Paeds - Gastroenterology (textbook) Flashcards
What are some “red flag” clinical features in a vomiting child?
- Bilious vomiting = intestinal obstruction
- Haematemesis = oesophagitis, peptic ulcer, oral/nasal bleeding, oesophageal variceal bleeding
- Projectile up to 2 months old = pyloric stenosis
- vomiting after paroxysmal coughing = whooping cough (pertussis)
- Abdo pain/ tenderness
- Abdo distension = obstruction, strangulated inguinal hernia
- Hepatosplenomegaly = CLD, inborn error of metabolism
- Blood in stool = bac gastroenteritis, Cows Milk Protein Allergy
- Severe dehydration/shock = severe gastroenteritis, systemic infection (eg. UTI, meningitis), DKA
- Bulging fontanelle/ seizures = Raised ICP
- Faltering growth = GORD, Coeliac, etc
- Chronic diarrhoea = cows milk protein allergy
- With or At risk of atopy = CMPA
Why is GORD common in infancy?
It is the involuntary passage of gastric contents into the oesophagus.
Caused in infants by inappropriate relaxation of the LOS as a result of functional immaturity, predominantly fluid diet, mainly horizontal posture, and short intra-abdo length of oesophagus.
What are some complications children with GORD can experience?
- faltering growth from severe vomiting
- oesophagitis (haematemesis, discomfort on feeding, heartburn, iron deficiency anaemia)
- Recurrent pulmonary aspiration (recurrent pneumonia, cough or wheeze, apnoea in preterm infants)
- Dystonic neck posturing (Sandifer syndrome)
How would you investigate GORD in children?
- 24 hour oesophageal pH monitioring to quantify degree of acid reflux
- Endoscopy with oesophageal biopsies to exclude other causes eg. oesophagitis
How would you decide who to refer with suspected GORD in children?
Refer for same day admission:
- haematemesis
- Melaena
- Dysphagia
Refer for speciliast asessment
- faltering growth
- unexplained distress
- GORD symptoms not responding to medical treatment
- unexplained iron deficiency anaemia
- No improvement in regurg after 1 year of age
- Suspected Sandifer’s syndrome (episodic torticollis + neck extension and rotation)
How would you manage a child with GORD
- breastfed infants = trial 1-2 week alginate therapy like Gaviscon
- then trial 4 weeks of PPI (omeprazole) or Histamine-2 Receptor Antagonist (Oral Ranitidine)
- formula fed infants =
- 1st = reduce the vol of feeds if they are excessive
- 2nd = trial 1-2 weeks of smaller more freq feeds
- 3rd = trial 1-2 weeks of feed thickeners like pre-thickened formula or adding thickener (Carobel)
- 4th = trial 1-2 weeks of alginate therapy added to formula
- 5th = trial 4 weeks of PPI or H2RA
- Children 1-2 years old = trial 4 weeks PPI or H2RA
Surgical = for complications unresponsive to medications or oesophgeal strictures
- Nissen Fundoplication either lap or abdo
What is pyloric stenosis?
Hypertorphy of the pyloric muscle, causing gastric outlet obstruction
How would pyloric stenosis present? (clinical and exam)
Clinical features
- hypochloraemic hypokalaemic metabolic alkalosis as a result of vomiting
- Vomiting which increases in freq and forcefulness over time, eventually projectile
- Hunger after vomiting until dehydration results in loss of interest in feeding
- weight loss
- not bilious
Exam
- Test feed is given to allow examination
- Gastric peristalsis from left to right across abdo
- Pyloric mass (feels like an olive) can be palpated in RUQ
- classical “scaphoid abdomen” due to weightloss
How would you manage pyloric stenosis?
Try investigating with an USS or Barium Meal.
Correct fluids and electrolyte disturbance with IV fluids
Definitive treatment = pyloromyotomy
Post op = child can be fed within 6 hours, discharged within 2 days
What are some features that would make you think - abdominal migraine?
- Recurrent abdo pain
- abdo pain in addition to headaches (abdo pain can predominate)
- midline pain + vomiting + facial pallor
- fhx migraines
- anti-migraine medication can benefit
How would you test for HPylori?
- Urea (13C) breath test
- Do not test within 4 weeks of treatment with an antibacterial or within 2 weeks of an antisecretory drug.
- Stool Helicobacter Antigen Test
- Serology tests
How would you manage peptic ulceration in children?
- PPI (eg. omeprazole)
- If investigations indicate H Pylori infection give eradication therapy:
- amoxicillin + metronidazole OR clarithromycin for 1 week
If unresponsive to treatment, do an upper GI endoscopy.
If normal, diagnose functional dyspepsia.
What is the typical clinical picture of gastroenteritis?
- sudden change to loose or watery stools
- vomiting
- contact with person with D/V or recent travel abroad
What are some common causes of gastroenteritis?
(Infective vomiting and diarrhoea)
- Commonly rotavirus, adenovirus, norovirus, etc.
- Bacterial suggested by blood in stools
- Campylobacter jejuni = severe abdo pain
- Shigella or salmonella = blood and pus in stool, pain, tenesmus. Shigella has high fever
- Cholera or EColi = profuse diarrhoea
- Parasite = Giardia or Cryptosporidium
What is the biggest danger in gastroenteritis and why are infants at risk
DEHYDRATION leading to shock
- Red flag symptoms to identify progression to shock =
- appears unwell, unresponsive, lethargic, sunken eyes, tahcycardia, tachypnoea, Reduced skin turgor
- infants have greater surface area to weight ratio
- higher basal fluid requirements
- immature renal tubular reabsorption
- unable to obtain fluids for themselves when thirsty
Give FLUIDS!!!!! but beware of hypernatraemic dehydration
(go slow or pontine myelinolysis)
What is coeliac disease?
Gliadin fraction of gluten provokes a damaging immunological response in the proximal small intestinal mucosa.
What is the classical presentation of coeliac disease?
Either Profound malabsorptive syndrome at 8-24 months of age after introduction of wheat containing weaning foods
- poor growth
- abdo distension
- buttock wasting
- abnormal stools
OR less acutely later in childhood
- non specific GI symptoms
- anaemia (iron/ folate deficiency)
- poor growth
- typically 1st degree relative with coeliac
- at risk kids are screened (T1DM, Autoimmune thyroid disease, Down syndrome)
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How would you investigate coeliac disease
- anti-tTG (Immunoglobulin A tissue transglutaminase antibodies) serological screening
- anti-EMA (anti-endomysial antibodies)
- Usually if these 2 are strongly positive, biopsy may be unnecessary and a gluten free diet can just be trialled
- Otherwise jejunal biopsy (while on gluten diet) is gold standard
- Check IgA levels
- Mucosal changes on s intestinal biopsy performed in endoscopy
- increased intraepithelial lymphocytes
- variable degree of villous atrophy and crypt hypertrophy
What are some clinical features of Crohns disease in kids?
- growth failure, delayed puberty
- Classical presentatiln = Abdo pain + Diarrhoea + Weight loss
- Extraintestinal = oral lesions, perianal skin tags, uveitis, arthralgia, erythema nodosum
What is Crohns disease?
- Transmural inflammation
- commonly affects distal ileum and proximal colon
- strictures of the bowel and fistulae can form between adjacent loops of bowel, skin, organs, etc.
How is Crohns disease investigated and diagnosed?
- Upper GI endoscopy
- Ileocolonoscopy
- Small bowel imaging
- narrowing, fissuring, mucosal irregularities, bowel wall thickening
- Histology = non-caseating epithelioid cell granulomata
- CRP and ESR can be raised in active inflammation
- Serum ferritin, vit B12, folate, vit D can be low due to malabsorption
- Coeliac serology to rule it out
- Stool Microscopy and Culture to rule out infective gastroenteritis
- Faecal calprotectin (raised in IBD. IBS has normal values)
How would you manage Crohns disease?
Induce Remission:
- nutritional therapy for 6-8 weeks
- normal diet replaced with whole protein modular feeds (polymeric diet)
- Systemic steroids (eg. prednisolone) if ineffective
Maintain Remission:
- immunosuppressants like azathioprine, mercaptopurine or methotrexate
- can trial antitumour necrosis factor agents like infliximab or adalimumab
- Supplemental enteral nutrition (eg. overnight NG or gastrostomy feeds) to correct growth failure
- Surgery for complications eg. obstruction, fistulae, abscess
What is Ulcerative Colitis?
- inflammatory and ulcerating disease involving the mucosa of the colon
What is a typical clinical presentation of UC?
- Rectal Bleeding + Diarrhoea + Colicky pain
- weight loss and growth failure less freq than Crohns
- Extra-intestinal = erythema nodosum and arthritis
How would you diagnose UC?
- Endoscopy (Upper GI and ileocolonoscopy)
- Histological = mucosal inflammation, crypt damage (abscess, loss, cryptitis), ulceration
How would you manage UC?
Mild
- aminosalicylates (eg. mesalazine) for induction and maintenance
confined to Rectum and sigmoid colon
- topical steroids eg. budesonide
Aggressive or extensive disease
- systemic steroids (eg. prednisolone) for acute exacerbations
- immunomodulators (eg azathioprine) to maintain remission
- can combine with low dose corticosteroids
- Trial Infliximab or Ciclosporin for resistant disease
Surgery for severe fulminating disease
Regular colonoscopic screening after 10 years from diagnosis due to increased incidence of adenocarcinoma of the colon
What are some red flag symptoms for a child that presents with constipation?
- Failure to mass meconium within first 24 hours = Hirschsprung
- Faltering growth = HypoThyroid, coeliac, etc
- Abdo distension = Hirschsprung, GI dysmotility
- Abnormal lower limb neurology or deformity (eg urinary incontinence) = Lumbosacral pathology
- Abnormal anorectal anatomy
- Perianal bruising or multiple fissures = sexual abuse
- Perianal fistulae, abscess, fissures = perianal crohns disease
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How would you generally manage constipation in a child?
- encourage good toileting habits, bowel habit diary, use of encouragement and rewards systems
- ensure adequate oral fluid intake
- lifestyle = high fibre, daily physical activity
- Coeliac screen and TFTs
Treat Impaction
- Oral laxative regimen and review in 1 week
- 1st line = Macragol
- If unresponsive in 2 weeks, add stimulant laxative (eg. Senna or sodium picosulphate)
If impaction is treated or not present
- Maintenance laxative treatment
- 1st line = Macragol
- Add Stimulant laxative like senna if constipation persists
SE = if diarrhoea occurs, reduce laxatives as prolonged diarrhoea can cause hypokalaemia.
Ensure child has easy access to toilet as disimapction can initially increase symptoms of soiling and abdo pain.
What are some common surgical causes of acute abdominal pain?
- acute appendicitis
- intestinal obstruction eg. intussusception
- Inguinal hernia
- Peritonitis
- Inflamed Meckel Diverticulum
- Pancreatitis
- Trauma
What is biliary atresia?
It is when there is progressive fibrosis and obliteration of the extrahepatic and intrahepatic biliary tree.
How would biliary atresia present?
- mild jaundice
- pale stools (become paler as disease progresses)
- normal birthweight followed by faltering growth
- Hepatomegaly often present initially
- Splenomegaly develops due to portal HTN
- Eventual Chronic Liver Failure and death within 2 years
How would you investigate biliary atresia?
- abnormal LFTs with raised conjugated bilirubin
- Fasting abdo US may show contracted or absent Gallbladder
- Confirmed with cholangiogram (Endoscopic Retrograde Cholangiopancreatography or Operative)
- will fail to outline a normal biliary tree
- Liver biopsy initally shows neonatal hepatitis
- features of extrahepatic biliary obstruction will develop
How would you treat biliary atresia?
- Palliative surgery = Kasai Hepatoportoenterostomy
- if unsuccessful, consider liver transplant
- Nutrition and fat soluble vitamin supplementation
How would an acute viral hepatitis present?
- nausea, vomiting
- abdo pain
- lethargy
- jaundice sometimes
- large tender liver
- 30% have splenomegaly
- LFTs elevated
- Normal coagulation
How would you diagnose Hepatitis A?
Detection of the IgM antibody to the virus
How is hepatitis B spread?
- perinatal transmission from carrier mothers
- inoculation with infected blood via blood transfusion, needlestick injuries, renal dialysis
- sexually transmitted among adults through body fluids
How would you test for Hep B?
- HBV antigens and antibodies
- anti-HBc are positive in acute infection (these are the IgM antibodies)
- HbsAg (Hepatitis B surface antigen) are positive in ongoing infectivity
How would you manage Chronic Hep B and prevent the spread?
30%-50% asymptomatic carrier children will develop chronic HBV liver disease, which progresses to cirrhosis in 10%.
(monitor risk of hepatocellular carcinoma with AFP and Liver US)
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Symptom control in adults
- paracetamol/ ibuprofen for pain relief
- metoclopramide or cyclizine for nausea in mild liver impairment
- chlorphenamine or ursodeoxycolic acid for itch
Management
- Interferon or pegylated interferon
- Or oral antivirals eg. lamivudine and adefovir
Prevention of spread
- antenatal screening for HBsAg in all pregnant women
- All babies from HbsAg +ve women are given Hep B Vaccine
- also give Hep B Immunoglobulin if mother is also HBeAg +ve
- Vaccinate other members of the family too
How is Hep C Spread?
- Post-transfusion hepatitis from donor blood before 1991
- Intravenous Drug Users
- Vertical Transmission most common cause to children
How would you manage Hep C?
(Almost always chronic carriers, rarely an acute infection)
- Combination of pegylated interferon and ribavirin
- Monitor for cirrhosis and hepatocellular carcinoma risk
How does hepatitis D work?
Hep D is a defective RNA virus that needs Hep B virus for replication.
Only occurs in coinfection with Hep B or can cause an acute exacerbation in someone with a chronic hep B infection.
Chronic HDV has a 70% chance of developing to cirrhosis
How is Hep E transmitted?
- enterally transmitted, usually by contaminated water
- known to be transmitted by blood transfusion or eating infected pork
How does acute liver failure happen in kids?
- development of massive hepatic necrosis and loss of liver function
- Can present within hours-weeks with jaundice, encephalopathy, coagulopathy, hypoglycaemia, electorlyte disturbance
- mostly due to metabolic or infective conditions.
- can also have hepatic encephalopathy
- early signs = periods of irritability, confusion, drowsiness
What are some common causes of acute liver failure in children below and above 2 years old?
Below 2 years old
- infection eg. herpes simplex
- Metabolic disease (Galactosemia, Fatty Acid Oxidation Defect, Tyrosinemia etc)
- Seronegative hepatitis
- Drug induced
- Neonatal haemochromatosis
Above 2 years old
- Seronegative hepatitis
- Paracetamol overdose
- Mitochondrial disease
- Wilsons Disease
- Autoimmune hepatitis
How would you diagnose acute liver failure in children?
- Transaminases are hugely elevated (10-100x)
- Alkaline Phosphatase is increased
- Coagulation is abnormal
- Plasma ammonia is elevated
- EEG can show hepatic encephalopathy
- CT can show cerebral oedema (a complication)
- other complications = haemorrhage from gastritis or coagulopathy, sepsis, pancreatitis
How would you manage acute liver failure?
- early referral to national paediatric liver centre
- Stabilise the child prior to transfer
- IV dextrose to maintain blood glucose >4mmol/L
- Broad spec antibiotics to prevent sepsis
- IV Vitamin K to prevent haemorrhage
- H2 blockers or PPIs to prevent haemorrhage from GI tract
- Fluid restriction to prevent cerebral oedema
- Mannitol diuresis if oedema develops
What are some common causes of chronic liver disease in older children?
- Postviral Hepatitis B or C
- Autoimmune hepatitis (and sclerosing cholangitis)
- Non alcoholic fatty liver disease
- Drug induced liver disease (NSAIDs)
- Cystic Fibrosis
- a1-antitrypsin deficiency
- Fibropolycystic liver disease
- Wilsons disease should always be excluded
How would autoimmune hepatitis (and sclerosing cholangitis) present, be diagnosed, and be treated?
Presentation
- acute hepatitis/ fulminant hepatic failure/ CLD with autoimmune features (skin rash, arthritis, haemolytic anaemia, nephritis)
Diagnosis
- elevated total protein (= inflammation or infection like hep)
- hypergammaglobulinaemia (= commonly seen in CLD)
- best diagnostic marker for AIH is elevated levels of serum immunoglobulin G (IgG)
- positive autoantibodies (eg. ANA)
- low serum complement (low levels of C4)
Management
- AIH = Prednisolone and azathioprine
- Sclerosing cholangitis = ursodeosycholic acid
What is Wilsons disease and how does it present?
- autosomal recessive disorder
- reduced synthesis of caeruloplasmin (copper binding protein)
- defective excretion of copper in bile = accumulation of copper in liver, brain, kidney, cornea
Presentation
- childhood = hepatic presentation eg. acute hepatitis, fulminant hepatitis, cirrhosis, portal HTN
- >7 years old Copper accumulation in cornea (Kayser-Fleischer rings)
- >20 years old = neuropsychiatric features (mood change, behaviour change, extrapyramidal signs eg. incoordination, tremor, dysarthria)
- Renal tubular dysfunction
- Vit D resistant rickets
- Haemolytic anaemia
How would you diagnose and manage Wilsons disease?
Investigations
- low serum caeruloplasmin and copper
- Urinary copper excretion is increased (further increases after adminstering penicillamine)
- Diagnostic = elevated hepatic copper on liver biopsy OR identification of gene mutation
Management
- Penicillamine or trientine (promote urinary copper excretion)
- Zinc reduces copper absorption
- Pyridoxine prevents peripheral neuropathy
How would you generally manage the complications of chronic liver disease?
- Fat malabsorption
- Fat soluble vitamins (K, A, E, D) should be given orally
- Protein malnutrition due to poor intake & high catabolic rate of diseased liver
- do not restrict protein intake unless child is encephalopathic
- Severe Pruritus is associated with cholestasis
- loose cotton clothing, avoid overheating, keep nails short
- moisturising skin with emollients
- Drugs =
- phenobarbital to stimulate bile flow
- Cholestyramine to absorb bile salts
- Ursodeoxycholic acid
- Rifampicin
- Encephalopathy
- oral lactulose can help reduce ammonia
What is cirrhosis?
Extensive fibrosis with regenerative nodules.
Results in diminished hepatic function and portal HTN with splenomegaly, varices, ascites.
What are some signs of cirrhosis and why may it not be obvious until later?
Sometimes in compensated cirrhosis children may be asymptomatic if liver function is adequate.
Eventually due to increasing cirrhosis, deteriorating liver function and increasing portal HTN become obvious.
Physical signs:
- jaundice
- palmar/ plantar erythema
- telangiectasia
- spider naevi
- malnutrition
- hypotonia
- dilated abdo veins and splenomegaly suggest portal HTN
- liver can be shrunken and impalpable
How would you investigate cirrhosis?
- screening for known causes
- upper GI endoscopy to detect oesophageal varices or erosive gastritis
- Abdo US = shrunken liver and splenomegaly with gastric and oesophageal varices
- Liver biopsy can indicate aetiology eg. copper storage
- LFTs (elevated AST and ALP, plasma albumin falls, prothrombin time becomes prolonged)
Pathophysiology of oesophageal varices and how you manage them.
- consequence of portal HTN
- Diagnosis = gastrointestinal endoscopy
Management
- acute bleeding = blood transfusions, H2 blockers (eg. ranitidine) or omeprazole
- persistent bleeding = octreotide infusion, vasopressin analogues, endoscopic band ligation, sclerotherapy
- Surgery = portacaval shunts are a temporary measure while considering liver transplantation
How would you manage ascites in cirrhosis?
- sodium and fluid restriction
- Diuretics
- Refractory ascites = try albumin infusions or paracentesis
What is spontaneous bacterial peritonitis what would you do?
- an infection of the ascitic fluid that cannot be attributed to any intra-abdo, ongoing, inflammatory, or surgically correctable condition
- Suspect it in undiagnosed fever, abdo pain, tenderness, vomiting, altered mental status, GI bleeding, unexplained deterioration in hepatic/renal function
- Do a diagnostic paracentesis
- Defined as an ascitic fluid absolute neutrophil count >250cells/mm3
- Treat with broad spectrum antibiotics
A kid comes in with a rash, low grade fever, and abdo pain. He has bloody diarrhoea and swollen painful joints.
He has a hx of a past strep infection.
What do you suspect?
Henoch-Schonlein Purpura
- it is a small vessel vasculitis
- typically post streptococcal infection eg. Group A Strep, EBV
- Starts with a low grade fever and abdo pain, then purpuric rash.
- Can have blood diarrhoea and swollen painful joints
- The rash is macular but progresses to papaulae in the classic buttock and back of leg location
- Renal involvement
How would a congenital diaphragmatic hernia present?
Herniation of abdo viscera into chest due to incomplete formation of diaphragm
- scaphoid abdo due to herniation of abdo contents into cleft
- classical concave abdo appearance
- dyspnoea and tachypnoea
- reduced breath sounds bilaterally due to pulmonary hypoplasia and compression of lungs due to abdo contents
Most common is the L sided posterolateral Bochdalek hernia
