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Pediatrics > Perinatal Period > Flashcards

Perinatal Period Flashcards

1
Q

What are components of the initial newborn assessment?

A
  • Determination of gestational age and growth
  • Comprehensive newborn assessment within 24 hours of birth
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2
Q

What is considered a preterm infant?

A

At or before 36 weeks 7 days

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3
Q

What is considered late preterm?

A

34 0/7 and 36 6/7 weeks gestation

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3
Q

What is considered term?

A

between 37 weeks 0 days and 41 weeks 7 days

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4
Q

What is considered post term?

A

42 weeks 0 days and longer

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5
Q

What conditions is the late preterm infant at higher risk for?

A
  • Hypoglycemia
  • Jaundice
  • Respiratory distress
  • Temperature instability
  • Feeding challenges
  • Readmission
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6
Q

What is the general protocol for late preterm infants?

A
  • Must be monitored for 48 hours
  • Pass a car seat trial

Car seat challenge = placed in car seat for 1 hr with pulse ox on

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7
Q

What are post term newborns at risk for?

A
  • fetal growth restriction
  • uteroplacental insufficiency
  • meconium aspiration
  • intrauterine infection
  • dysmaturity
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8
Q

How is growth measured?

A
  • Weight
  • Length
  • Head circumference
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9
Q

What is considered small for gestational age? Large?

A
  • Small for gestational age: birthweights less than 10th percentile
  • Large for gestational age: Birthweights greater than 90th percentile

Appropriate = 10th to 90th percentil

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10
Q

What typically causes symmetrical FGR (fetal growth restriction)/IUGR?

A

Early first-trimester insults such as chromosomal abnormalities or congenital infection –> global growth delay

Means that both length/weight and head circumference impacted

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11
Q

What typically causes asymmetrical FGR?

A
  • Uteroplacental insufficiency
  • Maternal malnutrition
  • Later in second or third trimester –> head sparing d/t fetal blood flow redistribution to vital organs
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12
Q

What are neonates who are LGA (large for gestational age) at risk for?

A
  • Birth trauma ie brachial plexus injuries, clavicular fractures, scalp hematomas
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13
Q

What supplies fetus with oxygen and nutrients essential for growth and development intrauterine?

A

Placenta

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14
Q

Describe fetal oxygen delivery

A
  • Lungs filled with fluid
  • Oxygen comes from placenta
  • Arteries in lung constricted and vascular resistance in lungs increased –> little blood reaching lungs

hypoxic pulmonary vasoconstriction

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15
Q

What is the pathway of blood flow from the umbilical vein?

A
  • Ductus venosus
  • Inferior vena cava bypassing liver
  • R atrium
  • L atrium
  • Body/organs
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16
Q

How do fetal lungs prepare for extrauterine life at the end of gestation?

A
  • Increased production of surfactant prevents collapse of alveoli
  • Decreased production of fetal lung fluid –> lungs start removing fluid out of alveoli and into interstitial space
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17
Q

How does respiratory adaption occur during birth?

A

Stimuli
1) Thermal –> change in temp stimulates respiratory center in medulla
2) Light and Sound
3) Tactile stimulation from labor contractions

–> trigger infant’s first breath and increased intrapulmonary pressure forcing remaining fluid out of lungs

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18
Q

What occurs during cardiovascular adaptation at birth?

A

Umbilical cord is cut and onset of respirations causes:
* O2 content of blood to increase –> pulmonary vasodilation –> decreased pulmonary vascular resistance –> increased blood flow to lungs
* Increased venous blood flow to left atrium –> increased L atrial pressure closes foramen ovale
* O2 constricts ductus arteriosus and begins to close with first breath
* Umbilical vein and ductus venosus collapse
* Increased SVR and systemic oxygen content causes umbilical arteries to vasoconstrict
* Fetal shunts and umbilical arteries and veins undergo fibrotic changes and close completely

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19
Q

What is the function of crying in adaptation of the newborn?

A

Promotes lung expansion and protects lung volume

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20
Q

What is the initial breathing pattern after birth?

A
  • Irregular, modulation of chemoreceptors and stretch receptors makes it rhythmic
  • Preterm infants may not be rhythmic due after birth b/c of poor respiratory drive, weak muscles, flexible ribs, surfactant deficiency, and impaired lung liquid clearance
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21
Q

What is required for successful gas exchange and initiation of respiration in a newborn?

A
  • adequate pulmonary gas exchange surface area and well-developed pulmonary vasculature
  • Compliant lungs, mature airways, chest wall, respiratory muscles, and neural mechanisms
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22
Q

What are the new 2020 recommendations for neonatal resuscitation?

A
  • Intubation and suctioning is not recommended for not crying babies born through meconium unless concern for airway obstruction post PPV
  • Umbilical vein is preferred vascular access point for IV meds
  • All births should be attended by 1+ people who can perform neonatal resuscitation
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23
Q

What are the 3 considerations for resuscitation at birth? If the answer to all of these questions is yes, what should you do?

A
  • Is the baby term?
  • What is the tone? (want flexion of extremities)
  • Is the baby breathing or crying?

If yes: no resuscitation needed: routine care with mother

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24
Q

What is considered routine care with mother?

A
  • Dry, warm
  • Position airway and clear secretions if needed
  • Preferably skin to skin with mother
  • Ongoing observation and evaluation
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25
Q

What should you do if the answer to any of the 3 considerations for resuscitation in the first 30 seconds of life are no? What are those questions again?

A

Is the baby to term? What is the tone? Is the baby breathing or crying?

  1. Cut cord immediately and take baby to warmer
  2. Stabilize: warm, dry, stimulate, position airway, clear secretions
  3. Tactile stimulation while drying and suctioning (no more than 30 s)
  4. Suction if necessary with bulb suction (mouth before nose)
  5. Start APGAR monitor clock and begin resuscitation
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26
Q

If labored breathing or persistent cyanosis in 30 seconds to 1 minute of life, what do you do?

A
  • Position and clear airway
  • Place SPO2 monitor on right hand or wrist
  • Provide supplemental O2 as needed
  • Consider CPAP
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27
Q

What should you do if apnea/gasping and HR <100 BPM

A
  • Begin PPV with BVM rate of 40-60 breaths per minute
  • If PPV not effective: MR SOPA
  • M: Mask repositioning
  • R: Repositioning
  • S: Suction
  • O: Open the mouth
  • P: Increase the pressure
  • A: Change the airway (ie transition to laryngeal mask or ET tube)
  • Place on SPO2 monitor and continuous ECG
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28
Q

When would you perform chest compressions on a newborn?

A
  • HR <60 despite adequate PPV for 30 s
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29
Q

What is the preferred way to do chest compressions on a newborn?

A
  • 3:1 (3 compressions before or after each inflation)
  • Hands encircling chest while thumbs depress sternum
  • FiO2 should be increased to 100%
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30
Q

What can you consider during chest compressions?

A
  • Umbilical vein catheterization

If HR persistently below 60 BPM:
* Administer IV epinephrine .01-.03 mg/kg through umbilical vein or .05-.1 mg/kg ET tube
* Always at 1:10,000 conc

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31
Q

If a neonate is still not responding to resuscitation after PPV, chest compressions, and epi what do you do?

A
  • Consider hypoglycemia and correct with 2 mL/kg D10W
  • Consider hypovolemia
  • Assess for potential pneumothorax
  • If no response to resuscitation efforts in 20 minutes may consider termination of efforts
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32
Q

How do you correct hypovolemia in neonates?

A
  • Volume expander of normal saline
  • If substantial blood loss consider uncross matched type O- blood volume of 10 mL/kg given IV over 5-10 minutes
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33
Q

What should you do if HR >100 bpm and effective spontaneous respirations?

A
  • Discontinue PPV
  • Administer supplemental O2 as needed to maintain target preductal SpO2
  • Maintain close monitoring with SpO2 and ECG

1 min: 60-65
2 min: 65-70
3 min: 70-75
4 min: 75-80
5 min: 80-85
10 min: 85-95

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34
Q

What is post resuscitation care of infant?

A
  • Infant >36 weeks estimated getational age who received resuscitation should be examined for HIE (hypoxic ischemic encephalopathy)to determine if they meet criteria for therapeutic hypothermia
  • Monitor temperature
  • Monitor glucose level
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35
Q

What are risk factors for neonatal respiratory distress?

A
  • C-section deliveries
  • Decreased gestational age
  • Low birth weight
  • Male sex
  • Maternal asthma
  • Maternal gestational diabetes
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36
Q

What causes increased work of breathing in neonates?

A
  • Decreased lung compliance or airway resistance
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37
Q

What should be in your differential diagnosis of a neonate with respiratory distress?

A
  • Transient tachypnea of the newborn
  • Respiratory distress syndrome
  • Pneumonia
  • Meconium aspiration syndrome
  • Sepsis
  • Meningitis
  • Respiratory rate suppression from maternal narcotics
  • Congenital airway anomalies

Less common: congenital heart defects, airway malformation, inborn errors of metabolism use

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38
Q

What is a normal respiratory rate for newborns?

A

30-60 breaths per minute

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39
Q

What causes transient tachypnea of the newborn?

A
  • Elective c-sections –> delay in reabsorption of lung fluid during delivery
  • Pulmonary edema due to delayed resorption of alveolar fluid leading to decreased lung compliance and tachypnea
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40
Q

What is seen on a CXR of a newborn with TTN?

A
  • Hyperexpansion
  • Perihilar densities with fissure fluid
  • Pleural effusions
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41
Q

How long should TTN last?

A

first 2 hours of life to up to 72 hours, but normally resolves within 24 hours

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42
Q

How is TTN diagnosed?

A
  • Pulse oximetry, physical examination, and chest radiograph
  • Labs such as blood cultures, CBC, and CRP
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43
Q

How is TTN managed?

A

Self-limiting, supportive care

DO NOT use furosemide (may cause weight loss and hyponatremia)

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44
Q

At what point in gestations does the risk for meconium aspiration increase?

A
  • After 41 weeks gestation
  • After 39 weeks, healthy women should consider induction
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45
Q

What is meconium?

A

Sterile substance produced in fetus’ intestines prior to birth and becomes newborn’s first stool after birth

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46
Q

What can cause early release of meconium?

A

Uterine stress during delivery

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47
Q

What can meconium aspiration cause?

A
  • Airway obstruction
  • Inactive surfactant
  • Trigger inflammatory changes

Symptoms: respiratory distress and hypoxia

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48
Q

What is the diagnostic criteria for MAS?

A
  • Respiratory stress AND
  • Meconium present in amniotic fluid or trachea if intubated
  • Chest X-ray with bilateral fluffy densities with hyperinflation
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49
Q

Meconium aspiration syndrome management

A
  • Newborn dried, warmed, and stimulated
  • Oxygen supplementation if not breathing or HR <100 bpm
  • If HR <60, CPR
  • Suction
  • Full neonatal resuscitation protocol if respiratory distress does not improve after initial management

Routine intubation not recommended

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50
Q

What is the leading respiratory disorder in preterm infants that causes severe symptoms and can lead to lasting impaired gas exchange

A

Respiratory distress syndrome

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51
Q

Risk factors for respiratory distress syndrome

A
  • Preterm infants <37 weeks (due to insufficient surfactant), younger –> more at risk
  • Environmental and genetic factors for late preterm and term infants
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52
Q

Presentation of respriatory distress syndrome

A
  • Minutes to hours after birth
  • Retractions, nasal flaring
  • Cyanosis
  • Grunting
  • Tachypnea
  • Symptoms worse by third day
53
Q

Diagnostics used for respiratory distress syndrome

A
  • Pulse oximetry
  • Chest radiographs: ground glass appearance
  • Blood gas
  • Blood culture
  • CRP
  • Glucose level
  • Echocardiogram
54
Q

Management of respiratory distress syndrome

A
  • Prenatal glucocorticoids
  • Postnatal sufactant for early preterm infants
  • Ventilation, NCPAP, or NIPPV for respiratory support after birth with supplemental oxygen if needed for hypoxemia
55
Q

What is the pathway of persistent pulmonary hypertension of newborn

A

Pulmonary vascular resistance abnormally elevated after birth –> right to left shunting of blood through fetal circulatory pathways (foramen ovale, ductus arteriosus) –> severe hypoxemia primarily in term or late preterm infants (older than 34 weeks)

56
Q

Respiratory diagnoses associated with PPHN

A
  • Meconium aspiration syndrome
  • Pneumonia
  • RDS
  • Prenatal: intrauterine/perinatal asphyxia, in utero exposure of SSRIs during second half of pregnancy
57
Q

Pathophysiology of PPHN

A
  1. Vasoconstriction secondary to perinatal hypoxia related to acute event (sepsis or asphyxia)
  2. Prenatal increase in pulmonary vascular smooth muscle development (meconium aspiration syndrome
  3. Lung hypoplasia (diaphragmatic hernia)

All due to ventilation perfusion mismatch

58
Q

Clinical findings of PPHN

A
  • Respiratory distress in first 24 hours of life
  • Tachypnea
  • Retractions
  • Grunting
  • Cyanosis
  • Meconium staining of skin and nails (may have)
  • Harsh systolic murmur at lower left sternal border (cardiac exam)
59
Q

Diagnosis of PPHN

A
  • ABGs
  • Pulse oximetry
  • Chest radiograph: lung infiltrates
  • Echocardiogram: normal cardiac anatomy with pulmonary hypertension
  • Blood cultures and empiric antimicrobial therapy
60
Q

Management of PPHN

A
  • Goal: decrease pulmonary arterial pressure
  • Supportive cardiorespiratory care (O2 ventilation, fluid therapy, correction of acidosis)
  • Severe: vasodilatory agents (nitric oxide, sildenafil)
  • ECMO if above fails
  • Specific treatment for any associated parenchymal lung disease
61
Q

What is the purpose of ECMO in PPHN?

A
  • Respiratory support when heart/lungs unable to provide adequate gas exchange or perfusion
  • Removes blood, waste, and oxygenates
62
Q

If PPHN is very severe, what are the babies at risk for?

A

Developmental delay

63
Q

What are AAP glucose concentration targets for neonatal hypoglycemia?

A
  • 0-4 hours: blood glucose >40
  • 4-24 hours: blood glucose >45
  • No established threshold at which to intervene
64
Q

How does glucose change over the first few hours of life in a healthy newborn?

A
  • falls during first 1-2 hours due to discontinuation of placental nutrients –> physiologic hypoglycemia (glucose as low as 30)
  • Lowest in first 2-4 hours and stabilizes around 4-6 hours at 45-79 mg/dL
  • Often transient and asymptomatic and compensated by fat
  • Breastfed infants often have NH for first 24 hours of life without symptoms or abnormal exam
65
Q

Risk factors for neonatal hypoglycemia

A
  • Infant of diabetic mother
  • Large for gestational age
  • Small for gestational age
  • Late preterm babies
  • Babies exposed to certain maternal meds such as labetolol or terbutaline
  • Babies with certain genetic syndromes (Turner, Beckwith-Wiedermann, glycogen storage diseases, galactosemia)
66
Q

Physical exam for NH

A

Evaluate for high-risk symptoms
* High pitched cry
* Cyanosis
* Floppiness
* Exaggerated moro reflex
* Lethargy
* Seizures
* Jitteriness
* Abnormal feeding
* Irritability
* Apnea

67
Q

What are recommendations for NH in healthy term newborns?

A
  • Routine glucose screening not recommended in asymptomatic, healthy, term newborn after uncomplicated pregnancy and delivery
68
Q

What are high-risk infants that require screening for NH, even if asymptomatic

A
  • Preterm and late preterm infants
  • LGA or SGA
  • Infants of mothers with diabetes
69
Q

What are factors that can cause you to consider screening infants for NH`

A
  • Low birthweight
  • Fetal growth restriction
  • Birth asphyxia
  • Maternal eclampsia or hypertension
  • Meconium aspiration
  • Postmature infants
  • Infant requiring intensive care
  • Infant with congenital syndrome associated with hypoglycemia
70
Q

How would you screen for NH

A

POC glucose can be used for screening but should be confirmed with serum glucose

71
Q

How would you treat NH if symptomatic and <40 mg/dL

A

IV glucose

72
Q

What should be done if an asymptomatic infant at birth to 4 hours of age after initial feed presents with a <25 mg/dL initial glucose screen

A
  • Feed and check in 1 hour
  • If <25 mg/dL after 1 hour give IV glucose
  • If 25-40 mg/dL refeed and give IV glucose as needed
73
Q

If an asymptomatic infant 4-24 hours of age has glucose <40, what should you do?

A
  • Continue feeds q 2-3 hours
  • Screen glucose prior to each feed
  • If <35 mg/dL give IV glucose
  • If 35-45 mg/dL refeed and IV glucose as needed
74
Q

What diagnosis should you consider if glucose levels don’t normalize after 24 hours?

A

Hyperinsulinemic hypoglycemia

Most common cause of persistent hypoglycemia in newborn period

75
Q

Unconjugated hyperbilirubinemia that arises after 24 hours of age

A

physiologic jaundice

76
Q

When does neonatal jaundice tend to peak?

A

day 3-4 of age, may persist for up to a week

77
Q

What causes physiologic neonatal jaundice?

A

Catabolism of red blood cells, increased RBC volume, immature hepatic conjugation, and delayed establishment of feedings –> reduced excretion of bilirubin and increased enterohepatic circulation of bilirubin

78
Q

Any sign of jaundice within the first 24 hours of life should prompt what

A

Investigation for pathologic etiology

79
Q

Risk factors for hyperbilirubinemia

A
  • Lower gestational age
  • Jaundice within the first 24 hours of life
  • Predischarge bilirubin close to phototherapy threshold
  • Hemolysis
  • High rate of bilirubin rise
  • Phototherapy prior to discharge
  • Parent or sibling who had phototherapy or exchange transfusion
  • G6PD deficiency
  • Exclusive breastfeeding with suboptimal intake
  • Scalp hematoma or significant bruising
  • Trisomy 21
  • Macrosomic infant of a diabetic mother
80
Q

What are neurotoxicity (hyperbilirubinemic encephalopathy) risk factors?

A
  • Gestational age <38 weeks (more premature –> greater risk)
  • Albumin <3 g/dL
  • Isoimmune hemolytic disease, G6PD, or other hemolytic conditions
  • Sepsis, significant clinical
  • Instability in previous 24 hours
81
Q

How is hyperbilirubinemia diagnosed

A
  • Visual assessment for jaundice every 12 hours
  • TSB or TcB measured as soon as possible for infants jaundiced <24 hours after birth
  • TcB or TSB measured between 24-48 hours after birth or before discharge, if that occurs earlier
  • TSB measured if TcB exceeeds or is within 3 mg/dl of phototherapy threshold or if TcB is >15 mg/dL
  • Use TSB as definitive test to guide phototherapy and escalation of care decisions, including exchange transfusion
82
Q

Conjugated or direct bilirubin level greater than 1 mg/dL when TSB level is less than 5 mg/dL or 20% of TSB if the TSB level is greater than 5 mg/dL is significant and needs evaluation

A

IDK what this means exactly but I’ll come back to it

83
Q

What additional labs can be ordered to evaluate neonatal hyperbilirubinemia?

A
  • Alkaline phosphatase
  • y-glutamyl transpeptidase
  • Aminotransferase
  • Albumin
  • Coag tests
  • TORCH serology
  • Urine test for CMV
  • Blood and urine cultures
  • Fasting abdominal US to evaluate for evidence of biliary atresia or choledochal cyst
  • Check newborn screen for galactosemia, repeat test
  • Thyroid function
  • Metabolic studies
84
Q

Occurs in first week after birth from inadequate feeding. Intestinal hypomotility and poor elimination of bilirubin in stool are underlying causes

A

Breastfeeding jaundice

85
Q

What do neonates with breastfeeding jaundice need?

A

If evidence of significant weight loss, supplementation with expressed breast milk or formula

86
Q

What is the cause of breast milk jaundice?

A
  • Occurs after 1st week and can persist for up to 3 weeks
  • Inhibition of uridine diphosphate glucuronosyltransferase by pregnanediol and deconjugation of conjugated bilirubin by B-glucuronidase in breast milk are possible underlying causes
87
Q

Presentation of breast milk jaundice and management?

A

Adequate feeding and good weight gain with jaundice
Don’t withold breast milk

88
Q

What is treatment for neonatal jaundice?

A
  • Phototherapy and discontinuing when TSB decreased by 2 mg/dL and longer if risk factors for rebound hyperbilirubinemia
    Feeding
89
Q

What is rebound hyperbilirubinemia

A

TSB that reaches phototherapy threshold for infant’s age within 72-96 hours after discontinuing phototherapy

90
Q

Risk factors for rebound hyperbilirubinemia

A
  • Gestational age <38 weeks
  • <48 hours old at start of phototherapy
  • Hemolytic disease
91
Q

What should all families with neonatal hyperbilirubinemia receive before discharge?

A
  • Education about neonatal jaundice
  • Information to facilitate postdischarge care
  • Birth hospitalization information, including the TcB or TSB and the age at which it was measured, and DAT results should be transmitted to the primary care provider who will see the infant at follow-up
92
Q

What is G6PD deficiency?

A
  • X-linked recessive disorder
  • Ancestry from Sub-saharan africa, middle east, mediterranean, arabian peninsula, and southeast asia may be helpful in predicting risk
93
Q

There may be a false normal G6PD assay after what?

A

Hemolytic event or transfusion

If high clinical suspicion, repeat in 3 months

94
Q

What is the most common cause of hemolytic disease in the newborn?

A

Isoimmune hemolytic disease: ABO incompatibility

95
Q

What causes isoimmune hemolytic disease?

A
  • Transplacental passage of maternal antibodies that destroy fetal RBCs
  • Neonatal hemolysis if mother has IgG antibodies from previous exposure to A or B antigens
96
Q

If the maternal antibody screen is positive or unknown for isoimmune hemolytic disease, what shoul dthe infant have?

A

Direct antiglobin test and blood typing ASAP

97
Q

What can severe Rh incompatibility cause?

A
  • Jaundice
  • Anemia
  • Hypoalbuminemia
  • High-output heart failure
  • Fetal death
98
Q

Treatment of Rh incompatibility

A
  • Prevention!
  • Screen for ABO and Rh at first prenatal visit
  • 28 week antibody screening if Rh negative, RhoGAM given
  • 40 weeks: optional injection given
  • Postpartum: if infant Rh positive, mother given RhoGAM within 72 hours postpartum
99
Q

Clinical findings of polycythemia

A
  • Hematocrit >65% at term
  • Plethora
  • Tachypnea
  • Retractions
  • Hypoglycemia
  • Irritability, lethargy, poor feeding
  • Hyperbilirubinemia
  • Hyperviscosity with decreased perfusion of capillary beds
  • Renal vein, deep vein, or artery thrombosis = severe complication
100
Q

Etiology of polycythemia

A
  • Delayed cord clamping MCC
101
Q

Specific system effects of polycythemia

A
  • CNS: irritability, jitteriness, seizures, lethargy
  • Cardiopulmonary: respiratory distress, CHF, PPH
  • GI: vomiting, heme-positive stools, distension
  • Renal: decreased urinary output, renal vein thrombosis
  • Metabolic: hypoglycemia
  • Hematologic: hyperbilirubinemia, thrombocytopenia
102
Q

Screening and treatment of polycythemia

A

Screening with capillary heelstick
If hematocrit >68%, do venous
Tx with isovolemic partial exchange transfusion with normal saline if symptomatic
Tx for asymptomatic infants not indicated

103
Q

Considerations in determining whether to screen for disorders on newborn screening

A
  • Disease can be missed clinically at birth
  • High enough frequency in population
  • Delay in diagnosis will induce irreversible damage
  • Simple and reasonably reliable test exists
  • Treatment/intervention makes a difference if disease detected early
104
Q

How will patients with inborn errors of metabolism present in acute crisis?

A
  • Acidosis
  • Hyperammonemia
  • Hypoglycemia

Most common in patients with dysfunction related to protein, lipid, or carbohydrate metabolism

105
Q

What symptoms of inborn errors of metabolism are non specific but must be considered with an index of suspicion

A
  • Rapid deterioration in otherwise well infants
  • Emesis, poor feeding
  • Tachypnea, apnea
  • Irritability, lethargy, seizures
  • Sepsis with lack of fever
106
Q

What labs are common for inborn errors of metabolism?

A
  • Blood gas
  • Serum electrolytes
  • BUN and Cr
  • Blood glucose
  • LFT
  • CrK
  • Ammonia
  • Serum uric acid
  • Serum lactate
  • Urine ketones
  • Urinalysis
107
Q

What specific labs are seen in inborn errors of metabolism?

A
  • Elevations in amino acids in amino acidopathies and urea cycle disorders
  • Elevations in glycine with organic acidemias
  • Elevated urine acid metabolites –> organic acidemias and fatty acid oxidation disorders and amino acidopathies (most sensitive while patient in catabolic state)
108
Q

What causes inborn errors of metabolism?

A
  • Defects in metabolism of energy sources (proteins, lipids, carbohydrates)
  • Dysfunction in pathways within cellular organelles (lysosomes, peroxisomes, mitochondria
109
Q

What should be on your differential list for a lethargic infant?

A
  • Inborn error of metabolism
  • Sepsis
  • Non accidental trauma
  • Congenital heart disease
110
Q

What is phenylketonuria?

A

Deficiency in phenylalanine hydroxylase that is responsible for hydroxylation of phenylalanine to tyrosine

111
Q

What can untreated PKU cause?

A
  • Accumulation of phenylalanine (phe) and phenylketones causing permanent brain injury
  • Microcephaly, global developmental delay, eczematous rash
112
Q

What is treatment of PKU?

A
  • Lifelong restriction of phenylalanine (phe) via dietary protein restriction
  • Supplementation with phe free protein containing foods/beverages to prevent protein deficiency
  • CABs (ABCs lol did not know what this was at first)
  • Fluid resuscitation with D10
  • If patient has seizures, give rescue med and watch for respiratory depression
  • For MUSD, may need to consider hemodialysis for elevated ammonia
113
Q

What are carbohydrate disorders?

A
  • Galactosemia
  • Glycogen storage disorders
114
Q

What is galactosemia?

A
  • Deficiency in GALT (galactose-1-phosphate uridyltransferase) –> accumulation of galactose and galactose-1-phosphate
115
Q

Presentation of galactosemia

A

Initiation of lactose formula in newborn –> metabolic decompensation
* Liver dysfunction
* Jaundice
* Coagulopathy
* E. Coli sepsis
* Cataracts
* Delayed diagnosis –> intellectual disability

116
Q

chronic management of classic galactosemia

A

lifelong dietary restriction of galactose

117
Q

How are most thyroid issues in infants identified

A
  • newborn screening
  • may have diffusely enlarged, symmetrical goiter
118
Q

Presentation of neonatal hypothyroidism

A
  • Goiter
  • If severe: persistent jaundice or myxedema
119
Q

Presentation of neonatal hyperthyroidism

A
  • Irritability
  • Hyperphagia
  • Poor weight gain
  • Tachycardia
  • Hepatomegaly
  • Splenomegaly
120
Q

Diagnostics for neonatal hypo/hyperthyroidism

A
  • TSH
  • Free T4
  • Thyrotropin Receptor Antibodies (TRAbs) - stimulating and blocking antibodies. If negative, cause likely inborn error of thyroid hormone metabolism or excess maternal iodine ingestion
121
Q

If euthyroid status identified on labs (normal TSH and free T4), what additional evaluation should be performed?

A
  • Ultrasound for congenital goiter
  • Further eval by endocrinologist
122
Q

When to perform hearing screening

A
  • Joint Committee on Infant Hearing recommendations: prior to 1 month of age and rescreen within 3 months if any ear did not pass so interventions before 6 months of age
  • Screen infants admitted to NICU for longer than 5 days and those readmitted to hospital for hyperbilirubinemia requiring exchange transfusion or sepsis
123
Q

What is gastroschisis

A

Defect in abdominal wall with protruding abdominal organs without a protective membranous sac, almost always to the right of the umbilicus

124
Q

Risk factors for gastroschisis

A
  • Teratogens
  • Poor prenatal care
  • Maternal infection
  • Young maternal age
125
Q

Definition of omphalocele

A
  • Defect in abdominal wall with protruding abdominal organs through the umbilicus with thin membranous sac covering
  • Half of infants with omphalocele have genetic anomaly or genetic syndrome
  • Mortality rate 20%
126
Q

Diagnosis of omphalocele

A
  • AFP elevated in mother’s blood
  • Defects seen on prenatal ultrasound

causes of elevated AFP: dating errors, underestimation of gestational age and multiple gestation, neural/abdominal wall defects

127
Q
A
128
Q

Esophageal atresia

A

Blind esophageal pouch with or without fistulous connection between proximal or distal esophagus and airway
Present in first hours of life with copiou secretions, choking, cyanosis, respiratory distress
Hx polyhydramnios

129
Q

Diagnosis of esophageal atresia

A
  • CXR after placement of NG tube to point of resistance
130
Q
A

Pediatrics (12 decks)

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