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Pediatrics > Perinatal Period > Flashcards

Perinatal Period Flashcards

1
Q

infants born at or before 36 weeks 7 days are called?

A

preterm infants

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2
Q

infants born between 34 0/7 and 36 6/7 weeks’ gestation are called?

A

Late preterm (near-term)

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3
Q

gestations between 37 weeks 0 days and 41 weeks 7 days are called?

what type of infant

A

term infants

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4
Q

gestations of 42 weeks 0 days and longer are called?

what type of infant

A

Post term infants

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5
Q

what type of infant is at higher risk for more conditions?

A

Late preterm

hypoglycemia, jaundice, respiratory distress, temperature instability, feeding challenges, and increased rates of readmissions compared with a term counterpart.

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6
Q

most hospital systems have protocols that require late preterm infants to be monitored for how long, in addition to interventions such as passing a car seat trial before discharge?

A

48 hours

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7
Q

what type of infants are at risk for FGR secondary to uteroplacental insufficiency plus increased risk of meconium aspiration, intrauterine infection, and dysmaturity?

A

Post term neonates

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8
Q

what components are evaluated on standardized growth curves

A
  • wt
  • length
  • head circumference
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9
Q

3 categories of the standardized growth curves

A
  • Small for gestational age (SGA): Birthweights < 10th percentile.
  • Large for gestational age (LGA): Birthweights > 90th percentile
  • Appropriate for gestational age (AGA): Birthweights within 10-90th percentiles.
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10
Q

MC caused by early first-trimester insults, such as chromosomal abnormalities or congenital infection, resulting in a global growth delay.

A

Symmetrical FGR/IUGR

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11
Q

characteristic of uteroplacental insufficiency or maternal malnutrition often occurring later in 2nd or 3rd trimester, which results in “head-sparing” growth delays due to fetal blood flow redistribution to vital organs.

A

Asymmetrical FGR

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12
Q

what type of neonates are at increased risk for birth trauma such as brachial plexus injuries, clavicular fractures, or scalp hematomas

A

Neonates who are LGA

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13
Q

an important part of the transitional process; it helps promote lung expansion and protect lung volume.

A

crying

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14
Q

initially, breathing pattern is irregular, how does it become rhythmic?

A

soon after birth, modulation of chemoreceptors and stretch receptors makes it rhythmic

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15
Q

For successful gas exchange, newborn lungs require what two things?

A
  1. adequate pulmonary gas exchange surface area
  2. well-developed pulmonary vasculature
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16
Q

the primary muscle used during quiet breathing.

A

diaphragm

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17
Q

Major physiologic changes during the first 6 hrs after birth lead to ?

A

increase in oxygenation
decrease in partial pressure of carbon dioxide, arterial (PaCO2)

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18
Q

what two factors play an important role in alveolar fluid clearance

A
  • ion exchange across the pulmonary and airway epithelium
  • sodium uptake

Glucocorticoids, catecholamines, and oxygen play an important role in regulating the activity of this uptake

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19
Q

what is the preferred vascular access point for IV medications for neonates?

A

umbilical vein

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20
Q

for resuscitation, what are the 3 considerations at birth?

A
  • Is the baby term?
  • What is the tone? You want to see flexion of the extremities.
  • is the baby breathing or crying?

If yes to all —› no resuscitation needed

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21
Q

if answers no to resuscitation questions, what is the next step?

A
  • cut the cord immediately and take the baby to the warmer
  • Stabilize: warm, dry, stimulate, position airway, clear secretions
  • Tactile stimulation is typically performed while drying and suctioning infant. Should take no more than 30 seconds
  • Suction if necessary. If bulb suction needed clear mouth before nose
  • Start the APGAR monitor clock and begin resuscitation
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22
Q

if infant has labored breathing or persistent cyanosis, what are the next steps?

A
  1. position and clear airway
  2. place SpO2 monitor on right hand or wrist
  3. provide O2 if needed
  4. consider CPAP
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23
Q

If apnea/gasping and HR <100 bpm, what are the next steps?

A
  • Begin Positive Pressure Ventilation (PPV) x 40-60 breaths per minute - if not effective - MR. SOPA (M-Mask adjustment, R- Reposition, S- Suction, O- Open the mouth, P- Increase the pressure, A- Change the airway)
  • possible laryngeal mask or endotracheal intubation
  • Place on SpO2 monitor and continuous ECG
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24
Q

when to start compressions on an infant?

A

HR < 60 bpm despite adequate PPV for 30 seconds

3:1 ratio (3 compressions before or after each inflation). 30 inflations and 90 compressions per minute

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25
Q

what is the compression technique for infants?

A

hands encircling chest while the thumbs depress sternum

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26
Q

If HR is persistently below 60 bpm what is the next tx?

A

give IV EPI

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27
Q

if still no response to resuscitation after EPI and how to correct?

A
  • hypoglycemia - 2 mL/kg of D10 W
  • hypovolemia - volume expander (blood, saline)
  • potential pneumothorax
  • If no response to resuscitation efforts in 20 minutes may consider termination of efforts
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28
Q

Once HR increases to > 100 bpm and there are effective spontaneous respirations after resuscitation, what are the next steps?

A

º DC PPV
º Administer O2 as needed to maintain target preductal SpO2
- 1 min: 60-65%
- 2 min: 65-70%
- 3 min: 70-75%
- 4 min: 75-80%
- 5 min: 80-85%
- 10 min: 85-95%
º close monitoring with SpO2 and ECG

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28
Q

Infants ≥ 36 weeks estimated gestational age who received resuscitation should be examined for ?

post resuscitation care

A
  • signs of HIE to determine if they meet criteria for therapeutic hypothermia.
  • monitor temp
  • monitor glucose
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29
Q

RF of neonates with respiratory distress?

A

c-section deliveries
decreased gestational age
low birth weight
male sex
maternal asthma & gestational diabetes.

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30
Q

Differential diagnosis of A Neonate With Respiratory Distress

A
  1. Transient tachypnea of the newborn (TTN)
  2. Respiratory distress syndrome,
  3. Pneumonia
  4. Meconium aspiration syndrome
  5. Sepsis
  6. Meningitis
  7. Respiratory rate suppression from maternal narcotics
  8. Congenital airway anomalies
  9. Less common: congenital heart defects, airway malformations, inborn errors of metabolism use
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31
Q

For newborns, a normal respiratory rate is ?

A

30-60 breaths/minute

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32
Q

An increase in the number of elective c-sections has caused an increased incidence of transient tachypnea cases, why?

A

due to the delay in reabsorption of lung fluid during the delivery

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33
Q

a disease of the lung parenchyma with pulmonary edema due to delayed resorption of the alveolar fluid, leading to decreased lung compliance and tachypnea

A

Transient tachypnea (TTN)

Presents within first 2 hours of life and can continue for up to 72 hours, normally tachypnea should resolve within 12-24 hours

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34
Q

diagnostics for TTN

A

pulse ox
PE and CXR
labs - blood cx, CBC, CRP

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35
Q

management for TTN?

A

self-limiting, supp

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36
Q

what medicine should you avoid in TTN and why?

A

Furosemide

may cause wt loss and hyponatremia, and it is CI despite excess pulmonary fluid present in newborns with TTN.

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37
Q

when does the risk for meconium increase during gestation and what is recommended?

A
  • 41 wks gestation
  • after 39 wks, healthy women should consider induction if no contraindications exist
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38
Q

sterile substance that is produced in the fetus’ intestines prior to birth and becomes the newborn’s first stool after birth

A

Meconium

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39
Q

what may cause the early release of meconium

during delivery

A

uterine stress

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40
Q

diagnostic criteria for MAS?

Meconium aspiration

A

Rsp distress + one of the following:

  • Meconium present in the amniotic fluid or the trachea if intubated
  • CXR shows bilateral fluffy densities with hyperinflation.
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41
Q

management for MAS

A

º Newborn dried, warmed and stimulated
º Oxygen supplementation if not breathing and/or if HR < 100 (< 60 = CPR)
º Routine intubation is not recommended
º no indications suctioning
º Full neonatal resuscitation protocol should begin if rsp distress does not improve after the initial management

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42
Q

what is the leading respiratory disorder for preterm infants

A

Respiratory distress syndrome

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43
Q

Preterm infants are at highest risk for Respiratory distress syndrome, why?

A

insufficient amounts of surfactant present in their lungs

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44
Q

s/s of respiratory distress syndrome

A

Presentation: minutes to hours after birth
º Retractions, nasal flaring, cyanosis, grunting, tachypnea
º sx worsen by the third day

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45
Q

diagnostics for respiratory distress syndrome

A

º Pulse oximetry
º CXR —› “ground glass” appearance
º Blood gas, blood culture, CRP, glucose level
º ECG (rule out cardiac problems with similar symptoms).

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46
Q

management for respiratory distress syndrome

A
  • glucocorticoids and postnatal surfactant therapy for early preterm infants
  • Ventilation, NCPAP, NIPPV - respiratory support after birth, with supplemental oxygen if required for hypoxemia
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47
Q

etiology of persistent pulmonary HTN of newborn

A
  • pulmonary vascular resistance (PVR) remains abnml elevated after birth
  • Resulting in R to L shunting of blood through fetal circulatory pathways (foramen ovale, ductus arteriosus)
  • Causes severe hypoxemia that may not respond to conventional rsp support
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47
Q

what other rsp conditions are associated with PPHN

A
  1. Meconium aspiration syndrome
  2. Pneumonia
  3. RDS
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47
Q

Associated prenatal factors for PPHN

A
  • intrauterine/perinatal asphyxia
  • in utero exposure of SSRIs during second half of pregnancy
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48
Q

PPHN pathophys

A
  1. Vasoconstriction sec perinatal hypoxia related to an acute event (sepsis or asphyxia)
  2. prenatal increase in pulmonary vascular smooth muscle development (associated with meconium aspiration syndrome)
  3. lung hypoplasia (diaphragmatic hernia)

All due to ventilation/perfusion mismatch

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49
Q

s/s of PPHN

A
  • present within first 24 hrs of life
  • Respiratory distress - tachypnea, retractions, grunting, and cyanosis
  • Meconium staining of skin and nails
  • Cardiac - harsh systolic murmur at lower left sternal border
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50
Q

diagnostics for PPHN

A
  • ABGs
  • Pulse oximetry
  • CXR: lung infiltrates related to lung pathology
  • Echo (confirms): demonstrates normal cardiac anatomy with pulmonary hypertension
  • Blood cultures and empiric antimicrobial therapy
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51
Q

management for PPHN

A

Goal: decreasing pulmonary arterial pressure

  1. General supportive cardiorespiratory care (O2 ventilation, fluid therapy, correction of acidosis)
    - Severe - vasodilators (NO, sildenafil)
  2. ECMO - if above therapies fail
    - provides rsp support when heart/lungs are unable to provide adequate gas exchange or perfusion; removes blood, removes waste, oxygenates
  3. Specific tx for any associated parenchymal lung disease
  4. if very severe, these children are at increased risk for developmental delay
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52
Q

one of the most common reasons for admission to neonatal units in term infants worldwide

A

neonatal hypoglycemia

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53
Q

AAP glucose concentration targets:

A

º 0-4 hours: blood glucose > 40 mg/dl
º 4-24 hours: blood glucose > 45 mg/dl

No established threshold has been identified

54
Q

what is “physiologic hypoglycemia”

A
  • In a healthy, term newborn glucose falls during first 1-2 hrs of life in relation to the DC of placental nutrient source
  • glucose levels as low as 30 mg/dL
55
Q

Breastfed infants can often have NH for how long w/o any symptoms or abnormal findings on physical exam.

A

first 24 hours of life

56
Q

RF for neonatal hypoglycemia

A
  • DM mother
  • LGA
  • SGA
  • Late preterm babies
  • babies exposed to certain maternal meds (labetalol, terbutaline)
  • genetic syndromes (Turner Syndrome, Beckwith-Wiedemann Syndrome, glycogen storage diseases and galactosemia)
57
Q

High risk PE findings of neonatal hypoglycemia

A
  • High pitched cry
  • Cyanosis
  • Floppiness
  • Exaggerated Moro reflex
  • Lethargy
  • Seizures
  • Jitteriness
  • Abnormal feeding
  • Irritability
  • Apnea
58
Q

what pts warrant for neonatal hypoglycemia screening?

A

Even if asx

  • Preterm and late preterm infants (any < 37 weeks)
  • LGA or SGA
  • Infants of mothers with DM

Routine glucose screening is not recommended in asx, healthy, term newborn after uncomplicated pregnancy and delivery.

59
Q

May consider screening infants with these risk factors, based on clinical status for neonatal hypoglycemia:

A
  • Low birthweight (< 2500 grams)
  • Fetal growth restriction
  • Birth asphyxia
  • Maternal eclampsia or hypertension
  • Meconium aspiration
  • Postmature infants (risk for placental insufficiency)
  • Infant requiring intensive care
  • Infant with congenital syndrome associated with hypoglycemia
60
Q

diagnostic for neonatal hypoglycemia

A

POC glucose as a screening method, confirmed with serum glucose given variation in reads

61
Q

If glucose levels are unable to be normalized after 24 hrs, what is the next step?

neonatal hypoglycemia

A

possible hyperinsulinemic hypoglycemia, MCC persistent hypoglycemia in the newborn period

62
Q

what is physiologic jaundice?

A

unconjugated hyperbilirubinemia that arises after 24 hrs of age, typically peaking at approximately day 3 or 4 of age, and may persist for up to 1 week.

63
Q

how does physiologic jaundice happen?

A
  • catabolism of RBC (half-life of RBCs in neonates is 90 d)
  • increased RBC volume
  • immature hepatic conjugation
  • delayed establishment of feedings

= reduced excretion of bilirubin and increased enterohepatic circulation of bilirubin

64
Q

Any signs of jaundice within the first 24 hours after birth should prompt investigation for ?

A

pathologic etiology

65
Q

Rf 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 (increase of 0.3 mg/dL/hour in first 24 hrs or > 0.2 mg/dL/hr after the first 24 hrs)
  • 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
66
Q

neurotoxicity RFs

A
  1. Gestational age < 38 weeks (the more premature, the greater the risk)
  2. Albumin < 3 g/dL
  3. Isoimmune hemolytic disease, G6PD or other hemolytic conditions
  4. Sepsis, significant clinical
  5. Instability in the previous 24 hours.
67
Q

what is used as the definitive test to guide phototherapy and escalation of-care decisions, including exchange transfusion

hyperbilirubinemia

A

TSB

67
Q

diagnostic work-up for hyperbilirubinemia

A
  • All visually assessed for jaundice q12h following delivery until DC. TSB/TcB ASAP for infants w/ jaundiced < 24 hrs after birth.
  • TcB/TSB w/n 24-48 hours after birth or before DC, if that occurs earlier
  • TSB measured if TcB exceeds/within 3 mg/dL of phototherapy tx threshold or ≥15 mg/dL
68
Q

when are additional labs warranted for hyperbilirubinemia?

A
  1. conjugated/direct bilirubin > 1 mg/dL + TSB < 5 mg/dL
  2. 20% of TSB (if TSB > 5 mg/dL)

galactosemia, and repeat testing for galactosemia and thyroid function, and perform metabolic studies (glucose, lactate, ammonia, ferritin, and serum amino acid levels)

69
Q

what work up should be considered to evaluate for evidence of biliary atresia or a choledochal cyst.

A

Fasting abdominal ultrasonography

70
Q
  • occurs in the 1st wk after birth from inadequate feeding
  • Intestinal hypomotility and poor elimination of bilirubin in stool are underlying causes
  • Affected neonates with evidence of significant wt loss need supplementation with expressed breast milk or formula.

what type of jaundice?

A

breastfeeding jaundice

71
Q
  • occurs after 1st wk and can persist for 3 wks.
  • Inhibition of uridine diphosphate glucuronosyltransferase by pregnanediol and deconjugation of conjugated bilirubin by β-glucuronidase in breast milk
  • adequate feeding and good wt gain in infants

what type of jaundice?

A

breask milk jaundice

72
Q

tx for hyperbilirubinemia

A

phototherapy

There are two curves, one of infants with neurotoxicity risk factors (outlined above) and one for infants without neurotoxicity risk factors. Both curves are organized by gestational age.

73
Q

For all babies with jaundice, what is the most important first intervention?

A

feeding

IV fluids are not routinely recommended.

74
Q

clinical findings of the bilirubin neurotoxicity phases

A
  • poor sucking, high-pitched cry, stupor, hypotonia, seizures
  • hypertonia of extensor muscles, opisthotonus, retrocollis, fever
  • generalized hypertonia
75
Q

DC phototherapy is an option when the TSB has decreased by ? below the hour-specific threshold at the initiation of phototherapy.

A

at least 2 mg/dL

76
Q

what is rebound hyperbilirubinemia?

A

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

77
Q

Risk factors for rebound hyperbilirubinemia:

A
  • Gestational age < 38 weeks
    • < 48 hours old at the start of phototherapy
    • Hemolytic disease
78
Q

before discharge, all families should receive:

hyperbilirubinemia

A
  • Education about neonatal jaundice (written and verbal).
  • Info to facilitate postdischarge care
  • Birth hospitalization info - last TcB or TSB and what age, and DAT results (if any) to PCP for f/u
79
Q

what is G6PD deficiency

A

x-linked recessive, MC no FHx
Genetic ancestry - Sub-Saharan Africa, Middle East, Mediterranean, Arabian Peninsula and SE Asia

80
Q

there might be a false normal G6PD assay shortly after what?

A
  • hemolytic event or has been transfused
  • repeat testing at 3 mo post discharge.
81
Q

the most common cause of hemolytic disease in the newborn

A
  • ABO incompatibility
  • results from transplacental passage of maternal antibodies that destroy fetal red cells
82
Q

pathophys of RH incompatibility

A
  1. father passes down Rh+ to baby, mother is Rh-, Fetal red blood cells pass into mother’s circulation
  2. IgG antibodies develop, cross placenta causing significant hemolysis
  3. Severe disease may cause jaundice, anemia, hypoalbuminemia, high-output HF, and or fetal death
  4. Anemia stimulates fetal bone marrow to produce and release immature RBCs (erythroblasts) into the fetal circulation (erythroblastosis fetalis)
83
Q

tx for RH incompatibility

A

Best treatment is prevention

  • first prenatal visit: all pregnant women should be scheduled for ABO blood group and Rh (D) antigen
  • 28 weeks: Antibody screening performed if RH negative, anti-D immunoglobulin (RhoGam) given
  • 40 weeks: optional injection given if 12 wks have passed since first
  • Postpartum: If infant is Rh+, give mother RhoGam shot within 72 hrs postpartum
84
Q

clinical findings of polycythemia

A
  • Hematocrit > 65% (venous) at term
  • Plethora, tachypnea, retractions
  • Hypoglycemia, irritability, lethargy, poor feeding
  • Hyperbilirubinemia
  • hyperviscosity with decreased perfusion of capillary beds
  • several organ systems affected
  • Renal vein, other deep vein, or artery thrombosis is a severe complication
85
Q

MCC of benign neonatal polycythemia

A

delayed cord clamping

86
Q

clinical findings of polycythemia

A
  • Can affect several organ systems
  • CNS: irritability, jitteriness, seizures, lethargy
  • Cardiopulmonary: respiratory distress, chf, pph
  • GI: vomiting, heme-positive stools, distention
  • Renal: decreased urinary output, renal vein thrombosis
  • Metabolic: hypoglycemia
  • Hematologic: hyperbilirubinemia, thrombocytopenia
87
Q

diagnostic and tx for polycythemia

A
  1. diagnostic - measure capillary heelstick hematocrit; If > 68%, do venous
  2. Tx when infant symptomatic
    - Isovolemic partial exchange transfusion with normal saline - “dilutes” blood, effectively decreasing the hematocrit
  3. Tx for asx strictly on hematocrit is not indicated as there is no proven long term benefit
88
Q

3 routine newborn screenings

A
  1. Metabolic testing
  2. Newborn hearing screening
  3. Universal newborn screening for critical congenital heart disease (CCHD)
89
Q

for newborn screening, common considerations in determining whether to screen for disorders:

A
  • disease that can be missed clinically at birth
  • high enough frequency in population
  • delay in dx will induce irreversible damage
  • simple and reasonably reliable test exists
  • tx/intervention makes a difference if the disease is detected early
90
Q

newborn pts often present in acute crisis with one or more of the following errors of metabolism: ?
MC in who?

A
  1. acidosis
  2. hyperammonemia
  3. hypoglycemia

MC in dysfunctions related to protein, lipid, or carb metabolism

91
Q

what s/s are good index of suspicion in inborn errors?

A
  1. rapid deterioration in otherwise well infants
  2. emesis, poor feeding
  3. tachypnea, apnea
  4. irritability, lethargy, seizures
  5. “sepsis” with LACK OF FEVER
92
Q

what specific lab can be used to support dx fatty acid oxidation disorders (FAOD)?

A

urine organic acids

93
Q

what specific lab is the most sensitive when performed while pt in a catabolic state?

A

urine organic acids

94
Q

inborn error disorders are due to what 2 pathophys?

A
  1. defects in metabolism of energy sources - protein, lipid, carbs
  2. dysfunction in pathways within cellular organelles - lysosomes, perioxisomes, mitochondria
95
Q

deficiency in phenylalanine hydroxylase (PAH)
what is this disorder

A

phenylketonuria (PKU)

96
Q

what happens if PKU is left untreated?

A

accumulation of phe and pheylketones = permanent brain injury

96
Q

tx for PKU

A
  1. strict lifelong restriction of phe - protein restriction
  2. supplementation with phe-free protein-containing foods/beverages to prevent protein deficiency
  3. CAB
  4. fluid resuscitation
  5. dextrose containing isotonic IVF (D10) - promotes anabolic state
    - avoid hypotonic fluids d/t risk of cerebral edema
  6. if seizure - resure meds and watch for rsp depression
  7. if MUSD - hemodialysis for elevated ammonia
96
Q

2 carbohydrate disorders

A
  1. glactosemia
  2. glycogen storage disorders (GSDs)
97
Q

what is classic galactosemia?

A

def in galactose-1-phosphate uridyltransferase (GALT)

98
Q

presentation of classic galactosemia?

A

start of lactose formula in newborn = metabolic decompensation

  • liver dysfunction, jaundice, coagulopathy
  • escherichia coli sepsis and cataracts
99
Q

what may happen with a delayed dx who survive initial episode of classic galactosemia?

A

metabolic decomposition

intellectual disability

100
Q

Clinically apparent goiters are more commonly associated with ?

A

inborn errors of thyroid hormone metabolism

Presentation: Typically is a diffusely enlarged, symmetrical goiter

101
Q

difference between hypothyroid vs hyperthyroidism presentation?

A
  • Hypothyroid: many will have no other symptoms outside of goiter; if severe, may have persistent jaundice or myxedema
  • Hyperthyroid: irritability, hyperphagia, poor weight gain, tachycardia, hepatomegaly, splenomegaly
102
Q

diagnostics for neonatal thyroid disease?

hypo, hyper, euthyroid

A
  1. Hypothyroid: TSH; or normal free T4
    - Check Thyrotropin Receptor Antibodies (TRAbs)
  2. Hyperthyroid: TSH; or normal free T4
    - Check TRAbs
  3. Euthyroid: Normal TSH and free T4
    - US for congenital goiters
    - Further eval by endocrinologist
103
Q

at what age is recommended for hearing screening

A

prior to 1 month of age
rescreening within 3 months if any ear did not pass, so that appropriate intervention can occur before 6 months of age.

104
Q

additional recommendations on hearing screenings are for who?

A
  • NICU > 5 days
  • readmitted to hospital for hyperbilirubinemia requiring exchange transfusion
  • sepsis
105
Q

Defect in the abdominal wall with protruding abdominal organs (typically the small intestine, but can include the stomach and colon) without a protective membranous sac, this opening is almost always to the right of the umbilicus

what type of GI anomality?

A

gastroschisis
Risk factors: teratogens, poor prenatal care, maternal infection, young maternal age

106
Q

Defect in the abdominal wall with protruding abdominal organs through the umbilicus however thin membranous sac overlies the procuring organs (small intestine, liver, stomach, spleen, bladder, uterus, ovaries)

which type of GI abnormlity?

A

omphalocele

107
Q

w/u for GI abnormalities (opmhalocele, gastroschisis)

A
  • elevated AFP (maternal)
  • Prenatal US
108
Q

MCC of elevated maternal serum AFP levels?
Other causes?

GI anomalities

A

dating errors

  • underestimation of gestational age
  • multiple gestation
  • neural tube defects and abdominal wall defects.
109
Q

Characterized by a blind esophageal pouch w/wo a fistulous connection between proximal or distal esophagus and airway

what congenital anomaly?

A

esophageal atresia

tracheoesophageal distula MC

110
Q

Present in first hours of life with copious secretions, choking, cyanosis, respiratory distress-hx of polyhydramnios (excess amniotic fluid)

dx?
w/u?
tx? definitive tx?

congenital anomaly

A
  • esophageal atresia
  • Confirmed with CXR after careful placement of NG tube to point of resistance is met (tube seen in blind pouch)
  • suction to drain secretions, elevate HOB, IV glucose and fluids
  • definitive: surgical ligation of fistula and ends of esophagus anastomosed
111
Q

MC intestinal obstructions are?

A

bowel atresias

112
Q

the most common surgical emergency seen in neonate

A

Intestinal obstruction

113
Q

difference between presentations of high intestinal obstruction vs lower intstinal obstruction

A
  • high - present soon after birth with emesis; Less prominent abdominal obstruction
  • Lower - abdominal distention and late onset of emesis, often with delayed or absent stooling
114
Q

two common intestinal atresia types are ? Where else can it happen?

A
  • duodenal and jejunoileal atresia
  • could also happen in the colon or anus
115
Q

duodenal atresia is linked to ____ while jejunoileal atresia is linked to _____

conditions

A

Down syndrome
cystic fibrosis

116
Q

RF for duodenal and jejunoileal atresia

A

Smoking and premature birth

117
Q

presentation of intestinal atresia

A
  • result in a blind pouch and intestinal obstruction
  • dilation proximal to the obstruction, causing abdominal distension, while no air can be found distal to the obstruction
  • failure to pass meconium
118
Q

radiography shows a double bubble sign where both the duodenum and the nearby stomach become filled with air.

which intestinal atresia

A

duodenal atresia

119
Q

XR shows a triple bubble sign where the jejunum is also dilated

which intestinal atresia

A

jejunal atresia

120
Q

If the obstruction is before the major duodenal papilla, what type of vomitting will result?

A

non-bilious vomiting

it is where bile and pancreatic juices are emptied into the duodenum, the infant will have

121
Q

If the obstruction is distal to the major duodenal papilla, they’ll have what type of vomitting?

A

bilious vomiting
This often occurs just hours after birth.

122
Q

neural tube RF

A

inadequate folic acid, maternal diabetes, maternal obesity, maternal hyperthermia, exposure to valproate

123
Q

the anterior neuropore doesn’t close properly, the forebrain fails to develop
an absence of structures derived from the forebrain and skull, forehead is absent or shortened

which neural tube defect?

A

ancencephaly

124
Q

subtypes of spina bifida

A

spina bifida occulta, meningocele, myelomeningocel

125
Q

Caused by failure to close the posterior spinal portion of the neural tube, often affects the lumbar region

what type of neural tube defect

A

Spina bifida (aka myelomeningocele)

126
Q
  • cystic mass containing neural tissues protrudes from a bony defect in the vertebral arches
  • Important to obtain an ultrasound if there are any
  • abnormalities on physical exam
  • May be associated with motor and sensory deficits below the spinal lesion
  • Bladder and rectal incontinence and sexual dysfunction may also be present

dx?

A

Spina bifida (aka myelomeningocele)

127
Q

hair dimple or birth mark above lesion
which type of spina bifida

A

spina bifida occulta

128
Q

meninges NOT spinal nerves slip between vertebrae

which type of spina bifida

A

meningocele

129
Q

spinal cord and meninges protrude out of vertebrae,

which type of spina bifida

A

myelomeningocele

130
Q

w/u for neural tube defects

A
  1. US
  2. maternal serum AFP
  3. MRI after birth
131
Q

which spina bifida would NOT show an increase of AFP?

A

spina bifida occulta - nml AFP

132
Q

tx for neural tube defects

A
  1. C-section followed by early surgical closure of meningocele and meningomyelocele
  2. management to avoid complications and restore as much as neuro function as possible
  3. lifelong course of surgery, PT, orthopedic management
  4. additional tx for chronic dx (kyphosis, scoliosis, paresis of LE)
133
Q

All women of childbearing age should take ?, which can prevent neural tube defects

A

prophylactic folate

Pediatrics (23 decks)

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