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Neonates Flashcards

1
Q

Definition of low birth weight?

A

born weighing less than 5 pounds, 8 ounces (2,500 grams)

less than 3 pounds, 5 ounces (1,500 grams) at birth are considered very low birth weight

extremely low - less than 1000g

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2
Q

Causes of low birth weight?

A

Often caused by premature birth

Substance use (alcohol, cigarettes, cocaine, heroin)

ACEi, carbamazepine, phenytoin, warfarin

Infections (malaria)

Placental insuff: smoking, DM, HTN, anaemia, AN, APS, SLE, sickle cell, Rh incompatibility, pre-eclampsia

Placenta previa, multiple gest, placenta abruption, umbilical a thrombosis/ infarction, uterine malf e.g. fibroids.

Fetal cyanotic heart defects

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3
Q

Signs and symptoms of low birth weight/small baby?

A

Asymmetric: more common, abdo circ lower centile than head, due to placenta insuff

Symmetric: head equally ↓, prolonged IUGR. TORCH, drug use, Chr abnormalities.

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4
Q

What is TORCH?

A

toxoplasmosis, other agents, rubella cytomegalovirus, herpes simplex, and HIV

causes Sx of: fever, difficulty feeding, small areas of bleeding under skin, small reddish or purplish sports, hepatosplenomegaly, jaundice, hearing impairment, abnormalities of eyes

if foetus infected by TORCH agent - outcome of pregnancy may be miscarriage, stillbirth, IUGR, premature birth

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5
Q

Complications of low birth weight/small baby?

A

Metabolic maladaptation

Use reserves (SC fat, ↓glycogen in liver ↓protein in muscle) to maintain brain growth.

Fetal hypoxia + hypoglycaemia, shunting blood to vital organs.
Anaerobic glycolysis, met acidosis, lactic acid damages organs

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6
Q

Diagnosis of low birth weight/small baby?

A

Doppler USS: reversed/absent flow suggests fetal distress

Small baby with normal doppler is fine.

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7
Q

Treatment of low birth weight/small baby?

A

Deliver if sig restriction

Tx of underlying cause

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8
Q

Risk factors for preterm birth?

A 
multiple gest
pre-eclamp 
cervical incompetency, preterm PROM
preg HTN
IUGR
↑ uterine size
bleeding in 1st or 2nd trim
placenta previa
IU infection
polyhydramnios
maternal systemic disease (UTI)
psychological stress
domestic violence
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9
Q

Complications of premature birth?

A

CP, RDS, NE

LD, behav problems

Chronic health issues: epilepsy, DM

Hypothermia

Infection: maternal IgG crosses 30wk, thin skin, immature immune system

Feeding: no suck/ swallow reflex until 34wks. IV nutritional gradual introduction of breast milk

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10
Q

Diagnosis of premature birth?

A

Identify risk: cervical assessment, fetal fibronectin (shouldn’t be present > 20 wks), screening for infections

Investigate maternal infection/haem

CTG/USS

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11
Q

Prevention of premature birth?

A

Abx for asymptomatic bacteriuria

Cervical cerclage, removed 36-37 wks.

Progesterone: antagonises oxytocin, relaxation of smooth muscle

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12
Q

Treatment of premature birth?

A

Tocolysis: nifedipine, indomethacin etc

24mg betamethasone/ dexamethasone 2 IM injections 24hrs apart.

Delayed cord clamping

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13
Q

What is macrosomia?

A

Birth weight >4000g

95th centile

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14
Q

Causes of macrosomia?

A

Mother had previous large baby before

FHx of large babies

BMI >35

Diabetic/gestational diabetes

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15
Q

Diagnosis of macrosomia?

A

Symphysis-fundal height - greater than expected >2 then offered growth scan

If >90th centime and under 36 wks - GTT

more than 36 wks, monitor BG levels over 7 days

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16
Q

Risks of macrosomia?

A

Shoulder dystocia > fractured clavicle, Erb’s palsy

PPH

Uterine rupture

C-section, instrumental delivery

Perineum tears

Neonatal hypoglycaemia

Metabolic syndrome

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17
Q

Management of macrosomia?

A

Induction at 39-40wks

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18
Q

How does GDM cause macrosomia?

A

increased insulin resistance of the mother

so a higher amount of blood glucose passes through the placenta into the fetal circulation

as a result, extra glucose in the fetus is stored as body fat causing macrosomia

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19
Q

What is hydrops fetalis?

A

abnormal accumulation of fluid in two or more fetal compartments, including ascites, pleural effusion, pericardial effusion, and skin edema

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20
Q

What causes immune hydrops?

A

Rh incompatiblity - Rh positive baby, Rh -ve mother

Causes haemolytic anaemia. If baby cannot overcome this, causes hydrops as heart starts to fail.

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21
Q

What causes non-immune hydrops?

A

Severe anemia

Infections present before birth

Heart or lung defects

Chromosomal abnormalities and birth defects

Liver disease

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22
Q

S+S of hydrops fetalis?

A

During pregnancy:

  • polyhydramnios
  • thickened placenta
  • US shows enlarged liver, spleen, heart, may show fluid build-up

After birth:

  • pale colouring
  • severe swelling - especially in abdomen
  • trouble breathing
  • hepatosplenomegaly
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23
Q

Diagnosis of hydrops fetalis?

A

USS

Increased abdominal fluid

Fetal blood sampling

Amniocentesis

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24
Q

Treatment of hydrops fetalis?

A

Depends on cause

Early delivery

Newborn - O2/ventilator, paracentesis

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25
Q

How long for baby to breath after vaginal and C-section?

A

Normal vaginal: breathing in 30s.

CS: several hrs to clear fluid from lungs

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26
Q

Causes of failure to develop normal respirations?

A

Asphyxia > lack of O2 to developing brain > prevents infant breathing

Prolonged uterine contractions /delivery, birth trauma

Preterm

Cong malformation

Poor oxygenation in delivery: maternal ↓BP, poor maternal oxygenation (anaesthesia induced hypoventilation, resp/heart disease), XS oxytocin, placental insuff, umbilical prolapse.

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27
Q

What is persistent pulmonary hypertension of the newborn?

A

Disorder in which the arteries to the lungs remain narrowed after delivery, and so limits the amount of blood flow to the lungs

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28
Q

Pathophysiology of PPHN?

A

RV pressure increases

Then LV

FO and DA don’t close as body chooses low pressures over high

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29
Q

Causes of PPHN?

A

Severe distress during delivery - meconium aspiration syndrome

Respiratory distress syndrome

Other causes of low O2 in foetus before, during or after delivery > infection, diaphragmatic hernia, collapsed lung, underdeveloped lungs, pneumonia

Primary PPHN - hypertrophy of muscular layer in PA. Placenta insuff, maternal NSAID use, poor prognosis

Congen abnormalities of heart + lungs eg diaphragmatic hernia, blocked heart valve, smaller lungs, pul hypoplasia

Pleural effusions

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30
Q

Risk factors for PPHN?

A

perinatal asphyxia

prolonged PROM

more common among new-borns who are full term (37-42) or post-term (>42)

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31
Q

Features of PPHN in new-born?

A 
Persistently low sats despite intensive O2 therapy
Cyanosis
Tachypnoea
Retractions, 
Within 24hr of birth,
Systolic murmur, 
Low APGAR.
Meconium staining
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32
Q

Diagnosis of PPHN?

A

ECHO: R>L shunting, patent FO + DA/

Difference of > 10% between pre + postductal O2 sat. Pre-ductal measured R hand, blood before DA, post-ductal > measured feet. If there is difference in them, means mixing of blood through duct

CXR: assess lung disease, congen diaphragmatic hernia

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33
Q

Treatment of PPHN?

A

Supplemental oxygen - environment with 100% O2

Sometimes a ventilator

Sometimes nitric oxide gas - opens arteries in newborn’s lungs and reduces pulmonary HTN

Sometimes extracorporeal membrane oxygenation - machine adds O2, removes CO2, slowly opens vessels

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34
Q

Causes of apnoea in newborn?

A 
Prematurity, LBW
Hypothermia, hypo/HTN
Aspiration, airway obstruction
Congenital HD, PDA
Anaemia 
Infections 
Pain 
GORD
↑↓Ca/Na
Maternal drugs 
Abnormal responses to hypoxia, hypercapnia, obstructed airflow or reflex laryngospasm
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35
Q

S+S of apnoea in newborn?

A

O2 sats typically <85% + HR <80 BPM, apnoeic spells.

Resp pauses at least 20 secs, or under 20s associated with bradycardia,

Cyanosis, pallor.

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36
Q

Treatment of apnoea in newborn?

A

HF nasal cannula, PEEP, CPAP, ventilation
Dry bay, rub back + feet, head neutral
Incubator
Suction secretions
Methylxanie: caffeine/ theophylline: stim resp centre, CNS, + CVS. ↑sensitivity to CO2 ↑skeletal muscle tone. Enhanced diaphragm contractility, ↑ventilation, MR, O2 consumption.
Supplementary O2 to maintain sats.
Usually settles within 1-2 days.

Prevention: CS

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37
Q

What is transient tachypnoea of newborn?

A

benign, self-limited condition that can present in infants of any gestational age, shortly after birth.

It is caused due to delay in resorption of fluid in lungs after birth which leads to ineffective gas exchange, respiratory distress, and tachypnea

Commonest cause of resp distress in newborn

More common after CS, fluid not squeezed out by contractions.

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38
Q

Diagnosis of TTN?

A

CXR: hyperinflation of lungs, fluid in horizontal fissure.

39
Q

Management of TTN?

A

Supplementary O2 to maintain sats.

Usually settles within 1-2 days.

40
Q

What is choanal atresia?

A

Congen narrowing of back of nasal cavity. Unilat or bilat.

Completely bony or composed of both bone + membranes.

1 in 7000 births

41
Q

What is CHARGE syndrome?

A 
coloboma
heart defects
atresia choanae (also known as choanal atresia)
growth retardation
genital abnormalities
ear abnormalities.
42
Q

Symptoms of choanal atresia?

A 
Immediately after birth, later if unilat
Cyclical RD
Improved with crying
Worse when feeding 
Noisy breathing

Unilateral - persistent nasal drainage, recurrent sinus infections

B/L - respiratory distress, cyanosis

43
Q

Diagnosis of choanal atresia?

A

Laryngeal mirror - fogging to suggest air flow or nasal obstruction

Inability to pass catheter into nasopharynx

CT for specifics

Diagnosis late in unilateral

44
Q

Treatment of choanal atresia?

A

Surgical repair ASAP in bilat, can wait in unilat > Transnasal endoscopic surgery, placing stent for few wks

Bilat intubation ASAP

Unilat > supplemental O2 nasal saline, keep nasal linings free of discharge.

45
Q

What is congenital cystic lung disease?

A

a benign lung lesion that appears before birth as a cyst or mass in the chest.

It is made up of abnormal lung tissue that does not function properly, but continues to grow.

CCAM is also frequently referred to as a congenital pulmonary airway malformation (CPAM)

46
Q

Complications of congenital cystic lung disease?

A

Lung hypoplasia
Recurrent infections
HF
Compression of heart

47
Q

Investigations and treatment of congenital cystic lung disease?

A

Prenatal USS

Steroid prevent growth

Prenatal removal of fluid/shunt placement

Prenatal surgery

CS with resection

48
Q

Summary of pneumothorax in neonates?

A

Can be spontaneous or secondary to: meconium, RDS, cystic lung disease, high pressure ventilation

Features - tachypnoea, grunting, cyanosis, chest on affected side more prominent

Investigations - CXR, ABG, positive transillumination

Management - give O2, aspirate, chest tube

49
Q

What is meconium aspiration syndrome?

A

refers to respiratory distress in the newborn as a result of meconium in the trachea.

It occurs in the immediate neonatal period

It is more common in post-term deliveries

Resp distress > meconium in trachea, airway obstruction > surfactant dysfunction > pul vasoconstriction > pul HTN.

Higher rates occur where there is a history of maternal hypertension, pre-eclampsia, chorioamnionitis, smoking or substance abuse.

50
Q

Features of meconium aspiration syndrome?

A

Immediate neonatal period

Post-maturity: green/ yellow skin + UC, long, stained nails, dry peeling skin, loss of SC tissue

Cyanosis

Systolic murmur. Rales, ↓BS, rhonchi

↑RR + HR, ↓BP

Chest wall asymmetry ↓air entry > pneumothorax

Barrel shaped chest, retractions. Grunting

51
Q

Complications of meconium aspiration syndrome?

A

Infection,
Chemical pneumonitis (oedema),
Pneumothorax,
Atelectasis.

52
Q

Diagnosis of meconium aspiration syndrome?

A

CXR: patchy infiltrations, atelectasis, hyperexpanded lung fields, areas of collapse, consolidation, pneumothorax

53
Q

Management of meconium aspiration syndrome?

A

Endotracheal suction only if flat at birth

Surfactant

O2 therapy, ventilation > CPAP, ECMO, mechanical ventilation + inhaled NO

Abx: ampicillin + gentamicin

Chest drain

Vasopressor: dopamine, dobutamine

54
Q

What is retinopathy of prematurity?

A

Disorder of developing retina

Abnormal fibrovascular prolif of retinal vessels > retinal detachment > visual loss

55
Q

Risk factors for retinopathy of prematurity?

A

prematurity (<31 wks), anaemia, blood transfusions, LBW (<1500g), hypotension, exposure to supplemental oxygen + fluctuations in O2

56
Q

Features of retinopathy of prematurity?

A

May appear normal, visual loss as child grows

1) Mildly abnormal BV growth, normal vision, no Tx
2) Mod abnormal, normal vision, no Tx
3) Severely abnormal, BVs grow towards centre of eye instead of along surface of retina. Tx to prevent retinal detachment
4) Partially detached retina, traction from scar produced by bleeding, abnormal vessels pull retina away from wall of eye
5) Completely detached retina, severe visual impairment + blindness

57
Q

Diagnosis of ROP?

A

Regular ophthalmology screening of high risk = wkly <32 wks / <1500g, until risk of developing ROP requiring Tx has passed

58
Q

Management of ROP?

A

Tx: laser therapy

photocoagulation > less myopia than cryotherapy,

Intravitreal anti-VEGF monoclonal antibodies (bevacizumab),

Vitrectomy with lensectomy

59
Q

What is Phenylketonuria?

A

an autosomal recessive condition caused by a disorder of phenylalanine metabolism.

This is usually due to defect in phenylalanine hydroxylase, an enzyme which converts phenylalanine to tyrosine

High levels of phenylalanine lead to problems such as learning difficulties and seizures.

The gene for phenylalanine hydroxylase is located on chromosome 12.

The incidence of PKU is around 1 in 10,000 live births.

60
Q

Features of PKU?

A

Presents by 6 mnths > developmental delay

Blue eyes, blonde hair

Seizures - typically infantile spasms

Eczema

Musty odour to urine + sweat

Microcephaly

61
Q

Diagnosis of PKU?

A

Guthrie test: the ‘heel-prick’ test done at 5-9 days of life - also looks for other biochemical disorders such as hypothyroidism

Hyperphenylalaninaemia

Phenylpyruvic acid in urine

62
Q

Management of PKU?

A

Restriction of dietary protein + phenylalanine.

Supplementation with phenylalanine-free AA mixtures

Dietary restrictions are however important during pregnancy as genetically normal fetuses may be affected by high maternal phenylalanine levels

63
Q

What is haemorrhagic disease of newborn?

A

aAbleeding problem that occurs in a baby during the first few days of life

Babies are normally born with low levels of vitamin K

Early or later (1-8 wks PP)

64
Q

Risk factors for haemorrhagic disease of newborn?

A

BF

65
Q

Symptoms of haemorrhagic disease of newborn?

A

Mild in most: melena/ haematemesis, bruising, prolonged bleeding of umbilical stump

Severe: IC haem, permanent disability, death

66
Q

Diagnosis and management of haemorrhagic disease of newborn?

A

↑PTT + PT
Platelets normal

It’s why vit K IM is given to all newborn infants (IM or oral)

Vit K 1mg ± FFP

67
Q

Jaundice in neonate in first 24 hours?

A

Always pathological

Causes of jaundice in the first 24 hrs:

  • rhesus haemolytic disease
  • ABO haemolytic disease
  • hereditary spherocytosis
  • glucose-6-phosphodehydrogenase
  • sepsis
  • CNJ syndrome
  • Gilbert’s
  • Red cell abnormalities
  • pyruvate kinase deficiency
  • congenital infection
68
Q

Investigations for jaundice in neonate in first 24 hours?

A

Direct coombs,

Maternal IgA,

AntiA AntiB for Rh

FBC,

Blood film,

Syphilis, TORCH

May rise >15mg/dL, 5mg/dL/day

69
Q

Causes of jaundice in neonate from days 2-14?

A

Common (up to 40%) and usually physiological

It is due to a combination of factors, including more red blood cells, more fragile red blood cells and less developed liver function.

It is more commonly seen in breastfed babies due to decreased fluid intake and inadequate bowel movements to remove bilirubin from body

Hepatic immaturity in BR conjugation, removal/ haemolysis of fetal RBCs. If ↓albumin, UBR unbound

Infection. Dehydration

Absence of gut flora impedes elimination of bile pigment

Total peak <15mg/L
<5mg/dL/day

70
Q

Causes of jaundice in neonate 14+ days?

A

If there are still signs of jaundice after 14 days (21 days if premature) a prolonged jaundice screen is performed, including:

  • conjugated and unconjugated bilirubin: the most important test as a raised conjugated bilirubin could indicate biliary atresia which requires urgent surgical intervention
  • direct antiglobulin test (Coombs’ test)
  • TFTs
  • FBC and blood film
  • urine for MC&S and reducing sugars
  • U&Es and LFTs

Causes of prolonged jaundice:

  • biliary atresia (conjugated and pale stools!)
  • hypothyroidism
  • galactosaemia
  • urinary tract infection
  • breast milk jaundice (thought to be due to high concentrations of beta-glucuronidase → increase in intestinal absorption of unconjugated bilirubin)
  • prematurity
  • due to immature liver function
  • increased risk of kernicterus
  • congenital infections e.g. CMV, toxoplasmosis
  • CF, Hirschsprung’s, pyloric stenosis
  • bile duct obstruction
  • neonatal hepatitis
  • Gilberts, CNJ syndrome, rotor syndrome
71
Q

Investigations for prolonged jaundice in neonate?

A

CBR/UBR: ↑conjugated = biliary atresia

Direct Coombs’ test

TFTs

FBC + blood film

Urine MC+S + reducing sugars

U+Es

LFTs

72
Q

What is Kernicterus?

A

a type of brain damage that can result from high levels of bilirubin in a baby’s blood

UBR crosses BBB, permanent neurological damage, deposits in BG or brain stem nuclei.

if smaller levels - less likely permanent, little effect on IQ unless preterm or SGA

73
Q

Risk factors for Kernicterus?

A

premature, co-morbid hypoalbuminaemia

74
Q

Symptoms of Kernicterus?

A

Sleepy ± poor suck/ feed

Setting sun lid traction

No moro reflex

Apnoea

Hypotonia

Odd movements

CP > choreoathetoid

Sensorineural deafness

Vertical gaze palsy

Movement (athetosis)

Dental enamel hypoplasia

Low IQ, LD

Irritability

Opisthotonos: UMN damage, seizures, coma

Bronze baby syndrome: rare, ↑BR following phototherapy, accumulation of bronze-coloured pigments (photoisomers of bilirubin) within skin

75
Q

Management of Kernicterus?

A

Phototherapy

Exchange transfusion

IV immunoglobulin

76
Q

What is neonatal hypoglycaemia?

A

Normal term babies often have hypoglycaemia especially in the first 24 hrs of life but without any sequelae, as they can utilise alternate fuels like ketones and lactate

< 2.6 mmol/L

Transient hypoglycaemia in the first hours after birth is common.

Persistent/severe: premature, SGA, poor stores, GDM, IUGR, hypothermia, neonatal sepsis, inborn errors of metabolism, Nesidioblastosis (β cell hyperplasia), maternal BB, Beckwith-Wiedemann synd, illness, ↑ demand, GH def, congen adrenal hypoplasia

77
Q

Sx of neonatal hypoglycaemia?

A

May be asymptomatic

Autonomic: jittery, irritable, ↑RR, pallor

Neuroglycopenic: poor feed/suck, weak cry, drowsy, hypotonia, seizures

Apnoea

Hypothermia

78
Q

Management of neonatal hypoglycaemia?

A

asymptomatic:
- encourage normal feeding (breast or bottle)
monitor blood glucose

symptomatic or very low blood glucose:
- admit to the neonatal unit
intravenous infusion of 10% dextrose

If <1.6 - give immediate glucose

79
Q

What is hypoxic ischaemic encephalopathy?

A

Sub-acute brain damage due to systemic hypoxaemia, causes ↓cerebral perfusion

80
Q

Causes of HIE?

A

↓placental gas exchange: abruption/ uterine rupture, prolonged contractions

UC: compressed, prolapsed, nuchal (wrapped around neck of baby)

Maternal hypotension (shock, intrapartum haemorrhage)

Fetal issues: cardioresp/ asphyxia

Metabolic issues: inborn errors of metabolism. hypoglycaemia,

Congenital infections

Maternal: DM, PE, CHD
Traumatic delivery, CS with GA

81
Q

Grading of HIE? (Sarnat staging)

A

Mild - weak sucking reflex, impaired feeding, good prognosis, hyperalert, resolves within 24 hrs, normal prognosis

Moderate - lethargic, ↓tone periodic apnoea, weak reflexes, feeding issues, seizures within 24 hrs birth, recovery possible after 1-2 wks, up to 40% develop cerebral palsy

Severe - reduced consciousness, flaccid tone, decerebrate, absent reflexes, irreg breathing and apnoeas, generalised seizures ↑ 24 – 48hrs after birth. Pupil abnormalities, death (50% mortality) or disability (90% develop CP)

82
Q

Diagnosis of HIE?

A

MRI: deep nuclear gray matter injury, parasagittal injury of cerebral cortex + watershed cortical injury

Clinical + cerebral function monitor (EEG).

MRI at 1 wk = dysfunction suggests highly likely CP

83
Q

Management of HIE?

A

Supportive care - neonatal resuscitation, ongoing optical ventilation, circulatory support, nutrition, acid base balance and Tx of seizures

Therapeutic hypothermia - actively cooling the core temperature of the baby. emperature is carefully monitored with a target of between 33 and 34°C, measured using a rectal probe. This is continued for 72 hours, after which the baby is gradually warmed to a normal temperature over 6 hours. It reduces the inflammation and neurone loss after the acute hypoxic injury. It reduces the risk of cerebral palsy, developmental delay, learning disability, blindness and death.

84
Q

What is Rhesus haemolytic disease?

A

Rh- mother gives birth to RH+, sensitisation event (mother + baby’s blood mixing)

Mother produces anti-D IgG, in later pregnancies, can cross placenta in successive Rh+ preg

Events: APH, CVS, threatened miscarriage, amnio, ECV, abdo trauma, termination, ectopic, miscarriage gestation >12wks

85
Q

Features of foetus in Rhesus haemolytic disease?

A

Oedematous: hydrops fetalis, liver devoted to RBC production albumin↓

Jaundice, anaemia, hepatosplenomegaly

HF

Kernicterus

86
Q

Investigations of Rhesus haemolytic disease?

A

All babies born to Rh- mother have cord blood taken RBC, blood group, direct coombs test.

Coombs test: direct antiglobulin, IG on RBCs of baby

Kleihauer test: add acid to maternal blood, fetal cells are resistant

87
Q

Management of Rhesus haemolytic disease?

A

Anti-D: within 72hrs of senitising events, + at 28 +34wks. Neutralises RhD pos antigens that enter mother’s blood in so mother doesn’t produce antibodies.

Tx of affected fetus: transfusions, UV phototherapy. Drain ascites + pleural effusion, limit IV fluids

88
Q

What are neural tube defects?

A

Failure of NT to close 3-4th wk IU.

Spina bifida: incomplete vertebral arch, spine split - cystica (meningocele and myelomeningocele) and occulta (when meninges do not herniate through opening)

Myelocele: failure of cord fusion - open spinal cord with meningeal cyst

Meningocele: herniation of dura + arachnoid through bony defect - protrusion of meninges through defect in skull/spine

Anencephaly: most common, incompatible with life - open brain and lack of skull vault

Encephalocele - herniation of meninges and brain

Craniorachischisis - completely open brain and spinal cord

RF: maternal folate def, vit B2 def, prev Hx of infant with NTD, smoking, DM, obesity + AED (valproic acid, carbamazepine, methotrexate)

Open (not covered by skin), closed (covered by skin)

89
Q

Features of neural tube defect?

A

Variable paralysis, sensory loss in legs

Scoliosis

Neurogenic bladder/ bowel.

Absence of anal wink/ rectal tone

Stool/ meconium leakage

Hydrocephalus: bulging fontanelle, rapid head growth, downward deviation of eyes, abnormal/ stridulous cry

Arching of neck: pressure on brainstem, shunt malfunction/ dysfunction

Asymmetry of spont arm + leg movements. Pain in limbs, muscle weakness, atrophy

90
Q

Complications of neural tube defect?

A

Fecal + urinary incontinence, sexual dysfunction

If higher than lumbosacral might never walk

Facial asymmetry > CN lesion

Club foot: common deformity with lumbar or ↑ lesions imbalance of muscles around foot + ankle.

Abnormal muscle tone + bulk in arms + legs, spasticity

91
Q

Investigations for neural tube defect?

A

USS: mostly found IU. Size, location, hydrocephalus. Flattened/ inwardly scalloped frontal bones (lemon sign), obliteration of cisterna magna + loss of roundness of cerebellar hemispheres (banana sign)

Antenatal/quadruple test: elevated

Fetal MRI

92
Q

Management of neural tube defects?

A

Termination offered at any stage

Surgical closure shortly after birth > prevent CNS infx

Further ops = fix spinal deformity

Hydrocephalus = ventriculoperitoneal CSF shunts

Prevention: 400mg folic acid normally until 13 wks, high risk mothers = 5mg folic acid

93
Q

What is umbilical granuloma?

A

a type of scar tissue that forms in the belly button. Most umbilical granulomas form when the belly button is healing after the umbilical cord falls off. They look like small red lumps in your child’s navel

Usually separates around day 7 but can persist up to 6 wks

Cherry red lesion surrounding umbilicus
May bleed on contact
Seropurulent discharge

Apply salt
Don’t cauterise with silver nitrate

Paediatrics (11 decks)

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