Gastro D-G

Question 1

What is Exomphalos and gastroschisis?

Answer 1

Congenital anterior wall defects resulting in herniation of abdominal viscera.

Question 2

What is the background of Exomphalos and gastroschisis?

Answer 2

Exo: 3/10k, Gastrosch: 5/10k.

Embryology: abdominal wall forms after the infolding of caudal and rostral and two lateral embryonic folds. This starts at 6/40 and ends at 12/40, when the intestine undergoes 270deg clockwise rotation and then returns into abdominal cavity.

Exomphalos: failure of migration of bowel back into abdomen, remaining in umbilical cord. Failure of abdominal wall folding.

Gastroschisis: ischaemic injury to developing anterior abdominal wall leading to evisceration of bowel through a defect in the right side of abdominal wall.

Question 3

What are the associations of Exomphalos and gastroschisis?

Answer 3

General: history of ischaemia in the foetus, may be associated with maternal smoking and drug use, alcohol.

Exomphalos: associated with chromosomal abnormalities (commonly trisomy 18/13). Increased maternal age. Pentalogy of Cantrell: cranial fold defects, exomphalos, diaphragmatic hernias, sternal clefts, pericardial and cardiac defects.

Gastroschisis: Rare associated abnormalities, intestinal atresia, cryptorchidism, low maternal age.

Question 4

What are the history and exam findings of Exomphalos and gastroschisis?

Answer 4

Antenatal: USS detection in utero, transfer to paediatric surgical centre with antenatal counseling.

Exomphalos: Herniation of the bowel, liver or other organs into umbilical cord. Herniated viscera enveloped in a membrane.

Gastroschisis: Intatct umbilical cord but evisceration through a defect to the right of the cord. No membrane covering. Red matted bowel loops.

Question 5

What investigations would you do for Exomphalos and gastroschisis?

Answer 5

USS: screening antenatally

Amniocentesis: if associated with chromosomal abnormalities.

Question 6

What is the management of Exomphalos and gastroschisis?

Answer 6

General: resusc, NGT with frequent aspirations, IV access with dextrose feeding. Intubation and ventilation with surfactant therapy. Prophylactic antibiotics. Cling film therapy to reduce water losses.

Surgical: prompt assessment to make diagnosis and ensure bowel is not compromised. Compromise requires urgent surgery.

Definitive surgical management: Majority of lesions are fixed by primary closure. Larger lesions may require spring loaded silastic silo applied in the NNU. Staged reduction then achieved over two weeks, with eventual complete closure and reduction of intra abdominal pressure / intra gastric pressure.

Question 7

What is the prognosis and complications of Exomphalos and gastroschisis?

Answer 7

Adhesions, SBS, syndrome related cmx, volvulus antenatally.

Good with antenatal diagnosis, and appropriate surgical management.

Question 8

What is Encopresis (fecal soiling)?

Answer 8

Voluntary or involuntary passing of faeces in places and moments when inappropriate, in a child of age at which fecal control is expected (>4y).

Question 9

What is the background of Encopresis (fecal soiling)?

Answer 9

3/100 children, reduces with age.

Retentive encopreis: occurs with chronic constipation: rectal fullness -> distension -> muscle weakness and distension -> loss of normal sensory information and muscle control -> fecal soiling.

Non retentive encopresis: without constipation

Emotional: due to conflict at home, psychological distress, neglect.

Related to surgical treatment for Hirschprungs, anorectal malformations, neuropathy, behavioral problems, low birthweight and enuresis.

Question 10

What are the history and exam findings of Encopresis (fecal soiling)?

Answer 10

Detialed history of encopresis, neonatal and birth, social history important too.

Abdominal: distension and impacted feces if constipated.

DRE: only by senior doctors, can feel impacted feces if constipation, enel fissures or tears, anal tone and wink, (lax if both retentive of ARM etc related).

Question 11

What investigations would you do for Encopresis (fecal soiling)?

Answer 11

Anorectal manometry: to measure defecation dynamics, exclusion of ultra short Hirschprings.

Radionuclear transit scintiography: identifies slow colonic transit.

Question 12

What is the management of Encopresis (fecal soiling)?

Answer 12

Medical: constipation management with diet, activity, routines, enemas, colonic evacuation (disimpaction). Laxative (ie Senna) at night encouraging motion after breakfast.

Behavioral strategies: if psychosocial cause suspect. Scheduled toileting, resolving conflict and stress.

Parental child education: avoiding conflict and anger, positive reinforcement of patterns.

Biofeedback training: to resolve paradoxical constriction of external anal sphincter in children with chronic constipation. Allows EAS relaxation.

Surgical intervention: anterograde continence enema in Hirschprungs, aloowing administration of enema directly into caecum or distal colon.

Question 13

What is the prognosis and complications of Encopresis (fecal soiling)?

Answer 13

Low self esteem, psychological, fall behind in school.

Depends on cause, unusual to persist after teenage years.

Question 14

What is Food allergy?

Answer 14

Immune mediated hypersensitivity reaction to food proteins.

Question 15

What is the background of Food allergy?

Answer 15

6-8% of children. 90% are caused by the big eight: cows milk, peanuts, sesame, kiwi, eggs, wheat, fish, soybean, shellfish, nuts.

Associated with parental atopy and atopic eczema, allergy, allergic rhinitis.

Question 16

What are the history and exam findings of Food allergy?

Answer 16

Same as CMPA

Question 17

What investigations would you do for Food allergy?

Answer 17

Same as CMPA

Question 18

What is the management of Food allergy?

Answer 18

Avoidance: once confirmed, dietitian input is key. Advice on eating out, food labels etc.

Emergency plan: in IgE mediated, training on how to assess severity of reaction. Wearing MedicAlert bracelet. Epipen is indicated in children with proven cardiorespiratory symptoms as a result of contact with allergen. Often indicated in peanut or tree nut allergy, or in teenagers.

Question 19

What is the prognosis and complications of Food allergy?

Answer 19

Anaphylaxis.

Children often grow out of all, apart form nut/peanut allergies and shellfish.

Question 20

What is Functional abdominal pain?

Answer 20

Abdominal pain of enough severity to interfere with daily activities but with no proven underlying pathological disease.

Question 21

What is the background of Functional abdominal pain?

Answer 21

4-25% of school children.

Intermittent or continuous (Rome III criteria). Chronic >2/12. Proposed mechanisms:

· Enteric nervous system ENS: response to noxious or stressful stimuli (inflammatory) psychological (anxiety) or physiological (distension from meal)

· Visceral hyperplasia: low pain threshold to high interluminal pressure, altered sensation in nerves by infection or inflammation.

· Biopsychosocial model: response to biological factors, governed by interaction with environment.

Pthology: marked basal hyperplasia, vascular ectasia and numerous intraepithelial eosinophils / lymphocytes. Lymphoid aggregates , crypt hyperplasia, villous atrophy, increased intraepithelial lymphocytes in duodenum.

Question 22

What are the history and exam findings of Functional abdominal pain?

Answer 22

Needs to be distinguished from anatomica, infectious, inflammatory or metabolic cuase of pain. May be present with dyspepsia, IBS, migraine of FAPS.

· IBS: pain worse before and relieved after defecating. Stools with excess mucus, bloating, incomplete defecation and constipation.

· Functional dyspepsia: epigastric pain, postprandial vomiting, early satiety and GOR.

· Abdominal migraine: paroxysmal pain with anorexia, N&V, pallor.

· Functional abdominal pain syndrome: FAP without the three above syndromes. (IBS, FD, AM).

Question 23

What investigations would you do for Functional abdominal pain?

Answer 23

If symptoms and signs indicate organic cause (weight loss, deceleration of growth, GO blood loss, significant vomiting, localized pain, pyrexia, FHx IBD.

Endoscopy with negative biopsy may exclude organic disease. USS for RIF / RUQ pain for gallstones / ovarian cyst / appendix.

Question 24

What is the management of Functional abdominal pain?

Answer 24

Supportive: positive diagnosis, not by exclusion. Careful explanation, headache parallel, reasonable goals establishment, absence of organic disease.

Psychological: may require therapy to work out stresors, biofeedback, CBT.

Medical: time limited analgesia use. H2 antagonists of PPI.

Dietary modifications: no evidence.

Question 25

What is the prognosis and complications of Functional abdominal pain?

Answer 25

Psychological, school missing, family dynamics.

Self limiting, resolves in most.

Question 26

What is Gastroenteritis?

Answer 26

Inflammation of the GI tract secondary to acute infection by enteropathogen

Question 27

What is the background of Gastroenteritis?

Answer 27

Viral: rotavirus, norovirus, adeovirus, coronavirus

Bacteria:

· Neurotoxin producing: Staph Areus and Bacillus Cereus, cause severe neurogenic vomiting after ingestion

· Enterotoxin producing: E coli and V cholera, act on secretory mechanisms by increasing cAMP and therefore Cl- and subsequent H2O secretion in lumen.

· Cytotoxin producing: Shigella dysenteriae, V parahemolitycus, C difficile, EHEC, lead to enterocyte destruction and damage to brush border.

· Mucosal inflammation: Shigella, Campylobacter, EIEC, cause mucosal destruction and inflammatory diahrrea.

· Mucosal invasion causing enteric fever: Salmonella and Yrsenia invade enterocytes but do not cause cell death, so no dysentery occurs. However, bacterial translocation via lamina propria may occur, leading to enteric fever

Related to poor sanitation, nutrition and antibiotic use and immunocompromise.

Epidemiology
UK: average 2-3 per year per child.

Question 28

What are the history and exam findings of Gastroenteritis?

Answer 28

General: pyrexia, D&V, unwell, no appetite, pain

Specific: diahrrea (color/character/frequency question) depending on pathogen. Establish time lapse between food consumption and onset.

Assess dehydration status: Mild (<4% no signs), Moderate (>5%) dry MM, low skin turgor, cool peripheries. Severe (10%) skin lax, sunk eyes and fontanelle, impaired circulation. Extreme (10-15%) leads to shock and coma.

Stool exam: blood, consistency, colour, mucu.

Question 29

What investigations would you do for Gastroenteritis?

Answer 29

General: monitor vitals and temperature.

Blood: FBC, WCC, LFT.

Stool MCS

Question 30

What is the management of Gastroenteritis?

Answer 30

General: mild to moderate dehydration may require fluids, try to encourage drinking if keeping down

Oral rehydration therapy (ORT) with ESPGHAN

Mild dehydration: short term ora glucose electrolyte solution (dioralyte)

Moderate dehydration: 6h trial of ORT, if no improvement, IV.

Severe dehydration: IV. Treat shock with plasma expanders, K supplementation to be considered.

Question 31

What is the prognosis and complications of Gastroenteritis?

Answer 31

Dehydartion, post gastroenteritis syndrome, acute renal failure, severe dehydration.

Developing countries: 5 million children <5 die per year

Developed countries: very low <1% mortality.

Question 32

What is Gastro oesophageal reflux disease?

Answer 32

Abnormal retrograde flow of gastric contents through LOS into oesophagus.

Question 33

What is the background of Gastro oesophageal reflux disease?

Answer 33

1/3k infants. GORD over-diagnosed due to difficulty to differentiate.

GOR: Normal in 60% infants, physiological due to underdeveloped sphincter. Predisposed by continuous supine position, short and straight intra abdominal oesophagus (angle of His – between gastric cardia and LO).

GORD: When frequency and duration produce symptoms. Due to delay in neuro maturation (preterm), neuro impairment (palsy, tri21, HIE), excessive spontaneous reductions in sphincter pressure (crying, coughing, defecation)

Related to CMPA, oesophageal atresia and hiatus hernia.

Question 34

What are the history and exam findings of Gastro oesophageal reflux disease?

Answer 34

Wide range of presentations, mild to severe. May cause respiratory symptoms.

General: feeding issues, discomfort, constant eating and drinking (milk is alkali) irritable, fail to thrive, tooth decay, may present as ALTEs.

GI: difficulty or pain on swallowing, sitting up or vomiting after meal, haematemesis, gastric/abdo/retrosternal pain

Resp: aopnea, stridor, chest infection

Question 35

What investigations would you do for Gastro oesophageal reflux disease?

Answer 35

24h pH monitoring of oesophagus (reflux index) / Impendance testing (accurate)

Contrast studies: of upper GI if anatomical abnormalities should be excluded.

Endoscopy: confirms oesophagitis, biopsies of LO, fundus and DD.

Question 36

What is the management of Gastro oesophageal reflux disease?

Answer 36

Conservative: unless failing to thrive. Thick feeds, positioning, low volume feeds.

Pharmacological: H2 antagonists (ranitidine/domperidone) also prokinetic.

Surgical: if fail conservative or medical management, Fundoplication preformed (nieesn 360 ot Toupet 180 or Belsey 270.) May involve gastrostomy.

Question 37

What is the prognosis and complications of Gastro oesophageal reflux disease?

Answer 37

Fail to thrive, Sandifer syndrome (dystonig head and neck movements). Oesophagitis, peptic stricture, Barrett oesophagus.

Aspiration pneumonia

60% resolve by 6month.