NICU HR Flashcards

1
Q

Which infants to screen for ROP? When to screen?

A
  • GA <30+6 OR BW < 1250g
  • For >26+6: At 4 weeks
  • For <26+6: At 31 weeks
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2
Q

Broadly, what is ROP?

A

Proliferative disorder of developing retinal blood vessels

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3
Q

Risk factors for ROP?

A
  • Hypotension
  • Prolonged ventilation
  • Oxygen therapy
  • Slow postnatal growth
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4
Q

Which patients to treat for ROP?

A
  • Type 1 ROP:
  • -Zone I - any stage ROP with plus disease as well as stage 3 ROP without plus disease
  • -Zone II - stage 2 or 3 ROP with plus disease
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5
Q

Which patients to monitor closely for ROP?

A
  • Type 2 ROP:
  • -Zone 1 - stage 1 or 2 ROP without plus disease
  • -Zone 2 - stage 3 ROP without plus diseaase
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6
Q

Treatment for ROP?

A
  • Laser photocoagulation
  • -within 72h of Type I ROP
  • Antivascular endothelial growth factor
  • -Proven in Zone 1
  • -Possible risk of delayed ROP
  • -Informed consent
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7
Q

Most common locations for NEC?

A

Terminal ileum, sigmoid colon

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8
Q

Diagnosis? Clinical features?

A
  • Gold standard - pathology
  • Clinical features: Lethargy, apnea, temp instability, bile-stained aspirates, abdominal distension, blood/mucous per rectum, shock
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9
Q

Risk factors for NEC?

A
  • Prematurity
  • Ischemia (asphyxia, CHD, PDA, severe IUGR, exchange transfusions)
  • Complication Hirshsprungs
  • Infectioin
  • Feeding (breast milk is protective)
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10
Q

Treatment for NEC?

A
  • Supportive
  • NPO
  • NG decompression
  • Antibiotics
  • +/- Surgery
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11
Q

Longterm complications of NEC?

A

-Short gut (surgical), stenosis/obstruction, recurrence

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12
Q

Criteria for safe discharge prem?

A
  • Physiologic maturity
  • -Thermoregulation (around 1700g to cot)
  • -Control of breathing (Spell free period off caffeine: 5-7days at least)
  • -Respiratory stability (25% of <1500g inifants on O2 at 36weeks cGA; Targe sats 90-95%)
  • -Feeding skills and weight gain
  • –Cue based feeding: earlier to full feeds, decreased length of stay
  • –Iron 2mg/kg/day, Vitamin D 400-1000 IU supplements
  • –GERD: little evidence of association with pathology
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13
Q

Considerations for investigations/treatment prior to discharge from NICU?

A
  • Assessment for RSV prophylaxis
  • Cranial imaging at near-term, if indicated by GA
  • ROP screening, if indicated
  • Immunizations according to chronological age
  • Pre discharge P/E: Weight, length and HC
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14
Q

Indications for therapeutic hypothermia?

A

Indications: (≥35-36 weeks)
Criteria A or B AND C
A. Cord pH≤7 or BD≥ -16or
B. pH 7.01 – 7.15 of -10 to -16 (cord
or 1 hour gas) AND Hx of acute perinatal event AND APGAR ≤ 5 at 10m or at least 10m of PPV
C. Signs of moderate to severe encephalopathy

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15
Q

Timing for therapeutic hypothermia?

A

ASAP, within 1st 6 hours

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16
Q

Complications of therapeutic hypothermia?

A
  • Hypotension
  • Bradycardia
  • Coagulopathy
  • PPHN
  • Fat necrosis
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17
Q

DDx for neonatal seizures?

A
  • HIE (term)
  • IVH (preterm)
  • Metabolic/IEM (intractable)
  • Stroke
  • Drugs (SSRIs)
  • NAS (opiates, benzos)
  • Infection
  • Brain malformations
  • Benign neonatal seizures (family hx, dx of exclusion)
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18
Q

Which of the following are true?
A. The pattern of injury associated with HIE in term infants including basal ganglia, internal capsule, and cerebellar hemorrhages predicts motor and cognitive outcomes.
B. Neonatal stroke is acutely seen as loss of grey white matter differentiation on MRI followed by eventual volume loss +/- cyst formation after 1 month.
C. In a term infant with encephalopathy a normal T1/T2 MRI at 72 hours rules out metabolic disorders i.e. maple syrup urine disease, non-ketotic hyperglycinemia, or creatine deficiency.
D. MRI is the modality of choice in trauma when detection of bony fractures is a priority.

A

B

19
Q
All of the following are recognized causes of ‘floppy baby’ except:
A. Trisomy 21
B. Zellweger syndrome
C. Becker muscular dystrophy 
D. Spinal muscular atropy
E. Prader Willi syndrome
A

C

20
Q

DDx for “floppy baby”?

A
  • Central/brain: Perinatal depression/HIE
  • Spinal cord: Trauma, stenosis
  • Anterior horn cell: SMA, face-sparing
  • Nerve root: Brachial plexus injury
  • NMJ: Myasthenia gravis (transient)
  • Muscle: Congenital muscular dystrophy (AR), congenital myotonic dystrophy (mother affected)
  • Genetic: Trisomy 21, Prader Willi
21
Q

Which of the following is true?
A. Erb’s palsy involves C6, C7, & C8
B. Klumpke’s palsy involves C7, C8, & T1
C. Facial nerve palsy–>persistently closed eye
D. In full nerve injury, neuroplasty is advised at the end of the first year of life

A

B

22
Q

Nerves in Erb Palsy? Clinical picture? Prognosis?

A
  • Upper/middle, C5, 6, 7
  • Waiter’s tip
  • Favourable - wach for phrenic n. (respiratory distress)
  • 75% recover completely in first month, if not, refer to brachial plexus team
23
Q

Nerves in Klumpke’s palsy? Clinical picture? Prognosis?

A
  • Lower C8-T1
  • Claw hand
  • Rare
  • Favourable
  • 75% recover completely in first month, if not, refer to brachial plexus team
24
Q

Nerves in flail arm? Clinical picture? Prognosis?

A
  • Complete C5-T1
  • Often associated with Horner’s syndrome
  • Less favourable prognosis
25
Q

On day 1 of life, you are managing a 39 week infant with APGARS 3, 8. Growth parameters: Weight 2.1kg and HC 34cm. Current fluids at 10 hours of age are D12.5W at 100ml/kg/day. Serum glucose is now 1.8.
What is the baby’s glucose infusion rate and what is the likely physiologic diagnosis?
A. GIR: 8-9 mg/kg/min; Diagnosis: inborn error of glucose metabolism
B. GIR 5-6 mg/kg/min; Diagnosis: inborn error of glucose metabolism
C. GIR 8-9mg/kg/min; Diagnosis: hyperinsulinism
D. GIR 5-6 mg/kg/min; Diagnosis: hyperinsulinism

A

C

26
Q

Formula for calculating GIR?

A

(IV rate (ml/kg/day) x % of dextrose)/144

27
Q

A 1 week old male presenting to the emergency department with normal HR, BP, and saturations, but altered level of consciousness and acidosis.
What additional test should be included in the initial evaluation to help make the diagnosis and guide treatment?
A. Cortisol level
B. Serum ketones
C. Thyroid function test
D. Ammonia level

A

D

28
Q

Clinical features suggestivec of IEM in newborn?

A
  • Signs/symptoms
  • -Encephalopathy
  • -Seizures
  • -Cardiomyopathy
  • -Liver, GI (vomiting)
  • -Eye (cataracts, retina)
  • -Neonatal hydrops
  • -Dysmorphic features
  • Lab abnormalitties
  • -Hypoglycemia
  • -Acidosis
  • -Hyperammonemia
  • -Hyperbilirubinemia (prolonged/late)
29
Q

Constellation of lab findings for urea cycle defect? Organic acidemias? Galactosemia?

A
  • Urea cycle defect: Normal gas - high ammonia
  • Organic acidemias: Acidotic +/- high ammonia
  • Galactosemia: Low glucose, normal BG, normal ammonia
30
Q

Red flags for jaundice? Investigations?

A
  • Onset before 24h
  • Pallor, unwell
  • HSM
  • Pale stools, dark urine
  • Conjugated
  • Hemolysis = predictor of severity

-Total and conjugated bili
-CBC, blood group, DAT
+/- G6PD, blood film
-Liver function, metabolic/endocrine work up, MRI if signs of acute encephalopathy

31
Q

Clinical signs of acute bilirubin encephalopathy? Management?

A

– Lethargy, decreased tone & suck
– Increased tone, opisthoclonus, retrocollis
– High pitched cry, seizure, coma
– MRI: increased T1 signal globus pallidus & subthalamic nuclei (low predictive value / high false-positives)

-Mgmt: Immediate exchange transfusion

32
Q

Clinical features of chronic bilirubin encephalopathy?

A
– Athetoid CP
-Seizures
-DD/MR
-hearing
-oculomotor
-dental
dysplasia
33
Q

Baby M is a 37+2 week infant, born to an A positive mother, following a normal pregnancy. At 24 hours total bilirubin is 135. She is feeding well, and mother is ready for discharge. Which of the following are most appropriate?
A. Routine care, discharge home to follow up with family physician within 48 hours
B. Discharge home to return for a bilirubin check in the postnatal clinic in 24 hours
C. Keep in hospital and recheck bilirubin in 24 hours
D. Start phototherapy and recheck bilirubin in 24 hours

A

B

34
Q

You are paged by a family physician in the community about a baby with a bilirubin level of 350. Baby was born at 36+6 weeks and is now 96 hours old. Birth weight was 3100g and current weight is 3000g. GBS positive in previous pregnancy, and blood type O. Baby is exclusively breastfeeding.
Which of the following is the correct next step?
A. Perform a full septic workup including LP (this is significant jaundice with risk factors for sepsis)
B. Send a CBC and coombs test now
C. Start phototherapy and recheck bilirubin in 12 hours with a CBC and coombs test
D. Baby is older now, the risk of kernicterus is much lower than in the first 24 hours, if she is feeding well, with good hydration, can repeat in 24 hours

A

B - need to know which line to use

35
Q

A 34 week infant was born to an A negative mother with anti-D antibodies. Maternal titers were up to 1:256 in the pregnancy.
Cord hemoglobin was 90, with a bilirubin of 130. His jaundice and hemolysis were treated appropriately. On day 4 of life, he develops feeding intolerance and abdominal distension.
These GI symptoms are most likely due to:
A. Acquired sepsis from multiple blood product exposure and invasive lines
B. Portal vein thrombosis secondary to invasive catheters causing portal hypertension and ascites
C. Necrotizing enterocolitis secondary to ischemia/bowel hypoperfusion as a result of anemia or exchange transfusion
D. An inborn error of metabolism, causing neonatal hepatitis, jaundice, and hyperammonemia

A

C

36
Q
Question: jaundice
All of the following are usually associated with congenital hypothyroidism except:
A. Prolonged jaundice
B. Umbilical hernia
C. Small anterior fontanelle
D. Hypotonia
A

C

37
Q

Causes of neonatal anemia? What investigations to do? Treatment?

A

– Physiologic anemia (HbF)
– Anemia of prematurity
– Hemorrhage (feto-maternal, Twin-twin, internal)
– Hemolysis
• Immune (Coombs +) Rh, ABO, Minor blood groups, maternal autoimmune (SLE)
• Non-immune (Coombs -) DIC, infection, G6PD, pyruvate kinase deficiency, hereditary spherocytosis, alpha-thal

-CBC, Hb, Hct, blood groups, coagulation studies – Kleihauer test on maternal blood (for fetal Hb)

• Treatment
– Transfusion (single vs. exchange), IVIG (immune)
– Monitor CBC, jaundice

38
Q

Transfusion thresholds for resp support vs no resp support based on postnatal age? How is resp support defined?

A

Resp support:
Week 1 - 115
Week 2 - 100
Week 3 and older - 85

No resp support:
Week 1 - 100
Week 2 - 85
Week 3 and older - 75

Resp support: Inspired O2 requirement in excess of 25% or need for mechanical increase in airway preessure

39
Q

Definition of hydrops fetalis? Causes?

A

• Definition:
– Fluid in 2 or more fetal compartments

• Causes
– Immune:
• hemolytic disease of the newborn
– Non-immune:
• Chronic anemia (alpha-thal)
• Cardiac failure
• Renal disease
• TORCH – CMV (send pleural fluid)
• Congenital malformations,
• Genetic syndromes (Trisomies 21,18,13, Turner, Noonan)
40
Q

Which statement is correct regarding Neonatal Alloimmune Thrombocytopenia?
A. Mother is often also thrombocytopenic
B. Risk of intracranial hemorrhage highest during first 96 hours
C. IVIG is not an effective treatment
D. Expect a higher platelet count than in autoimmune thrombocytopenia

A

B

41
Q

Causes of neonatal thrombocytopenia? Treatment?

A

– Infection: bacterial, TORCH
– Neonatal alloimmune thrombocytopenia
– Other maternal causes
• toxemia, ITP, SLE, Drugs (hydralazine, thiazides)
– Consumption: DIC, Kassabach-Merrit (hemangioma) – Syndromes: IUGR, TAR, Fanconi’s
– Bone marrow suppression: pancytopenia, leukemia

Treatment:
– Transfusion if platelets < 20-30 or bleeding or procedures
– NAIT – IVIG, maternal washed or antigen negative platelets, follow-up CBCs
– Consider brain imaging (r/o ICH)

42
Q

You are caring for twins with an antenatal history of moderate (stage III) twin-twin transfusion syndrome.
Twin A had a hematocrit of .75, Twin B had a Hct .30. Which of the following is true?
A. Twin A had a history of oligohydramnios
B. Twin A is at increased risk of congenital heart disease
C. Twin B’s bladder was visualized antenatally
D. Twin B will require an partial exchange transfusion with saline

A

B

43
Q

Clinical features of polycythemia? Management?

A
• Clinical features
– Hyperviscosity S&amp;S
• CNS: apnea, lethargy, tremors, irritability, sz 
• Renal: RVT, decreased GFR, oliguria
• Cardiopulm: PPHN
• GI: NEC
– Other: acidosis, hypoxia, thrombocytopenia
– Hyperbilirubinemia
– Hypoglycemia

• Treatment:
– Measure central Hct (venous/arterial)
– Hct > 75% repeated or symptomatic – partial exchange transfusion (controversial – rarely done)
– Volume = (actual – desired Hct) x wt (kg) x 90 actual Hct