Vomiting and Malabsorption in Children Flashcards by Chloe Mackle

Types of vomiting

Vomiting with retching
Projectile vomiting
Bilious vomiting
Effortless vomiting

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Phases and features of these phases of vomiting with retching

Pre-ejection phase

pallor
nausea
tachycardia

Ejection phase

retch
vomit

Post-ejection phase

weakness, pale and limp
shivering
lethargy

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What stimulates vomiting centre?

enteric pathogens 
Intestinal inflammation 
Metabolic derangement 
Infection 
Head injury 
Visual stimuli 
Middle ear stimuli

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Features of bilious vomiting

Should always ring alarm bells

Due to intestinal obstruction until proven otherwise

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Causes of bilious vomiting

Intestinal atresia 
Malrotation +/- volvulus 
Intussusception 
Ileus 
Crohn's disease with strictures

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Investigations of bilious vomiting

Abdominal x-ray
Consider contrast meal
Surgical opinion re exploratory laparotomy

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Daily, how much fluid enters the duodenum, and how much of this gets to the colon and is lost in faeces?

9L enters duodenum each day
1.5L gets to colon
< 200ml lost in faeces

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What causes the 600-fold increase in surface area of the small intestine?

Mucosal folds

Villi

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Essential secretory component of GI tract

Water for fluidity/enzyme transport/absorption
Ions
Defence mechanism against pathogens

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Features of pyloric stenosis

Babies
4-12 weeks old
Boys > girls 
Projectile non-bilious vomiting 
Weight loss
Dehydration +/- shock

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Characteristic electrolyte disturbance in pyloric stenosis

Metabolic acidosis
Hypocholoraemia
Hypokalaemia

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Features of gastro-oesophageal reflux

Movement of gastric contents into the oesophagus - GORD occurs when this causes inflammation
Effortless vomiting
Very common problem in infants
Usually self-limiting and resolves spontaneously

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Presenting symptoms of gastro-oesophageal reflux/GORD

vomiting
haematemesis

Nutritional

feeding problems
failure to thrive

Respiratory

apnoea
cough
wheeze
chest infections

Neurological
- Sandifer’s syndrome

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What is Sandifer’s syndrome?

Association of GORD with spastic torticollis and dystonic body movements
Nodding and rotation of the head, neck extension, gurgling sounds, writhing movements of limbs and severe hypotonia have been reported
Causal relation between GORD and neurological manifestations of Sandifer’s syndrome is supported by the resolution of the manifestations on successful treatment of GORD

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Medical assessment of GORD

History and examination often sufficient
Radiological investigations
- Video fluoroscopy (only if swallowing problems)
- Barium swallow

pH study - gold standard
Oesophageal impedance monitoring
Endoscopy if not resolved in 2 years or severe symptoms

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What features or GORD can be picked up on radiology?

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Dysmotility
Reflux
Gastric emptying
Strictures

Treatment of gastro-oesophageal reflux

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Feeding advice
Nutritional support
Medical treatment
Surgery

Feeding advice for gastro-oesophageal reflux

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Feed thickeners e.g. carobel
Appropriateness of foods - texture and amount
Behavioural programme - oral stimulation, removal of aversive stimuli
Feeding position - 45 degrees

Nutritional support for gastro-oesophageal reflux

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Calorie supplements
Exclusion diet
Nasogastric tube
Gastrotomy

Medical treatment of gastro-oesophageal reflux

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Feed thickener e.g. gaviscon
Prokinetic drugs
Acid-suppressing drugs

Indications for surgery for gastro-oesophageal reflux

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Failure of medical treatment

Persistent

failure to thrive
aspiration
oesophagitis

Vomiting without complications is not an indication

Features of Nissen Fundoplication

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Children with cerebral palsy are more likely to have complications of bloat, dumping and retching after surgery
Successful surgery may unmask more generalised GI motility problems in the child
Post-operative course may be more complicated in children with cerebral palsy

Chronic diarrhoea definition

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4 or more stools per week

< 1 week = acute diarrhoea
2-4 weeks = persistent diarrhoea
> 4 weeks = chronic diarrhoea

Causes of chronic diarrhoea

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Motility disturbance

toddler’s diarrhoea
irritable bowel syndrome

Active secretion

acute infective diarrhoea
IBD
secretory

Malabsorption of nutrients

food allergy
CF
coeliac disease
osmotic

Features of osmotic diarrhoea

Movement of water into the bowel to equilibrate osmotic gradient Usually a feature of malabsorption - enzymatic defect or transport defect Mechanism of action of lactulose/movicol Generally accompanied by macroscopic and microscopic intestinal injury Clinical remission with removal of causative agent

Types of carbohydrate malabsorption

``` Primary lactose malabsorption very rare Secondary lactose malabsorption e.g. rotavirus infection Glucose-galactose malabsorption Fructose malabsorption Disaccharidases deficiency ```

Causes of fat malabsorption

Pancreatic Disease - Diarrhoea due to lack of lipase and resultant steatorrhoea - Classically cystic fibrosis Hepatobiliary Disease - Chronic liver disease - Cholestasis

Features of secretory diarrhoea

Classically associated with toxin production from vibrio cholerae and enterotoxigenic E. coli - in cholera, can lose 24L per day Intestinal fluid secretion predominantly driven by active Cl- secretion via CFTR

Features of motility diarrhoea

Classically toddler's diarrhoea | Other causes - irritable bowel syndrome, congenital hyperthyroidism, chronic intestinal pseudo-obstruction

Features of inflammatory diarrhoea

Mixed bag Malabsorption due to intestinal damage Secretory effect of cytokines Accelerated transit time in response to inflammation Protein exudate across inflamed epithelium

Important features of history of a child with diarrhoea

``` Age at onset Abrupt/gradual onset Family history Nocturnal defaecation - suggests organic pathology Consider growth and weight gain of child ```

Components of faeces analysis

Appearance Stool culture Determination of secretory vs osmotic

What percentage of Western population are affected by coeliac disease?

Presentation of coeliac disease

``` Abdominal bloating Diarrhoea Failure to thrive Short stature Constipation Tiredness Dermatitis herpatiformis ```

Susceptible asymptomatic group to coeliac disease

Type 1 DM Autoimmune thyroid disease Down syndrome First degree relatives of people with coeliac disease

Screening tests for coeliac disease

Serological screens - anti-tissue transglutaminase - anti-endomysial - concurrent IgA deficiency in 2% may result in false negatives Gold standard - duodenal biopsy Genetic testing - HLA DQ2, DQ8

ESPCHAN/BSPCHAN Guidelines for coeliac disease

``` Symptomatic children Anti-TTG > 10 times upper limit of normal Positive anti-endomysial antibodies Normal serum IgA HLA DQ2, DQ8 positive Diagnose coeliac disease without biopsy ```

Treatment of coeliac disease

Strict gluten-free diet for life - avoid rye, wheat and barley Gluten must not be removed prior to diagnosis as serological and histological features will resolve In very young (< 2 years) re-challenge and re-biopsy may be warranted Increased risk of rare small bowel lymphoma if untreated

Vomiting and Malabsorption in Children Flashcards

(38 cards)