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Neonatology Flashcards

1
Q

What is the newborn period defined as?

A

First 28 days of life

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2
Q

Key components of newborn medical history?

A
  1. Parents medical/genetic hx
  2. Maternal past obstretic hx
  3. Current antepartum and intrapartum obstretic hx
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3
Q

What is the Apgar score?

A

Infant evaluation at birth (0 is not good, 2 is good)

  • HR
  • Respiratory effort
  • Muscle tone
  • Response to catheter in nostril
  • Color
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4
Q

Describe circumcision’s place in medicine

A

Elective procedure to be performed only in healthy, stable infants

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5
Q

Medical benefits of circumcision

A
  • Prevention of phimosis, paraphimosis, balanoposthitis, UTI

- Later benefits: decreased penile cancer, STIs

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6
Q

Risks of circumcision

A
  • Local infection
  • Bleeding
  • Removal of too much skin
  • Urethral injury
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7
Q

What circumcision techniques are preferred?

A

Ones that allow visualization (Plastibell and Gomco clamps) preferred over blind techniques (Mogen clamp)

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8
Q

Mogen clamp use in circumcision

A
  • Blind technique
  • Not preferred
  • Risk of glans amputation
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9
Q

Contraindications to circumcision

A

Infants with genital abnormalities (e.g. hypospadia)

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10
Q

How are newborns screened for hearing abnormalities?

A

Universal screening with auditory brainstem recording

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11
Q

General causes of pathologic unconjugated hyperbilirubinemia

A
  • Overproduction of bilirubin (either hemolytic or nonhemolytic)
  • Decreased rate of conjugation
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12
Q

What are the hemolytic causes of increased bilirubin production?

A
  • Immune mediated (positive Coombs)
  • Nonimmune (negative Coombs)
  • Bacterial or viral sepsis
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13
Q

How to tell if the overproduction of bilirubin is hemolytic or nonhemolytic?

A
  • Hemolytic causes will have an increased retic count

- Nonhemolytic causes will have normal retic count

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14
Q

Nonhemolytic causes of increased bilirubin production?

A
  • Extravascular hemorrhage (cephalohematoma)
  • Polycythemia
  • Exaggerated enterohepatic circulation (bowel obstruction)
  • Breast feeding associated jaundice (inadequate intake)
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15
Q

Main causes of decreased rate of bilirubin conjugation

A
  1. Crigler-Najjar syndrome (rare and severe)
  2. Gilbert syndrome (common, milder)
  3. Hypothyroidism (maybe?)
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16
Q

What is MC: Crigler-Najjar or Gilbert syndrome?

A

Gilbert syndrome

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17
Q

What do Crigler-Najjar and Gilbert syndromes cause?

A

Decreased rate of bilirubin conjugation

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18
Q

What is kernicterus? What is it characterized by?

A

Chronic bilirubin encephalopathy of the neonatal period

  • Extrapyramidal movement disorder
  • Gaze abnormality
  • Auditory disturbances
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19
Q

What is considered neonatal hypoglycemia?

A

Blood glucose under 45 mg/dL

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20
Q

Clinical presentation of hypoglycemia in infants

A
  • May be asymptomatic

- Lethargy, poor feeding, irritability, seizures

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21
Q

Which infants are at risk for hypoglycemia?

A
  • Large for gestational age (LGA)
  • Small for gestational age (SGA)
  • Preterm
  • Stressed
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22
Q

Clinical presentation of respiratory distress in a term infant

A
  • Tachypnea (RR over 60)
  • Intercostal and sternal retractions
  • Expiratory grunting
  • Cyanosis in room air
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23
Q

Describe neonatal murmurs

A

Heart murmurs are common in the first days of life and do not usually signify structural heart problems

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24
Q

What does a murmur present at birth indicate?

A

A valvular problem

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25
Q

What is recommended to identify congenital heart disease in newborns?

A

Pulse ox prior to discharge (anything under 95% at sea level needs echo)

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26
Q

MC birth injuries?

A
  • Soft tissue bruising
  • Fractures (clavicle, humerus, femur)
  • Cervical plexus palsies
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27
Q

Features observed in fetal alcohol syndrome

A
  • Short palpebral fissures
  • Thin vermillion of upper lip
  • Pre and postnatal growth deficiency
  • Microcephaly
  • Optic nerve hypoplasia
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28
Q

Why have multiple births increased in the US?

A

Assisted reproductive technologies

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29
Q

What type of twins are more at risk for twin-twin transfusion syndrome and congenital anomalies?

A

Monochorial (identical)

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30
Q

What is twin to twin transfusion syndrome?

A
  • Disease of the placenta that affects identical twins

- Disproportionate blood supply

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31
Q

When can intrauterine growth restriction start in twins?

A

32 weeks

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32
Q

When can intrauterine growth restriction start in triplets?

A

26-27 weeks

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33
Q

Cerebral palsy is MC in what type of twins?

A

Monochorial (identical)

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34
Q

How does the length of gestation relate to multiple births?

A

More fetuses typically results in shorter gestation period

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35
Q

What are potential obstretic complications in multiple births?

A
  • Polyhydramnios
  • Pregnancy induced HTN
  • PROM
  • Abnormal fetal presentations
  • Prolapsed umbilical cord
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36
Q

When asphyxia occurs at birth, what best predicts neurologic outcome (risk of CP)?

A

10 min Apgar score (better predictor than the 5 min score)

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37
Q

What is the MC cause of respiratory distress in preterm infants?

A

Hyaline membrane disease (RDS type 1)

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38
Q

Describe hyaline membrane disease (RDS type 1)

A
  • Surfactant deficiency in alveoli (in production and inactivation due to protein leak)
  • MC cause of resp distress in preterm infants
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39
Q

CXR findings of hyaline membrane disease

A
  • Hypoaerated
  • Air bronchograms
  • Ground glass (reticulogranular)
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40
Q

Describe transient tachypnea of the newborn (RDS type 2) including how to treat

A
  • AKA retained fetal lung fluid
  • A/w precipitous or C-section without labor
  • O2 support w/resolution usually in 12-24 hrs
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41
Q

What is bronchopulmonary dysplasia?

A
  • Major sequelae of neonatal respiratory distress
  • Used to be MC in premies that required prolonged mechanical ventilation
  • Less severe now bc of surfactant, prenatal glucocorticoids, revised ventilation strategies
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42
Q

What is the pathology of bronchopulmonary dysplasia?

A

Inflammation, hypercellularity then fibrosis

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43
Q

Risk factors for bronchopulmonary dysplasia

A
  • Oxygen required over 28 days
  • History of PPV or CPAP
  • Premature gestational age
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44
Q

What reduces the risk of bronchopulmonary dysplasia in newborns?

A

Early use of surfactant

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45
Q

Signs of PDA?

A
  • Hyperdynamic precordium
  • Widened pulse pressure
  • Hypotension
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46
Q

When does PDA usually present in a newborn?

A

Days 3-7 as the respiratory distress from hyaline membrane disease (HMD) is improving

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47
Q

Treatment of PDA

A
  • Medical ligation (initially effective in 2/3 pts, indomethacin)
  • Surgical ligation if indomethacin fails (mortality of 1-10%)
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48
Q

What is the MC acquired GI emergency in the newborn?

A

Necrotizing enterocolitis (NEC)

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49
Q

Risk factors for NEC

A
  • Preterm infants

- Full term infants with polycythemia, congenital heart disease, birth asphyxia

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50
Q

Signs of NEC

A
  • Feeding intolerance w/gastric residuals
  • Vomiting
  • Bloody stools
  • Abd distention/tenderness
  • Pneumatosis intestinalis on KUB
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51
Q

Symptoms of anemia in infants

A
  • Poor feeding
  • Lethargy
  • Tachycardia
  • Poor weight gain
  • Periodic breathing (?)
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52
Q

What to know about treatment of an asymptomatic infant with low hematocrit?

A

Transfusion is NOT indicated

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53
Q

Clinical presentation of intraventricular hemorrhages in infants?

A
  • Small bleeds can be asymp

- Larger cause hypotension, metabolic acidosis, altered neuro status

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54
Q

Periventricular-intraventricular hemorrhage occurs almost exclusively in _____

A

Premature infants (20-30% in infants under 31 weeks EGA and under 1500 g)

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55
Q

Describe an intraventricular hemorrhage

A

Ischemia with reperfusion injury to the capillaries in the germinal matrix in the immediate perinatal period

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56
Q

CNS complications a/w an intraventricular hemorrhage are MC in which pts?

A

Preterm infants exposed antenatally to intrauterine infection

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57
Q

Describe retinopathy of prematurity (ROP)

A

Occurs only in the incompletely vascularized premature retina

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58
Q

Describe the risk of severe ROP

A

Inversely proportional to gestational age

59
Q

How is ROP graded?

A

Stages of abnormal vascular development and retinal detachment

60
Q

Rate of preterm births in the US?

A

Increased over 30% in the past 30 years

61
Q

Which type of preterm births have increased the most in the US?

A

Late preterm births (34 0/7 to 36 6/7 weeks EGA)

62
Q

How do cyanotic congenital heart defects present in newborns?

A
  • Cyanosis (initially w/o associated resp distress)
  • Failure to increase PaO2 w/supplemental O2
  • Decreased lung markings on CXR suggests R heart obstruction
63
Q

What CXR finding suggests right heart obstruction?

A

Decreased lung markings

64
Q

What are the cyanotic congenital heart defects?

A
  1. Truncus arteriosus
  2. Transposition of great vessels
  3. Tricuspid atresia
  4. Tetralogy of Fallot
  5. Total anomalous pulm venous return
65
Q

Describe acyanotic heart disease in newborns

A
  • Most have L sided outflow obstruction

- Metabolic acidemia

66
Q

CXR findings of acyanotic heart disease in newborns

A

Large heart and pulmonary edema

67
Q

Describe persistent pulmonary hypertension

A
  • Newborn with some pulm condition (aspiration of meconium, pneumonia)
  • Pulm vascular resistance does NOT decrease
  • This leads to hypoxia with poor response to high concentrations of inspired oxygen
68
Q

What is persistent fetal circulation most often associated with?

A

Parenchymal lung disease

69
Q

Which infants are MC affected by persistent fetal circulation?

A

Full term or postterm

70
Q

Treatment goals of persistent fetal circulation

A
  • Increase systemic arterial pressure

- Decrease pulm arterial pressure to reverse the R-L shunt

71
Q

Treatment of persistent fetal circulation

A
  • Oxygen/ventilation and crystalloid infusions (1st)
  • Systemic pressors if compromised cardiac function (2nd line)
  • Correction of metabolic acidemia
72
Q

Why does metabolic acidemia need to be corrected in persistent fetal circulation?

A

Acidemia exacerbates pulmonary vasoconstriction

73
Q

If conventional therapy fails, what should be used as treatment for persistent fetal circulation?

A

Extracorporeal membrane oxygenation (ECMO) - lungs put at rest

74
Q

Complications of persistent fetal circulation

A

10-15% will develop neuro sequelae:

  • Cerebral palsy or cognitive delays
  • Chronic lung disease, sensorineural hearing loss, feeding problems (all less common)
75
Q

MC arrhythmias seen in newborns?

A

PACs (less often PVCs)

76
Q

Describe PACs in newborns

A
  • Irregularly irregular
  • Common during 1st few days of life
  • Benign and resolve within 1st week
77
Q

Treatment of tachyarrhythmias in newborns?

A
  • Ice to the face (vagal)
  • IV adenosine
  • Long term therapy is digoxin or propranolol
78
Q

Describe intestinal atresia in newborns. How is it diagnosed? What can cause it?

A
  • Narrowing or absence of a portion of intestine
  • Surgical emergency!
  • Often diagnosed prenatally by US
  • Can be caused by polyhydramnios
79
Q

X-ray findings of intestinal atresia

A

Double bubble

80
Q

Clinical presentation of intestinal atresia

A

Bilious (green, yellow) vomiting and distention soon after birth

81
Q

What do most cases of intestinal atresia present with?

A

Other congenital anomalies (54% of cases)

82
Q

Treatment of intestinal atresia

A

Duodenoduodenostomy

83
Q

Clinical presentation of intestinal malrotation

A
  • Usually present in first 3 wks of life with bilious vomiting
  • Later presentations may be undiagnosed (intermittent obstruction, malabsorption, diarrhea)
84
Q

Imaging of intestinal malrotation

A
  • Plain film (double bubble or just no distal gas)
  • UGI (gold standard, 96% sensitive)
  • Barium enema for confirmation (to locate cecum)
85
Q

What is the gold standard imaging for intestinal malrotation?

A

UGI - 96% sensitive

86
Q

What is the Ladd procedure?

A
  • Treatment of intestinal malrotation
  • Duodenum mobilized
  • Mesenteric root extended
  • Bowel fixed in more normal layout
87
Q

Treatment of intestinal malrotation

A

Ladd procedure

88
Q

Describe cystic fibrosis

A
  • Autosomal recessive
  • 1 in 40 people are carriers
  • Causes defects in water and salt movement leading to thick secretions
89
Q

Effects of CF on lungs, GI, and male reproductive?

A
  • Lungs: mucus plugging, poor clearance
  • GI: meconium ileus, pancreatic insufficiency
  • Male infertility
90
Q

Clinical presentation of CF in infants

A
  • Meconium ileus (15% pts)
  • Failure to thrive (FTT) with good appetite and frequent stools
  • Chronic airway infections start in 1st year leading to bronchiectasis
91
Q

Describe Hirschsprung disease

A
  • Congenital megacolon

- Absence of ganglion cells in colon

92
Q

Clinical presentation of Hirschsprung disease

A
  • Colonic muscles fail to relax in front of advancing bolus
  • Vomiting, distention, failure to pass meconium
  • Toxic megacolon in 50% pts (enterocolitis w/fever, explosive diarrhea)
93
Q

Diagnosis of Hirschsprung disease

A

Unprepped barium enema

-Shows distinct transition point between narrow distal and dilated proximal colon

94
Q

Treatment of Hirschsprung disease

A

Surgical resection with diversion or pull through

95
Q

What is an omphalocele?

A
  • Abdominal wall defect

- Membrane covered herniation of abd contents into base of umbilical cord

96
Q

What do most cases of omphalocele present with?

A

Either an abnormal karyotype or an associated syndrome (over 50% cases)

97
Q

What is gastroschisis?

A
  • Abdominal wall defect
  • Uncovered intestine through abdominal wall to the right of umbilical cord
  • NO membrane or sac (like omphalocele)
98
Q

How does gastroschisis differ from omphalocele?

A

Both are abdominal wall defects in newborns, but omphalocele is membrane covered and gastroschisis is UNCOVERED

99
Q

Epidemiology of gastroschisis

A
  • Prevalence increasing worldwide

- Environmental risk factors: illicit drugs (meth, cocaine) and COX inhibitors (ASA, ibuprofen)

100
Q

Treatment of gastroschisis

A
  • Silastic bowel bag to decrease fluid and electrolyte losses
  • Surgery
101
Q

Prognosis of gastroschisis

A

Bowel motility, especially duodenal, may be slow to return

102
Q

Describe congenital diaphragmatic hernia

A
  • Abdominal wall defect
  • Herniation of abd contents through posterolateral defect
  • Failure of diaphragm fusion
  • Bowel blocks space for lungs to grow resulting in lung hypoplasia
  • 80% involve L diaphragm
103
Q

Clinical presentation of congenital diaphragmatic hernia

A
  • Can be found incidentally at autopsy

- Respiratory distress with scaphoid abdomen

104
Q

How to treat congenital diaphragmatic hernia

A

Early intubation WITHOUT bag and mask (this causes bowel to inflate and makes lung function even worse)

105
Q

What should be considered in GI bleeds of newborns?

A

Could be maternal blood (not even from the infant)

106
Q

When is GERD in an infant pathologic and should be treated?

A
  • Failure to thrive
  • Poor intake d/t dysphagia and irritability
  • Apnea or cyanotic episode
  • Wheezing and recurrent PNA
107
Q

How to diagnose GERD in infant?

A

Clinical diagnosis

108
Q

What should be considered in the treatment of GERD in infants?

A

Most antireflux therapies have NOT been studied enough in infants (especially premature)

109
Q

Treatment options for GERD in the infant

A
  • Thickened feeds
  • Gastric acid suppressants
  • Prokinetic agents are of little benefit and have significant side effects
  • Aging (GERD improves w/time)
110
Q

What are the major routes of perinatal infection?

A
  1. Bloodborne transplacental
  2. Disruption of the barrier provided by amniotic membranes allowing infection to ascend
  3. Passage through an infected birth canal or exposure to infected blood at delivery
111
Q

What provides passive protection to a fetus against some infectious organisms?

A

Transfer of IgG across the placenta (particularly during 3rd trimester)

112
Q

Describe early onset sepsis in a newborn including presentation

A
  • First 7 days of life
  • Resp distress MC
  • Hypotension, acidemia, neutropenia
113
Q

Describe late onset sepsis in a newborn

A
  • More subtle than early onset

- Poor feeding, lethargy, hypotonia, temp instability, altered perfusion

114
Q

What increases newborn infection rates?

A
  • ROM over 24 hrs prior to delivery
  • Early rupture w/chorioamnionitis
  • Preterm infant (5 times higher risk)
115
Q

MC pathogens of early onset infection in newborns?

A
  • Group B hemolytic strep (GBS)

- Gram neg enteric (E coli)

116
Q

MC pathogens of late onset sepsis in newborns?

A

Coagulase-negative staph (MC in infants w/indwelling central lines)

117
Q

Treatment of early onset infections in newborns

A

Ampicillin and aminoglycoside (or 3rd generation cephalosporin)

118
Q

Treatment of late onset infections in newborns

A
  • Same coverage as early onset but expanded coverage for staph
  • Vancomycin esp for preterm infants w/indwelling line
119
Q

Describe neonatal meningitis

A
  • Low risk for infant presenting in first 24 hrs
  • Late onset infection is MC
  • MC organisms are GBS and gram negative enteric (E coli)
120
Q

Early onset neonatal infection is usually associated with what?

121
Q

Neonatal pneumonia is usually a/w what type of infection?

A
  • Early onset infection

- May be bacterial OR viral

122
Q

Describe neonatal UTIs

A
  • UNCOMMON in first days of life
  • Can suggest GU anomalies
  • MC Gram negative enteric (E. coli) or Enterococcus
123
Q

Describe neonatal omphalitis

A
  • Infection of the umbilical stump
  • Strep, staph, or gram negative organisms
  • Erythema and edema around stump
124
Q

Possible complications of neonatal omphalitis

A
  • Septic thrombophlebitis
  • Hepatic abscess
  • Necrotizing fasciitis
  • Portal vein thrombosis
125
Q

Describe neonatal conjuctivitis caused by N. gonorrhoeae

A
  • Colonizes an infant during passage through infected canal

- Presents at 3-7 days w/copious purulent conjunctivitis

126
Q

Describe neonatal conjuctivitis caused by C. trachomatis

A
  • Acquired at birth after passage through infected birth canal
  • Presents at 5 days to several weeks of age w/congestion, edema, minimal discharge
127
Q

Topical optho treatment of neonatal conjunctivitis caused by C. trachomatis?

A

Alone it will NOT eradicate nasopharyngeal carriage and leaves risk for pneumonitis

128
Q

Which infants are MC affected by Vit K deficiency?

A

Exclusively breast fed children

129
Q

How can early (0-2 weeks) vitamin K deficiency bleeding be prevented?

A

Either parenteral or oral vit K

130
Q

How can late (2 wks-6 mos) vit K deficiency be prevented?

A

Parenteral vit K

131
Q

Describe neonatal thrombocytopenia

A
  • Platelets under 10-20,000

- Generalized petechiae, oozing at cord or puncture sites

132
Q

In a well infant, what should be suspected if thrombocytopenic?

A

Isoimmune thrombocytopenia

133
Q

In a sick or asphyxiated infant, what should be suspected if thrombocytopenic?

134
Q

Treatment of neonatal thrombocytopenia

A

Transfusion of platelets indicated if:

  • Clinical bleeding
  • Plt ct under 10-20,000
  • Preterm infant at risk for intraventricular hemorrhage (or plt under 40-50,000)
135
Q

Prognosis of infants who have mothers with ITP?

A

Low risk for serious hemorrhage despite thrombocytopenia

136
Q

Describe neonatal anemia and causes

A

Hct under 40% at term birth

  • Acute blood loss
  • Chronic blood loss
  • Hemolytic anemia
137
Q

Labs to work up neonatal anemia?

A
  • CBC
  • Blood smear
  • Retic count
  • Type
  • Direct and indirect Coombs
138
Q

How does neonatal polycythemia present?

A

Plethora, tachypnea, retractions, hypoxemia

139
Q

Pathophys of polycythemia

A

Hyperviscosity with decreased perfusion of capillary bed

140
Q

Etiology of neonatal polycythemia

A

50% are appropriate weight for gestational age (AGA) so etiology is indeterminant

141
Q

Treatment of neonatal polycythemia

A

Only recommended for symptomatic

-Isovolemic partial exchange transfusion with normal saline (decreases Hct)

142
Q

Clinical presentation of neonatal renal failure

A
  • Birth depression, hypovolemia, hypotension, shock
  • Low or delayed urine output
  • Rising serum Cr
143
Q

Role of prenatal US for renal issues?

A

Identifies many renal anomalies prior to birth - MC hydronephrosis

144
Q

Describe neonatal stroke

A
  • Often occurs antenatally

- MC clinical presentation: seizures (focal or generalized)

Special Pops - Peds (10 decks)

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