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Child health > Neonatology 4 > Flashcards

Neonatology 4 Flashcards

1
Q

What is rhesus haemolytic disease. affect on baby

A

condition where antibodies in a pregnant woman’s blood destroy her baby’s blood cells

also known as haemolytic disease of the foetus and newborn (HDFN)

Baby may become anaemic and jaundiced.
Hydrops, hepatosplenomegaly and rapid jaundice are rare nowadays due to antenatal care

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2
Q

When can ABO incompability occur

A

Most ABO antibodies are IgM and do not cross the placenta.

Some group O women have an IgG anti-A haemolysin in the blood - it can cross placenta and haemolyse group A infant RBCs

(occasionally there is a group B infant affected by anti-B haemolysis)

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3
Q

Effects of ABO incompability (haemolysis)

A

Severe jaundice
Peak 12-72 hrs
Hb level usually normal
NO hepatosplenomegaly (in contrast to Rhesus)

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4
Q

Diagnosis of Rhesus/ABO haemolysis

A

Bloods:
biochemistry for jaundice
antibody screen

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5
Q

Treatment of ABO/Rhesus incompability

A 
Before birth:
intrauterine transfusion (RBCs) or early induction of labour once there is pulmonary maturity

Mother can undergo plasma exchange to lower circulatory antibodies by 75% .
Anti-D prophylaxis after first Rhesus +ve child in a Rhesus -ve mother

Treatment of baby may be treatment of jaundice with phototherapy.
Transfusion with RBC may be needed
Bicarbonate for acidosis

Most complications arise from high bilirubin

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6
Q

Important RF for congenital abnormalities

A

Large number are due to genetic conditions.

There are a huge number.

Maternal and paternal age.
Infections (TORCH - toxoplasmosis, others, rubella, CMV and HSV)
Toxins (alcohol, smoking, mercury, prescription drugs)
Dietary deficiencies eg. folic

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7
Q

What is CHARGE?

A

Acronym that describes a set of unusual congenital features seen in many newborn children.

Coloboma (hole in one of the eye structures - retina, choroid, iris, optic disc)
Heart defects
Atresia of the nasal choanase
Retarded growth and development
Genitourinary abnormalities
Ear abnormalities and hearing loss

Leading cause of congenital deafness. Very few people will have all features

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8
Q

Genetics of CHARGE

A

Autosomal dominant

Chromosome affeced is 8q12 and gene CHD7

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9
Q

What is VACTERAL

A

Acronym that describes a syndrome/associated of birth defects

Vertebral (hypoplastic vertebrae(scoliosis)
Anal atresia
Cardiac defects (ASD, VSD, tetralogy of Fallot)
Tracheo-oesophagel fistula
Esophageal atresia
Renal abnormalities (eg 1 umbilival vein causing outflow obstruction)
Limb defects (hypoplastic thumbs, extra digits, fusion)

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10
Q

What is VACTERAL associated with

A

trisomy 18
Diabetic mothers

Most babies have normal development and intelligence, but can be quite small

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11
Q

What is Patau syndrome

A

trisomy 13
Most are detected on 2nd trimester scan

Structural defect of brain
Scalp defects
Small eyes (microphthalmia)
Cleft lip and palate
Polydactyly
Cardiac and renal malformations
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12
Q

What is Edward syndrome

A

Trisomy 18
Most detected on antenatal scan

Low birthweight
Prominent occiput
Small mouth+chin
Short sternum
Flexed overlapping fingers
Rocker-bottom feet
Cardiac and renal malformation
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13
Q

Pathology of cleft lip/palate

A

Unilateral or bilateral
Failure of fusion of the frontonasal and maxillary processes

Some associated with maternal anticonvulsant therapy

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14
Q

Clinical features of fetal alcohol syndrome

A

Growth restriction
Characteristic facies
Developmental delay
70% have cardiac defects

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15
Q

What is neural tube defects

A

result from failure of normal fusion of the neural plate to form the neural tube during the first 28 days following conception

Folic acid supplementation reduces risk

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16
Q

Different types of neural tube defect

A 
Anencephaly
Encephalocoele
Spina bifida occulta
Meningocoele
Myelomeningoceles
17
Q

What is anencephaly

A

Failure of development of most of the cranium and brain

Affected infants stillborn or die shortly after birth

Detected on antenatal screening with TOP

18
Q

What is encephalocele

A

Extrusion of brain and meninges through a midline skull defect which can be corrected surgically

However, often there are associated cerebral malformations

19
Q

What is spina bifida occulta

A

Failure of fusion of vertebral arch.

There may be an associated skin lesion in the lumbar region - tuft of hair, lipoma, birthmark

May be underlying tethering of the cords: cause neurological deficits of bladder function and lower limbs

20
Q

What are myelomeningoceles associated with

A

variable paralysis of the legs
Muscle imbalance which can cause dislocation of hips
Sensory loss
Bladder denervation (neuropathic bladder)
Bowel denervation (neuropathic bowel)
Scoliosis
Hydrocephalus

21
Q

Features of gastroschisis

A

Defect in anterior abdominal wall through which the abdominal contents freely protrude

No overlying sac or peritoneum

Size of defect usually <4cm

22
Q

Features of exomphalos

A

Weakness of abdominal wall where the umbilical cord joins it

Allows abdominal contents (mainly bowel and liver) to protrude outside the abdominal cavity where they are contained in a loose sac

23
Q

What is bowel atresia

A

Narrowing or absence of a portion of the intestine

Can occur in either small or large intestine

24
Q

Recognize biliary tree atresia from history and investigations

A

Normal birthweight but FTT as disease progresses

Mild jaundice with pale stools and dark urine

Hepatosplenomegaly often present

LFTs are of little value
Fasting USS may show contracted/absent gallbladder

Radioisotope scan with TIBIDA shows good uptake in the lvier, but no excretion into bowel

Liver biopsy may show features of extrahepatic biliary obstruction

Treatment - surgical bypass of fibrotic ducts (hepatoportoenterostomy aka Kasa procedure)

25
Q

Main causes of haemolytic disease of the newborn

A

Immune - haemolytic disease of the newborn

Red cell membrane disorders - hereditary spherocytosis

Red cell enzyme disorders - G6PD deficiency

Haemoglobinopathies - alpha thalassaemia major

26
Q

Which events can potentially sensitise a Rhesus -ve mothers to a rhesus +ve child?

A

When mother is sensitised to fetal RBCs:

Fetal-maternal haemorrhage:

  • Abortion
  • Childbirth
  • rupture in placenta during pregnancy
  • medical procedures in pregnancy that breach the uterine wall

When mother receives blood transfusion.. although ABO and Rh typing is routine

Mothers with type O blood are more prone to make IgG anti-A and anti-B antibodies which can cross the placenta

27
Q

FBC results in haemolytic anaemia. Other tests?

A

Increased reticulocyte count to compensate for anaemia

Increased unconjugated bilirubin

other diagnostic clue is positive direct anti-globulin test (Coombs test): only positive in antibody-mediated anaemias (can differentiate from other causes of haemolytic anaemia)

28
Q

What is perinatal asphyxia

A

Gas exchange (pulmonary or placental) is compromised or ceases altogether. Results in cardiorespiratory depression. Causes hypoxia, hypercapnia and metabolic acidosis

Compromised cardiac output diminishes tissue perfusion causing hypoxic-ischaemic injury

29
Q

Aetiology of HIE (hypoxic ischaemic encephalopathy)

A

Most follow a significant hypoxic event immediately before or during labour or delivery:

Reduced umbilical blood flow - cord compression including cord prolapse and shoulder dystocia

Reduced placental gas exchange - placental abruption, excessive/prolonged uterine contractions, ruptured uterus

Reduced maternal placental perfusion - IUGR

Maternal hypoxia

Compromised fetus (IUGR or anaemia)

Inadequate postnatal cardiopulmonary circulation - failure to breath

30
Q

Presentation of hypoxic ischaemic encephalopathy

A

Varies depending on severity of cerebral hypoxia

Level of consciousness
Muscle tone
Posture
Tendon reflexes
Suck
Heart rate
CNS homeostasis

Start <48hrs after asphyxia.
Mild: infant is irritable, responds excessively to stimulation, may have staring of eyes and hyperventilation and has impaired feeding

Moderate - infant shows marked abnormalities of tone and movement, cannot feed and may have seizures

Severe - there are no normal spontaneous movements or response to pain, tone in limbs may fluctuate between hypo & hypertonia, seizures are prolonged and often refractory to treatment and multi-organ failure is present

31
Q

Management of Hypoxic Ischaemic Encephalopathy

A

Respiratory support
Record amplitude-integrated EEG to detect abnormal background activity to confirm early encephalopathy or identify seizures

Treat clinical seizures with anti-convulsants

Treat hypotension by volume and inotrope support

Monitor and treat hypoglycaemia and electrolyte imbalance, especially hypocalcaemia

THERAPEUTIC HYPOTHERMIA

32
Q

Explain therapeutic hypothermia

A

If A and B are met, then assess for C.

A. >36/40. >1800g. <6hr old with:

  • Apgar<5 or continued need for resuscitation at 10 min
  • acidosis - cord pH<7/BE
33
Q

Long-term neurodevelopmental risks of HIE

A

mild - complete recovery

Moderate - if feeding by 2 weeks, prognosis is excellent. If clinical abnormalities persist, full recovery unlikely

Severe - mortality of 30-40%. 80% survivors have neurodevelopmental disabilities, particularly CP.
If MRI at 4-14 days shows significant brain abnormalities, the risk of CP is very high

34
Q

Effects of multi-orgn dysfunction in HIE

A

Encephalopathy:
seizures, abnormal signs

Resp:
Persistent pulmonary HTN of the newborn (PPHN)

Myocardial:
Hypotension

Metabolic:
hypoglycaemia
hypocalcaemia
hyponatraemia

Other:
renal failure
DIC

Child health (51 decks)

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