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NICU Flashcards

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1
Q

What does NIPT test for and when can you do it?

A

Non-invasive prenatal testing (NIPT)
¤ NOT for ONTDs, only aneuploidies (T21/18/13) and sex chromosome abnormalities
¤ Available after 10 weeks GA
¤ Measures cell-free fetal DNA in maternal blood (“liquid” placental sample)
¤ Considered a screening test only, results must be confirmed by invasive testing

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2
Q

What does chorionic villus sampling test for and when can you do it?

A

Chorionic villous sampling
¤ Earliest prenatal diagnostic technique (10-13
weeks)
¤ Biopsy of chorionic villi for chromosomal analysis
¤ Cannot assess for ONTDs
¤ Higher rate of fetal loss, risk of infection,
PROM, limb anomalies

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3
Q

What does amniocentesis test for and when can you do it?

A

Amniocentesis
¤ Typically performed at 15-20 weeks
¤ Aspiration of amniotic fluid forchromosomal analysis +AFP levels + acetylcholinesterase
¤ Canalso be used to assess fetal lung maturity (L:Sratio > 2), measure bilirubin, TORCH infections

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4
Q

What does decreased FHR variability mean on the prenatal tracing?

A

decreased cerebral oxygenation

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5
Q

What are some common causes of fetal tachycardia?

A 
¤Fever (maternal)
¤ Arrhythmia
¤ Thyrotoxicosis
¤Infection (chorioamnionitis)
¤Medications (e.g. beta-agonists, parasympathetic blockers)
¤ Anemia 
¤Hypoxia/Fetal distress

̈ A sinusoidal FHR tracing = anemia until proven otherwise!

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6
Q

List some neonatal effects of a mom who smokes during pregnancy

A
  • Growth restriction
  • Preterm labour and delivery
  • Premature ROM
  • Placental abruption
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7
Q

What are some post natal effects of cigarette smoking?

A
  • SIDS

- No convincing evidence that nicotine exposure associated with neonatal withdrawal syndrome

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8
Q

What is the definition of FASD?

A

Fetal alcohol spectrum disorder
¤ Leading known cause of preventable developmental disability
¤ Describes FAS, partial FAS, and “neurobehavioural disorder associated with prenatal alcohol exposure” (ND-PAE)

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9
Q

What are the postnatal complications of alcohol use in pregnancy?

A

¤ Exposure in 1st trimester associated with facial anomalies and major structural anomalies
¤ Exposure in 2nd trimester increases risk of spontaneous abortion
¤ Exposure in 3rd trimester predominantly affects weight, length, and brain growth

̈ However, neurobehavioral effects may occur with a range of exposures throughout gestation, even in the absence of facial or structural brain anomalies.

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10
Q

List some facial features of FASD?

A 
small palpebral fissure
smooth philtrum
thin upper lip
microcephaly
low nasal bridge
epicentral folds
minor ear abnormalities
micrognathia
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11
Q

How long does an infant with a mom who had SSRI use during pregnancy need to be observed?

A

48 hours

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12
Q

What neonatal and post natal effects are seen if mom uses cocaine?

A

Cocaine
¤Use during pregnancy linked with spontaneous abortion, fetaldemise, placental abruption, prematurity and IUGR

Neonatal effects
¤Neurobehavioural abnormalities (tremors, high-pitched cry, irritability, hyper-alertness, episodes of apnea/tachypnea)
¤Usually present by 48-72 hours
¤Abnormal auditory brainstem responses and transient abnormal EEG changes

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13
Q

What are some symptoms of NAS?

A

Opioids
¤ High pitched cry/irritability
¤ Sleep and wake disturbances
¤ Alterations in tone or movement (eg: hyperactive primitive reflexes, hypertonicity, and tremors with resultant skin excoriation)
¤ Feeding difficulties
¤ Gastrointestinal disturbances (eg: vomiting and loose stools)
¤ Autonomic dysfunction (sweating, sneezing, mottling, fever, nasal stuffiness, and yawning)
¤ Failure to thrive

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14
Q

When does NAS present?

A

̈ Timing of symptoms depends on half life of opioid being used (e.g. delayed onset of NAS due to longer half life of methadone (5 days)
̈ Breast-feeding is generally supported with some exceptions

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15
Q

How do we treat NAS?

A

̈ Pharmacological therapy (morphine, phenobarbital, clonidine) may be required if high NAS scores
despite comfort care measures
̈ NOTE: Never give naloxone in mother with chronic opioid use

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16
Q

Describe the syndrome seen with fetal dilantin exposure?

A

Fetal hydantoin syndrome
Facial: cleft lip/palate, short nose, depressed bridge, mild hypertelorism
Extremities: digit and nail hypoplasia
Other: IUGR

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17
Q

Describe some findings if mom was using lithium during pregnancy?

A

Lithium
Ebstein anomaly
Fetal goitre, hypotonia, arrhythmia,seizures, diabetes insipidus, preterm birth

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18
Q

Describe some symptoms of in utero phenobarbital exposure

A

Phenobarbital
¤ Cleft lip/palate
¤ Cardiac anomalies
¤ Hemorrhagic disease of the newborn

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19
Q

What are some findings from in utero VPA exposure

A

Valproic Acid
¤ Neural tube defects
¤ Face narrow bi-frontal diameter, telecanthus, anteverted nostrils ¤ Cardiac defects, Long thin fingers/toes

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20
Q

In utero warfarin exposure causes what in the baby?

A

Warfarin
¤ Nasal hypoplasia
depressed bridge
Stippled bone epiphyses

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21
Q

Neonatal effects of pregnancy induced hypertension

A

Neonatal Effects
Increased risk of mortality, IUGR, RDS (mixed evidence), BPD, Thrombocytopenia, Neutropenia, NEC, behavioural problems, adult-onset cardiovascular disease

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22
Q

What is hydrops fetalis?

A 
Abnormal fluid accumulation in ≥2 fetal compartments
¤Skin thickening
¤Fetal ascites 
¤Pleural effusion 
¤Pericardial effusion
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23
Q

Causes of Hydrops?

A

Etiologies
¤ Immune: due to Rh(D) incompatibility (uncommon)
¤ Non-immune
- Hematological (Feto-maternal hemorrhage, thalassemia, RBC enzyme deficiencies/membrane defects, TTTS)

  • Cardiac (Congenital heart disease, cardiomyopathy, arrhythmia)
  • Vascular malformation (AVM, lymphatic obstruction (congenital chylothorax,cystic hygroma)
  • Infection (TORCH, Parvovirus B19, congenital syphilis)
  • Genetic (Aneuploidies, Turner syndrome, Noonan syndrome)
  • Metabolic (Lysosomal storage disorders, Glycogen storage diseases)
  • Pulmonary (CCAM, pulmonary sequestration)
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24
Q

Fetal side effects to maternal diabetes?

A

Fetal and Neonatal effects
¤ Still birth, polyhydramnios, preterm delivery
¤ LGA, birth trauma (may be SGA if significant vascular disease) ¤Transient hyperinsulinism and hypoglycemia
¤ Respiratory distress syndrome
¤ Congenital heart disease
¤ Polycythemia, hyperbilirubinemia
¤ Early neonatal hypocalcemia
¤ Caudal regression, hydrocephalus, NTDs, situs inversus, small left colon syndrome, renal anomalies

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25
Q

What symptoms may a baby have if mom has lupus?

A

Mostly present if she’s anti ro or anti la positive

Signs and symptoms:
¤ Cutaneous rash (may or may not be present at birth)
- Discoid-type rash (Disappears (generally without scarring) by 4 months age)
¤ Cardiac (heart block, cardiomyopathies)
-The only permanent sequelae
¤ Hepatobiliary (transaminitis)
¤ Hematological (anemia, thrombocytopenia)

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26
Q

Most common etiology of IUGR *but not SGA

A

placental insufficiency in large stature parents

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27
Q

Definition of IUGR

A

IUGR – rate of growth less than fetus’ genetic potential

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28
Q

Definition of SGA

A

SGA – fetus weight lower than standard population

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29
Q

Most common etiology if baby SGA but not IUGR

A

baby of small parents

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30
Q

List some neonatal effects of SGA/IUGR?

A 
Neonatal effects
¤ Hypoglycemia, hyperglycemia
hypocalcemia
depressed immune function
hypothermia
risk of perinatal asphyxia
polycythemia (with concomitant neutropenia and thrombocytopenia)
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31
Q

In discussion with the parents, what are some reasons to not resuscitate a fetus?

A

“GA, BW or congenital anomalies associated with almost certain early death and an unacceptably high morbidity … among rare survivors”
¤ Appropriate for:
- Confirmed GA <23 wks, BW <400 grams, anencephaly
- Confirmed trisomy 13 & 18

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32
Q

Which children MUST you resuscitate

A

¤ High rate of survival and “acceptable” morbidity

¤ e.g. GA ≥25 wk or most congenital malformations

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33
Q

When can you stop resuscitation?

A

In newly born baby with no detectable HR, consider stopping after 10 minutes if no HR remains undetectable

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34
Q

Factors that lead to a favourable outcome with prem deliveries

A 
Factors beside GA that are favourable:
¤ Female sex
¤ Antenatal steroids
¤ Appropriate EFW
¤ Singleton pregnancy
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35
Q

Rate of PPV in NRP

A

PPV at 40-60 bpm

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36
Q

Ratio of PPV and chest compressions in NRP

A

Chest compression: PPV breath ratio = 3:1

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37
Q

What are oxygen saturation targets for 1, 3, 5 mons of age

A

Oxygen saturation targets (1 min: 60-65%, 3 min 70-75%, 5 min 80-85%)

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38
Q

FiO2 for resus for infants >35 weeks?

A

For babies born >35 weeks, best to initiate resuscitation at 21%

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39
Q

FiO2 for resus for infants <35 weeks?

A

¤For < 35 weeks, start between 21-30% if blended O2 available and titrate to achieve recommended target saturations

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40
Q

Most sensitive sign for effective resuscitation?

A

¤Prompt increase in HRis most sensitive indicator of efficacy of resuscitation

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41
Q

Risk factor for birth injuries/trauma to baby

A 
Risk factors:
¤ Macrosomia
¤Maternal obesity
¤Abnormal fetal presentation
¤Operative vaginal delivery (Vacuum/Forceps) ¤Cesarean delivery
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42
Q

Brachial Plexus is supplied by which nerves?

A

Brachial plexus supplied by C5-T1

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43
Q

How many children have residual brachial plexus injuries?

A

20-30% with residual deficits, especially if incomplete recovery by 3-4 weeks

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44
Q

Management of Brachial Plexus injury

A

Careful monitoring for clinical recovery of function
̈ If no recovery by 3 months do MRI at 4 months
̈ EMG not helpful (false positive & negative)
̈ If poor recovery by 4 months, surgery at 6-9 months (before 9 months) due to concerns re: muscle atrophy

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45
Q

FOr HIE what GA and how many hours old do they have to be to start cooling?

A

Therapeutic hypothermia (33-34 °C x 72 hours, start by age 6 hours, must be 36 weeks or greater GA)

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46
Q

Who qualifies for cooling for HIE?

A

36 WGA or greater. Before 6 hours of life.

Any TWO of the following:
• APGAR score < 5 at 10 min
• Continued need for ventilation and resuscitation at 10 min of age
• Metabolic acidosis (pH < 7 or BD > 16 in cord or ABG within 1 hour

AND

Moderate or Severe encephalopathy (see SARNAT Scoring Table: seizures or 3/6 categories positive)

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47
Q

What are indications to stop cooling early (before 72 Horus)

A

uncontrollable bleeding

uncontrollable PPHN

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48
Q

What are some complications associated with HIE?

A

Resp: PPHN, secondary surfactant deficiency
• Cardiac: myocardial ischemia, valve insufficiency
• Renal: oliguria, acute tubular necrosis (hematuria), fluid overload
• Heme: DIC, low platelets
• Metabolic: hypoglycemia, hypocalcemia, hyperkalemia
• GI: NEC
• Neurodevelopmental disability:
• Mild: usually no deficits
• Moderate: 30-50%
• Severe: 80%

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49
Q

When do most IVH occur?

A

first 72 hours of life (80%)

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50
Q

What preventative measures can decrease IVH?

A
  • Antenatal steroids

* Delayed cord clamping

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51
Q

Most common cause of spastic diplegia in children?

A

PVL

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52
Q

Most common cause of hemiplegia CP?

A

stroke

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53
Q

Most common cause of athetoid/dyskinetic CP?

A

kernicterus

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54
Q

Babe with cleft, harsh systolic murmur is seizing…what do you do?

A

Calcium infusion
Vit D

This baby has digeorge

55
Q

Diagnostic work up for neonatal seizure

A
  • Diagnostic work-up • Neuroimaging
  • EEG
  • Infection workup
  • Metabolic workup
56
Q

Treatment for neonatal seizure?

A
  • Treatment
  • Treat underlying etiology (e.g. infection) if known
  • Limited evidence:
  • Lorazepam
  • Phenobarbital
57
Q

What does this baby have? Hypotonia, poor feeding and cryptocordism?

A

Prader Willi

58
Q

Mom on carbamazepine, what is one fetal complication?

A

NTD

59
Q

Neural tube defect Risk factors

A
  • Neural tube defect risk factors
  • Lack of maternal folate
  • Diabetes
  • Medications (e.g. VPA, carbamazepine)
60
Q

What are some External signs of spinal dysraphisms

A
  • Dimple
  • Sinus tract
  • Hemangiomas/Lipomas
  • Hair tuft
61
Q

Complications in childhood of open NTD

A 
urinary incontinence
UTI
constipation/diarrhea
ID
Leg impairment
Hydrocephalus
62
Q

Causes of craniosynostosis

A 
Conditions to consider:
• Hypophosphatemia
• Rickets
• Syndrome(Crouzon,
Pfeiffer, Apert, Carpenter’s)
63
Q

How to treat positional plagiocephaly

A

(ear moved forward on flat side)
̈ Lying on each side in the supine position = used for moderate.
̈ Important maneuvers involve positioning for sleep and use of tummy time / alternate sides to bed.
¤Tummy time, 2-3/day x 10-15min ̈ Alternate head of crib
̈ Most will go away on their own

64
Q

What causes hydrocephalus and has adducted thumbs?

A

Aqueductalstenosis
• X-linked with adducted thumbs
• Auto recessive associated with VACTERL

65
Q

What is a vein of Galen malformation and how does it present?

A

Large intracranial arteriovenous fistulas most often occur in newborn infants

Presentation:
̈ Hydrocephalus: can expand to become large and, because of its midline position, obstruct the flow of CSF
̈ The large intracranial left-to-right shunt results in heart failure secondary to the demand for high cardiac output. Patients with smaller communications may not have cardiovascular manifestations but may later be disposed to hydrocephalus or seizure disorders
̈ DX: A cranial bruit is audible

66
Q

Centrally mediated facial nerve palsy will present how?

A

Centrally mediated facial nerve palsy: only lower 2/3 face involved; forehead sparing

67
Q

Peripherally mediated facial nerve palsy will present how?

A

Whole side of face, including eye, will be involved

68
Q

Congenital absence of depressor angularis oris muscle presents how?

A

causes facial asymmetry, especially when infant cries

associated with congenital anomalies involving cardiac issues.

69
Q

How does Mobius Syndrome present?

A

Möbius syndrome can have bilateral (or unilateral) facial palsies (most have complete facial palsies)

  • inability to move the eyes from side to side.
  • Limb and chest wall abnormalities sometimes occur with the syndrome.
  • normal intelligence
    – symmetric calcified infarcts of pons/medulla
70
Q

Risk Factors for Meconium stained fluid?

A
  • Advanced GA (post-maturity)
  • Acute/Chronic in-utero hypoxic insult
  • Small for gestational age
  • Vaginal breech delivery
71
Q

Risk for MAS if MSAF?

A 
Thick MSAF
NRFHR tracing
Low APGAR score at 5 min 
Instrumental delivery 
Emergency C/S 
Planned home delivery
72
Q

What is the mechanism of lung injury in MAS?

A

What are mechanisms of lung injury in MAS?

  1. Mechanical obstruction of airways (partial vs. complete)
  2. Chemical pneumonitis and inflammation
  3. Infection
  4. Inactivation & decreased endogenous production of surfactant
  5. Ventilation-perfusion mismatch- pulmonary vasoconstriction/PPHN
73
Q

What are the CXR findings for MAS?

A
  • Diffuse or local linear or patchy infiltrates
  • Consolidation or atelectasis
  • Hyperaeration with or without air leaks
74
Q

Any special management for MAS?

A

• NRP 7th edition: No AUTOMATIC tracheal suction with non- vigorous infant
• Supplemental oxygen as required
• Target pre-ductal saturations
• CPAP support as required
• Patient (often term/post-term) may be uncomfortable
• Mechanical ventilation support and call your local tertiary care
centre
• Surfactant: if on >50% FiO2 (CPS)

75
Q

CXR findings for RDS?

A

Typical Radiographic Features:
Low FRC
Diffuse reticulogranular appearance
Air bronchograms

76
Q

Risk factors for RDS

A
  • Low Gestational Age (including late preterm)
  • Low birth weight
  • Male gender
  • Elective delivery in absence of labour
  • Maternal diabetes
  • Perinatal hypoxia-ischemia
77
Q

What can be done to prevent and treat RDS?

A 
Antenatal corticosteroids (recommended for GA 24-34 weeks) 
• Ventilation support as needed
• Surfactant replacement (Selective administration of surfactant to infants requiring intubation is now the preferred alternative to prophylactic surfactant)
78
Q

What complications does sufactant help decrease?

A
  • Decreases risk of:
  • Neonatal mortality
  • Pneumothorax
  • Pulmonary interstitial emphysema
79
Q

Who qualifies for surfactant?

A

Preterm
• Intubated patients with RDS
• Consider prophylactic if outborn & <29 weeks
• Preterms on non-invasive with CPAP with FiO2 >50%

80
Q

How often can you repeat surfactant?

A

• Rapid weaning and extubation to CPAP within one hour
• Repeat doses to max 3, up to 72 hours of age
• Consider re-treatment if persistent or recurrent oxygen
requirement; FiO2 >30%
• Timing of repeat dose: early as 2 hours usually 4-6 hours after first dose

81
Q

What are some risk factors for TTN?

A
  • Elective caesarean delivery without labour
  • Prematurity
  • Large birth weight
  • Maternal diabetes
  • Twin pregnancy
  • Male gender
  • Maternal asthma
82
Q

CXR findings for TTN?

A

Peri-hilar streaking
• Fluid in interlobar fissues (Oblique and Horizontal)
• Bilateral infiltrates
• Fluid filled alveoli

83
Q

What is the definition of BPD?

A

Definition

• For exam – oxygen requirement at 36 weeks post- menstrual age (PMA)

84
Q

CXR findings for BPD?

A

cysts
hyperinflated
gas trapping

85
Q

Management of BPD

A
  • Gentle ventilation with minimization of endotracheal ventilation
  • Nutritional support and supportive care
  • Corticosteroids (Controversial due to link with Cerebral Palsy)
  • Limited evidence for inhaled corticosteroids

Volutrama»>barotrauma
Beware of oxygen toxicity

86
Q

Long term sequelae of BPD?

A
  • Frequent hospitalizations
  • Increased pulmonary problems • Reactive airway disease
  • Pulmonary hypertension
  • More severe infections
  • Poorer neurodevelopment
87
Q

Choanal atresia presentation?

A

Gets better with bagging!! KEY

88
Q

What is CPAM?

A
  • CPAM (congenital pulmonary adenomatous malformation)
  • Numerous cysts within lung tissue
  • Communicates with trachea-bronchial tree
  • Blood supply from pulmonary circulation
  • Risk of hamartomas and/or infection

May look like a mass on CXR

Management controversial
• Surgical resection
• Surveillance with serial CTs (many regress over time)

89
Q

What is Bronchopulmonary sequestration?

A
  • Bronchopulmonary sequestration
  • Non-functioning lung tissue that receives blood supply from anomalous systemic vessels
  • Does NOT communicate with tracheobronchial tree
  • Majority lower lobe (intra- or extra-lobar)
  • Risk of respiratory distress, recurrent pneumonias in childhood

Management
• Surgical resection
• May observe, particularly if extralobar

90
Q

Management of CDH

A 
Management
• Intubate away
• Surgical repair
• Avoid bag mask ventilation: Intubate
• Insert large bore NG
• Minimize ventilation pressures: PIP <25 cm
• Pre-ductal sat >85%
• Sedation: minimize risk of pneumothorax
• Transfer to tertiary care centre
91
Q

Long term complication fo CDH

A

• Long term complications include neurodevelopmental/behavioural impairment, GERD/nutritional problems and pulmonary disease

92
Q

Most common defect in CDH?

A

Congenital diaphragmatic hernia
• Developmental defect in formation of diaphragm at 8-10 weeks GA
• Left posterior defect most common
• Pulmonary hypoplasia which leads to pulmonary hypertension

93
Q

What is PPHN?

A

Increased pulmonary vascular resistance

• R to L shunt at atrial or ductal level

94
Q

Causes of PPHN?

A 
MAS
Pneumonia
RDS
Idiopathic
CDH
Pulmonary hypoplasia
95
Q

Clinical presentation fo PPHN

A

Presents with hypoxemia, severe cyanosis, respiratory distress, labile oxygenation, gradient in pre- and post-ductal oxygen saturation
Cannot handle them easily
̈ Note: may be difficult to distinguish from congenital heart defect

96
Q

Management of PPHN

A
  • Optimal lung expansion
  • Reduction of PVR (iNO)
  • Maintenance of systemic perfusion
  • Optimization of cardiac function
  • Optimizing oxygenation (PaO2) and ventilation
  • Treatment of underlying lung disease
97
Q

Muffled heart sounds and HR drops
Breath sounds equal and symmetric
What is happening?

A

Fluid around the heart!
Needs pericardiocentesis
Can be caused by PICC!

98
Q

Management of Pneumothorax

A 
• Ventilation support as required
• Low flow oxygen or CPAP (not for the pneumothorax
per se)
• Mechanical ventilation
• Use lowest possible pressure
• Reduce PIP, PEEP, i-time
  • Thoracentesis
  • Typically used as emergent treatment of symptomatic PTX
  • May be a temporizing measure while stabilizing patient before chest tube placement
  • Sometimes may be sufficient alone
  • Chest tube placement
  • Generally required in mechanically ventilated patient
  • Resolution in 2 – 3 days as underlying lesion heals
  • 4th or 5th intercostal space (mid-axillary line)
99
Q

Treatment of pneumomediastinum

A
  • Air in mediastinal space
  • Most cases are asymptomatic
  • Resolves spontaneously and requires no specific treatment
  • Reports of need for US-guided drainage in tension pneumomediastinum
100
Q

Presentation of pneumopericardium

A
  • Air in pericardial space
  • Abrupt onset of hemodynamic compromise due to cardiac tamponade
  • Tachycardia to Bradycardia, narrowed pulse pressure, hypotension, cyanosis
  • Distant/muffled heart sounds
  • Low voltage of ECG/rhythm strips
101
Q

Diagnosis of pneumonia in neonates?

A

• Extremely difficult and subjective: no validated criteria

  • Standards of diagnosis:
  • Bronchoalveolarlavage
  • Aspirate using protected specimen brush
  • Lung biopsy
  • Pleural fluid culture

• Seldom performed in neonates

  • High C-reactive protein
  • WBC counts (neutropenia, high I/T ratio)
  • Pleural effusions on radiograph
  • Positive gram stain on ETT aspirates
  • Tracheal cultures
  • May have value if performed early
  • However, limited evidence for tracheal cultures for late onset pneumonia
102
Q

What is malrotation?

A

Failure of normal rotation with abnormal fixation of bowels

103
Q

When does volvulus typically present?

A

• 80% with symptoms in first month of life

104
Q

How does volvulus present?

A

• Bilious vomiting – must rule out malrotation (± volvulus)

105
Q

How do you diagnose volvulus?

A
  • Diagnosis
  • X-ray may show decreased bowel gas
  • Definitive diagnosis with upper GI series
106
Q

What is the treatment for volvulus?

A
  • Surgical emergency – may lead to rapid necrosis of bowel if volvulus present
  • Ladd’sprocedure
107
Q

What condition is associated with meconium ileus

A

Impaction of thick tenuous meconium in distal small bowel
• 10-15% of patients with CF have MI
• 90% of patients with MI have CF

108
Q

How do you diagnose Meconium Ileus

A

• Contrast enema required to establish diagnosis

Dilated proximal to the ileus, with micro colon after

109
Q

Treatment of meconium ileus

A
  • Hypertonic enema (gastrografin) may lead to disimpaction

* Mucomyst (N-acetylcysteine)

110
Q

Duodenal atresia is associated with what syndromes?

A

Duodenal atresia
• Failure of recannulization
• Trisomy 21 in ~1/3

111
Q

What do you see on X-ray for duodenal atresia?

A

• Classical sign: double bubble

NOT ALWAYS BILIOUS VOMITING

112
Q

How do you manage Duodenal/jejunal/ileal atresia?

A
  • Management
  • Abdominal decompression
  • Surgery
113
Q

How do jejunal/ileal atresia present thats different from DA?

A

Jejunal/Ileal atresia
• In utero mesentericvascular occlusion
• Presents with bilious vomiting, abdominal distension

DA not always bilious

114
Q

What is Hirschsprung disease?

A

Failure of complete cranial to caudal migration of neural crest cells
• No parasympathetic innervation to distal colon to abnormal peristalsis and functional constipation
- part of colon without neural crest cells is tiny.

115
Q

How does Hirschsprungs disease present?

A
  • Clinical
  • No meconium in first 24-48 hours, abdominal distension
  • Acute bacterial enterocolitis (megacolon)
116
Q

How do you diagnose hirschsprungs?

A
  • Diagnosis
  • Barium enema
  • Anal manometry
  • Biopsy (definitive)
117
Q

What syndromes are associated with hirschrpungs?

A

Down syndrome
Central Hypoventilation Syndrome
Wardenburg

118
Q

What are risk factors for NEC?

A
  • Prematurity
  • Formula
  • Intestinal ischemia
  • Abnormal bacterial colonization
119
Q

How does NEC present?

A
  • Clinical
  • Abdominal distension, feeding intolerance, emesis, hematochezia, loose stools, abdominal wall erythema, systemicinstability
  • Leukopenia, thrombocytopenia, metabolic acidosis, DIC, glucose instability
120
Q

Complications of NEC?

A

Complications
• Mortality rate 30-40%
• Intestinal strictures, short bowel syndrome, TPN related cholestatis, neurodevelopmental impairment

121
Q

Radiographic findings of NEC?

A

pneumatosis intestinal
portal air
football sign (seeing falciform ligament)
pneumoperitoneum

122
Q

What is an omphalocele?

A

Intestinal loops fail to return to abdominal cavity (or lack of formation of anterior abdominal wall)
Has covering to the bowel
midline
involves the umbilicus

123
Q

What conditions is omphalocele associated with?

A

80% associated with anomalies
• Beckwith Weidemann
• Trisomy 13 and 18

124
Q

What is gastroschisis?

A

“Abdominal wall hernia”
• More common in young mothers
• High risk of concomitant intestinal atresia

125
Q

What conditions are gastroschisis associated with?

A

Usually none

Well baby otherwise

126
Q

Long term complications of gastroschisis?

A
  • Long term complications (more common in gastroschisis)
  • Decreased GI motility
  • Bowel obstruction
  • Perforated bowel/strictures • GERD
  • Sepsis
  • Cholestasis
  • Short Bowel
127
Q

What is short gut?

A

Defined as prolonged parenteral nutrition following bowel resection
• Usually more than 3 months
• Malabsorption secondary to bowel resection

128
Q

Complications of short gut?

A
  • Complications
  • Intestinal hyperplasia
  • Gastric hypersecretion
  • Bacterial overgrowth
  • Colitis
  • Watery diarrhea
  • Electrolyte imbalance
  • Cholestasis/Cholelithiasis
  • Renal stones
  • Failure to thrive
129
Q

Which babies are at risk of hypoglycemia and why?

A

IDM (hyperinsulinism)
• LGA infants (hyperinsulinism)
• Prematurity (reduced fat and glycogen stores)
• Infants SGA (reduced fat and glycogen stores)
- IUGR/Asphyxia (hyperinsulinism because of stress)

130
Q

What investigations would show hyperinsulinism as a cause of hypoglycaemia?

A

Hyperinsulinism: normal or elevated insulin level in face of hypoglycemia; low ketones and free fatty acids,
urine negative for ketones

131
Q

When can you stop screening at risk babies for hypoglycemia?

A

Discontinue screen if levels ≥2.6
• SGA after 36 h
• LGA & IDM after 12h

132
Q

What is in a critical sample for hypoglycemia?

A 
Critical Sample
• 1. Glucose
• 2. Insulin
• 3. Cortisol
• 4.GH
• 5. Beta OH Butyrate
• 6. FFAs
• 7. Lactate, Gas
• 8. Urine Ketones
133
Q

What is the etiology of most congenital hypothyroidism?

A
  • Incidence rate: 1:2,000 – 1:4,000
  • Most newborn babies with congenital hypothriodism have few or no clinical manifestations
  • Majority of cases are sporadic
  • Thyroid dysgenesis (sporadic, ~85%)
  • Ectopia (most common), aplasia or hypoplasia of thyroid
  • Inborn errors of thyroid hormone synthesis (hereditary, ~15%)
  • Central hypothyroidism (extremely rare)

Royal College Study (13 decks)

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