GASTROENTEROLOGY PAEDS Flashcards
Medical differentials for abdo pain in children
Constipation UTI, pyelonephritis, hydonephrosis, renal calculus DKA Coeliac IBD, IBS Mesenteric adenitis Henoch-schonlein purpura Infantile colic Gynae in pubertal females Sickle cell Etc.
Surgical differentials for abdominal pain
Acute appendicitis Intussusception Bowel obstruction Testicular torsion Inflamed meckles diverticulum
RED FLAGS for abdominal pain
Persistent or bilious vomiting Severe chronic diarrhoea Fever Rectal bleeding Weight loss/faltering growth Dysphagia Nighttime pain Abdominal tenderness
What is abdominal migraine?
Central abdo pain lasting more than 1 hour
Normal examination
May be Associated with: N&V, Anorexia, Pallor, Headache, Photophobia, Aura
Treating abdominal migraine
Similar to typical migraine
Treating attack: Low stimulus environment, ibuprofen, SUMATRIPTAN, PARACETAMOL
Preventative (started by specialist) PIZOTIFEN (serotonin agonist)
Other preventative (less commonly used): PROPRANOLOL (non-selective beta-blocker), FLUNARAZINE (ca channel blocker), CYPROHEPTADINE (antihistamine)
Causes of constipation in paeds
Idiopathic/functional
Secondary causes: Hirschsprung’s disease, cystic fibrosis, hypothyroidism, coeliac
What is Desensitisation of the rectum ?
Poor bowel habits + ignoring the sensation of a full rectum —> loss of sensation —> less frequent opening of bowels —> faecal impaction —> further desensitisation of rectum from stretching
Constipation red flags
Not passing meconium within 48hrs of birth (Hirschsprung’s, CF)
Neurological signs or symptoms (Cerebral palsy, spinal cord lesion)
Vomiting (obstruction, Hirschsprung’s)
Ribbon stool (Anal stenosis)
Abnormal anus (anal stenosis, IBD, Sexual abuse)
Abnormal lower back or buttocks (Spina bifida, spinal cord lesion etc.)
Acute severe abdo pain and bloating (obstruction or intussusception)
Complications of constipation
Pain Reduced sensation Anal fissures Haemorrhoids Overflow and soiling Psychosocial morbidity
Management of constipation
- Correct any reversible contributing factors (Diet, hydration)
- Start laxatives (MOVICOL first line)
- Faecal impaction may require disimpaction regime + high dose laxatives
- Encourage and praise visiting toilet - scheduling visits, bowel diary, star charts
Laxatives continued long term and slowly weaned off
What is Hirschsprung’s disease?
Congenital condition - nerve cells of the myenteric plexus are absent in the distal bowel and rectum
Forms part of the enteric nervous system - the brain of the gut and responsible for stimulating peristalsis of the large bowel.
ABSENCE OF PARASYMPATHETIC GANGLION CELLS - severity varies as could be small amount of colon or the full length
Hirschsprung’s disease: Presentation
Can present as acute intestinal obstruction shortly after birth, or more gradually developing symptoms such as:
- Delay in passing meconium (>24hrs)
- chronic constipation from birth
- abdo pain and distension
- vomiting
- poor weight gain and failure to thrive
Hirschsprung-associated enterocolitis (HAEC)
Inflammation and obstruction of instestimes in neonates with Hirschsprung’s
Typically presents in first 2-4 weeks of life
Fever, abdo distension, diarrhoea, features of sepsis
LIFE THREATENING - can lead to toxic mega colon and perforation of the bowel
Management of Hirschsprung-associated enterocolitis
Urgent antibiotics, fluid resuscitation and decompression of the bowel
Management of Hirschsprung’s disease
ABDO X-RAY - identify intestinal obstruction / features of HAEC
RECTAL BIOPSY - confirm diagnosis (absence of ganglion)
FLUID RESUSCITATION and MANAGEMENT OF OBSTRUCTION
Definitive management: SURGICAL REMOVAL OF AGANGLIONIC SECTION OF THE BOWEL
Signs of problematic gastro-oesophageal reflux
Chronic cough Hoarse voice Distress/crying or unsettled after feeding Reluctance to feed Pneumonia Poor weight gain
GOR - Red Flags
Not keeping down any feed (Pyloric stenosis, intestinal obstruction)
Projectile or forceful vomiting (Pyloric stenosis, intestinal obstruction)
Bile stained vomit (Intestinal obstruction)
Reduced consciousness, bulging fontanelle, neurological signs (Meningitis, RICP)
Resp symptoms (Aspiration, infection)
Blood in stools (gastroenteritis, cows milk protein allergy)
Signs of infection
Rash, angiooedema, and other signs of allergy (Cow’s milk protein allergy)
Apnoeas
GOR: Management
Small frequent meals
Burping regularly to help milk settle
Not over-feeding
Keeping baby upright after feeding
Gaviscon mixed with feeds
Thickened milk/formula (Anti-reflux)
Ranitidine
Omeprazole where ranitidine is inadequate
Where is the pyloric sphincter
Ring of smooth muscle that forms the canal between the stomach and the duodenum
What is pyloric stenosis?
Hypertrophy (therefore narrowing) of the pylorus
Prevents food travelling from the stomach to the duodenum as normal
After feeding there is powerful peristalsis in the stomach - becomes to powerful it ejects the food into the oesophageal and out the mouth - PROJECTILE VOMITING
Pyloric stenosis characteristics
First few weeks of life
Baby - hungry, thin, pale, failing to thrive
Projectile vomiting
Peristalsis can sometimes be seen on examination
Upper abdo: firm round mass (feels like a large olive)
Blood gas: hypochloric METABOLIC ALKALOSIS (baby vomiting hyperchloric acid)
Pyloric stenosis: diagnosis
ABDO ULTRASOUND
Pyloric stenosis: treatment
Laparoscopic pyloromyotomy
- incision made into muscle to widen canal
Define acute gastritis
Inflammation of stomach
Nausea & Vomiting
Define Enteritis
Inflammation of intestines
Diarrhoea
Define Gastroenteritis
Inflammation all the way from the stomach to the intestines
Nausea, vomiting, and diarrhoea
Key conditions to consider if child presents with LOOSE STOOLS
INFECTION (gastroenteritis) IBD LACTOSE INTOLERANCE COELIAC DISEASE CYSTIC FIBROSIS IBS MEDICATIONS
Most common causative agents of gastroenteritis
VIRAL most common - Rotavirus - Norovirus - Less common: adenovirus Others: Bacterial - E. Coli, campylobacter Jejuni, shigella, salmonella, bacillus cereus, staphylococcus aureus toxin, giardiasis
Why should antibiotics be avoided in E.Coli gastroenteritis?
Increases the risk of HAEMOLYTIC URAEMIC SYNDROME
- E. Coli produces the Shiga toxin which destroys blood cells and leads to HUS
Coeliac disease: IgA Antibodies
Anti-tissue transglutinase (anti-TTG)
Anti-endomysial (anti-EMA)
Coeliac diease: Presentation
Often Asymptomatic- low threshold for testing Failure to thrive Diarrhoea Fatigue Weight loss Mouth ulcers Anaemia secondary to iron, B12 or folate deficiency Dermatitis herpetiformis
What conditions are often linked to coeliac disease
Type 1 diabetes Thyroid disease Autoimmune hepatitis Primary biliary cirrhosis Primary sclerosing cholangitis Down’s syndrome
Coeliac disease: Genetic association
HLA-DQ2 gene (90%)
Coeliac disease: Diagnosis
Pt. Must remain on diet containing gluten !
Check total IgA levels (to exclude a deficiency)
Check coeliac specific antibodies (Anti-TTG, Anti-EMA)
Endoscopy and intestinal biopsy (Crypt hypertrophy, Villious atrophy)
Complications of untreated coeliac disease
Vitamin deficiency Anaemia Osteoporosis Ulcerative jejunitis Enteropathy-associated T-cell lymphoma of the intestine Non-Hodgkin Lymphoma Small bowel adenocardinoma (rare)
Features of Crohn’s disease (NESTTS)
N - No blood or mucus (less common in crohns)
E - Entire GI tract
S - Skip lesions (on endoscopy)
T - Terminal ilium most affected
T - Transmural (full thickness) inflammation
S - Smoking is a risk factor (Don’t set the NEST on fire!)
Ulcerative colitis characteristics (U-C- CLOSEUP)
C - Continuous inflammation L- Limited to colon or rectum O - Only superficial mucosa affected S - Smoking is preventative E - Excrete blood and mucus U - Use AMINOSALICYLATES P - Primary sclerosing cholangitis
Extra-intestinal manifestations of IBD
Finger clubbing Erythema nodosum Pyoderma gangrenous Episcleritis and iritis Inflammatory arthritis Primary sclerosing cholangitis (UC)
IBD: Investigations
Blood tests: Anaemia, infection, thyroid, kidney, LFT
FAECAL CALPROTECTIN - released by intestines when inflamed (more sensitive and specific in adults
Endoscopy (ODG and colonoscopy) with biopsy - gold standard
Imaging (Ultrasound, CT and MRI) - to look for any complications
Crohns: Management - inducing remission
STEROIDS
Enteral nutrition: alternative to steroids in children where there are concerns about growth or side effects (taken orally, via NG tube, ND tube or NJ tube, or gastronomy)
If steroids don’t work alone —> immunosuppressant medication can be given: Azathioprine, infliximab, mercaptopurine, methotrexate, adalimumab
Crohns: management - maintaining remission
Treatment tailored to individual patients
First line: Azathioprine, mercaptopurine
Alternatives: Methotrexate, infliximab, Adalimumab
Crohns: Managment - surgery
If disease only affects distal ilium - possible to resect the area to prevent flares
Crohns typically affects entire GI tract - surgery used to treat strictures and fistulas secondary to the disease
UC: Management - inducing remission
Mild to mod disease:
1st line: AMINOSALICYLATE ( e.g. mesalazine oral or rectal)
2nd line: CORTICOSTEROIDS (e.g. prednisolone)
Severe disease:
1st line: IV CORTICOSTEROIDS (e.g. hydrocortisone)
2nd line: IV CICLOSPORIN
UC: management - maintaining remission
AMINOSALICYLATE (e.g. mesalazine oral or rectal)
AZATHIOPRINE
MERCAPTOPURINE
UC: Management - surgery
UC only affects colon and rectum
Removing colon and rectum (panproctocolectomy) - removes disease
Permanent iliostomy or ilio-anal anastomosis (J-pouch)
What is biliary atresia?
Congential condition
Bile duct narrowed or absent —> cholestasis (bile cannot be transported from liver to bowel
Unconjugated bilirubin therefore cant be excreted
Biliary atresia: Presentation
Significant jaundice shortly after birth - HIGH LEVELS OF CONJUGATED BILIRUBIN
Suspect biliary atresia in babies with PERSISTANT JAUNDICE - lasting more than 14 days in term babies, and more than 21 days in pre-term babies
Biliary atresia: Management
KASI PORTOENTEROSOMY
- attach a section of the small intestine to the opening of the liver (where the bile duct usually attaches)
Patients often require a full liver transplant to resolve the problem
Causes of intestinal obstruction
Meconium Ileus Hirschsprung’s disease Oesophageal atresia Duodenal atresia Intussusception Imperforate anus Mallo at ion of the intestines with a volvulus Strangulated hernia
What is Intussusception
The bowel invaginates/ telescopes into itself
Thickens the overal size of the bowel and narrows lumen in the folded areas
What conditions are Intussusception associated with ?
Concurrent viral illness Henoch-Schonlein Purpura Cystic fibrosis Intestinal polyps Meckles diverticulum
Intussusception presentation
Severe colicky abdo pain Pale, lethargic and unwell child REDCURRENT JELLY STOOL RUQ mass on palpating (sausage shaped) Vomiting Intestinal obstruction
Intussusception diagnosis
USS and contrast enema
Intussusception management
THERAPEUTIC ENEMAS - force folded bowel back into right position
SURGICAL RESECTION - may be needed in enema doesn’t work, or if the bowel becomes gangrenous or perforated
Peak incidence of appendicitis
Age 10-20
Classic features of appendicitis
Central abdo pain that moves down to the RIF overtime and eventually becomes localised in the RIF
Tenderness at McBurney’s point (1/3 distance from ASIS to umbilicus)
Other features:
Anorexia, N&V, Rovsing’s sign (Palpation on LIF causes pain in RIF), Guarding on abdo palpation, Rebound tenderness, percussion tenderness (these 2 types of tenderness suggest peritonitis)
