1. No category

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GUIDELINES FOR WRITTEN PATIENT CASE REPORT
Write a case study of a patient of your choice. Include all of the topics below and relate the information in your own words with complete
sentences and paragraphs. Anything taken directly from the medical record or a reference text that is longer than five words needs quotation
marks and documentation. I expect you to paraphrase everything in your own words unless cited. The report need not be in the order below.
However, all topics should be covered; additional information that is relevant should be added where you feel it belongs. There is no length
requirement or limit, however the report should be Concise, i.e. enough to cover all relevant areas completely. Text should be 12pt single or
1.5 spacing, one sided.
1.
Summarize the patient’s presenting diagnosis and the development of any
2.
Summarize the patient’s history.
3.
Summarize the patient’s presenting signs and symptoms.
4.
Summarize pertinent laboratory data including chest x-ray, ABG’s with interpretation, other significant blood work, cultures,
spirometry, EKG’s, hemodynamics, etc. and any other data. INTERPRET all results.
5.
Describe YOUR examination of the patient.
6.
Summarize drug therapy the patient is receiving including indications and results. Include all respiratory meds & any other
meds pertinent to the case study. Non relevant meds need not be included.
S
N am
ot
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tu R
al ep
pa or
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nt
secondary diagnoses.
7.
Summarize respiratory therapeutic modalities the patient is receiving
results. Use generic names. Describe
how they work.
including indications, actions, and
8.
Provide an overview of every disease state the patient has. This should be concise & include the definition, how it is
diagnosed, how it is treated, & how it relates to the primary diagnosis & the current patient condition. [APA format]
9.
Provide an in depth Definition, etiology (cause), pathophysiology (physiological changes associated with), how to diagnose,
& treatment for the primary disease you chose to cover. Again, this should be related to your current case throughout your
discussion. [Must be in APA format]
10.
Patient Assessments: Minimum 3, no closer than 6hrs of each other, ideally each on separate days, but if more are included
multiple assessments from the same day are ok, this should only be done if there is some major change/procedure that would
indicate fully reassessing the patient on the same day.
Initial Assessment: should be fully inclusive. Similar to how the Physicians do assessments for their H&P’s (Refer to Wilkins
assessment text & assessment forms)
Follow-up Assessment: should portray the major elements of assessment, i.e. vitals, sats, breath sounds, WOB, SOB,
appearance, Current days or most current days labs, etc. other assessments should be noted if there has been a change in
them. Should be presented in SOAP format.
11.
Recommended Action in hospital based on your assessments & H&P, etiology, & pathophysiology. Be specific including
rationale; be sure to treat all previously documented abnormalities/ailments. Include medications, procedures, tests, therapies,
etc. as it relates to your case.
10.
Referances: follow APA guidelines found at http://owl.english.purdue.edu/owl/resource/560/01/
Especially in regards to electronic sources, i.e. internet.
Remember the pt chart as a reference as well. You should give me the exact info I need to find the information you
referenced, i.e. the exact web address for the page that has the info you used on it. Same goes for texts, include page numbers
& section headings if applicable.
Additional guidelines
a.
Tell a story. Start with a “thumbnail” of the patient so that Joe Schmoe, RRT. knows by the end of the first paragraph what
your report is about. After that follow above guidelines.
b.
Use initials for the person’s name. If their name is “John Doe,” call them JD.
c.
Present this as a narrative, a story. For example if in the ER certain drugs are
used, talk about and describe what
they are in that paragraph.
If certain labs and blood work are done in the ER present that right there as well. As you are going through your report relate
the procedures, definitions, pathophysiology, etc. to your current case. When doing the etiology, etc. on secondary disease
states discuss how that is affecting the patient & the primary diagnosis. Do the same for tests & procedures; discuss why,
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what, results, significance, plans, etc. Prove to me that you understand the full picture & what each individual therapy, test,
procedure, result etc. means individually & to the patient as a whole as well as the corrective action.
d.
Use “Day one” and “Day two” rather than calendar days. It’s easier to follow.
PATIENT CASE REPORT EVALUATION GRADE SHEET
Student______________________________
SCORE
1.
Diagnosis (es)
__15_____
2.
Patient’s history
_____20__
3.
Presenting signs & symptoms, Diff Dx
_______18
4.
Description of student’s examination/assessments
_______18
5.
Summary of laboratory data
_______20
6.
Drug therapy including indications
and results
_______19
7.
Respiratory modalities including
indications and results
_______20
8.
Research of diseases
_______18
9.
Impression, Discharge, & Comments
10.
Overall presentation
11.
Spelling & Grammar
12.
References’ & Citations
*13.
Overall ability to relay research to your Pt’s case
_______60
Total points obtained
_______285
Total points possible
__300__
S
N am
ot
ac ple
tu R
al ep
pa or
tie t
nt
AREA OF CASE STUDY
_______19
Percentage grade
*60pts available for #13, 20pts available for each section
Additional Comments:
_19
_______19
_______20
______95%_
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MSU - GREAT FALLS
RESPIRATORY CARE PROGRAM
CASE STUDY
Student:
Hospital:
Patient (Initials):
Diagnosis: RDS, Sepsis, PDA, PFO,
Age: 33 wks
Sex: M
AdmitDate:
PROM, PREMATURITY
HISTORY & ADMIT PHYSICAL EVALUATION (In Your own words):
Include at least
History of Present Illness:
Maternal history: Maternal age is 34 years with a G/P of G5, P4. Mother presented with limited prenatal care and an
estimated date of delivery of 11/20/10. Infants estimated gestation by OB is 33 weeks 3 days. Prenatal labs obtained
by St. James hospital in Butte, Montana reveal: Blood type A positive, SyphillisSyphilis, Hepatitis B, HIV, and
Rubella screens were all negative, with a positive Hepatitis C screen. Mother admits to poly drug abuse during
pregnancy with admission to the use of methamphetamine and marijuana on the day of her delivery. The mother
presented at St. James Hospital with spontaneous PROM (premature rupture of membranes) dilated to 7cm, and double
footling breech. An emergent cesarean section was immediately preformed.
The infant was born on 10/5/10 at 0938 hours at St. James Hospital at 33 weeks gestation. He was appropriate
for gestational age with Apgar scores of 1, 3, and 7 at 1, 5, and 10 minutes. Full resuscitation with chest compressions
was required and vascular access was achieved with fluid bolus and additional stabilization efforts. The infant
responded and was immediately placed in hood oxygen. Blood cultures were then drawn. The infant’s respiratory
distress progressed requiring positive pressure nasal cannula (CPAP) and ultimately endotracheal intubation with
mechanical ventilation and Curosurf administration was required. The infant was then transported to Benefis Health
System. The admitting diagnosis at Benefis were premature infant at 33 weeks gestation, respiratory distress
syndrome, clinical sepsis, poly drug abuse of mother during pregnancy with methamphetamine positive infant,
Jaundice secondary to bruising, and patent ductus arteriosus.
Once admitted to Benefis Health System, the infant was immediately placed on a Puritan Bennett 840 ventilator
in SIMV mode. The settings were as follows: rate of 35, PC of 20, PEEP of 5, PS of 4, iTime of 0.35 sec, and 0.50
FiO2. Pulse oximetry and Transcutaneous monitoring were also placed. The infant received three additional doses of
surfactant over the next two days. After surfactant administration, the infant greatly improved ultimately being
extubated to a HFNC on 4lpm at 0.28 FiO2, five days after admission. The infant is now placed in the custody of DFS
andDFS and will remain on the HFNC for the next 30 plus days. At this point, the infant is unable to be weaned from
the HFNC past 2lpm, and will remain admitted in the NICU until further notice.
Comment [BC1]: Meaning 30days past or still at
5days past admission?
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Past Medical History: The patient has no past medical history as he was recently born. Mothers past history is
vague due to her living in Butte, however; she admits to poly drug use in the past and throughout her
pregnancy.
Surgeries / dates: No dates of surgery.
Social & Family History: The mother is TE. Department of Family Services is involved and the infant will be
removed as all of her other children have been removed from her custody as well. Mother is hepatitis C positive
and admits to methamphetamine and marijuana use during her pregnancy, as well as methamphetamine use at
the time of delivery.
Comment [BC2]: Unfamiliar with this?
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PRESENTING PROBLEM LIST:
This should include all signs and symptoms presenting on ADMIT
1. Post Cardiac arrest
2. Hypoxia
3. Respiratory distress
4. Hypotension
5. PDA
6. Possible Sepsis
7. Mild Jaundice
8. Surfactant deficiency syndrome
9. Methamphetamine positive
10. Prematurity
11. Maternal Hepatitis C positive
12. Maternal drug abuse
13. Grunting
14. Flaring
15. Retracting
16. Respiratory Failure types I and II
17. Lethargy
18. Diminished breath sounds with fine crackles
PROBLEMS THE PATIENT COULD HAVE: (Disease state possibilities)
1. Death
2. Brian hemorrhage/ decreased brain activity
3. Pulmonary hypertension
4. Atelectasis
5. Jitters from withdrawlwithdrawal
6. Hepatitis C
7. Apnea
8. Pneumothorax
9. Pulmonary air leaks
10. Fever
11. Periodic breathing
12. Absent breath sounds
13. Prenatal asphyxia
14. Tachycardia
15. Cyanosis
16. Failure to thrive
17. Hypercarbia
18. Aspiration
19. Mild hypertension
20. Edema
21. Oliguria
22. Shock
Comment [BC3]: Great list, but format it using
the Dz state presented with as a header to identify
which problem the pt could have underneath. This
will serve to qualify it as a possible manifestation of
that dz.
Formatted: Position: Horizontal: 0.34",
Relative to: Page, Vertical: 4.95", Relative to:
Page
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Based on the ADMITTING DIAGNOSIS, what problems could the patient present with that they did not.
(clinical manifestations of that diagnosis that did not manifest in this patient)
PROBLEMS THE PATIENT COULD HAVE: (Disease state possibilities)
DIFFERENTIAL DIAGNOSIS: (Through this process what differential diagnosis could have been made or ruled out)
Based on your PRESENTING PROBLEMS LIST, what different diagnosis could be made or would need to be
ruled out in order to confirm your current diagnosis.
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1. Brain Hemorrhage: obtain a cranial ultrasound to ensure no hemorrhage or hydrocephalus is present.
2. PIE: obtain multiple chest x-rays to ensure the infant did not develop PIE due to PPV.
3. CLD: Continue to monitor chest x-rays to ensure infant is not developing CLD due to mechanical
ventilation, oxygen therapy, hypoxemia, cyanosis, and failure to thrive. Closely watch for an increase in
respiratory rate, retractions, diffuse fine crackles, expiratory wheeze, and irritability.
4. Patent PDA: Obtain an echo to determine if the infant’s PDA is gradually closing or continuing to cause a
left-to-right shunt due to a chronically patent PDA.
5. ROP: obtain an eye exam with the ret cam. The patient fits the criteria for ROP due to immaturity,
requiring high PaO2, and oxygen therapy. Maintain appropriate oxygen saturation between 85-92%.
6. Group B strep: This infant is pre-term and born with PROM, increasing the infant’s risk for Group B strep.
Obtain a Group B test and watch for shock, early apnea, and pulmonary hemorrhage.
7. Tetralogy of Fallot: This infant is at risk for the pathology of TOF. A decrease in blood pressure due to
hypoxia, decrease in vascular markings due to the decrease in blood flow to the lungs, and decrease in
oxygenation. I would obtain an echo immediately to ensure the infant does not have any other serious
cardiac abnormality other than the common PDA.
8. Pleural effusions: Obtain a chest x-ray.
9. Pneumothorax: obtain a chest x-ray.
10. NEC: obtain an abdominal x-ray and continue to monitor for chronic acidosis and a steady rise in fever and
WBC count.
Comment [BC4]: Please expand
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PATIENT ASSESSMENT: (Must see & assess patient over a 3 DAY period of time): Your 1st day of
assessment should be a thorough PT Assessment; The subsequent 2 Assessments should be in SOAP
format.
Adult Patient Assessment
HOSPITAL DAY # & TIME: Day 1 at Benefis
Age/sex 33 week M
Height 43.0cm (33rd percentile) Weight 1.8871 kg (31.2 percentile) IBW
Admitting Diagnosis: Prematurity, RDS, Clinical sepsis
Secondary Diagnosis: Jaundice, Poly drug use by mother with methamphetamine positive infant, PDA
Pulmonary Diagnosis: RDS
Other Diagnosis:
Subjective Data:
sedated and intubated.
Oxygen Therapy
Device: 840 Ventilator
FiO2: 0.60
Flowrate: 60lpm
Aerosol & Humidity Therapy Ventilated
Device: Heated wick
Temp:
Appropriate Rel Humid.: Yes
Hyperinflation Therapy
Device: Ventilated
Bronchial Hygiene
Technique: None
Ventilator Settings
Mode SIMV
Rate 35 /
Vol/Press PC 20
PS 4
PEEP 5
FiO2 0.60
I:E 1:5.39
Flow 60lpm
Waveform descending ramp
SpO2: 93
EtCO2: TCM: 57
Resp Medications:
None
Actual Values
RRtot 74
Vt 12/6
Min Vent4.20
I:E 1:5.39
PIP 25
MAP 5.6
Static P & Compliance: /
Additional Settings:
Tube Size & Depth: 2.5
Graphics Interpretation:
Additional Therapies/Procedures/Lines
UVC and percutaneous central venous catheter and IV placed
Cardiac monitors placed and pulse oximeter placed on left foot
@
7 cm
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Physical Assessment
Interpretation of Physical Assessment
Initial Impression & General Appearance:
Sensorium: mechanically ventilated and
sedated
Cough: slight cough during suctioning
Sputum: Amt
Color
Consistency
Small white
thick
PS is intubated and sedated. He has a fair general
appearance. He appears to be at rest at this time,time;
however, he is still retracting. PS does have a slight cough
reflex during suctioning. The cloudy thick sputum that has
been suctioned could easily be due to the patients RDS or his
previous surfactant administration in Butte. This is to be
expected on a mechanically ventilated patient.
The infantsinfant’s saturation on 0.60 FiO2 appears adequate
at this point, I would continue to try to wean ventilator as
possible. Pulse rate and respirations are all within normal for
a premature infant but continue to closely monitor. BP
seems to be adequate but needs to be closely monitored as
well. The infant’s temperature is slightly elevated, most
likely due to the patients’ possible sepsis from the PROM. I
would continue to monitor this and start on antibiotics.
The infants’ neck, extremities, and abdomen are all within
normal for an infant in his gestational age. I would continue
to closely monitor for any changes that would be detrimental
to the infant.
Vital Signs:
Pulse rate 160
BP 58/32
Resp. rate 75
Sat 92%
Temp. 99.7 degrees Fahrenheit
Neck: nothing abnormal
Extremities: no edema or deformity present
Abdomen: Liver at costal margin. No
splenomegaly. Umbilicus benign. Nondistended
and no masses
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Thorax: Slight retractions present
Breath Sounds: Equal breath sounds with
bilateral fine crackles. Some rhonchi present.
Slight retractions are present, which is a clear sign of
respiratory distress. Considering the patient underwent chest
compressions and is now being mechanically ventilated I
would expect his retractions to decrease drastically within the
next 24-48 hours, since the patient is receiving adequate
oxygenation. Also, having surfactant
insufficiency,insufficiency makes it much more difficult to
oxygenate areas of the lung that are collapsed. Surfactant
helps the elasticity of the lung allowing the lung to remain
open after exhalation and preventing collapse, when
surfactant is not present, it requires much greater pressures to
reopen the lungs for oxygen exchange. This causes major
exhaustion in infants often seen by retractions, and ultimately
leads to respiratory failure. The fine crackles heard
throughout are expected with RDS. I would expect this due
to the lack of surfactant and the immediate collapse of the
alveoli after exhalation. The fine crackles are heard when
the alveoli are trying to reopen for air exchange. I would
expect these crackles to lessen after adequate surfactant
administration by providing a barrier to help reduce friction
and keep the alveoli open for air exchange. The rhonchi
could be transmitted from the endotracheal tube or from
secretions. The moving air can easily vibrate the mucus
causing the rhonchi sound. It can also be from the surfactant
administration as well, since we are only suctioning a small
amount from him.
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Complete Blood Count:
WBC
12.9
(3.2-9.7 k/ul)
Bands 3
10%)
RBC
Hgb
HCT
3.47
(4.5-6.0 M/ul)
14.6
(14.5-17.9 g/dl)
42
(42.6-51%)
Platelets 182
COAGS:
PT
PTT
N/A
INR
D-Dimer
Hepatic:
AST 27
ALT 6
AP
104
Bili
7.6
Cardiac:
CK-MB
Trop I
(11.4-14.5sec)
(25-39sec)
(0.9-1.2)
( 0-0.49 ug/ml)
(15-37 IU/L)
(30-65 IU/L)
(50-136 IU/L)
(0.2-1.0 mg/dl)
Blood Chemistry:
Na
142
K
3.1
Cl
108
CO2
25
Glu:
105
Renal:
BUN
Cr
I/O’s:
(146-360 k/ul)
6
0.7
-2.7ml
(136-145 mEq/L)
(3.5-5.1 mEq/L)
(98-107 mEq/L)
(21-32 mEq/L)
(74-106)
(7-18 mg/dl)
(0.5-1.1 mg/dl)
(<4-6%)
N/A
(<0.4)
(0-
Interpretation
1. Low RBC: Normally the bone marrow
does not produce new RBC’s between birth
and 3-4 weeks of age. This causes a slow
drop in the RBC count over the first 2-3
months of life. Premature infants have a
slightly greater drop in RBC count. This is
a normal process called physiologic
anemia. This infant also has jaundice,
which is caused by RBC’s being broken
down too fast causing an elevation in
bilirubin levels. This process can also
cause a decline in the number of RBC’s. I
would expect this to be normal for this
preterm infant. I would continue to
monitor his CBC and ensure that his RBC
level does not continue to decline.
2. Elevated Bili: elevated bilirubin levels are
common in infants. There is no exact
normal level of bilirubin since it is an
excretion product and the levels found in
the body reflect the balance between
production and excretion. Usually jaundice
shows if the bilirubin level is above 2-3
mg/dl. Infection, hypoxia, and traumatic
labor are all indications for an elevated
level of bilirubin. This infant needs to
receive phototherapy and continue to
monitor his bili levels on a regular basis.
3. Hypokalemia: A decrease in potassium is
one of the side effects of one of the
medications this infant is receiving for his
possible sepsis. I would continue to
monitor his potassium to ensure no further
decline, however; I would expect this
normal for now.
4. Low BUN: BUN evaluates kidney
function and is directly related to protein
intake and nitrogen metabolism and is
inversely related to the rate of excretion of
urea. Usually a decrease in BUN is
generally not cause for concern however; it
can be indicative of hepatic failure,
nephrotic syndrome, and cachexia. I
believe that his BUN is not a cause for
concern. I would expect his BUN to
stabilize after he becomes more stable. I
would expect this number to be falsely
reported due to his arrest and extreme
hypoxia.
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Blood Gases:
This blood gas is from capillary blood,blood; therefore, it will slightly differ
from arterial blood. This infant shows a respiratory acidosis, however; in
the neonatal population a PaCO2 in the 50’s is perfectly acceptable. His
PO2 is low and should continue to increase while being mechanically
ventilated. Continue to monitor and obtain another blood gas at least every
24 hours.
pH 7.299
PaCO2 52.1
HCO3 25.2
PaO2 30.0
Hb N/A
HbO2 N/A
Abnormal Hb’s
A-a gradient
N/A
O2 cont
Oximetry/Pleth: 92%
Capnography: TPO2 44/ TCO2 57
Micro:
Sputum C/S & GS
Other: none
Hemodynamic Data & EKG’s No EKG performed
CVP(RA)
PAsys
Rythym
PAdias
Rate
PAmean
PCWP
COL/m
CI
PVR
SVR
SvO2
Echo 10/8/10
Interpretation:NormalInterpretation: Normal systemic and pulmonary venous returns. Normal atrial chambers
with a patent foramen ovale with a left to right shunt. Normal atrioventricular valves by echo Doppler and color
flow mapping. Normal atrioventricular and ventricular great vessel relationships. Mildly dilated right ventricle
without hypertrophy with normal function. Normal pulmonary valve flow patterns. Closing ductus arteriosus
with left to right shunt. Normal left ventricular size and function. Normal interventricular septum. Normal
aortic balvevalve by echo Doppler and color flow mapping. Coronary arteries not visualized. Normal aortic
arch without coarctation. No pericardial effusion. No intracardiac masses. LA: AO ratio 1.86.
Impression: Patent ductus arteriosus with left to right shunt with mildly dilated left atrium. Mildly dilated
right ventricle consistent with delayed transitional circulation with estimates of right ventricular and pulmonary
artery pressures of mild to moderately elevated. Patent FO with L to R shunt.
Pulmonary Function Results
Spirometry: SVC
FVC
Lung Volumes: TLC
Interpretation: N/A
FRC
FEV1
RV
FEV1/FVC
FEF 25-75
Diffusion: DLCO
PEFR
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Imaging
X-rays: 10/6/10 Single Chest
Other:
Interpretation: Diffuse granular opacities persist. There is no pneumothorax. Cardiothymic silhouette size is
stable. Endotracheal tube is in good position. Enteric tube has been removed. The presumed umbilical venous
line is favored to be unchanged given differences in patient positioning. There are scattered nondistended gas
filled loops of bowel within the abdomen. An indeterminantindeterminate prominent gas collection within the
left lower quadrant of the abdomen, caudal to the stomach is of uncertain etiology but is unchanged. There are
no other findings of pneumoperitoneum or pneumatosis.
Impression: Persistent diffuse pulmonary opacities, presumably related to surfactant disorder if this is a
premature infant. Bowel gas pattern.
Assessment & Plan
Assessment & Plan:
1. Prematurity: Follow the infant for complications and support proper growth.
2. RDS: This infant prompted intubation and surfactant prior to transport. Chest x-ray
revealed bilateral reticular granular opacities, left more than right and surfactant deficiency is
suspected. Continue to mechanically ventilate and oxygenate. Adjust the ventilator as
needed and consider a second dose of surfactant this evening. Continue to closely monitor
chest x-rays for further progression along with blood gases and saturation. Try to wean the
ventilator as much as possible to reduce the risk of acquiring barotrauma. Continue to
administer Fentanyl infusion to ensure the infant remains comfortable while intubated.
3. Possible sepsis: The infant is receiving Ampicillin and Gentamicin antibiotic therapy.
Continue to administer antibiotics and continue to follow the blood culture until final.
Monitor for daily changes.
4. PDA: The echo reported a left-to-right shunting PDA. Continue to monitor and obtain a
follow up echo if clinically needed. If the PDA does not close on its own and becomes
symptomatic, we can administer ibuprofen to help close the ductus. The infant is already
receiving indomethacin which should help as well.
5. Maternal Hepatitis C positive: Consider HCV RNA PCR at 3-4 months, or antibody testing
at 18 months. Until testing can be performed, take precaution and continue to monitor for
changes.
6. Maternal drug abuse/ methamphetamine positive: Obtain a high risk infant screen and send
meconium for toxicology as soon as possible.
Closely watch for signs of
withdrawlwithdrawal and if present administer medications to make infant comfortable.
Also, I would obtain a brain ultrasound to ensure no major defect at this point due to poly
drug abuse.
7. Jaundice: This is most likely secondary to bruising. Continue to follow bilirubin levels and
begin phototherapy.
8. Nutritional support: Keep infant NPO and closely follow electrolytes, I/O’s, and begin
TPN.
9. Low RBC: I would continue to closely monitor and obtain regular CBC’s to ensure this is a
normal physiologic anemia.
10. Hypokalemia: Although only slightly decreased, continue to closely monitor. I would
suspect this slight decline due to the side effects of Gentamicin.
11. Surfactant deficiency: Continue to monitor and obtain regular chest x-rays for further
decline and improvement. I would consider another dose of Curosurf tonight since there has
been no real improvement since his transfer here.
12. Hypoxia/Post cardiac arrest/ lethargy: Continue to monitor this infant closely. He is
receiving adequate oxygenation and ventilation due to mechanical ventilation, however; he is
could rapidly decline and need immediate attention. Continue to get daily CBC, Hepatic, and
Chemistry panels to ensure no drastic changes. Although he is stable at this point.
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Comment [BC5]: Bold headers and subjects but
do not bold body text as a whole.
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P a g e | 13
13. Low BUN: I would expect this value to normalize after his condition becomes more stable.
I would expect this number to be false due to his arrest and extreme hypoxia, causing a false
reading from the kidneys. I would continue to monitor with routine blood work to ensure no
significant changes.
13.14. Patent Foramen ovale – because of left to right shunting, surgery is not indicated.
Continue to monitor with echoes as the FO may close spontaneously given other intracardiac
pressures stabilize normally.
SOAP ONE
SUBJECTIVE: hospital day # day 2
The infant was born on 10/5/10 at 0938 hours at St. James Hospital in Butte, Montana, by double footling breech
presentation with spontaneous rupture of membranes, emergency cesarean section, 33-week gestation appropriate for
gestational age infant with Apgar scores 1,3, and 7 at 1,5, and 10 minutes respectively. Full resuscitation with chest
compressions required and vascular access achieved with fluid bolus and additional stabilization efforts. The infant
responded ansand was put into hood oxygen. Respiratory distress progressed requiring nasal CPAP and ultimately
endotracheal intubation with mechanical ventilation and Curosurf administration. He was then transported to Benefis Health
system. Last night 10/6/10 the infant received another dose of Curosurf that he tolerated well. After Curosurf
administration, PS was placed back on the ventilator with his previous settings. PS was also given another dose of surfactant
this morning 10/7/10. PS appears comfortable and his previous retractions appear to have subsided. PS appears alert and
startles easily.
Comment [BC6]: Great review of HxPI while
updating on the current events since the last
assessment.
OBJECTIVE:
1.
PS weighs 1.829 kg, heart rate currently sinus rhythm at 168 bpm, respirations 50 with blood pressure 70/24
mmHg.
2.
PS remains on the ventilator with SIMV mode of 34, PC of 23, PEEP of 5, with mean of 9, and FiO2 of 0.6. Equal
breath sounds with bilateral fine crackles. Some ronchirhonchi present also, but this appears to be transmitted
from the endotracheal tube.
PDA shows acyanotic (acrocyanosis?) and the heart reveals no dysrhythmia. Heart sounds are normal, with a
slight outflow murmur. Pulses and perfusion are normal.
There are contusions about the head on both sides likely secondary to emergent delivery efforts. Mild jaundice
but no rashes are apparent.
Moderate pulmonary hypertension is present and consistent with delayed transitional circulation.
Surfactant deliver y on 10/6/10: 4.5ml Curosurf via ET tube at 2054. 2.25ml with left side down and 2.25 with
right side down. Ventilated with bag using pressures of 20/5. RR 60, SaO2 of 93%, HR 159. Infant tolerated
well.
Additional surfactant delivery done this morning 10/7/10. 2.6 ml of Curosurf via ET tube at 1116. 1.3ml with
left side down and 1.3 with right side down. Infant was ventilated with bag using pressures of 23-26/5-7. RR
was 34-40, FiO2 of 0.30, HR 156-167, SaO2 93-95%. PS tolerated well and placed back on previous settings.
Chest x-ray on 10/7/10 reveals endotracheal tube is between the sternal notch and carina. Left PICC line has
been placed and this extends to the expected location of the right atrium and could be retracted approximately
1 to 1.5cm. Umbilical catheter extends to the T11 level. Lung volumes remain low with air bronchograms, left
greater than right. Heart is not enlarged. No dilated bowel loops are seen within the upper abdomen. Chest xray consistent with RDS and surfactant deficiency disorder.
Labs reveal: normal CBC with Hemoglobin 15 and Hematocrit 41 respectively with 211,000 platelets. Most
recent capillary blood gas with pH of 7.31, CO2 48, O2 43, bicarbonate 23.9. Na 135, K 3.4, Cl 107, and BUN 8
with Cr 0.6. Blood culture at St. James Hospital reportedly negative. Glu 106, Phos 3.3, and Bili is 6.9. AST 27,
ALT 6, and AP 104.
3.
4.
5.
6.
7.
8.
9.
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Comment [BC7]: Try to be consistent between
using dates or day #’s when describing the
chronological order of things.
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P a g e | 14
10.
ECG: reveals a patent ductus arteriosus with left-to-right shunt with increased left atrial size. Moderate
pulmonary hypertension with mildly dilated right ventricle. Biventricular function is normal. Structure of heart
is normal.
10.11.
No recent ECHO so PDA & FO are assumed to remain open with L to R shunt? Or is there other evidence
to suggest closure?
ASSESSMENT/PLAN
1. RDS: Continue to mechanically ventilate the infant and provide adequate oxygenation. Monitor daily
chest x-rays to evaluate progress or deterioration. Follow blood gases and wean ventilator as much as
tolerated.
2. Prematurity: Continue to closely monitor and provide optimal environment to enhance growth and
development.
3. PDA/ Pulmonary hypertension: Continue to monitor with follow up echo and treat with ibuprofen if
natural closure does not occur and if it becomes symptomatic. The infant is already receiving
indomethacin which should help as well. Continue to provide oxygen therapy. I would expect this
pulmonary hypertension to subside and most likely due to delayed transitional circulation.
4. Hypoxemia/ post cardiac arrest: Continue to mechanically ventilate until able to wean. Ensure adequate
oxygenation and ventilation and monitor with routine blood gases. Closely watch saturation, heart rate,
and respirations.
5. Maternal Hepatitis C: Consider HCV RNA PCR at 3-4 months or antibody testing at 18 months.
Continue to take precautions.
6. Sepsis: Continue to administer Ampicillin and Gentamicin. Follow blood culture until results are final.
Closely monitor CBC, Chemistries, and Hepatic panel to ensure no rapid decline.
7. Surfactant deficiency: Continue to mechanically ventilate and monitor with routine chest x-rays. PS has
received three total doses of Curosurf. Continue to administer Curosurf if clinically indicated.
8. Hypokalemia: Continue to monitor with regular chem panels to ensure no rapid decline. I would expect
this to be somewhat normal for this preterm infant. Continue to closely monitor.
9. Decreased BUN: I would expect this to be normal and not generally a cause for concern. I would
continue to monitor with daily blood work.
10. Increased Bilirubin/Jaundice: Continue to administer phototherapy and monitor with daily blood work.
Elevated bilirubin is common in infants.
11. Low RBC/ Anemia: I would consider this physiologic anemia, and normal in newly born infants. I
would expect his RBC’s to increase within a month.
12. Methamphetamine positive: Continue to monitor for withdrawlwithdrawal and administer medications
to provide comfort. Closely monitor for appropriate responses and obtain aan infant drug screen.
13. Nutritional support: Keep NPO as patient is being mechanically ventilated. Closely follow electrolytes,
I/O’s, and continue TPN to ensure adequate nutrition.
Comment [BC8]: Make sure to f/u on prior days
abnormalities to state that they have either improved,
regressed, stayed the same, or were not assessed.
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Formatted: Tab stops: 0.5", Centered + Not
at 3.75"
Comment [BC9]: You are certainly doing great
so far on this study…………….but make sure that if
you list data In the S & O sections you address it in
the A & P sections. Or if you talk about something in
the A&P section that you are providing data of that
in the S&O sections.
You really are doing great here and therefore I have
to be pretty picky to find things to point out to help
you improve. 
P a g e | 15
SOAP TWO
SUBJECTIVE: hospital day # 6 days in hospital
This is the infants sixth day in the NICU. PS appears comfortable and there is no evidence of retractions or any distress. He
is sleeping but startles easily. PS received an additional dose of surfactant on 10/8/10 and did not tolerate well. After
administration the infant dropped his saturation and brady down to the 60’s. At that point, breath sounds were not heard.
PS then coughed and a CO2 detector was placed on the ET tube and revealed a positive color change. PS then had breath
sounds throughout with saturation and heart rate returning to baseline. After surfactant administration, PS was placed back
on the ventilator to his previous settings. The next two consecutive days, the patient continued to improve and ultimately
the decision to extubate was made on 10/11/10. After extubation, the infant was placed on a high flow nasal cannula on
4lpm with ana FiO2 of 0.28.
OBJECTIVE:
1.
Weight 1.859 kg, heart rate currently sinus rhythm at 165bpm, respirations 43, with a blood pressure of 75/30
mmHg.
2.
Last vent settings before extubation: SIMV rate of 20, PC 15, PEEP of 5, pressure support of 4, and FiO2 of
0.21. TPO2 40, TCO2 48. Saturation 97%.
Last blood gas before extubation: pH 7.321, PCO2 45.3, PO2 42.9, HCO3 22.9, total CO2 24.3, BE -3.3.
Chest x-ray reveals: The left PICC line has been pulled back and now extends into the lower superior vena
cava. An enteric tube extends below the diaphragm. Endotracheal tube is unchanged. Diffuse pulmonary
opacities persist. There is slightly increased volume loss within the left lung. Cardiothymic silhouette size in
unchanged. Osseous structures are age appropriate. No new focal consolidation or pneumothorax.
Impression: Support equipment as detailed above and surfactant deficiency disorder.
Current echocardiogram reveals: Normal systemic and pulmonary venous returns. Normal atrial chambers
with a patent foramen ovale with a left-to-right shunt. Normal atrioventricular and ventricular great vessel
relationships. Normal right ventricular size and function. Normal pulmonary valve. Normal left ventricular
size and function. Normal interventricular septum and aortic valve. No pericardial effusion or intracardiac
masses. Impression reveals a closed ductus arteriosus. Normal right heart pressures. Overall normal 2dimensional Doppler color-flow echocardiogram.
Cranial ultrasound performed 10/11/10 reveals: No hemorrhage is noted. Sulci and gyri appear
unremarkable. No anomaly is noted. There is no hydrocephalus. Periventricular white matter appears
normal. Impression: findings are within normal limits.
Blood cultures reveal no growth as of this point.
New labs reveal: WBC 9.3, RBC 3.54, Hgb 14.5, Na 134, K 4.1, Cl 100, BUN 17, Glu 94, Ca 9.3, Bili 5.5.
After adequate blood gas and clinical status, PS was extubated to 4l HFNC on 0.28 FiO2. Blood gas after
extubation reveals: pH 7.279, PCO2 42.4, PO2 42.9, HCO3 19.4, total CO2 20.7, BE -7.0. Saturation from pulse
oximetry 95%. A-a gradient was 93.1. TPCO2 47, TPO2 56.
Lung sounds reveal fine crackles throughout and suctioning reveals a small amount of oral secretions.
3.
4.
5.
6.
7.
8.
9.
10.
ASSESSMENT/PLAN
1. RDS: Continue to monitor with daily chest x-rays to ensure no decline in the progress that has been
made. Continue to provide adequate oxygenation and follow with routine capillary blood gases.
Maintain appropriate saturation and closely monitor no new increase in respirations or a rapid decline in
heart rate. Keep the infant on the HFNC but try to wean the flow as much as tolerated. FiO2 appears
adequate at 0.28 but continue to wean as tolerated to room air.
2. Prematurity: continue to monitor the infants’ growth to ensure proper growth and development of an
infant of his gestational age.
3. Pulmonary hypertension: The PDA has closed naturally with the help of indomethacin however; there is
evidence of mild hypertension. I would expect this to subside as it is most likely due to delayed
transitional circulation. Continue to monitor and obtain a follow up Echo if clinically indicated.
4. Hypoxemia/post cardiac arrest: Hypoxemia is not present however, with an infant that has had have
resuscitation, they can rapidly decline. Continue to administer oxygen supplementation through HFNC
Comment [BC10]: Great update, but still provide
a very brief description of HxPI.
P a g e | 16
and wean as much as tolerated.
5. Maternal Hepatitis C: Continue to closely monitor and vaccinate for other hepatitis. Obtain Hep C testing
when infant is old enough.
6. Sepsis: Although the blood cultures to this point are negative, infants born from PROM are at an
increased risk, therefore; continue to treat with Ampicillin and Gentamicin. Continue antibiotics until
further indicated and closely monitor for any other decline.
7. Surfactant deficiency: The infant has received four total doses of surfactant (three here at Benefis).
Continue to monitor the progress through daily chest x-rays. Closely monitor for an increase in work of
breathing, tachypnea, and tachycardia.
8. Anemia: Continue to monitor with CBC’s for any changes, however; I believe this to be normal physiologic
anemia and will subside when the infant ages.
9. Maternal drug use and methamphetamine positive: continue to monitor for signs of
withdrawlwithdrawal and make the infant comfortable.
10. Labs all appear normal but continue to monitor with daily blood work and ensure no drastic changes.
11. Nutritional support: At this point the infant has been NPO I would continue to keep him this way until Dr.
Kenney decides he can nipple. He appears nutritionally adequate, continue; continue to monitor I/O’s,
electrolytes, and TPN.
11.12. Continue to follow Patent Foramen Ovale - follow up echoes.
Comment [BC11]: some PFO’s will not close
and with a left to right shunt a person can progress
normally. It will not be surgically closed unless some
other open heart surgery is performed. Often times
not until adulthood.
P a g e | 17
Medication
Indication
Mechanism of Action
Possible Complications
Amino
Supply all daily
IV infusion/ nutrition
Thrombosis of peripheral veins,
Acids/
nutritional
Electrolyt
requirements.
1.
Sepsis, Glucose abnormality
es/
Dextrose
TPN
Q24h
2.
A
Ampicilli
Used to treat a
Penicillin type antibiotic that
Dark urine, nausea, vomiting,
n Sodium
wide variety of
works by stopping the growth
stomach or abdominal pain, easy
250mg
bacterial
of bacteria
bruising, and persistent sore
vial
infections
throat.
190mg IV
Q12H
3.
F
Fat
Used to provide
IV infusion/Calories
Persistent fever, pain, swelling,
emulsion
calories to
sudden weight gain, shortness of
Intraveno
patients who
breath, back or chest pain.
us 18 ml
are getting their
0.75
nutrition
mls/hr IV
through a vein
Q24H
4.
F
Fentanyl
Used to treat
Produces its effects
Respiratory depression, diarrhea,
Citrate
pain and aide in
predominantly via agonist
nausea, fatigue, weight loss,
actions at the mu receptor.
dyspnea, and apnea.
200mcg in sedation
dextrose/
water
25mls
Q24h
5.
G
Nephrotoxicity, auditory or
Gentamic
Used to treat
Inhibits bacterial protein
vestibular ototoxicity,
in Sulfate
severe
synthesis
hypersensitivity reactions.
P a g e | 18
20 mg
infections
8.4mg IV
caused by
Q36H
organisms
6.
sensitive to
I
Indometh
gentamicin.
acin
Used to relieve
Stops the body’s production of
Headache, dizziness, vomiting,
Sodium
moderate to
a substance that causes pain,
diarrhea, and ringing in the ears.
1.8mls IV
severe pain/ to
fever, and inflammation.
Q12H
help close a
7.
PDA
Curosurf
Comment [BC12]: How does it help close the
PDA, this cases indication.
C
The treatment
Reduces surface tension at the
Bradycardia, hypotension,
or rescue of
air-liquid interface of the
oxygen desaturation, ET tube
Respiratory
alveoli during ventilation and
blockage, and pulmonary
distress
stabilizes the alveoli against
hemorrhage.
syndrome in
collapse at resting
premature
transpulmonarytrans
infants.
pulmonary pressures.
P a g e | 19
PATHOPHYSIOLOGY (Research): (In your own words, Definition, Etiology, Pathology, Clinical
manifestations, Complications, Mortality/ prognosis, Treatment & Special procedures. You MUST be specific to
your patient when relating researched material to your clinical case. Include in text Citations and then
Reference your citations in APA format at end of study):
1. Respiratory Distress syndrome (RDS)
Definition: RDS is a common complication seen in premature infants. It is mainly caused by a lack of
surfactant, which helps the lungs inflate with air and keep the air sacs from collapsing.
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Etiology: RDS occurs in infants whose lungs have not yet fully developed. Surfactant is not produced in
adequate amounts until relatively late in gestation; thus, the risk of RDS increases with greater prematurity.
The earlier the infant is born, the less developed the lungs are and the higher the chance of developing RDS.
Most cases are seen in babies born before 28 weeks of gestation (1).
PS was born at 33 weeks gestation, although greater than the common 28 weeks, he was still premature and had
poor underdeveloped lungs.
Pathophysiology: Pulmonary surfactant is a mixture of phospholipids and lipoproteins secreted by the type II
pneumocytes. Its primary role is to diminish the surface tension of the water film that lines the alveoli, thereby
lowering the tendency of the alveoli to collapse and the work required to inflate them. Because much of the
infants’ lungs are stiff, newborns are unable to begin breathing. Over a period of hours, the respiratory distress
tends to become more severe as the muscles used for breathing tire, the small amount of surfactant in the lungs
is used up, and increasing numbers of air sacs collapse (1).
PS was born prematurely without adequate surfactant. This was easily seen after birth when his respiratory
distress began. He was then placed in hood oxygen and over the next couple of hours continued to decline. His
work of breathing continued to increase and he became fatigued, ultimately requiring intubation.
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Signs/symptoms: There are many signs and symptoms for RDS: Bluish color of the skin and mucus
membranes, apnea, decreased urine output, grunting, nasal flaring, puffy or swollen arms or legs, rapid
breathing, shallow breathing, retractions, and shortness of breath accompanied by grunting and retractions.
Without being in Butte at his time of delivery, I cannot determine the extent of his symptoms. We do know that
he became increasingly short of breath and fatigued, requiring intubation and mechanical ventilation to alleviate
his work of breathing.
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Diagnosis: Diagnosis of RDS is based on symptoms, oxygen levels in the blood, and chest x-ray results.
PS was diagnosed originally in Butte based on his rapid decline in oxygenation and increase in work of
breathing. After transfer to Benefis, the diagnosis was confirmed via chest x-ray.
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Complications: Some complications with RDS are: intraventricular hemorrhage, periventricular white matter
injury, tension pneumothorax, bronchopulmonary dysplasia, sepsis, and death (1).
Thankfully, PS has not displayed any indication of these complications, at this point.
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Prevention: The risk of RDS is greatly reduced if delivery can be delayed until the fetus’ lungs have produced
sufficient surfactant.
Treatment: After birth, infants with severe RDS may require CPAP or even intubation and mechanical
ventilation. The use of surfactant can be lifesaving and helps reduce complications such as a pneumothorax.
Surfactant can be given immediately after birth or several times during the first days until RDS resolves.
After birth PS was placed in hood oxygen but after further distress he was switched to nasal CPAP. According
to St. James Hospital, his distress continued to increase and he ultimately was intubated and soon thereafter
received his first dose of surfactant therapy.
Prognosis: RDS with rapid treatment is excellent; mortality is less than 10% with adequate ventilator support
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Comment [BC13]: You could discuss possible
ways we can delay childbirth, of course in this case
there was no prenatal care however in good prenatal
care we have ways to both delay birth and increase
maturity as well.
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P a g e | 20
alone. Surfactant production eventually begins and once production begins, RDS usually resolves within 4-5
days. However, severe hypoxemia can result in multiple organ failure and death (1).
PS was soon transported to Benefis, where he remained intubated and received three additional doses of
surfactant over the next three days. Thankfully, he was able to be stabilized and extubated to a HFNC, which
he continues to be on.
2. Prematurity: An infant born before 37 weeks gestation.
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Etiology: The cause of premature labor and delivery whether preceded by PROM or not, is usually unknown.
However, maternal history commonly shows low socioeconomic status, inadequate prenatal care, poor nutrition,
poor education, unwed state, and previous pre-term birth or infection (2).
PS was born with many of these risks. His birth was preceded by PROM and his birth mother proved to have
poor prenatal care, poor education, unwed state, and from a low socioeconomic status.
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Signs/Symptoms: Some of the common signs are: prior to estimated delivery date, small, think skin, little
subcutaneous fat, hair, and little external ear cartilage. Spontaneous tone and activity are all reduced and
extremities are not held in the flexed position.
PS presented with many of these signs including small, little subcutaneous fat, little external ear cartilage, and
reduced tone and activity were evidenced by his low Apgar scores.
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Complications: Most complications are due to the dysfunction of immature organ systems. Surfactant
production is often inadequate to prevent alveolar collapse and atelectasis, which results in RDS. Infants less
than 34 weeks have I adequate coordination of sucking and swallowing reflexes and need to be fed by IV. They
are also at an increased risk for developmental and cognitive delays, particularly those with a history of sepsis,
hypoxia, and intraventricular or periventricular hemorrhages (3).
PS did have a surfactant deficiency that resulted in RDS. It will not be until the infant ages to determine if there
are any developmental and cognitive delays. Unfortunately, he is at an increased risk due to his RDS, sepsis,
and hypoxia.
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Prognosis/Treatment: Prognosis varies with the severity of complications but usually mortality and likelihood
of complications decreases greatly with greater gestational age and weight.
PS has greatly improved since he was first admitted, however; I would expect many struggles to arise through
his growth and development.
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3. Sepsis: Sepsis is defined as an invasive infection, usually bacterial, occurring during the neonatal period.
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Etiology: Sepsis can be early onset (within 7 days of birth) or late onset (after 7 days of birth). Group B
streptococcus and gram negative enteric organisms account for most cases of early onset. Late onset is usually
acquired from the environment (5).
PS was diagnosed with sepsis right after birth, most likely due to his emergent birth from PROM, therefore; he
would be classified as early onset sepsis. His blood cultures came back negative but with his increased risk
from the PROM, prophylaxis was necessary.
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Pathophysiology: Certain maternal perinatal and obstetric factors can increase the risk for sepsis. Some
common risks are: PROM, maternal bleeding, preeclampsia, precipitous delivery, maternal infection, heavy
colonization with GBS, and preterm delivery (4).
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Signs and symptoms: Early signs are frequently nonspecific and subtle and do not distinguish among
organisms. Some common signs are: diminished spontaneous activity, less vigorous suckling, apnea,
bradycardia, temperature instability, fever, RDS, neurologic findings, vomiting, diarrhea, and abdominal
distention.
PS presented with diminished spontaneous activity, bradycardia, and RDS.
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P a g e | 21
Diagnosis: Diagnosis of Sepsis is primarily based on a high index of suspicion, blood, urine, and CSF cultures.
PS was initially diagnosed with sepsis due to his birth from PROM and symptoms that correlated with sepsis.
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Prognosis: The fatality rate is 2-4% times higher in low birth weight infants than in full term infants. The
overall mortality rate of early onset sepsis is 3-40% and of late onset is 2-20 %( 5).
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Treatment: Sepsis is commonly treated with antibiotic and supportive therapy.
PS immediately started to receive antibiotic therapy (Ampicillin and Gentamicin) and supportive therapy.
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4. Patent Ductus Arteriosus: A persistence of the fetal connection between the aorta and pulmonary artery after
birth, resulting in a left-to-right shunt.
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Etiology: PDA accounts for 5-10% of congenital heart anomalies, the male to female ratio is 1:3. PDA is very
common in preterm infants.
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Pathophysiology: The ductus arteriosus is a normal connection between the pulmonary artery and aorta and is
necessary for proper fetal circulation. At birth, the increase in PaO2 and the decrease in prostaglandin
concentration causescause closure of the ductus. If this normal process does not occur than the patent ductus
arteroisus exists. A small ductus rarely causes consequences where a large ductus causes a large left to right
shunt. Over time, the large shunt results in pulmonary artery hypertension and elevated pulmonary vascular
resistance, ultimately leading to Eisenmenger’s syndrome (6).
PS had a PDA that was evidenced via echo. PDA is common in preterm infants like PS. His PDA was large
enough to require indomethacin and eventually closed.
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Signs/ Symptoms: Clinical presentation depends on PDA size and gestational age at delivery. Infants with a
small PDA are often asymptomatic where infants with a large PDA can present with: Heart failure, failure to
thrive, poor feeding, tachypnea, dyspnea, respiratory distress, apnea, and worsening mechanical ventilation
requirements (7).
This was present in PS where he became increasingly dyspnic and required intubation.
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A large ductal shunt in the premature infant often is a major contributor to the severity of the lung disease of
prematurity. Premature infants with a significant shunt often have bounding pulses and a hyper dynamic
precordium. A heart murmur occurs in the pulmonary area.
The PDA in PS could have been a contributor to his severe RDS.
Diagnosis: Chest x-ray, ECG, and an Echocardiogram are the standard for diagnosis of a PDA. It is suggested
by clinical exam and is supported by the chest x-ray and ECG. This is established by a 2-dimensional echo with
color flow and Doppler studies.
PS had a confirmed PDA by obtaining an Echo. After initial diagnosis, he continued to have routine echo’s to
ensure that the PDA eventually closed and was not becoming more symptomatic.
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Treatment: Prostaglandin synthesis inhibitor therapy such as Indomethacin or ibuprofen is often used to close
the patent ductus arteriosus. Sometimes TransTran’s catheter occlusion devices or surgical repair are needed to
close a large PDA. In preterm infants with compromised respiratory status, the PDA can sometimes be closed
by using a prostaglandin synthesis inhibitor (7).
PS did receive indomethacin and oxygen to help close the ductus.
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5. Jaundice: A yellow discoloration of the skin and eyes caused by hyperbilirubinemia.
Etiology: There are several ways to classify and discuss causes of hyperbilirubinemia. Transient jaundice is
common among healthy neonates. Hyperbilirubinemia can be classified as physiologic or pathologic. Some of
the most common causes of neonatal jaundice include: physiologic hyperbilirubinemia, breast feeding jaundice,
breast milk jaundice, and pathologic hyperbilirubinemia due to hemolytic disease.
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P a g e | 22
Pathophysiology: The majority of bilirubin is produced from the breakdown of hemoglobin into unconjugated
bilirubin. This then binds to albumin in the blood for transport to the liver, where it is taken up by hepatocytes
and conjugated with glucuronic acid by the enzyme UGT to make it water soluble. It is then excreted in the bile
and into the duodenum. Physiologic hyperbilirubinemia occurs in almost all neonates. Shorter neonatal RBC
life span increases bilirubin production. Deficient conjugation due to the deficiency of UGT decreases
clearance and decreases bacterial levels in the intestine. This combined with an increase in hydrolysis
conjugated bilirubin causes an increase in enterohepatic circulation (8).
PS had jaundice most likely secondary to bruising. I would expect this jaundice to be normal for this infant and
is most likely physiologic hyperbilirubinemia.
Diagnosis: Diagnosis is generally based on the overall clinical appearance and serum bilirubin blood test.
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Comment [BC14]: Provide more discussion
comparing pathological and physiological jaundice.
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Signs/symptoms: The most common symptom is yellowing of the skin and eyes. Hyperbilirubinemia can also
cause fever, tachycardia, respiratory distress, lethargy, and hypotonia.
PS presented with a slight yellowing of the skin and eyes, however, I do not believe that his slight fever,
tachycardia, respiratory distress, and lethargy, were related to his jaundice.
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Treatment: Treatment is directed at the underlying disorder; in addition, treatment for hyperbilirubinemia
itself may be necessary. Physiologic jaundice is usually not significant and will resolve in one week. Definitive
treatment includes: phototherapy and exchange transfusion. Phototherapy remains the standard of care, most
commonly using blue light.
PS did receive phototherapy for roughly two days. After this treatment, his serum bili level decreased enough
that treatment was not needed and the jaundice would subside on its own.
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6. Methamphetamine use during pregnancy/ Infant positive for methamphetamine
There is little known about the effects of methamphetamine on the fetus, however; there are some
significant health concerns.
Pathology: Methamphetamine has been shown to easily penetrate the placental barrier. If the mother uses
methamphetamine prior to the birth of the child it will assure that the child has an intrauterine exposure to
methamphetamine (9).
Signs/Symptoms: Some possible health effects include: increased maternal blood pressure, decreased birth weight,
and prematurity. It can also cause an increase in biological risk for developmental delays and learning impairments,
whether or not poor outcomes become evident depends largely on the post-natal environment. Heavy
methamphetamine use during pregnancy is related to poor fetal movement, decreased arousal, lethargy and an increase
in physiological stress. Evidence that lifelong breathing, hearing, vision, and learning disabilities are also being related
to methamphetamine use during pregnancy. There has also been an increase in SIDS in infants born positive for
methamphetamine. Meth may cause the infant to be jittery, floppy, and have trouble sleeping (10).
Treatment & prognosis: Thankfully, PS has had excellent post-natal care and has had help sleeping with the use of
Fentanyl. If he has had jitteriness that can easily be addressed as well. It will be vital to obtain testing when he ages to
determine if there are any developmental or learning impairment.
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Comment [BC15]: Due to the reasons you
already listed.
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Comment [BC16]: Include patent Foramen
Ovale and PROM. You discussed prom briefly in
prematurity but only in mention. You should add
prom as a diagnosis discussing it in depth since it
was a precipitating factor to the premature birth\,
P a g e | 23
PLAN MOVING FORWARD (Include rationale):
1. RDS: Continue to treat with the HFNC and wean flow as much as tolerated until the infant no longer requires
oxygen supplementation. Monitor with routine chest x-rays to ensure nothing new develops.
2. Sepsis: The infant has completed antibiotic therapy for the sepsis. Continue to monitor with routine blood work
such as CBC, Chem panels, and Hepatic panels to ensure no new developments or any rapid decline.
3. Methamphetamine positive: Continue to monitor and make comfortable. When the infant is a little older, I
would recommend testing to see if there are any delays or disabilities that the infant has.
This infant has a long road ahead of him. Hopefully he has already been through the worst, as I can’t imagine
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P a g e | 24
being born into the world in the way that he did. Thankfully he is no longer in his mother’s custody and has
been receiving exceptional care. I believe the most important thing for this child is to continue to monitor him
regularly and ensure growth and development as much as possible until he is able to be discharged.
Unfortunately, with as many problems as he has already had, he is at a much higher risk for developing other
life threatening illnesses.
4. PFO - Include f/u echo to assess for cardiac blood flow abnormalities that may still persist.
Formatted: Numbered + Level: 1 +
Numbering Style: 1, 2, 3, … + Start at: 1 +
Alignment: Left + Aligned at: 0.25" + Indent
at: 0.5"
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OVERALL IMPRESSION/STUDENT COMMENTS OR DISCUSSION:
PS is a very strong kid. I cannot imagine being born with RDS, prematurity, sepsis, and positive for
methamphetamine. It is incredibly sad that almost all of his complications could have been avoided if his
mother had made better choices. I think that PS is a fighter and has done extremely well considering his
rapid decline with RDS, having to be intubated and mechanically ventilated, and now only requiring a
HFNC. My hope is that he will continue to grow and soon be able to be weaned from the HFNC, ultimately,
being adopted into a good home. I fear that he will have many complications and struggles throughout his
life due to his mothers’ selfish decisions. This was an extremely hard case initially for me. It is hard for me
to believe that there are infants born into life like this. The only positive point is that he is receiving much
better care than he would if he were with his natural mother.
REFERANCES: (Minimum 3)
1. Kantak, Anand D. M.D., (March 2009) Respiratory Distress Syndrome. Retrieved from
http://www.merck.com
2. Kendig, James W. M.D., (March 2007) Prematurity. Retrieved from http://www.merck.com
3. Lee, Kimberly G. M.D., (26 October 2010) Premature infant. Retrieved from www.nlm.nih.gov
4. Caserta, Mary T. M.D., (October 2009) Sepsis. Retrieved from http://www.merck.com
5. Berry-Anderson, Ann L. M.D., (23 February 2010) Neonatal sepsis. Retrieved from
www.emedicine.medscape.com
6. Beerman, Lee B. M.D., (March 2010) Patent Ductus Arteriosus. Retrieved from http://www.merck.com
7. Neish, Steven R. M.D., (1 June 2010) Patent Ductus Arteriosus. Retrieved from
http://www.emedicine.medscape.com/article/891096-overview
8. Jospe, Nicholas M.D., (December 2009) Neonatal Jaundice. Retrieved from http://www.merck.com
9. Prenatal Methamphetamine Use and Neonatal Neurobehavoral Outcome. (2008) Smith, L.M., LaGasse,
L., Deraut, C., Grant P., Shah, R., Arria, A., et al. Neurotoxicol Teratol. 30 (1): 20-28.
10. Organization of Teratology Information Specialists. (2005) Methamphetamine/Dextroamphetamine and
Pregnancy Fact Sheet. Retrieved from http://health.utah.gov/meth/html/healthconcerns/children.html
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