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TN Pédiatrie > 13. Neonatology > Flashcards

13. Neonatology Flashcards

1
Q

Define preterm, term and post-term

A
  • preterm: <37 wk (extremely preterm <28 wk, very preterm 28-32 wk, moderate-late preterm 32-37 wk)
  • term: 37-42 wk
  • post-term: >42 wk
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2
Q

Define small for gestational age (SGA), AGA and large for gestational age (LGA)

A
  • SGA: 2 SD < mean weight for GA or <10th percentile
  • AGA: within 2 SD of mean weight for GA
  • LGA: 2 SD > mean weight for GA or >90th percentile
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3
Q

Describe classification of preterm infants by birth weight (3)

A
  • low birthweight (LBW) <2500 g
  • very low birthweight (VLBW) <1500 g
  • extremely low birthweight (ELBW) <1000 g
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4
Q

Describe: Dubowitz/Ballard Scores (5)

A

GA can be determined after birth using Dubowitz/Ballard scores:

  • Assessment at delivery of physical maturity (e.g. plantar creases, lanugo, ear maturation) and neuromuscular maturity (e.g. posture, arm recoil) translates into a score from -10 to +50
  • Higher score means greater maturity (increased GA)
  • -10 = 20 wk; +50 = 44 wk
  • Ideal = 35-40, which corresponds to GA 38-40 wk
  • Only accurate ± 2 wk
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5
Q

Name causes: Pre-Term Infants​ <37 wk (5)

A
  • Spontaneous: cause unknown
  • Maternal disease: HTN, DM, cardiac and renal disorders
  • Fetal conditions: multiple pregnancy, congenital abnormalities, macrosomia, red blood cell isoimmunization, fetal infection
  • Pregnancy issues: placental insufficiency, placenta previa, uterine malformations, previous preterm birth, infection, placental abruption
  • Behavioural and psychological contributors: smoking, EtOH, drug use, psychosocial stressors Sociodemographic factors: age, socioeconomic conditions
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6
Q

Name problems: Pre-Term Infants​ <37 wk (6)

A
  • RDS, apnea of prematurity, chronic lung disease, bronchopulmonary dysplasia
  • Feeding difficulties, necrotizing enterocolitis (NEC)
  • Hypocalcemia, hypoglycemia, hypothermia
  • Anaemia, jaundice
  • Retinopathy of prematurity intracranial hemorrhage (ICH)/intraventricular hemorrhage (IVH)
  • patent ductus arteriosus (PDA)
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7
Q

Name causes: Post-Term Infants >42 wk (4)

A
  • Most cases unknown
  • Increased in first pregnancies
  • Previous post-term birth
  • Genetic factors
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8
Q

Name problems: Post-Term Infants >42 wk (5)

A
  • Increased risk of stillbirth or neonatal death
  • Increased birthweight
  • Fetal “postmaturity syndrome”: impaired growth due to
  • placental dysfunction
  • Meconium aspiration
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9
Q

Name causes: SGA Infants <10th percentile (7)

  • Asymmetric (head-sparing): late onset,growth arrest
A

Extrinsic causes:

  • placental insufficiency
  • poor nutrition,
  • HTN
  • multiple pregnancies
  • drugs
  • EtOH
  • smoking
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10
Q

Name problems: SGA Infants (7)

A
  • Perinatal hypoxia
  • Hypoglycemia
  • hypocalcemia
  • hypothermia,
  • hyperviscosity (polycythemia)
  • jaundice
  • hypomotility
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11
Q

Name causes: SGA Infants <10th percentile (4)

  • Symmetric: early onset, lower growth
A

Intrinsic causes:

  • maternal infections (TORCH)
  • congenital abnormalities
  • syndromal
  • idiopathic
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12
Q

Name problems: SGA Infants <10th percentile (1)

A

patent ductus arteriosus (PDA)

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13
Q

Describe: Routine Neonatal Care (9)

A
  • history taking
    • passage of meconium in 24-48 h, urination/number of wet diapers
    • feeding: breast milk or formula, route (breast or bottle), duration, frequency and volume of feeds
    • issues: jaundice, poor feeding, difficulty breathing, cyanosis, seizures
    • weight: discharge weight (close follow-up if >10% below birth weight), initial weight gain (goal 20- 25 g/d), number of days until birth weight regained (should regain by day 10 of life)
  • erythromycin ointment: applied to both eyes for prophylaxis of ophthalmia neonatorum (of questionable efficacy)
  • vitamin K IM: prophylaxis against HDNB
  • newborn screening tests in Ontario
    • in Ontario, newborn screening tests for:
      • metabolic disorders (amino acid disorders, organic acid disorders, fatty acid oxidation defects, biotinidase deficiency, galactosemia)
      • blood disorders (SCD, other hemoglobinopathies)
      • endocrine disorders (CAH, congenital hypothyroidism)
      • others (CF, severe combined immunodeficiency)
      • congenital hearing loss
  • if mother Rh negative: send cord blood for blood group and direct antiglobulin test
  • if household contact is hepatitis B surface antigen positive: start hepatitis B vaccine series (and if mother is positive, give HBIg within 12 h of birth)
  • assess Apgar score at 1 and 5 min
  • if <7 at 5 min then reassess q5min, until >7
  • do not wait to assign Apgar score before initiating resuscitation
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14
Q

Describe: Apgar Score

A
  • Appearance (colour)
  • Pulse (heart rate)
  • Grimace (irritability)
  • Activity (tone)
  • Respiration (respiratory effort) Or: “How Ready Is This Child?”
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15
Q

Describe: Initial Resuscitation (9)

A
  • anticipation: know maternal history, history of pregnancy, labour, and delivery
  • steps to take for all infants
    • pre-delivery team debriefing including assigning roles, checking equipment, and discussing possible complications and management plan
    • warm (radiant heater, warm blankets) and dry the newborn (remove wet blankets)
    • stimulate infant: rub lower back gently or flick soles of feet
    • position airway (“sniffing” position) and clear or suction if necessary
    • assess breathing and heart rate
    • if no response to stimulation: bag and mask ventilation. Continue until HR >100 and breathing spontaneously
    • if HR <60: establish effective ventilation and start chest compressions
    • if meconium present: a team with advanced resuscitation skills should be present. If the newborn is hypotonic with ineffective respirations, routine intubation for tracheal suction is not suggested. Do initial resuscitation and administer PPV as required
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16
Q

Describe this intervention used in neonatal resuscitation: Epinephrine (adrenaline)

  • Schedule
  • Indications
  • Comments
A
  • Schedule:
    • 0.1-0.3 mL/kg/dose of 1:10,000
    • (0.01-0.03 mg/kg) IV
    • 0.5-1 mL/kg/dose of 1:10,000 (0.05-0.1 mg/ kg) endotracheally can be considered while awaiting IV access (IV preferred)
    • Can be repeated q3-5 min prn
  • Indications: HR <60 and not rising
  • Comments: Side effects: tachycardia, HTN, cardiac arrhythmias
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17
Q

Describe this intervention used in neonatal resuscitation: Fluid Bolus (NS, whole blood, Ringer’s lactate)

  • Schedule
  • Indications
A
  • Schedule:
    • 10 ml/kg
    • May need to be repeated
    • Avoid giving too rapidly as large volume rapid infusions can be associated with intraventricular haemorrhage
  • Indications: Evidence of hypovolemia
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18
Q

Described: Approach to the Depressed Newborn (2)

A
  • a depressed newborn lacks one or more of the following characteristics of a normal newborn
    • pulse >100 bpm
    • cries when stimulated
    • actively moves all extremities
    • has a good strong cry
  • approximately 10% of newborn babies require assistance with breathing after delivery
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19
Q

Describe: Corrective Actions for positive pressure ventilation (PPV) in Neonatal Resuscitation (6)

A

MR SOPA

  • Mask readjustment
  • Reposition airway
  • Suction mouth and nose
  • Open mouth
  • Pressure increase
  • Alternative airway
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20
Q

Name etiologies of Respiratory Depression in the Newborn (7)

A
  • Respiratory Problems
    • RDS/hyaline membrane disease
    • Pulmonary hypoplasia
    • CNS depression
    • meconium aspiration syndrome MAS
    • Pneumonia
    • Pneumothorax
    • Pleural effusions
    • Congenital malformations
  • Anemia (severe)
    • Erythroblastosis fetalis
    • Secondary hydrops fetalis
  • Maternal causes
    • Drugs/anesthesia (opiates, magnesium sulphate)
    • DM
    • Maternal myasthenia gravis
  • Congenital Malformations/Birth injury
    • Nuchal cord, perinatal depression
    • Bilateral phrenic nerve injury
    • Potter’s sequence
  • Shock: Antepartum hemorrhage
  • congenital heart defect (CHD): Transposition of the great arteries with intact ventricular septum
  • Other:
    • Hypothermia
    • Hypoglycemia
    • Infection
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21
Q

Name: Targeted Preductal SpO2 After Birth

  • ​1/2/3/4/5/10 minutes
A
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22
Q

Describe diagnosis: Neonatal Resuscitation (6)

A
  • vital signs including pre- and post-ductal oxygen saturations and 4 limb blood pressure
  • detailed maternal history: include prenatal care, illnesses, use of drugs, previous high risk pregnancies, infections during pregnancy (including GBS status), duration of ruptured membranes, maternal fever or signs of chorioamnionitis during labour/delivery, blood type and Rh status, amniotic fluid status, GA, meconium, Apgar scores
  • clinical findings (observe for signs of respiratory distress such as cyanosis, tachypnea, retractions, grunting, temperature instability)
  • laboratory results (CBC, blood gas, blood type and DAT, glucose)
  • transillumination of chest to evaluate for pneumothorax
  • CXR, ECG, echocardiogram
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23
Q

Define: Apnea (3)

A
  • periodic breathing: normal respiratory pattern seen in newborns in which periods of rapid respiration are alternated with pauses lasting 5-10 s
  • apnea: absence of respiratory gas flow for >20 s (or less if associated with bradycardia or desaturation)
  • three types of apnea
    • central: no chest wall movement, no signs of obstruction
    • obstructive: chest wall movement continues against obstructed upper airway, no airflow
    • mixed: combination of central and obstructive apnea
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24
Q

Name DDX: Apenia (9)

A
  • in term infants, apnea requires full septic workup (CBC and differential, blood and urine cultures ± LP, CXR)
  • other causes
    • CNS: seizures, ICH
    • apnea of prematurity (<34 wk): combination of CNS immaturity and obstructive apnea; resolves by 36 wk GA; diagnosis of exclusion
    • hypoxic injury
    • infectious: sepsis, meningitis, NEC
    • GI: GERD, aspiration with feeding
    • metabolic: hypoglycemia, hyponatremia, hypocalcemia, inborn error of metabolism
    • cardiovascular: anemia, hypovolemia, PDA, heart failure
    • medications: morphine
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25
Q

Describe management: Apenia (5)

A
  • O2, ventilatory support, maintain normal blood gases
  • tactile stimulation
  • correct underlying cause
  • medications: methylxanthines (caffeine) stimulate the CNS and diaphragm and are used for apnea of prematurity (not in term infants)
  • if apnea of prematurity is diagnosed, infants should receive cardiorespiratory monitoring in a neonatal intensive care unit
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26
Q

Name clinical features: Bleeding Disorders in Neonates (5)

A
  • oozing from the umbilical stump
  • excessive bleeding from peripheral venipuncture/heel stick sites/IV sites
  • large caput succedaneum
  • cephalohematomas (in absence of significant birth trauma)
  • subgaleal hemorrhage and prolonged bleeding following circumcision
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27
Q

Name etiologies: Bleeding Disorders in Neonates (3)

A
  • 4 major categories
    • increased platelet destruction: maternal ITP or SLE, infection/sepsis, DIC, neonatal alloimmune thrombocytopenia, autoimmune thrombocytopenia
    • decreased platelet production/function: pancytopenia, bone marrow replacement, Fanconi anemia, Trisomy 13 and 18
    • metabolic: congenital thyrotoxicosis, inborn error of metabolism
    • coagulation factor deficiencies (see Hematology, H53): hemophilia A/B, HDNB
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28
Q

Describe epidemiology: Neonatal Alloimune Thrombocytopenia (1)

A
  • 1 per 4000-5000 live births
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29
Q

Describe pathophysiology: Neonatal Alloimune Thrombocytopenia (3)

A
  • platelet equivalent of Rh disease of the newborn
  • occurs when mother is negative for HPA and fetus is positive
  • development of maternal IgG antibodies against HPA antigens on fetal platelets
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30
Q

Describe clinical features: Neonatal Alloimune Thrombocytopenia (2)

A
  • petechiae, purpura, thrombocytopenia in otherwise healthy neonate
  • severe disease can lead to intracranial bleeding
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31
Q

Describe diagnosis: Neonatal Alloimune Thrombocytopenia (1)

A
  • maternal and paternal platelet typing and identification of platelet alloantibodies
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32
Q

Describe tx: Neonatal Alloimune Thrombocytopenia (3)

A
  • IVIg to mother prenatally starts in second trimester ± steroids ± fetal platelet transfusions
  • if transfusion required, use washed maternal platelets or donor HPA negative platelets
  • treat neonate with IVIg (less effective than platelet transfusions)
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33
Q

Describe pathophysiology: Autoimmune thrombocytopenia (2)

A
  • caused by antiplatelet antibodies from maternal immune thrombocytopenic purpura (ITP) or SLE
  • passive transfer of antibodies across placenta
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34
Q

Describe clinical features: Autoimmune thrombocytopenia (1)

A
  • similar presentation to neonatal alloimmune thrombocytopenia, but thrombocytopenia usually less severe
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35
Q

Describe tx: Autoimmune thrombocytopenia (3)

A
  • steroids to mother for 10-14 d prior to delivery or IVIg to mother before delivery
  • treat neonate with IVIg (usually if platelets <60,000)
  • transfusion of infant with maternal/donor platelets only in severe cases, as antibodies will destroy transfused platelets
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36
Q

Describe Pathophysiology: Hemorrhagic disease of the newborn (2)

A
  • caused by vitamin K deficiency
  • factors II, VII, IX, X are vitamin K-dependent, therefore both PT and PTT are abnormal
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37
Q

Describe Etiology and Clinical Feature: Hemorrhagic disease of the newborn (2)

A
  • neonates at increased risk of vitamin K deficiency due to:
    • poor transfer of vitamin K across the placenta
    • insufficient bacterial colonization of colon at birth to synthesize vitamin K
    • breastfeeding (inadequate vitamin K intake)
    • additional risk if maternal use of antiepileptics
  • neonate may present with hematomas, ICH (causing apnea or seizures), internal bleeding, hematuria, bruising, prolonged bleeding (often from mucous membranes, umbilicus, circumcision, and venipunctures)
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38
Q

Describe prevention: Hemorrhagic disease of the newborn (1)

A
  • vitamin K IM administration at birth to all newborns
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39
Q

Define: Bronchopulmonary Dysplasia (3)

A
  • also known as chronic lung disease
  • clinically defined as O2 requirement for >28 d plus persistent need for oxygen and/or ventilatory support at 36 wk corrected GA
  • damage to developing lungs with prolonged intubation/ventilation, high levels O2, infections
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40
Q

Describe investigations: Bronchopulmonary Dysplasia (1)

A
  • CXR findings may demonstrate decreased lung volumes, areas of atelectasis, signs of inflammation, and hyperinflation
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41
Q

Describe tx: Bronchopulmonary Dysplasia (3)

A
  • no good treatments
  • gradual wean from ventilator, optimize nutrition
  • dexamethasone may help decrease inflammation and encourage weaning, but use of dexamethasone is associated with increased risk of adverse neurodevelopmental outcomes
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42
Q

Describe prognosis: Bronchopulmonary Dysplasia (4)

A
  • chronic respiratory failure may lead to pulmonary HTN, poor growth, and right-sided heart failure
  • patients with bronchopulmonary dysplasia may continue to have significant impairment and deterioration in lung function late into adolescence
  • some lung abnormalities may persist into adulthood including airway obstruction, airway hyper- reactivity, and emphysema
  • associated with increased risk of adverse neurodevelopmental outcomes
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43
Q

Describe: Approach to neonatal cyanosis (Figure)

A
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44
Q

Describe management: Cyanosis (2)

A
  • ABGs
    • elevated CO2 suggests respiratory cause
    • hyperoxia test (to distinguish between cardiac and respiratory causes of cyanosis): get baseline PaO2 in room air, then PaO2 on 100% O2 for 10-15 min
      • PaO2 <150 mmHg: suggests cyanotic CHD or possible PPHN (see Cardiology, P20)
      • PaO2 >150 mmHg: suggests cyanosis likely due to respiratory or non-cardiac cause
  • CXR: look for respiratory abnormalities (pneumothorax, respiratory tract malformations, evidence of shunting, pulmonary infiltrates) and cardiac abnormalities (cardiomegaly, abnormalities of the great vessels)
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45
Q

Describe: Carboxyhemoglobinemia (2)

A
  • (secondary to carbon monoxide poisoning) results in impaired binding of oxygen to hemoglobin but does not discolour the blood.
  • Therefore it may not register on pulse oximetry and cyanosis may not be evident clinically
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46
Q

Describe: Methemoglobinemia (2)

A
  • typically reads higher on pulse oximetry than the true level of oxyhemoglobin.
  • Methemoglobin alters the absorption of red light at the two wavelengths that pulse oximetry uses to predict oxygen saturation
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47
Q

Define: Diaphragmatic Hernia (2)

A
  • developmental defect of the diaphragm with herniation of abdominal organs into thorax
  • associated with pulmonary hypoplasia and persistent pulmonary hypertension of newborn (PPHN)
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48
Q

Describe clinical features: Diaphragmatic Hernia (8)

A
  • respiratory distress, cyanosis
  • scaphoid abdomen and barrel-shaped chest
  • affected side dull to percussion and breath sounds absent, may hear bowel sounds instead
  • heart sounds shifted to contralateral side
  • asymmetric chest movements, trachea deviated away from affected side
  • may present outside of neonatal period
  • often associated with other anomalies (cardiovascular, CNS, chromosomal abnormalities)
  • CXR: bowel loops in thorax (usually left side), displaced mediastinum
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49
Q

Describe tx: Diaphragmatic Hernia (3)

A
  • immediate intubation required at birth: DO NOT bag mask ventilate because air will enter stomach and further compress lungs
  • place large bore orogastric tube to decompress bowel
  • initial stabilization and management of pulmonary hypoplasia and PPHN if present, hemodynamic support and surgery when stable
50
Q

Define: Hypoglycemia (1)

A
  • glucose <2.6 mmol/L
51
Q

Describe etiology: Hypoglycemia (4)

A
  • decreased carbohydrate stores: premature, SGA, RDS, maternal HTN
  • endocrine: hormonal deficiencies (GH, cortisol, epinephrine), insulin excess (infant of diabetic mother, Beckwith-Wiedemann syndrome/islet cell hyperplasia), HPA axis suppression (panhypopituitarism)
  • inborn errors of metabolism: fatty acid oxidation defects, galactosemia
  • miscellaneous: sepsis, hypothermia, polycythemia
52
Q

Describe clinical findings: Hypoglycemia (7)

A
  • signs often non-specific and subtle:
    • lethargy
    • poor feeding
    • irritability
    • tremors
    • apnea
    • cyanosis
    • seizures
53
Q

Describe management: Hypoglycemia (4)

A
  • identify and monitor infants at risk (pre-feed blood glucose checks) until blood glucose stable and for at least 12 h (for infant of diabetic mother or LGA) or 36 h (if preterm or SGA)
  • begin oral feeds as soon as possible after birth and ensure regular feeds
  • if significant and/or symptomatic hypoglycemia, provide glucose IV and titrate according to blood sugar levels
  • if persistent hypoglycemia or no predisposing cause, send “critical blood work” during an episode of hypoglycemia: ABG, ammonia, β-hydroxybutyrate, cortisol, free fatty acids, GH, insulin, lactate, urine dipstick for ketones
54
Q

Define: Neonatal Hyperbilirubinemia (1)

A

total serum bilirubin >95th percentile (high risk zone) on Bhutani nomogram in infants >35 wk GA

55
Q

Describe clinical features: Neonatal Hyperbilirubinemia (2)

A
  • jaundice typically visible at serum bilirubin levels of 85-120 µmol/L
  • visual assessment is often misleading and should confirm with blood test
56
Q

Jaundice in the first 24 h of life and conjugated hyperbilirubinemia are always physiological OR pathological?

A

Jaundice in the first 24 h of life and conjugated hyperbilirubinemia are always pathological

57
Q

Jaundice must be investigated when? (4)

A

if:

  • It occurs within 24 h of birth
  • Conjugated hyperbilirubinemia is present
  • Unconjugated bilirubin rises rapidly or is excessive for patient’s age and weight
  • Persistent jaundice lasts beyond 1-2 wk of age
58
Q

Describe: Approach to neonatal hyperbilirubinemia (Figure)

A
59
Q

Describe epidemiology: Physiologic Jaundice (2)

A
  • term infants: onset 3-4 d of life, resolution by 10 d of life
  • premature infants: higher peak and longer duration
60
Q

Describe pathophysiology: Physiologic Jaundice (3)

A
  • increased hematocrit and decreased RBC lifespan
  • immature glucuronyl transferase enzyme system (slow conjugation of bilirubin)
  • increased enterohepatic circulation
61
Q

Define: Breastfeeding Jaundice (1)

A
  • common: due to a lack of milk production s dehydration s exaggerated physiologic jaundice
62
Q

Define: Breast Milk Jaundice (3)

A
  • 1 per 200 breastfed infants
  • glucuronyl transferase inhibitor found in breast milk
  • onset 7 d of life, peak at 2-3 wk of life, usually resolved by 6 wk
63
Q

Name: MATERNAL Risk Factors for Jaundice (4)

A
  • Ethnic group (e.g. Asian, Indigenous)
  • Complications during pregnancy (infant of diabetic mother, Rh or ABO incompatibility)
  • Breastfeeding
  • Family history/previous child required phototherapy
64
Q

Name: PERINATAL Risk Factors for Jaundice (2)

A
  • Birth trauma (cephalohematoma, ecchymoses)
  • Prematurity
65
Q

Name: NEONATAL Risk Factors for Jaundice (5)

A
  • Difficulty establishing breastfeeding
  • Infection (sepsis, hepatitis)
  • Genetic factors
  • Polycythemia Drugs
  • total parenteral nutrition (TPN)
66
Q

Name: Causes of Neonatal Jaundice if < 24h (5)

A

ALWAYS PATHOLOGIC

  • Hemolytic
  • Rh or ABO incompatibility
  • Sepsis
  • Congenital infection (TORCH)
  • Severe bruising/hemorrhage
67
Q

Name: Causes of Neonatal Jaundice if 24h - 72h (8)

A
  • Physiologic, polycythemia
  • Dehydration (breastfeeding jaundice)
  • Hemolysis
  • G6PD deficiency
  • Pyruvate kinase deficiency
  • Spherocytosis
  • Bruising, hemorrhage, hematoma
  • Sepsis/congenital infection
68
Q

Name: Causes of Neonatal Jaundice if 72h-96h (2)

A
  • Physiologic ± breastfeeding
  • Sepsis
69
Q

Name: Causes of Neonatal Jaundice if age prolonged (>1wk) (6)

A
  • Breast milk jaundice Prolonged physiologic jaundice in preterm
  • Hypothyroidism
  • Neonatal hepatitis
  • Conjugation dysfunction
    • e.g. Gilbert syndrome, Crigler-Najjar syndrome
  • Inborn errors of metabolism
    • e.g. galactosemia
  • Biliary tract obstruction
    • e.g. biliary atresia
70
Q

Describe investigations: Pathologic Jaundice (5)

A
  • unconjugated hyperbilirubinemia
    • hemolytic workup: CBC, reticulocyte count, blood group (mother and infant), peripheral blood smear, Coombs test
    • if baby is unwell or has fever: septic workup (CBC and differential, blood and urine cultures ± LP, CXR)
    • other: G6PD screen (especially in males), TSH
  • conjugated hyperbilirubinemia must be investigated without delay
    • consider liver enzymes (AST, ALT), coagulation studies (PT, PTT), serum albumin, ammonia, TSH, TORCH screen, septic workup, galactosemia screen (erythrocyte galactose-1-phosphate uridyltransferase levels), metabolic screen, abdominal U/S, HIDA scan, sweat chloride
  • predicting occurrence of severe hyperbilirubinemia
    • measure either TSB or TcB concentration in all infants between 24 h and 72 h of life and plot on appropriate hyperbilirubinemia treatment graph. If infant does not require immediate treatment, results should be plotted on predictive nomogram to determine the risk of progression to severe hyperbilirubinemia and need for repeat measurement (refer to: http://www.cps.ca/documents/position/hyperbilirubinemia-newborn)
71
Q

Describe the treatment of unconjugated hyperbilirubinemia (6)

A
  • to prevent kernicterus
  • breastfeeding does not usually need to be discontinued, ensure adequate feeds and hydration
  • lactation consultant support, mother to pump after feeds
  • treat underlying causes (e.g. sepsis)
  • phototherapy (blue-green wavelength, not UV light) – standard intensive or multiple intensive protocol depending on severeity of hyperbilirubinemia
    • insoluble unconjugated bilirubin is converted to excretable form via photoisomerization
    • serum bilirubin should be monitored during and immediately after therapy (risk of rebound because photoisomerization reversible when phototherapy discontinued)
    • contraindicated in conjugated hyperbilirubinemia: results in “bronzed” baby
    • side effects: skin rash, diarrhea, eye damage (eye shield used routinely for prevention), dehydration
    • use published guidelines and nomogram for initiation of phototherapy
  • exchange transfusion
    • indications: high bilirubin levels as per published graphs based on age, weeks gestation
    • most commonly performed for hemolytic disease and G6PD deficiency
    • use of IVIg in case of severe hyperbilirubinemia (DAT+) becoming evidence-based practice
72
Q

Name etiologies: Kernicterus (3)

A
  • unconjugated bilirubin concentrations exceed albumin binding capacity and bilirubin is deposited in the brain resulting in tissue necrosis and permanent damage (typically basal ganglia or brainstem)
  • incidence increases as serum bilirubin levels increase above 340 µmol/L
  • can occur at lower levels in presence of sepsis, meningitis, hemolysis, hypoxia, acidosis, hypothermia, hypoglycemia, and prematurity
73
Q

Describe clinical features: Kernicterus (4)

A
  • up to 15% of infants have no obvious neurologic symptoms
  • early stage: lethargy, hypotonia, poor feeding, emesis (bilirubin encephalopathy)
  • mid stage: hypertonia, high pitched cry, opisthotonic posturing (back arching), bulging fontanelle, seizures, pulmonary hemorrhage
  • late stage (during first year and beyond)
    • hypotonia, delayed motor skills, extrapyramidal abnormalities (choreoathetoid CP), gaze palsy, mitral regurgitation, sensorineural hearing loss
74
Q

Describe prevention: Kernicterus (1)

A
  • exchange transfusion, IVIg if indicated
75
Q

Define: Biliary Atresia (2)

A
  • atresia of the extrahepatic bile ducts which leads to cholestasis and increased conjugated bilirubin after the first wk of life
  • progressive obliterative cholangiopathy
76
Q

Describe epidemiology: Biliary Atresia (2)

A
  • incidence: 1:10,000-15,000 live births
  • associated anomalies in 10-35% of cases: situs inversus, congenital heart defects, polysplenia
77
Q

Describe clinical features: Biliary Atresia (5)

A
  • dark urine
  • pale stool
  • jaundice (persisting for >2 wk)
  • abdominal distension
  • hepatomegaly
78
Q

Describe diagnosis: Biliary Atresia (3)

A
  • conjugated hyperbilirubinemia, abdominal U/S, operative cholangiogram
  • HIDA scan (may be bypassed in favour of biopsy if timing of diagnosis is critical)
  • liver biopsy
79
Q

Describe tx: Biliary Atresia (4)

A
  • surgical drainage procedure
  • hepatoportoenterostomy (Kasai procedure; most successful if <8 wk of age)
  • two-thirds will eventually require liver transplantation
  • vitamins A, D, E, and K; diet should be enriched with medium-chain triglycerides to ensure adequate fat ingestion
80
Q

Define: Necrotizing Enterocolitis (2)

A
  • intestinal inflammation associated with focal or diffuse ulceration and necrosis
  • primarily affecting terminal ileum and colon
81
Q

Describe epidemiology: Necrotizing Enterocolitis (1)

A
  • affects 1-5% of preterm newborns admitted to NICU
82
Q

Describe pathophysiology: Necrotizing Enterocolitis (2)

A
  • postulated mechanism of bowel ischemia:
    • mucosal damage and enteral feeding -> bacterial growth -> bowel necrosis/gangrene/perforation
83
Q

Name risk factors: Necrotizing Enterocolitis (5)

A
  • prematurity (immature defenses)
  • asphyxia, shock (poor bowel perfusion)
  • hyperosmolar feeds
  • enteral feeding with formula (breast milk can be protective)
  • sepsis
84
Q

Describe clinical features: Necrotizing Enterocolitis (5)

A
  • usually presents at 2-3 wk of age
  • distended abdomen, diminished bowel sounds, feeding intolerance
  • increased amount of gastric aspirate/vomitus with bile staining
  • frank or occult blood in stool
  • signs of bowel perforation (sepsis, shock, peritonitis, DIC)
85
Q

Describe investigations: Necrotizing Enterocolitis (3)

A
  • AXR: pneumonitis intestinalis (intramural air is a hallmark of NEC), free air, fixed loops, ileus, thickened bowel wall, portal venous gas
  • CBC, ABG, lactate, blood culture, electrolytes
  • high or low WBC, low platelets, hyponatremia, acidosis, hypoxia, hypercapnea
86
Q

Describe tx: Necrotizing Enterocolitis (6)

A
  • NPO (7-10 d), vigorous IV fluid resuscitation, decompression with NG tube, supportive therapy
  • total parenteral nutrition (TPN)
  • antibiotics (usually ampicillin, gentamicin ± metronidazole if risk of perforation x 7-10 d)
  • serial AXRs detect early perforation (40% mortality in perforated necrotizing enterocolitis NEC)
  • peritoneal drain/surgery if perforation
  • surgical resection of necrotic bowel and surgery for complications (e.g. perforation, strictures)
87
Q

Define: Persistent Pulmonary Hypertension of the Newborn (2)

A
  • persistence of fetal circulation as a result of persistent elevation of pulmonary vascular resistance
  • classified as primary (absence of risk factors) or secondary
88
Q

Describe epidemiology: Persistent Pulmonary Hypertension of the Newborn (1)

A
  • incidence 1.9/1000 live births
89
Q

Describe clinical features: Persistent Pulmonary Hypertension of the Newborn (1)

A

Usually presents within 12 h of birth with severe hypoxemia/cyanosis; may have only mild respiratory distress

90
Q

Describe pathophysiology: Persistent Pulmonary Hypertension of the Newborn (1)

A
  • elevated pulmonary pressures cause R -> L shunt through patent ductus arteriosus, foramen ovale -> decreased pulmonary blood flow and hypoxemia -> further pulmonary vasoconstriction
91
Q

Name risk factors: Persistent Pulmonary Hypertension of the Newborn (6)

A
  • secondary persistent pulmonary hypertension of newborn:
    • asphyxia
    • meconium aspiration syndrome
    • respiratory distress syndrome RDS
    • sepsis
    • pneumonia
    • structural abnormalities (e.g. diaphragmatic hernia, pulmonary hypoplasia)
  • more common in term or post-term infants
92
Q

Describe investigations: Persistent Pulmonary Hypertension of the Newborn (4)

A
  • measure pre- and post-ductal oxygen levels
  • hyperoxia test to exclude CHD
  • ECG (RV strain)
  • Echo reveals increased pulmonary arterial pressure and a R s L shunt across PDA and patent foramen ovale; also used to rule out other cardiac defects
93
Q

Describe tx: Persistent Pulmonary Hypertension of the Newborn (5)

A
  • maintain good oxygenation (SaO2 >95%) in at-risk infants
  • O2 given early and tapered slowly, minimize stress and metabolic demands, maintain normal blood gases, circulatory support
  • mechanical ventilation, high frequency oscillation in a sedated muscle-relaxed infant
  • nitric oxide, surfactant
  • extracorporeal membrane oxygenation used in some centres when other therapy fails
94
Q

Describe clinical features: Respiratory Distress in the Newborn (4)

A
  • tachypnea: RR >60/min; tachycardia: HR >160/min
  • grunting, subcostal/intercostal indrawing, nasal flaring
  • duskiness, central cyanosis
  • decreased air entry, crackles on auscultation
95
Q

Describe investigations: Respiratory Distress in the Newborn (3)

A
  • labs: CBC, blood gas, glucose, blood culture
  • imaging: CXR
  • if indicated: ECG, Echo, LP (CSF cell count, culture, and chemistry)
96
Q

Distinguishing Features of respiratory distress syndrome (RDS), transient tachypnea of the newborn (TTN) and meconium aspiration syndrome (MAS): Etiology

A
  • RDS:
    • Surfactant deficiency -> poor lung compliance due to high alveolar surface tension -> atelectasis -> ⬇️ surface area for gas exchange-> hypoxia + acidosis -> respiratory distress

“Hyaline membrane disease”

  • TTN:
    • Delayed resorption of fetal lung fluid -> accumulation of fluid in peribronchial lymphatics and vascular spaces -> tachypnea “Wet lung syndrome”
  • MAS:
    • Meconium is sterile but causes airway obstruction, chemical inflammation, and surfactant inactivation leading to chemical pneumonitis
97
Q

Distinguishing Features of respiratory distress syndrome (RDS), transient tachypnea of the newborn (TTN) and meconium aspiration syndrome (MAS): Gestational Age

A
  • RDS: Preterm
  • TTN: Usually term and late preterm
  • MAS: Term and post-term
98
Q

Distinguishing Features of respiratory distress syndrome (RDS), transient tachypnea of the newborn (TTN) and meconium aspiration syndrome (MAS): Risk Factors

A
  • RDS:
    • Maternal DM
    • Preterm delivery
    • Male sex
    • low birth weight LBW
    • Acidosis, sepsis
    • Hypothermia
    • Second born twin
  • TTN:
    • Maternal DM
    • Maternal asthma
    • Male sex
    • Macrosomia (>4500 g)
    • Elective Cesarean section or short labour
    • Late preterm delivery
  • MAS:
    • Meconium-stained amniotic fluid
    • Post-term delivery
99
Q

Distinguishing Features of respiratory distress syndrome (RDS), transient tachypnea of the newborn (TTN) and meconium aspiration syndrome (MAS): Clinical Feature

A
  • RDS:
    • Respiratory distress within first few hours of life, worsens over next 24-72 h
    • Hypoxia
    • Cyanosis
  • TTN:
    • Tachypnea within the first few hours of life ± retractions, grunting, nasal flaring
    • Often NO hypoxia or cyanosis
  • MAS:
    • Respiratory distress within hours of birth
    • Small airway obstruction, chemical pneumonitis tachypnea, barrel chest with audible crackles
    • Hypoxia
100
Q

Distinguishing Features of respiratory distress syndrome (RDS), transient tachypnea of the newborn (TTN) and meconium aspiration syndrome (MAS): CXR Findings

A
  • RDS:
    • Homogenous infiltrates
    • Air bronchograms
    • Decreased lung volumes
    • May resemble pneumonia (GBS) If severe, “white-out” with no differentiation of cardiac border
  • TTN:
    • Perihilar infiltrates
    • “Wet silhouette”; fluid in fissures
  • MAS:
    • Hyperinflation
    • Patchy atelectasis
    • Patchy and coarse infiltrates 10-20% have pneumothorax
101
Q

Distinguishing Features of respiratory distress syndrome (RDS), transient tachypnea of the newborn (TTN) and meconium aspiration syndrome (MAS): Prevention

A
  • RDS:
    • Prenatal corticosteroids (e.g. Celestone® 12 mg q24h x 2 doses) if risk of preterm delivery <34 wk
    • Monitor lecithin:sphingomyelin (L/S) ratio with amniocentesis, L/S >2:1 indicates lung maturity
  • TTN:
    • Where possible, avoidance of elective
    • Cesarean delivery, particularly before 38 wk GA
  • MAS:
    • If infant is depressed at birth, intubate and suction below vocal cords
    • Avoidance of factors associated with in utero passage of meconium (e.g. post term delivery)
102
Q

Distinguishing Features of respiratory distress syndrome (RDS), transient tachypnea of the newborn (TTN) and meconium aspiration syndrome (MAS): Treatment

A
  • RDS:
    • Resuscitation
    • Oxygen
    • Ventilation
    • Surfactant (decreases alveolar surface tension, improves lung compliance, and maintains functional residual capacity)
  • TTN:
    • Supportive
    • Oxygen if hypoxic
    • Ventilator support (e.g. CPAP) IV fluids and NG tube feeds if too tachypneic to feed orally
  • MAS:
    • Resuscitation Oxygen Ventilatory support Surfactant
    • Inhaled nitric oxide Extracorporeal membrane oxygenation for PPHN
103
Q

Distinguishing Features of respiratory distress syndrome (RDS), transient tachypnea of the newborn (TTN) and meconium aspiration syndrome (MAS):

A
  • RDS:
  • TTN:
  • MAS:
104
Q

Distinguishing Features of respiratory distress syndrome (RDS), transient tachypnea of the newborn (TTN) and meconium aspiration syndrome (MAS): Complications

A
  • RDS: In severe prematurity and/or prolonged ventilation, increased risk of bronchopulmonary dysplasia
  • TTN:
    • Hypoxemia
    • Hypercapnea
    • Acidosis
    • persistent pulmonary hypertension of newborn (PPHN)
  • MAS:
    • Hypoxemia
    • Hypercapnea
    • Acidosis
    • PPHN
    • Pneumothorax Pneumomediastinum
    • Chemical pneumonitis Secondary surfactant inhibition
    • Respiratory failure
105
Q

Distinguishing Features of respiratory distress syndrome (RDS), transient tachypnea of the newborn (TTN) and meconium aspiration syndrome (MAS): Prognosis

A
  • RDS: Dependent on GA at birth and severity of underlying lung disease; long-term risks of chronic lung disease
  • TTN: Recovery usually expected in 24-72 h
  • MAS: Dependent on severity, mortality up to 20%
106
Q

Describe pneumonia in newborns (5)

A
  • consider in infants with prolonged (≥18 h) or premature rupture of membranes, maternal fever or other signs and symptoms of chorioamnionitis, or if mother is GBS positive
  • suspect if infant exhibits respiratory distress, temperature instability, or WBC is low (<5 x 109/L), elevated (>30 x 109/L, or left-shifted)
  • symptoms may be non-specific
  • CXR: hazy lung and/or distinct infiltrates (may be difficult to differentiate from RDS)
  • neonates with pneumonia should be admitted to the neonatal ICU (NICU) with blood and CSF cultures and antibiotics for management
107
Q

Name sepsis Considerations in the Neonate: Early Onset (< 72h) (3)

A
  • Vertical transmission, 95% present within 24 h after birth
  • Risk factors:
    • Maternal infection: UTI, GBS positive, previous child with GBS, sepsis, or meningitis
    • Maternal fever/leukocytosis/chorioamnionitis
    • Prolonged rupture of membranes (>18 h)
    • Preterm labour
  • Pathogens: GBS, E. coli, Listeria are most common Pneumonia more common with early onset sepsis
108
Q

Name sepsis Considerations in the Neonate: Late Onset (72h - 28d) (3)

A
  • Acquired after birth
  • Most common in preterm infants in NICU (most commonly due to coagulase negative Staphylococcus)
  • Other pathogens implicated include GBS, anaerobes, E. coli, Klebsiella
109
Q

Name: Chronic Perinatal Infections (10)

A

CHEAP TORCHES

  • Chicken pox/shingles
  • Hepatitis B
  • Epstein-Barr virus AIDS (HIV)
  • Parvovirus B19 (erythema infectiosum)
  • Toxoplasmosis
  • Other
  • Rubella virus Cytomegalovirus/Coxsackievirus
  • HSV
  • Every STI
  • Syphilis
110
Q

Name clinical features: Sepsis in the Neonate (8)

A
  • no reliable absolute indicator of occult bacteremia in infants <3 mo, most specific result has been WBC <5
  • temperature instability (hypo/hyperthermia)
  • respiratory distress, cyanosis, apnea
  • tachycardia/bradycardia
  • lethargy, irritability
  • poor feeding, vomiting, abdominal distension, diarrhea
  • hypotonia, seizures, lethargy
  • jaundice, hepatomegaly, petechiae, purpura
111
Q

Describe investigations: Sepsis in the Neonate (2)

A
  • suspicion of neonatal sepsis requires “full septic workup”
    • CBC, blood and urine cultures, CXR, ± LP (CSF analysis: cell count, glucose, protein, culture, and PCR for viruses)
    • LP must be conducted if blood culture is positive due to increased risk of meningitis
112
Q

Describe management: Sepsis in the Neonate (5)

A
  • supportive care
  • IV antibiotics: typically ampicillin + cefotaxime or ampicillin + gentamicin chosen as first-line empiric therapy
  • choice of antibiotic and duration of treatment dependent on symptoms, culture results, maternal GBS status, local resistance patterns
  • if meningitis suspected, consider IV ampicillin + cefotaxime ± vancomycin
  • addition of IV acyclovir if HSV infection suspected
113
Q

Name: Common Neonatal Skin Conditions (9)

A
  • Vasomotor Response (Cutis Marmorata, Acrocyanosis)
  • Vernix Caseosa
  • Congenital Dermal Melanocytosis (‘Mongolian Spots’)
  • Capillary Hemangioma
  • Erythema Toxicum
  • Milia
  • Transient Pustular Melanosis
  • Nevus Simplex (Salmon Patch)
  • Neonatal Acne
114
Q

Describe: Vasomotor Response (1)

A

Transient mottling when exposed to cold; usually normal, particularly if premature

115
Q

Describe: Vernix Caseosa (1)

A

Soft, creamy, white layer covering baby at birth

116
Q

Describe: Congenital Dermal Melanocytosis (‘Mongolian Spots’) (1)

A

Slate grey macules over lower back and buttocks (may look like bruises); common in dark skinned infants

117
Q

Describe: Capillary Hemangioma (1)

A

Raised red lesion, which increases in size after birth and involutes; 50% resolved by 5 yr, 90% by 9 yr

118
Q

Describe: Erythema Toxicum (1)

A

Yellow-white papules/pustules surrounded by erythema, eosinophils within the lesions; common rash, resolves by 2 wk

119
Q

Describe: Milia (1)

A

Lesions 1-2 mm firm white pearly papules on nasal bridge, cheeks, and palate; self- resolving

120
Q

Describe: Transient Pustular Melanosis (1)

A

Brown macular base with pustules, seen more commonly in African American infants; may be present at birth

121
Q

Describe: Nevus Simplex (Salmon Patch) (2)

A
  • Transient macular vascular malformation of the eyelids and/or neck (“Angel Kiss” or “Stork Bite”)
  • most lesions disappear by 1 yr of life
122
Q

Describe: Neonatal Acne (2)

A
  • Inflammatory papules and pustules mainly on face
  • self-resolving usually within 4 mo

TN Pédiatrie (14 decks)

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