vomiting and malabsorption Flashcards
what is vomiting
forceful ejection of gastric contents through the mouth
3 phases of vomiting
pre-ejction: pallor, nausea, tachycardia
ejection: retch (deep breaths taken against a closed glottis), vomit (contractions of abdo muscles, contraction of upper part of S intestine and stomach)
post ejection: lethargy, pallor, sweathing
why does vomiting occur
stimulation of vomiting centre in medulla oblongata
chemoreceptor trigger zone (base of 4th ventricle) is stimulated by certain chemical and toxins
triggers for vomiting
- enteric pathogens
- infection e.g. meningitis, encephalitis, otitis media, UTI, sepsis
- visual/olfactory stimuli, fear
- head injury, raised ICP
- inner ear stimuli
- metabolic derangements/chemotherapy
how do GI triggers stimulate vomiting
impulses sent to vomiting centre via vagus nerve
types of vomiting
- vomiting w/ retching - associated w/ IC pathology if also in early morning
- projectile
- bilious
- effortless/regurgitation
- haematemesis
causes of vomiting in children
GOR
cow’s milk allergy
infection
intestinal obstruction
causes of vomiting in children
gastroenteritis
infection
appendicitis
intestinal obstruction
raised ICP
coealic disease
causes of vomiting in young adults
gastroenteritis
infection
H. pylori infection
appendicitis
raised ICP
DKA
cyclical vomiting syndrome
bulimia
what does palpation of an ‘olive’ tumour indicate
thickened pylorus - classical of pyloric stenosis
what does hypochloraemic metabolic acidosis indicate
large amounts of vomiting
losing HCl from stomach
when does pyloric stenosis typically occur
babies 4-12wks
M>F
features of pyloric stenosis
projectile non-bilious vomiting
weight loss
dehydration +/- shock
electrolyte disturbance
electrolyte disturbance in pyrloric stenosis
metabolic alkalosis
hypochloraemia
hypokalaemia
what is effortless vomiting
prognosis
almost always due to GOR
very common in infants
self-limiting and resolves spontaneously in the vast majority
when may effortless vomiting not resolve
cerebral palsy
progressive neurological problems
oesophageal atresia +/- TOF operated - associated oesophageal dysmotility, altered use of gastro-oesophageal junction
generalised GI motility issues
pathophysiology of reflex
lower oesophageal sphincter and diaphragmatic crura prevent expulsion of gastric contents into oesophagus
in babies LOS is lax and they are generally lying down
feeds are mainly liquid
- predisposes to GOR
improves w/ age as solids are introduced and more sitting/standing posture
presenting symptoms of effortless vomiting
- vomiting, haematemesis
- feeding problems, FTT
- apnoea, cough, wheeze, chest infection - aspiration pneumonia
- Sandifer’s syndrome
what is sandifer’s syndrome
rare pediatric manifestation of gastro-esophageal reflux (GER) disease characterized by abnormal and dystonic movements of the head, neck, eyes and trunk
diagnosis of GOR and further investigations
hx and examination often enough
oesophageal pH/impendance monitoring - assess severity
endoscopy
radiological investigations - video fluroscopy (aspiration pneumonia, look for pharyngeal pouch or incoordination of swallowing mechanism) , barium swallow (rule out hiatus hernia or malrotation)
management of GOR
often child is thriving well, reassurance
usually starts ~2w/o, worse 4-6m/o, improves 1y/o
investigate for causes if not improving at 1y/o or FTT/growth faltering
- look for severity and oesophagitis, rule out anatomical problems e.g. hiatus hernia
aims of barium swallow
dysmotility
hiatus hernia
reflux
gastric emptying
strictures
problems w/ barium swallow
inadequate contrast taken, may require NG tube
what does a pH study detect
- pH sensor place ~5cm above gastro-oesophageal junction or LOS
- measures number of times pH drops below 4 - suggesting reflux of acid into oesophagus
- don’t detect weak or non-acid reflux
why is pH studies combined w/ impendance monitoring
impendance monitoring detects acid, non-acid and air monitoring
when would an upper GI endoscopy be carried out in children
persistent symptoms, faltering growth, non-response to anti-reflux therapy
done under GA
what is looked for on upper GI endoscopy
reflux oesophagitis
oesophagitis due to other causes
treatment for GOR
feeding advice
nutritional support
medical treatment
surgery
treatment for GOR - feeding advice
thickeners for liquid
appropriateness of food - texture, amount
behavioural programme - oral stimulation, removal of aversive stimuli
feeding position
check feed volumes - neonates: 150ml/kg/day, infants: 100ml/kg/day
treatment for GOR - nutritional support
calorie supplements
exclusion diet - cow milk protein free trial for 4wks
NG tube
gastrostomy
- NG tube/gastrostomy for severe reflux or unsafe swallow
treatment for GOR - nutritional support
calorie supplements
exclusion diet - cow milk protein free trial for 4wks
NG tube
gastrostomy
- NG tube/gastrostomy for severe reflux or unsafe swallow
treatment for GOR - medical treatment
feed thickener - gaviscon, thick and easy
prokinetic drugs e.g. domperidone (usually not recommended due to cardiac side effects)
acid suppressing drugs - H2 receptor blocker, PPI
treatment for GOR - indications for surgery
failure of medical treatment
persistent: FTT, aspiration, oesophagitis
vomiting w/o complications may not be an indication
treatment for GOR - surgical treatment
Nissen fundoplication
- fundus is wrapped round oesophageal sphincter
- usually required in children w/ cerebral palsy or neurodisabilities
complications of Nissen fundoplication
children w/ cerebral palsy are more likely to have complications - bloat, dumping, retching
successful surgery may unmask more generalised GI motility problems
what does billous vomiting indicate
intestinal obstruction until proven otherwise
should always be investigated
causes of billous vomiting
intestinal atresia - neonates
malrotation +/- volvulus
intussusception
ileus
Crohn’s disease w/ strictures
investigations for billous vomiting
abdo XR
consider contrast meal
surgical opinion - exploratory laparotomy
fluid passage in intestines
9L enters duodenum
1.5L gets to colon
<200ml lost
SA of small intestine
v. large for absorption functions
600x increase in SA through mucosal folds and villi
- S intestine resection or necrotising enterocolitis causes malabsorption - short gut syndrome
secretory component of S intestine
water for fluidity/enzyme transport/absorption
ions e.g. duodenal bicarbonate
defense mechanisms against pathogens/toxins/antigens
small intestine histology
- stem cells arise from crypts of Leiberkuhn
- extruded into lumen at tip of villi
what is chronic diarrhoea
≥4 stools/day for >4wks
<1wk - acute
2-4wks - persistent
>4wks - chronic and requires investigation for cause
causes of diarrhoes
- motility disturbance: toddler diarrhoea, IBS
- active secretion (secretory): acute infective, IBD
- malabsorption (osmotic): food allergy, coeliac, CF
what is osmotic diarrhoea
movement of water into the bowel to equilibrate osmotic gradient
what is osmotic diarrhoea usually a feature of
malabsorption
- enzymatic defect e.g. 2y lactase deficiency
- transport deficit e.g. glucose galactose transporter deficit
how can ostomic diarrhoea be utilised
mechanism of action of lactulose/movicol
clinical remission of osmotic diarrhoea
seen w/ removal of causative agent
what is secretory diarrhoea classically associated with
toxin production from vibrio cholerae and enterotoxigenic escherichia coli
causes XS secretion of water and ions
- can lose 24L/day in cholera
what is intestinal fluid secretion driven by in secretory diarrhoea
predominantly driven by active chloride secretion via CFTR
clinical approach to chronic diarrhoea
HX:
- age at onset
- abrubt/gradual onset
- FHx
- travel Hx, local outbreaks
- noctural defecation - organic pathology
consider growth and weight gain of child - growth faltering shouldn’t be missed
faeces analysis
- appearance, stool culture, determination of secretory vs osmotic
faeces analysis
undigested food
greasy/frothy/foul smelling - malabsorption
differentiation of osmotic and secretory diarrhoea
when is fat malabrosption seen
pancreatic disease - diarrhoea due to lack of lipase and resultant steatorrhoea
classically CF
hepatobiliary disease - chronic liver disease, cholestasis
what is the commonest cause for malabsorption in children
coeliac disease
what is coeliac disease
AI
gluten sensitive enteropathy - wheat, rye, barley
how common is coeliac disease
1% of western population affected
genetic susceptibility to coeliac
DQ2/DQ8
- not everyone w/ susceptibility will develop disease
- if you don’t have genetics - unlikely to develop coeliac - high -ve predictive value
symptoms of coeliac disease
abdo bloating
diarrhoea
FTT
short stature
constipation
fatigue
dermatitis herpatiformis
- usually seen between 12-14mths but can be diagnosed later
- more common in children w/ other AI conditions and 1st degree relatives
screening tests for coeliac disease
serological screens:
- anti-tissue transglutaminase - high sensitivity
- anti-endomysial - high specificity
- serum IgA
- concurrent IgA deficiency in 25% may result in false -ve
gold standard = duodenal biopsy
genetic testing - HLA DQ2/DQ8
endoscopic findings in coeliac
oedema
erythematous mucosa
blunting of villi
scalloping and dipping
histology in coeliac disease
lymphocytic infiltration of surface epithelium
partial/total villous atrophy
crypt hyperplasia
diagnosing coeliac - ESPGHAN/BSPGHAN guidelines
symptomatic children
anti TTG >10x upper limit of normal
+ve anti-endomysial ab
HLA DQ2/DQ8 +ve
- if all above are present - diagnosis made w/o biopsy
- if any of the above aren’t present, proceed to endoscopy
treatment of coeliac disease
- gluten free diet for life
- gluten must not be removed prior to diagnosis as serological and histological features will resolve
- <2y/o - rechallenge and rebiopsy may be warranted
what is the risk in untreated coeliac disease
rare small bowel lymphoma
