Running head: CASE STUDY 1: NNP II
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Case study 1: NNP II
Marissa Hampton and Gabriela Olivas
University of Texas Medical Branch at Galveston School of Nursing
Neonatal Nurse Practitioner II
GNRS 5623
Dr. Debra Armentrout PhD, RN, MSN, NNP-BC
And
Dr. Leigh Ann Cates PhD, APRN, NNP-BC, RRT-NPS, CHSE
June 23, 2014
CASE STUDY 1: NNP II
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Case study 1: NNP II
Case Study #1: [12 points]
Michael Washington is a 715 gram, 27 week African American male infant born by
emergency caesarean section (C/S) secondary to significant fetal distress after a failed
attempt to stop preterm labor. Post delivery, baby Washington was intubated, received
positive pressure ventilation with 22/5x 40 FIO2 1.00 via Neo puff, and given tactile
stimulation. APGARS were 4,5,8 at 1, 5, 10 minutes respectively. Baby Washington was
admitted to the NICU and placed on SIMV with a PIP of 22, PEEP of 5, rate 40, I-time 0.30.
Maternal history is significant for the development of preterm labor at 26 weeks. Mrs.
Washington had been hospitalized 3 days prior to delivery with tocolytics and bedrest.
The tocolytics were discontinued at 27 weeks due to maternal fever, leaking membranes,
meconium-stained fluid, and fetal heart rate decelerations. An emergency C/S was
performed as above.
1. Would you have done anything differently in the delivery room? Why, why not?
In the delivery room, if the infant did not initially cry, then I would ensue with intubation. In a
delivery with meconium stained fluid intubation and suctioning below the vocal cords infant is
the recommended practice for an infant who is not vigorous (Pappas & Walker, 2010).
If the infant cried after delivery, then I would have deep suctioned and continued positive
pressure ventilation per neonatal resuscitation guidelines. A vigorous infant with meconium
stained fluid requires clearing of fluid from mouth, even if it is wiping while drying (Pappas &
Walker, 2010).
With either treatment modality, resuscitation would have begun at room air. With the use of
a portable pulse oximetery, we could determine if our intervention was effective. If the infant did
not have a change in oxygen saturation, then I would gradually increase the FiO2, remembering
that infants may initially have a lower preductal oxygen saturation according to minutes old
(Gomella, Cunningham, Eyal, 2014). If the infant continued to have poor or no respiratory effort
then I would consider intubation.
Once intubation was successful, I would have immediately tried to wean our FiO2. If infant
was unable to wean or still continued to have difficulty exchanging gas, then I would consider
administering a dose of surfactant to the infant. Early prophylactic surfactant administration
helps restore pulmonary function and helps prevent further tissue injury (Gomella, et al, 2014). I
would have administered…
2. What are your admitting diagnoses?
 27 week African American preterm male, appropriate for gestational age (AGA),
day of life (DOL) 1
 Respiratory distress syndrome
 Suspected sepsis
 Suspected meconium aspiration syndrome
3. What are your differential diagnoses for the respiratory distress?
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Suspected meconium aspiration syndrome
Suspected hyaline membrane disease
CASE STUDY 1: NNP II
4. Write your admitting orders (if you would place on different respiratory support from that
provided in the scenario, please write for that).
Admit infant to NICU.
Place infant in isolette.
Initiate humidity at 70 percent, after 2 weeks may
decrease humidity by 10 percent each day until reach
40 %, then off.
Admission vital signs every (q) 15 minutes x 4, then q
30 minutes x 4, then hourly x 4, then q 3 hours.
Admission weight, length and occipital frontal
circumference (FOC).
Admission four point blood pressures (bp), then hourly
bp.
Daily weight and weekly FOC.
Strict intake and output (I&O’s).
Intubate with 2.5 endotracheal tube (ETT).
Ventilator settings: SIMV rate of 40 breaths per minute
(bpm), peak inspiratory pressure (PIP) of 22, (PEEP)
Of 5, inspiratory time of 0.30 seconds.
Blood gases Q 6 hours.
STAT chest x ray for ETT and umbilical line placement.
Infasurf 2.1 ml via ETT x1 (in delivery room, 3ml/kg)
Hold suctioning by ETT for 6 hours.
Nothing by mouth (NPO).
Place orogastric tube (OGT).
Place umbilical arterial/venous catheters (UAC/UVC).
Infuse clear IVF of 4 mEq of Na Acetate in sterile water + 0.25 units heparin/ml at rate of
0.5ml/hr (~15 ml/kg/day)
Infuse D10% + 2 g/kg protein +1 meq KCl/100 + 2 mEq NaCl/ 100 +0.25 units heparin/ml at a
rate of 2 ml/hr (~65 ml/kg/day, GIR 4.5)
Admission laboratory:
Admission blood culture
Complete blood count (CBC),
Arterial blood gas
Type and screen
Bedside glucose.
In am obtain:
CBC
C reactive protein (CRP)
Complete metabolic panel (CMP)
Begin antibiotics:
Ampicillin 50 mg/kg/day q 12 hours..
Gentamicin 5 mg/kg/dose Q 48 hours. .
Admission medications:
Erythromycin ointment both eyes(OU) x 1
Vitamin K IM injection 0.25 mg x 1
Caffiene citrate
Loading dose: 8.9 mg IV q 12 hours times 2 doses (25 mg/kg/day)
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CASE STUDY 1: NNP II
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Maintence dose: 3.6 mg IV q 24 hours (5 mg/kg/day)
AM chest/ abdominal xray
Initial CXR to left. Initial CBC reveals a low WBC with an increased number of immature
to mature neutrophils.
5. What are your differential diagnoses?
 Respiratory distress syndrome
 Pneumonia
 Sepsis of the newborn
 Situs Inversus
6. Based on the concerns for sepsis, would you order any additional diagnostic tests at this
point? If so, what; if not, why not?
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Serial CRPs: will identify worsening sepsis. Increased CRP is elevated in 50-90 % of
septic infants and usually peaks within 24 hours (Gomella et al, 2013). Serial CRPs
may be helpful in determining duration of antibiotic therapy.
Tracheal aspirate: Obtaining a tracheal aspirate may help identify our suspicion for
pneumonia. Tracheal aspirate will use a gram stain to identify if any bacterial
organisms exist and may therefore guide in determining antibiotic therapy and
duration.
Additionally, I would like to obtain mothers prenatal labs. These labs will identify any
positive bacterial or viral infections, and if appropriate treatment was given.
Case Study #2: [26 points]
Lily Jones was born at 34 5/7 weeks (BW 2 kg) following an uncomplicated vaginal
delivery. Pregnancy was complicated by premature labor and an upper respiratory
infection 2 days prior to delivery. A maternal throat culture was done but results are
unavailable. Lily was admitted to the Level II nursery for observation and was tolerating
bottle feedings. She was noted to be jaundiced on DOL 1 and lab studies were ordered
with the following results:
Hct 43%; BBT B+/Direct Coombs negative; Bili T/D 12.8/0.7 @ 24 hours.
7. Based on the above information, what preliminary admission diagnoses would you
consider for this infant?
 34 week preterm AGA female infant DOL1
 Hyperbilirubinemia
 Suspected hemolytic disease of the newborn
 Suspected sepsis
8. What additional diagnostic tests, if any, would you order at this time, and why?
 Mothers blood type
 Blood culture
 CBC with differential
 Reticulocyte count
 Liver function tests
 Q 4 hour T/D bilirubin levels
 Peripheral red blood smear
 Indirect coombs test ( pg 404)
CASE STUDY 1: NNP II
9.
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Briefly describe the bilirubin production cycle.
Bilirubin is the product of erythrocyte destruction (Stokowski, 2011). More specifically,
bilirubin is derived from the degradation of heme contained in the red blood cells (Wong,
DeSandre, Sibley & Stevenson, 2011). When destruction of the red blood cell occurs,
hemoglobin is released. Hemoglobin further breaks down and yields heme as a byproduct.
Heme is then oxidized to biliverdin by enzymes. Bilirubin binds to albumin as is transported to
the liver as unconjugated bilirubin. Transportation occurs as the molecule binds to albumin.
While in the liver, bilirubin travels to hepatic cell membranes. Conjugation takes place here.
Liver enzymes conjugate bilirubin, therefore making it water soluable for excretion. Conjugated
bilirubin is then excreted into the bile, and exits the body via the intestines and kidneys during
normal elimination patterns. Bilirubin that is not excreted may be reabsorbed and may revert to
unconjugated bilirubin. Reabsoprtion occurs as unconjugated bilirubin enters the blood and
recirculates for uptake back into the liver. This cycle is known as enterohepatic circulation and
may cause an influx in unconjugated bilirubin levels (Stokowski, 2011).
10. What is the difference between physiologic jaundice, conjugated, and unconjugated
jaundice?
Physiologic jaundice is a progressive increase of serum unconjugated bilirubin levels that
occur gradually over the first week of life. Increase in bilirubin levels typically occur after the first
24 hours of life. Normal red blood cell destruction in infants occurs 2-3 times that of adults.
Decreased transport, enterohepatic circulation and breastfeeding are also contributing factors to
physiologic jaundice.
Conjugated jaundice is a measurement of direct bilirubin that is at least 20% of the total
bilirubin value. An increased level of direct bilirubin level is a biochemical marker of cholestasis
or hepatobiliary dysfunction (Gomella et al, 2013). Increased levels of direct bilirubin are not
normal and are less common than physiological unconjugated bilirubinemia. Risk factors of
conjugated jaundice include congenital infections, sepsis, neonatal hepatitis, ABO
incompatibility and using total parenteral nutrition (Gomella et al, 2013). Infant clinically presents
with prolonged jaundice, pale stools and darkened urine (Gomella et al, 2013).
Unconjugated jaundice reflects the value of total serum bilirubin (TSB); that is the value of
both indirect and direct circulating serum bilirubin level. Unconjugated bilirubin is derived from
byproducts of hemoglobin metabolism. Conjugation in the liver must occur in order for the
bilirubin to be excreted and for a decline in the overall TSB level. Depending on age, an
increase in TSB levels may describe the disease process.
11. Interpret the following normal CBC and differential. Briefly discuss the significance of
each parameter.
WBC 7.6
RBC 5.6
Hgb 17.8
Hct 55%
MCV 99
MCH 33
MCHC 33
Retic 1-3
Plts 213,000
Segs 55
Bands 0
Lymphs 9
Eos 2
Monos 5
CASE STUDY 1: NNP II
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WBC- normal WBC has a wide range; 5,000- 30,000/mm3. Values lower than 5,000
may be indicative of leukopenia. Leukopenia is a significant finding in sepsis or
pregnancy induced hypertension (PIH) (Lott, 2010).
RBC- normal RBC range is 4-6 mm3. Total RBC equal production or destruction of
circulating cells. RBCs are lower for earlier gestational age (Diehl-Jones & Askin,
2010).
Hgb- Hemoglobin values depend on gestational age. Hemoglobin levels can be
increased by delayed cord clamping and are typically highest in the first week after
birth. Hemoglobin values are significant because this is the major iron containing
component of the RBC. Hemoglobin carries oxygen to the tissues (Diehl-Jones &
Askin, 2010). Hemoglobin levels are usually one -third of the hematocrit.
Hct- Adequate hematocrit levels should be maintained to promote oxygenation to the
tissues. Values usually rise soon after birth, then decline. Depending on current
respiratory needs/ disease p
rocess higher hematocrit levels may need to maintained. Normal hematocrit values
are 40-55%. Higher hematocrit values (>65%) are indicative of polycythemia.
MCV- Mean corpuscle volume- This is the average size and volume of a single RBC
(Diehl-Jones & Askin, 2010). Either increase or decrease in values characteristically
describes the size of the RBC. This value may be indicative of specific types of
anemia.
MCH- Mean Corpuscle Hemoglobin are average hemoglobin molecules in each
RBC(Diehl-Jones & Askin, 2010). This values is also indicative of specific types of
anemia.
MCHC- Mean Corpuscle Hemoglobin Concentration is the concentration of
hemoglobin in each RBC(Diehl-Jones & Askin, 2010). Helps identify anemia.
Reticulocyte count- Measurement of how fast red blood cells are made from bone
marrow fro replacement back into blood supply. Normal ranges of term infants are
lower (4-5%) as opposed to preterm infants (up to 10%). Increased ranges above
these levels may indicate hemolytic anemia (Gomella et al, 2013).
Platelets- Normal range is 150,000-400,000/mm3 although total counts may be lower
in infants who are small for gestational age. Lower platelet count prolongs bleeding
times. Platelets may also be lowered due to maternal disease such as PIH and
autoimmune diseases, such as lupus. Neonatal conditions that have significantly low
platelet counts include alloimmune thrombocytopenia, sepsis, DIC or birth asphyxia
(Diehl-Jones & Askin, 2010).
WBC smear
o Overall relevance of WBC differential determines the presence of infection
using the I:T ratio. This ratio calculates the amount of immature WBC over
the total WBC. The presence of increased immature WBC indicates infection,
specifically a value over 0.2. Increased presence of immature WBC
demonstrates the mature WBC pool is depleted due to decreased production
or use. With lingering infection, the body must mount a response and does so
with whatever kind of WBC is left, for example, immature cells.
o Segs- Mature WBC responsible for inflammatory processes as seen with
infection.
o Bands-Immature WBC
o Lymphs- T and B cell immunity
o Monos- Immature WBC that macrophage invading cells. Monocytes are
responsible for clearing old or invading cells from the circulation.
o Eosinophils-
CASE STUDY 1: NNP II
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12 hours later, Lily suddenly became pale and voided a small quantity of burgundy
colored urine. Vital signs were: HR 165; RR 45; BP 40/28; T 98.2. A UAC was placed and
showed a MAP of 22 mmHg. Additional labs were done with the following results:
Hgb
Hct
Retic Ct
Peripheral smear
D. Coombs
Platelet count
Prothrombin time (PT)
Partial thrombo-plastin time
(PTT)
Thrombin time (TT)
Fibrinogen
Fibrin split products
D-dimer
Factor VIII
Factor V
Blood culture (prelim)
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31%
17.1%
Fragmented erythrocytes, decreased
platelets
Negative
35,000/mm
20.5 seconds
85.7 seconds
17.3 seconds
95 mg/dl
12 ug/ml
0.7 ug/mL
1.02 U/mL
0.99 U/mL
Many Gm-positive organisms in clumps
12. What is the significance of the platelet count, PT, PTT, thrombin time, fibrinogen, fibrin
split products, and d-dimer?
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Platelet count of 35,000 is significantly low. Normal platelet counts are between
150,000 to 400,000/ uL. Platelets provide a patchwork for intital blood vessel injury.
A decreased platelet count inhibits the body’s ability to provide clot formation and
therefore is unable to control bleeding. Risk factors for thrombocytopenia include
infections, particularly TORCH or other bacterial/viral infections, disseminated
intravascular coagulation (DIC), antiplatelet antibodies or situations that involve a
considerable amount of hypoxemia.
Pt level of 20.5 seconds is prolonged. Normal PT values are 10.6-16.2 seconds of an
infant who is 30-36 weeks, DOL 1 (Nock & Patra, 2011). Prolonged PT levels
indicate higher risk for bleeding.
PTT level of 85.7 seconds is prolonged. Normal PTT values are 27.5-79.4 seconds
for an infant who is 30-36 weeks on DOL 1 (Nock & Patra, 2011). Delayed PTT
levels are also indicative of prolonged bleeding times due to decreased plasma
levels of factors V to factor XI (Gomella et al, 2013).
Thrombin times of 17.3 are prolonged. Normal ranges for thrombin times are 12-14
seconds. Thrombin times are significant because they help evaluate the level of
fibrinogen present. If thrombin times are prolonged, this indicates a decreased
fibrinogen level or functionality, which ultimately means increased risk for bleeding or
DIC().
Fibrinogen levels of 95 mg/dL are low. Normal values are 200-400 mg/dL. Fibrinogen
levels are uses to determine blood clot formation. Fibrinogen converts into insoluable
fibrin, which inevitably forms a clot. A decrease in fibrinogen level signifies an
inability for clot formation, and therefore increases the likelihood of DIC().
CASE STUDY 1: NNP II
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Fibrin split products also help determine clotting stages. A level of 12 mcg/mL
signifies an increase in clotting time, and predisposes the infant to DIC. Normal
ranges for fibrin split products are levels less than 10 mcg/mL().
D-dimer: Clinical test that estimates fibrin lysis by plasmin. D-dimer is a sensitive
marker of coagulation activation, particularly DIC. Increased D dimer values indicate
DIC (Gomella et al, 2013). Varying ranges of normal noted.
13. What is the significance of Factor VIII and Factor V in the clotting cycle?
The F5 gene is responsible for the production of Factor V. Factor V plays a significant role,
along with other coagulation factors, in clot formation. Hepatic cells are responsible for Factor V
cell production. After production, these cells remain relatively inactive until the coagulation
system is activated and there is a need for clot formation. When Factor V is activated, it works in
conjunction with other clotting factors, to convert prothrombin to its active form, thrombin.
Thrombin then converts fibrinogen to fibrin, which essentially allows clot formation (Genetics
Home Reference a, 2014). Secondly, factor V, in conjunction with activated protein C (APC),
also plays a self-limiting role in regulating clot formation. APC controls clot formation by further
inactivating Factor V, once clot formation is established. This regulation controls the size of clot
formation at the site of injury (Genetics Home Reference a, 2014). .
Deficiency of Factor V results in inability of normal clotting cascade. Factor V Leiden is a
specific clotting abnormality that slows the rate of APC production. Slowed APC production
inadvertently causes prolonged circulation of Factor V and Factor VIII. Prolonged circulation of
these factors will cause abnormal clot size and formation. Increased formation of blood clots
may unintentionally block narrowed blood vessels in the circulation. This abnormality is known
as thrombophilia (Genetics Home Reference a, 2014).
Like Factor V, Factor VIII also plays a crucial role in clot formation. Liver is major site of
factor VIII production. Factor VIII is bound to von Willebrand factor in the circulatory system, and
remains dormant until the clotting cascade is activated. Once activated, Factor VIII separates
from von Willebrand factor and begins to interact with Factor IX This process initiates clot
formation. Abnormalities in Factor VIII lead to reduced protein levels that result in an inefficient
clotting cascade. These abnormalities lead to inability to form clots and control bleeding
processes. This inability is also referred to hemophilia. The severity of disease is related to
abnormality in Factor VIII production (Genetics Home reference b, 2014).
14. List your differential diagnoses for Baby Jones at this point, with a brief rationale for
each.
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34.5 week preterm AGA female infant DOL 2
DIC: Diagnosis of DIC is related to Baby Jones thrombocytopenia, prolonged PT
and PTT levels, reduced fibrinogen and elevated D dimer levels. Additionally,
baby Jones intial Hct level was 43% at birth and then decreased to 31 % by 36
hours of age. Infant is also pale and has a decreased urine output.
Hypotension: As evidenced by central bp with mean of 22 mmHg. Possible
bleeding may have occurred due to DIC.
Thrombocytopenia: Decreased platelet levels are due to DIC cascade.
Anemia: Decrease in Hct level from 43% to 31% in 12 hours.
CASE STUDY 1: NNP II
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Hyperbilirubinemia: Increased T/D Bili level 12.8/0.7 at 24 hours of age. If bleed
is suspected we can anticipate that this value will increase without the use of
phototherapy.
Suspected Viral infection: Due to mothers history of throat culture and upper
respiratory infection 2 days prior to delivery. Suspected sepsis is eliminated due
to many gram positive organisms in clumps as seen on the blood culture.
Presence of clumps indicates contamination
Suspected Pre-renal Failure: Due to decreased blood flow and perfusion to
kidneys. Decreased blood flow maybe due to hemorrhage, hypoxia, and
hypotension. Burgendy urine is a characterisitic finding.
15. Briefly discuss the etiology for the pathophysiological processes that underlie the
primary problem(s) that Baby Girl Jones is experiencing.
DIC is an inappropriate cascade of activation and dysregulation of clotting factors. In DIC,
active coagulation and accelerated fibrinolysis occurs simultaneously. The patient experiences
both bleeding and thrombosis at the same time. Thrombocytopenia is common as the body is
depleted of platelets and clotting factors. Contributors to the disease include exposure of blood
to tissue factor, vascular injury, liver disease, thrombosis, birth trauma, hypoxia, acidosis, tissue
necrosis or sepsis (Luchtman-Jones, Schwartz & Wilson, 2011). In baby girl Jones case, viral
illness or hypoxia maybe the underlying cause of DIC. Our suspicion is greater with suspected
viral infection as the mother presented with an upper respiratory infection 2 days prior to
delivery. Furthermore, Baby Jones delivery was uncomplicated, indicating that birth trauma,
hypoxia and acidosis are unlikely causes.
Further complications of DIC include inappropriate bleeding events, therefore contributing to
the infant’s hypotension and suspected pre renal failure. As hemorrhage ensues, less blood
remains in the intra vascular space, causing hypovolemia and hypotension. Decreases blood in
the vascular system leads to poor circulation. As a result, hypotension and a diminished
perfusion to the infant’s organs occur.
Hyperbilirubinemia
16. What treatment modalities are indicated at this point, and why?
 Treatment for suspected Viral infection:
 Treatment for hypotension
o Hydration. Will give replacement with platelets and FFP. Begin IVF. Total fluid
volume of 100 ml/kg/day
 Through UVC infuse D10 + ¼ NS +1 mEq KCl/100+ 1 Meq NaCl/100
+ 0.25 units heparin/ml to run at 5 ml/hr (~60 ml/kg/day)
o Consider NS fluid bolus of 10 mg/kg over 1 hour if still hypotensive after FFP
and platelet transfusion.
o Monitor hourly bp with UAC.
o Keep MAP between 30 to 45 mmHg.
o Consider dopamine if have reached near total fluid volume for the day and
still hypotensive with MAP under 30 mmHg.
 Treatment for hyperbilirubinemia:
o Begin single bank phototherapy
o Apply eye shields.
CASE STUDY 1: NNP II
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Recheck serum T/D bilirubin level q 4 hours (as infant current is in high risk
zone for age.
Treatment modality for DIC:
o Treat underlying disease
o Type and Cross for blood product administration
o Platelet transfusion for thrombocytopenia: 10ml/kg (20 ml) over 1 hour IV x 1
o Redraw platelets 1 hours after completed infusion.
o Fresh Frozen Plasma transfusion: Infuse 20 mL/kg over 2 hours IV x 1 (40
ml/kg/day total fluid)
o Redraw D-dimer, PT, PTT, fibrinogen levels
Case Study #3: [15 points]
Sarah Jane Hill is a former 23 week gestation infant (BW 543 gm) who is now 32 wks
PCA. Her hospital course is notable for RDS treated with 2 doses of surfactant; and
continued oxygen requirement/vent support with chronic lung changes apparent on CXR.
Other problems thus far include:
 PDA treated with unsuccessfully with indocin; followed by ligation
 HUSs have been negative X2
 Numerous sepsis “rule-outs” – none proven. Treated with either Amp/Gent or
Vancomycin & Tobramicin
 Feedings were started at 10 days of life with EBM/Premature Enfamil 24. These
have been interrupted several times for “feeding intolerance” with no evidence of
NEC.
Yesterday, DOL 62, Sarah Jane began having more apnea/bradycardia episodes, and
developed temperature instability. A CBC showed a left shift and a full sepsis w/u was
done; Baby Hill was started on Vancomycin & Tobramicin. Feedings were stopped
overnight for a bilious residual and IVFs were begun. KUB at the time showed enlarged
& dilated loops of bowel.
Today is DOL #63, current wt = 1320 gm. Sarah Jane is on NCPAP 6 cm with FiO2
ranging from 0.35-0.60 with O2 sats 82-98%. There are 3 A’s and B’s recorded for the
past 24 hours, one which required vigorous stimulation to reverse. On exam this AM,
you note that she is arousable and cries with abdominal palpation. There are few, if any,
BS present. Lungs have the “usual” fine crackles throughout, and there is no murmur.
The remainder of the exam is unchanged from previous exams. Morning labs are still
pending, but the blood culture report shows “budding yeast”. CSF and gram stain is
negative so far. KUB this AM shows a gasless abdomen.
17. Discuss the significance of the above events, the PE, X-ray findings, and the lab results.
Preterm infants at 30-32 weeks postconceptual age have increased risks for necrotizing
enterocolitis (Gomella et al, 2013). Baby Hill is a former 23 week, chronic lung infant who is now
32 weeks. Her age and contributing factors of chronic lung disease place her at an increased
susceptibility to NEC.
Although premature, Baby Hill’s course was relatively stable. Initial warning signs of illness
presented as increased events of A/B episodes, abdominal tenderness and feeding intolerance.
First, worsening A/B episodes indicate a change in status, possibly sepsis. The development of
CASE STUDY 1: NNP II
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bilious residuals with abdominal distention and discomfort indicate feeding intolerance.
Decreased bowel sounds indicate decreased perfusion to the gut, as well as altered
functionality.
This am, Baby Hill’s assessment along with xray studies provided progressive worsening
bowel disease. Initial worrisome films include visible and dilated bowel loops. Normal KUB
should reveal gas patterns, however the presence of dilation indicates a change in abdominal
status. Furthermore, Baby Hills abdominal xray continued to progressively worsening by
displaying a gasless pattern. Abnormal gas patterns visualized on abdominal xrays are
supportive findings of NEC (Gomella et al, 2013).
Pending morning labs may either show an increased or decreased WBC, decreased platelet
level and a left shift. These laboratory values may provide clues to whether NEC was a result of
bacterial infection. Blood culture with budding yeast suggests a systemic candida infection.
Negative CSF and gram stain indicate that the infection has not reached the meninges, and
therefore has not crossed the blood brain barrier to suggest meningitis.
18. Discuss your differential diagnosis and plan of care at this point.
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Former 23 week, now 32 week female infant AGA DOL 63
Chronic Lung disease
Apnea of prematurity
Necrotizing entercolitis
Confirmed Candida Sepsis
The culture ID comes back the later that afternoon as C. parapsilosis in the blood. CSF
remains no growth thus far.
19. Briefly discuss the etiology, risk factors, and usual treatment for fungal infections.
Etiology
Risk factors for obtaining C. parapsilosis in the blood are extreme prematurity, colonization
with candida, the use of more than 2 or long duration of antibiotic therapy, long term parenteral
nutrition(>5 days) or lipid administration (>7 days), invasive indwelling catheters or extended
NICU stay (Chow, Linden & Bliss, 2012). As pertains to antibiotic therapy, the use of third
generation cephalosporins place the infant at increased risk for C. parapsilosis (Chow, Linden &
Bliss, 2012).
With long term antibiotic therapy, the use of Diflucan is used to prevent Candida infections in
the neonate. Diflucan is a potent fungistatic medication, however it is most effective against C.
albanis, rather than C. parapsilosis. For Candidad prophylaxis, 3-6 mg/kg/dose IV infusion twice
weekly is administered to extremely low birth weight infants who are at a high risk for fungal
infection (Gomella et al, 2013).
Antifungal medication for treatment of C. parapsilosis is the use of caspofungin.
Caspofungin is a fungicidal agent that acts by inhibiting synthesis of the cell wall. Caspofungin is
particularly effective against invasive organisms or those who have been resistant to other
antifungal agents. Preterm infants should receive 2 mg/kg/dose IV q 24 hours over at least one
CASE STUDY 1: NNP II
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hour. Length of therapy should consist of 14 days from the last positive blood culture result
(Gomella et al, 2013).
Final efforts for antifungal treatment include the use of Amphotericin B. Amphotericin B is an
antifungal agent that acts by disrupting the fungal membrane. Its broad spectrum properties
allow for activity against Candida and other fungal infections (Gomella et al, 2013). Initial dose is
0.5 mg/kg iver 2-6 hours and maintence administration is 1-1.5 mg/kg IV q 24 hours for 2-6
weeks or longer. Continued monitoring of electrolytes, renal function tests, CBC and liver panel
are necessary due to the drugs toxic nature (Gomella et al, 2013).
Sarah Jane is now on day #14 of the treatment for C. parapsilosis that you prescribed
above. She again develops increasing A’s and B’s. Blood cultures X2 are drawn and a
cathed urine specimen is obtained with some difficulty, there is only enough urine for a
culture. A bagged specimen was sent for routine U/A, which showed: “yellow, clear. pH
6.5, Sp gr 1.025; 3-5 WBCs and 2-3 RBCs; few hyaline casts.”
20. Discuss your plan of care at this point, giving rationales.
Our plan of care will be guided at treatment of a urinary tract infection (UTI). Presenting
factors of UTIs include respiratory distress with A/B episodes, and nonspecific findings include
lethargy, irritability and poor feeding (Gomella et al, 2013). Obtaining and following urine culture
results will indicate if the infant has current UTI. Blood cultures will monitor if the infection has
become systemic. Additionally we will order a CBC, CRP. Consideration of a lumbar puncture
will be necessary if the blood cultures have a positive result.
The urine analysis results report normal color, pH and specific gravity. Small WBC and RBC
indicate the presence of either urinary tract or kidney infection. The few hyaline casts present in
her urinary sample are normal. Treatment for the suspected UTI is warranted due to WBC/RBC
presence. Broad spectrum antibiotic treatment is indicated until the urine culture identifies a
bacteria.
That afternoon, the urine culture is reported as growing “gram-negative rods in pairs”.
21. Giving rationales for each, discuss your:
a. differential diagnosis at this point



Former 23 week, now 34 week female infant AGA DOL 77
Urinary tract Infection with E coli. as indicated by the presence of gram-negative rods
in pairs in the urine culture.
Confirmed candida sepsis: Continuing treatment, no on Day 14 of treatment.
b.
plan of care, including pharmacotherapeutics and further diagnostic w/u, if
warranted.
Further lab work
 CBC now and in am x 2
 CRP now and in am x 2
 BMP now (to identify pyelonephritis)
 Renal function studies now
 Electrolytes now
 Blood sugar now
CASE STUDY 1: NNP II

13
Monitor blood cultures and obtain LP if blood culture negative
Antibiotic therapy



Begin Gentamycin for gram negative coverage: 4 mg/kg/dose IV q 24 hours
Begin Cefotaxime (third generation cephalosporin with bactericidal activity
against gram negative organisms including E.Coli) 100 mg/kg/day divided q 6-8
hours for 7-10 days.
Begin Cefoxitin (second generation cephalosporin for gram negative enteric
organisms including E.coli) 100 mg/kg/day divided q 6-8 hours for 7-10 days.
Case Study #4: [16 points]
Johnny Fields was delivered by emergency cesarean section; Apgar scores were 7/8 at
1/5 minutes respectively. Birth weight 834 grams, ~26 weeks gestation on exam. Initially
Johnny was dried, stimulated, and suctioned orally. He developed increased work of
breathing requiring intubation and surfactant administration. On admission to the NICU,
he is noted to be lethargic with only occasional spontaneous respiratory effort,
tachycardic to 190 BPM, with a peripheral BP of 30/20, MAP 24, axillary temp of 35.8 C.
He is cyanotic with poor peripheral perfusion. Umbilical lines are placed, IVFs started at
80 ml/kg. Blood cultures are drawn and he is started on appropriate doses of antibiotics.
A blood glucose of 20 mg/dl is treated with an IV bolus of D10W (2 ml/kg).
22. Identify, per system, possible signs/symptoms of sepsis that Johnny is demonstrating.
 Neurology: lethargy
 Cardiovascular: tachycardic with HR up to 190bpm, peripheral blood pressur of
30/20 with MAP 24, poor perfusion
 Respiratory: Increased WOB requiring surfactant administration, occasional
spontaneous respiratory effort, cyanotic
 GI/FEN: Initial blood sugar of 20 mg/dL
 Other: Axillary temp of 35.8 C
23. What laboratory information do you want to order?
 CBC
 Blood culture
 Blood gas
 Repeat blood glucose 30 minutes after IV bolus of D 10
 Type and screen
The initial CBC shows:
Hemoglobin 15.3 g/dL
Hematocrit 46%
WBCs 5000/mm3
Neutrophils 26%
Bands 22%
Metamyelocytes 1%
Myelocytes 1%
Lymphocytes 40%
Monocytes 10%
nRBCs 20/100 WBCs
Platelet count 149,000/mm3
CASE STUDY 1: NNP II
14
Blood cultures drawn at the time of the sepsis evaluation grew GBS. Subsequent blood
cultures drawn at 24 and 48 hours following the initial culture grew GBS as well. A
lumbar puncture (performed once stable) demonstrated 3 WBC/mm3, normal CSF
chemistries, a negative gram stain, and no growth at 48 hrs. A CXR revealed a white-out
with small lung volumes and the presence of air bronchograms.
24. Calculate Johnny's absolute neutrophil count and his immature to total neutrophil ratio
(I:T).
25. How would you interpret the a) blood culture results; b.) CXR findings; c.) CSF results?
26. Which antibiotics did you order on admission?
27. Based on the above lab results, would you change the antibiotics – why, why not. If so,
to what?
How long do you plan to treat Johnny with antibiotics?
28. What other supportive therapies should Johnny receive? Address all body systems.
Johnny's HUSs obtained during his hospitalization were reportedly normal. He weaned
from the ventilator, doubled his birth weight in 2 months, and was ready for discharge at
3 months post birth. He was discharged to the care of his local pediatrician as well as
the high risk follow-up program.
29. How would you counsel Johnny's parents regarding his prognosis?
Case Study #5: [3 points]
Carlos Villareal is a newborn term infant born to a 22 year old, AB positive, antibody
screen negative, gravida 2 para 2 Hispanic mother via repeat cesarean section at 38
weeks gestation. The infant required blow-by oxygen and positive pressure ventilation
for 30 seconds before spontaneous respirations occurred. Apgar scores were 6 at 1
minute and 7 at five minutes. Birth weight was 2710 grams. On physical examination
heart rate was 178 bpm, respiratory rate 64, temperature 36.9, and blood pressure 58/34
mm Hg. Carlos was pale, not jaundiced, and in moderate respiratory distress. Oxygen
saturation with NC at 1 LPM @ 35% was 98%. The cardiac examination reveals a 2/6
systolic ejection murmur over the lower left sternal border, a liver edge 3.5 cm below the
right costal margin, and decreased pulses. The rest of the physical examination is
normal.
30. Highlight which of the following diagnoses would be consistent with this clinical
picture:
A. Perinatal hypoxic injury
B. Septic shock
C. Acute hemorrhage
D. Congenital heart disease
31. Highlight what your first step would be in Carlos' management:
A. Transfuse with 10mL/kg type O negative PRBCs
B. Obtain a blood gas analysis for acid-base and ventilation status
C. Intubate and provide 100% oxygen
D. Administer prostaglandins
CASE STUDY 1: NNP II
15
A spun hematocrit is determined to be 16% and the CBC has a hematocrit of 14.8%,
hemoglobin 5 g/dL, MCV 94 fL, MCHC 32 g/dL, RDW 21%. Carlos' CBG shows: pH 7.10,
PCO2 32 mm Hg, PO2 41 mm Hg, bicarbonate 8, and base deficit 16. Further maternal
information reveals that Carlos' mother had noted decreased fetal movement during the
last 2 days prior to birth. External monitoring prior to the cesarean section showed a
sinusoidal pattern. There was no evidence of abruption or trauma to the placenta or cord.
32. Which of the following maternal lab tests would you want to order and why?
A. Peat antibody screen
B. Maternal CBC and RBC indices
C. Kleihauer-Betke (KB) test
D. GBS status
E. Maternal LFTs
Case Study #6: [2 points]
Megan Kubiak is a newborn infant born at 34 weeks gestation to a 29 year old Caucasian
mother. Initial CBC shows a hematocrit 28%, hemoglobin 9.1 g/dL, MCV 102 fL, MCHC 33
g/dL, RDW 11%, and peripheral smear shows moderate polychromasia. On examination
Megan appears pale and in moderate respiratory distress. Vital signs reveal: HR 170
bpm, RR 65, BP: 44/33 mm Hg. Cardiac exam is significant for quiet heart sounds, a 2/6
systolic murmur, and equal pulses. Lung sounds are slightly diminished bilaterally.
Abdomen is slightly protuberant with a spleen palpable 1 cm below the left costal margin
and a liver palpable 2 cm below the right costal margin.
33. Highlight which of the following statements are true:
A. This infant has nonimmune hydrops fetalis
B. This infant has immune-mediated hydrops fetalis
C. This infant has evidence of hydrops fetalis
D. Rh hemolytic disease is a common cause of immune-mediated hydrops
E. Tachy arrhythmia can be a cause of nonimmune hydrops fetalis
34. Highlight which of the following you would ask Megan's mother's obstetrician to
order:
A. IgG and IgM for CMV
B. PCR for parvovirus B 19
C. Cervical culture for GBS
D. Rapid plasma reagin and rubella screen
E. Sputum for RSV and influenza
Case Study #7: [5 points]
There is a Rubella outbreak in the community. Mrs. Trevino wants to know if you can give
the MMR immunization early to her 8 month old son.
35. What is rubella?
36. What diagnostic features (history and physical) are associated with rubella?
37. How will you respond to Mrs. Trevino's request?
Case Study #8:
[10 points]
CASE STUDY 1: NNP II
16
Fifteen month old Adelaide Stevens is due to receive a MMR vaccine; however, she
received immune globulin 2 months ago.
38. What is immune globulin?
39. Under what circumstances might Adelaide have received immune globulin?
40. What is MMR and how is it administered?
41. Are the components of this vaccine ever given as separate vaccines?
42. Can Adelaide receive her MMR vaccine today? If not when?
Need to wait 10 months to received MMR vaccine after receiving IVIG.
Case Study #9: [1 point]
Danny Houston was a normal newborn born at tem. For the first six months of life he was
only fed a commercially available infant formula which he tolerated well. At 6 months of
age Danny's mother introduced fruit juices into Danny's diet after which he developed
jaundice, hepatomegaly, vomiting, lethargy, irritability, and seizures. Tests for reducing
substances were positive.
43. Highlight which of the following likely explains Danny's condition:
A. Tyrosinosis
B. Galactosemia
C. Fructosemia
D. Alpha -1 - antitrypsin
E. Glucose -6-phosphatase deficiency
Case Study #10: [10 points]
On a routine screen, 2 week old Mia Harden is noted to have sickle cell disease (SCD).
44. How would you confirm that Mia has SCD?
45. Describe the pathology associated with SCD.
46. What is the inheritance pattern of this disease?
47. What aspects of Mia's physical exam would be important to include and note in your
findings?
Provide rationale
48. What lab work would you order to establish a baseline for future comparison?
Provide
rationale
49. Would you recommend that Mia's parents start her on folic acid? If so why?
50. Would you recommend starting Mia on an antibiotic for prophylaxis? If so, why? If so,
what
antibiotic, what dose, how often?
CASE STUDY 1: NNP II
17
References
Chow, B. D., Linden, J. R., & Bliss, J. M. (2012). Candida parapsilosis and the neonate:
epidemiology, virulence and host defense in a unique patient setting. Expert Review of
Anti- Infective Therapy 10(8), 935-46. Doi: 10.1586/eri.12.74.
Diehl-Jones, W. & Askin, D. F. (2010). Hematologic disorders. In M. T. Verklan, & M. Walden
(Eds.), Core Curriculum for Neonatal Intensive Care Nursing (4th ed., pp. 91-109). St.
Louis, MO: Saunders Elsevier.
Genetics Home Reference a.(2014). F5. Retrieved from http://ghr.nlm.nih.gov/gene/F5
Genetics Home Reference b. (2014). F8. Retrieved from http://ghr.nlm.nih.gov/gene/F8
Gomella, T. L, Cunningham, M. D. & Eyal, F. G. (2013). Neonatology: Management,
procedures, on-call problems, diseases and drugs (7th Ed.). New York: McGraw
Hill Education
Lott, J. W. (2010). Imunnology and infectious disease. In M. T. Verklan, & M. Walden (Eds.),
Core Curriculum for Neonatal Intensive Care Nursing (4th ed., pp. 91-109). St. Louis,
MO: Saunders Elsevier.
Luchtman-Jones, L., Schwartz, A. L. & Wilson, D. B (2011). The blood and hematopoietic
system. In R. J. Martin, A. A. Fanaroff, & M. C. Walsh (Eds.), Neonatal-Perinatal
Medicine: Diseases of the fetus and infant (9th ed., pp.1287- 1356). Philadelphia: PA:
Mosby Elsevier.
Pappas, B. E., & Walker, B. (2010). Neonatal delivery room resuscitation. In M. T. Verklan, &
M. Walden (Eds.), Core Curriculum for Neonatal Intensive Care Nursing (4th ed., pp.
91-109). St. Louis, MO: Saunders Elsevier.
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Stokowski, L. A. (2011). Fundamentals of phototherarpy for neonatal jaundice. Advances in
Neonatal Care, 11(5s), 10-21. http://dx.doi.org/10.1097/ANC.0b013e31822ee62c
Wong, R. J., & DeSandre, G.H., Sibley, E., & Stevenson, D. K. (2011). Neonatal jaundice and
liver disease. In R. J. Martin, A. A. Fanaroff, & M. C. Walsh (Eds.), Neonatal-Perinatal
Medicine: Diseases of the fetus and infant (9th ed., pp. 1419-1465). Philadelphia: PA:
Mosby Elsevier.