Gastroenterology Flashcards
Causes of prolonged neonatal jaundice
Unconjugated: Breast milk jaundice Infection Haemolytic anaemia Hypothyroidism High GI obstruction Critter-Najjar Syndrome
Conjugated:
Biliary atresia
Neonatal hepatitis syndrome - CF, inborn errors of metabolism, congenital infection
Intrahepatic biliary hypoplasia
Why is it important to investigate prolonged neonatal jaundice
To distinguish bw conjugated and unconjugated
Because conjugated means liver disease - need early detection and treatment to prevent permanent liver damage
What is biliary atresia
Progressive, idiopathic fibrosis and obliteration of extra and intrahepatic biliary tree
Clinical features of biliary atresia
Prolonged neonatal jaundice
Pale stools
Faltering growth
Hepatomegaly - late stage w significant progression
Splenomegaly - portal hypertension in late stage
Investigations for biliary atresia
Raised conjugated bilirubin Normal LFTs Liver uss ERCP Liver biopsy
Management of biliary atresia
Surgical intervention as soon as possible - earlier the intervention, better the outcome due to permanent liver damage
Hepatoportoenterostomy - loop of jejunum anastamosed to porta hepatis to bypass fibrosed biliary tree
Liver transplantation - Most common indication for liver transplantation
Normal frequency of defecation in neonates, infants, >1yo?
4/day in 1st week of life
2/day up to 1 year
1/day after 1 year
Definition of constipation
Infrequent passage of stools leading to 1 or more of: painful defecation, overflow incontinence, rectal fecal impaction, active defecation avoidance behaviour
Red flag clinical features of constipation
Failure to pass meconium within 24 hrs of life
Faltering growth/growth failure
Gross abdominal distension
Abnormal lower limb neurology or deformity
Sacral dimple, naevus/hairy patch/central pit over spine
Absent/ectopic anus
Perianal bruising of fissures
Perianal fistulae, abscess, fissures
Causes of constipation
Functional - majority Hirschsprung disease Anorectal anomaly Anal sexual abuse Hypothyroidism, coeliac Lumbosacral pathology Spina bifida occulta Crohn’s disease
Pathophysiology of constipation
Combination of painful defecation and sufficient rectal capacity to withhold stools
- Hard stools produced - low fibre diet, low hydration, excessive colonic transit time allowing water reabsorption
- Pain on passing stool and Learned sphincter contraction
- Increasing delays bw defecation, enlargement of stool volume in rectum
- Increase in size of rectum
- Increase in pain and fear
- Overflow incontinence - rectum becomes overdistended, loss of feeling the need to defecate, involuntary soiling occifsndue to contractions of full rectum inhibit internal sphincter, leading to overflow with passage of softer stool around retained hard stool
General Management of constipation
Coeliac screen and TFTs
Dietary modification - fluid intake, fibre intake
Management of constipation with no impaction
Dietary modification
1. Macrogol laxative: polyethylene glycol + electrolytes (movicol) Low dose regimen
2. Stimulant laxative: senna
Maintenance: minimum 6month laxative therapy - PEG
Management of constipation with impaction
Education:
soiling is involuntary, recovery of normal rectal size and sensation achieved but takes long time, long term use of laxatives is safe
Dietary modification no benefit, fibre not helpful
Behavioural modification: star chart for motivation p
Disimpaction:
1. Polyethylene glycol 3350 + electrolytes disimpaction regimen
2. + stimulant laxative: senna, sodium pocosulphate
Maintenance:
osmotic laxative at least 6 moths until regular bowel movements achieved
What is disimpaction regimen
- Movicol given in escalating dose over 1-2 weeks or until impaction resolves
- Stimulant laxative If unsuccessful
What is the maintenance treatment for constipation
Polyethylene glycol for at least 6 months
To ensure regular pain free defecation
Dose reduced in response to improvement in stool consistency and frequency
Management of relapse of constipation
Disimpaction regimen:
Early aggressive and prolonged use of laxatives
Ensure passage of large soft stool once a day
Define Hirschsprung disease
congenital condition characterised by partial or complete colonic functional obstruction associated with Absence of ganglion cells from myenteric and submucosal plexuses
Location of Hirschsprung disease
At rectum and extends proximally
Rectosigmoid - 75%
Entire colon - 10%
Pathophysiology of Hirschsprung disease
Absence of ganglion cells and presence of hypertrophic nerves and increase in acetylcholinesterase
Uncoordinated contraction of affected bowel leads to spasms and tonic contraction
Partial or total functional colonic obstruction
Clinical features of Hirschsprung disease
Neonate:
failure to pass meconium first 24 hrs, distension, bilious vomiting
Explosive passage of liquid stools on PR exam
Hirschsprung enterocolitis
Childhood:
profound chronic constipation, distension, growth failure
Investigations for Hirschsprung disease
AXR - colonic distension
Contrast enema - non-distended aganglionic portion, distended proximal Bowel
Diagnosis of Hirschsprung disease
Suction rectal biopsy - absence of ganglion cells + presence of large acetylcholinesterase-positive nerve trunks
Management of Hirschsprung disease
Initial colostomy and anastamosis of normally innervated bowel to anus
