Gastroenterology Flashcards
Non-organic/ functional abdominal pain
Very common in over 5
No disease process can be found to explain the pain
Medical causes of abdominal pain
Constipation is very common UTI Coeliac disease IBD IBS Mesenteric adenitis Abdominal migraine Pyelonephritis Henoch-Schonlein purpura Tonsilitis DKA Infantile colic
Causes of abdominal pain in adolescent girls
Dysmenorrhea (period pain) Mittelschmerz (ovulation pain) Ectopic pregnancy PID Ovarian torsion Pregnancy
Surgical causes of abdominal pain
Appendicitis: central abdo pain-> RIF
Intussusception: red jelly stools, colicky non-specific pain
Bowel obstruction: pain, distension, absolute constipation, vomiting
Testicular torsion
Red flags for serious abdominal pain
Persistent or bilious vomiting Severe chronic diarrhoea Fever Rectal bleeding Weight loss or faltering growth Dysphagia Nighttime pain Abdominal tenderness
Abdominal pain investigations
Anaemia: IBD, coeliac disease ESR/CRP: indicates IBD Raised anti-TTG or anti-EMA; coeliac disease Raised faecal calprotectin: IBD Positive urine dipstick: UTI
Recurrent abdominal pain
Repeated episodes of abdominal pain
No identifiable underlying cause
Non-organic/ functional pain
Effects of recurrent abdominal pain
Psychosocial problems
Missed days at school
Parental anxiety
Association of recurrent abdominal pain
Abdominal migraine
IBS
Functional abdominal pain
Causes of recurrent abdominal pain
Stressful life events
Loss of relative or bullying
Inappropriate pain signals from visceral nerve
Management of recurrent abdominal pain
Distract child
Encourage parents to not ask about the pain
Advice about sleep, regular meals, healthy balanced diet, staying hydrated, exercise and reduced stress
Probiotics with IBS
Avoid NSAIDs
Address triggers, psychosocial
Support from school counsellor and child psychologist
Abdominal migraine
Occur in young children before traditional migraines
Episodes of central abdominal pain
Lasting >1hr
Normal examination
Associated features of abdominal migraine
N/V Anorexia Pallor Headache Photophobia Aura
Management of acute abdominal migraine
Low stimulus environment (quiet, dark room)
Paracetamol
Ibuprofen
Sumatriptan
Medications to prevent abdominal migraine
Pizotifen, serotonin agonist
Propanolol
Cyproheptadine: antihistamine
Flunarazine: CCB
Pizotifen for abdominal migraine
Main preventative measure
Needs to be withdrawn slowly
Withdrawal symptoms; depression, anxiety, poor sleep and tremor
Secondary causes of constipation
Hirschsprung’s disease
CF
Hypothyroidism
Features in history and examination
Constipation
<3 stools/week Hard stools are difficult to pass Rabbit dropping stools Straining and passage of stools Abdominal pain Retentive posturing Rectal bleeding Overflow soiling from faecal impaction, incontinence of loose smelly stools Hard stools palpable in abdomen Loss of sensation of need to open the bowel
Encopresis
Faecal incontinence
Not pathological in <4
Chronic constipation-> rectum stretched and lose sensation
Loose stools bypass blockage of hard stools, soiling
Causes of encoparesis
Chronic constipation Spina bifida Hirschsprung’s disease Cerebral palsy Learning disability Psychosocial stress Abuse
Lifestyle factors causing constipation
Habitually not opening bowels Low fibre diet Poor fluid intake and dehydration Sedentary lifestyle Psychosocial problems: safeguarding
Desensitisation of rectum
Develop habit of not opening bowels Ignore sensation of full rectum Over time lose sensation of needing to open bowels Open bowels even less frequently Retain faeces in rectum Faecal impaction Rectum stretches Leads to more desensitisation Need to treat constipation
Secondary causes of constipation
Hirschsprung’s disease CF (meconium ileus) Hypothyroidism Spinal cord lesions Sexual abuse Intestinal obstruction Anal stenosis Cow’s milk intolerance
Constipation red flags
Delayed passing of meconium (>48hrs): CF/ Hirschsprung’s
Neurological signs or symptoms: cerbral palsy, spinal cord lesion
Vomiting; intestinal obstruction, Hirschsprung’s disease
Ribbon stool: anal stenosis
Abnormal anus: anal stenosis, IBD, sexual abuse
Abnormal lower back or buttocks: spina bifida, spinal cord lesion, sacral agenesis
Failure to thrive: coeliac disease, hypothyroidism, safeguarding
Acute severe abdominal 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
High fibre and good hydration
Movicol
Disimpaction regimen for faecal impaction With high laxative dose
Encourage and praise visiting toiletry
Scheduling visits, bowel diary, start charts
Long-term laxative and slowly weaned off
GORD
Contents from stomach reflux through lower oesophageal sphincter into oesophagus, throat and mouth
Babies have an immature LOS, normal to reflux contents
Should be better by 1 year
Regurgitation
Reflux of stomach contents beyond the oesophagus
Epidemiology of GORD
Regurgitation and GORD usually appear in the first 2 weeks of life
Why is tone of LOS too low in infants in GORD
Anatomical and physiological features
Short, narrow oesophagus
Delayed gastric emptying
Shorter, lower oesophageal sphincter that is slightly above the diaphragm
Liquid diet and high calorie requirement, distending the stomach and increasing pressure gradient between stomach and oesophagus
Larger ratio of gastric volume to oesophageal volume
Spending significant periods recumbent
Risk factors for GORD
Prematurity
Parental history of heartburn or acid regurgitation
Obesity
Hiatus hernia
Hx of congenital diaphragmatic hernia (repaired)
Hx of congenital oesophageal atresia
Neurodisability (cerebral palsy)
History of GORD
Distressed behaviour: excessive crying, unusual neck posture, back arching
Unexplained feeding difficulties: refusing feeds, gagging, choking
Hoarseness and/or chronic cough in children
Single episode of pneumonia
Faltering growth
Retrosternal/ epigastric pain
Feeding history
Feeding history GORD
Position, attachment, technique, duration, frequency, type of milk
Calculate volume of milk being given: can be over-fed and have gastric over-distension
Frequency and volume of vomits
Relationship of symptoms to feeds
Examination of GORD
Hydration status
Signs of malnutrition
Abnormalities indicating DD
Assess growth charts
GORD dd
Pyloric stenosis Intestinal obstruction Any acute surgical abdominal issue Upper GI bleed: haematemesis Sepsis RICP Bacterial gastroenteritis, cows milk protein allergy Chronic diarrhoea UTI If onset >6 months of age or if symptoms persist beyond 1 year then reflux is unlikely
Investigations GORD
Not needed to diagnosis
Barium swallow
Ph study
Endoscopy
Causes of vomiting
Over feeding GORD Pyloric stenosis Gastritis or gastroenteritis Appendicitis Infections such as UTI, tonsilitis or meningitis Intestinal obstruction Bulimia
Management of GORD if breast fed with frequent regurgitation causing marked distress
Self-resolve by 1 year of age
- Use alginate (Gaviscon) mixed with water immediately after feeds for 2 week trial
- Start PPI or histamine antagonist (e.g. omeprazole or ranitidine)
- If symptoms persist refer to paediatrics and reconsider differential diagnosis
Management of GORD in formula-fed with frequent regurgitation causing marked distress
- Ensure infant isn’t over-Fed (<150ml/kg/day)
- Decrease feed volume be increasing frequency (2-3hourly)
- Use feed-thickened (or pre-thickened formula)
- Stop thickener and start alginate added to formula
- Start PPI or histamine antagonist (e.g. omeprazole or ranitidine)
- If symptoms persist refer to paediatrics and reconsider differential diagnosis
Red flags for GOR
Not keeping down any food: pyloric stenosis or intestinal obstruction
Projectile or forceful vomiting: pyloric stenosis or intestinal obstruction
Bile stained vomit: intestinal obstruction
Haematemesis or malaena: peptic ulcer, oesophagitis or varices
Abdominal distension: intestinal obstruction
Reduced consciousness, building fontanelle, neurological sign: meningitis or RICP
Respiratory symptoms: aspiration and infection
Blood in stools: gastroenteritis or Cows milk protein allergy
Signs of infection: pneumonia, UTI, tonsilitis, otitis, meningitis
Rash, angioedema, signs of allergy: cows milk protein allergy
Apnoea
Simple cases of GORD mx
Small, frequent meals
Burping regularly to help milk settle
Not over-feeding
Keep baby upright after feeding
Complex cases of GORD mx
Gaviscon mixed with feeds
Thickened milk or formula
Ranitidine
Omeprazole with ranitidine is inadequate
Barium meal
Endoscopy
Fundoplication
Complications of GORD
90% will resolve in first year: older, more solid diet, more upright
Reflux oesophagitis
Recurrent aspiration pneumonia
Recurrent acute otitis media (>3 episodes in 6 months)
Dental erosion (children with neuro disability)
Apnoea
Apparent life-threatening events: apnoea, colour change, change in muscle tone, choking and gagging
Sandifers syndrome
Brief episodes of abnormal movements
Associated with GORD in infants
Infants usually neurologically normal
Key features of sandifers syndrome
Torticolis: forceful contraction of neck muscles causes twisting of neck
Dystonia: abnormal muscle movements causing twisting movements, arching of back or unusual postures
Self-resolves
DD: infantile spasms and seizures
Epidemiology of gastroenteritis
Common isolates: Rotavirus and Campylobacter
Adenovirus, respiratory infections
Acute gastroenteritis
Inflammation of stomach and intestines
Main concern is dehydration
Viral causes of gastroenteritis
Rotavirus
Norovirus
Adenovirus (less common), more subacute diarrhoea
Highly contagious
When to consider Differential diagnosis of gastroenteritis
Temperature >38 if <3months Temperature >39 of >3 months Breathlessness or tachypnoea Altered GCS Blood/ mucous in stool Bilious vomit Severe/ localised abdominal pain Abdominal distension or guarding
Differential diagnosis of diarrhoea
Infection IBD Lactose intolerance Coeliac disease CF Toddlers diarrhoea IBS Medications
Rotavirus gastroenteritis
Most common cause
<5 years
Uncommon in adults, vaccine given at 8 and 12 weeks
Faecal oral route or by environmental contamination
Incidence peaks over winter months
Norovirus gastroenteritis
Single stranded RNA viruses
Commonest cause of gastroenteritis in all age groups
Faecal oral contamination and environmental contamination
Adenovirus gastroenteritis
Infections of respiratory system
<2 years
E.coli for gastroenteritis
Most strains are harmless
VTEC E.coli 0157:H7 can cause haemorrhagic colitis and haemolytic uraemic syndrome
Spread through contaminated food, person-to-person contact, contact with infected animals
E.coli 0157 produces the Shiga toxin
Shiga toxin
Produced by Ecoli 0157 Abdominal cramps Bloody diarrhoea Vomiting Shiga toxin: destroys blood cells and leads to HUS, ax increases this risk
Campylobacter jejuni
Travellers diarrhoea
Most common cause of bacterial gastroenteritis in the UK
Gram negative bacteria: curved or spiral shape
Campylobacter transmission
Raw or improperly cooked poultry
Untreated water
Unpasteurised milk
Campylobacter incubation
2-5 days
Symptoms resolve after 3-6days
Campylobacter symptoms
Abdominal cramps
Diarrhoea, often with blood
Vomiting
Fever
Campylobacter management
Severe symptoms
Other risk factors: HIV, heart failure
Azithromycin, ciprofloxacin
Clinical features of gastroenteritis
Sudden onset of loose/ watery stool with/without vomiting
Abdominal pain/crams
Mild fever
Recent contact with someone with diarrhoea or vomiting
Which diarrhoea children are more at risk of dehydration
Young children <6 months
Children who have passed >5 diarrhoea stools in last 24hrs
Children who have vomited >2x in last 24 hrs
Children who have stopped breast feeding during illness
Symptoms of dehydration
Appears to be unwell or deteriorating Altered responsiveness Decreased urine output Skin colour unchanged Warm extremities
Symptom of shock
Decreased level of consciousness Pale or mottled skin Cold extremities Decreased urine output Appears to be unwell or deteriorating
Signs of clinical dehydration
Altered responsiveness Skin colour unchanged Warm extremities Sunken eyes Dry mucous membranes Tachycardia Tachypnoea Normal, peripheral pulses Normal CRT Reduced skin turgor Normal blood pressure
Signs of clinical shock
Decreased level of consciousness Pale or mottled skin Cold extremities Sunken eyes Dry mucous membranes Tachycardia Tachypnoea Weak peripheral pulses Prolonged CRT Reduced skin Turgor Hypotension
Investigations for gastroenteritis
Stool sample if:
Septicaemia suspected
Blood and/or mucus in stool
Immunocompromised child
Measure Na, K, Cr, Ur and glucose if:
IV fluids are going to be used
Symptoms/signs of hypernatraemia (jittery, increased muscle tone, hyperreflexia, convulsions, drowsiness or coma)
Measure acid-base status
Chloride concentration
Shock
Management of gastroenteritis
Immediate if not clinically dehydrated
Continue breast feeding/ other milk feeds
Encourage fluid intake
Discourage fruit juices and carbonated drinks
Oral rehydration salt solution as supplemental fluid to those at risk of dehydration
Management of gastroenteritis
Immediate if dehydrated
Use IV therapy if shock is suspected, red flags, evidence of dehydration, vomiting persistently
Oral therapy:
ORS solution: 50mL/kg over 4 hours
Plus maintenance fluid
If child is refusing oral fluid, consider NG tube
Maintenance fluid calculation Childs weight 0-10kg 10-20kg >20kg
0-10kg: 100ml/kg/day
10-20kg: requirement for first 10kg + 50mL/kg/day
>20kg: requirement for first 20kg (1500ml) + 20ml/kg/day
Following rehydration after gastroenteritis
Advise parents to give full strength milk straight away
Slowly re-introduce the child’s solid food
Suggest that fruit juices and carbonated drinks are avoided until the diarrhoea has resolved
Advice on hand washing and avoiding towel sharing
Wait 48hours since last D/V before school
Child shouldn’t swim for 2 weeks after last episode
Complications of gastroenteritis
Haemolytic uraemic syndrome
Reactive complications with bacterial gastroenteritis
Toxic mega colon
Acquired/ secondary lactose intolerance
Diarrhoea lasts 5-7 days
Vomiting lasts 1-2 days
Haemolytic uraemic syndrome (HUS)
Rare but serious complication of acute infectious gastroenteritis that occurs mostly in young children and the elderly.
This can be a life-threatening complication causing:
acute renal failure,
haemolytic anaemia
Reactive complications of bacterial gastroenteritis
Including arthritis, carditis, urticaria, erythema nodosum and conjunctivitis.
REMEMBER: Reiter’s syndrome (the combination of urethritis, arthritis, and uveitis).
Toxic mega colon
Rare but significant complication of rotavirus gastroenteritis
Acquired /secondary lactose intolerance
Occurs due to the lining of the intestine being damaged.
Leads to symptoms of bloating, abdominal pain, wind and watery stools after drinking milk.
Improves when infection resolves and gut lining heals (5).
Gastroenteritis complication
Shigella gastroenteritis
Spread by faces contaminated drinking water, swimming pools and food
Incubation: 1-2days
Symptoms resolve within 1 weeks without treatment
Causes bloody diarrhoea, abdominal cramps and fever
Shiga toxin: HUS
Mx: azithromycin or ciprofloxacin
Salmonella gastroenteritis
Transmission: raw eggs, poultry, faeco-oral
Incubation: 12hrs-3days, symptoms resolve at 1week
Watery diarrhoea associated with mucus or blood, abdominal pain and vomiting
Ax: stool culture and sensitivities
Bacillus cereus gastroenteritis
Gram positive rod Spread through inadequately cooked food Fried rice left out at room temperature Produces toxin:: cereulide Vomiting within 5 hours, diarrhoea within 8 hours, resolution within 24hours
Cereulide
Produced by bacillus cereus
Within 5 hours of ingestion: Causes abdominal cramping and vomiting
8 hours after ingestion: Produces toxins in intestine, watery diarrhoea
Usually all symptoms resolve within 24hours
Yersinia enterocolitis
Gram negative bacillus
Pigs, raw or uncooked pork can cause infection
Also spread through contamination with urine or faeces of other mammals, such as rats and rabbits
Yersinia clinical presentation
Most frequently affects children
Watery or blood diarrhoea, abdominal pain, fever and lymphadenopathy
Incubation 4-7days, illness can last longer that other causes of enteritis
Symptoms lasting 3 week or more
Older children: can present with fever and right sided abdominal pain due to Mesenteric lymphadenitis
Impression of appendicitis
Staphylococcus aureus toxin
S.aureus produces enterotoxin when growing on eggs, dairy and meat
Small intestine inflammation
Symptoms: diarrhoea, perfuse vomiting, abdominal cramps and fever
Symptoms start within hours of ingestion
Settle within 12-24hours
Enterotoxin causes enteritis
Giardiasis
Giardia lambia Parasite Small intestines of mammals Releases cysts, Falcon oral Diagnosis with stool microscopy Metronidazole
Principles of gastroenteritis management
Good hygiene
Isolate patients
Barrier nursing and rigorous infection control
No school for 48hrs after symptoms have resolved
Faecal sample: microscopy, culture and sensitivities
Attempt fluid challenged
Diorylate rehdration fluid
Complications post-gastroenteritis
Lactose intolerance
IBS
Reactive arthritis
Guillian-Barre syndrome
Coeliac disease
Autoimmune condition
Gluten causes an immune response
And inflammation in small intestine
Usually develops in childhood
Pathophysiology of coeliac disease
Immunological response (antibodies) to gliadin in gluten
Antibodies: anti-TTG, anti-EMA
Genetic factors (HLA-DQ2/DQ8)
Antibodies target epithelial cells, damage villi of small intestine
Lead to inflammation and Malabsorption
Epithelial cell destruction and villous atrophy
T-cell mediated immune disorder
Development of inflammatory anti-gluten CD4 T-cell response, anti-gluten ab, autoantibodies against tissue transglutaminase, endomysium, activation of intraepithelial lymhphocytes
Risk factors coeliac disease
Wheat, barley, rye Bread, beer, squash, biscuits, cereal, cake, pasta, pies TY1 diabetes Down syndrome Turner syndrome Thyroid disease, RA, Addison’s disease HLA-DQ2 gene
Classic coeliac presentation
9-24months presentation Malabsorption Failur yo thrive Diarrhoea Steatorrhea Anorexia Abdominal pain Abdominal distension Muscle waste Crypt hyperplasia and villous atrophy on histology Mouth ulcers Anaemia
Coeliac disease neurological symptoms
Rare
Peripheral neuropathy
Cerebellar ataxia
Epilepsy
Extra-intestinal symptoms coeliac
Dermatitis herpetiformis Dental enamel Hypoplasia Osteoporosis Short stature Iron-deficient anaemia- resistant to oral Fe Liver and biliary tract disease Arthritis Peripheral neuropathy, epilepsy, ataxia
DD coeliac
Tropical spruce CF IBD Post-gastroenteritis Autoimmune encephalopathy Eosinophilic enteritis
Genetic associations coeliac
HLA-DQ2
HLA-DQ8
Coeliac autoantibodies
Anti-TTG: tissue transglutaminase antibodies
EMAs: endomysial antibodies
Anti-DGPs: deaminated gliadin peptides antibodies
Also check IgA deficiency
Diagnosis coeliac
Need patient having gluten in diet, 6 weeks before testing
IgA TOTAL
IgA TTG
IgA EMA
Avoid HLA DQ2/8 testing
Endoscopic intestinal biopsy if serology positive
Duodenal biopsy
Duodenal biopsy coeliac disease
Crypt hypertrophy
Villous atrophy
Management of coeliac
Lifelong diet free of gluten
Iron supplements
Annual follow up: compliance, development, growth and long-term complications
Complications coeliac
Vitamin deficiency Anaemia Osteoporosis Refractory coeliac, need steroid treatment Malignancy: Non-Hodkin lymphoma Ulcerative jejunitis Fertility problems Depression/ anxiety Enteropathic-associated T-cell lymphoma of the intestine Small bowel adenocarcinoma
Crohn’s disease
Crows NESTS No blood or mucus Entire GI tract Skip lesions on endoscopy Terminal ileum most affected and transmural inflammaiton Smoking is a risk factor
Also weight loss, strictures, fistula
Ulcerative colitis
U-C-CLOSEUP Continuous inflammation Limited to colon and rectum Only superficial mucosa affected Smoking is protective Excrete blood and mucus Use aminosalicylates Primary sclerosing cholangitis
Presentation of IBD
Diarrhoea Abdominal pain Bleeding Weight loss Anemia Systemically unwell during flares, fever, malaise, dehydration
Extra-intestinal manifestations IBD
Finger clubbing Erythema nodosum Pyoderma gangrenosum Episcleritis and iritis Inflammatory arthritis Primary sclerosing cholangitis (UC)
IBD testing
Blood tests for: anaemia, infection, thyroid, kidney, liver function
Raised CRP: indicates active inflammation
Faecal calprotectin: released by intestines when inflamed
Endoscopy (OGD and colonoscopy) with biopsy is Gold-standard
Imaging with US, CT, MRI: look for fistula, abscesses, strictures
General management IBD
MDT
Monitor growth and pubertal development, especially for exacerbations or when treated with steroids
Inducing remission during flares
Maintaining remission
Inducing remission Crohn’s
Steroids: oral prednisolone,v IV hydrocortisone
Enteral nutrition to improve gut microbiome
Azathioprine
Mercaptopurine
Methotrexate
Infliximab
Adalimumab
Maintaining remission Crohn’s
First line: azathioprine, mercaptopurine
Alternatives: methotrexate, infliximab, adalimumab
Surgery for Crohn’s
Surgically resect distal ileum
Surgery to treat strictures and fistula
Inducing remission in ulcerative colitis
Mild/moderate disease
First line: aminosalicylate (e.g. mesalazine oral or rectal)
Second line: corticosteroids (e.g. prednisolone)
Inducing remission in ulcerative colitis
Severe disease
First line: IV corticosteroids (e.g. hydrocortisone)
Second line: IV cyclosporin
UC maintaining remission
Aminosalicylate (e.g. mesalazine)
Azathioprine
Mercaptopurine
Surgery UC
Remove colon and rectum (panproctocolectomy)
Patient left with permanent ileostomy or ileo-anal anastomosis (J-pouch)
J-pouch collects stools prior to patient passing motions
Cows milk protein allergy
Immune-mediated allergic response to naturally-occurring milk proteins casein and whey.
Pathophysiology of Cow’s milk protein allergy
IgE mediated: TY1 hypersensitivity reactions, histamine and cytokines released from mast cells and basophils
Non-IgE-mediated: involves T cell activation against cows milk protein
Risk factors CMPA
Personal history of atopy (eg. asthma, eczema, allergic rhinitis, other food allergies)
Family history of atopy (only allergic predisposition is inherited, not specific allergies)
IgE mediated cows milk protein allergy
Acute and frequently rapid onset Pruritis Erythema Acute urticaria Angio-oedema Oral pruritis Nausea Colicky abdominal pain V/D LRT symptoms: cough, chest tightness, wheezing, SoB URT symptoms: nasal itching, sneezing, rhinorrhea, congestion
Non-IgE mediated CMPA
Non-acute and generally delayed onset Pruritis Erythema Atopic eczema GORD Loos or frequent stools Blood/mucus in stools Abdominal pain Infantile colic Food refusal or aversion Constipation Perianal redness Pallor/tiredness Faltering growth LRI symptoms: cough, chest tightness, wheezing, SoB
CMPA history
Personal and family history of atopy Diet and feeding history of infant Mother’s diet if breastfed Any previous management used for symptoms Which milk/foods Age of onset Speed of onset following exposure Duration Severity and frequency of occurrence Setting of reaction Reproducibility of symptoms
CMPA examination
General physical examination of patient with a focused gastrointestinal examination, specifically signs of malnutrition.
Review growth charts
Signs of atopic comorbidities such as asthma, eczema, allergic rhinitis.
DD CMPA
Food intolerance (eg. lactose) may present as abdominal pain and diarrhoea following exposure to certain foodstuffs
Allergic reaction to other food or non-food allergens
Anatomical abnormalities such as Meckel’s diverticulum
Chronic gastrointestinal disease (e.g. gastro-oesophageal reflux disease, coeliac disease, inflammatory bowel disease, constipation, gastroenteritis)
Pancreatic insufficiency (eg. as a complication of cystic fibrosis)
Urinary tract infections
Investigations CMPA
RAST-radioallegosorbent test: looks for IgE antibodies
Non-IgE CMPA is clinically diagnosis diagnosed
Check for iron deficiency anaemia
Mx CMPA
Avoidance of Cow’s milk for 6 months until infant is 9-12months MAP guidance milk ladder Nutritional counselling Extensively hydrolysed formula Amino acid formula
Complications of CMPA
Malabsorption
Reduced intake
When to suspect spontaneous bacterial peritonitis
Undiagnosed fever
Abdominal pain
Tenderness
Unexplained deterioration in hepatic/renal function
How to diagnose bacterial peritonitis
Diagnostic paracentesis
Send fluid for WCC, differential and culture
How to treat bacterial peritonitis
Broad spectrum antibiotics
Clinical feature of viral hepatitis
Nausea Vomiting Abdominal pain Lethargy Jaundice Hepatomegaly Splenomegaly ALT/AST elevated Coagulation normal
Hepatitis A
RNAvirus
Faeco-oral transmission
Vaccination for travellers to endemic areas
Clinical features of HepA
May be asymptomatic Majority have mild illness, 2-4weeks Prolonged cholestatic hepatitis (self-limiting) Fulminant hepatitis No chronic liver disease
HepA diagnosis
Detect IgM antibody to virus
HepA Mx
No treatment
Vaccinate close contacts within 2 weeks of illness onset
At risk (CLD), giving human normal immunoglobulin
HepB
DNA virus
Sub-Saharan Africa and Far East
HepB transmission
Sexually
Blood
Perinatal, horizontal spread: infants become chronic carriers
Clinical features HepB
Infants who contract perinatally are asymptomatic chronic carriers
Classic features of hepatitis or asymptomatic
Small chance of developing hepatic failure
HepB diagnosis
Detect HBV antigens and antibodies
IgM antibodies (anti-HBc) are positive in acute infection
Hepatitis B surface Antigen (HBsAg) denotes ongoing infectivity
HepB mx
No treatment for acute HBV infection
Chronic HepB
Asymptomatic carrier children-> chronic HBV liver disease
Progress to cirrhosis
Risk of hepatocellular carcinoma
Management of chronic HepB
Interferon
Pegylated interferon
>2s: entecacir, tenofovir
Prevention of chronic HepB
Immunisation
Screen pregnant women for HBsAg: if +ve give infant additional vaccine doses at birth
HBeAg+ve: give infant HepB Ig after birth
Hepatitis C
RNA virus
Post-transfusion hepatitis
IVDU
HepC transmission
Vertical transmission
Transmission more common if HIV+ve
Majority becom,e chronic carriers
HepC clinical features
Chronic carriers
Can progress to cirrhosis or hepatocelllar carcinoma
HepC Mx
Sofosbuvir
Ledipasvir
Treatment not indicated ~<3years, may resolve spontaneously
HepD
RNA virus
Depends on HepB for replication
Superinfection
Cirrhosis occurs in chronic HDV infection
HepE virus
RNA virus
Low-income countries
HepE transmission
Enterally, contaminated water
Mild self-limiting illness
Blood transfusion
Infected pork
HepE presentation
Fulminant hepatic failure in pregnant wo en
High mortality rate
Acute liver failure (fulminant hepatitis)
Development of massive hepatic necrosis
Loss of liver function
With/without hepatic encephalopathy
High mortality
Presentation acute liver failure (fulminant hepatitis)
Preceding infection/ metabolic condition
Hours/weeks later with jaundice, encephalopathy, coagulopathy, hypoglycaemia, electrolyte disturbance
Early signs of encephalopathy: irritability/ confusion with drowsiness
Older children may be aggressive and difficult
Complications of acute liver failre
Cerebral oedema Haemorrhage from gastritis Coagulopathy Sepsis Pancreatitis
Causes of acute liver failure in <2
Infection (herpes simplex) Metabolic disease Sero negative hepatitis Drug-induced Gestational alloimmune liver disease
Children >2years causes of acute liver failure
Sero-negative hepatitis Paracetamol overdose Mitochondrial disease Wilson disease Autoimmune disease
Diagnosis of acute liver failure
Elevated transaminases Alkaline phosphatase is increased Coagulation is very abnormal Plasma ammonium is elevated Monitor acid-base balance Blood glucose Coagulation times EEG: acute hepatic encephalopathy CT: cerebral oedema
Management of acute liver failure
Refer to national paediatric liver centre
Maintain blood glucose >4mmol/L
Prevent sepsis: Ax, antifungal
Prevent haemorrhage with IV vitK, and PPI, H2 antagonists
Prevent cerebral oedema with fluid restriction and mannitol diuresis if oedema develo[s
Features suggestive of poor prognosis in acute liver failure
Shrinking liver Rising bilirubin Failing transaminases Worsening coagulopathy Progression to coma Liver transplantation needed
Peptic ulcer diseae
Duodenal ulcers uncommon in children
When to consider peptic ulcers
Epigastric pain
Wakes them at night
Pain radiating to back
FH of peptic ulceration
Diagnosis of peptic ulcer disease
Gastric biopsy on endoscopy for H.pylori
Carbon 13 breath test, detects urea s produced
Stool antigen tests for H.pylori
Management of peptic ulcer disease in children
PPI: omeprazole
Antibiotics if H.pylori
