med Int Health. 2002
Singh,RK. Emergence of chloroquine-resistant vivax malaria in south Bihar (India).
Trop Med Hyg. 2000
Trans R Soc
Kurcer,MA, Simsek,Z, Kurcer,Z. The decreasing efficacy of chloroquine in the treatment of
Plasmodium vivax malaria, in Sanliurfa, south-eastern Turkey. Ann Trop Med Parasitol. 2006
The American Academy of Orthopedic Surgeons: Treating Clavical Fractures
Sinden,REG. The malaria parasites.In: Warrell DA, Gilles HM, eds. Essential Malariology. 4th ed.
London, England: Arnold; 2002:26, 30
Molineaux,L. The epidemiology of human malaria as an explanation of its distribution, including some
implications for its control. In: Wernsdorfer WH, ed. Malaria, Principles and Practice of Malariology,
Volume 2. Edinburgh, Scotland: Churchill Livingstone; 1988
225
Garnham,P. Malaria parasites of man: life-cycles and morphology. In: Wernsdorfer WH, McGregor I,
eds. Malaria: Principles and Practice of Malariology, Volume 1. London, England: Churchill
Livingstone; 1988
Dorsey,G, Gandhi,M, Oyugi,JH, Rosenthal,PJ. Difficulties in the prevention, diagnosis, and treatment
of imported malaria. Arch Intern Med. 2000
Moore,TA, Tomayko,JF Jr, Wierman,AM, Rensimer,ER, White,AC Jr. Imported malaria in the 1990s: a
report of 59 cases from Houston, Tex. Arch Fam Med. 1994
Singh,K, Wester,WC, Trenholme,GM. Problems in the therapy for imported malaria in the United
States. Arch Intern Med. 2003
Svenson JE, MacLean,JD, Gyorkos,TW, Keystone,J. Imported malaria: clinical presentation and
examination of symptomatic travelers. Arch Intern Med. 1995
Lynk,A, Gold,R. Review of 40 children with imported malaria. Pediatr Infect Disease J. 1989
McCaslin,RI, Pikis,A, Rodriguez,WJ. Pediatric Plasmodium falciparium malaria: a ten-year
experience from Washington, DC. Pediatr Infect Dis J. 1994
World Health Organization. WHO Guidelines for the Treatment of Malaria. Geneva, Switzerland:
WHO Press; 2000
World Health Organization. WHO Guidelines for the Treatment of Malaria. Geneva, Switzerland:
WHO Press; 2006
Beg,MA, Khan,R, Baig,SM, Gulzar,Z, Hussain,R, Smego,RA Jr. Cerebral involvement in benign
tertian malaria. Am J Trop Med Hyg. 2002
Curlin,ME, Barat,LM, Walsh,DK, Granger,DL. Noncardiogenic pulmonary edema during vivax
malaria. Clin Infect Dis. 1999
Islam,N, Qamruddin,K. Unusual complications in benign tertian malaria. Trop Geogr Med. 1995
Kochar DK, Saxena V, Singh N, Kochar SK, Kumar SV, Das A. Plasmodium vivax malaria. Emerg
Infect Dis. 2005
Muhlberger, Jelinek T, Gascon J. et al. Epidemiology and clinical features of vivax malaria imported
to Europe: sentinel surveillance data from TropNetEurop. Malar J. 2004
Sachdev HS, Mohan M. Vivax cerebral malaria. J Trop Pediatr. 1985
Tanios MA, Kogelman L, McGovern B, Hassoun PM. Acute respiratory distress syndrome
complicating Plasmodium vivax malaria. Crit Care Med. 2001
Zingman BS, Viner BL. Splenic complications in malaria: case report and review. Clin Infect
Dis. 1993
Moody A. Rapid diagnostic tests for malaria parasites. Clin Microbiol Rev. 2002
226
Greenwood BM, Bradley AK, Greenwood AM. et al. Mortality and morbidity from malaria among
children in a rural area of The Gambia, West Africa. Trans R Soc Trop Med Hyg. 1987
Kain KC, Gadd E, Gushulak B, McCarthy A, MacPherson D. Errors in treatment recommendations for
severe malaria. Committee to Advise on Tropical Medicine and Travel (CATMAT). Lancet. 1996
D’Acremont V, Landry P, Mueller I, Pecoud A, Genton B. Clinical and laboratory predictors of
imported malaria in an outpatient setting: an aid to medical decision making in returning travelers with
fever. Am J Trop Med Hyg. 200
Caillon E, Schmitt L, Moron P. Acute depressive symptoms after mefloquine treatment. Am J
Psychiatry. 1992
Ekue JM, Simooya OO, Sheth UK, Wernsdorfer WH, Njelesani EK. A double-blind clinical trial of a
combination of mefloquine, sulfadoxine and pyrimethamine in symptomatic falciparum malaria. Bull
World Health Organ. 1985
Harinasuta T, Bunnag D, Wernsdorfer WH. A phase II clinical trial of mefloquine in patients with
chloroquine-resistant falciparum malaria in Thailand. Bull World Health Organ. 1983
Hennequin C, Bouree P, Bazin N, Bisaro F, Feline A. Severe psychiatric side effects observed during
prophylaxis and treatment with mefloquine. Arch Intern Med. 1994
Luxemburger C, Nosten F, ter Kuiile F, Frejacques L, Chongsuphajaisiddhi T, White NJ. Mefloquine
for multidrug-resistant malaria. Lancet. 1991
Patchen LC, Campbell CC, Williams SB. Neurologic reactions after a therapeutic dose of
mefloquine. N Engl J Med. 1989
Phillips-Howard PA, ter Kuile FO. CNS adverse events associated with antimalarial agents: fact or
fiction? Drug Saf. 1995
Price R, van Vugt M, Phaipun L. et al. Adverse effects in patients with acute falciparum malaria
treated with artemisinin derivatives. Am J Trop Med Hyg. 1999
Rendi-Wagner P, Noedl H, Wernsdorfer WH, Wiedermann G, Mikolasek A, Kollaritsch H. Unexpected
frequency, duration and spectrum of adverse events after therapeutic dose of mefloquine in healthy
adults. Acta Trop. 2002
Rouveix B, Bricaire F, Michon C. et al. Mefloquine and an acute brain syndrome. Ann Intern
Med. 1989
Sowunmi A. Acute psychosis after mefloquine: a case report. East Afr Med J. 1994
Sowunmi A, Adio RA, Oduola AM, Ogundahunsi OA, Salako LA. Acute psychosis after mefloquine:
report of six cases. Trop Geogr Med. 1995
Sowunmi A, Salako LA, Oduola AM, Walker O, Akindele JA, Ogundahunsi OA. Neuropsychiatric side
effects of mefloquine in Africans. Trans R Soc Trop Med Hyg. 1993
Speich R, Haller A. Central anticholinergic syndrome with the antimalarial drug mefloquine. N Engl J
Med. 1994
227
Weinke T, Trautmann M, Held T. et al. Neuropsychiatric side effects after the use of mefloquine. Am
J Trop Med Hyg. 1991
Stuiver PC, Ligthelm RJ, Goud TJ. Acute psychosis after mefloquine. Lancet. 1989
Bunnag D, Karbwang J, Na-Bangchang K, Thanavibul A, Chittamas S, Harinasuta T. Quininetetracycline for multidrug resistant falciparum malaria. Southeast Asian J Trop Med Public
Health. 1996
Clyde DF, Gilman RH, McCarthy VC. Antimalarial effects of clindamycin in man. Am J Trop Med
Hyg. 1975
Colwell EJ, Hickman RL, Kosakal S. Quinine-tetracycline and quinine-bactrim treatment of acute
falciparum malaria in Thailand. Ann Trop Med Parasitol. 1973
Hall AP, Doberstyn EB, Nanokorn A, Sonkom P. Falciparum malaria semi-resistant to clindamycin. Br
Med J. 1975
Karbwang J, Molunto P, Bunnag D, Harinasuta T. Plasma quinine levels in patients with falciparum
malaria when given alone or in combination with tetracycline with or without primaquine. Southeast
Asian J Trop Med Public Health. 1991
Karbwang J, Na-Bangchang K, Thanavibul A, Bunnag D, Chongsuphajaisiddhi T,
Harinasuta T. Comparison of oral artesunate and quinine plus tetracycline in acute uncomplicated
falciparum malaria. Bull World Health Organ. 1994
Kremsner PG, Winkler S, Brandts C, Neifer S, Bienzle U, Graninger W. Clindamycin in combination
with chloroquine or quinine is an effective therapy for uncomplicated Plasmodium falciparum malaria
in children from Gabon. J Infect Dis. 1994
Kremsner PG, Zotter GM, Feldmeier H, Graninger W, Rocha RM, Wiedermann G. A comparative trial
of three regimens for treating uncomplicated falciparum malaria in Acre, Brazil. J Infect Dis. 1988
Looareesuwan S, Vanijanonta S, Viravan C. et al. Randomised trial of mefloquine-tetracycline and
quinine-tetracycline for acute uncomplicated falciparum malaria. Acta Trop. 1994
Looareesuwan S, Wilairatana P, Vanijanonta S, Kyle D, Webster K. Efficacy of quinine-tetracycline for
acute uncomplicated falciparum malaria in Thailand. Lancet. 1992
McGready R, Cho T, Samuel . et al. Randomized comparison of quinine-clindamycin versus
artesunate in the treatment of falciparum malaria in pregnancy. Trans R Soc Trop Med Hyg. 2001
Metzger W, Mordmuller B, Graninger W, Bienzle U, Kremsner PG. High efficacy of short-term
quinine-antibiotic combinations for treating adult malaria patients in an area in which malaria is
hyperendemic. Antimicrob Agents Chemother. 1995
Miller LH, Glew RH, Wyler DJ. et al. Evaluation of clindamycin in combination with quinine against
multidrug-resistant strains of Plasmodium falciparum. Am J Trop Med Hyg.
229
Parola P, Ranque S, Badiaga S. et al. Controlled trial of 3-day quinine-clindamycin treatment versus
7-day quinine treatment for adult travelers with uncomplicated falciparum malaria imported from the
tropics. Antimicrob Agents Chemother. 2001
Pukrittayakamee S, Chantra A, Vanijanonta S, Clemens R, Looareesuwan S, White NJ. Therapeutic
responses to quinine and clindamycin in multidrug-resistant falciparum malaria. Antimicrob Agents
Chemother. 2000
Pukrittayakamee S, Chotivanich K, Chantra A, Clemens R, Looareesuwan S, White NJ. Activities of
artesunate and primaquine against asexual- and sexual-stage parasites in falciparum
malaria. Antimicrob Agents Chemother. 2004;48:1329-1334
Reacher M, Campbell CC, Freeman J, Doberstyn EB, Brandling-Bennett AD. Drug therapy for
Plasmodium falciparum malaria resistant to pyrimethamine-sulfadoxine (Fansidar): a study of alternate
regimens in Eastern Thailand, 1980. Lancet. 1981
Vaillant M, Millet P, Luty A. et al. Therapeutic efficacy of clindamycin in combination with quinine
for treating uncomplicated malaria in a village dispensary in Gabon. Trop Med Int Health. 1997
Vanijanonta S, Chantra A, Phophak N, Chindanond D, Clemens R, Pukrittayakamee S. Therapeutic
effects of chloroquine in combination with quinine in uncomplicated falciparum malaria. Ann Trop
Med Parasitol. 1996
Andersen SL, Oloo AJ, Gordon DM. et al. Successful double-blinded, randomized, placebo-controlled
field trial of azithromycin and doxycycline as prophylaxis for malaria in western Kenya. Clin Infect
Dis. 1998
Baudon D, Martet G, Pascal B, Bernard J, Keundjian A, Laroche R. Efficacy of daily antimalarial
chemoprophylaxis in tropical Africa using either doxycycline or chloroquine-proguanil: a study
conducted in 1996 in the French Army. Trans R Soc Trop Med Hyg. 1999
Karwacki JJ, Shanks GD, Kummalue T, Watanasook C. Primaquine induced hemolysis in a Thai
soldier. Southeast Asian J Trop Med Public Health. 1989
Ohrt C, Richie TL, Widjaja H. et al. Mefloquine compared with doxycycline for the prophylaxis of
malaria in Indonesian soldiers: a randomized, double-blind, placebo-controlled trial. Ann Intern
Med. 1997
Pang L, Limsomwong N, Singharaj P. Prophylactic treatment of vivax and falciparum malaria with
low-dose doxycycline. J Infect Dis. 1988
Pang LW, Limsomwong N, Boudreau EF, Singharaj P. Doxycycline prophylaxis for falciparum
malaria. Lancet. 1987
Rieckmann KH, Yeo AE, Davis DR, Hutton DC, Wheatley PF, Simpson R. Recent military experience
with malaria chemoprophylaxis. Med J Aust. 1993
Sanchez JL, DeFraites RF, Sharp TW, Hanson RK. Mefloquine or doxycycline prophylaxis in US
troops in Somalia. Lancet. 1993
Shamiss A, Atar E, Zohar L, Cain Y. Mefloquine versus doxycycline for malaria prophylaxis in
intermittent exposure of Israeli Air Force aircrew in Rwanda. Aviat Space Environ Med. 1996
230
Shanks GD, Barnett A, Edstein MD, Rieckmann KH. Effectiveness of doxycycline combined with
primaquine for malaria prophylaxis. Med J Aust. 1995
Taylor WR, Richie TL, Fryauff DJ. et al. Malaria prophylaxis using azithromycin: a double-blind,
placebo-controlled trial in Irian Jaya, Indonesia. Clin Infect Dis. 1999
Adehossi E, Parola P, Foucault C. et al. Three-day quinine-clindamycin treatment of uncomplicated
falciparum malaria imported from the tropics. Antimicrob Agents Chemother. 2003
Ramharter M, Oyakhirome S, Klouwenberg PK. et al. Artesunate-clindamycin versus quinineclindamycin in the treatment of Plasmodium falciparum malaria: a randomized controlled trial. Clin
Infect Dis. 2005
Duarte EC, Fontes CJ, Gyorkos TW, Abrahamowicz M. Randomized controlled trial of artesunate plus
tetracycline versus standard treatment (quinine plus tetracycline) for uncomplicated Plasmodium
falciparum malaria in Brazil. Am J Trop Med Hyg. 1996
Silamut K, Molunto P, Ho M, Davis TM, White NJ. Alpha 1-acid glycoprotein (orosomucoid) and
plasma protein binding of quinine in falciparum malaria. Br J Clin Pharmacol. 1991
Winstanley P, Newton C, Watkins W. et al. Towards optimal regimens of parenteral quinine for young
African children with cerebral malaria: the importance of unbound quinine concentration. Trans R Soc
Trop Med Hyg. 1993
White NJ. The treatment of malaria. N Engl J Med. 1996
Di Perri G, Allegranzi B, Bonora S. Quinine-induced blindness reversed by an increase in alpha1-acid
glycoprotein level. Ann Intern Med. 2002
Severe falciparum malaria: World Health Organization, Communicable Diseases Cluster. Trans R Soc
Trop Med Hyg. 2000
Anabwani G, Canfield CJ, Hutchinson DB. Combination atovaquone and proguanil hydrochloride vs.
halofantrine for treatment of acute Plasmodium falciparum malaria in children. Pediatr Infect Dis
J. 1999
Blanchard TJ, Mabey DC, Hunt-Cooke A. et al. Multiresistant falciparum malaria cured using
atovaquone and proguanil. Trans R Soc Trop Med Hyg. 1994
Bouchaud O, Monlun E, Muanza K. et al. Atovaquone plus proguanil versus halofantrine for the
treatment of imported acute uncomplicated Plasmodium falciparum malaria in non-immune adults: a
randomized comparative trial. Am J Trop Med Hyg. 2000
Bustos DG, Canfield CJ, Canete-Miguel E, Hutchinson DB. Atovaquone-proguanil compared with
chloroquine and chloroquine-sulfadoxine-pyrimethamine for treatment of acute Plasmodium
falciparum malaria in the Philippines. J Infect Dis. 1999
Lacy MD, Maguire JD, Barcus MJ. et al. Atovaquone/proguanil therapy for Plasmodium falciparum
and Plasmodium vivax malaria in Indonesians who lack clinical immunity. Clin Infect Dis. 2002
231
Llanos-Cuentas A, Campos P, Clendenes M, Canfield CJ, Hutchinson DB. Atovaquone and proguani
hydrochloride compared with chloroquine or pyrimethamine/sulfodaxine for treatment of acute
Plasmodium falciparum malaria in Peru. Braz J Infect Dis. 2001
Mulenga M, Sukwa TY, Canfield CJ, Hutchinson DB. Atovaquone and proguanil versus
pyrimethamine/sulfadoxine for the treatment of acute falciparum malaria in Zambia. Clin Ther. 1999
Radloff PD, Philipps J, Nkeyi M, Hutchinson D, Kremsner PG. Atovaquone and proguanil for
Plasmodium falciparum malaria. Lancet. 1996
Sabchareon A, Attanath P, Phanuaksook P. et al. Efficacy and pharmacokinetics of atovaquone and
proguanil in children with multidrug-resistant Plasmodium falciparum malaria. Trans R Soc Trop Med
Hyg. 1998
Uchiyama H, Okamoto A, Sato K. et al. Quinine-resistant severe falciparum malaria effectively
treated with atovaquone and proguanil hydrochloride combination therapy. Intern Med. 2004
van Vugt M, Leonardi E, Phaipun L. et al. Treatment of uncomplicated multidrug-resistant falciparum
malaria with artesunate-atovaquone-proguanil. Clin Infect Dis. 2002
Farnert A, Lindberg J, Gil P. et al. Evidence of Plasmodium falciparum malaria resistant to
atovaquone and proguanil hydrochloride: case reports. BMJ. 2003
Wichmann O, Muehlen M, Gruss H, Mockenhaupt FP, Suttorp N, Jelinek T. Malarone treatment failure
not associated with previously described mutations in the cytochrome b gene. Malar J. 2004
Schwobel B, Alifrangis M, Salanti A, Jelinek T. Different mutation patterns of atovaquone resistance to
Plasmodium falciparum in vitro and in vivo: rapid detection of codon 268 polymorphisms in the
cytochrome b as potential in vivo resistance marker. Malar J. 2003
Boggild AK, Parise ME. et al. Atovaquone-proguanil: report from a CDC expert meeting on malaria
chemoprophylaxis (II). Am J Trop Med Hyg. 2007
Health Information for International Travel 2007-2008. Atlanta, Ga: Elsevier; 2007
Hall AP, Doberstyn EB, Karnchanachetanee C. et al. Sequential treatment with quinine and
mefloquine or quinine and pyrimethamine-sulfadoxine for falciparum malaria. Br Med J. 1977
Murphy GS, Basri H, Purnomo HB. et al. Vivax malaria resistant to treatment and prophylaxis with
chloroquine. Lancet. 1993
Rieckmann KH, Davis DR, Hutton DC. Plasmodium vivax resistance to chloroquine? Lancet. 1989
Whitby M, Wood G, Veenendaal JR, Rieckmann K. Chloroquine-resistant Plasmodium vivax. Lancet.
Collignon P. Chloroquine resistance in Plasmodium vivax. J Infect Dis. 1991
Dixon KE, Pitaktong U, Phintuyothin P. A clinical trial of mefloquine in the treatment of Plasmodium
vivax malaria. Am J Trop Med Hyg. 1985
232
Hanna J. Chloroquine-resistant Plasmodium vivax: how common? Med J Aust. 1993
Harinasuta T, Bunnag D, Lasserre R, Leimer R, Vinijanont S. Trials of mefloquine in vivax and of
mefloquine plus “fansidar” in falciparum malaria. Lancet. 1985
Pukrittayakamee S, Chantra A, Simpson JA. et al. Therapeutic responses to different antimalarial
drugs in vivax malaria. Antimicrob Agents Chemother. 2000
Baird JK, Basri H, Subianto B. et al. Treatment of chloroquine-resistant Plasmodium vivax with
chloroquine and primaquine or halofantrine. J Infect Dis. 1995
Glucose-6-phosphate dehydrogenase deficiency. Bull World Health Organ. 1989
Hill DR, Baird JK, Parise ME, Lewis LS, Ryan ET, Magill AJ. Primaquine: report from CDC expert
meeting on malaria chemoprophylaxis I. Am J Trop Med Hyg. 2006
Povinelli L, Monson TA, Fox BC, Parise ME, Morrisey JM, Vaidya AB. Plasmodium vivax malaria in
spite of atovaquone/proguanil (malarone) prophylaxis. J Travel Med. 2003
Miller KD, Greenberg AE, Campbell CC. Treatment of severe malaria in the United States with a
continuous infusion of quinidine gluconate and exchange transfusion. N Engl J Med. 1989
Phillips RE, Warrell DA, White NJ, Looareesuwan S, Karbwang J. Intravenous quinidine for the
treatment of severe falciparum malaria: clinical and pharmacokinetic studies. N Engl J Med. 1985
van Hensbroek MB, Onyiorah E, Jaffar S. et al. A trial of artemether or quinine in children with
cerebral malaria. N Engl J Med. 1996
Newton PN, Angus BJ, Chierakul W. et al. Randomized comparison of artesunate and quinine in the
treatment of severe falciparum malaria. Clin Infect Dis. 2003
Molyneux ME, Taylor TE, Thomas CG, Mansor S, Wirima JJ. Efficacy of quinine for falciparum
malaria according to previous chloroquine exposure. Lancet. 1991
Zucker JR, Campbell CC. Malaria: principles of prevention and treatment. Infect Dis Clin North
Am. 1993
White NJ, Looareesuwan S, Warrell DA, Chongsuphajaisiddhi T, Bunnag D, Harinasuta T. Quinidine in
falciparum malaria. Lancet. 1981
Availability and use of parenteral quinidine gluconate for severe or complicated malaria. MMWR
Morb Mortal Wkly Rep. 2000
White NJ, Warrell DA. Managing cerebral malaria. Br Med J (Clin Res Ed). 1982
Powell VI, Grima K. Exchange transfusion for malaria and Babesia infection. Transfus Med Rev. 2002
Pasvol G, Jacobs M. What is the future of exchange transfusion for falciparum malaria? J Infect. 1999
Prasad K, Garner P. Steroids for treating cerebral malaria. Cochrane Database Syst Rev. 2000;
(2):CD000972
233
Borochovitz D, Crosley AL, Metz J. Disseminated intravascular coagulation with fatal haemorrhage in
cerebral malaria. Br Med J. 1970
Hemmer CJ. Neither heparin nor acetylsalicylic acid influence the clinical course in human
Plasmodium falciparum malaria: a prospective randomized study. Am J Trop Med Hyg. 1991
Thuma PE, Olivieri NF, Mabeza GF. et al. Assessment of the effect of the oral iron chelator
deferiprone on asymptomatic Plasmodium falciparum parasitemia in humans. Am J Trop Med
Hyg. 1998
Parise M, Lewis LS. Severe malaria: North American perspective. In: Feldman CSG, ed. Tropical and
Parasitic Infections in the ICU. New York, NY: Springer Science+Business Media Inc; 2005
Phillips RE, Looareesuwan S, White NJ. et al. Hypoglycaemia and antimalarial drugs: quinidine and
release of insulin. Br Med J (Clin Res Ed). 1986
White NJ, Warrell DA, Chanthavanich P. et al. Severe hypoglycemia and hyperinsulinemia in
falciparum malaria. N Engl J Med. 1983
White N. Controversies in the management of severe falciparum malaria. In: Pasvol G, ed. Balliere's
Clinical Infectious Diseases: Malaria [Volume 2]. London, England: Baillière Tindall; 1995
Marino P. The ICU Book. 2nd ed. Baltimore, Md: Williams & Wilkins; 1998
Newton CR, Hien TT, White N. Cerebral malaria. J Neurol Neurosurg Psychiatry. 2000
U.D.E. Group, ed. USP DI Drug Information for the Healthcare Provider. 23rd ed. Taunton, Mass:
Micromedex Inc; 2003
Conchie JM, Munroe JD, Anderson DO. The incidence of staining of permanent teeth by the
tetracyclines. Can Med Assoc J. 1970
Canadian recommendations for the prevention and treatment of malaria among international travellers.
Committee to Advise on Tropical Medicine and Travel CATMAT), Laboratory for Disease
Control. Can Commun Dis Rep. 2000;26:(suppl 2)
Sources: WHO Management of Severe Malaria (2000) and WHO Guidelines for the Treatment of
Malaria (2006).
PARARESCUE MEDICATION AND PROCEDURE HANDBOOK Second Edition
28 February, 2001 EDITOR Robert C. Allen, DO, FACEP Lt Col, USAF MC
CONTRIBUTORS:
James P. Bagian, MD Col, USAFR MC,
Lewis Neace, DO Col, USAFR MC,
John M. McAtee, PA-C Lt Col, USAF BSC
Gus Varnivas, MD Maj, USAF MC
Gary C. Perez, PA-C Capt, USAF BSC
Michael L. Fleming, NREMT-P TSgt, USAF
Brady Paramedic Emergency Care, Bledsoe, et al., Prentice Hall
234
Emergency Medicine: A Comprehensive Study Guide, 4th Ed., Tintanelli, et al. McGraw-Hill
Lippencott Nursing Manual, J. B. Lippencott Co.
Physicians' Desk Reference, Medical Economics Data Production Co.
Physicians GenRx, Mosby, 1998
Advanced Cardiac Life Support, American Heart Association, 2000 edition
Wilderness Medicine: Management of Wilderness and Environmental Emergencies, 3rd Ed., PA
Auerbach, Mosby 1995.
Emergency Medicine Concepts and Clinical Practice, 4th Ed., Rosen, et al., Mosby 1998
Medical Management of Chemical Casualties Handbook, US Army Medical Research Institute of
Chemical Defense, Sept 1995.
Medical Management of Biological Casualties Handbook, US Army Medical Research
Institute of Infections Diseases, August 1996
Skills and Training Manual, Adapted by COL Warren Whitlock, MC, USA
US Army Special Forces Medical Handbook ST 31-91B 1982
MAJ Daniel Schissel, MC, USA
COL Roland J. Weisser, Jr., MC, USA
MAJ Daniel Schissel, MC, USA
CAPT Robert Johnson, MC, USN
MAJ John Hlavnicka, AN, USA
Lt Col Robert Allen, USAF, MC
CAPT Kurt Strosahl,COL
COL Richard Tenglin, MC, USA,
Maj. Frederick Shuler, USAF, MC
1LT Harold Becker, SP, PA, USAR
LTC Lee Cancio, MC, USA
CAPT Kurt Strosahl, MC, USN & COL Warren Whitlock, MC, USA
LTC David DuBois, DC, USA
LTC Lee Cancio, MC, USA & 1LT Harold Becker, SP, USAR
Lt Col John Wightman, USAF, MC
Maj Michael Curriston, USAF, MC
LTC Lee Cancio, MC, USA
1LT Harold Becker, SP, PA, USAR
LTC Duane Hospenthal, MC, USA
COL (Ret) Peter McNally, MC, USA
LTC John Holcomb, MC, USA and SFC Dominique Greydanus, USA
Col Stephen Brietzke, USAF, MC
Lt Col John McAtee, USAF, BSC
COL Theodore Cieslak, MC, USA & COL Edward Eitzen, MC, USA
Lt Col Aimee Hawley, USAF, MC
COL Warren Whitlock, MC, USA
235
CPT Brooks Morelock, MC, USA
MAJ Ann Friedmann, MC, USA
LTC Michael Matthews, MC, USA & COL Warren Whitlock, MC, USA
LCDR (sel) Edward Moldenhauer, MSC, USN
MAJ Victor Yu, SP, USA & LCDR (sel) Edward T. Moldenhauer, MSC, USN
MAJ Ann Friedmann, MC, USA
COL Naomi Aronson, MC, USA
MAJ Joseph Wilde, MC, USAR
LTC Glenn Wortmann, MC, USA
CDR Scott Flinn, MC, USN
CDR David Llewellyn, MC, USN
CAPT Leo Kusuda, MC, USN
COL (Ret) Joel Gaydos, MC, USA & SFC Jeffrey Crainich, USA
LTC Duane Hospenthal, MC, USA & MAJ Daniel Schissel, MC, USA
CDR Robert Wall, MC, USN
COL Naomi Aronson, MC, USA
CAPT Elwood Hopkins, MC, USN
LTC Howard Burtnett, AN, USA & MAJ Steven Hendrix, AN, USA
MAJ Michael Doyle, MC, USA
LCDR Christopher Jankosky, MC, USN
COL Warren Whitlock, MC, USA
LTC Niranjan Kanesa-thasan, MC, USA
Lt Col Gerald Peters, USAF, MC
COL Clifford Cloonan, MC, USA
State of Wisconsin Standards & Procedures of Practical Skills Manual
July 2008
Cousins MJ, Mather LE. Clinical pharmacology of local anesthetics. Anesth Intens Care 1980
Saltzman, M., Mercer, D., Bertelsen, A., Warme, W., & Matsen, III, F. (2009). Bilateral posterior
sternoclavicular dislocations Radiology Case Reports
Jacques B. Jougon, MD, Denis J. Lepront, MD, Claire E. H. Dromer, M. Posterior Dislocation of the
Sternoclavicular Joint Leading to Mediastinal Compression.
Hoekzema N. Torchia M. Adkins M Cassivi SD. Posterior sternoclavicular joint dislocation
Mirza AH, Alam K, Ali A Posterior sternoclavicular dislocation in a rugby player as a cause of silent
vascular compromise: a case report. Br J Sports Med. 2005 May
Asplund C, Pollard ME. Posterior sternoclavicular joint dislocation in a wrestler. Mil Med. 2004 Feb
Wirth MA, Rockwood CA Jr. Acute and Chronic Traumatic Injuries of the Sternoclavicular Joint.J Am
Acad Orthop Surg. 1996 Oct
Brinker MR, Bartz RL, Reardon PR, Reardon MJ. A method for open reduction and internal fixation of
the unstable posterior sternoclavicular joint dislocation. J Orthop Trauma. 1997
236
Saltzman, M., Mercer, D., Bertelsen, A., Warme, W., & Matsen, III, F. (2009). Bilateral posterior
sternoclavicular dislocations Radiology Case Report
O’Connor PA. Nölke L. O’Donnell A. Maha Lingham A. Retrosternal dislocation of the clavicle
associated with a traumatic pneumothorax
Cooper A. A treatise on dislocations and on fractures of the joints. In: Longman, Hurst, Orme, Brown,
Green, eds. London, 1824:359
International Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiac Care,
Circulation 2000, Aug 22 102(8 suppl))
Joint Reduction, Elbow Dislocation, Posterior
Author: Nina Chicharoen, MD; Chief Editor: Erik D Schraga, MD
Tham, E.T., & Brenner, B.E. (n.d.). Hip dislocation in emergency medicine.
PubMed U.S. National Library of Medicine & National Institutes of Health, (n.d.). Bethesda, MD:
National Center for Biotechnology Information.
National Center for Biotechnology Information & U.S. National Library of Medicine, Agency for
Healthcare Research and QualityAgency for Healthcare Research and Quality. (n.d.). Rockville, MD
"Agency for Healthcare Research and Quality." HCUPnet. 2011.
Media Partners. (2010, July 28). Hip anatomy, function and common problems
Floyd, R.T. (2009). Manual of structural kinesiology. New York, NY: McGraw-Hill
Matta, Joel M. "Periacetabular Osteotomy - Page 1." Hip and Pelvis Institute. 2000.
"Hip Dislocation - Your Orthopaedic Connection - AAOS." AAOS - Your Orthopaedic Connection.
Aug. 2007.
McCarthy, James and Jaff, William L."Developmental Dysplasia of the Hip". Medscape Reference.
March 2011.
"Congenital Hip Dislocation." Zimmer Oct. 14, 2008.
French, Linda M. and Dietz, Frederick. "Screening for Developmental Dysplasia of the Hip". American
Academy of Family Physicians. July 1999.
"Definition of Congenital Hip Dislocation". MedicineNet. August 2000.
“Hip Dislocation”.. American Academy of Orthopadeic Surgeons. 2007.
Gammons, Matthew. “Hip Dislocation Treatment and Management”.
Rihn JA, et al. "The Acutely Dislocated Knee: Evaluation and Management" J. Am. Acad. Ortho. Surg.,
September/October 2004
237
Elisa M Aponte, MD; Chief Editor: Erik D Schraga, MD
Joint Reduction, Shoulder Dislocation, Anterior
Benjamin T Milligan, MD, FAAEM; Chief Editor: Erik D Schraga, MD
Joint Reduction, Shoulder Dislocation, Posterior
Sternoclavicular Joint Dislocation February 6, 2010 by Mike Cadogan
Wilderness Environ Med. 1997 May;8(2):111-6. Strimple PD, Tomassoni AJ, Otten EJ, Bahner D.
Saltzman, M., Mercer, D., Bertelsen, A., Warme, W., & Matsen, III, F. (2009). Bilateral posterior
sternoclavicular dislocations Radiology Case Reports, 4 (1)
Jacques B. Jougon, MD, Denis J. Lepront, MD, Claire E. H. Dromer, M. Posterior Dislocation of the
Sternoclavicular Joint Leading to Mediastinal Compression.
Hoekzema N. Torchia M. Adkins M Cassivi SD. Posterior sternoclavicular joint dislocation
Mirza AH, Alam K, Ali A Posterior sternoclavicular dislocation in a rugby player as a cause of silent
vascular compromise: a case report. Br J Sports Med. 2005 May;39(5)
Asplund C, Pollard ME. Posterior sternoclavicular joint dislocation in a wrestler. Mil Med. 2004
Feb;169(2)
Wirth MA, Rockwood CA Jr. Acute and Chronic Traumatic Injuries of the Sternoclavicular Joint.J Am
Acad Orthop Surg. 1996 Oct;4(5)
Brinker MR, Bartz RL, Reardon PR, Reardon MJ. A method for open reduction and internal fixation of
the unstable posterior sternoclavicular joint dislocation. J Orthop Trauma. 1997 Jul;11(5)
Saltzman, M., Mercer, D., Bertelsen, A., Warme, W., & Matsen, III, F. (2009). Bilateral posterior
sternoclavicular dislocations Radiology Case Reports, 4
O’Connor PA. Nölke L. O’Donnell A. Maha Lingham A. Retrosternal dislocation of the clavicle
associated with a traumatic pneumothorax
Cooper A. A treatise on dislocations and on fractures of the joints. In: Longman, Hurst, Orme, Brown,
Green, eds. London, 1824
MacGillivray JD (February 2005). "Traumatic shoulder dislocation in the adolescent athlete: advances
in surgical treatment". Curr. Opin. Pediatr.
Shoulder Dislocations at eMedicine
Kelley SP, Hinsche AF, Hossain JF (November 2004). "Axillary artery transection following anterior
shoulder dislocation: classical presentation and current concepts". Injury
Posterior Shoulder Dislocation Hawkins RJ, Neer CS, Pianta RM, Mendoza FX (January 1987).
238
Dislocated shoulder: Treatment - MayoClinic.com
Miljesic, Kelly; Kelly, Anne-Maree (1998). "Reduction of anterior dislocation of the shoulder: the
Spaso technique". Emergency Medicine Australasia
Yuen, Gap, Chan, Tung (2001). . Emerg"An easy method to reduce anterior shoulder dislocation: the
Spaso technique" Med J
Murrell GA (October 2003). "Treatment of shoulder dislocation: is a sling appropriate?". Med. J. Aust.
Murrell GA. "We got it wrong on shoulder dislocation. Don't use a sling". Orthopaedic Research
Institute, Dept. Orthopaedic Surgery and Sports Medicine, University of New South Wales.
Chalidis B, Sachinis N, Dimitriou C, Papadopoulos P, Samoladas E, Pournaras J (June 2007). "Has the
management of shoulder dislocation changed over time?". Int Orthop
"Anterior glenoid reconstruction for unstable dislocating shoulders." . University of Washington:
Orthopaedics and Sports Medicine.
Burkhead Jr, WZ; Rockwood Jr, CA (1992). "Treatment of instability of the shoulder with an exercise
program". The Journal of bone and joint surgery. American volume 74
Townsend: Sabiston Textbook of Surgery, 18th ed
Matsen Fa, 3rd; Harryman Dt, 2nd; Sidles, JA (1991). "Mechanics of glenohumeral instability". Clinics
in sports medicine
Owens, B. D.; Nelson, B. J.; Duffey, M. L.; Mountcastle, S. B.; Taylor, D. C.; Cameron, K. L.;
Campbell, S.; Deberardino, T. M. (2010). "Pathoanatomy of First-Time, Traumatic, Anterior
Glenohumeral Subluxation Events". The Journal of Bone and Joint Surgery
EMED Publications
Petron DJ, et al. Distal radius fractures in adults.
Hand fractures. American Academy of Orthopaedic Surgeons.
Anderson BC. Evaluation of the adult patient with wrist pain.
Wrist fractures. American Society for Surgery of the Hand.
Scaphoid fracture of the wrist. American Academy of Orthopaedic Surgeons.
Lewiecki EM. Prevention of osteoporosis.
Good CR, MacGillivray JD (February 2005). "Traumatic shoulder dislocation in the adolescent athlete:
advances in surgical treatment". Curr. Opin. Pediatr. 17
Kelley SP, HShoulder Dislocation sinsche AF, Hossain JF (November 2004).
"Axillary artery transection following anterior shoulder dislocation: classical presentation and current
concepts". Injury 35
Neer CS, Pianta RM, Mendoza FX (January 1987). "Locked posterior dislocation of the shoulder". J
Bone Joint Surg Am 69
Yuen, Gap, Chan, Tung (2001). "An easy method to reduce anterior shoulder dislocation: the Spaso
technique". Emerg Med J 18
239
Chalidis B, Sachinis N, Dimitriou C, Papadopoulos P, Samoladas E, Pournaras J (June 2007). "Has the
management of shoulder dislocation changed over time?". Int Orthop 31
"Bankart repair for unstable dislocating shoulders:". University of Washington: Orthopaedics and
Sports Medicine.
"Anterior glenoid reconstruction for unstable dislocating shoulders.". University of Washington:
Orthopaedics and Sports Medicine.
Department of Family Medicine at Naval Hospital Jacksonville, Jacksonville, Fla.
CORRY J. KUCIK, LT, MC, USN,
TIMOTHY CLENNEY, CDR, MC, USN
JAMES PHELAN, CDR, MC, USN
Timothy Clenney, CDR, MC, USN,
Anthony J. Viera, LCDR, MC, USNR.
Timothy Clenney, CDR, MC, USN.
Bartkiw TP, Pynn BR, Brown DH. Diagnosis and management of nasal fractures. Int J Trauma Nurs.
1995
Smith JA. Nasal emergencies and sinusitis. In: Tintinalli JE, Ruiz E, Krome RL, American College of
Emergency Physicians. Emergency medicine: a comprehensive study guide. 4th ed. New York:
McGraw-Hill, 1996
Ellis E III, Scott K. Assessment of patients with facial fractures. Emerg Med Clin North Am. 2000;
Hester TO, Campbell JP. Diagnosis and management of nasal trauma for primary care physicians. J Ky
Med Assoc. 1997
Cummings CW, ed. Otolaryngology—head & neck surgery. 3d ed. St Louis: Mosby, 1998:
Bailey BJ, ed. Head and neck surgery—otolaryngology. Philadelphia: Lippincott, 1993
Cox AJ III. Nasal fractures—the details. Facial Plast Surg. 2000
Rodriguez JO, Lavina AM, Agarwal A. Prevention and treatment of common eye injuries in sports. Am
Fam Physician. 2003
Rhea JT, Rao PM, Novelline RA. Helical CT and three-dimensional CT of facial and orbital injury.
Radiol Clin North Am. 1999
Sargent LA, Rogers GF. Nasoethmoid orbital fractures: diagnosis and management. J
Kneecap Dislocation By Jonathan Cluett, M.D.
Craniomaxillofac Traum. 1999;5:19–27.
Rohrich RJ, Adams WP Jr . Nasal fracture management: minimizing secondary nasal deformities. Plast
Reconstr Surg. 2000;106:266–73
240
Gilpin T, Carley S. Toward evidence based emergency medicine: best BETs from the Manchester Royal
Infirmary. Early management of displaced nasal fractures. J Accid Emerg Med. 2000;17:286.
Canty PA, Berkowitz RG. Hematoma and abscess of the nasal septum in children. Arch Otolaryngol
Head Neck Surg. 1996;122:1373–6.
Jacobson JA, Kasworm EM. Toxic shock syndrome after nasal surgery. Case reports and analysis of
risk factors. Arch Otolaryngol Head Neck Surg. 1986;112:329–32.
Kane AP, Kane LA. Open reduction of nasal fractures. J Otolaryngol. 1978;7:183–6.
Chegar BE, Tatum SA III. Nasal fractures. In: Flint PW, Haughey BH, Lund LJ, et al, eds. Cummings
Otolaryngology: Head & Neck Surgery. 5th ed. Philadelphia, Pa: Mosby Elsevier; 2010:chap 35.
Riviello RJ. Otolaryngologic procedures. In: Roberts JR, Hedges JR, eds. Clinical Procedures in
Emergency Medicine. 5th ed. Philadelphia, Pa: Saunders Elsevier; 2009:chap 64.
McKay MP, Mayersak RJ. Facial trauma. In: Marx JA, Hockberger RS, Walls RM, et al, eds. Rosen's
Emergency Medicine: Concepts and Clinical Practice. 7th ed. Philadelphia, Pa: Mosby Elsevier;
2009:chap 39.
Update Date: 8/31/2011
Updated by: Linda J. Vorvick, MD, Medical Director, MEDEX Northwest Division of Physician
Assistant Studies, University of Washington, School of Medicine; Seth Schwartz, MD, MPH,
Otolaryngologist, Virginia Mason Medical Center, Seattle, Washington. Also reviewed by David Zieve,
MD, MHA, Medical Director, A.D.A.M., Inc.