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Paeds > Neonatal > Flashcards

Neonatal Flashcards

1
Q

What is Hypoxic Ischaemic Encephalopathy (HIE)?

A

Clinical manifestation of brain injury 48hrs after hypoxic event. Occurs if perinatal asphyxia has occurred (> cardiorespiratory depression)

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2
Q

What is the difference between HIE and CP?

A

HIE = neonatal condition
Cerebral palsy = post-neonatal condition (i.e. severe HIE that is not tx)

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3
Q

What are the causes of HIE?

A
  • Placental abruption
  • Shoulder dystocia > cord compression
  • Maternal hypotension
  • Compromised foetus (i.e. IUGR)
  • Failure to breath at birth
  • Hypotension > maternal haemorrhage (placental abruption, placental praevia)
  • Hypertension > fulminant pregnancy-induced HTN
  • Obstructed labour > malpresentation, cephalopelvic disproportion, multiple births, postmature neonates

Infants at risk > preterm, infants with CHD

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4
Q

What are the S/S of HIE?

A

Response within first 48hrs grades the HIE level

Mild

  • Infant irritable, responds excessively to stimulation, staring eyes, hyperventilation, hypertonia
  • Complete recovery expected

Moderate

  • Abnormalities of movement, hypotonic, cannot feed, has seizures
  • If fully resolved by 2wks of age > good long-term prognosis
  • If persistent past 2wks > bad prognosis

Severe

  • No normal movements or response to pain, tone in limbs fluctuates hypo- to hypertonic, seizures prolonged and refractory to tx, multi-organ failure may be present
  • 30-40% mortality
  • Over 80% have neurodisability (if not cooled) > cerebral palsy
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5
Q

What is the management of HIE?

A

Therapeutic hypothermia

  • > 36wks, mild hypothermia can reduce morbidity from HIE
  • Requires NICU

Supportive

  • Resp support
  • Anticonvulsants
  • Fluid restriction (transient renal impairment)
  • Inotropes (tx of hypotension)
  • Electrolytes and glucose (tx hypoglycaemia and electrolyte imbalances)
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6
Q

What is Cerebral Palsy?

A

A disorder of movement and posture due to a non-progressive lesion of the motor pathways in the developing brain.

If brain injury occurs after 2yrs > diagnosed as acquired brain injury (not CP)

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7
Q

What are the causes of cerebral palsy?

A

Antenatal (80%)

  • Congenital infection e.g. rubella, toxoplasmosis, CMV
  • Cerebral dysgenesis/malformation

Perinatal (10%)

  • HIE, birth trauma/asphyxia

Postnatal (10%)

  • Intraventricular haemorrhage, meningitis, head-trauma, NAI
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8
Q

What are the RFs for cerebral palsy?

A

Antenatal

  • Preterm birth, chorioamnionitis, maternal infection

Perinatal

  • LBW, HIE, neonatal sepsis

Postnatal

  • Meningitis
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9
Q

What are the S/S of cerebral palsy?

A
  • Delayed milestones +/- persistent primitive reflexes
  • NON-PROGRESSIVE condition so NO LOSS of previously attained milestones
  • Abnormal posture / tone / gait
  • Feeding difficulties > slow, gagging, vomit
  • Associated non-motor problems e.g. learning difficulties, epilepsy, squints, hearing impairment
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10
Q

What is the classification of cerebral palsy?

A

Spastic (70%) > MUSCLES STIFF/TIGHT

  • Damage to UMNs
  • Increased tone, brisk reflexes, extensor plantar/Babinski’s, ‘clasp knife’ rigidity
  • Scissor gait

Subtypes:

  • Hemiplegia > unilateral arm and leg, face spared
  • Diplegia > legs affected to greater degree, but all 4 limbs affected
  • Quadriplegia > all 4 limbs, often severe

Dyskinetic (10%) > INVOLUNTARY MOVEMENTS

  • Damage to basal ganglia and substantia nigra
  • Athetosis (slow, involuntary, convoluted, writhing movements of the fingers, hands, toes, and feet) / dystonia
  • Random, slow, uncontrolled movements
  • Repetitive and patterned movements
  • Oro-motor problems e.g. drooling
  • Difficulty holding onto objects due to fluctuating muscle tone

Ataxic (10%) > SHAKY / UNBALANCED

  • Damage to cerebellum
  • Hypotonia, ataxia of trunk and limbs, postural imbalance, intention tremor / shaky movements
  • Clumsiness / instability

Mixed (10%)

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11
Q

What are the investigations for cerebral palsy?

A

1st to order:

  • MRI brain

Also consider:

  • Assessment of hearing and vision
  • EEG if seizure prone
  • Bloods > FBCs, U&Es, TFTs, coagulation screen
  • Metabolic screen > IEM
  • XR > if severe deformity
  • Gait analysis
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12
Q

What is the management of cerebral palsy?

A

»MDT orientated

1st line:

  • PT > encourage movement, improve strength and stop muscles from losing range of motion
  • SALT > improve language abilities
  • OT > identify everyday tasks that may be difficult and help make these tasks more accessible
  • Consider adaptive equipment

Medical:

  • Oral diazepam (good for transient use for acute spasms) / baclofen
  • Botulinum toxin type A injections (for spasticity)
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13
Q

What is necrotising enterocolitis (NEC)?

A

Acquired inflammatory disease affecting the gut of newborns

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14
Q

What is the incidence of NEC?

A
  • Most common surgical emergency in newborns
  • One of the leading causes of death in prem infants
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15
Q

What are the RFs for NEC?

A
  • Premature
  • LBW
  • PDA
  • Perinatal stress
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16
Q

What are the S/S of NEC?

A

Onset often after initiating feeds

Early signs:

  • Feeding intolerance
  • Bilious vomiting
  • Abdominal distension
  • Bloody stools

Can quickly progress to:

  • Abdominal discolouration
  • Perforation
  • Peritonitis
  • Shock
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17
Q

What are the investigations for NEC?

A

Abdominal XR:

  • Pneumatosis intestinalis (intramural gas)
  • Dilated bowel loops
  • Portal venous gas
  • Bowel wall oedema
  • Pneumoperitoneum resulting from perforation
  • Air both inside and outside of the bowel wall > Rigler sign
  • Air outlining the falciform ligament > football sign

Bloods + culture:

  • Depends on stage
  • Hb low, platelets low, high WCC, metabolic acidosis, electrolyte derangement, coagulopathy
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18
Q

What is the management of NEC?

A

Conservative:

  • NBM + NGT decompression
  • IV broad spec abx > cefotaxime/tazocin and vancomycin
  • Blood and platelet transfusions
  • Electrolyte imbalances correction

Surgical (if bowel perforation / necrosis):

  • Resection of necrotic bowel with formation of a stoma and mucous fistula / primary anastomosis
  • Extensive disease may be left as balance of resection vs short gut syndrome
  • Consequences > strictures, malabsorption
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19
Q

What is neonatal jaundice?

A

Excess amount of bilirubin in the neonatal circulation causing a yellow discolouration of the skin and sclera

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20
Q

How common is neonatal jaundice?

A

Over 50% of newborns become visibly jaundiced

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21
Q

What are the RFs for neonatal jaundice?

A
  • Previous affected sibling
  • Prematurity
  • Breastfeeding
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22
Q

What are the causes of neonatal jaundice?

A

Physiological unconjugated hyperbilirubinemia
(functional immaturity)

  • Instability of foetal Hb (increased RBC volume but decreased survival)
  • Defective BR metabolism / excretion in first few days of life
    > > Peaks at 5d, resolves by 1-2w

Breast milk jaundice

  • Only >24hrs
    > > Peaks in week 2, resolves very slowly (3m)

Unconjugated haemolytic hyperbilirubinaemia

  • ABO or Rh incompatibility (immune-related)
  • Hereditary spherocytosis, G6PDD (defect)
  • Congenital infection, bacterial sepsis (acquired)

Unconjugated non-haemolytic hyperbilirubinaemia

  • Haemorrhage, polycythaemia
  • Galactosaemia, hypothyroidism

Conjugated hyperbilirubinaemia

  • Biliary atresia, choledochal cyst (bile duct obstruction)
  • Neonatal hepatitis (congenital infection, CF, alpha-1-antitrypsin deficiency)
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23
Q

What does the age of onset tell you about neonatal jaundice?

A

<24hrs = always pathological (ABO/Rh incompatibility, G6PDD, HS)

>24hrs = probably physiological (but beware sepsis and galactosaemia)

>2wks = perform prolonged jaundice screen (biliary atresia, hypothyroidism, galactosaemia, UTI, congenital infection)

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24
Q

What are the S/S of neonatal jaundice?

A
  • May be asx in physiological jaundice
  • Visible jaundice seen at 80umol/L
  • cBR > dark urine, pale stools
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25
Q

What are the S/S of kernicterus?

A
  • Lethargy, irritability
  • Poor feeding
  • Increased muscle tone (arched back)
  • Seizures
  • Coma

> > May develop into CP (dyskinetic), learning difficulties, sensorineural deafness

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26
Q

What is kernicterus?

A

uBR deposits in basal ganglia

  • Form of encephalopathy
  • Causes spectrum from severe damage to death
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27
Q

What are the investigations for neonatal jaundice?

A

Early jaundice (<24hrs)

  • Direct (total) serum BR
  • FBC/blood film (HS), maternal and infant ABO/Rh, DAT, infection screen (blood culture, TORCH screen), G6PD levels

Jaundice >24hrs

  • Transcutaneous BR
  • If normal Hx and examination > monitor only

Persistent jaundice (>2wks)

  • Direct and indirect serum BR
  • Conjugated fraction should be obtained
  • TFTs, LFTs, U&Es, DAT, G6PD levels, MC&S of blood/urine/CSF

Conjugated hyperbilirubinaemia

  • Requires urgent investigation > USS billary tree +/- liver biopsy isotope scanning HIDA/DISIDA and referral to a paediatric liver centre
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28
Q

What is the management of neonatal jaundice?

A

Sometimes no treatment necessary (cBR does NOT cause harm > although cause of cBR can be bad)

(1) Phototherapy > breaks down uBR so it can be excreted in urine

  • Neonate under series of lights on radiant warmer bed (eye protection, short breaks for breastfeeding, monitor temp)
  • Repeat BR measurements every 4-6hrs (until drops 50 below threshold for tx)
  • Use single PT unless SBR rising rapidly (>1 box per hour), SBR within 5 boxes of exchange transfusion threshold, SBR fails to respond to single PT
  • +/- IVIG (used in Rh / ABO incompatibility)

(2) Exchange transfusion + PT +/- IVIG

  • If signs of kernicterus, if intensive PT fails to lower BR, or in conjunction with PT with extremely elevated BR levels
  • Give folic acid after (prevent anaemia)
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29
Q

What is transient tachypnoea of the newborn (TTN)?

A

Acute, self-limiting tachypnoea in the absence of other causes

Commonest cause of respiratory distress in term infants

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30
Q

What causes TTN?

A

Delayed resorption of lung fluid

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31
Q

What are the RFs for TTN?

A

C-section
Maternal asthma

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32
Q

What are the S/S of TTN?

A

Usually occurs in first 1-3hrs following uneventful normal preterm, term vaginal or elective C-section delivery

  • Early onset tachypnoea (RR>60)
  • +/- signs of respiratory distress
  • Cyanosis in severe cases
  • O/E = crackles, diminished breath sounds
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33
Q

What are the investigations for TTN?

A

CXR:

  • Fluid in horizontal fissure
  • Hyperinflation of the lungs
  • Flat diaphragms
  • Occasional pleural fluid

ABG:

  • Degree of decreased pO2 > depends on amount of fluid on the lungs

Blood cultures:

  • Exclude infectious cause
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34
Q

What is the management of TTN?

A

· Observation
· Supportive care
· Additional O2 if required
> > Usually settles within 1-2d

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35
Q

What is the F pneumonic for TTN?

A

Full-term neonate
First day of life
Fissures Filled with Fluid
DiFFuse crackles

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36
Q

What is persistent pulmonary HTN?

A

The failure of the normal circulatory transition that occurs after birth

Persistent raised pulmonary vascular resistance > R-L shunting of blood away from the lungs > life-threatening

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37
Q

What are the causes of persistent pulmonary HTN?

A

Primary = idiopathic

Secondary = birth asphyxia, meconium aspiration, septicaemia, RDS, diaphragmatic hernia, congenital pneumonia

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38
Q

What is persistent pulmonary HTN associated with?

A

· IUGR
· Foetal distress
· Down Syndrome

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39
Q

What are the S/S of persistent pulmonary HTN?

A
  • Signs of respiratory distress
  • Signs of cardiogenic shock (lethargy, hypotension, oliguria)
  • Absent heart murmurs and signs of HF

> > Should be suspected in all infants when hypoxaemia is out of proportion to the severity of parenchymal lung disease on CXR

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40
Q

What are the investigations for persistent pulmonary HTN?

A

CXR
- Some pulmonary oligaemia (reduction in pulmonary volume)

Bloods
- Hb, WCC, glucose, clotting screen

Echo
- Urgent to ensure no cardiac defect

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41
Q

What is the management of persistent pulmonary HTN?

A

Antenatal > at-risk infants should be identified

  • Correct any predisposing conditions (hypoglucaemia, polycythaemia)

Postnatal

  • Most infants require mechanical ventilation and circulatory support
  • Inhaled nitric oxide (potent vasodilator)
  • Prostaglandins (keep DA patent)
  • Sildenafil (viagra) has also been introduced recently
  • High-frequency (oscillatory) ventilation may be useful
  • For severe but reversible cases, extracorporeal membrane oxygenation (ECMO) (where the infant is placed on heart and lung bypass for several days) may be used
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42
Q

What is the prognosis of persistent pulmonary HTN?

A

Mortality <10%

25% likely to have some impairment such as learning difficulties / deafness

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43
Q

What is chronic lung disease of prematurity / bronchopulmonary dysplasia (BPD)?

A

Oxygen still required at corrected age of term with characteristic radiological changes (bronchopulmonary dysplasia)

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44
Q

What are the causes of CLD/BPD?

A
  • Premature
  • Mechanical ventilation
  • Oxygen therapy - prolonged exposure to high concentrations
  • Inflammation and infection - pneumonia, sepsis, RDS
  • Maternal factors - smoking, infection
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45
Q

What are the RFs for CLD/BPD?

A
  • Premature
  • LBW
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46
Q

What are the S/S of CLD/BPD?

A

Signs of respiratory distress, poor feeding, poor weight gain

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47
Q

What are the investigations for CLD/BPD?

A

CXR
- Widespread opacification - atelectasis
- Hyperinflation and cystic changes
- Ground glass appearance

ABG / VBG / CBG
- Compensated respiratory acidosis reflecting chronic high pCO2
- Hypercapnia
- Hypoxia

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48
Q

What is the management of CLD/BPD?

A

Respiratory support

  • Prolonged artificial ventilation
  • Wean to CPAP
  • Wean to additional O2

+/- corticosteroid therapy

  • Dexamethasone for short term clinical improvement

Prevention

  • If baby does not need intubation or ventilation, it is important to minimise ventilation-associated lung injury using strict monitoring and maintaining of tidal volume

Long-term

  • Home O2 supported by community children’s nurses
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49
Q

What is respiratory distress syndrome (RDS)?

A

Respiratory compromise in a neonate secondary to surfactant deficiency

Surfactant deficiency > lungs more likely to collpase

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50
Q

What are the RFs for RDS?

A
  • PREMATURITY
  • Maternal diabetes
  • Male
  • C-section
  • 2nd born premature twin
  • FHx
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51
Q

How does the risk of RDS change with gestation?

A

Risk decreases with gestation

  • Common if born <24w
  • 50% born 26-28w
  • 25% born 30-39w
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52
Q

What are the causes of RDS?

A

Primary surfactant deficiency:

  • Prematurity and intrapartum hypoxia
  • Acidosis
  • Hypothermia
  • Hypotension

Secondary:

  • Intrapartum asphyxia
  • Pulmonary infections
  • Haemorrhage
  • Meconium aspiration pneumonia
53
Q

What are the S/S of RDS?

A

> > At delivery or within 4hrs of birth

  • Early onset tachypnoea (>60)
  • Respiratory distress
  • Prominent grunting (baby trying to make +ve airway pressure)
  • Cyanosis (if severe)
  • Extremely premature infants > apnoea +/- hypothermia
  • May progress rapidly to fatigue, apnoea, hypoxia
  • O/E = harsh breath sounds, fine inspiratory crackles
54
Q

What are the investigations for RDS?

A

Blood gas

  • Respiratory acidosis
  • Metabolic acidosis (lactic acidosis secondary to poor tissue perfusion)
  • Hypoxia (right-to-left shunting)
  • Hypercapnia

CXR

  • Pneumothorax (from ventilation)
  • Bilateral diffuse reticular or ‘ground-glass’ appearance
  • Pulmonary oedema
  • Poor lung expansion
  • Indistinct heart border

Biopsy

  • Hyaline membrane (pink) protein

Echo

  • PDA is a complication
55
Q

What is the management of RDS?

A

Prevention / Antenatal > identify at-risk infants (neonatologist/NICU early involvement)

  • Amniocentesis for estimation of foetal lung maturity
  • Antenatal steroids to stimulate foetal surfactant production (when preterm delivery expected <34w)
  • Tocolytic therapy so steroids have at least 24hrs to work

Postnatal

  • Surfactant replacement therapy via endotracheal tube (ETT)
  • Oxygen and ventilation > CPAP, nasal cannula, conventional mechanical ventilation
  • Other: High frequency oscillatory ventilation (HFOV) may be used, high flow humidified oxygen therapy may be used

Also

  • Prophylactic abx after blood cultures
  • Gentle / minimal handling
  • Enteral or parenteral nutrition
56
Q

What are the causes of pneumothorax?

A
  • Can occur from RDS
  • Can occur from the ventilation used to treat RDS

> pulmonary intestinal emphysema

57
Q

How is pneumothorax prevented when using oxygen therapy?

A

Infants should be ventilated with the lowest possible pressures that provide adequate chest movement and blood gases

58
Q

What is the management of pneumothorax?

A
  • Immediate decompression
  • O2 therapy
  • Chest drain if tension pneumothorax
59
Q

What is meconium aspiration?

A

Respiratory distress in the neonate secondary to the presence of meconium (foetal intestinal contents) in the trachea.

Causes mechanical obstruction and/or chemical pneumonitis > pneumonia / infection

60
Q

When does meconium aspiration occur?

A
  • Occurs exclusively in the immediate neonatal period
  • Risk increases with increasing gestational age
61
Q

What are the RFs for meconium aspiration?

A
  • GA >42wks (44%)
  • Foetal distress / hypoxia
  • Maternal hx of HTN / PET / smoking / substance abuse / pre-eclampsia
  • Meconium-stained amniotic fluid
  • Oligohydramnios
  • Chorioamnionitis
62
Q

What are the S/S of meconium aspiration?

A

Respiratory distress > increased RR, chest retraction, recessions, grunting, overinflated chest, cyanosis (severe)

63
Q

What are the investigations for meconium aspiration?

A

CXR (diagnostic)

  • Patchy infiltrations
  • Atelectasis
  • Hyperinflation
  • Patches of collapse and consolidation
  • May show cardiomegaly, pneumothorax, pneumomediastinum

Bloods

  • FBC, CRP, culture > rule out infection

Blood gas

  • Reduced O2
64
Q

What is meconium ileus?

A

Bowel obstruction caused by thick, sticky meconium that has a prolonged passing time

  • Usually passes within 24hrs of delivery
  • Neonate may vomit meconium instead of passing it as stool
  • Associated with CF (90%) and biliary atresia
65
Q

What is the management of meconium ileus?

A

1st line = Gastrograffin enema
2nd line = Surgical decompression

66
Q

What is cleft lip / palate ?

A

Congenital malformation resulting in clefts that involve the lip, hard palate, and soft palate

67
Q

What is the aetiology of cleft lip / palate ?

A

Cleft lip = failure of fusion of the frontonasal and maxillary processes - when the tissue that makes the lip doesn’t completely join before birth, results in an opening of the upper lip

Cleft palate = failure of the palatine processes and the nasal septum to fuse

68
Q

What are the types of cleft lip / palate ?

A
  • Combined cleft lip and palate (45%)
  • Isolated cleft palate (40%)
  • Isolated cleft lip (15%)
69
Q

What are the RFs for cleft lip / palate ?

A
  • Maternal antiepileptic and BDZ use
  • Maternal smoking
  • Patau’s syndrome
70
Q

What are the S/S of cleft lip / palate ?

A

At birth = overt clefts of the hard and soft palate

Postnatal = feeding, airway, and speech difficulties, increased risk of otitis media

71
Q

What are the investigations for cleft lip / palate ?

A
  • 75% detected 20w anomaly scan
  • Also detected during new-born baby check
72
Q

What is the management of cleft lip / palate ?

A

MDT approach > Plastic surgeon, ENT surgeon, paediatrician, orthodontist, audiologist, SALT

Pre-surgical concerns:

  • Specialised feeding = slower, use of cleft palate feeders, semi-upright positioning
  • Watch out for airway problems (e.g. Pierre-Robin sequence)
  • Pre-surgical lip tapping, oral appliances or pre-surgical nasal alveolar moulding (PNAM) to narrow cleft

Surgery (definitive):

  • 3m for lip
  • 6-12m for palate
73
Q

What is a diaphragmatic hernia?

A

Congenital defect in the formation of the diaphragm that leads to the protrusion of abdominal contents into the thoracic cavity > pulmonary hypoplasia and HTN > respiratory distress

74
Q

When does a diaphragmatic hernia occur?

A

6-8wks of pregnancy (when diaphragm does not form correctly)

75
Q

What is the most common type of diaphragmatic hernia?

A

Left-sided Bochdalek hernia

  • 85%
  • Part of intestine moves through left chest area > stops lungs developing properly
76
Q

What does the prognosis of a diaphragmatic hernia depend on?

A

Prognosis depends on liver position and lung-to-head ratio
Only around 50% survive

77
Q

What are the S/S of a diaphragmatic hernia?

A
  • Concave chest at birth
  • Respiratory distress in the neonate
  • May be a maternal hx of polyhydramnios

Complications = intestinal obstruction, volvulus of stomach, ARDS > collapse

78
Q

What are the investigations for a diaphragmatic hernia?

A

> Diagnosed on routine USS or after respiratory distress at birth

CXR:

  • Displaced mediastinum to the L
  • Collapsed L lung
  • Bowel loops in thorax

Also:

  • Blood gas
  • U&Es
  • Chromosomal studies
  • Cardiac echo
  • Renal USS
79
Q

What is the management for a diaphragmatic hernia?

A

(1) Large NGT to decompress bowel + respiratory support
(2) Surgical reduction and repair > re-expansion of lung > TPN / ventilatory support during recovery

80
Q

What is oesophageal atresia (OA)?

A

Malformation of the oesophagus so it does not connect to the stomach

81
Q

What is transoesophageal fistula (TOF)?

A

Congenital malformation where part of the oesophagus is joined to the trachea

TOF often occurs alongside OA

82
Q

What complications are associated with OA/TOF?

A
  • Stomach acid can regurgitate and go into the lungs > CLD/BPD
  • Polyhydramnios
  • Other developmental issues
  • Take longer to adjust to solids
  • Tracheomalacia (collapse of the airway while breathing)
  • Feeding issues > stricture formation
  • GORD
83
Q

What are the S/S of OA/TOF?

A
  • Hx of polyhydramnios prenatally
  • Excess mucus
  • Coughing / choking / cyanosis with first feed
  • Abdominal distension (TOF)
  • Scaphoid abdomen (if OA present alone)
84
Q

What are the investigations for TOF/OA?

A

First line:

  • Antenatal USS > polyhydramnios (if present > MRI)
  • Antenatal MRI > oesophageal pouch and small stomach
  • XR chest and abdomen (obtained immediately after birth if TOF/OA suspected) > nasogastric tube coiled in upper pouch

Consider:

  • Barium swallow
  • Echo for cardiac abnormalities
85
Q

What is the management of TOF/OA?

A

Immediate = Stabilisation:

  • Infant should be placed in a slight reverse Trendelenburg position to avoid regurg / aspiration pneumonia
  • NBM
  • Suction catheter in upper pouch

Surgical:

  • Surgical repair within a few days of birth
  • NICU and ventilator support
86
Q

What is biliary atresia?

A

Malformation of the bile ducts which causes the ducts to be abnormally narrow, blocked or absent > obstruction of bile flow > neonatal cholestasis

87
Q

What is biliary atresia associated with?

A

CMV infections and aflatoxin B

88
Q

What are the 3 types of biliary atresia?

A

Type I = common bile duct atresia

Type II = cystic duct atresia

Type III = full atresia (>90%)

89
Q

What are the S/S of biliary atresia?

A

Patients typically present in first few weeks of life with:

  • Mild jaundice (>2wks) (obstructive picture)
  • Pale stools, dark urine
  • NO vomiting
  • Normal birth weight > faltering growth
  • Appetite disturbance
  • Hepatosplenomegaly
  • Swollen abdomen
  • Irritability
90
Q

What are the investigations for biliary atresia?

A

Raised cBR >2wks (serum total and direct or conjugated BR)

1st = Abdominal USS (triangular cord sign)
TIBIDA isotope scan
Confirmation = ERCP +/- biopsy
Bloods = LFTs (raised), FBC, INR, PT, plasma or serum amino acids
Sweat chloride test > CF?

91
Q

What is the management of biliary atresia?

A

Surgical intervention is recommended ASAP (ideally within the first 60 days of life)

  • 1st line = Hepatoportoenterostomy (HPE) - Kasai procedure
  • 2nd line / end stage liver disease = liver transplant
  • Ongoing = abx prophylaxis (prevent cholangitis), nutritional support, vitamin supplementation, ursodeoxycholic acid (promotes bile flow)
92
Q

What are the complications of biliary atresia?

A
  • Growth failure
  • Portal HTN
  • Cholangitis
  • Ascites
  • Progressive liver disease
  • Cirrhosis with eventual hepatocellular carcinoma
93
Q

What is small bowel atresia?

A

Congenital malformation of the small bowel resulting in the absence or complete closure of a portion of its lumen

94
Q

What are the 2 types of small bowel atresia?

A

Duodenal atresia = associated with polyhydramnios, Down’s, congenital cardiac abnormalities

Duodenal stenosis = no vomiting, potential for obstruction and ‘double bubble’ on AXR

95
Q

What are the S/S of small bowel atresia?

A
  • Bile-stained vomiting (jejunal or ileal atresia) > tx as intestinal obstruction until proven otherwise
  • Non-bilious or bilious vomiting (duodenal atresia)
  • Abdominal distension
96
Q

What are the investigations for small bowel atresia?

A

Bloods:

  • LFTs, total serum BR (uBR), INR, serum amino acids

Urinary:

  • Organic acids, succinyl acetone, bile acids, lactate : pyruvate ratio

AXR:

  • “Double bubble” sign
  • Absent or reduced gas past the obstructions
  • Dilated loops of bowel (jejunal)
97
Q

What is the management of small bowel atresia?

A

General:

  • ABCDE approach > stabilise neonate with NGT decompression + NBM

Surgical:

  • Primary anastomosis or Ladd procedure if malrotation present
  • Need to examine entire bowel to exclude other multiple atretic segments
98
Q

What are the complications of small bowel atresia?

A
  • Pulmonary aspiration
  • Anastomotic complications (stenosis or leak)
  • Proximal bowel may have abnormal peristalsis > may need prolonged post-op TPN
99
Q

What are the S/S of urinary tract abnormalities?

A

Antenatal:

  • Oligohydramnios, decreased foetal urine output

Postnatal:

  • Irritability, infections

Also > intra-abdominal masses, haematuria, renal calculi, renal failure, HTN, hepatosplenomegaly

100
Q

What are the investigations for urinary tract abnormalities?

A
  • Renal USS
  • DMSA scan > detect scarring and functional defects (only 2m after UTI)
  • Nuclear renal imaging > assessment of kidney function and perfusion
    1. MCUG > visualise anatomy, see VUR and urethral obstruction, not past infancy
    2. MAG3 renogram > see MAG3 excreted from blood into urine
  • IV urogram (IVG) > visualisation of majority of anomalies
  • Genetic karyotyping > Potter sequence (renal problems > oligohydramnios > problems seen)
101
Q

What is the management of urinary tract abnormalities?

A

General

  • Antenatal counselling with screening for associated anomalies or kayotyping as appropriate

Medical

  • Sx control (HTN), abx (UTI/prophylaxis), dialysis (renal failure)

Surgical

  • Tx of cause
102
Q

What are anorectal malformations?

A

Wide spectrum of congenital disorders affecting the distal anus and rectum as well as the urinary and genital tracts > all have absence of an anus in the normal position

103
Q

What is a low anorectal anomaly?

A

Anus closed over, in a different position or narrower than usual, and fistula to ski

104
Q

What is a high anorectal anomaly?

A

Bowel has closed end at high level, does not connect with anus, usually associated with bladder / urethral / vaginal fistula.

105
Q

What are the S/S of an anorectal malformation?

A

No/delayed meconium > swollen abdomen, vomiting

If fistula > may pass stool from abnormal area

106
Q

What are the investigations for an anorectal malformation?

A

Clinical, checked on neonatal check
Screen for associated abnormalities

107
Q

What is the management of anorectal malformation?

A

Surgical correction by 9m (depending on specific abnormality)

108
Q

What is cryptorchidism?

A

Failure of normal descent of the testicle to a scrotal position by 3m of age

109
Q

What is a RF for cryptorchidism?

A

Prematurity

110
Q

What is cryptorchidism associated with?

A

Patent processus vaginalis, abnormal epididymis, cerebral palsy, mental retardation, Wilms tumour, abdominal wall defects

111
Q

What are the differential diagnoses of cryptorchidism?

A

Retractile testes, intersex conditions

112
Q

What are the S/S of cryptorchidism?

A
  • Asx
  • Picked up during examination
  • May have associated inguinal hernia
  • Most common location of the cryptorchid testis is in the inguinal canal, may also be in the prescrotal and abdominal regions
113
Q

What are the investigations for cryptorchidism?

A

Clinical diagnosis

  • USS abdomen to aid location of the testis
  • In bilateral absence, conduct hormonal tests (B-HCG) and chromosomal mapping
114
Q

What is the management of cryptorchidism?

A

Unilateral, at birth:

  • Commonly idiopathic and will resolve spontaneously
  • Arrange RV for 6-8wks
  • If still undescended, arrange RV at 3m
  • If still undescended, refer to paediatric surgeon to be seen before 6m

Bilateral, at birth:

  • Pituitary causes > refer to paediatricians / endocrinologists
  • If concern of disorder of sexual development e.g. ambiguous genitalia or hypospadias > refer to senior paediatrician for endo and genetic ix

Retractile (testes have descended but come in and out of scrotal sac)

  • Detect at 3m and advise annual follow-up throughout childhood

Surgical:

  • Orchidopexy (palpable testes = inguinal approach, non-palpable = laparoscopy)
  • 6-18m

Medical:

+/- b-hCG

Reasons for correction:

  • Reduce risk of infertility
  • Allows the testes to be examined for testicular cancer (40x more likely)
  • Avoid testicular torsion
  • Cosmetic appearance
115
Q

Describe newborn resuscitation

A
  1. Dry baby and maintain temperature
  2. Assess tone, respiratory rate, heart rate
  3. If gasping or not breathing give 5 inflation breaths
  4. Reassess (chest movements)
  5. If the heart rate is not improving and <60bpm start compressions and ventilation breaths at a rate of 3:1
116
Q

What are the components of APGAR?

A
  • A = Appearance (colour)
  • P = Pulse (HR)
  • G = Grimace (reflex irritability)
  • A = Activity (tone)
  • R = Respiratory effort
117
Q

How is colour scored in APGAR?

A

2 = pink
1= body pink, extremities blue
0 = blue all over

118
Q

How is pulse scored in AGPAR?

A

2 = >100
1 = <100
0 = absent

119
Q

How is reflex irritability scored on APGAR?

A

2 = cries on stimulation / sneezes / coughs
1 = Grimace
0 = nil

120
Q

How is tone scored on AGPAR?

A

2 = active movement
1 = limb flexion
0 = flaccid

121
Q

How is respiratory effort scored on AGPAR?

A

2 = strong, crying
1 = weak, irregular
0 = nil

122
Q

What is Caput succedaneum?

A

Oedema of the scalp at the presenting part of the head, typically the vertex.

123
Q

What causes Caput succedaneum?

A
  • Mechanical trauma of the initial portion of the scalp pushing through the cervix in a prolonged delivery
  • Secondary to the use of ventouse (vacuum) delivery
124
Q

What are the S/S of Caput succedaneum?

A
  • Fluid collection with poorly defined margins
  • Soft, puffy swelling due to localised oedema
  • Crosses suture lines
125
Q

What is the management of Caput succedaneum?

A
  • It resolves within a few days - no intervention is necessary.
126
Q

What is Cephalhaematoma?

A

A swelling on the newborns head

  • Develops several hours after delivery
  • Due to bleeding between periosteum and skull
  • Most common site affected is parietal region
  • Does not cross suture lines
127
Q

What is the management of Cephalhaematoma?

A
  • Managed conservatively
  • May take a few months to resolve
128
Q

What causes Cephalhaematoma?

A

More common following difficult / prolonged deliveries

129
Q

What are the complications of Cephalhaematoma?

A

If severe - jaundice

Paeds (18 decks)

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