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Year 5: Conditions > Paediatrics- Neonatal Medicine > Flashcards

Paediatrics- Neonatal Medicine Flashcards

1
Q

What is biliary atresia

A

Rare, congenital disorder involving the obliteration/discontinuity of the extrahepatic biliary tree; resulting in bile flow obstruction

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2
Q

What is the cause of biliary atresia

A

• Unknown aetiology
• ?genetics, ?perinatal viral infection, ?toxin exposure during pregnancy, ?immune-mediated

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3
Q

When does biliary atresia typically present

A

• Typically presents in the first 2-8weeks of life

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4
Q

What is the most common cause of neonatal jaundice for which surgery is indicated

A

Biliary atresia

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5
Q

What is pathophysiology of biliary atresia

A

• Fibrosis of bile ducts causes bile flow obstruction (cholestasis)
◦ Bile accumulation leads to hepatic injury
‣ Causing fibrosis and eventually cirrhosis of liver
• Leads to chronic liver failure

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6
Q

What is presentation of biliary atresia

A

• Born at normal birth weight

• Persistent jaundice:
◦ Very soon infant develops jaundice that persists beyond normal 2 weeks (3 weeks if preterm)
◦ Does NOT resolve with phototherapy
◦ Pale stools
◦ Dark urine
• Hepatomegaly
• Splenomegaly
• Failure to thrive: Due to malabsorption of fats and fat-soluble vitamins (A,D,E,K)- lack of bile in intestines

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7
Q

What vitamin deficiencies are associated with biliary atresia

A

• Vitamin deficiencies:
◦ Vitamin K: bruising
◦ D: rickets
◦ A: blindness
◦ E: neuropathy

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8
Q

Investigations for biliary atresia

A

• LFTs:
◦ Raised conjugated bilirubin
◦ Raised GGT (disproportionality raised)
◦ Raised ALT, AST, ALP
• Prolonged prothrombin time

• Abdominal ultrasound:
‣ Can identify absence of gallbladder, hepatomegaly, splenomegaly
‣ Triangular cord sign
‣ Cannot definitively diagnose biliary atresia

• HIDA scan:
• Can be done if USS inconclusive (looks at lack of excretion into intestines)

• Liver Biopsy:
• Often needed for definitive diagnosis

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9
Q

Definitive management of biliary atresia

A

1) Kasai Hepatoportoenterostomy:
◦ Restores bile flow from liver to duodenum
◦ Should be done ideally before 60 days of life

2) Liver transplant:
◦ Do if Kasai HPE is unsuccessful or late presentation of infant with end-stage liver disease

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10
Q

What is the post-operative management of biliary atresia

A

• Ursodeoxycholic acid: To promote bile flow

• Fat-soluble vitamin supplementation: Levels should be monitored and doses adjusted accordingly

• Prophylactic antibiotics (co-trimoxazole): To prevent cholangitis in the first year

• Nutritional support: High caloric diet with triglycerides

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11
Q

Risk factors for neonatal jaundice

A

RISK FACTORS:
• Decreased gestational age
• Low infant birth weight
• Maternal diabetes
• Breastfeeding
• Male

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12
Q

Is jaundice within first 24 hours of life pathological or not

A

Pathological

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13
Q

What is raised in jaundice within first 24 hours of life

A

Unconjugated bilirubin

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14
Q

What is the raised unconjugated bilirubin in the first 24 hours of life usually caused by

A

• Usually due to haemolysis:
• ABO Incompatibility:
◦ Mismatch between maternal and foetal blood- DAT positive
◦ Typically occurs in Group O women

					• Rhesus haemolytic disease:
						◦ Occurs when Rh negative mother is exposed to Rh antigen 

					• G6PD deficiency, pyruvate kinase deficiency, hereditary spherocytosis
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15
Q

Is jaundice from 2 days to 2 weeks pathological?

A

Can be normal

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16
Q

Causes of jaundice from 2 days to 2 weeks of life

A

• Physiological Jaundice:

• Breastfeeding jaundice:

• Breastmilk jaundice:

• Dehydration

• Infection

• Haemolysis:

• Metabolic:

• Congenital hypothyroidism

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17
Q

What is physiological jaundice

A

‣ Immature liver
‣ Combination of increased RBC breakdown and immature hepatic enzymes causes build up of unconjugated bilirubin
‣ Peaks on days 3-5 and decreases by day 10

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18
Q

What is breastfeeding jaundice

A

◦ Common in healthy, breastfed babies (now have reduced breast-feeding)
◦ Peaks on day 3-5
◦ Can be caused by enterohepatic recycling due to reduced breast milk intake
◦ Causes unconjugated hyperbilirubinaemia

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19
Q

What haemolysis can cause jaundice at 2 days to 2 weeks of life

A

• G6PD deficiency
• Pyruvate kinase deficiency
• Hereditary spherocytosis
• (Less likely to be ABO incompatibility at this point)

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20
Q

What metabolic syndromes can cause jaundice at 2 days to 2 weeks of life

A

‣ Gilbert’s syndrome
‣ Crigler-Najjar

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21
Q

Is jaundice at >2 weeks (3 weeks if pre-term) of life pathological?

A

Can be normal

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22
Q

What are causes of raised unconjugated bilirubin at >2 weeks of life

A

• Breast milk jaundice (can be ongoing)
• Infections (particularly UTI)
• Congenital hypothyroidism (diagnosed via Guthries test)
• Pyloric stenosis

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23
Q

What are causes of raised conjugated bilirubin at >2 weeks of life

A

• Biliary atresia
• Neonatal hepatitis
• Cystic fibrosis
• Inherited metabolic conditions (e.g. Alpha-1-antitrypsin deficiency)

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24
Q

What is classed as prolonged jaundice

A

• Prolonged= 2 weeks term, 3 weeks preterm

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25
General investigations for jaundiced baby
• Visibly inspect baby in natural light • Bilirubin levels must be taken within <6 hours of presentation
26
Investigations if jaundice within 24 hours of life
• Urgent neonatal admission ‣ 1) Serum Bilirubin: • Direct= Total Br • Indirect= Unconjugated Br • Assume Total Br = Unconjugated Br ‣ FBC and Blood film: • Haematocrit <45% + raised reticulocyte count = Haemolysis Signs • Can show hereditary spherocytosis ‣ Blood group: ‣ From baby and mother ‣ Test for ABO incompatibility ‣ DAT (Coomb’s test): • Tests for ABO or Rh incompatibility by detecting antibodies on RBCs ‣ LFT: • Congenital infection ‣ G6PD
27
Investigations if jaundice at >1 day to 2 weeks of life
• Transcutaneous Bilirubin: • Can assume that TC-Br=UBr • Is non-invasive • Uses spectroscopy to measure light reflection from skin • If elevated reading, then confirm with serum bilirubin • Good for screening • TFTs, TSH • FBC + blood film • DAT
28
Investigations if jaundice at >2 weeks of life
• Split Serum Bilirubin: ◦ Direct= total Br ◦ Indirect= Unconjugated Br • TFTs, TSH • FBC + Blood Film • LFT • Urinary MCS or CSF
29
What is used to determine treatment of jaundiced baby
• Threshold Table: Plot to see if phototherapy or exchange transfusion needed ◦ Lower limits in preterm due to less albumin, therefore less ability to bind to Br ◦ And due to leaky BBB
30
Management of high conjugated bilirubin
• No treatment required • High cBr is not harmful • Treat the underlying cause • Bronzing after phototherapy indicates cBr
31
Management of raised unconjugated bilirubin
1) Phototherapy: • Converts uBr into water-soluble pigment that is excreted in urine • Br measurement repeated every 4-6 hours • Stop treatment once Br drops below threshold • Protect eyes • Check for rebound hyperbilirubinaemia after 12-18 hours • Consider IVIG: • If Rhesus Disease, ABO incompatibility, low albumin (cannot bind to Br)
32
When to give intensive phototherapy
‣ Do if: • Rapidly rising Br • Br level within umol/L of exchange transfusion threshold • Br levels fail to respond after 6 hours of therapy
33
What to do if very high bilirubin or if signs of Kernicterus
Exchange Transfusion + Phototherapy +/- IVIG: ◦ Give folic acid after to prevent anaemia
34
Complication of raised unconjugated bilirubin
Kernicterus
35
What is Kernicterus
• Unconjugated bilirubin passes through BBB • Causes neurotoxicity • Causes bilirubin encephalopathy
36
Symptoms of Kernicterus
‣ Poor suck ‣ Abnormal muscle tone and posture (opisthotonos) ‣ High pitched cry ‣ Apnoea
37
What is chronic lung disease of a newborn (bronchopulmonary dysplasia)
A chronic lung disorder where there is damage to the lungs of a newborn/child.
38
What causes lung damage in chronic lung disease of newborn
◦ Extreme preterm: especially <26 weeks- would cause delay in lung maturation ◦ Ventilator induced injury: Barotrauma to the lungs ◦ High oxygen requirements ◦ Sepsis: including NEC ◦ Chorioamnioitis ◦ Pulmonary haemorrhage ◦ Pulmonary fluid overload ◦ Nutritional deficits
39
Risk factor of chronic lung disease of newborn
• Highest rate in low birthweight infants (incidence decreases with gestational age)
40
Presentation of chronic lung disease of newborn
• Breathing difficulties and is oxygen dependent at 36 weeks • Poor growth • Feeding problems
41
Investigations for chronic lung disease of newborn
• Chest X-ray: • Hyperinflated lungs • Widespread opacification • Streaky infiltrates • Cystic changes
42
Prophylactic measures to prevent chronic lung disease of newborn
• Corticosteroids: ◦ For women expected or have had preterm labour (<34 weeks). ◦ Low dose-short course due to risk of abnormal development ◦ Dexamethasone • Early surfactant • Respiratory support: ◦ NIV preferred (CPAP) ◦ Target saturations 88-94% (be careful of hyperoxia due to risk of CLD) ◦ If ventilator: keep low ventilation pressures and tidal volume • Adequate nutrition: to promote lung growth and repair • Diuretics: ‣ Loop or thiazide diuretics can help with weaning of oxygen • RSV immunisations and palivizumab prophylaxis, flu vaccine (at 6 months)
43
What is neonatal respiratory distress syndrome
Respiratory distress caused by a deficiency of endogenous surfactant. Respiratory cause of neonatal cyanosis
44
Risk factors for neonatal respiratory distress syndrome
• Increasing prematurity (common if <28 weeks) • Maternal diabetes: Due to delayed lung maturation • Multiple gestation • Birth asphyxia
45
Pathophysiology of neonatal respiratory distress syndrome
• Surfactant produced by Type 2 pneumocytes • Lack of endogenous surfactant causes: ◦ Increased surface tension within alveoli and reduced lung compliance ◦ Causes widespread distal collapse of alveoli (actelectasis) • This would cause a decreased Functional Residual Capacity • Collapsed alveoli require higher opening pressures that can damage the endothelial lining
46
Presentation of neonatal respiratory distress syndrome
• At delivery or within 4 hours of birth: ◦ Untreated can lead to respiratory failure in 48-72 hours • Increased RR (>60) • Increased work of breathing: • Nasal flaring • Tracheal tug • Subcostal recession • Intercostal recessions • Head bobbing • Grunting: baby making +ve airway pressure to keep alveoli open • Cyanosis • Poor peripheral perfusion • Decreased breath sounds
47
Investigations for neonatal respiratory distress syndrome
• Prompt clinical diagnosis • Pulse Oximetry • Chest X-Ray: • Homogenous lung disease with ground-glass appearance • Air bronchograms (shown by arrows)
48
Antenatal prophylaxis for neonatal respiratory distress syndrome
• Glucocorticoid therapy: ‣ If delivery anticipated <34 weeks ‣ Will stimulate foetal surfactant production
49
Postnatal management of neonatal respiratory distress syndrome
• Immediate respiratory support: ◦ CPAP (delivers constant PEEP to keep airway open), high-flow humidified oxygen or mechanical ventilation (if severe) ◦ Continuous monitoring via arterial catheter ◦ Aim for 91-95% sats for preterm ◦ Lie prone ◦ Minimal handling ◦ Risk of pneumothorax • Exogenous Surfactant Therapy: ◦ Less Invasive Surfactant Adminstration ◦ Give following intubation ◦ Can reduce O2 demands and alveolar collapse
50
What is a pneumothorax
Collection of air between the thoracic cage and the parietal pleura
51
Different types of pneumothorax
• Primary Spontaneous: ‣ No underlying respiratory pathology • Secondary Spontaneous: ‣ Occurs as complication of underlying lung disease ‣ E.g. asthma, cystic fibrosis, interstitial lung disease, necrotising pneumonia, neonatal respiratory distress syndrome • Ventilator-Associated Pneumothorax: ◦ To prevent pneumothoraces, infants should be ventilated at the lowest pressures that provide adequate chest movement and gas exchange
52
Presentation of pneumothorax
• Sudden onset dyspnoea • Pleuritic chest pain • Pain radiates to ipsilateral shoulder • Tension pneumothorax: ‣ Tracheal deviation away from affect side ‣ Tachycardia ‣ Hypotension ‣ Cyanosis
53
Investigations for pneumothorax
• Translumination of chest wall using bright fibre optic light • Chest X-Ray: • Air in pleural space • Lack of lung markings
54
Management of pneumothorax
• Immediate decompression: • Primary: Needle aspiration • Secondary: Chest drain • Tension: Emergency needle aspiration and chest drain • Oxygen therapy
55
What is transient tachypnoea of the newborn
Commonest cause of respiratory distress in term infants characterised by pulmonary oedema from delayed resorption of foetal alveolar fluid.
56
Pathophysiology of transient tachypnoea of newborn
• Pulmonary oedema causes reduced pulmonary compliance + bronchiole collapse ◦ Results in compensatory tachypnoea
57
Risk factors for transient tachypnoea of newborn
• C-Section • Maternal diabetes • Prematurity <39weeks • Male • Maternal asthma
58
Presentation of transient tachypnoea of newborn
• Tachypnoea: • Onset: time of birth and 2 hours post-delivery • Respiratory distress: ‣ Nasal flaring ‣ Subcostal and intercostal recessions ‣ Tracheal tug ‣ Expiratory grunting ‣ Cyanosis
59
Investigations for transient tachypnoea of newborn
• Chest X-Ray: • Fluid in horizontal fissure • Clinical diagnosis: ◦ Respiratory distress shortly after delivery + X ray changes
60
Management of transient tachypnoea of newborn
• Supportive therapy: ◦ Usually RESOLVES within first day of life ◦ Supplemental O2 via hood/nasal cannula (keep O2 >90%) ◦ Provide nutrition if high RR (>60)
61
Management of tachypnoea in newborn that persists for >4-6 hours
• Ampicillin + Gentamicin
62
Prevention of transient tachypnoea of newborn
• Antenatal corticosteroids to mother (Dexamethasone) can reduce risk of TTN in late preterm or term neonates.
63
What is meconium aspiration
Respiratory distress in the newborn due to presence of meconium in respiratory tract
64
Pathophysiology of meconium aspiration
• Intrauterine passing of meconium into the amniotic fluid ◦ Neonate aspiration ‣ Mechanical obstruction via meconium plug causing hypoxaemia and persistent pulmonary hypertension of the newborn or ‣ Chemical pneumonitis • Meconium can be passed in response to foetal distress- leads to gasping and inhalation of amniotic fluid
65
Risk factors for meconium aspiration
RISK FACTORS: • Post-term infants: ◦ (>41 weeks) ◦ Increased risk with increasing gestational age ◦ Rare in preterm • Vaginal breech delivery • Caesarean delivery • Chorioamnioitis • Foetal distress/hypoxia
66
Presentation of meconium aspiration
• Respiratory distress: Immediately after birth ◦ Tachypnoea ◦ Tracheal tug ◦ Grunting ◦ Subcostal + intercostal recessions • Barrel shaped chest: Hyperinflated lungs • Evidence of meconium staining: ◦ Vernix (substance covering skin of newborn) and nails become stained • Perinatal asphyxia: Foetal respiratory depression • Post-maturity: peeling skin, less vernix, long fingernails
67
Investigations for meconium aspiration
• Chest X-Ray: • Diagnostic • Overinflated lungs • Streaky linear densities • Patches of collapse and consolidation • May have pneumothorax or pneumomediastinum (from air leak) • Culture/FBC etc: ?pneumonia
68
Management of meconium aspiration in infant with no history of GBS
• Observation • O2 Therapy: may need NIV (CPAP) in severe cases
69
Management of meconium aspiration if features of infection present
• IV ampicillin + IV Gentamicin • O2 Therapy
70
Complication of meconium aspiration
• Persistent pulmonary hypertension of the newborn
71
What is persistent pulmonary hypertension of newborn
Life-threatening condition that occurs when pulmonary vascular resistance remains abnormally elevated after birth.
72
Causes of persistent pulmonary hypertension of newborn
‣ Birth asphyxia ‣ Meconium aspiration ‣ Septicaemia ‣ Neonatal respiratory distress syndrome
73
What shunt created with persistent pulmonary hypertension of newborn
‣ Blood bypasses lungs via ductus arteriosus (forming right-to-left shunt) • Acidosis due to deoxygenated blood in systemic circulation
74
Presentation of persistent pulmonary hypertension of newborn
• Cyanosis right after birth • Respiratory distress: Tachypnoea, tracheal tug, Subcostal + intercostal recessions, grunting, head bobbing • No murmurs • No signs of heart failure
75
Investigations of persistent pulmonary hypertension of newborn
• Pre- and post-ductal O2 saturations: ◦ More than 10% difference due to right-to-left shunt through PDA • Chest X-Ray: • Normal sized heart • May be pulmonary oligaemia • Echo: Confirms no cardiac cause
76
Management of persistent pulmonary hypertension of newborn
• Oxygen: ‣ High PO2 ‣ Likely will need mechanical ventilation • Inhaled nitric oxide: Potent vasodilator • Sildenafil: also can be used as vasodilator • High frequency oscillatory ventilation
77
What is intraventricular haemorrhage
Bleeding into the lateral ventricles seen in preterm infants
78
Risk factors of intraventricular haemorrhage
• Increasing prematurity (<33 weeks) • Antenatal maternal haemorrhage • Vaginal delivery • ECMO in preterm babies with severe respiratory distress syndrome • Congenital CMV infection
79
Pathophysiology of intraventricular haemorrhage
‣ Due to fragile, thin-walled blood vessels in brain ‣ Hypoperfusion-reperfusion injury can damage as CO2 can vasodilate neural blood vessels, and removal of it will cause them to vasoconstrict ‣ Bleeding arises from germinal matrix ‣ Can block CSF and cause hydrocephalus
80
Time of incidence of intraventricular haemorrhage
• Most occur in first 3 days (uncommon after 1st week)
81
Presentation of intraventricular haemorrhage
• May be initially asymptomatic • Hypoactivity/lethargy/sleepiness • Respiratory distress • Apnoea • Seizures • Bulging fontanelle • Reduced/absent Moro reflex
82
Investigations for intraventricular haemorrhage
• Trans-cranial USS: ‣ Dilation of ventricles ‣ White flare indicating blood
83
Management of intraventricular haemorrhage
• Fluid replacement • Anticonvulsants • Reduce CSF: • Lumbar puncture • Acetazolamide • Consider Ventriculo-Peritoneal Shunt if hydrocephalus
84
What is necrotising enterocolitis
Neonatal surgical emergency characterised by the necrosis of intestinal tissue due to inflammation
85
Risk factors of necrotising enterocolitis
• Tends to affect: ◦ Preterm babes ◦ Very low birth weight babies ◦ Growth restricted babies ◦ Only formula-fed babies ◦ Black infants
86
Time of incidence of necrotising enterocolitis
• Occurs in first few weeks of life • Rarely affects term infants
87
Presentation of necrotising enterocolitis
• Around 9 days of age • Feeding intolerance • Bilious vomiting • Lethargy/Quiet • Abdominal distention • Bloody stools: Comes slightly later Rapidly progress into (within hours): ◦ Abdominal discolouration ◦ Bilious gastric aspirate ◦ Peritonitis ◦ Hypotensive ◦ Shock
88
Investigations for necrotising enterocolitis
• Abdominal X-Ray: ◦ Asymmetrical dilated bowel loops ◦ Paucity of gas ◦ PNEUMATOSIS INTESTINALIS: Intramural air, pathognomic finding (can see sharp lines on x-ray) ◦ Portal venous gas • Blood cultures
89
Management of necrotising enterocolitis
• Supportive Treatment: ‣ Stop entral feeding and switch to total PARENTRAL feeding ‣ Then gently introduce breast-milk feeds to prime the gut ‣ Broad-Spectrum Antibiotics: ◦ Penicillin + Gentamicin + Metronidazole ◦ For 10-14 days ‣ Gastric decompression: ◦ With NG tube • Mechanical ventilation with volume and inotropic support often needed • Surgical Assessment: ‣ Laparotomy if perforated or failure to respond to medical management
90
Complications of necrotising enterocolitis
• Stricture development • Short bowel syndrome (if surgery done)

Year 5: Conditions (17 decks)

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