1. family and parenting
2. motherhood
3. pregnancy

Notes Obs &Gynae
HYPEREMESIS GRAVIDARUM
not a lot of detail to find
Aetiology
Unclear
Possibly related to high oestrogen levels
Clinical
Diagnosis of exclusion
Severe intractable vomiting
Peak 8 – 12 weeks
Usually resolves by week 16
Investigations
FBP
U&E
U/A - ketosis
Management
Rehydration
Antiemetics
Metoclopramide
class A
Promethazine
C
Prochlorperazine
C
Ondansetron
B1
Admit
Marked dehydration
Unable to tolerate oral fluids
Significant electrolyte abnormalities
Ketosis
1
Miscarriage
25% all pregnancies have bleeding in first trimester
- 50% of these will abort
Threatened - pv bleeding +/- abdo pain + os closed
3 - 5 weeks - empty uterus
5 - 6.5 weeks - empty gestational sac
> 6.5 weeks - cardiac activity
Complete - pv bleeding + os closed + hCG falling
Incomplete - pv bleeding + falling/ plateau hCG
irregular endometrium on USS
Inevitable - pv bleeding + os opened
Missed abortion - embryo CRL >5mm but no cardiac activity
Blighted ovum - gestational sac >20mm but no embryo
Septic abortion - abdo tenderness + cervical excitation + pv discharge / bleeding
Thickened, irreg endometrium
Investigations
Urine hCG testing 99.4% accurate at time of missed menses
- most detect >25 IU/l [hCG]
Urine analysis essential even if asymptomatic
- UTI is a risk factor for miscarriage
FBE
Rhesus status - anti-D if necessary (250 Iunits)
Quant hCG
- incr by 66% every 48 days in 85% of normal pregnancy
USS Eccentric gestational sac with double ring sign in uterus
Discriminatory zone - transvaginal USS : 1000 - 1500 IU/l hCG
Transabdominal USS : 6000 - 6500 IU/l hCG
Findings seen on TA USS lags one week behind TV USS
hCG >1500 : 4.5 weeks = gestational sac
hCG 1000 - 7500 : 5.5 weeks = yolk sac
hCG >7000 : 6.5 weeks = embryo with cardiac activity
Management
Resuscitation
Remove products from os if able
Gynaecological referral
Psychological issues
Broad-spectrum Abs for septic - all poymicrobial
2
INVESTIGATION OF SUSPECTED ECTOPIC PREGNANCY
ECTOPIC SUSPECTED ON CLINICAL FINDINGS
1. Always do quantitative β-HCG.
-
If neg, consider other diagnoses
Level > 10mIU/ml is 100% sensitive for detecting pregnancy
“Discriminatory zone” is > 700mIU.ml(700-1500 depending on text)
2. If β-HCG is > 700 – do TVUSS or TAUSS( TAUSS lags 1 week behind TVUSS)
-
TVUSS – Absence of IU gestational sack
- Sens 100%
- Spec 96%
- PPV 90%
- NPV 100% for diagnosis of EP
- IUP confirmed
- ~ 1:3000 pregnancies heterotopic
- ~ 7% of IVF pregnancies heterotopic
- Refer if high risk for EP and EP suspected
USS findings
Small amt free pelvic fluid
Echogenic adnexal mass
Med/large amt free fluid
Any mass + echogenic fluid
Risk of EP
52%
70%
86%
97%
3. If β-HCG > 700 and no IUP detected on TVUSS, refer for operative management
4. If β-HCG < 700 or initial USS equivocal in stable patient, can consider serial β-HCG’s
-
β-HCG increase by more than 66% every 2 days(should more or less double every 2 days)
If fails to double only suggests EP and warrants further investigation
13% of EP’s will have increase in β-HCG of at least 66%
ALTERNATIVE INVESTIGATIONS
1. culdocentesis
- Only if USS not available (stable or unstable patients)
- Positive if 5ml unclotted blood aspirated
- 85-90% of ruptured EP’s will have + test
- 70% of unruptured EP’s will have + test
- + β HCG and + culdocentesis has PPV of 99% for EP
- 20% false neg
2. Laparoscopy
- Low false neg rates
- Operator dependant
- Can be diagnostic and curative
- Low morbidity
3. D&C
- Definite diagnosis for IUP if chorionic villi obtained
- Where termination of pregnancy is desired or non viable pregnancy
5. Progesterone measurements
-
During first 8-10 weeks levels remain relatively constant
Most pathological pregnancies has P ≤ 10ng/ml
Nearly 100% of abnormal pregnancies has P ≤ 5ng/ml
No normal pregnancies with P ≤ 2.5 ng/ml
Levels > 25 have sens of 97% for viable IUP
•
3
ECTOPIC PREGNANCY DIAGNOSIS AND DISCRIMINATORY ZONES.
THE LAST WORD (FOR NOW) (early 2007 )
The following is a one page condensed version of some detailed background work by Mike Cadogan. If you wish to
read the more detailed evidence base he has compiled on this, please contact him or Trevor directly.
Important background principles
•
•
•
•
At the same gestational age, nonviable intrauterine pregnancies (NVIUP) and ectopic pregnancies (EP)
tend to have lower quantitative ß-hCG values than viable intrauterine pregnancies. (VIUP)
VIUPs usually show doubling of the serum quantitative ß-hCG about every 48 hours. EPs tend to show
lower increase rates, and 15% will show decreasing serial levels.
About half of all EPs are not detected when the patient first presents, with diagnosis and intervention reliant
upon on close serial follow-up.
EP can (rarely) exist in the setting of a negative ß-hCG and ultrasound report.
Discriminatory zones
As a new pregnancy develops, ß-hCG levels rise, leading to ß-hCG levels or zones in which the quantitative serum
level of ß-hCG will accurately predict the ability to demonstrate a VIUP on ultrasound in > 98.5% of cases. The
absolute value of these zones varies among institutions as it is based on the expertise of the ultrasonographer and
the equipment used. Transvaginal USS (TVS) diagnoses intrauterine pregnancies around one week earlier than
transabdominal USS. (TAS)
The two most important levels or zones are:
•
A zone of > 1000-1500 IU for TVS.
This means if you can't visualize an intrauterine pregnancy on TVS when the quantitative ß-hCG is > 10001500 IU, then an abnormal, nonviable gestation is diagnosed with the differential diagnosis of spontaneous
miscarriage or ectopic pregnancy.
•
A zone of > 6000-6500 IU for TAS
As above, but with a higher ß-hCG level reflecting the lower accuracy of TAS.
Important note:
Levels in the intermediate zone between 1500 - 6000 IU are non-diagnostic and must be assessed on an individual
patient basis with their ultrasound findings (TAS +\- TVS). A definitive diagnosis may rest on serial US examinations,
ß-hCG levels and the results of other investigations for example Progesterone levels.
-
4
Antenatal Care
The aim of antenatal care:
a) Prevent the pregnancy from having deleterious effect on maternal health
b) To ensure as far as possible that the mother takes home a healthy baby
The first visit
1. A full history
2. A full physical examination
3. Duration of the pregnancy must be established
4. Important screening tests must be done
5. The first assessment of risk factors must be done
History:
• Any previous obstetric history
o Gravity, parity, ectopics, miscarriages
o Birth weights etc
o Previous complications of pregnancy
o Thromboembolic disease
• The present obstetric history
o Problems, symptoms of pregnancy, planned
• A medical history
• History of medications and allergies
• A surgical history
• A family history
• Social circumstances
Physical examination:
• In addition to a full examination the following organs must be carefully examined
o Thyroid gland
o Breasts
o Respiratory system
o Cardiovascular system
o Abdomen
o External and internal genitalia
Determining the duration of the pregnancy:
• Last normal menstrual period
• Size of the uterus on bimanual or abdominal examination up to 24 weeks
• Height of fundus after 24 weeks
• The size of the fetus
• Ultrasound
Side room and special investigations:
• BP->140/90 on 2 occasions over several hours
• Mid- dipstix, midstream mcs
o Testing for asymptomatic bacteriuria, chronic renal disease, glycosuria, proteinuria
• Blood sugar
• Blood group and RH determination
• RPR, Hepatitis, HIV, rubella antibodies,
• PAP smear
• Blood tests (FBP, UE, Iron, LFT)
• Ultrasound (to confirm pregnancy but the 18-22w is the important scan)
Assessment of risk:
Will determine the required follow up and monitoring through the pregnancy
Second and subsequent visits:
• To review and act on results of the special investigations done at previous visits
• To monitor both mother and fetus
o Assessment of fetal movements, fetal heart rate
o Growth of the uterus
o Lie of the fetus
o Systemic well being of the mother
Generally- low risk mothers- visit every 6w until 24w, again at 28w, then 2 weekly till 36w and weekly till delivery
5
PHYSIOLOGICAL CHANGES IN PREGNANCY
(Relevance to EM & Trauma)
Trauma
General
Two lives at risk, fetal survival depends on management of mother
Tilt patient 15 degrees to left side after 20 weeks gestation – remember ‘spinal
precautions’
Airway
Increased risk for ‘difficult airway’
Increased BMI, large breasts and capillary dilatation
- Swollen cords, engorged airway and upper respiratory tract
- Increased risk for bleeding from ‘spongy gums’ and upper airway
- Increased risk for stomach contents regurgitation / aspiration due to relaxation of lower
esophageal sphincter
Breathing
Increased risk for compromised ventilation / oxygenation
- Engorged upper respiratory tract = increased resistance
- Increased weight = more chest to ‘move’
- Decreased chest compliance cancelled by Increased lung compliance
- Large uterus / abdomen elevating the diaphragm
Decreased oxygen ‘reserve’
- 20 % increase in O2 consumption
- Functional Residual Capacity decreased
- ‘Dilutional’ anemia = decreased O2 carrying capacity
Mild respiratory alkalosis is ‘normal’ , pCO2 +- 32 mmHg
- Increased Tidal Volume by 40%
Circulation
Large uterus in supine patient compromising IVC venous return causing hypotension
‘Delayed’ maternal signs of significant blood loss
- 40% increase in blood volume and 20% increase Rbc
- Physiologic / Dilution anemia, Hct decrease to +- 30%
- Early ‘shunting’ of blood away from placenta = fetal compromise
- Engorged pelvic veins = massive retroperitoneal bleed
Obstetrics / Fetus
- Importance of Fetal Heart rate as part of ‘physiological assessment’
- Fetus easily affected by maternal hypoxia / hypovolemia
Tests
- NB – Bedside tests: Urine B-Hcg to dx ‘unknown’ pregnancy and CTG
- Radiology & Issues of ‘radiation exposure’ risk and fetal gestation / development. Fetus
maximally at risk 2 – 7 weeks after conception
- Dose > 10 rad associated with marked increase adverse effects for fetus
- ‘Trauma series’ = very low dose of radiation (pelvis view is highest at 0.1 - 0.5 rad). Weigh
benefit – risk and err on side of assessing patient properly
- Avoid CT abdo & pelvis, exposure may be up to 10 rad
- Distinguish maternal from fetal blood e.g. Kleihauer, Apt tests
- Check Rhesus status and prevention of Iso-immunisation
Note - ‘Peri-mortem’ c/section > 23 / 40 may improve chances for both
6
Relevance to EM in General
General
-
Assessment of acute illness requires more urgent priority
Additional need for skilled staff with O&G experience
Additional need for equipment (CTG) and special tests (Kleihauer)
Incr BMI, decreased mobility, stressed hubby & family
Difficult to perform effective CPR
Neurological
- Increased risk of ‘seizure’ e.g. Eclampsia, not taking anti-convulsants
Cardiovascular
nd
rd
BP reduces 5-10 mmHg in 2 trimester, return to normal in 3
- Cardiac output increases 40% (15% increase heart rate, 25% increase stroke volume) and
decreased peripheral resistance (accounting for decr DBP)
- Increased risk for ‘thrombo-embolic disease’, see hematology below
- See above for blood volume / Rbc
- Premature atrial contractions are common
- ECG may show Left axis deviation, Inferior Q waves with T wave inversion
Respiratory
- 1/3 of asthma patients have ‘worse’ asthma during pregnancy
Gastro-intestinal
- Increased reflux / regurgitation
- Pregnancy = constipation, so NOT appropriate diagnosis for ‘abdo pain’
- Increased rate for ‘missed’ diagnosis of Acute Appendicitis
st
- Gastric acid secretion increased during the 1 trimester
- Increased risk for gallstone formation
Renal / Urological
- Increased UTI risk, increased residual volume in bladder, ureters & kidneys
- Increased renal GFR with glucosuria in 50% of pregnancies
- Decreased baseline Urea and Creatinine (so mild increases are abnormal)
- Increased Renin – Aldosterone = Water & Salt retention
Endocrine & Metabolic
- Pituitary gland doubles in size (Risk of Sheehan syndrome)
- Resting metabolic rate 10-15 % higher than non-pregnant women
- Increased Insulin resistance / undetected Gestational Diabetes
- Mild decrease in s-Albumin with further oncotic / edema implications
Hematological
- Increase of several clotting factors and fibrinogen, decreased fibrinolytic activity =
‘hypercoaguable’ state (? Up to 6/52 post partum)
- White Cell Count increases above normal (12 – 16)
Other – Pharmacology
- Altered pharmacokinetics (especially - absorption, Vd, elimination)
- Issues with drug safety (FDA classes A-B-C-X)
7
TRAUMA in PREGNANCY
Notes:
1 .Trauma in pregnancy is most common cause of non-obstetric maternal death with most mortality due to
head injury and haemorrhagic shock.
2. Foetal death occurs much more often than maternal death, most due to placental abruption and direct
foetal trauma.
3. Common causes = MVCs, falls assaults
4. Physiological changes including relative hypervolaemia, borderline tachycardia and gravid uterus may
make Ax difficult.
5. Maternal resuscitation is the best method of foetal resuscitation.
6. Premature labour may go unnoticed especially if intubated, paralysed or mentally obtunded.
Problems unique to pregnant patient:-
-
placental abruption
laceration of cord or placenta
premature labour
premature rupture of membranes
amniotic fluid embolism
uterine rupture
foetomaternal haemorrhage.
foetal distress
direct foetal injury
Specific injuries:
1. Pelvic fracture- usually due to high speed MVC. Massive haemorrhage can occur form uterus, bladder,
urethra and ureteric lacs.
2. Placental abruption: in 1-5% of minor trauma, 20-50% of major trauma.
Due to shearing forces especially from high speed (>80kmph) and broad side collisions.
Thromboplastin release may lead to DIC
3. Uterine rupture: rare, but leads to considerable haemorrhage and almost 100% foetal mortality rate.
Suspect if: maternal shock, foetal death, easily palpable foetal parts and +ve DPL.
ASSESSMENT
History:
- Severity/ type of trauma: direct trauma to abdo more likely to cause liver/ splenic injury, indirect( via
shearing forces) more likely to cause abruption.
? penetrating: stab wounds have a better prognosis for foetus than stab wounds.
-current gestation
- problems this pregnancy and ultrasonographic results
- obstetric history
- Sxs now: abdo/ pelvic pain, contractions, vaginal bleeding
-AMPLE
Examination:
Primary survey with concurrent resuscitation:
Airway: intubation may be difficult because of aspiration risk/ possible C-spine injury/ enlarged breasts.
Breathing: supplemental O2 to improve both maternal and foetal oxygenation
Circulation: if > 20/40, place on L lateral side ( foam wedge under spinal board if spinal precautions
required)
N.B. Signs of shock may present late because of relative hypervolaemia.
Disability: GCS and any other major neuro deficits.
Secondary survey: head to toe as in non-pregnant patient but must include obstetric exam:
-Abdo: fundal ht, uterine tenderness, contractions, foetal position/ movements/ heartbeat.
- Pelvic: preferably by obstetrician.
?lacerations/ trauma to genital tract
cervical dilatation
foetal presentation and station
test for presence of amniotic fluid on nitrazine paper
- rectal exam and U/A also essential.
Investigations:
Bedside: ECG, U/A
8
Lab.:
Imaging:
FBP, U&Es, coags, G&H (or X-match), Kleihauer in rhesus –ve pts.
Trauma series with abdo shielding in severe trauma.
U/S: gestational age/ foetal well-being/ placental position/ amniotic fluid volume.
(CTG more sensitive for placental abruption)
CT to assess uterine and retroperitoneal structures
Other:
CTG if > 20/40: institute early and continuously for 4 hours.
Frequent uterine contractions and foetal distress suggestive of abruption.
DPL: incision above fundus.
Management:
- Resusc area, team approach, oximetry, bp , ECG and CTG monitoring.
- Early obstetric and surgical consultation
- Attention to adequate positioning, oxygenation and fluid resusc.
- NGT and IDC
- Ixs as indicated
- If patient remains HD unstable -> laparotomy
- If vaginal bleeding/ abdo pain and tenderness/ hypotension/ foetal distress/
absent foetal heart beat/
amniotic fluid leakage-> may need urgent C/S.
- ? DIC ( from abruption/ amniotic fluid embolism/ foetal death) -> replace factors
- Surgical exploration of penetrating wounds.
- Post-mortem C/S should be performed within 4 mins
Disposition:
- Haemodynamically unstable and major injuries-> surg. Intervention and ICU
- Mother stable, but foetal distress-> C/S
- Mother with minor injuries and stable-> CTG for 4 hours.
9
DRUGS IN PREGNANCY
General
If possible try non-drug therapy first for minor conditions, especially in first trimester
Choose the safest category as possible
Use lowest effective dose
Use for shortest time as possible
Classification
Category
Interpretation
A
Safe in large numbers of pregnant women
B1
Safe in small numbers of women. No adverse effects in animals
B2
Safe in small numbers of women. Inadequate animal studies
B3
Safe in small numbers of women. Animal studies show increased risk of uncertain human
significance.
C
Suspected of causing or cause reversible harmful effects. No malformations. Consult
experts prior to use.
D
Suspected of causing or cause irreversible harmful effects, including malformations. Consult
experts prior to use.
X
High risk of permanent foetal damage. DO NOT USE if possibility of pregnancy.
Drugs covered
Antiemetics
Analgesics
Antibiotics
Antireflux drugs
Antimigrainous drugs
Anticoagulants
Thrombolytics
Benzodiazepines
Anticonvulsants
Corticosteroids
Bronchodilators
Antihistamines
Anaesthetic agents
Antidotes
Common Category X Drugs
Misoprostol (gastric ulcer)
Dienoestrol (OCP)
Ribavirin (antiviral)
Isotrentin, finasteride, Acitretin (dermatology)
Common Category D drugs
ACE inhibitors
nd
rd
- Previously thought to be 2 and 3 trimesters, now C/I in all
Angiotensin 2 antagonists (losartan,irbesartan etc.)
- As ACEI
Warfarin
- Embropathy, CNS foetal bleeding, spontaneous abortion
Lithium
- increased birth defects in first trimester
Anticonvulsants Phenytoin, Na Valproate, Carbamezepine, phenobarbitone
10
- Lamotrigine (B3)and gabapentin (B1) safe
Quinine, Chloroquine
- risk of abortion, damage at toxic levels
Tetracycline, doxycycline
- safe in first 18 weeks only, bone ,teeth abnormalities after this
Aminoglycosides (gentamycin, tobramycin etc.)
- nephrotoxicity, ototoxicity
Ganciclovir
-teratogenic
Azathiaprine, methotrexate
- foetal malformations and bone marrow suppression
Antineoplastic and Sex or pituitary hormones should generally be avoided (D)
Other drugs to avoid
Erythromycin(estolate)- maternal hepatotoxicity but azithromycin is safe
Fluoroquinolones
- cartilage abnormalities eg ciprofloxacin
Metronidazole
- facial defects in first trimester
Trimethoprim
- folate antagonist, neural tube defects
Sulphonamides - foetal haemolysis
Aspirin
NSAID’s
- foetal bleeding
- premature ductus closure if post 32 weeks
Antiemetics
Metoclopramide is safe and should be used as first line therapy. Ondansetron is reasonable second line (B1). Either
tropisetron (B3) or stemetil (C) is third line.
Antihistamines (Promethazine-cat C) have also been shown to be safe in recent meta-analyses of 20,000 women.
Note that abdominal pain is rare in hyperemesis gravidarum, and should prompt investigation.
Analgesics
Paracetamol is the initial analgesic of choice. Codeine and opiates are safe, but prolonged use, especially near term
should be avoided. NSAIDs and Digesic (Dextropropoxyphene) should be avoided if possible. Tramadol (C) has not
been studied.
Antibiotics
Cephalosporins and penicillins are considered safe in any trimester and should be used as first line where indicated.
Azathiaprine and Nitrofurantoin are also safe. Ciprofloxacin, tetracyclines, aminoglycosides, metronidazole,
sulphonamides, trimethoprim are all contraindicated.
Antireflux drugs
nd
Reflux is common in pregnancy 2 to LOS relaxation. Antacids are generally safe including Gaviscon. H2 blockers
are safe. PPI’s (B3) have caused foetal death in rats at high doses, but no malformations in humans, and should
rd
probably be considered 3 line.
Antimigrainous drugs
Generally migraine gets better in pregnancy. Treatment involves Paracetamol, codeine +/- other opioid, and
antiemetic. Pizotifen and B-Blockers may be used for prophylaxis. Chlorpromazine is category C. Ergotamine should
not be used as it causes uterine contraction.
Anticoagulants
Pregnancy is a risk factor for PE (doubles risk of DVT). USS should be used for Dx. Tc-99m venography (and V/Q)
are also safe. CT can be used with shielding. Iodine-125 fibrinogen scanning should not be used as it concentrates
in the foetal thyroid. Either unfractionated or LMWH heparin should be used for anticoagulation. Warfarin should not
be used as it causes a first trimester embryopathy, and CNS and ophthalmological abnormalities in the second and
third trimesters.
Thrombolytics
Risk: benefit should be assessed. Pregnancy is a minor contraindication to thrombolysis unless delivery is imminent.
(Unknown? <10 days). Case reports of no placental bleeding <12 hrs post administration.1995 review found no
increased risk of premature rupture, placental bleeding or premature labour with Strep, Urokinase or Alteplase. No
adverse foetal development noted. Aprotinin should be used for reversal if life threatening haemorrhage.
11
Benzodiazepines
No hard evidence that benzo’s cause any foetal developmental defects, including cleft palate. If taken recreationally
they are usually used in combination with other illicit drugs and at higher doses for a prolonged time. If used
perinatally cause hypotonia, resp. depression and hypothermia in newborn (Floppy infant). Withdrawal is a problem
in the neonate in 24-48 hrs, especially with shorter T1/2 drugs eg. Temazepam, which manifests as tremors,
irritability, hypertonicity, and D&V. n.b Benzo dependant mothers should not breastfeed.
Anticonvulsants
Frequency of seizures tends to slightly increase during pregnancy. Treatment of a pregnant patient with a seizure
does not differ from the non-pregnant patient, however Oxygenation should be optimized, and the patient should be
placed in the Left lateral position post-ictally. Carbamezepine, Na Valproate, and Phenytoin reduce the efficacy of
the OCP (require higher oestrogen dose). Once a patient has discovered she is pregnant, the highest risk of
teratogenicity has probably passed. If possible monotherapy at lowest dose should be used. Levels tend to fall in
pregnancy and if seizures a problem, increasing the dose may be required. All patients should have folate
supplementation prior to pregnancy if possible (high risk neural tube defects). The risk of an uncontrolled seizure is
generally a lot higher than the risk of malformations.
Corticosteroids
The use of corticosteroids in pregnancy to accelerate foetal lung maturation may dramatically increase insulin
resistance in diabetics. It may also be a risk factor for gestational diabetes and pre-eclampsia at high doses. Thus
BSL and BP should be closely monitored. All inhaled corticosteroids in asthma are safe. Oral corticosteroids for
asthma are safe in small doses, and the patient should also be on inhaled corticosteroids to minimise oral dose. Less
than 10% of active Prednisolone reaches the foetus as it is metabolised by the placenta, and thus it is the oral
steroid of choice in pregnancy. Betamethasone crosses the placenta more readily. There is no evidence for
suppression of foetal hypothalamic/pituitary/adrenal axis. Steroids should not be withheld in pregnancy if asthma is
severe.
Bronchodilators
Inhaled B2 agonists are safe in pregnancy. Although B2 agonists are proven tocolytics when given intravenously,
there is no evidence that they provide tocolysis at inhaled doses. Inhaled anticholinergics are also safe, but they do
nd
cause a slight increase in foetal HR, and so should be 2 line therapy. There is insufficient evidence for LT
antagonists eg. Montelucast. Theophylline crosses the placenta, but does not cause malformations. Some studies
indicate a transient tachycardia in neonates, but this is refuted in other studies. Sodium cromoglycate is safe.
Antihistamines
Meta-analysis of 20,000 women showed that antihistamines are safe. If a systemic antihistamine is required,
Promethazine or chlorpheniramine may be used safely. Avoid high doses late in pregnancy if possible.
Anaesthetic agents
Local anaesthetics are all safe. For G.A.’s, Ketamine, thiopentone, and Nitrous oxide are safe. Propofol (C) should
be only used if necessary. All G.A.’s have the potential to cause CNS and respiratory depression, but clinically this
does not seem to occur. Suxamethonium is safe.
Antidotes
NAC, Digibind, Desferrioxamine, Naloxone, Flumazenil safe. Beware inducing withdrawal in foetus. Penicillamine
(lead poisoning)should not be used if possible due to risk of foetal cutis laxis.
12
ANALGESIA CHOICES \ PROBLEMS IN PREGNANCY
Acute pain during pregnancy
Analgesic drugs almost always cross the placenta
- Most drugs are safe
- Particular times of concern
 Organogenesis weeks 4-10
 Just before delivery
- Non-pharmacologic options considered first where possible
- Ongoing analgesic requirements by liaising with obstetrician and GP
Drugs used in pregnancy
- Categorized according to foetal risk by ADEC
 A, B1, B2, B3, C, D, X
 For B1-3 human data are lacking or inadequate and subcategorisation is based on animal
data
 B doesn’t imply greater safety then C
 D drugs are not contraindicated in pregnancy (some cases are categorised on the basis of
“suspicion”)
- Paracetamol
 Analgesic of choice, safe
- NSAIDS
 Relatively safe in early and mid pregnancy
 Caution in the last trimester and avoided after the 32/40 (interfere with foetal brain
development and production of amniotic fluid)

Late in pregnancy may cause premature closure of ductus arteriosus, delayed labour and
birth
 Use during pregnancy is associated with increased risk of miscarriage and foetal pulmonary
HT
- Aspirin
 Should be avoided in the last trimester
 Late in pregnancy may cause premature closure of ductus arteriosus, delayed labour and
birth
 Increases the bleeding time in the mother and infant (except in low-dose – 100mg/kg)
- Opioids
 Overall the use appears to be safe
 Most of the experience relating to effects on neonates comes from opioid abuse
 Neonatal abstinence syndrome occurs in 30-90% infants exposed to heroin or methadone
but not with buprenorphine
 May cause respiratory depression in the newborn infant
- LA
 Lignocaine, bupivacaine, prilocaine are safe
 Ropivacaine and procaine human data is lacking
- Antidepressants – SSRI’s, TCA’s
 Limited use in pregnancy without a reported increase in birth defects
rd
 Use in the 3 trimester may result in withdrawal in the newborn
- Anticonvulsants
o Carbamazepine
 Use is associated with spina bifida, minor craniofacial defects, fingernail hypoplasia,
developmental disability, coagulation defects (risk of bleeding in the foetus; prophylactic
vitamin K prior to delivery)
o Phenytoin
• Same as above and less frequently oral clefts and cardiac anomalies
o Na valproate
st
 In the 1 trimester risk of neural tube defects
o Clonazepam
 Hypotonia, respiratory depression and hypothermia in the newborn if used in high dose
during labour
13
PRE-ECLAMPSIA AND ECLAMPSIA
14% incidence in primips; 5.5% incidence in multips
Occurs after 23 weeks gestation
Raised BP early in pregnancy usually represents chronic hypertension
- 20% of women with chronic hypertension develop pre-eclampsia during pregnancy
Fetal complications :
intrauterine growth retardation (head-sparing) + oligohydramnios; placental
infarction and necrosis; placental abruption; premature labour; fetal death
Maternal complications :
Seizures
Intra-cerebral haemorrhage
Pulmonary oedema
Renal failure
Thrombocytopaenia and haemoconcentration
DIC
Hepatic oedema with subcapsular infarction
HELLP – HTN + Elevated liver enzymes + Low platelets
Hypertension can persist for up to three months post-partum
Presentation :
High blood pressure – diastolic > 110mmHg >>> urgent delivery
Headache
Scotomas and scintillations
Oedema – sudden weight gain; hands and face more than feet
Epigastric pain – hepatic swelling
Seizure differentiates eclampsia from pre-eclampsia
ED Investigation :
FBE; UEC; LFTS; Coag profile; Uric acid – sensitive but non-specific
ECG if pre-existing HTN
Consider – CXR; CT head
Urine dipstick - > 1+ protein
Fetal well-being : biophysical profile
Treatment :
Anti-hypertensives commenced if systolic > 160mmHg or diastolic >100mmHg
Beta-blockers eg labetalol; alpha-blockers eg methyldopa
If systolic >170mmHg or diastolic >110mmHg then urgent lowering of BP
IV – labetalol; hydralazine; nitroprusside
Severe pre-eclampsia / Eclampsia
IV Magnesium preferred ; 4-6g IV load then 2-3g/hr
Phenytoin second alternative
Other therapies - low-dose acetylsalicylic acid (ASA), supplemental calcium, salt restriction, supplemental
magnesium, and fish oil therapy. None have demonstrated any significant preventive benefit.
One recent trial demonstrated some preventive benefit to supplemental antioxidants (vitamins C and E), but
results remain to be confirmed
14
HELLP SYNDROME
-Form of PIH that develops in 5% to 10% of females who have preeclamptic symptoms.
-0.3% of all pregnancies (U.S data)
-Considered a complication of Preeclampsia/Eclampsia
3
-Characterised by haemolysis, elevated liver enzymes, and low platelets (fewer than 100,000/mm ).
-Aetiology unclear; probable vasospasm is basis progressing to endothelial injury and leaky vessels;
ultimately local tissue hypoxia, necrosis, haemorrhage and end organ damage.
Usually second trimester and in older pregnant women
Multiparous > primiparous (c.f. pre-eclampsia and eclampsia)
Liver disease is hallmark
Severity directly related to Platelet count
Class 1: <50,000
Class 2: 50-100,000
Class 3: >100,000
-Perinatal and maternal mortality is greater with HELLP syndrome and greatest in Class 1.
Presentation:
Nausea, vomiting
Severe epigastric or RUQ pain – the chief complaint.
Visual disturbance
Most are Hypertensive but may be normal initially.
Examination:
-signs of cardiac and non-cardiogenic pulmonary oedema
-Pulmonary embolus
-Myocardial ischaemia
-Mental state changes
-hypertensive encephalopathy
-Cerebral oedema
-seizures
-blindness
Renal: haematuria, ARF
GIT: Jaundice, Ascites
Signs of thrombocytopenia
Investigations
FBC: haemolytic anaemia schistocytes
Plts: <100,000 but suspicious if <150,000
LFTs: ALT elevated but <500 IU/L, LDH and Bilirubin raised (haemolysis)
Renal fx: Normal or elevated Urea, Creatinine
Coagulation: Abnormal (DIC)
Urine analysis: haematuria, urobilinogen.
Imaging: CXR
CT head: cerebral oedema, haemorrhage
USS: foetal viability, gestational age, placenta position, amniotic fluid quantity.
Differential Diagnosis
-GIT: cholecystitis, biliary colic, hepatitis, pancreatitis, GORD,
-Haem: ITP, HUS, TTP, Gestational Thrombocytopenia
-Neuro: epilepsy, meningitis, encephalitis, encephalopathy, tumour, haemorrhage
-Other: Drug abuse, UTI, sepsis
Management
-As for Pre-eclampsia/Eclampsia (see other List)
-control BP, control seizures, urgent delivery
-Platelet transfusion recommended if <20,000 as high risk of PPH and to >50,000 if emergency LSCS
15
PLACENTAL ABRUPTION
= premature separation of placenta from uterine wall (1% of pregnancies)
Clinical
- sudden onset pv bleeding
- tender uterus
- ↑ resting uterine tone
- hypertonic/hyperactive uterine contractions
- spontaneous or secondary to trauma
risk factors for spontaneous placental abruption
- hypertension
- maternal trauma
- ↑ maternal age
- multiparity
- smoking / cocaine
- previous abruptions
classification
- complete
- partial
- concealed (no pv bleeding)
complications
- foetal distress
- foetal distress (separation of >50% placental area)
- hypotension
- dic (coags abnormal in 50%)
- foetomaternal transfusion
- amniotic fluid embolism
investigation
- uss unreliable!!! - have high index of suspicion if story and findings consistent
treatment
- rest
- correct hypertension and coagulopathy
- anti-d if required
- monitor foetal progress
- consider early delivery if diagnosis confirmed and >23/40 with foetal distress
PREMATURE RUPTURE OF MEMBRANES
Definition
Rupture of membranes before the onset of labour – irrespective of gestation
Causes
Amnionitis, trauma, polyhydramnios, multiple pregnancy
Risks
Infection - chorioamnionitis
Prem labour if < 37 weeks gestation
Cord prolapse or abnormal fetal presentation esp if head not engaged
Diagnosis
Speculum examination – pooling of fluid in vagina
Amniotic fluid is basic and will turn nitrazine paper blue
Will also see ferning pattern if plated on slide
Management in the ED
Obstetric review
If < 34 weeks
Betamethasone 11.4mg IM and repeat in 24
Ampicillin 1g QID
Further investigation
FBC CRP / HVS ? GpB Strep / CTG / Ultrasound
Obstetric management
80-90% will progress into labour – not a problem provided they are > 37 weeks
Those less than 34 weeks get steroids, prophylactic antibiotics, and delivery at 37 weeks (variable
depending on institution)
Those that are >37 weeks and don’t go into labour get augmentation with a syntocinon infusion
16
PREMATURE LABOUR
Definition - Onset of labour (regular contractions that results in cervical effacement and dilatation)
before 37 weeks gestation
Causes
Idiopathic
Prem rupture of membranes
Antepartum haemorrhage/trauma
Infection anywhere but esp chorioamnionitis
Polyhydramnios
Multiple pregnancies
Use of stimulants – amphetamines/cocaine
Hypertensive disease of pregnancy
Risks
Perinatal death and morbidity, which increases in a non-linear fashion with increasing prematurity.
Gestational age <22 weeks = 5% survival, >30 weeks = 80% survival
Treatment - In conjunction with obstetric unit
Less than 34 weeks and no fetal distress or infection – tocolytics and obstetric admission
Less than 34 weeks also require steroids – betamethasone 11.4mg IM and repeat in 24hrs
Less than 37 weeks – contentious re tocolysis vs delivery
Greater than 37 weeks is not premature labour - transfer to obstetric unit for delivery (if
obstetric unit not onsite and patient >5cm dilated do not transport long distances –can
deliver in ED and summon appropriate help to you – obstetric and paediatric/neonatal)
Tocolytics
Nifedipine 20mg orally and repeat X3 in first hour
Salbutamol 2-5mcg/
Magnesium sulphate 2mg and repeat up to 6mg
Indomethacin 100 PR
GTN infusion
All have been used and each has pros and cons. None completely effective!
Preferred agent depends on experience and preference
Indications for tocolysis → discuss with obstetric unit
Temporary use for transport to appropriate facility if in labour (term or preterm)
Premature labour
Contraindications = foetal distress or chorioamnionitis → requires urgent delivery
17
ISOIMMUNISATION
Defn: development of antibodies against an antigen derived from a genetically dissimilar individual of the
same species.
Most serious is Rh., then Kell, Duffy etc least of all ABO.
Rhesus blood group, most complex, antigens grouped in 3 pairs, Cc, Dd, Ee.
45% Rh+ve homozygous for D, 55% Rh+ve heterozygous.
Incidence: of Rh-ve, 15%of Caucasians, 30% Basques, 4% African blacks.
Mechanisms: -Foetomaternal haemorrhage – most common. Risk of Isoimmunisation, related to the volume
of trans placental h/hage, as little as 0.5ml of Rh+ve cells, and ABO compatibility ie.,15% (1.5-2%
nd
antepartum, 7% post partum, 7% early 2 Pregnancy) in ABO compatible infant, 1.5 -2% in ABO
incompatible.
-Incompatible blood transfusion. 30% will not become sensitised.
st
nd
rd
For no apparent reason foetal RBC are detected in maternal blood in, 6.7% 1 trimester, 15.9 2 , 28.9% 3 .
Sensitising Events:- Delivery accounts for 90%, Amniocentesis 10%, Abortion 4%,
Miscarriage 2%,
Abdo trauma, Abruptio placentae, Placenta praevia, Foetal death, Multiple pregnancy, Caesarian section,
Manual removal of placenta, given blood products containing Rh+ve RBCs eg platelets.
Post sensitisation it takes 6 weeks to 6 months for IgG to cross placentae and it takes 1 month for Rh IgG
A/bodies in maternal circulation to equilibrate in foetal circulation.
Effects on foetus:- Lysis of foetal RBCs, => Bilirubin (neurotoxic), stimulation extramedullary erythropoietic
sites, high reticulocyte count, Ht. failure, Oedema, Ascites, Pericardial effusion.
Anti-D:- derived from a limited No. of sensitised individuals who donate every 2 weeks.
st
Usual doses: 1 Trimester 250IU subsequently 1ml (625IU = 125ug) given IMI.
Indications:- Rh-ve woman with no anti-D antibodies following a sensitising event, some effect if
given upto 9 days after. Unless father is known to be Rh-ve !!!
If given w/in 72hrs of full term delivery (once baby blood gp known) reduces IsoI from 12% to 2%, if given at
28wks and delivery <0.1%.
Kleihauer Test is an acid elution technique that differentially stains foetal vs maternal cells. Used in
sensitising event later in pregnancy to determine dose of Anti-D. 100 IU Anti-D per 1ml of Rh+ve RBCs. If
mothers serum has Anti-D present 36 hours after injection the dose has been adequate.
ABO Haemolytic Disease:- milder than IsoI by Rh and other Antigens. 25% of pregnancies have potential,
<10% of those have problems, usually A or B infants of O mothers. 40% in the first born, usually jaundice in
first 24hrs, requiring phototherapy in 10% hepatosplenomegaly, exchange t/fusion in 1%.
18
CARDIOTOCOGRAPHY
Introduction:- A Cardiotocograph (CTG) is a record of the fetal heart rate (FHR) either measured from a transducer
on the abdomen or a probe on the fetal scalp. In addition to the fetal heart rate another transducer measures the
uterine contractions over the fundus
Literature review
•
The non-stress CTG is an evaluation tool used in antenatal care for both screening and diagnosis
•
Antenatal CTG is commonly used in conjunction with ultrasound imaging and Doppler measurements in high
risk pregnancy
•
Antenatal fetal heart recordings only provide assessment of the immediate fetal condition
•
The use of antenatal CTGs has not been found to affect the rates of induction of labour or elective
caesarean section
•
It is reported that the use of antenatal CTGs reduces hospital admissions and duration of inpatient stay
(Pattison and McCowan 2006)
•
Antenatal CTG is of no value as a screening test in an apparently normal obstetric population (Trimbos and
Keirse 1978)
•
Current evidence suggests that antenatal cardiotocography has no beneficial effect on rates of perinatal
mortality or morbidity (Pattison and McCowan 2006)
•
10 % of CTGs may be uninterpretable due to:
o
Gestational age
o
Normal rest phases (may be up to 90 minutes)
o
The use of certain medications (e.g. CNS sedatives such as methadone, pethidine) (Mohide and
Keirse 1989; Pattison and McCowan 2006)
The CTG :
The CTG trace generally shows two lines. The upper line is a record of the fetal heart rate in beats per minute. The
lower line is a recording of uterine contractions from the toco. The vertical scale of this trace depends on how the
transducer is picking up the contractions so interpretation needs to be in relation to the rest of the trace. The trace
may also have markings on it that are indications that the mother has felt a fetal movement (operated by a switch
given to the mother). When recording often indicate
Baseline Rate:- This should be between 110 and 150 beats per minute (BPM) and is indicated by the FHR when
stable (with accelerations and decelerations absent). It should be taken over a period of 5 - 10 minutes. The rate
may change over a period of time but normally remains fairly constant.
Bradycardia:- This is defined as a baseline heart rate of less than 110 bpm. If between 110 and 100 it is suspicious
whereas below 100 it is pathological. A steep sustained decrease in rate is indicative of fetal distress and if the
cause cannot be reversed the fetus should be delivered.
Tachycardia:- A suspicious tachycardia is defined as being between 150 and 170 whereas a pathological pattern is
above 170. Tachycardias can be indicative of fever or fetal infection and occasionally fetal distress (with other
abnormalities). An epidural may also induce a tachycardia in the fetus.
Baseline variations:- The short term variations in the baseline should be between 10 and 15 bpm (except during
intervals of fetal sleep which should be no longer than 60 minutes). Prolonged reduced variability along with other
abnormalities may be indicative of fetal distress.
Accelerations:- This is defined as a transient increase in heart rate of greater than 15 bpm for at least 15 seconds.
Two accelerations in 20 minutes is considered a reactive trace. Accelerations are a good sign as they show fetal
responsiveness and the integrity of the mechanisms controlling the heart.
Decelerations:- These may either be normal or pathological. Early decelerations occur at the same time as uterine
contractions and are usually due to fetal head compression and therefore occur in first and second stage labour with
decent of the head. They are normally perfectly benign. Late decelerations persist after the contraction has finished
19
and suggest fetal distress. Variable decelerations vary in timings and shape with respect to each other and may be
indicative of hypoxia or cord compression.
Interpretation of EFM
Categorisation of fetal heart rate traces
Category
Normal
Suspicious
Pathological
Definition
A CTG where all four features fall into the reassuring category.
A CTG whose features fall into one of the non-reassuring categories and the remainder of the
features are reassuring.
A CTG whose features fall into two or more non-reassuring categories or one or more abnormal
categories.
Categorisation of fetal heart rate (FHR) features
Feature
Baseline (bpm)
Reassuring
110-160
Non-reassuring 100-109
Variability
(bpm)
= >5
Decelerations
Accelerations
None
Present
< 5 for >40 to
<90 minutes
Early deceleration
The absence of accelerations with
an otherwise normal CTG are of
uncertain significance
161-180
Abnormal
<100
>180
Sinusoidal
pattern >= 10
minutes
Variable deceleration
Single prolonged
deceleration up to 3
minutes
<5 for>= 90
minutes
Atypical variable
decelerations
Late decelerations
Single prolonged
deceleration >3 minutes
In cases where the CTG falls into the suspicious category, conservative measures should be used.
In cases where the CTG falls into the pathological category, conservative measures should be used and fetal blood
sampling be undertaken where appropriate/feasible. In situations where fetal blood sampling is not possible or
appropriate then delivery should be expedited. If foetal blood sample pH < 7.20 then delivery indicated.
Indications
Continuous CTG monitoring is recommended whenever there is evidence of fetal compromise
Abdominal trauma (minimum of 4 hrs in minor cases, minimum 24 hrs in major trauma)
Further recommendations are:
There are a number of antenatal and intrapartum risk factors that have been shown to be associated with the
development of neonatal encephalopathy, cerebral palsy or even perinatal death.
B
Continuous EFM should be offered and recommended for high-risk pregnancies where there is an increased
risk of perinatal death, cerebral palsy or neonatal encephalopathy.
C
Continuous EFM should be used where oxytocin is being used for induction or augmentation of labour.
Appropriate monitoring in an uncomplicated pregnancy
A
For a woman who is healthy and has had an otherwise uncomplicated pregnancy, intermittent auscultation
should be offered and recommended in labour to monitor fetal wellbeing. If decelerations develop then should
have continuous CTG.
B
Current evidence does not support the use of the admission cardiotocography (CTG) in low-risk pregnancy and
it is therefore not recommended.
DYSTOCIA
20
Definition
Cause
Dystocia is defined as ‘Difficult labour’
a) Power
Inadequate uterine contractions
b) Pelvis
Abnormal pelvic anatomy
c) Passenger
Macrosomia, malposition, fetal anomalies
Dystocia cannot be accurately diagnosed until active labour has commenced
Dystocia is further defined, in women in active labour as
a) Protraction of labour
Slow rate of dilatation or descent
Reduced by sedation, anaesthesia, malposition
b) Arrest of labour
Complete cessation of progress
2 hours of active labour without dilatation
1 hour of active labour without descent
Risk
No one factor accurately predicts dystocia
Increased in nulliparous women / increased birth weight, infection, gestational age
/ malpresentation and pelvic disproportion
Diabetes / Excessive weight gain in pregnancy / History of large babies
Increased risk with epidural anaesthesia
Restricted ambulation in labour (size, anaesthesia) both increase risk
Prediction
Predicting dystocia is difficult but enhanced by
a) Use of partograph (labour curve)
b) Frequent vaginal examinations
c) Maintaining continuity of examiner
Specific ED problems - Shoulder dystocia / Cord prolapse /Breech presentation
CORD PROLAPSE
Incidence
Mortality
Nature
0.2% of pregnancies
Perinatal mortality 15-20%
Protrusion of cord from birth canal
Occult (beside presenting part)
Overt (Below presenting part)
Risks
Malpresentation
Breech increased risk x 10
High lie and membrane rupture (not engaged)
Multiple gestation
Foetal malformation
Premature labour and rapid progression of labour
AROM (especially with high head)
Polyhydramnios / Intrauterine manipulation / Placenta praevia
Management (PPPP)
Position patient
Deep Trendelenberg
Knees on chest
Palpate presenting part, push posteriorly
Vaginal examination
Feel pulsation of cord
Confirm cord present and presenting part
Replace presenting part and keep in uterus
Try not to handle cord too much as will increase spasm and reduce foetal circulation
Maintain hand in vagina with presenting part distraction and transport to theatre
Peritoneal pressure
Bladder (IDC and fill)
Fill with 500-700ml
Assists in manual decompression
Prevent contraction
Tocolysis will reduce contractions and reduce risk of uterine rupture
21
SHOULDER DYSTOCIA
Definition
Impaction of the anterior presenting shoulder against the pubic symphysis after the foetal
head has been delivered
Associated with bisacromial diameter (breadth of shoulders) is greater than the diameter of
the pelvic inlet
Incidence
<2% of vaginal deliveries
True obstetric emergency
0.3-1% in birth weights 2500 to 4000grams
5-7% with birth weight >4000grams
Risks:
Not predictable in most cases
Prior shoulder dystocia
Gestational diabetes (lower risk if insulin requiring diabetic)
Post dates pregnancy
Macrosomia
Short stature
Abnormal pelvic anatomy
Signs:
Warning signs of
Protracted active phase of labour
Prolonged second stage with ‘head bobbing’ in and out of pelvis
Failed forceps and vacuum delivery
Morbidity
Maternal
Soft tissue injuries most common maternal complication
rd
th
Increased rates of 3 and 4 degree tears
Increased risk of recto-vaginal fistula
Increased risk of PPH and uterine atony
Rarely associated with uterine rupture
Symphysial separation with McRoberts manoeuvre
Foetal
Foetal hypoxia (cord compression)
Once head is delivered it must be assumed that the cord is compressed
Foetal scalp pH drops by 0.4 pH per minute
Takes 7 minutes to fall from 7.25 to danger level 6.97
Increasingly difficult to resuscitate with persistence of foetal circulation
Prolonged hypoxia associated with neurological deficits
Foetal chest compression (inhibition of respiration)
Brachial plexus palsies (7-20%)
Most recover in 12 months 1% permanent disability
Erb palsy commonest C5-6 palsy
Klumpke palsy rare C8-T1
May not be delivery but lie of foetus in utero
Clavicular fracture
May damage underlying lung and vasculature
Humeral fractures
Usually heal without complication
Management
Anticipation
a) Patient and family
Patient education as to expected manoeuvres, procedures and implications
Empty patient bladder (self-void and IDC decompression)
b) Staff and department
Organising key personnel
Institutional plan (who to call and when)
OG registrar, Paeds registrar, team leader midwife
Theatre staff and anaesthetist
Clear roles and responsibilities
22
Patient assessment
Turtle sign (head retraction after contraction)
Head delivery without anterior shoulder
Arrest of labour
Procedural manoeuvres
Use HELPERR mnemonic to remember the list of procedures and order in which to attempt
Each procedure moves slickly onto the next and a maximum of 30-60 seconds is allowed for
each manoeuvre
Help
Episiotomy
Legs (McRoberts) (continue position for each manoeuvre)
Pressure (Additive to success if applied with each manoeuvre)
Enter for internal manoeuvres
Rubin
Woods screw
Remove posterior arm
Roll patient
Last resort manoeuvres
Deliberate clavicle fracture
Zavanelli
Symphysiotomy
Caesarean section and abdominal screw
HELPERR
H
Call for Help
Pre-planned personnel (OG, anaesthetist, midwife, paediatrician)
Equipment available for paediatric resuscitation
Equipment available form maternal procedures
Theatre prepared for operation
E
Episiotomy
Either midline or lateral (Usually midline)
Consideration to early performance
Impaction is usually bony, but release prior to head pushing into vaginal vault will
allow hand to be inserted easily into vagina for internal manoeuvres
Early episiotomy reduces maternal tear complications
L
Legs (The McRoberts manoeuvre)(Relieves 40% SD)
Simple and easy to perform with good success
Hip flexion with thighs onto abdomen
Simulates the squatting position
Aims to
Increase the pelvic diameter
Flatten the lumbosacral lordosis
Allow vertical contraction aimed through pelvic vault
Posterior foetal shoulder in sacral hollow for anterior shoulder disimpaction
Attempt delivery with head traction for 30-60 seconds
P
Pressure (Suprapubic)
(for 30-60 seconds) (In McRoberts position)
External manual Suprapubic pressure
Associated with traction and McRoberts will reduce further 50% of SD
Hand placed over the foetus anterior shoulder
Directed effort of push dependent on clinicians direction of head traction
Initially pressure continuous but if this fails use a gentle rocking motion
NEVER apply fundal pressure (increased maternal and foetal injury)
E
Enter for internal manoeuvres
Procedures to rotate anterior shoulder to oblique plain and under maternal symphysis
Again each procedure can be applied fro a maximum of 30-60 seconds then move directly
on to next procedure
a) Rubin procedure
23
1) Place fingers vaginally behind anterior shoulder and push towards foetal chest
to collapse/adduct shoulder
2) Simultaneously apply suprapubic pressure (assistant) to rock the shoulder from
the side and assist in dislodging impaction
b) Woods screw manoeuvre
Combined anterior and posterior shoulder movement
Needs large episiotomy!!
1) Maintain fingers pushing forwards on anterior shoulder from behind
2) Place other hand internally to push backwards on posterior shoulder form in
front
3) Combination of pressures forces screw-like motion and extraction of foetus
c) Reverse Woods screw
If Woods fails after 60 seconds then try the opposite direction
Replace fingers to apply pressure form opposite direction to try to disimpact
R
Remove the posterior arm
Attempt to clear the posterior shoulder to facilitate delivery of the anterior shoulder
Insert hand high into the vagina and locate posterior arm
Sweep across the anterior chest and remove hand first
Never attempt to remove the anterior arm as this will definitely result in humeral # and
brachial plexus injury
R
Roll the patient
Roll form existing position into an ‘all-fours’ position
Gaskin position
Alters pelvic diameter when changing position
Sometimes causes the anterior shoulder to disimpact
Gravity assists in traction of the foetal head and anterior shoulder
Last resort
1) Clavicular fracture
Break with direct upward pressure in mid-clavicle
2) Zavanelli
Cephalic replacement followed by LSCS
Turn head to OA position and flex neck and push backwards
Maintain hand in vagina with persistent upward pressure on the way to theatre
Requires tocolysis as adjunct
MUST have theatre ready and standing by
3) Symphysiotomy
Direct cut to the fibrous symphysis
Takes 2 minutes
Must be thought about early in complications
Abdominal Woods screw
Take to theatre
Open uterus
Twist baby out for vaginal birth through abdominal wound and direct pressure (bit more invasive than
suprapubic pressure)
24
POST PARTUM HAEMORRHAGE
PRIMARY
Within 24 hours post delivery
Bleeding from birth canal >500ml
Incidence 5%
Causes uterine atony 50%
Trauma uterine ,cervical, vaginal, vulval.(episiotomy) 20%
Retained products(placental accreta)
Coag defect DIC(eclampsia, amniotic fluid embolism, placental abruption)
Multiple pregnancy
Polyhydramnios
Prolonged labour
Management
Anticipate patients at risk
Resus ABC ,fbc,coag,crossmatch
Oxytocic agent-syntocinon 10u
Remove placenta, clots manually
Massage uterine fundus
If local bleed –direct pressure/suture
Uterine packing temporary measure
Correct coags
Foley catheter 24,80ml.
Exploration in OR/hysterectomy
Pelvic vessel embolisation
External abdominal aortic compression
Temporary measure
Fist patients abdomen just above the umbilicus
Successful in 50%
Secondary PPH
After 24hrs
Cause-retained products
Infection
Clinically –bleed,pain,offensive discharge,fever ,rigors,sepsis.
Management-RESUS ABC
Fluids analgesia
Triple antibiotics
DandC
Retained Placenta
-Cause of PPH 10%
-Iatrogenic inappropriate traction on the placenta in stage 3 labour.
-abnormal placenta-accreta(placenta adheres without the intervening deciduas basalis)
-percreta(villi extend in to the myometrium)
-increta(villi extend full thickness through the myometrium)
-risk factors multigravida,prior caesarean section, placenta previa, uterine infections,d&c
25
PELVIC INFLAMMATORY DISEASE
Every female who is sexually active with abdominal pain is pregnant until proven
otherwise, and whether pregnant or not, can have PID
Sequelae include infertility (most common cause, especially Chlamydia), chronic pelvic
pain (in up to 18% of patients), ectopic pregnancies from scarring (12-15%
increased risk following PID)
History
Abdominal pain most common, but also abnormal PV bleed or discharge, dysuria or dyspareunia
Increased risk if – early age or first sexual intercourse, multiple partners, high frequency
of sexual intercourse and recent instrumentation of the cervix (TOP, insertion of IUD in last 20 days).
Also more likely during menses or shortly after
Need to take good history of sexual contacts (overseas, esp. SE Asia have high incidence of penicillin
resistance in Gonococcus)
Examination
Fever (high, moderate or may be non-existent)
Adnexal tenderness (95% sensitive for PID)/cervical excitation
A finding of RUQ tenderness in someone with associated PID is consistent with a condition called
Fitz-Hugh-Curtis syndrome where there is tracking of inflammatory fluid into the abdomen
Can present with peritonitis
Investigation
Pregnancy test
CRP/WBC/ESR – non-specific markers which will often (usually) be raised, but sometimes not in atypical
or mild cases (which still need treatment)
Urinalysis (pyelonephritis/UTI can present with similar pain)
First pass urine for PCR (Chlamydia and Gonococcus)
Cervical swabs for Chlamydia trachomatis and gonococcus should always be taken (Endocervical swab
(brush) for culture – note needs charcoal for gonococcus, and special media for Chlamydia)
Ultrasound to look for tubo-ovarian abscesses or other causes for pain. Newer techniques
becoming sensitive and specific for diagnosis
Laparoscopy is used if diagnosis in doubt, but do not wait for this test
Treatment
Early aggressive broad-spectrum treatment important in avoiding sequelae
If suspicious for PID then take swabs and start treatment
Need to cover Gonococcus, Chlamydia and anaerobes
Mild / Moderate disease
Non-sexually acquired (e.g. instrumentation)
Augmentin Duo Forte 1 tab bd for 7-10 days plus Doxycycline 100mg bd for 7-10 days (unless
pregnant in which case substitute Roxithromycin 300mg daily for 14 days)
Sexually acquired
Azithromycin 1g po stat or Doxycycline 100mg bd for 14 days
plus Metronidazole 400mg bd for 14 days plus Ceftriaxone 250mg IV/IM
Severe disease
Ceftriaxone 1g IV daily or Cefotaxime 1g IV tds plus Metronidazole 500mg IV bd plus
Doxycycline 100mg bd or Azithromycin 1g stat. When improved, then above regimen
Contact tracing important if Chlamydia or Gonococcus confirmed with treatment of at risk contacts (and
their at risk contacts, etc.)
Referral to G.P. for followup in next 1-2 days, or referral to Family Planning Association (FPWA) or other
sexual health clinic for appropriate followup (including Pap smears etc. when infection treatment
concluded). These services can also do the contact tracing very effectively.
Proof of cure testing – at 3 weeks for proof of cure (use condoms in mean time or abstinence)
Notifiable diseases – both Chlamydia and gonorrhoea are notifiable diseases
26
SEXUALLY TRANSMITTED INFECTIONS
Introduction:
Sexually transmitted infections (STIs) remain endemic in Australia and have significant individual and public
health consequences. For instance, infection with C. trachomatis was the third most common notifiable
disease in Australia in 2000.
Most STIs are asymptomatic or produce mild symptoms that do not bring affected people to medical
attention. These are detected only through screening and contact tracing. Patients with suspected or
diagnosed STI should be screened for other STIs. Their partners and sexual contacts should be screened
and treated empirically.
Chlamydia
-often asymptomatic especially in women
-may cause cervicitis, endometritis and pelvic inflammatory disease in women and lead to infertility and
ectopic pregnancy.
-urethritis, epididymo-orchitis and prostatitis in men
Laboratory diagnosis
-DNA probe assays and other rapid antigen assays are now the "gold standard"
-Samples collected from the cervix and vagina, self-sampling with self-inserted swabs, tampons or first-void
urine.
-results take < 24 hours, with most tests being "batched" and performed several times a week.
Management
-azithromycin as a single oral dose has equivalent efficacy to a seven-day course of twice-daily oral
doxycycline. Both achieve cure rates >95%. Use azithromycin if compliance is likely to be suboptimal.
-Azithromycin is also effective for non-specific urethritis (ie, cases with negative
results for chlamydia and gonococcus).
- azithromycin is categorised as B1 in pregnancy (can be used safely during pregnancy and
breastfeeding).
-chlamydia related epididymitis or pelvic inflammatory disease (PID) requires longer therapy
-PID requires treatment with broad-spectrum antimicrobials (ampicillin, metronidazole and gentamicin), as
the infection usually involves mixed endogenous vaginal flora, particularly if postpartum or after
gynaecological instrumentation, miscarriage, termination of pregnancy or insertion of an IUCD. If PID is
sexually acquired, an antibiotic to cover Neisseria gonorrhoeae is also required. Untreated PID leads to
chronic pelvic pain, infertility and ectopic pregnancy.
Gonorrhoea
Gonorrhoea presents similarly to chlamydia, although symptomatic disease is more common, especially in
men. Three groups are affected: men who have sex with men, Indigenous Australians in remote settings,
and people with heterosexual contact overseas.
Laboratory diagnosis
-Culture of Neisseria gonorrhoeae from a urethral or endocervical swab remains the standard diagnostic
method
-nucleic acid amplification of urine, cervical and vaginal specimens has an important role in diagnosis where
prevalence is high.
- PCR assay for both C. trachomatis and N. gonorrhoeae as a single test.
- positive results for N. gonorrhoeae should be confirmed by culture and antibiotic susceptibility is
determined.
Trichomonas vaginalis
-most common treatable STI in the world.
-women living in remote areas of Australia: prevalence as high as 25%
-associated with premature rupture of membranes and premature labour.
Human papillomavirus infection
-very common, although the vast majority are asymptomatic.
-most frequently HPV 16, followed by 6 and 11
-the most frequent manifestation of HPV infection is genital warts
-"oncogenic" strains (HPV16 and 18) is a risk factor for cervical cancer
Diagnosis and management
-Diagnosis of external genital warts is clinical. Pap smear remains the cornerstone of screening for cervical
precancerous lesions.
- out-patient therapy cryotherapy, cautery/laser ablation, podophyllin solution (25%) or trichloroacetic acid.
-topical imiquimod is an immune-response modifier that reduces relapse
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-Condoms reduce the risk of HPV transmission.
Herpes simplex
-Genital herpes usually due to HSV-2 rarely HSV-2
-recurrent in 20%
-15% of women attending antenatal clinics
-55% of those attending STI clinics
-Genital herpes caused by HSV-1 is transmitted by oro-genital sex
-HSV transmission may occur in the absence of genital lesions (asymptomatic carrier)
Laboratory diagnosis
-Viral culture and direct immunofluorescence are the definitive tests for HSV diagnosis
-HSV PCR is highly sensitive and specific
-HSV antibody testing is used to determine whether sexual contact is already infected with HSV-2:
precautions against transmission are then unnecessary
-Pap smears not recommended for women <18 years unless they have been sexually active for >two years.
Management
-Aciclovir, valaciclovir and famciclovir are all effective in primary and recurrent HSV
-Primary episodes should be treated regardless of duration of symptoms
-symptoms and duration of recurrence is reduced by two days if treatment begins within 72 hours of
symptom onset
-Suppressive therapy prevents 75% of attacks and reduces asymptomatic shedding.
For all STI’s, there are public health implications, with partner notification, disease surveillance, health
promotion and outbreak investigation being essential.
Treatment of sexually transmitted infections
Chlamydial and other non-gonococcal urethritis and cervicitis:
Azithromycin (1 g orally, as a single dose) or doxycycline (100 mg orally, 12-hourly for 7 days).
Gonorrhoea
Ceftriaxone (250 mg intramuscularly) or ciprofloxacin (500 mg orally, as a single dose) plus either
azithromycin (1 g orally, as a single dose) or doxycycline (100 mg orally, 12-hourly for 7 days).
Pelvic inflammatory disease (sexually acquired)
Mild-moderate: Doxycycline (100 mg orally, 12-hourly for 14 days) plus either metronidazole (400 mg orally,
12-hourly) or tinidazole (500 mg orally, daily for 14 days) plus either ceftriaxone (250 mg intramuscularly) or
ciprofloxacin (500 mg orally, as a single dose).If adherence to a 2-week course of doxycycline is likely to be
suboptimal, doxycycline may be replaced by azithromycin (1 g orally on Days 1 and 8)
Severe infection: Metronidazole (500 mg intravenously, 12-hourly) plus doxycycline (100 mg orally, 12hourly) plus either cefotaxime (1 g intravenously, 8-hourly) or ceftriaxone (1 g intravenously, daily).
Pelvic inflammatory disease (non-sexually acquired)
Mild to moderate: amoxycillin clavulanate (875/125 mg orally, 12-hourly for 7–10 days) plus doxycycline (100
mg orally, 12-hourly for 7–10 days).
If the patient is pregnant or breastfeeding substitute roxithromycin (300 mg orally, daily for 14 days) for
doxycycline.
Trichomoniasis
Tinidazole or metronidazole (2 g orally, as a single dose).
Candidiasis
Clotrimazole (2% vaginal cream for 3 nights or 500 mg pessary as a single dose)
Herpes simplex types 1 and 2
Initial infection: Famciclovir (125 mg) or valaciclovir (500 mg) (both orally, 12-hourly) for 5–10 days or
aciclovir (200 mg orally, 5 times daily, or 400 mg 8-hourly) for 5 days
Episodic therapy: Famciclovir (125 mg) or valaciclovir (500 mg) (both orally, 12-hourly) for 5–10 days or
aciclovir (400 mg orally, 3 times daily) for 5 days
Suppressive therapy: Famciclovir (250 mg orally, 12-hourly) or valaciclovir (500 mg orally daily [if < 10
recurrences per year] or aciclovir (200 mg orally 8-hourly or 400 mg orally 12-hourly) for up to 6 months.
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OVARIAN HYPERSTIMULATION SYNDROME
Sudden multiplication of follicles in response to GnRH used in assisted reproduction.
Commoner in conceptional cycles
Clinical
Diffuse lower abdominal pain
Cystic ovarian enlargement
Incidence
0.5-2% of women having ovarian hyperstimulation
Complications
Ascites
Reduced intravascular volume
Pulmonary effusions
ARDS
Pericardial effusions
Thromboembolic disease
Hyponatraemia
Renal failure / Liver failure
Grade
Severe
Hct >45% / WCC>15
Massive ascites
Oliguria
Mild liver/renal dysfunction
Critical
Hct>55% / WCC>25 / Tense ascites
Renal failure / ARDS /Thromboembolism
Investigations
FBC / U&E’s Cr / LFTs / coags / ABGs / CXR
USS - Ovarian size is a guide to severity
Management
General
Morphine IV
IDC -Measure urine output
Fluid resuscitation
Specific
Ascites
Paracentesis of ascites to improve renal function
Thromboembolism
Antiembolic stockings
Encourage leg mobility
s.c. heparin
ARDS/Pleural effusions
Ventilate
ICC
Distributive shock
Aim at 3L/24hr
Electrolyte imbalance
Correct hyponatraemia
Termination of pregnancy
Disposition
+
Admit /- ICU / OT
Severity of effusions determine time to recovery
Non-conception cycles generally end with menstruation
Conceptional cycles may persist for weeks and require TOP
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ENDOMETRIOSIS
Because periods aren’t bad enough !
Second most common cause of pelvic pain in women behind dysmenorrhoea, affects 11% .
70% sufferers are nulliparous.
60% of those investigated for infertility have it.
Affects age 20-45 more common in 30’s.
Initially cyclic then acyclic and continuous as adhesions develop.
Caused by seeding of endometrium outside uterine cavity.
Diagnosis – USS can be suggestive but laparoscopy is both diagnostic and therapeutic.
Also amenable to hormone manipulation .
OVARIAN CYSTS & ACCIDENTS
Introduction
Ovarian cyst = sac with liquid / semi-liquid material arising in female ovary that can occur at any age in
females. Increasingly common finding due to regular physical examination and ultrasound investigation. Vast
majority benign but important to rule out ectopic pregnancy and infections, ensure hemodynamic stability
and consider malignant disease.
Functional ovarian cysts Follicular ovarian cyst develops prior to ovulation
Corpus luteum cyst develops after ovulation
Never in post-menopausal females
Neoplastic ovarian cysts
Benign or malignant growth that may originate from all ovarian cell types /
tissues
Malignancy most common from mesothelium, benign counterparts are
mucinous & serous cystadenoma
Clinical Presentation
Majority of cysts are asymptomatic but is an important cause for acute pelvic pain and possible
complications including:
Intra-ovarian hemorrhage
Rupture
Torsion of adnexae
Ovarian infection secondary to Pid.
Can present with evidence of infection / sepsis, acute surgical abdomen +- haemodynamic instability. Caveat
! – abdo pain out of proportion to clinical findings = ? torsion / ischaemia
Differential Diagnosis & Causes of acute pelvic pain
Gynecological
Complication of pregnancy: ectopic, miscarriage
Complication of ovarian & adnexal cysts / masses
PID, Adnexal torsion, Leiomyoma complication
Intestinal
Appendicitis, Diverticulitis, IBD, Gastro-enteritis
Bowel obstruction, Constipation
Cystitis, Acute urinary retention, Urolithiasis,
Pyelonephritis
Hernia, Porphyria, Pelvic vein thrombophlebitis
Abdominal abscess, Psychogenic (dx of exclusion)
Urological
Other
ED evaluation
Standard process of ‘resus’ -- history – physical exam – investigations with particular focus on:
Resuscitation
History
Exam
Investigations
of the acutely unwell patient
abdo pain history, gynae history, psyche / social issues
vitals, abdominal & pelvic (chaperone)
urine analysis & B-hcg, swabs, bloods as indicated
Imaging: Uss = non invasive extension of physical exam
CT to delineate pelvic masses (malignancy / abscess), urinary
calculi, spigelian hernias, abdo tuberculosis, appendicitis
ED management
Patient care includes: ensuring adequate iv access, analgesia & hemodynamic stability, early anti-biotics for
infection, early consultation with Gynaecological / General surgical specialties
Disposition
Admit unwell patient needing surgery / iv therapy / further investigation
Home well patient with no evidence of acute \ serious illness with appropriate out patient f/up &
further investigation
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