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Yr 5 - Paeds > Revision - Neonatal Jaundice, Sepsis, Prematurity > Flashcards

Revision - Neonatal Jaundice, Sepsis, Prematurity Flashcards

1
Q

1st line abx for suspected or confirmed early onset neonatal sepsis?

A

IV benzylpenicillin + gentamicin

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2
Q

What should be measured 18–24 hours after neonatal sepsis presentation in babies given antibiotics?

A

CRP

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3
Q

How long are Abx continued for in neonatal sepsis if:

a) blood cultures are positive
b) CSF is positive

A

a) 7-10 days

b) 14 days

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4
Q

1st line Abx for suspected or confirmed LATE onset neonatal sepsis?

A

IV flucloxacillin (or vancomycin) + gentamicin

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5
Q

What Abx are given if meningitis is suspected in neonates?

A

IV cefotaxime + amoxicillin

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6
Q

Early vs late onset neonatal sepsis?

A

Early: <72h after birth

Late: >72h - 28 days after birth

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7
Q

What is the most common bacteria causes late onset neonatal sepsis?

A

Coagulase negative Staphylococci

e.g. Staph epidermis (colonises lines)

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8
Q

What are 2 ABSOLUTE contraindications to lumbar puncture in neonates?

A

1) GCS <8

2) Signs of raised ICP

Note - a bulging fontanelle alone, without other signs of raised ICP, is not a contraindication.

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9
Q

What are 2 metabolites of conjugated bilirubin?

A

1) Stercobilinogen
2) Urobilinogen

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10
Q

Is physiological jaundice conjugated or unconjugated?

A

Unconjugated

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11
Q

Give 3 haemolytic causes of neonatal jaundice

A

1) Haemolytic disease of the newborn –> ABO or rhesus incompatibility

2) G6PD deficiency

3) Hereditary spherocytosis

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12
Q

What is hereditary spherocytosis?

A

An inherited disease where defects in RBC skeletal proteins cause RBCs to assume a spherical shape with a reduced lifespan.

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13
Q

Inheritance of G6PD deficiency?

A

X-linked recessive

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14
Q

What happens in G6PD deficiency?

A

A lack of G6PD makes RBCs susceptible to oxidative damage and haemolysis. It can cause severe neonatal jaundice.

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15
Q

Give 4 endocine or metabolic causes of unconjugated neonatal jaundice

A

1) Gilbert’s syndrome

2) Crigler-Najjar syndrome

3) Congenital hypothyroidism

4) Galactosaemia and other inborn errors of metabolism (these may also cause conjugated jaundice)

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16
Q

Inheritance of Gilbert’s syndrome?

A

Autosomal recessive

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17
Q

What happens in Gilbert’s syndrome?

A

There is reduced activity of UGT in the liver.

This causes reduced ability to conjugate bilirubin, resulting in mild episodes of jaundice throughout life in response to certain triggers.

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18
Q

Inheritance of Crigler-Najjar syndrome?

A

Autosomal recessive

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19
Q

What happens in Crigler-Najjar?

A

NO functioning UGT is produced in the liver.

It presents with severe, prolonged jaundice that often results in neurological damage and death within one year of life.

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20
Q

What are 2 causes of conjugated neonatal jaundice?

A

1) Biliary atresia

2) Neonatal hepatitis (e.g. CMV, hepatitis B, rubella or HSV)

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21
Q

What is a common cause of neonatal jaundice within the first 24 hours?

A

Neonatal sepsis

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22
Q

What does ‘rhesus’ refer to?

A

Various types of rhesus antigens on the surface of RBCs.

These antigens vary between individuals.

The rhesus antigens are SEPARATE to the ABO blood groups.

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23
Q

What is the most relevant antigen within the rhesus blood group system?

A

Rhesus-D antigen

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24
Q

Do women who are rhesus-D positive need any additional treatment during pregnancy?

A

No

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25
Q

What do you need to consider when a woman who is rhesus-D negative becomes pregnant?

A

The possibility that her child will be rhesus positive.

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26
Q

Why is it an issue if a rhesus-D negative woman is pregnant with a rhesus-D positive baby?

A

1) As it is likely at some point in the pregnancy (i.e. childbirth) that the blood from the baby will find a way into the mother’s bloodstream.

2) When this happens, the baby’s RBCs display the rhesus-D antigen.

3) The mother’s immune system will recognise this rhesus-D antigen as foreign, and produce antibodies to the rhesus-D antigen.

4) The mother has then become sensitised to rhesus-D antigens.

5) Usually, this sensitisation process does not cause problems during the first pregnancy.

6) During subsequent pregnancies, the mother’s anti-rhesus-D antibodies can cross the placenta into the fetus.

7) If that fetus is rhesus-D positive, these antibodies attach themselves to the RBCs of the fetus and causes the immune system of the fetus to attack them (haemolysis).

8) The RBCl destruction caused by antibodies from the mother is called haemolytic disease of the newborn.

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27
Q

When can the sensitisation process in a rhesus D negative mother be a problem in their first pregnancy?

A

If the sensitisation happens early on, such as during antepartum haemorrhage

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28
Q

Is maternal diabetes a risk factor for neonatal jaundice?

A

Yes

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29
Q

What is biliary atresia?

A

Congenital inflammatory condition.

Results in complete obliteration of extra-hepatic ducts after birth –> cirrhosis –> death.

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30
Q

How does biliary atresia present?

A

1) prolonged conjugated jaundice

2) pale stools

3) dark urine

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31
Q

What defines prolonged neonatal jaundice?

A

> 14 days in term babies

> 21 days in preterm babies

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32
Q

What is the gold standard diagnostic method for biliary atresia?

A

Percutaneous biopsy

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33
Q

Management of biliary atresia?

A

1) portoenterostomy (Kasai procedure)

or

2) liver transplant

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34
Q

What investigations are required in prolonged neonatal jaundice?

A

1) conjugated and unconjugated bilirubin levels

2) direct antiglobulin test (Coombs’ test): for haemolysis

3) TFTs

4) FBC and blood film: for polycythaemia or anaemia

5) urine for MC&S and reducing sugars

6) U&Es and LFTs

7) G6PD levels for G6PD deficiency

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35
Q

Causes of prolonged neonatal jaundice?

A

1) Hypothyrodism

2) Biliary atresia

3) Galactosaemia

4) Breast milk jaundice

5) Prematurity

6) UTI

7) Congenital infections e.g. CMV, toxoplasmosis

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36
Q

Which neonates require routine bilirubin checking?

A

All babies who are visibly jaundiced

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37
Q

What are 2 options for measuring bilirubin levels in neonates?

A

1) Transcutaneous bilirubinometry

2) Serum bilirubin

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38
Q

When would transcutaneous bilirubinometry be used to over serum bilirubin and vice versa?

A

Transcutaneous bilirubinometer:
- >35 weeks gestation
- >24 hours old
- Can be used for all subsequent measurements, providing the level remains <250 µmol/L and the child has not required treatment

Serum bilirubin:
- Babies who are visibly jaundiced <24 hours of life
- Gestational age <35 weeks
- Monitoring bilirubin after starting treatment.

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39
Q

What bilirubin monitoring is required in babies with jaundice <24h after birth?

A

Serum bilirubin

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40
Q

Which investigation is used to monitor bilirubin levels AFTER starting treatmnet?

A

Serum bilirubin

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41
Q

Which investigation is used to monitor bilirubin levels in jaundiced neonates with a gestational age <35 weeks?

A

Serum bilirubin

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42
Q

Purpose of a blood packed cell volume (PCV) in neonatal jaundice?

A

To assess the degree of anaemia or polycythaemia

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43
Q

What does a positive Coombs test indicate?

A

Suggests immune-mediated haemolysis (i.e. haemolytic disease of the newborn).

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44
Q

What does a negative Coombs test indicate?

A

suggests non-immune-mediated haemolysis (e.g. hereditary spherocytosis or G6PD deficiency)

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45
Q

What is neurotoxic unconjugated bilirubin converted to in phototherapy?

A

Lumirubin (water-soluble isomer which is readily excreted in the bile and urine).

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46
Q
A
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47
Q

What is found on a treatment threshold charts for neonatal jaundice?

A

Age of baby - x axis

Total bilirubin level - y axis

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48
Q

How often should bilirubin levels be monitored during treatment for neonatal jaundice?

A

Repeat bilirubin 4-6 hours post initiation to ensure not still rising, 6-12 hourly once level is stable or reducing.

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49
Q

When can phototherapy for neonatal jaundice be stopped?

A

Stop phototherapy once level >50µmol/L below treatment line on the threshold graphs.

Check for rebound of hyperbilirubinaemia 12-18 hours after stopping phototherapy.

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50
Q

What should you check for 12-18h after stopping phototherapy?

A

rebound hyperbilirubinaemia

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51
Q

What can be used as adjunct to intensified phototherapy in rhesus haemolytic disease or ABO haemolytic disease?

A

IV immunoglobulin

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52
Q

What is the key complication of neonatal jaundice?

A

Kernicterus (bilirubin encephalopathy)

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53
Q

How does bilirubin encephalopathy (kernicterus) present?

A
  • lethargy
  • hypotonia
  • poor suck reflex

This progresses to:
- hypertonia
- opisthotonos
- fever
- seizures
- a high-pitched cry

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53
Q

Long term complications of kernicterus?

A
  • cerebral palsy
  • sensorineural hearing loss
  • cognitive impairment
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54
Q

1st line investigation in suspected pathological neonatal jaundice?

A

Coombs test

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55
Q

When are doses of anti D given?

A

1) 28 weeks gestation

2) Within 24 hours of birth

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56
Q

If the Coombs test is negative in neonatal jaundice, what is the next step?

A

Check Hb level

Low –> may be a blood collection outside vessels e.g. cephalohaematoma due to trauma during delivery.

High –> increased load of RBCs is slowly getting broken down e.g. common in babies of diabetic mothers, twin-twin transfusion syndrome, delayed cord clamping.

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57
Q

If Hb is normal in neonatal jaundice, what is next step?

A

Check reticulocyte count, LDH & haptoglobin.

Then consider blood film.

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58
Q

Define preterm birth

A

<37 weeks gestation

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59
Q

Define:

1) extreme preterm

2) very preterm

3) moderate to late preterm

A

1) <28w

2) 28-32w

3) 32-37w

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60
Q

In women with a history of preterm birth or an US demonstrating a cervical length of 25mm or less before 24 weeks gestation, what are the two options of trying to delay birth?

A

1) prophylactic vaginal progesterone –> putting a progesterone suppository in the vagina to discourage labour

2) prophylactic cervical cerclage –> putting a suture in the cervix to hold it closed

61
Q

Where preterm labour is suspected or confirmed, what are the options for improving the outcomes?

A

1) Tocolysis with nifedipine

2) Maternal corticosteroids

3) IV Magnesium sulphate

4) Delayed cord clamping or cord milking

62
Q

Define tocolytics

A

medications used to suppress premature labor

63
Q

When should maternal steroids be given in premature delivery?

A

<34w gestation

64
Q

Role of IV Magnesium sulphate in preterm delivery?

A

Neuroprotective for baby

65
Q

Role of delayed cord clamping or cord milking in preterm?

A

Can increase the circulating blood volume and haemoglobin in the baby

66
Q

At what gestation age should resuscitation not be performed in premature babies?

A

<23w

Between 23 and 23+6 weeks then there may be a decision not to start resuscitation in the best interests of the baby, especially if parents have expressed this wish.

Between 24 and 24+6 weeks, resuscitation should be commenced unless the baby is thought to be severely compromised

67
Q

What respiratory complications may be caused by prematurity?

A

1) Respiratory distress syndrome

2) Surfactant deficiency lung disease

3) Chronic lung disease / bronchopulmonary dysplasia

4) Recurrent apnoea

68
Q

What age gestation does RoP typically present?

A

<32w gestation

69
Q

At what gestational age does retinal blood vessel development start?

A

Around 16 weeks, is complete by 37 – 40 weeks gestation.

70
Q

What is retinal blood vessel development stimulated by?

A

Hypoxia (which is a normal condition in the retina in pregnancy)

71
Q

How does prematurity cause RoP?

A

1) When the retina is exposed to higher oxygen concentrations in a preterm baby, particularly with supplementary oxygen during medical care, the stimulant for normal blood vessel development is removed.

2) When the hypoxic environment recurs, the retina responds by producing excessive blood vessels (neovascularisation), as well as scar tissue.

3) These abnormal blood vessels may regress and leave the retina without a blood supply.

4) The scar tissue may cause retinal detachment.

72
Q

What are the 3 key risk factors for RoP?

A

1) Prematurity (<32w)

2) Low birth weight (<1500g)

3) Uncontrolled hyper-oxygenation

73
Q

How can high flow oxygen in premature infants cause RoP?

A

Over oxygenation (e.g. during ventilation) results in a proliferation of retinal blood vessels (neovascularisation).

74
Q

Under what circumstances would babies be screened for RoP?

A

1) Infants born <31 weeks gestational age

OR

2) Infants born <1.5kg birth weight

75
Q

What are the 2 mainstays of management of RoP?

A

1) Transpupillary laser photocoagulation

2) Anti-VEGF

76
Q

Role of laser therapy in the management of RoP?

A

Involves use of laser to “burn” abnormal areas of the retina in which there is inadequate vascularisation.

This burning process prevents abnormal blood vessel proliferation.

77
Q

What are the 3 key complications of RoP?

A

1) Infection
2) Cataracts
3) Retinal detachment

Children who are diagnosed with ROP are more likely to be short-sighted and develop a squint.

78
Q

What is the most common surgical emergency in neonates?

A

NEC

79
Q

What are the 2 key risk factors for NEC?

A

1) Prematurity

2) Low birth weight

80
Q

What is NEC?

A

Death (necrotising) of intestinal tissue (entero-) due to inflammation (colitis). This can lead to bowel perforation, peritonitis and shock.

It is a life threatening emergency that predominantly affects preterm infants.

81
Q

Is NEC more common in breastfed or bottlefed babies?

A

Bottlefed

82
Q

What does the classic presentation of NEC include?

A

1) a new feeding intolerance

2) vomiting (may be bile or blood-stained)

3) abdo distension

4) haematochezia

5) if progresses: abdominal tenderness, abdominal oedema, erythema and palpable bowel loops (due to loop dilation)

6) systemic symptoms: apnoea, lethargy, bradycardia and decreased peripheral perfusion

82
Q

Exam findings in NEC?

A

1) Shiny distended abdomen, tender to palpation and can feel tense or “wooden”

2) Periumbilical erythema

3) Abdominal tenderness

4) Bilious gastric aspirate

5) Shock

6) Reduced bowel sounds

83
Q

How may abdo feel in NEC?

A

Tense or ‘wooden’

84
Q

What are 4 key differentials for NEC?

A

1) Sepsis

2) Intussusception

3) Volvulus

4) Hirschsprung’s disease

85
Q

What is the diagnostic investigation for NEC?

A

AXR

86
Q

AXR features in NEC?

A

1) distended bowel loops

2) thickened bowel wall (bowel oedema)

3) intramural gas (pneumatosis intestinalis)

4) gas in the portal vein

5) pneumoperitoneum: in the later stages due to bowel perforation

87
Q

Lab investigations in NEC?

A

1) FBC: thrombocytopenia and neutropenia

2) CRP

3) ABG: metabolic acidosis or raised lactate

4) Blood culture: for sepsis

88
Q

If the bowel has perforated in NEC, Rigler’s sign may be visible.

What is this?

A

This occurs when both sides of the bowel wall are visible due to the presence of gas inside the lumen and within the peritoneal cavity.

89
Q

Key principles of MEDICAL management of NEC?

A

1) NBM

2) NG tube for bowel decompression

3) 3) Assess and manage sepsis

4) IV fluid resuscitation

5) IV Abx (broad-spectrum cover is recommended as first-line, such as cefotaxime and metronidazole)

6) Circulatory support and ventilation may be required

90
Q

What is the main indication for surgical intervention in NEC?

A

Perforation

91
Q

Surgical mx of NEC?

A

A laparotomy is carried out to remove the perforated and necrotic bowel from the abdomen.

91
Q

What criteria is used to stage NEC?

A

Bell’s staging criteria

92
Q

Bell’s staging criteria for NEC:

A

Stage I: suspected NEC

Stage II: proven NEC

Stage III: advanced NEC

93
Q

General complications of NEC?

A

1) Bowel perforation

2) DIC

3) Sepsis

4) Adverse neurodevelopmental outcomes (especially in infants who undergo surgery)

5) Long term stoma

94
Q

Post-op complications of NEC?

A

1) Short bowel syndrome

2) Formation of intestinal strictures

3) Enterocolic fistulae

4) Abscess formation

5) Death –> In infants who undergo surgery for NEC, a 29% post-surgical mortality rate has been reported at one year.

94
Q

What will U&Es show in NEC?

A

Hyponatraemia

95
Q

What is the key risk factor for apnoea in neonates?

A

Prematurity

96
Q

What does apnoea indicate in preterm vs term neonates

A

Preterm –> very common

Term –> usually indicates underlying pathology.

97
Q

What causes apnoea?

A

Apnoea occur due to immaturity of the autonomic nervous system that controls respiration and heart rate. This system is more immature in premature neonates.

98
Q

Management of apnoea of prematurity?

A

1) Tactile stimulation

2) IV caffeine

99
Q

Prognosis of apnoea of prematurity?

A

Episodes will settle as as the baby grows and develops.

100
Q

What is used to prompt the baby to restart breathing in apnoea or prematurity?

A

Tactile stimulation

101
Q

What can be used to prevent apnoea and bradycardia in babies with recurrent episodes of apnoea of prematurity?

A

IV caffeine

102
Q

What staging system is used in HIE?

A

Sarnat staging

103
Q

What are the 3 stages of Sarnat Staging for HIE?

A

1) Mild

2) Moderate

3) Severe

104
Q

Features of ‘mild’ HIE?

A

1) Poor feeding, generally irritability and hyper-alert

2) Resolves within 24 hours

3) Normal prognosis

105
Q

Features of ‘moderate’ HIE?

A
  • Poor feeding, lethargic, hypotonic and seizures
  • Can take weeks to resolve
  • Up to 40% develop cerebral palsy
106
Q

Features of ‘severe’ HIE?

A
  • Reduced consciousness, apnoeas, flaccid and reduced or absent reflexes
  • Up to 50% mortality
  • Up to 90% develop cerebral palsy
107
Q

What long term complication is HIE associated with?

A

Cerebral palsy

108
Q

Management of HIE?

A

1) Specialised care in neonatal unit

2) Therapeutic hypothermia

3) Following up by a paediatrician and the MDT to assess their development and support any lasting disability

109
Q

What gestational age does respiratory distress syndrome (RDS) typically affect?

A

<32w gestation

Due to inadequate surfactant production

110
Q

CXR findings in neonate RDS?

A

Ground glass appearance

111
Q

Long term complications of RDS in premature neonates?

A

1) Chronic lung disease of prematurity

2) Retinopathy of prematurity occurs more often and more severely in neonates with RDS

3) Neurological, hearing and visual impairment

112
Q

How can meconium aspiration lead to respiratory distress?

A

Meconium inhibits surfactant

Also inflammatory response in lungs

113
Q

Clinical features of MAS?

A

1) Meconium-stained liquor

2) Respiratory distress at or shortly following birth: tachypnoea, tachycardia, cyanosis, grunting, nasal flaring

3) Increased oxygen requirements (mechanical ventilation may be required for severe cases)

4) Hypotension

114
Q

Key risk factor for MAS?

A

Post-term

115
Q

Bedside investigations in MAS?

A

1) Pre- and post-ductal saturations: to assess respiratory involvement and detect congenital cardiac lesions

2) ABG or VBG: to assess the degree of respiratory compromise and assist in decisions regarding respiratory support and systemic involvement

116
Q

1st line imaging in MAS?

A

CXR

117
Q

CXR findings in MAS?

A

1) hyperinflated lungs due to distal air trapping

2) asymmetrical patchy pulmonary opacities

3) may show pneumothorax or pneumomediastinum due to raised alveolar tension

4) pleural effusions

118
Q

What 2 intrapartum preventative measures may be taken to avoid meconium aspiration syndrome?

A

1) prevention of foetal hypoxia

2) prevention of postdates gestation

119
Q

For infants who are born through meconium-stained liquor, what preventative measures for MAS may be taken?

A

A vigorous infant –> requires no oropharyngeal suctioning despite the meconium-stained liquor as this does not reduce the risk of meconium aspiration syndrome.

A non-vigorous infant –> should not have routine endotracheal suction for meconiu BUT may require oropharyngeal suctioning if there is meconium obstructing the airway. The priority should be to rapidly initiate ventilation

120
Q

When is the Apgar score assessed?

A

1 and 5 minutes of age.

If the score is low then it is again repeated at 10 minutes.

121
Q

What does the Apgar scores indicate?

A

0-3: baby in bad state

4-6: moderately low

7-10: baby in good state

122
Q

What makes up the Apgar score?

A

Appearance:
- pink all over (2)
- pink body, blue extremities (1)
- blue all over (0)

Pulse:
- >100 (2)
- <100 (1)
- no pulse (0)

Grimace:
- strong regular cry (2)
- weak irregular cry (1)
- silence (0)

Activity:
- active movement = 2 points
- limb flexion = 1 point
- flaccid = 0 points

Reflex irritability:
- cries on stimulation/sneezes/coughs (2)
- grimace (1)
- nothing (0)

123
Q

What Apgras score indicates the need for additional monitoring after birth?

A

≤8

124
Q

Management of MAS?

A

1) supportive e.g. O2, ventilation

2) surfactant therapy

3) Abx - usually started whilst awaiting blood cultures result

125
Q

What is the medical treatment option for moderate to severe symptoms for opiate withdrawal?

A

Oral morphine sulphate

126
Q

What is the medical treatment option for moderate to severe symptoms for non-opiate withdrawal?

A

Oral phenobarbitone

127
Q

Does NAS from SSRI withdrawal require medical treatment?

A

Typically no

128
Q

What pregnancy risks does smoking cause?

A

1) Increased risk of miscarriage (increased risk of around 47%)

2) Increased risk of pre-term labour

3) Increased risk of stillbirth

4) IUGR

5) Increased risk of SIDS

129
Q

Maternal risks of cocaine use during pregnancy?

A

1) HTN in pregnancy including pre-eclampsia

2) Placental abruption

130
Q

Foetal risks of cocaine use during pregnancy?

A

1) prematurity

2) neonatal abstinence syndrome

131
Q

Vomiting in Hirschsprung’s?

A

Bilious

132
Q

In jaundiced babies <24h after birth, how quickly should serum bilirubin be measured?

A

Urgently - within 2 hours

133
Q

What drugs are contraindicated in G6PD deficiency?

A

1) anti-malarials: primaquine

2) ciprofloxacin

3) sulph- group drugs: sulphonamides, sulphasalazine, sulfonylureas (e.g. gliclazide)

134
Q

How can methotrexate affect the lungs?

A

Can cause pneumonitis

135
Q

What is the most common presentation of neonatal sepsis?

A

Grunting and other signs of respiratory distress

136
Q

If meconium is observed during birth, the presence of what features indicates that the baby must be assessed by the neonatal team?

A
  • RR >60/min
  • the presence of grunting
  • HR <100 or >160 beats/minute
  • CRT above 3 seconds
  • temperature of 38°C or above, or 37.5°C on 2 occasions 30 minutes apart
  • oxygen saturation below 95%
  • presence of central cyanosis
137
Q

If there are ‘reducing substances’ present in urine in neonatal jaundice, what does this indicate?

A

Galactosaemia

138
Q

What is the gold standard for diagnosis of Hirschsprung’s?

A

Rectal biopsy

139
Q

In what patients may ciprofloxacin cause haemolysis?

A

in those with G6PD deficiency

140
Q

What is the initial mx in Hirschprung’s disease?

A

rectal washouts/bowel irrigation

141
Q

What is the abx of choice for GBS prophylaxis?

A

Intrapartum IV benzylpenicillin

142
Q

What is sensitisation in terms of rhesus?

A

When foetal RBCs (RhD+ve) enter the maternal circulation, where the mother is RhD-ve.

This can cause antibodies to form in the maternal circulation that can haemolyse fetal RBCs.

The process of sensitisation usually affects subsequent pregnancies, if the fetus is RhD+ve. The immune response is much quicker and greater, resulting in complications such as HDN.

143
Q

How can the risk of sensitisation be reduced?

A

Anti-D injections in situations where sensitisation in likely

144
Q

Does anti-D work in a woman who is already sensitised?

A

no

145
Q

Give some potentially sensitising events in pregnancy

A
  • ectopic pregnancy
  • evacuation of retained products of conception and molar pregnancy
  • vaginal bleeding <12 weeks, only if painful, heavy or persistent
  • vaginal bleeding > 12 weeks
  • CVS & amniocentesis
  • anteparum haemorrhage
  • abdo trauma
  • external cephalic version
  • intrauterine death
  • post-delivery (if baby is RhD+ve)
146
Q

When is prophylactic anti-D routinely given to previously non-sensitised RhD-negative women?

A

28 weeks and 24 weeks

147
Q

Definitive mx of Hirschsprung’s?

A

Anorectal pullthroug

148
Q
A

Yr 5 - Paeds (10 decks)

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