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Gastroenterology Flashcards

1
Q

Guidelines on infant feeding?

A
  • WHO recommend exclusive breastfeeding for 1st 6m

- NICE guidelines state 1st feed ideally within 1h of birth

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2
Q

Advantages of breast feeding for infant? (5)

A
  • Ideal nutrition for 1st 4-6m
  • Life-saving in developing countries
  • Decrease in GI infection/preterm NEC
  • Enhances mother-child relationship
  • Decreased risk of IDDM, HTN and obesity in later life
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3
Q

Advantages of breast feeding for mother? (3)

A
  • Promotes close attachment
  • Increased time interval b/w children – important at reducing birth rate in developing countries
  • Possible decrease in pre-menopausal breast cancer
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4
Q

Potential complications/disadvantages of breast feeding? (8)

A
  • Unknown intake
  • Breast milk jaundice
  • Infection transmission (CMV, HBV, HIV)
  • Drug transmission - inc recreational
  • Nutrient inadequacies (if beyond 6m)
  • Vit K deficiency
  • Less flexible
  • Emotional upset
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5
Q

How is colostrum different from normal breast milk? (2)

A

Higher protein

Higher immunoglobulin

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6
Q

What maternal hormones are important in breast feeding? (2)

A

Prolactin - increased milk production
- Ant pituitary

Oxytocin - let down reflex
- Post pituitary

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7
Q

Why is unmodified cow’s milk unsuitable for babies?

A
  • Too much protein/electrolytes

- Inadequate iron/vitamins

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8
Q

From what age can pasteurised cow’s milk be given?

A

1y (formula before this)
- Still many vitamin deficiencies, so must have supplements unless on good mixed solid diet

  • Should have full-fat up to 5y
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9
Q

When may specialised infant formula be needed? (5)

A
  • Cow’s milk protein allergy/intolerance
  • Lactose intolerance
  • CF
  • Neonatal cholestatic liver disease
  • Following neonatal intestinal resection
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10
Q

Differences b/w cow’s milk formula and specialised formula?

A

Cow’s milk:

  • Protein derived from cow’s milk protein
  • CHO = lactose
  • Fat mainly long chain triglycerides

Specialised:

  • Protein either hydrolyzed cow’s milk protein, a-a’s or from soya
  • CHO = glucose polymer
  • Fat = combination of medium­ and long chain triglycerides
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11
Q

How is FTT categorised?

A

Mild - fall across 2 centile lines

Severe - fall across 3 centile lines

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12
Q

Causes of FTT? (broad categories) (5)

A
  • Inadequate intake
  • Inadequate retention - D/V, GORD
  • Malabsorption - coeliac, CF, NEC etc
  • Failure to utilise nutrients - Down’s, IUGR, metabolic disorders, storage disorders etc
  • Increased requirements - thyrotoxicosis, CF, malignancy, HIV, CKD etc
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13
Q

What is the MUST tool?

A

Malnutrition universal screening tool

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14
Q

What are the 2 types of protein/energy malnutrition?

A

Marasmus (no oedema)

Kwashiorkor (oedema)

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15
Q

Features of Kwashiorkor?

A

Generalised oedema
Severe wasting

Plus

  • A ‘flaky-paint’ skin rash with hyperkeratosis (thickened skin) and desquamation
  • Distended abdo and enlarged liver (fatty infiltration)
  • Angular stomatitis
  • Hair which is sparse and depigmented
  • Diarrhoea, hypothermia, bradycardia and 
hypotension
  • Low plasma albumin, potassium, glucose and magnesium
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16
Q

Recommended intake for different age groups?

A 
0-3m = 18-32 oz (530-950ml)
4-6m = 28-40 oz (830-1,180ml)
7-9m = 24-36 oz (710 – 1,060ml) + 1-2.5 cups solids
10-12m = 18-30 oz (530- 890ml) + 3-4.5 cups solids
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17
Q

Normal frequency of bowels opening in infants?

A

4/day in first few days
2/day by 1y
By 4y, have pattern of adults (3/d-3/w)

  • -> YET highly variable
  • Breast fed may not pass stools for days
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18
Q

4 things to consider if constipation in baby?

A
  • Hirschprung’s
  • Anorectal malformations
  • Hypothyroidism
  • Hypercalcaemia
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19
Q

Red flags in constipation? (8)

A
  • Failure to pass stools in 1st 24h
    (?Hirschprungs)
  • FTT (coeliac, hypothyroid)
  • Gross abdo distension (Hirschprung/other GI motility disorder)
  • Abnormal lower limb pathology/urinary incontinence - ?Lumbosacral
  • Sacral dimple - spina biffida etc?
  • Abnormal appearance of anus
  • Bruising around anus (?abuse)
  • Perianal fistulae/fissures/abscesses (Crohns?)
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20
Q

What is encoparesis?

A

Toilet-trained child soiling clothes

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21
Q

What is soiling due to overflow and aim of management?

A
  • Rectum becomes overdistended with loss of feeling the need to defecate
  • → Involuntary soiling may occur as contractions of full rectum inhibit internal sphincter
  • Initial aim is to evacuate rectum completely
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22
Q

What is functional encoparesis?

A

Repeated involuntary faecal soiling not caused by organic defect or illness

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23
Q

How do you differentiate b/w functional encoparesis and soiling due to overflow?

A
  • Check for s+s of constipation

- If yes –> overflow

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24
Q

What is Hirschprung’s disease and how much bowel is usually affected?

A
  • Absence of ganglion cells from myenteric and submucosal plexuses of part of large bowel
  • → Narrow, contracted segment
  • Abnormal bowel extends from rectum for variable distance, ending in normally innervated, dilated colon
  • 75% - confined to rectosigmoid
  • 10% entire colon is involved
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25
Q

Presenting features of Hirschprung’s disease?

A
  • Usually in neonatal period
  • Failure to pass meconium in 1st 24h
  • Abdo distension
  • Bile-stained vomit
  • PR may reveal narrowed segment
  • Withdrawal of examining finger often releases gush of liquid stool and flatus
  • Temporary improvement in obstruction following PR can delay diagnosis
  • Occasionally present with life-threatening Hirschprung enterocolitis during 1st few wks, sometimes due to C. Diff
  • Later childhood presentation = chronic constipation, usually profound + abdo distension (no soiling)
  • Growth failure may present
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26
Q

How is Hirschprung’s diagnosed?

A

Suction rectal biopsy

  • Absence of ganglion cells
  • Presence of large Ach-esterase +ve nerve trunks

Anorectal manometry or barium studies

  • May be useful
  • Give surgeon idea of length of a ganglionic segment
  • Unreliable for diagnosis
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27
Q

Management of Hirschprung’s?

A
  • Surgical
  • Initial colostomy
  • Followed by anastomosing normally innervated bowel to anus
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28
Q

Most common cause of gastroenteritis in children?

A

Rotavirus

- Esp winter/spring

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29
Q

What bacteria is most common cause of gastroenteritis?

A

Campylobacter jejuni

  • Associated w/ severe abdo pain
  • Yet bacterial causes much less common
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30
Q

Ddx of gastroenteritis? (6)

A
  • Systemic infection – septicaemia, meningitis
  • Local infection – resp tract, otitis media, Hep A, UTI
  • Surgical disorders – pyloric stenosis, intussusception, acute appendicitis, necrotizing enterocolitis, Hirschprung disease
  • Metabolic disorder – diabetic ketoacidosis
  • Renal disorder – haemolytic uraemic syndrome
  • Other – coeliac disease, cow’s milk protein intolerance, adrenal insufficiency

→ If in doubt, hospital referral essential

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31
Q

Indicators that diagnosis is not gastroenteritis?

A
  • Temp >38 (<3m) or <39 (<3m)
  • SOB or tachypnoeic
  • Altered conscious state
  • Neck stiffness
  • Bulging fontanelle
  • Non-blanching rash
  • Blood +/- mucus in stool
  • Bilious (green) vomit
  • Severe or localized abdo pain
  • Abdo distension or rebound tenderness
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32
Q

When is stool microscopy indicated in suspected gastroenteritis?

A
  • Suspect septicaemia
  • Blood or mucus in stool
  • Child is immunocompromised
  • Consider if recently abroad, diarrhea not improved in 7d, uncertain about diagnosis
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33
Q

Main complication of gastroenteritis?

A

Dehydration

Pos –> shock

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34
Q

What factors in gastroenteritis put the child at increased risk of dehydration? (5)

A
  • Infants, esp <6m or those with low birth weight (greater SA:weight → more water losses)
  • If passed >6 diarrhoeal stools in 24h
  • Vomitted ≥3x in 24h
  • Unable to tolerate (or not offered) extra fluids
  • If malnourished
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35
Q

3 categories of dehydration?

A
  1. No clinically detectable dehydration (usually <5% loss of body wt)
  2. Clinical dehydration (5-10%)
  3. Shock (>10%)
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36
Q

What do you look at when assessing hydration status? (13)

A
  • General appearance
  • Consciousness level
  • Urine output
  • Skin colour
  • Extremeties temperature
  • Eyes (sunken or not)
  • Mucous membranes
  • Heart rate
  • Resp rate
  • Peripheral pulses (strong/weak)
  • Cap refill
  • Skin turgor
  • BP
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37
Q

Red flags when assessing hydration? (6)

A
  • Appears unwell or deteriorating
  • Altered responsiveness eg irritable, lethargic
  • Sunken eyes
  • Tachycardia
  • Tachypnoea
  • Reduced skin turgor

–> Helps to identify those who may progress to shock

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38
Q

Signs of hypernatraemic dehydration? (5)

A
  • Jittery movements
  • Increased muscle tone with hyperreflexia
  • Altered consciousness
  • Seizures
  • Multiple, small cerebral haemorrhages
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39
Q

Treatment of

a) Clinical dehydration
b) Shock?

A

a) Oral rehydration solution
- Fluid deficit replacement fluids (50ml/kg)
- Over 4h
- + maintenance requirement
- Continue breast feeding
- IV therapy if deteriorate/continual vomiting

b) IV therapy
- Rapid infusion of 0.9%NaCl
- Repeat if nec
- Fluid deficit = 100ml/kg
- Maintenance fluids

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40
Q

When are abx indicated in gastroenteritis? (6)

A
  • Suspected or confirmed sepsis
  • Extra­intestinal spread
  • Salmonella if <6m
  • Malnourished
  • Immunocompromised
  • Specific bacterial or protozoal infections (e.g. C. Diff ­associated with pseudomembranous colitis, cholera, shigellosis)
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41
Q

Ddx for vomiting in infants? (8)

A
  • GORD
  • Feeding problems
  • Infection
  • Dietary protein intolerances
  • Intestinal obstruction
  • Inborn errors of metabolism
  • Congenital adrenal hyperplasia
  • Renal failure
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42
Q

Types of intestinal obstruction in infants? (8)

A
  • Pyloric stenosis
  • Atresia (duodenal, other)
  • Intussusception
  • Malrotation
  • Volvulus
  • Duplication cysts
  • Strangulated inguinal hernia
  • Hirschprung disease
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43
Q

Types of intestinal obstruction in preschool children? (5)

A
  • Intussusception
  • Malrotation
  • Volvulus
  • Adhesions
  • Foreign body
44
Q

Causes of vomiting in preschool children? (8)

A 
Infection (gastro most common)
Appendicitis
Intestinal obstruction
Raised ICP
Coeliac
Renal failure
Inborn errors of metabolism
Torsion of testes
45
Q

Causes of vomiting in school age children and adolescents? (13)

A 
Infection
Peptic ulceration (h pylori)
Appendicitis
Migraine
Raised ICP
Coeliac
Renal failure
DKA
Alcohol/drug
Cyclical vomiting syndrome
Bulimia/anorexia
Pregnancy
Torsion of testes
46
Q

Sx of GORD?

A
  • Frequent regurgitation/vomiting

- Putting on weight and otherwise well

47
Q

Severe reflux more common if? (3)

A

Cerebral palsy
Preterm
After surgery for oesophageal atresia

48
Q

Management of GORD?

A

If uncomplicated:

  • → Excellent prognosis
  • Thickening agents (e.g. Nestargel, Carobel) and positioning in a 30° head­up prone position after feeds

More significant GORD:

  • H2 receptor antagonists (e.g. ranitidine) or PPIs
  • Drugs which enhance gastric emptying (e.g. domperidone) may be tried
  • If no response, other diagnoses such as cow’s milk protein allergy should be considered and further Ix performed

Surgical management:
- Reserved for children with complications unresponsive to intensive medical treatment or oesophageal stricture

49
Q

Complications of GORD? (7)

A
  • FTT from severe vomiting
  • Oesophagitis – haematemesis, discomfort on feeding or heartburn, iron deficiency anaemia
  • Recurrent pulmonary aspiration – recurrent pneumonia, cough or wheeze, apnoea in preterm infants
  • Dystonic neck posturing – Sandifer syndrome
  • ALTE
  • SIDS
  • Barrett’s – v rare, managed with PPIs
50
Q

How does malabsorption manifest? (3)

A
  • Abnormal stools
  • FTT or poor growth in most but not all
  • Specific nutrient deficiencies, either singly or in combination
51
Q

Ddx with malabsorption? (9)

A
  • Coeliac
  • Food allergy/intolerance
  • Cholestatic liver disease/biliary atresia
  • Lymphatic leakage/obstruction
  • Short bowel syndrome
  • Loss of terminal ileal function
  • Exocrine pancreatic dysfunction
  • SI mucosal disease
  • Parasitic infection
52
Q

Classical presentation of coeliac?

A
  • Profound malabsorptive syndrome at 8–24m after introduction of wheat­containing weaning foods
  • →FTT, abdo distension, buttock wasting abnormal stools and general irritability
  • However, this is no longer the most common presentation and children are now more likely to present less acutely in later childhood
53
Q

Clinical features of coeliac?

A
  • Highly variable
  • Mild, non-specific GI sx eg diarrhea or vomiting
  • Anaemia (iron +/or folate deficiency)
  • Growth failure
  • Alternatively, identified on screening of children at increased risk (T1DM, autoimmune thyroid disease, Down syndrome) and 1st degree relatives of individuals with known coeliac disease
54
Q

Diagnosis of coeliac?

A
  • Serology (must eat gluten 6w prior) - IgA tissue transglutaminase antibodies
  • Confirmed by SI biopsy
55
Q

Difference b/w food allergy and food intolerance?

A

Food allergy = immune mediated (usually IgE)
–> Allergy sx = urticaria to anaphylaxis 10-15m after ingestion

Food intolerance = non-immunological hypersensitivity reaction
–> Sx= usually GI - D+V, hours after ingestion

56
Q

How is diagnosis of food allergy usually made? (3)

A

Skin prick test
Measurement of IgE in blood

Gold standard test = double blinded placebo controlled food challenge
- Rarely done

57
Q

What is a type 1 and type 2 reaction in food allergies?

A

Type 1 reaction:

  • Usually instant
  • Where body suffers notable itching, swelling, hives and breathing difficulties
  • Whilst most of these reactions are mild, some can be more serious and result in an anaphylactic shock

Type 2 reaction:

  • Not immediate → difficult to detect
  • Different foods breakdown at different rates so a reaction can be anywhere from 24-72 hours after ingestion
58
Q

How is food allergy managed?

A
  • Avoid food
  • Give parents written advice and training about how to manage allergic attack
  • Oral antihistamines if mild (no cardio-resp sx)
  • IM epinephrine if severe
59
Q

What is cow’s milk protein allergy and intolerance?

A 
Allergy:
Immune response to cow's milk protein
Most likely IgE mediated
--> hives, rashes, wheezing
- Within 2h

Intolerance:
Not immune mediated
–> GI reactions
- Usually much later

60
Q

How is cow’s milk protein allergy/intolerance managed?

A

If breast feeding eliminate from mother’s diet and take calcium supplements instead

If bottle fed, use hydrolysed (a-a) formula

Resolved in 90% by 6y

61
Q

What is toddler diarrhoea?

A

= Chronic non­-specific diarrhoea

  • Commonest cause of persistent loose stools in preschool children
  • Stools are of varying consistency, sometimes well formed, sometimes explosive and loose
  • Presence of undigested vegetables common
  • Affected children are well and thriving
  • No precipitating dietary factors

Aetiology:

  • Probably results from underlying maturational delay in intestinal motility which leads to intestinal hurry
  • Loose stools not due to malabsorption
  • Most grown out of their sx by 5y
  • Achieving faecal continence may be significantly delayed
62
Q

Management of toddler diarrhoea?

A
  • Some relief of symptoms can be achieved by ensuring that child’s diet contains adequate fat (which slows gut transit) and fibre
  • XS consumption of fresh fruit juice, esp those high in non-­absorbable sorbitol, can exacerbate sx
63
Q

Causes of diarrhoea in children? (6)

A
  • Toddler diarrhoea
  • Cow’s milk protein allergy
  • Coeliac
  • Gastroenteritis
  • Lactose intolerance
  • Following bowel surgery with malabsorption
64
Q

Where does Crohn’s most commonly affect?

A

Distal ileum

Proximal colon

65
Q

Presentation of Crohns in children/adolescents? (4)

A

Growth failure/ puberty delay

Classical presentation (25%)
- Abdo pain, diarrhoea, wt loss

Gen ill health
- Fever, lethargy, wt loss

Extra-intestinal
- Oral lesions, perianal skin tags, uveitis, arthralgia, erythema nodosum

66
Q

What do blood tests show in Crohn’s?

A
  • Raised inflammatory markers (platelet count, ESR and CRP)
  • Iron deficiency anaemia
  • Low serum albumin

→ Helpful in both making a diagnosis and confirming a relapse

67
Q

How is Crohn’s diagnosed?

A
  • Based on endoscopic and histological findings on biopsy
  • Upper GI endoscopy, ileocolonoscopy and small bowel imaging required
  • Histological hallmark = presence of non­ caseating epithelioid cell granulomata
  • → Although this is not identified in up to 30% at presentation
  • Small bowel imaging may reveal narrowing, fissuring, mucosal irregularities and bowel wall thickening
68
Q

How is Crohn’s remission induced?

A
  • Nutritional therapy
  • –> Normal diet replaced by whole protein modular feeds (polymeric diet) for 6–8w
  • Effective in 75% of cases
  • Systemic steroids required if ineffective
69
Q

How is relapses/ maintenance of Crohn’s managed?

A
  • Relapse common → immunosuppressant medication (azathioprine, mercaptopurine or methotrexate) may be required to maintain remission
  • Anti­-tumour necrosis factor agents (infliximab or adalimumab) when conventional treatments failed
  • Long­-term supplemental enteral nutrition (overnight NG or gastrostomy feeds) helpful in correcting growth failure
  • Surgery necessary for complications of Crohn disease – obstruction, fistulae, abscess formation or severe localised disease unresponsive to medical treatment, often manifesting as growth failure
  • Long-­term prognosis for Crohn’s beginning in childhood is good - most lead normal lives, despite occasional relapsing disease
70
Q

Clinical presentation of UC?

A

Characteristically:

  • Rectal bleeding
  • Diarrhoea
  • Colicky pain
  • Wt loss and growth failure may occur, although less frequent than Crohn’s
  • Extraintestinal complications include erythema nodosum and arthritis
71
Q

Extra-intestinal manifestations of

a) Crohns? (5)
b) UC? (2)

A 
a) Oral lesions
Perianal skin tags
Uveitis
Arthralgia
Erythema nodosum

b) Erythema nodosum
Arthritis

72
Q

How is UC diagnosed?

A
  • Endoscopy (upper and ileocolonoscopy) + histological features, after exclusion of infective causes of colitis
  • → Confluent colitis extending from rectum proximally for variable length
  • In contrast to adults, in whom colitis usually confined to distal colon, 90% of children have pancolitis
  • Histology reveals mucosal inflammation, crypt damage (cryptitis, architectural distortion, abscesses and crypt loss) and ulceration
  • Small bowel imaging required to check extra­ colonic inflammation suggestive of Crohn’s not present
73
Q

How is mild UC managed?

A
  • Aminosalicylates (balsalazide and mesalazine) used for induction and maintenance therapy
  • Disease confined to rectum and sigmoid colon may be managed with topical steroids
  • More aggressive or extensive disease requires systemic steroids for acute exacerbations and immunomodulatory therapy, e.g. azathioprine to maintain remission alone or in combination with low­ dose corticosteroid therapy
74
Q

How is severe fulminating UC managed?

A

= Medical emergency

  • IV fluids and steroids
  • If this fails to induce remission, may use ciclosporin
  • Colectomy with ileostomy or ileorectal pouch undertaken for severe fulminating disease which may be complicated by toxic megacolon, or for chronic poorly controlled disease
75
Q

What screening must be undertaken in those with UC?

A
  • Increased incidence of adenocarcinoma of colon in adults (1 /200 risk for each year of disease b/w 10-20y from diagnosis)
  • Regular colonoscopic screening performed after 10y from diagnosis
76
Q

What is colic?

A
  • Common sx complex that occurs during 1st few months of life
  • Paroxysmal, inconsolable crying or screaming often accompanied by drawing up of knees and passage of XS flatus takes place several times a day, esp in evening
  • No firm ev that cause is GI, but often suspected
  • Occurs in up to 40% of babies
77
Q

Features of colic?

A
  • Typically occurs in 1st few wks of life, resolves by 4m
  • Benign but v frustrating and worrying for parents → may precipitate NAI in infants already at risk
  • Gripe water often recommended but unproven benefit
  • If severe and persistent → may be due to cow’s milk protein allergy or GORD
  • → Empirical 2w trial of a whey hydrolysate formula followed by trial of anti­reflux treatment may be considered
78
Q

What is functional/recurrent abdo pain?

A

Pain sufficient to interrupt normal activities and lasts ≥3m

  • 10% of school aged children
  • Cause only identified in <10%
  • Pain characteristically periumbilical
  • Children otherwise well
  • May be manifestation of stress
79
Q

Prognosis of functional abdo pain?

A
  • ½ rapidly recover
  • ¼ take months to recover
  • ¼ remain into adulthood with migraine, IBS or functional dyspepsia
80
Q

Causes of recurrent abdo pain?

A

> 90% no cause found

GI
- IBS, constipation, dyspepsia, abdo migraine, gastritis, peptic ulcer, IBD, malrotation

Gynae
- Dysmenorrhoea, ovarian cysts, PID

Hepato-biliary/pancreatic
- Hepatitis, gall stones, pancreatitis

Urinary tract
- UTI, PUJ obstruction

Psychosocial
-Bullying, abuse, stress

81
Q

In abdo pain what do these sx suggest?
a) - Epigastric pain at night, haematemesis

b) Diarrhoea, wt loss, growth failure, blood in stools
c) Vomiting

A

a) Duodenal ulcer
b) IBD
c) Pancreatitis

82
Q

In abdo pain what do these sx suggest?
a) Jaundice

b) Dysuria, secondary eneuresis
c) Bilious vomiting and abdo distension

A

a) Liver disease
b) UTI
c) Malrotation

83
Q

Sx of gastritis? (7)

A
  • Epigastric pain
  • Abdo bloating
  • Diarrhoea
  • Nausea
  • Vomiting – coffee ground appearance = bleeding in stomach
  • Melaena
  • Loss of appetite
84
Q

Causes of gastritis? (5)

A
  • H Pylori – not as strong an association as in adults
  • NSAIDs
  • Chemotherapy
  • Pernicious anaemia
  • Infections
85
Q

How is H pylori detected? (3)

A
  • Urease breath test (13C)
  • Stool antigens
  • Serological testing is unreliable in children
86
Q

Lifestyle advice to be given in gastritis?

A
  • Eat smaller and more frequent meals
  • Avoid irritant foods (acidic, spicy, fried)
  • Drink alcohol in moderation
  • Avoid NSAIDs
  • Manage stress
  • Reduce smoking
87
Q

What is mesenteric adenitis?

A

Inflamed lymph glands in abdomen which cause abdo pain

- Not usually serious and gets better without treatment

88
Q

Sx of mesenteric adenitis? (4)

A
  • Pain in abdomen usually centrally or in RIF
  • Fever and generally unwell
  • N +/- D
  • Sore throat or sx of cold before pain started
89
Q

Ddx of mesenteric adenitis? (2)

A
  • Ectopic pregnancy

- Appendicitis

90
Q

Is it conjugated or unconjugated bilirubin that gives urine/stools colour?

A

Conjugated (water soluble)

91
Q

Is it conjugated or unconjugated bilirubin that can cause kernicterus?

A

Unconjugated

  • Normally bound to albumin
  • If albumin is saturated, it is free to cross BBB
92
Q

Causes of prolonged neonatal jaundice (unconjugated)? (6)

A
  • Breast milk jaundice
  • Infection (particularly urinary tract)
  • Haemolytic anaemia, e.g. G6PD deficiency
  • Hypothyroidism
  • High GI obstruction
  • Crigler–Najjar syndrome
93
Q

Causes of prolonged neonatal jaundice (conjugated)? (3 categories)

A

Due to liver disease, accompanied by pale stools, dark urine, FTT, bleeding tendency

Bile duct obstruction

  • Biliary atresia
  • Choledochal cyst

Neonatal hepatitis syndrome

  • Congenital infection
  • Inborn errors of metabolism
  • Alpha1-antitrypsin deficiency
  • Galactosaemia
  • Tyrosinaemia (type 1)
  • Errors of bile acid synthesis
  • Progressive familial intrahepatic cholestasis (PFIC)
  • CF
  • Intestinal failure-associated liver disease – associated with long term parental nutrition

Intrahepatic biliary hypoplasia
- Alagille syndrome

94
Q

What level of conjugated bilirubin is classed as jaundice?

A

> 20micromol/L

95
Q

What is kernicterus?

Manifestations? Prognosis?

A
  • Encephalopathy from deposition of unconjugated bilirubin in basal ganglia and brainstem nuclei
  • Usually occurs when level of bilirubin exceeds albumin binding capacity in blood
  • → Neurotoxic effect can vary in severity from transient disturbance to severe damage and death

Manifestations inc:

  • Poor feeding
  • Lethargy
  • Irritability
  • Increased muscle tone and an arched back

–> Infants who survive may develop choreoathetoid cerebral palsy, learning difficulties and sensorineural deafness

96
Q

What % newborns become visibly jaundiced and why? (3 reasons)

A

> 50%

  • Marked physiological release of Hb from breakdown of RBCs because of high Hb conc at birth
  • RBC life span of newborn infants (70 days) is shorter than in adults (120 days)
  • Hepatic bilirubin metabolism less efficient in 1st few days of life
97
Q

Likely causes of jaundice at <24h old? (2)

A

Haemolytic disorders:
- Rhesus haemolytic disease, ABO
incompatibility, spherocytosis and G6PD deficiency can all cause this

Congenital infection:
- Should inc other abnormal signs such 
as growth restriction, hepatosplenomegaly and thrombocytopenic purpura 


98
Q

Likely causes of jaundice 2d-2w old? (4)

A

Physiological jaundice: normal for most infants

Breast milk jaundice: most common cause affecting up to 15% of healthy breast fed infants and gradually disappears by 4-5w

Dehydration: exacerbated if milk intake poor from delay in establishing breastfeeding - sometimes IV fluids needed

Infection: unconjugated hyperbilirubinaemia from poor fluid intake, haemolysis and reduced hepatic function 


99
Q

Likely causes of jaundice >2w old?

A

= Persistent neonatal jaundice (5-10% newborns)

Biliary atresia (conjugated)
- Important to diagnose promptly as surgical treatment adversely affected by delay

Breast milk jaundice (unconjugated)

Infection (uncongugated)

Congenital hypothyroidism (unconjugated)

100
Q

How does assessing stool colour help in assessing jaundice?

A

Pale stool –> lack of conjugated bilirubin

- Most likely biliary tree or post-hepatic obstruction

101
Q

Management of jaundice?

A

Monitored

  • Check transcutaneous bilirubin, serum bilirubin
  • Chart to see if need phototherapy

Phototherapy

  • Single if not too high with breaks + feeding etc
  • Continuous if v high (IV/enteral feeding/hydration)

Exchange transfusion

  • If bilirubin dangerously high (rarely done)
  • Continuous phototherapy continued
102
Q

What is biliary atresia?

A
  • Progressive disease – destruction or absence of extrahepatic biliary tree and intrahepatic biliary ducts

→ Chronic liver failure + death unless surgical intervention

103
Q

Clinical features of biliary atresia?

A
  • Normal birth weight but FTT as disease progresses
  • Mildly jaundiced
  • Stools pale + urine dark (after meconium)
  • Pale stool warrants investigation always (even if no jaundice)
  • Hepatomegaly often present
  • Splenomegaly will develop (due to portal HTN)
104
Q

How is biliary atresia diagnosis confirmed?

A

Diagnosis confirmed at laparotomy by operative cholangiography → fails to outline normal biliary tree

105
Q

Treatment of biliary atresia?

A

Surgery

  • Success rate diminishes with age (80% <60d)
  • Even if successful often progression to cirrhosis and portal HTN

Liver transplant if fails
- Commonest reason for paediatric liver transplant

Paeds (15 decks)

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