Gastro Flashcards
Define coeliac disease
Primarily digestive disorder
Most common genetically related food intolerance
Life-long gluten-sensitive autoimmune disease of small intestine
Epidemiology of coeliac disease
Approx 1%
Often seen more in diabetes, autoimmune disorders and relative of Coeliac disease individuals
Pathophysiology of coeliac disease
Combination of immunological responses to an environmental factor (gliadin) and genetic factors (HLA-DQ2/DQ8)
Body’s immune system overreacts to in food
- damages villi of small intestine
T-cell mediated immune disorder
- anti-gluten CD4 T cell response
- anti-gluten antibodies
- autoantibodies against tissue transglutaminase
Epithelial cell destruction and villous atrophy
Which types of cereal is gluten found in?
Wheat
Barley
Rye
Presentation of coeliac disease
Classical form
- 9-24 months
- malabsorption, failure to thrive, weight loss, loose stool, steatorrhea, anorexia, abdo pain, abdo distention, muscle water
- histology reveals crypt hyperplasia and villous atrophy
Atypical form
- no intestinal symptoms a/w extra-intestinal symptoms
- osteoporosis, peripheral neuropathy, anaemia and infertility
- positive coeliac serology, limited abnormalities of small intestine
Latent form
- presence of predisposing gene
- normal intestinal mucosa and possible positive serology
Silent form
- damaged small intestinal mucosa
- positive serology but no clinical symptoms
Potential
- normal mucosal morphology, positive autoimmune serology and asymptomatic
- genetically predisposed to develop at some point
Extra-intestinal symptoms of coeliac disease
Dermatitis herpetiformis Dental enamel hypoplasia Osteoporosis Delayed puberty Short stature Iron-deficient anemia - resistant to oral Fe Liver and biliary tract disease Arthritis Peripheral neuropathy, epilepsy, ataxia
Differential diagnosis of coeliac disease
Tropical sprue Cystic fibrosis IBD Post-gastroenteritis Autoimmune enteropathy Eosinophilic enteritis
Investigations for coeliac disease
Serology
- test total immunoglobulin A (IgA) and IgA tissue transglutaminase (tTG)
- if IgA tTG weakly positive then use IgA endomysial antibodies
- must have gluten in diet at period of testing and for at least 6 weeks before
Biopsy
- duodenal biopsy gold standard to diagnose
- ensure findings improved on gluten free diet or diagnose different GI disorder
Who should be offered serological testing for coeliac disease
Children with
- persistent unexplained abdo or GI symptoms
- faltering growth
- prolonged fatigue
unexpected weight loss
- severe or persistent mouth ulcers
- unexplained iron, vit B12 or folate deficiency
- type 1 diabetes
- autoimmune thyroid disease
- IBS
First degree relatives of people with coeliac disease
Marsh classification of coeliac disease biopsy
Stage 0 = normal
Stage 1 = increased intraepithelial lymphocytes
Stage 2 = increased inflammatory cells and crypt hyperplasia
Stage 3 = all of the above plus mild to complete villous atrophy
Management of coeliac disease
Lifelong diet free of gluten
Supplementation if obvious malabsorption
Annual follow up to check symptoms, diet compliance, development, growth and long term complications
Complications of coeliac disease
Anaemia
Osteopenia/osteoporosis
Refractory coeliac disease - symptoms persist despite diet
Malignancy
Fertility problems / adverse events during pregnancy
Depression/anxiety
Define cow’s milk protein allergy
Immune-mediated allergic response to naturally-occuring milk proteins casein and whey
Epidemiology of cow’s milk protein allergy
Most common childhood food allergies
7% of formula/mixed-fed infants
Pathophysiology of cow’s milk protein allergy
IgE-mediated
- Type-1 hypersensitivity reaction
- CD4+ TH2 stimulate B cells to produce IgE antibodies against cow’s mild protein
- trigger release of histamine and other cytokines from mast cells and basophils
Non-IgE-mediated
- involves T cell activation against cow’s milk protein
Risk factors for cow’s milk protein allergy
Personal hx of atopy
Family hx of atopy
Exclusive breastfeeding is possible protective factros
Clinical features of IgE-mediated cow’s milk protein allergy
Acute and rapid onset (2 hours post ingestion) Skin reactions - pruritus - erythema - acute urticaria - acute angioedema GI symptoms - angioedema - oral pruritus - N+V - colicky abdo pain - diarrhoea Resp symptoms - lower - cough, chest tightness, wheezing or SOB - upper - nasal itching, sneezing, rhinorrhoea or congestion
Clinical features of Non-IgE-mediated cow’s milk protein allergy
Non-acute and generally delayed Skin reactions - pruritus - erythema - atopic eczema GI symptoms - GORD - loose or frequent stools - blood / mucus in stool - abdo pain - infantile colic - food refusal or aversion - constipation - perianal redness - pallor and tiredness - faltering growth Lower resp tract symptoms - cough - chest tightness - wheezing - SOB
Features of an allergy focused history
Personal or family history of atopy Diet and feeding hx 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
Differential diagnosis of cow’s milk protein allergy
Food intolerance Allergic reaction to other food/non-food allergens Anatomical abnormalities such as Meckel's diverticulum Chronic GI disease - GORD - coeliac disease - IBD - constipation - gastroenteritis Pancreatic insufficiency UTI
Investigations for cow’s milk protein allergy
Usually clinically diagnosed
Blood test looking for specific IgE antibodies - RAST
- low specificity resulting in false positives
Skin prick test
Refer for IgE antibody test for cow’s milk protein allergy
Faltering growth with symptoms
One or more acute systemic or severe delayed reactions
Confirmed IgE mediated food allergy with asthma
Persistent parental suspicion of a food allergy despite lack of clear hx
Clinical suspicion of multiple food allergies
Management of cow’s milk protein allergy
Avoidance of cow’s milk
- including from mother’s diet if breastfeeding
- elimination diet required for at least 6 months or until infant 9-12 months
- extensively hydrolysed formula - cheaper
- made from cow’s milk but casein and whey broken down into smaller peptides
- 90% of children ok
- amino acid formula - more expensive
- soy-based formulas not recommended in infants <6 months due to weak oestrogenic effects
Nutritional counselling and regular monitoring of growth
Complications of cow’s milk protein allergy
Malabsorption Reduced intake Chronic iron-deficiency anaemia Faltering growth Anaphylaxis - rare
Define GORD
Gastro-oesophageal reflux (GOR)
- passage of gastric contents into oesophagus
- normal in infants if asymptomatic
Gastro-oesophageal reflux disease (GORD)
- presence of symptoms or complications from reflux
Regurgitation (posseting)
- reflux of stomach contents beyond the oesophagus
Epidemiology of GORD
Regurgitation extremely common - occurs in approx 40% of infants
Usually appears in first 2 weeks of life
Pathophysiology of GORD
LOS muscle tone too low
-> uncontrolled reflux of stomach content
Features of infants that can contribute to GORD
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
History of (repaired) congenital diaphragmatic hernia
History of (repaired) congenital oesophageal atresia
Neurodisability - cerebral palsy
Clinical features of GORD
Distressed behaviour - excessive crying, unusual neck postures, back-arching
Unexplained feeding difficulties - refusing feeds, gagging, choking
Hoarseness and/or chronic cough in children
A single episode of pneumonia
Faltering growth
If child is able to they may report retrosternal or epigastric pain
Take feeding hx - check technique, calculate volume of milk and relationship between symptoms and feeds
Differential diagnosis of GORD
Pyloric stenosis - frequent forceful vomiting in < 2 months old Intestinal obstruction - bile-stained vomit Acute surgical abdo issue - abdo distention, tenderness or palpable mass Upper GI bleed - haematemesis Sepsis - altered responsiveness, severe prolonged vomiting, petechial rash, bulging fontanelle Raised ICP - rapid increasing head circumference, persistent headache and vomiting following periods of recumbence Bacterial gastroenteritis - blood in stool Cow's milk protein allergy - blood in stool - chronic diarrhoea UTI
Management of GORD
Effortless regurgitation
- reassurance
Breastfed
- alginate (Gaviscon) mixed with water immediately after feeds
Formula-fed
- ensure infant not over-fed - no more than 150ml/kg/day
- decrease feed volume by increasing frequency
- use feed thickener
- stop thickener and start alginate added to formula
If no improvement after 2 weeks trial PPI or histamine antagonist - omeprazole or ranitidine
Complications of GORD
90% spontaneously resolve by 1 year
Reflux oesophagitis
Recurrent aspiration pneumonia
Recurrent acute otitis media - >3 episodes in 6 months
Dental erosion - especially in children with neurodisability
Apnoea
Apparent life-threatening events (ALTE): a combination of symptoms including apnoea, colour change, change in muscle tone, choking and gagging
Define gastroenteritis
Inflammation of stomach and intestines
Infective gastroenteritis is a temporary disorder due to an enteric infection
- Most commonly caused by viruses, but can also be due to bacterial or parasitic infection
Typically characterised by sudden onset diarrhoea with or without vomiting
Epidemiology of gasteroenteritis
Viral causes
- rotavirus
- most common in infants - immunity long lasting
- oral vaccine part of UK vaccination programme at 8-12 weeks
- norovirus
- commonest in all age groups
- spread by faecal oral route or by environmental contamination
- adenovirus
Bacterial
- campylobacter
- bloody diarrhoea
- consumption of undercooked meat and unpasteurised milk
- Escherichia coli
- transmitted through contaminated food, person-to-person and contact with infected animals
Clinical features of gastroenteritis
Sudden onset of loose/watery stool with or without vomiting
Abdominal pain/cramps
Mild fever
Recent contact with someone with diarrhoea or vomiting
Groups at high risk for dehydration
Young children - under 6months
Children who have passed >5 diarrhoeal stools in the last 24 hours
Children who have vomited >2x in the last 24 hours
Children who have stopped breastfeeding during the illness
Differential diagnosis of gastroenteritis
Temperature higher than 38oC if < 3months or higher than 39oC if >3months Breathlessness or tachypnoea Altered GCS Meningism Blood/mucous in stool Bilious (green) vomit Severe/localised abdominal pain Abdominal distension or guarding
Investigations for gasteroenteritis
A stool sample should be sent for microbiological investigations if
- Septicaemia is suspected or
- blood and/or mucus is present in the stool or
- the child is immunocompromised
Do not routinely perform blood tests however measure Na+, K+, Cr, Ur and glucose if
- IV fluids are going to be used
- There are symptoms/signs of hypernatraemia - jittery, increased muscle tone, hyperreflexia, convulsions, drowsiness or coma
Measure acid-base status and chloride concentration is shock is suspected.
Management of gasteroenteritis
Immediate
- if not clinically dehydrated
- continue breastfeeding/formula
- encourage fluid intake
- discourage fruit juices and carbonated drinks
- offer oral rehydration salt solution as supplementation
- if dehydrated
- IV therapy - if suspected shock, evidence of red flags, no improvement or vomiting with oral/NG tube fluid
- oral therapy - ORS ml/kg over 4 hours plus maintenance fluid
Following rehydration
- give full strength milk straight away
- slowly introduce child’s solid food
- do not return to nursery/school at least 48hrs have passed since last symptoms
Complications of gastroenteritis
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 associated with bacterial gastroenteritis
- arthritis, carditis,4 urticaria, erythema nodosum and conjunctivitis.
- Reiter’s syndrome (the combination of urethritis, arthritis, and uveitis).
Toxic megacolon
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
Epidemiology of UC
Most prevalent among Caucasian population
Bimodal distribution between 15-25 years and 55-65 years
Follows remitting and relapsing course
Features of UC
Large bowel only Mucosa only Microscopic changes - crypt abscess formation - reduced goblet cells - non-granulomatous Macroscopic changes - continuous inflammation - proximal from rectum - pseudopolyps and ulcers from
Features of Crohn’s disease
Entire GI tract Transmural Microscopic changes - granulomatous - non-caseating Macroscopic changes - discontinuous inflammation - skip lesions - fissures and deep ulcers - cobblestone appearance - fistula formation
Clinical features of UC
Insidious onset Bloody diarrhoea and mucus discharge Systemic symptoms - malaise - anorexia - low-grade pyrexia
Extra-intestinal manifestations of UC
Musculoskeletal – enteropathic arthritis (typically affecting sacroiliac and other large joints) or nail clubbing
Skin – Erythema nodosum (tender red/purple subcutaneous nodules, typically found on the patient’s shins)
Eyes – Episcleritis, anterior uveitis, or iritis
Hepatobiliary – Primary sclerosing cholangitis (chronic inflammation and fibrosis of the bile ducts)
Ix of UC
Routine bloods
Faecal calprotectin - raised in IBD but not IBS
Imaging
- colonoscopy with biopsy
- AXR or CT in acute exacerbations - look for megacolon or bowel perforation
Mx of UC
Inducing remission
- fluid resuscitation, nutritional support and prophylactic heparin
- corticosteroid therapy and immunosuppressive agents - mesalazine or azathioprine
Maintaining remission
- immunomodulators - mesalazine or sulfasalazine
- colonoscopic surveillance
- IBD nurse specialists
Surgical
- total proctocolectomy is curative
Complications of UC
Toxic megacolon, present with severe abdominal pain, abdominal distension, pyrexia, and systemic toxicity
Decompression of the bowel is required as soon as possible, due to high risk of perforation, and failure to respond to medical management is an indication for surgery
Colorectal carcinoma
Osteoporosis, requiring regular assessment for fracture risk and treated as necessary
Pouchitis, inflammation of an ileal pouch, with typical symptoms include abdominal pain, bloody diarrhoea, and nausea
Pouchitis should be treated with metronidazole and ciprofloxacin
Risk factors for Crohn’s disease
Family history
Smoking
- Increases the risk of developing Crohn’s disease and risk of relapse
White European descent (particularly Ashkenazi Jews)
Appendicectomy
Clinical features of Crohn’s disease
Abdo pain and diarrhoea Systemic symptoms - malaise - anorexia - low-grade fever Oral aphthous ulcers Perianal disease - skin tags - perianal abscesses - fistulae - bowel stenosis
Extra-intestinal features of Crohn’s disease
Musculoskeletal
- Enteropathic arthritis or nail clubbing
- Metabolic bone disease (secondary to malabsorption)
Skin
- Erythema nodosum –
- Pyoderma gangrenosum – erythematous papules/pustules that develop into deep ulcers
Eyes
- Episcleritis, anterior uvetitis, or iritis
Hepatobiliary
- Primary sclerosing cholangitis (more associated with UC)
- Cholangiocarcinoma (due to association with primary sclerosing cholangitis)
- Gallstones
Renal
- Renal stones
Mx of Crohn’s disease
Inducing remission - fluid resuscitation, nutritional support and prophylactic heparin - corticosteroid therapy and immunosuppressive agents - mesalazine or azathioprine Maintaining remission - azathioprine - smoking cessation Surgical - ileocaecal resection - surgery for peri-anal disease - stricturoplasty - small or large bowel resections
Complications of Crohn’s disease
GI - fistula - stricture formation - recurrent perianal abscesses/fistulae - GI malignancy Extra-intestinal - malabsorption - osteoporosis - increased risk of gallstones - increased risk of renal stones
Define infantile colic
Benign condition without any known understanding or surgical cause
Typically begins in the first few weeks of life and resolves spontaneously by 4-5 months
Risk factors for infantile colic
Age under 5 months
Exposure to cigarette smoke
Formula-fed only
Clinical features of infantile colic
Paroxysms of crying, often worse in afternoons and evening - high pitched piercing Difficult to comfort Grimacing/frowning Red face Knees drawn up to chest Clenched fists Excessive gas Flatus - typically relieves symptoms
DDx of infantile colic
UTI Cow's milk protein intolerance GORD Anal fissure Intussusception Pyloric stenosis Acute otitis media Non-accidental injury Meningitis
Mx of infantile colic
No definitive management
Hold baby through crying episode
Bottle-fed infants may benefit from hydrolysed formula
Pathophysiology of constipation
95% functional
- low fibre, low-fluid diet resulting in hardening of school
- pain on defecation
- voluntary delay of defecation
- further hardening of stool
Risk factors for functional constipation
Low-fibre diet
Poor nutrition
Obesity
Childhood stressors
Clinical features of constipation
Painful passage of infrequent hard stool
Overflow faecal incontinence - small volume of soft stool
Indentable mass in left LLQ
Red flag symptoms for constipation
Present from birth Delayed passage of meconium > 48 hours Ribbon stools Neurological symptoms or signs - locomotor delay or falling over/ abnormal gait in older children Vomiting Abdominal distension
Key features to exclude on examination of constipation
Spine - hairy patches or lipomata - indicative of spina bifida Gluteal region - symmetry Perianal region - no fissures - anatomically normal anus Lower limbs - normal power, tone and reflexes
DDx of functional constipation
Infants - Hirschsprung disease - CF - hypothyroidism - spinal dysraphism - anogenital anomalies - imperforate anus Older children - neuromuscular disorders - spinal muscular atrophy, cerebral palsy - hypothyroidism - anorexia
Mx of functional constipation
Pharmacological disimpaction - polyethylene glycol 3350 (Movicol) - osmotic laxative - lactulose - if no improvement add stimulant laxative such as senna Maintenance - polyethylene glycol 3350 Dietary advice - regular scheduled toileting - increasing dietary fibre and fluids - increasing exercise
Commonly used laxatives in children
Macrogols - polyethylene glycol 3350 (Movicol)
- induces effect by retaining water in stool
- softens stool and increases bulk
- increasing frequency
Osmotic - lactulose
- broken down to lactic acid which raises osmotic pressure of bowel
Stimulant - senna
- breakdown products are directly irritant to the bowel wall causing increased fluid secretion and colonic motility
Pathophysiology of Hirschsprung disease
Absence of ganglion cells in bowel wall myenteric nerve plexus
- in utero cells migrate in craniocaudal fashion - distal bowel most often affected
Lack of peristalsis and muscle spasm
- impaired relaxation of bowel wall and internal anal sphincter
Functional bowel obstruction
Due to stasis of faeces - increased risk of enterocolitis - sepsis
Epidemiology of Hirschsprung disease
1.6 per 100,000 live births
Male predominance of 2:1
Significant association with Down’s syndrome
Clinical features of Hirschsprung disease
Delayed passage of meconium - greater than 48 hours
Vomiting - eventually bilious
When stool is passed usually foul (due to bacterial growth) and explosive
If complicated by enterocolitis child will be febrile
Distended abdomen
Ix for Hirschsprung disease
Bloods if febrile - raised WCC suggests enterocolitis
Abdo XRAY - bowel obstruction
Rectal biopsy - definitive investigation
Mx of Hirschsprung disease
NBM and commence IV maintenance fluids
Decompress stomach and bowel by NG tube and saline enemas
If enterocolitis present start broad-spec abx IV
Surgical resection of aganglionic segment with coloanal anastomosis
Epidemiology of anal fissures
Often < 2 years old
Common cause of rectal bleeding in childhood
Pathophysiology of anal fissures
Hard stool stretches the anal mucosa causing a tear
- pain during bowel movement
- spasm of internal anal sphincter causing reduced blood flow and poor healing
- avoidance of opening bowels - worsening constipation
Clinical features of anal fissures
Pain during defecation
Small volumes of bright-red blood on paper
Pain leads to toilet avoidance
Fissure seen on examination - break in anal mucosa - often in posterior midline
Mx of anal fissure
Aim is to soften stool
- increasing fluid and fibre in the diet is required
- laxatives - continued for 1 month after symptoms resolve
- sitting in warm bath 2-3 times per day
Epidemiology of threadworm
Enterobius vermicularis
Very common infection in childhood
Typically 5-10 years
Pathophysiology of threadworm
Highly contagious infection with Enterobius vermicularis
Live in bowel but migrate to anus to lay eggs
- highly irritant and cause child to scratch
- eggs on fingers passed to mouth to re-infect or transferred elsewhere to infect others
Clinical features of threadworms
Intense perianal itching, often worse at night
Disturbs sleep -> behavioural problems
Small, thread-like worms may be seen in perianal region
Ix for threadworms
If worms seen - not required
Tape-test - parent places piece of sticky tape briefly on child’s anus first thing in the morning which is sent for microscopy
Mx of threadworms
Antifungal - mebendazole
Measures taken to prevent transmission/prevent re-infection for 2 weeks post treatment as medication only kills like worms
- daily washing of bedding
- fastidious hand hygiene
- bathing every morning with cleansing of perianal region
- storing toothbrushes out of reach
IgE-mediated vs non-IgE-mediated cow’s milk allergy
IgE-mediated - within 2 hours onset - pruritus and erythema - urticarial rash - angioedema - N+V - colic - diarrhoea - lower resp symptoms - wheeze and dyspnoea - upper resp symptoms - sneezing, rhinorrhoea and nasal itching Non-IgE-mediated - between 48 hours and 2 weeks - pruritis and erythema - eczematous rash - angioedema unusual - colic - may mimic infantile colic - chronic diarrhoea - may be bloody - perianal redness - lower resp symptoms - wheeze and dyspnoea
Pathophysiology of lactose intolerance
Primary
- autosomal recessive condition leading to reduction in lactase activity
Secondary
- pathology of GI tract damages the villi in small bowel and causes a reduction of activity of lactase
Reduction in lactase activity in small bowel means lactose enters colon
- acts as osmolyte keeping water in bowel
- digested by bacteria to form short-chain fatty acids and gas
Risk factors for lactose intolerance
Gastroenteritis
FHx
Non-white ethnicity
25% Caucasians and up to 75% other ethnic groups
Clinical features of lactose intolerance
Watery diarrhoea that follows gastroenteritis
Abdo discomfort, distention and increased flatus
Ix for lactose intolerance
Stool sample - pH < 6.0 and reducing sugars
Hydrogen breath test or lactose tolerance test - older children
DDx for lactose intolerance
Cow's milk protein intolerance IBD IBS Gastroenteritis Coeliac disease Infantile colic Giardiasis Hyperthyroidism Meckel diverticulum
Mx of lactose intolerance
Lactose free diet/milk/formula
- varying degrees of lactose may be tolerated
- dietitian referral required
Consider vit D and calcium supplementation
In secondary disease cow’s milk can be reintroduced once symptoms have resolved
Define toddler diarrhoea
Very common cause of chronic diarrhoea
Children otherwise well
Self-limiting without long term significance
Clinical features of toddler diarrhoea
Chronic diarrhoea which classically contains particles of undigested food +- mucus
May be exacerbated by high-fibre diets and sugary juices
Examination normal
DDx of toddler diarrhoea
Malabsorptive disease - IBD, coeliac, pancreatic insufficiency
Food allergy - cow’s milk
Lactose intolerance
Mx of toddler diarrhoea
Reassurance
- typically resolve by 4-5 years
No medication
Dietary amendments
- limit intake of fruit juice, fizzy drinks, grapes, peas, baked beans, high-fibre cereals
- include full fat milk, lower fibre cereals
Pathophysiology of pyloric stenosis
Thickening of pyloric musculature leading to narrowing of gastric antrum and subsequent disruption of gastric outflow
Causes forceful vomiting of gastric contents - will not be bilious
Loss of hydrogen and chloride ions orally produces a hypochloraemic metabolic alkalosis
- potassium ions move intracellularly leading to hypokalaemia
Risk factors for pyloric stenosis
Typically presents between 4th and 6th week of life
Male sex (7:1)
Fhx
Clinical features of pyloric stenosis
Effortless projectile vomiting during or after feeds
- vomiting never bilious, maybe small amounts of blood
Visible peristaltic waves in upper quadrants of abdomen
Firm mobile olive-sized mass in epigastrium
Ix for pyloric stenosis
Bloods - blood gases and U+Es show hypochloraemia, hypokalaemia and metabolic alkalosis
Abdo USS
DDx for pyloric stenosis
GOR Overfeeding Duodenal atresia Gastroenteritis Food allergy
Mx of pyloric stenosis
IV access gained - fluid and metabolic derangements corrected
Definitive treatment - Ramstedt’s pyloromyotomy
