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Phase 3a Paediatrics > Neonatology > Flashcards

Neonatology Flashcards

1
Q

What is celft lip?

A

Cleft lip = a congenital condition where there is a split or open section of the upper lip. This opening can occur at any point along the top lip, and can extend as high as the nose.

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2
Q

What is celft palate?

A

Celft palate = a defect exists in the hard or soft palate at the roof of the mouth. This leaves an opening between the mouth and the nasal cavity.

Cleft lip and cleft palate can occur together or on their own.

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3
Q

Complications of cleft lip or palate

A

Problems with:
* Feeding
* Swallowing
* Speech
* Psychosocial implications

Children with cleft palates can be more prone to hearing problems, ear infections and glue ear.

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4
Q

Management of cleft lip or palate

A

The first priority is to ensure the baby can eat and drink. This may involve specially shaped bottles and teat

Definitive treatment: surgically correct the cleft lip or palate (cleft lip at 3 months, cleft palate at 6-12 months)

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5
Q

Info: Neonates with with duodenal atresia
(Risk factors)

A

Rule of 1/3s:
* 1/3 have trisomy 21
* 1/3 will have cardiac anomalies
* 1/3 will have associated malrotation (midgut rotation and volvulus)

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6
Q

Presentation of duodenal atresia

A

Antenatal diagnosis:
* Polyhydramnios + a double bubble (AXR)

Postnatally diagnosis:
* Bile-stained vomiting

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7
Q

What bowel abnormality seen antenatally in AXR is seen as ‘double bubble’

A

Duodenal atresia

‘Double bubble’ = sign of gas in stomach + proximal duodenum

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8
Q

Management of duodenal atresia

A

Surgery: duodenodeuodenostomy

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9
Q

Cause of small bowel atresias

A

Vascular insult

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10
Q

Pathology of small bowel atresias

A

Varies from an itraluminal obstructing membrane → to a widely separated atresia with a V-shaped mesenteric defect + loss of gut

About 10% are multiple

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11
Q

Presentation of small bowel atresias

A

Bile-stained vomiting + abdominal distenstion

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12
Q

Investigation for small bowel atresias

A

Abdominal x-ray (AXR)
Few dilated loops

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13
Q

Management for small bowel atresias

A

Laparotomy: End-to-end anastomosis

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14
Q

95% of neonates with meconium ileus will have what condition?

A

Cystic fibrosis (CF)

Lack of pancreatic enzymes = results in thick + viscous meconium → causing an intraluminal obstruction in the terminal ileum

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15
Q

How do babies present with meconium ileus at birth?

A

Babies present with intestinal obstruction

  • Failure to pass meconium (within the first 24-48 hours)
  • Abdominal distension (due to distension)
  • Vomiting (bile-stained)
  • Poor feeding
  • Absent or decreased bowel sounds
  • Signs of dehydration
  • Palpable abdominal mass
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16
Q

Management of meconium ileus

A
  • Simple MCI: Enema (hypertonic contrast) + fluid resuscitation
  • Unsuccessful enema or complicated MCI: Laparotomy
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17
Q

Define oesophageal atresia

A

Oesophageal atresia = oesophagus is discontinuous or blocked → ends in a blind pouch → preventing food from reaching the stomach

It is commonly associated with a tracheo-oesophageal fistula (TOF) in around 85% of cases, where there is an abnormal connection between the trachea and the oesophagus.

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18
Q

Clinical presentation of oesophageal atresia

A

Often presents immediately after birth:

  • Excessive salivation and drooling – due to the inability to swallow.
  • Choking and coughing – especially after feeding attempts, as milk or secretions can’t pass into the stomach and may spill over into the lungs.
  • Cyanosis – episodes of bluish skin, particularly when feeding, due to aspiration or airway obstruction.
  • Respiratory distress – difficulty breathing, especially if the baby aspirates food or saliva.
  • Inability to pass a feeding tube – failure to pass a nasogastric tube into the stomach is a common finding in neonatal units.
  • Abdominal distension – may occur in cases where there is a tracheo-oesophageal fistula, as air can enter the stomach from the trachea.
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19
Q

Investigation for oesophageal atresia

A

Chest + abdominal x-ray

  • Inability to pass NGT > 10cm from the mouth
  • CXR: NGT stops in the upper thorax. Air in stomach indicates a fistula between the trachea + distal oesophagus (TOF)
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20
Q

Management of oesophageal atresia

A

Acute management:
* Minimise risk of pneumonia: aspirate upper oesophageal pouch
* IV fluids
* Preoperative antibioticss

Surgery

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21
Q

What is brunchopulmonary dysplasia?

AKA chronic lung disease of prematurity (CLDP)

A

Bronchopulmonary dysplasia = occurs in premature babies - typically before 28 weeks gestation

  • These babies suffer with respiratory distress syndrome → requiring oxygen therapy or intubation + ventilation at birth
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22
Q

Diagnosis/Ix of bronchopulmonary dysplasia

A

Diagnosis is made based on chest xray changes + when the infant requires oxygen therapy after they reach 36 weeks gestational age

Also:
* A formal sleep study to assess their oxygen saturations during sleep supports the diagnosis and guides management

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23
Q

Clinical features of bronchopulmonary dysplasia

A
  • Low oxygen saturations
  • Increased work of breathing
  • Poor feeding + weight gain
  • Crackles + wheeze on chest auscultation
  • Increased susceptibility to infection
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24
Q

Prevention on bronchopulmonary dysplasia antenatally and after birth

A

Antenatally:
* Give mothers corticosteroids (betamethasone) that show signs of premature labour at less than 36 weeks → speeding up lung development (reducing risk of bronchopulmonary dysplasia)

Once neonate is born:
* Using CPAP rather than intubation and ventilation when possible
* Using caffeine to stimulate the respiratory effort
* Not over-oxygenating with supplementary oxygen

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25
Q

Management of bronchopulmonary dysplasia

A
  • Discharged with low dose of oxygen at home (e.g. 0.01 litres per minute via nasal cannula) → follow up weaning them off of oxygen for a year
  • Palivizumab (monoclonal antibody) injections: protect against respiratory syncytial virus (RSV)
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26
Q

A term newborn presents with poor muscle tone, weak cry, and seizures within hours of birth. The mother had a prolonged labour with meconium-stained amniotic fluid. The baby’s Apgar scores were 3 at 1 minute and 6 at 5 minutes. On examination, the infant has altered consciousness and poor responsiveness to stimuli. Possible diagnosis?

A

Hypoxic ischaemic encephalopathy

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27
Q

Pathophysiology of hypoxic ischaemic encephalopathy

A

Hypoxic-ischaemic encephalopathy (HIE) = occurs when there is a reduction in oxygen supply (hypoxia) and/or blood flow (ischaemia) to the neonate’s brain → leading to neuronal damage + dysfunction

Primary cause of HIE in neonates = asphyxia. This can be caused by:
* Prolapsed or nuchal cord
* Intrapartum haemorrhage
* Maternal shock

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28
Q

When should you suspect hypoxic ischaemic encephalopathy?

A
  • Hypoxic events occur during perinatal or intrapartum period
  • Acidosis (pH<7) on umbilical artery blood gas
  • Poor Apgar scores
  • Clinical presentation of HIE
29
Q

Staging system for hypoxic ischaemic encephalopathy

A

Sarnat staging

Stage 1 (Mild HIE):
* Poor feeding, irritable but alert, mild hypotonia, and no seizures
* Resolves within 24 hours
* Normal prognosis

Stage 2 (Moderate HIE):
* Lethargy, moderate hypotonia, and seizures
* Can take weeks to resolve
* Up to 40% develop cerebral palsy

Stage 3 (Severe HIE):
* Coma, severe hypotonia, and severe seizures
* Up to 50% mortality rate
* Up to 90% develop cerebral palsy

30
Q

Risk factors for HIE

A
  • Maternal risk factors: hypertension, diabetes, substance abuse, infection
  • Obstetric risk factors: prolonged labour, meconium-stained amniotic fluid, placental abruption, umbilical cord prolapse
  • Infant risk factors: prematurity, low birth weight, congenital anomalies
31
Q

Clinical features of hypoxic ischaemic encephalopathy

A

Signs:
* Altered level of consciousness
* Hypotonia
* Weak or absent reflexes
* Apnoea or irregular breathing

Symptoms:
* Poor feeding
* Irritability
* Lethargy
* Seizures

32
Q

Investigations for hypoxic ischaemic encephalopathy

A
  • Blood gas analysis: to assess oxygenation, carbon dioxide levels, and acid-base status
  • Blood tests: to evaluate electrolyte levels, glucose, and infection markers
  • Cranial ultrasound: to detect brain injury and rule out other intracranial pathologies.

Investigations to consider:
* MRI : to provide a detailed assessment of brain injury, including the extent and location of lesions . Routinely performed shortly after rewarming post-hypothermic treatment.
* EEG : To monitor seizure activity and assess brain function.

33
Q

Management for hypoxic ischaemic encephalopathy

A

First line:
* Oxygen therapy: to maintain adequate oxygenation and prevent further hypoxia
* Antiepileptic drugs : given to manage seizures and reduce the risk of further brain injury
* Therapeutic hypothermia: to decrease metabolic demands and protect against further brain injury. Recommended for moderate to severe HIE within 6 hours of birth
* Supportive care: to provide adequate nutrition, maintain body temperature, and manage any complications.
* Fluid and electrolyte management: to maintain hydration, electrolyte balance, and prevent hypoglycaemia

34
Q

Complications of hypoxic ischaemic encephalopathy

A
  • Cerebral palsy
  • Cognitive impairment
  • Epilepsy
  • Visual + hearing impairment
  • Developmental delay
  • Death
35
Q

A 5-day-old breastfed term infant presents with his mother to the GP as she is concerned that he “looks yellow”. On examination, the child is jaundiced but otherwise well. Possible diagnosis?

A

Neonatal jaundice

36
Q

Difference between onset of physiological and pathological neonatal jaundice

A

Majority:
* Physiological → after 24 hours of birth
* Pathological → occurs within the first 24 hours

37
Q

Define jaundice

A

Jaundice = describes the condition of abnormally high levels of bilirubin in the blood.

38
Q

Info: Jaundice

A
  • RBCs = contain unconjugated bilirubin
  • When red blood cells break down → release unconjugated bilirubin into the blood.
  • Unconjugated bilirubin = conjugated in the liver.
  • Conjugated bilirubin = excreted in two ways: via the biliary system into the gastrointestinal tract + via the urine.
39
Q

Physiological jaundice physiology

A
  • There is a high concentration of red blood cells in the fetus and neonate → that are more fragile than normal RBCs .
  • The fetus + neonate = also have less developed liver function
  • Fetal RBCs = break down more rapidly → releasing lots of bilirubin
  • Normally, this bilirubin = excreted via the placenta - however at birth the foetus no longer has excess to the placenta to excrete bilirubin
  • ** Leads to normal rise in bilirubin shortly after birth** → causing mild yellowing of skin + sclera from 2-7 days of age
  • Usually resolves completely by 10 days
  • Most babies remain otherwise healthy and well
40
Q

Causes of neonatal jaundice: increased production of bilirubin

A
  • Haemolytic disease of the newborn
  • ABO incompatibility
  • Haemorrhage
  • Intraventricular haemorrhage
  • Cephalo-haematoma
  • Polycythaemia
  • Sepsis and disseminated intravascular coagulation
  • G6PD deficiency
41
Q

Causes of neonatal jaundice: decreased clearance of bilirubin

A
  • Prematurity
  • Breast milk jaundice
  • Neonatal cholestasis
  • Extrahepatic biliary atresia
  • Endocrine disorders (hypothyroid and hypopituitary)
  • Gilbert syndrome
42
Q

Tom Tip: Jaundice

A
  • Jaundice in the first 24 hours of life = pathological.
  • This needs urgent investigations and management.
  • Neonatal sepsis is a common cause.
  • Babies with jaundice within 24 hours of birth need treatment for sepsis if they have any other clinical features or risk factors.
43
Q

Info: Jaundice in Premature Neonates

A

In premature babies = physiological jaundice is exaggerated due to the immature liver → increases risk of complications - particularly kernicterus

Kernicterus = brain damage due to high bilirubin levels

44
Q

Are breastfed more likely to have neonatal jaundice?

A

Yes!
* Components of breast milk inhibit the ability of the liver to process the bilirubin.
* Breastfed babies = more likely to become dehydrated if not feeding adequately.
* Inadequate breastfeeding may lead to slow passage of stools → increasing absorption of bilirubin in the intestines.

Breastfeeding should still be encouraged, as the benefits of breastfeeding outweigh the risks of breast milk jaundice. Mothers may need extra support and advice to ensure adequate breastfeeding.

45
Q

What is prolonged jaundice?

A

Jaundice is “prolonged” when it lasts longer than would be expected in physiological jaundice. This is:
* More than 14 days in full term babies
* More than 21 days in premature babies

46
Q

Should prolonged jaundice prompt further investigations?

A

Yes - looking for an underlying cause
These are particularly looking for conditions that will cause jaundice to persist after the initial neonatal period, such as:
* Biliary atresia
* Hypothyroidism
* G6PD deficiency

47
Q

Investigations for neonatal jaundice

A
  • Full blood count + blood film → polycythaemia or anaemia
  • Conjugated bilirubin: elevated levels indicate a hepatobiliary cause
  • Blood type testing of mother and baby for ABO or rhesus incompatibility
  • Direct Coombs Test (direct antiglobulin test) for haemolysis
  • Thyroid function, particularly for hypothyroid
  • Blood + urine cultures if infection is suspected (suspected sepsis needs treatment with antibiotics)
  • Glucose-6-phosphate-dehydrogenase (G6PD) levels for G6PD deficiency
48
Q

Management of neonatal jaundice

A

Total bilirubin levels = monitored + plotted on treatment threshold charts
* x-axis = age of baby
* y-axis = total bilirubin level

If the total bilirubin reaches the threshold on the chart, they need to be commenced on treatment to lower their bilirubin level.

  • Phototherapy = can usually correct neonatal jaundice
  • Extremely high levels = may require exchange transfusion
  • Exchange transfusions involve removing blood from the neonate and replacing it with donor blood.
49
Q

Info: Phototherapy

A
  • Phototherapy = converts unconjugated bilirubin into isomers - that can be excreted in the bile + urine - without requiring conjugation in the liver
  • Blue light is used in light box
  • Double phototherapy = 2 light boxes
  • Once phototherapy is complete, a rebound bilirubin should be measured 12 – 18 hours after stopping to ensure the levels do not rise about the treatment threshold again.
50
Q

What is kernicterus?

A
  • Kernicterus = type of brain damage - caused by excessive bilirubin levels
  • Bilirubin = can cross the blood-brain barrier
  • Excessive bilirubin = causes direct damage to the CNS

Kernicterus = main reason why we treat jaundice

51
Q

How does kernicterus present?

A
  • Less responsive
  • Floppy
  • Drowsy
  • Poor feeding

Damage to the CNS is permeant - causing cerebral palsy, learning disability, deafness

52
Q

What is gastroschisis?

A

Gastroschisis = a congenital defect in the abdominal wall where the intestines + sometimes other abdominal organs protrude outside the baby’s body through a hole near the belly button - without a protective covering

The intestines are not covered by a protective membrane → exposing them to amniotic fluid → lead to inflammation + damage.

53
Q

Risk factors for gastroschisis

A
  • Maternal age (more common in younger mothers - particularly under 20 years)
  • Lifestyle: Smoking, alcohol consumptio, drug use
  • Low maternal body mass index (BMI) + poor nutrition
54
Q

Clinical features for gastroschisis

A

Gastroschisis = usually diagnosed prenatally via routine ultrasound

Visible herniation of abdomina; organs:
* intestines (sometimes stomach or liver) = protrude outside of the neonate’s abdomen (typically to right of the umbilicus)
* Exposed bowel = appears inflamed + thickened matted appearance → due to contact with amniotic fluid

Normal umbilical cord insertion

55
Q

Management of gastroshisis

A
  • Monitored very closely antenatal → fetal growth restriction (common complication)
  • Delivery → vaginal unless otherwise (elective preterm delivery between 36-38 weeks) may be considered to minimise bowel damage
  • Postnatally → surgergical closure
56
Q

What infections are included in TORCH?

A

T - Toxoplasmosis
O - Other (VZV, parvovirus B19, HIV, Hep B)
R - Rubella
C - Cytomegalovirus (CMV)
H - Herpes simplex virus (HSV)

57
Q

Ix for TORCH infections (generally)

A

Antenatally:
* Ultrasound (can indicate unusual fetal findings, such as the enlargement of the ventricles in the fetus’ brain (i.e., ventriculomegaly), intracranial calcifications, and fetal growth restriction or retardation)
* PCR of amniotic fluid

Postnatally:
* Viral cultures, PCR testing, antibody measurement
* MRI (brain lesions, hydrocephalus, intracranial calcifications)
* Eye tests (cataracts)
* Hearing tests (hearing loss)

58
Q

Info: Congenital Toxoplasmosis

A
  • Infection with Toxoplasma gondii = usually asymptomatic
  • Primarily spread by contamination with faeces from a cat that is a host of the parasite
  • When infection occurs during pregnancy it can lead to congenital toxoplasmosis.
  • This risk is higher later in the pregnancy

Classic triad of features in congenital toxoplasmosis:
* Intracranial calcification
* Hydrocephalus
* Chorioretinitis

59
Q

Info: Congenital Varicella Syndorme

A

Chickenpox = caused by varicella zoster virus (VSV)

Dangerous in pregnancy, as can lead cause:
* Fetal varicella syndrome
* More severe cases in the mother - varicella pneumonitis, hepatitis, encephalitis
* Severe neonatal varicella infection (if mum is infected around delivery)

Management:
* If exposed → IV varicella immunoglobulins (within 10 days of exposure)
* If the chickenpox rash starts in pregnancy → ** oral aciclovir if they present within 24 hours** and are more than 20 weeks gestation.

Features of congenital varicella syndrome:
* Fetal growth restriction
* Microcephaly, hydrocephalus and learning disability
* Scars and significant skin changes following the dermatomes
* Limb hypoplasia (underdeveloped limbs)
* Cataracts and inflammation in the eye (chorioretinitis)

Mothers that have previously had chickenpox are immune and safe. If in doubt, IgG levels for VZV can be tested

60
Q

Info: Congenital Rubella Syndrome

Congenital rubella syndrome is caused by maternal infection with the rubella virus during pregnancy.

A
  • Women planning to get pregnant should get MMR
  • Pregnant women should not get MMR vaccine (as its a live vaccine)

Features of congenital rubella syndrome:
* Congenital cataracts
* Congenital heart disease (PDA and pulmonary stenosis)
* Learning disability
* Hearing loss
* Blueberry muffin rash

61
Q

Info: Herpes Simplex Virus (HSV)

A
  • Herpes Simplex Virus = usually infects a newborn during passage through the birth canal.
  • In infants, HSV can cause blisters + inflammation of the brain, known as meningoencephalitis.

Magangement: Iv Aciclovir

62
Q

Info: Congenital Cytomegalovirus

Congenital cytomegalovirus (CMV) infection occurs due to maternal CMV infection during pregnancy.

A

CMV = mostly spread via infected saliva or urine of asymptomatic children
* Most cases of CMV in pregnancy do not cause congenital CMV. The features of congenital CMV are:

  • Fetal growth restriction
  • Microcephaly
  • Hearing loss
  • Vision loss
  • Learning disability
  • Seizures

Management: ?Gancyclovir

63
Q

Info: Congenital Zika Syndrome

A

The zika virus is spread by host Aedes mosquitos in areas of the world where the virus is prevalent. It can also be spread by sex with someone infected with the virus. It can cause no symptoms, minimal symptoms or a mild flu like illness. In pregnancy it can lead to congenital Zika syndrome, which involves:

  • Microcephaly
  • Fetal growth restriction
  • Other** intracranial abnormalities**, such as ventriculomegaly and cerebellar atrophy

Pregnant women that may have contracted the Zika virus should be tested for the viral PCR and antibodies to the Zika virus. Women with a positive result should be referred to fetal medicine to monitor the pregnancy. There is no treatment for the virus.

64
Q

Non-specific signs and symptoms of TORCH infections

A
  • Fever
  • Lethergy
  • Cataracts
  • Jaundice
  • Microencephaly
  • Low birth weight
  • Hearing loss
  • Jaundice
  • Reddish-brown spots on skin
  • Heatosplenomegly
  • Congenital heart disease
65
Q

Transmission of TORCH infections

A
  • Via placenta
  • Via birth canal
  • Via breastmilk
66
Q

What can alcohol use lead to in pregnancy?

A
  • Miscarriage
  • Small for dates
  • Preterm delivery

Fetal alcohol syndrome

67
Q

Presentation of fetal alcohol syndrome

A
  • Microcephaly (small head)
  • Thin upper lip
  • Smooth flat philtrum (the groove between the nose and upper lip)
  • ** Short palpebral fissure** (short horizontal distance from one side of the eye and the other)
  • Learning disability
  • Behavioural difficulties
  • Hearing and vision problems
  • Cerebral palsy
68
Q

What is necrotising enterocolitis (NEC)?

A

Necrotising enterocolitis (NEC) = affects premature neonates → part of the bowel becomes necrotic → can lead to perforation → peritonitis → shock

Life-threatening emergency

Phase 3a Paediatrics (13 decks)

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