Gastro Flashcards
What causes GORD?
Inappropriate relaxation of oesophagael sphincter
When does GOR become GORD?
After 12 months, if doesn’t resolve –> GORD (Gastrooesophagael Reflux Disease)
NOTE: GOR is due to functional immaturity
PACES: Important question to ask when considering diagnosis of GORD
IS THE CHILD GROWING? (ASK ABOUT RED BOOK) –> HEIGHT?WEIGHT
How does GORD present?
Vomiting
Refusal to feed / irritability
Aspiration
Chronic cough or wheeze
Slow weight gain
How is GORD typically diagnosed?
USUALLY A CLINICAL DIAGNOSIS
Can use:
(24h LOS pH monitoring)
(OGD)
What red flag sx would warrant a same day referral to a paediatrician in GORD?
Red flags (SAME DAY REFERRAL):
Haematemesis
Melaena
Dysphagia
What concerning features would warrant referral to a paediatrician in GORD?
Faltering growth
Unexplained distress
Unresponsive to medical therapy
Unexplained IDA
What complications would warrant a referral to a paediatrician in GORD?
Recurrent aspiration pneumonia
Dental erosion
Unexplained apnoea
Recurrent acute otitis media
PACES: What should be told to parents during GORD counselling?
Reassure (very common condition) –> may be frequent, less frequent with time, resolves by 12m
Note: no positional management – baby must sleep on back (risk of SIDS)
How does management vary in GORD?
If breast fed, or formula fed
How to manage GORD if breast-fed?
1st –> breastfeeding assessment
2nd –> consider trial of alginate for 1-2 weeks
3rd –> pharmacological*
*Pharmacological Management
4-week PPI/H2 antagonist trial
E.g. Omeprazole or Ranitidine
How to manage GORD if bottle-fed?
1st –> review feeding history
2nd –> trial smaller, more frequent feeds (aim for 150-180 mL/kg/day)
3rd –> trial of thickened formula (e.g. containing rice starch Enfamil, Carabel)
4th –> trial of alginate (stop periodically to see if infant has recovered)
5th –> pharmacological*
*Pharmacological Management
4-week PPI/H2 antagonist trial
E.g. Omeprazole or Ranitidine
What causes pyloric stenosis?
Hypertrophy of pyloric muscle gastric outlet obstruction
When does pyloric stenosis present?
Presents age 2-8 weeks
Which sex does pyloric stenosis present most often in?
4:1 (Male:Female)
PACES: What is important to get a description of in pyloric stenosis?
Contents of vomit (R/O bile, blood)
Description of vomiting:
“Does it go everywhere” vs drip down child’s chin
How does pyloric stenosis present?
Projectile Vomiting (non-bilious)
Hunger after vomiting
Failure to thrive
What is seen on examination in pyloric stenosis?
palpable ‘olive’ mass in RUQ
Visible peristalsis in upper abdomen
What investigations are done in pyloric stenosis?
Bloods
Blood Gas: hypochloraemic metabolic alkalosis
U&E: hyponatraemia and hypokalaemia
Imaging
Ultrasound
What is the management of pyloric stenosis?
Fluid resuscitation
Surgery: laparoscopic Ramstedt pyloromyotomy
Palpable ‘olive mass’
Pyloric stenosis
Hypochloraemic hypokalaemic metabolic acidosis on blood gas
Pyloric stenosis
Projectile non-bilious vomit
Pyloric stenosis
Target sign on USS
Pyloric Stenosis
Laparoscopic Ramstedy pyloromyotomy
Pyloric Stenosis
What is Oesophagael atresia?
malformation of oesophagus so it does not connect to stomach
What is tracheooesophagael fistula?
part of oesophagus joined to trachea
What is oesophgaeal atresia associated with?
Associations: polyhydramnios (no swallow), other developmental issues
What are VACTERL associations?
Set of conditions that can occur together:
Vertebral defects
Anal atresia
Cardiac defects
Tracheo‐Esophageal fistula
Renal malformations
Limb defects
How does oesophagael atresia present?
Excessive drooling
Choking
Failure to swallow or pass an NG tube
What investigations are done for oesophageal atresia?
Prenatal USS
NG tube placement +/- aspirate
Gastrograffin swallow (Gold-Standard)
Gold standard investigation for oesophagael atresia
Gastrograffin swallow
Oesophageal condition associated with polyhdramnios
Oesophageal atresia
NOTE: Also has VACTERL association: Vertebral defects, Anal atresia, Cardiac defects, Tracheo‐Esophageal fistula, Renal malformations, and Limb defects
How is Oesophagael atresia managed?
Surgical repair –> NICU for I&V
Before: Replogle tube (Drain saliva from oesophagus)
What must be done before surgical management of oesophagael atresia?
Replogle tube
What causes Intussusception?
Invagination of proximal bowel into distal component
NOTE: 95% ileum through to caecum through ileocecal valve
Cause of recurrent Intussusception
Meckel’s diverticulum
NOTE: If recurrent intussusception, consider investigating for a lead point
(e.g. Meckel’s diverticulum)
Risk Factors for Intussusception
Gastroenteritis (viral illness enlarging Peyer’s patches)
HSP
CF
Why can gastroenteritis cause intusussception?
Viral illness enlarging Peyer’s patches
How does intussusception present?
Abdominal pain
Vomit (may be bile stained)
Red-currant jelly stool (late sign)
Abdominal distension (+ sausage shaped mass RUQ)
What is a late sign of intussusception?
Red-currant jelly stool
Red current jelly stool
Intussusception
Sausage shaped mass in RUQ
Intussusception
First line Investigation for intussusception
Abdominal USS (Target mass)
Target mass on Abdominal USS
Intusussception
Investigations for intussusception
First line: Abdominal USS (Target mass)
Alternative: barium (or gastrograffin) enema
Management for intussusception
“Drip and suck:
1st line: rectal air insufflation
Otherwise: barium/gastrograffin enema
2nd line (perforation): surgical reduction + Broad-spectrum antibiotics
1st line management for intussusception
1st line: rectal air insufflation
What causes malrotation?
Congenital issue: intestines do not (fully) rotate and fixate in mesentery as usually expected
What can malrotation lead to?
bowel twisting and causing obstruction (volvulus)
What is malrotation (& volvulus) associated with?
exomphalos
congenital diaphragmatic hernia
How does malrotation (& volvulus) present?
Signs of bowel obstruction:
Abdominal pain and peritonism
Vomiting (bilious)
Constipation
Bloody stools
Investigations for malrotation (& volvulus)
Upper GI contrast study (assess patency)
USS
Management of malrotation (& volvulus)
Urgent laparotomy (Ladd’s procedure) - Untwist volvulus, remove necrotic bowel and place bowel in non-rotation position
Ladd’s procedure
Malrotation (& volvulus)
Cause of Hirchsprung’s Disease
Absence of ganglion cells from the myenteric (Auerbach) and submucosal (Meissner’s) plexuses
Most common location of hirchsprung’s disease
100% start in rectum, 75% spread proximally to rectosigmoid
RFs for hirchsprung
Down’s
MEN2a
PACES: what question to ask in Hirchsprung’s?
Did baby pass any stool in the first day of life?
“Dark, sticky/tarry stool”?
How does hirchsprung’s present?
Failure to pass meconium <24hrs
Abdominal distension
Bilious vomiting
Explosive passage of liquid/foul stools
NOTE: May present later in first few weeks of life with severe, life-threatening Hirschsprung enterocolitis (C. diff)
What may people with Hirchsprung’s present in first few weeks of life with?
severe, life-threatening Hirschsprung enterocolitis (C. diff)
What causes severe, life-threatening Hirschsprung enterocolitis?
C. Diff
NOTE: May present later in first few weeks of life
What severe, life-threatening infection may people with Hirchsprung’s present with?
Hirschsprung enterocolitis (caused by C. Diff)
What is a delayed clinical features of Hirchsprung?
Chronic constipation (delayed presentation)
Investigations for Hirchsprung’s
AXR (if obstruction)
Contrast (barium) enema: –> dilated distal segment + narrowed proximal segment
Definitive = suction-assisted full-thickness rectal biopsy: –> absence of ganglion cells, ACh +ve nerve trunks
Definitive investigation for Hirchsprung
Suction-assisted full thickness rectal biopsy (visualise the absence of the ganglion cells)
Management of Hirchsprung
Initial management = bowel irrigation
Followed by: Endorectal pull-through (colostomy followed by anastomosing normally innervated bowel)
Initial management of Hirchsprung
Bowel irrigation
Followed by: Endorectal pull-through (colostomy followed by anastomosing normally innervated bowel)
Definitive management of Hirchsprung
Endorectal pull-through (colostomy followed by anastomosing normally innervated bowel)
Preceded by: bowel irrigation
What causes meconium ileus?
Thick, sticky meconium that has a prolonged passing time
When should meconium have passed by?
Meconium usually passes within 24hrs of delivery, if not, there may be an ileus
Causes of delayed meconium passage
Meconium Ileus
Hirchsprung’s Disease
What is meconium ileus associated with?
Cystic Fibrosis (90%) and biliary atresia
What GI condition is cystic fibrosis associated with heavily?
meconium ileus
How may meconium ileus present?
Child may vomit meconium instead of passing it as stool
What test should be done if diagnosis of meconium ileus is suspected>
Heel prick test for CF
Management of meconium ileus
1st line = gastrografin enema (N-acetylcysteine can also be used)
2nd line = surgery
1st line management for meconium ileus
1st line = gastrografin enema (N-acetylcysteine can also be used)
What causes meckel’s diverticulum?
An ileal remnant of the vitello-intestinal duct containing ectopic gastric mucosa (i.e. can form gastric ulcers that bleed) or pancreatic tissue
What type of tissue is meckel’s diverticulum made from?
Ectopic gastric mucosa or pancreatic tissue
MASSIVE PAINLESS PR BLEED
Meckel’s diverticulum
How does meckel’s diverticulum usually present?
Mostly asymptomatic!
Painless massive PR bleeding
May present with intussusception, volvulus or diverticulitis
What GI condition may Meckel’s Diverticulum increase the recurrence of?
Intusussception
NOTE: Can be the lead point for intussusception, thereby presenting with intermittent abdominal pain and vomiting
Who is Meckel’s diverticulum more common in?
More common in boys (2:1)
Investigations for meckel’s diverticulum
Technetium scan (increased uptake by gastric mucosa)
Abdominal USS ± laparoscopy
1st line investigation for meckel’s diverticulum
Technetium scan can demonstrate increased uptake by ectopic gastric mucosa found within the diverticulum.
Management of Meckel’s Diverticulum
Only treat if symptomatic
Bleeding: excision (with blood transfusion if needed)
Obstruction: excision of diverticulum and lysis of adhesions
Perforation/peritonitis: excision or small bowel segmental resection with perioperative antibiotics
Treatment of Meckel’s if bleeding
Only treat if symptomatic
Bleeding: excision (with blood transfusion if needed)
Treatment of Meckel’s if osbtruction
Only treat if symptomatic
Obstruction: excision of diverticulum and lysis of adhesions
Treatment of Meckel’s if perforation/peritonitis
Only treat if symptomatic
Perforation/peritonitis: excision or small bowel segmental resection with perioperative antibiotics
RFs for oesophagael atresia
Trisomy 18 and 21
What may occur recurrently in oesophagael atresia?
Aspiration
What is a hernia?
Hernia = A bulging of an organ or tissue through an abnormal opening
Types of hernia
indirect/direct inguinal
umbilical
epigastric
femoral
PACES: Questions to ask if hernia
Duration of bulge/lump
Always present vs on standing or straining
Does it retract alone? Can they push it back in?
Any pain?
Constipation?
PACES: what are you trying to assess in a hernia history?
History is to assess for any signs of incarceration or strangulation
What type of hernia requires instant referral?
Femoral
Investigations for inguinal hernia
Clinical Diagnosis + examination
What should be checked on examination of inguinal hernia
EXAMINATION SHOULD BE BILATERAL
Painful vs painless
Cough impulse
Reducible (if not: incarceration)
Auscultation (bowel sounds?)
NEED TO ASSESS IF DIRECT VS INDIRECT
How to differentiate between direct and indirect inguinal hernias?
Direct vs indirect:
1.Locate deep inguinal ring (midway between ASIS and pubic tubercle).
2.Manually reduce hernia
3.Apply pressure over the deep inguinal ring and ask the patient to cough.
If reappears = direct; if not = indirect
Management of inguinal hernias
If incarcerated: emergency surgery
Non-incarcerated: elective repair
Open or laparoscopic
Management of incarcerated inguinal hernias
Emergency surgery
Management of non-incarcerated inguinal hernias
Non-incarcerated: elective repair
Open or laparoscopic
What anatomical structure do indirect inguinal hernias go through?
deep inguinal ring
How investigate femoral hernia?
Clinical diagnosis
How does femoral hernia compare to inguinal hernia?
Femoral = infero-lateral to public tubercle
Inguinal – supero-medial to pubic tubercle
Management of femoral hernias
All should be managed surgically – high risk of incarceration
NOTE: FEMORAL HERNIAS ARE AT MUCH HIGHER RISK OF INCARCERATION
Investigations for umbilical hernia
Clinical diagnosis
Management of umbilical hernia
Incarceration: attempt reduction and surgical repair
Non-incarcerated:
Large or symptomatic: elective surgical repair (age 2-3 years)
Small and asymptomatic: most self-resolve by age 5. If have not resolved, may consider elective repair.
Management of incarcerated umbilical hernia
Incarceration: attempt reduction and surgical repair
Management of non-incaracertaed umbilical hernia
Depends on size and symptoms
Large or symptomatic: elective surgical repair (age 2-3 years)
Small and asymptomatic: most self-resolve by age 5. If have not resolved, may consider elective repair.
What type of hernia may self-resolve by the age of 5?
small and asymptomatic umbilical hernias
What is constipation?
Infrequent passage of stools, often associated with abdominal discomfort.
Risk factors for constipation
Dehydration
Toilet Anxiety
Hirschsprung Disease
Hypothyroidism
Coeliac Disease
Stress/emotional abuse
PACES: What conditions do you need to rule out in constipation?
Hirschsprung Disease
Hypothyroidism
Coeliac Disease
Cystic Fibrosis
PACES: What red flags should be ruled out in constipation?
Blood in stool
Weight loss
Investigations for constipation
Clinical diagnosis (rule out secondary causes)
AXR (impaction)
Clinical features of constipation
Abdominal pain
Difficult defecation
Soiling
PACES: What questions should be asked to rule out social causes of constipation?
Enquire about diet and lifestyle
Enquire about home and school life
What does management of constipation depend on
Presence of disimpaction:
If Faecal Impaction –> Disimpaction Regime
No Faecal Impaction –> Maintenance Regime
How to manage constipation if faecal impaction?
Disimpaction regime:
Movicol Paediatric Plain (polyethylene glycol + electrolytes) - escalating dose for 2 weeks (followed by maintenance dose until regular bowel habit re-established)
Add stimulant laxative (e.g. Senna)
NOTE: If Movicol is not tolerated: a stimulant laxative (e.g. senna) can be used with lactulose or docusate (stool softeners)
How to manage constipation if no faecal impaction?
Movicol with/without a stimulant laxative
Dose should be reduced over a period of months
What management must always be given in constipation?
Lifestyle & Behaviour (ALWAYS GIVE):
Advise behavioural interventions (scheduled toileting, bowel habit diary, reward system)
Diet and lifestyle advice (adequate fluid intake)
PACES: What advice should be given in constipation management?
Advice about establishing good toileting practices (e.g. positive reward schemes and regular toileting schedules)
Encourage good hydration and a balanced diet
Where can Crohn’s affect?
Affects any part of the GI tract mouth to anus
Where does Crohn’s most commonly affect?
distal ileum and proximal colon
Does Crohn’s go through the layers of the mucosa?
Yes it is transmural
What condition affects any part of the GI tract from mouth to anus?
Crohn’s
What condition is transmural and most commonly affects the distal ileum and proximal colon
Crohn’s
What social habit can make Crohn’s worse?
Smoking
NOTE: Makes UC better
Presentation of Crohn’s
Abdominal pain, diarrhoea, weight loss
Fever, lethargy
Aphthous ulcers, perianal skin tags
Growth failure, delayed puberty
Uveitis, arthralgia, erythema nodosum
Complications: strictures and fistulae
Extra-intestinal manifestations of Crohn’s
Aphthous ulcers
Perianal skin tags
Uveitis
Arthralgia
Erythema Nodosum
Complications of crohn’s
strictures and fistulae
Investigations for Crohn’s
Faecal calprotectin
FBC (including iron, B12 and folate), CRP and ESR
Upper GI and small bowel contrast scan
Colonoscopy and biopsy (cobblestones; non-caseating granulomas)
Gold standard investigation for Crohn’s
Colonoscopy and biopsy (cobblestones; non-caseating granulomas)
NOTE: Unlikely to do this in a child
What is seen on colonoscopy and biopsy of crohn’s?
cobblestones; non-caseating granulomas
Cobblestones and non-caseating granulomas on biopsy
Crohn’s
What does management of Crohn’s involve?
Inducing remission
Maintaining remission
Surgery for complications
How is remission induced in Crohn’s?
Pharmacological management –> steroids (prednisolone)
Nutritional management –> effective in 85-100% patients (crohns.org)
Replace diet with whole protein modular diet – excessively liquid, for 6-8 weeks
May need NG if the child struggles to drink that much
Products are easily digested, provide all nutrients needed to replace lost weight
How is remission maintained in Crohn’s
Aminosalicylates (e.g. mesalazine)
Immunosuppressive drugs (azathioprine, methotrexate, mercaptopurine)
Azathioprine cannot be given to people with a TPMT mutation
Must not have live vaccines
Must have pneumococcal and influenza vaccines
Anti-TNF antibodies in biologic therapies (e.g. infliximab
What must be tested before giving azathioprine?
Presence of TPMT mutation
What drug class must be avoided with azathioprine?
Xanthine oxidase inhibitors (e.g. allopurinol)
What steroids are used in Crohn’s?
Prednisolone –> used to induce remission alongside nutritional management (whole protein modular diet)
What aminosalicyclates are used to maintain remission in Crohn’s?
Mesalazine
Used alongside:
Immunosuppressive drugs (azathioprine, methotrexate, mercaptopurine)
Anti-TNF antibodies in biologic therapies (e.g. infliximab)
What immunosuppressive drugs are used to maintain remission in Crohn’s?
azathioprine, methotrexate, mercaptopurine
Used alongside:
Aminosalicylates (e.g. mesalazine)
Anti-TNF antibodies in biologic therapies (e.g. infliximab)
What biologic therapies are used to maintain remission in Crohn’s?
Infliximab (anti-TNF alpha)
Used alongside:
Aminosalicylates (e.g. mesalazine)
Immunosuppressive drugs (azathioprine, methotrexate, mercaptopurine)
What do the biologic therapies in Crohn’s target?
Anti-TNF alpha antibodies in biologic therapies (e.g. infliximab
When is surgery done for Crohn’s?
Surgery for complications: e.g. obstruction, fistula, abscess, severe localized disease
What requires monitoring in medical management of Crohn’s?
biochemical measures (e.g. ferritin, B12, calcium and vitamin
PACES: what support can be offered to those with Crohn’s?
Support: Crohn’s & Colitis UK (information leaflet and grants available)
Where is affected in UC?
Partial thickness inflammation in a distal to proximal pattern
Key features of UC
Crypt damage & ulceration
What GI condition causes Crypt damage & ulceration?
UC
What is UC associated with?
PSC, Toxic megacolon, enteric arthritis, haemorrhage, bowel cancer
GI condition associated with PSC and toxic megacolon
UC
How does UC present?
Classic presentation is rectal bleeding, diarrhoea, abdominal pain
Weight loss and growth failure
Erythema nodosum, arthritis
Extra-intestinal manifestations of UC
Erythema nodosum, arthritis
Investigations for UC
Endoscopy and histological features:
Confluent colitis extending from rectum proximally
Histology = mucosal inflammation/ulceration, crypt damage (abscesses, loss, architectural distortion)
Severity graded using:
Paediatric Ulcerative Colitis Activity Index (PUCAI) - N.B. be aware of coexistent depression
Truelove and Witts score
What is seen on histology in UC?
mucosal inflammation/ulceration, crypt damage
How is the severity of UC graded?
Paediatric Ulcerative Colitis Activity Index (PUCAI) - N.B. be aware of coexistent depression
Truelove and Witts score
What psychiatric condition can co-exist with UC?
Depression
NOTE: Paediatric Ulcerative Colitis Activity Index (PUCAI)
How is UC managed?
1st line: topical –> oral aminosalicylates – if no improvement 4 weeks after starting, move to oral, then 2nd line
Often used to maintain remission
Can use oral azathioprine or mercaptopurine if aminosalicylates insufficient
2nd line: topical –> oral corticosteroid (i.e. if aminosalicylates not tolerated/contraindicated)
Prednisolone
Beclomethasone
3rd line: oral tacrolimus
4th line: biological agents (infliximab, adalimumab and golimumab)
5th line (resistant disease) –> surgery (colectomy with ileostomy or ileojejunal pouch)
what is 1st line management of UC?
topical –> oral aminosalicylates
NOTE: If no improvement after 4 weeks, try oral, before 2nd line –> topical –> oral immunosuppressants
What is often used to maintain remission in UC?
aminosalicyclates
What is 2nd line in UC?
2nd line: topical –> oral corticosteroid (i.e. if aminosalicylates not tolerated/contraindicated)
Prednisolone
what is 3rd line in UC?
oral tacrolimus
Preceded by: topical+oral aminosalicyclates, topical+oral corticosteroids
What biologic agents used in UC?
infliximab, adalimumab and golimumab
NOTE: 4th line after aminosalicyclates, corticosteroids and oral tacrolimus
When is surgery used in UC?
Resistant disease
NOTE: after trialling oral aminosalicyclates, oral corticosteroids and oral tacrolimus and biologic agents
What surgery is used in UC?
colectomy with ileostomy or ileojejunal pouch
Management of severe fulminating disease in UC
IT IS AN EMERGENCY
MDT approach (medics and surgeons)
IV corticosteroids or ciclosporin and assess likelihood of needing surgery
Consider IV ciclosporin (if IV corticosteroids are contraindicated or ineffective)
When is an MDT approach needed in UC?
SEVERE FULMINATING DISESE - MEDICAL EMERGENCY
PACES: What support to offer in UC?
UC is associated with an increased risk of bowel cancer
Regular screening performed after 10 years of diagnosis
Support: Crohn’s and Colitis UK
Crohn’s vs UC (table)
What is the immune reaction against in coeliac?
Gliadin
Genetic associations of coeliac
HLA DQ2 (95%) and DQ8 (80%) association
How does coeliac present?
Malabsorption syndrome (failure to thrive, abdominal distension, bloating, irritability)
Malnutrition (check weight, height, BMI) –> wasted buttocks and distended abdomen
Pathogenomic = dermatitis herpetiformis (pruritic papulovesicular elbow/knee rash)
What skin condition is pathognomonic for coeliac?
dermatitis herpetiformis (pruritic papulovesicular elbow/knee rash)
Signs of malnutrition in coeliac
wasted buttocks and distended abdomen
GI condition that causes dermatitis herpetiformis
Coeliac disease
What does malabsorption syndrome present with in coeliac?
failure to thrive, abdominal distension, bloating, irritability
How is coeliac investigated?
Serological diagnosis:
Most sensitive = IgA tissue transglutaminase (anti-tTG)
Less sensitive = IgA anti-endomysial cell antibodies (anti-EMA)
If IgA deficient IgG DGP / Deiminated Gliadin Peptide
FBC and blood smear (iron deficient, vitamin B12/folate deficient, vitamin D deficient)
Confirmation of diagnosis (n.b. grading with the ‘Marsh’ system):
Older children / adults OGD + jejunal biopsy (villous atrophy, crypt hyperplasia, ↑ IELs)
What is the most sensitive serological test for coeliac?
Most sensitive = IgA tissue transglutaminase (anti-tTG)
Less sensitive = IgA anti-endomysial cell antibodies (anti-EMA)
NOTE: NEED TO TEST FOR IgA deficeincy
What needs to be tested for before serological diagnosis of coeliac?
serum IgA levels
If IgA deficient IgG DGP / Deiminated Gliadin Peptide
What serological test is done if IgA deficient in coeliac?
IgG DGP / Deiminated Gliadin Peptide
What deficiencies may be seen in coeliac?
Iron deficient, vitamin B12/folate deficient, vitamin D deficient
Gold standard investigation for coeliac
Older children / adults OGD + jejunal biopsy (villous atrophy, crypt hyperplasia, ↑ IELs)
What findings may be found on blood film in coeliac?
hyposplenism –> target cells
What is found on biopsy of coeliac?
villous atrophy, crypt hyperplasia, ↑ IELs
villous atrophy, crypt hyperplasia, ↑ IELs on biopsy
Coeliac
What is seen in coeliac disease if there is non-adherence to diet?
micronutrient deficiency (vitamin D, iron), osteoporosis, EATL, hyposplenism
Management of coeliac
Remove all products containing wheat, rye and barley
MDT – dietician, child psychologist, school involvement, GP, gastroenterologist
Dietician referral (if problems with adhering to the diet) and annual (6-12m) review:
Regular checks of height & weight, r/v symptoms, diet, consider bloods
Support sources: Coeliac UK
Most important management point in coeliac
REMOVAL OF TRIGGER
PACES: What support to offer in coeliac?
Support sources: Coeliac UK
What are the two types of cow’s milk protein allergy? When do they present?
Can be immediate (IgE mediated) or delayed (non-IgE mediated) – usually presents in first 3m of life in formula-fed children
What type of cow’s milk protein allergy presents immediately?
IgE mediated
NOTE: Non-IgE mediated is delayed, usually presents in first 3m of life in formula-fed children
What type of cow’s milk protein allergy has a delayed presentation?
Non-IgE mediated is delayed, usually presents in first 3m of life in formula-fed children
NOTE: IgE mediated presents immediately
PACES: What is important to classify in cow’s milk protein allergy?
Classify the reaction – speed of onset (and relation to food), age of onset, severity, location, reproducibility, history
NOTE: take an atopic and feeding history too
“3-month-old baby that vomits and has diarrhoea after every feed”
Cow’s milk protein allergy
How does IgE mediated cow’s milk protein allergy present?
urticaria, angioedema, rash, erythema, nausea, D&V, colicky abdominal pain, sneezing, rhinorrhoea, congestion, cough, tightness, wheeze, ANAPHYLAXIS
What type of cow’s milk protein allergy can anaphylaxis occur in?
IgE mediated
How does non-IgE mediated cow’s milk protein allergy present?
erythema, atopic eczema, GORD, change in frequency of stools, blood/mucus in stools, abdominal pain, FTT, infantile colic, constipation, food aversion, pallor
Investigations for cow’s milk protein allergy
Test 1: Skin prick allergy testing OR
Test 2: Measurement of specific IgE antibodies (RAST)
When to refer to a specialist in cow’s milk protein allergy?
Faltering growth with ≥1 GI symptoms of allergy
≥1 acute systemic or severe delayed reactions
Severe atopic eczema
Persisting suspicion
Multiple allergies
Management of cow’s milk protein allergy
1st Trial cows’ milk elimination from diet for 2-6 weeks:
Breastfed Babies: mother to exclude cow’s milk protein from her diet
Consider prescribing daily supplement of 1g of calcium and 10 mcg of vitamin D
N.B. it takes 2-3 weeks to fully eliminate cow’s milk from breastmilk
Formula-fed Babies: replacement of cows’ milk-based formula with hypoallergenic infant formula (e.g. extensively hydrolysed formula or amino acid formula if SEVERE: use amino-acid based formula)
Weaned infants/older children: exclude cows’ milk protein from their diet
2nd Regularly monitor growth, nutritional counselling with a paediatric dietician
3rd Re-evaluate tolerance to cows’ milk protein (every 6-12 months) re-introduce cows’ milk protein into the diet if tolerance is established, greater exposure of less processed milk is advised with ‘Milk Ladder’
1st line management of cow’s milk protein allergy
Trial cows’ milk elimination from diet for 2-6 weeks:
Breastfed Babies: mother to exclude cow’s milk protein from her diet
Consider prescribing daily supplement of 1g of calcium and 10 mcg of vitamin D
N.B. it takes 2-3 weeks to fully eliminate cow’s milk from breastmilk
Formula-fed Babies: replacement of cows’ milk-based formula with hypoallergenic infant formula (e.g. extensively hydrolysed formula or amino acid formula if SEVERE: use amino-acid based formula)
Weaned infants/older children: exclude cows’ milk protein from their diet
Initial management of cow’s milk protein allergy
Trial cows’ milk elimination from diet for 2-6 weeks:
How to manage breastfed babies with cow’s milk protein allergy?
Initially Trial cows’ milk elimination from diet for 2-6 weeks
Then Breastfed Babies: mother to exclude cow’s milk protein from her diet
Consider prescribing daily supplement of 1g of calcium and 10 mcg of vitamin D
N.B. it takes 2-3 weeks to fully eliminate cow’s milk from breastmilk
How to manage formula fed babies with cow’s milk protein allergy?
Initially Trial cows’ milk elimination from diet for 2-6 weeks
Then Formula-fed Babies: replacement of cows’ milk-based formula with hypoallergenic infant formula (e.g. extensively hydrolysed formula or amino acid formula if SEVERE: use amino-acid based formula)
How to manage weaned infants/older children with cow’s milk protein allergy?
Initially Trial cows’ milk elimination from diet for 2-6 weeks
Then Weaned infants/older children: exclude cows’ milk protein from their diet
What is the most common acuse of abdominal pain in childhood?
Appendicitis
NOTE: rare in <3 year old
What is the most common cause of appendicitis in pre-school children?
Faecolith
What is the most common cause of appendicitis post-preschool?
Perforation
What cause of appendicitis can be seen on AXR?
Faecolith
How does appendicitis present?
Anorexia, vomiting, nausea
umbilical–>RIF pain
Fever, tenderness, etc.
Investigations for appendicitis
FBC, pregnancy test (if female)
Clinical (watchful waiting observation)
Consider USS if diagnostic uncertainty
Mainstay of investigation for appendicitis
CLINICAL DIAGNOSIS
When to consider USS in appendicitis
If diagnostic uncertainty
NOTE: APPENDICITIS IS PREDOMINANTLY A CLINICAL DIAGNOSIS
Management of appendicitis
GAME:
G (Group & Save)
A (ABx IV)
M (MRSA screen)
E (Eat & drink – must be NBM)
THEN APPENDICECTOMY
Who does mesenteric adenitis affect?
Mainly in children <15yo; recent viral/bacterial infection (including UTIs)
What is usually the precursor to mesenteric adenitis?
Recent viral/bacterial infection (including UTIs)
How does mesenteric adenitis present?
Abdominal pain – central or RIF
(Nausea ± diarrhoea)
↓ appetite
Differential for appendicitis
Mesenteric adenitis –> May present with Nausea+Diarrhoea –> similar to appendicitis, hence bloods and USS can be used to differentiate
What can be used to differentiate mesenteric adenitis from appendicitis?
Bloods to exclude appendicitis (bloods, urine MC&S, USS)
How to confirm diagnosis of mesenteric adenitis
CLINICALLY
Definitive diagnosis of mesenteric adenitis
Large mesenteric lymph nodes seen at laparoscopy (w/ normal appendix)
NOTE: Never done
Management of mesenteric adenitis
Simple analgesia (symptoms usually resolve in a few days, maximum 2 weeks)
Safety net for increased pain or deterioration
PACES: What to safety net for in mesenteric adenitis?
increased pain or deterioration
What is the most common surgical emergency in newborn babies>
Necrotising enterocolitis
Who does necrotising enterocolitis tend to affect?
Premature babies and LBW
What does necrotising enterocolitis lead to?
Serious intestinal injury
When does necrotising enterocolitis often begin?
After starting enteral feeding, occurs due to immature/fragile bowels
How does necrotising enterocolitis present?
Early signs = biliary vomiting, feed intolerance
Abdomen distension
Blood-stained stool
Rapid deterioration and shock
Early signs of necrotising enterocolitis
biliary vomiting, feed intolerance
Investigations for necrotising enterocolitis
AXR – ‘gas cysts’ in bowel wall, distended loops of bowel with thickened walls
Blood cultures
AXR findings for necrotising enterocolitis
‘gas cysts’ in bowel wall, distended loops of bowel with thickened walls
AXR findings - ‘gas cysts’ in bowel wall, distended loops of bowel with thickened walls
Necrotising enterocolitis
Management of necrotising enterocolitis
Bowel rest (NPO (stop oral feed) and switch to parenteral nutrition)
Broad-spectrum antibiotics (cefotaxime/tazocin and vancomycin)
Stage IA/IB (3 days), stage IIA (7-10 days), stage IIB, III (14 days)
Laparotomy (if perforated as seen on AXR)
1st step in necrotising enterocolitis management
Bowel rest (NPO (stop oral feed) and switch to parenteral nutrition)
Followed by: Broad-spectrum antibiotics (cefotaxime/tazocin and vancomycin)
Which broad spectrum ABs are used in necrotising enterocolitis management?
Cefotaxime/tazocin and vancomycin
NOTE: Preceded by Bowel rest (NPO (stop oral feed) and switch to parenteral nutrition)
When is surgical management done in necrotising enterocolitis?
If perforation seen on AXR –> laparotomy
Long term consequences of necrotising enterocolitis
Development of strictures
Malabsorption (if extensive bowel resection is necessary)
NOTE: (20% mortality/morbidity acutely)
How do threadworms present?
Itchiness in anal/perianal region
PACES: Important question to ask in threadworm history
Who is in the house (highly transmissible)
Investigations for threadworms
Clinical
Stool sample (ova, cysts, parasites)
Management of threadworms
Single dose of an anti-helminth (mebendazole) for the whole household
Repeat dose 2 weeks alter if infection persists
Rigorous hygiene for 2 weeks if on mebendazole or 6 weeks if using hygiene measures alone:
Hand washing
Cut fingernails regularly, avoid biting nails and scratching anus
Shower everyday, including perineal area, to remove eggs from skin
Change bed linin and nightwear daily for several days after treatment (don’t shake bedsheets)
Thoroughly dust and vacuum
Exclusion from school/nursery is NOT required
Children <6 months should be treated with hygiene measures alone for 6 weeks (seek advice from ID)
Treating all household contacts
What medication should be given for threadworms?
Mebendazole (anti-helminth)
Who should the medication be given to in threadworms?
Entire household –> mebendazole (anti-helminth)
Is school exclusion required for threadworms?
NO EXCLUSION FROM SCHOOL/NURSERY IS NOT REQUIRED
How long are hygiene measures required for in threadworm management?
Rigorous hygiene for 2 weeks if on mebendazole or 6 weeks if using hygiene measures alone:
What is the commonest cause of loose stools in preschool kids?
Toddler’s diarrhoea
Cause of toddler’s diarrhoea
Underlying maturational delay in intestinal mobility
Presentation of toddler’s diarrhoea
Varying consistency stools (well-formed to explosive and loose ± presence of undigested vegetables in stool)
NOTE: Child is well and thriving (no precipitating dietary factors and normal examination)
Investigations for toddler’s diarrhoea
CLINICAL DIAGNOSIS
Management of toddler’s diarrhoea
Increased fibre and fat in diet (whole milk, yoghurts, cheeses) relieve symptoms
Avoid fruit juice and squash
What to avoid in toddler’s diarrhoea?
Avoid fruit juice and squash
What is infantile colic?
Paroxysms of uncontrollable crying in an otherwise healthy infant.
When does infantile colic typically resolve by?
3-12 months
Presentation of infantile colic
manifests as random inconsolable crying and drawing up on the hands and feet
PACES: Questions to ask in infantile colic
Clarify onset and duration of episodes
Clarify what happens in these episodes
Rule out any signs of illness
Check how parents are coping / support
How is infantile colic diagnosed?
CLINICALLY
Management of infantile colic
Soothe infant – hold with gentle motion, optimal winding technique, white noise
If persistent → consider cow’s milk protein allergy or reflux, consider:
(1) 2-week trial of whey hydrolysate formula; followed by
(2) 2-week trial of anti-reflux treatment
Support:
Self-help support group www.cry-sis.org.uk for families with excessive crying or sleepless children
Get support from health visitor, family, friends and other parents
What diagnoses to consider if infantile colic?
consider cow’s milk protein allergy or reflux
consider:
(1) 2-week trial of whey hydrolysate formula; followed by
(2) 2-week trial of anti-reflux treatment
PACES: What support to offer for infantile colic?
Self-help support group www.cry-sis.org.uk for families with excessive crying or sleepless children
Get support from health visitor, family, friends and other parents
What can be given as a trial medication for infantile colic?
Simeticone (anti-flatulant)
random inconsolable crying and drawing up of the knees
Infantile Colic
What is eosinophillic oesophogitis?
Inflammation of the oesophagus associated with activation of eosinophils within the oesophageal mucosa and submucosa.
Risk factors for eosinophillic oesophagitis
Atopic conditions (asthma, hay fever, eczema)
Clinical features of eosinophillic oesophagitis
dysphagia
Investigations for eosinophiliic oesophogitis
Imaging:
OGD and biopsy (to identify eosinophilic infiltration)
Management of eosinophilic oesophagitis
Oral Corticosteroids
What is IBS?
Chronic condition characterised by abdominal discomfort and issues with intestinal motility (diarrhoea or constipation or both).
what sex is IBS more common in?
Females
RFs for IBS
Depression
Anxiety
Female Sex
Family History
Presentation of IBS
Non-specific abdominal pain (often relieved by defecation)
Diarrhoea
Constipation
Bloating
How to diagnose IBS?
Diagnosis of exclusion
Management of IBS
Reassurance
Identify and attend to sources of stress and anxiety
Encourage fluid intake
FODMAP diet
Mebeverine (anti-spasmolytic)
