Child Development Lecture

MAA Paediatrics - Gastroenterology
Anorectal malformations (ARM)

Definition
Wide spectrum of disorders affecting the distal anus and rectum, with or without
involvement of the genitourinary tract.
Aetiology
Wide spectrum of disorders. Mild forms have a bowel outlet via a fistula in the
perineal region. Severe forms have bowel outlet in the genitourinary tract region
in males, or genital tract in females. Associated with other anomalies in 60%:
VACTERL, CHARGE, MURCS, OEIS, Trisomy 13/18/22, Hirschprungs,
vertebral/sacral abnormalities.
Wingspread classification: by the relation of the fistula or pouch to levator
muscle complex (low/intermediate/high)
Krickenbeck classification:
 Major group (wither with presence of fistula – perineal /rectourethral/
prostatic/ bulbar/ retrovescical/ vestibular. There may be no fistula, and
colaca or anal stenosis).
 Minor group (pouch colon, rectal atresia/stenosis, rectovaginal fistula, H
fistula and others).
Epidemiology
1/5k live births.
History/Examination
Clinical examination by surgeon to classify the type in 90%. Associated
abnormalities.
Specific for low lesions: prominent midline skin bridge (bucket handle),
subepithelial midline raphe fistula, rectovestibular fistula, anal membrane. A flat
perineum (absence of gluteal fold and anal dimple) may indicate absence of
perineum muscle and therefore high ARM.
Investigations
General: Screning for other abnormalities: CXR, ECHO, RUSS, Karyotype, USS for
hydrometytrocolpos/spinal abnormalities, sacral XR, urinalysis.
Specific: Prone cross table lateral XR with specific marker for perineum (air
column to marker <1cm low lesion, >1cm colostomy). High pressur distal
colostography.
Management
Medical (neonatal): REsuscitaiton, abnormalities screening, NBM, IVI, Abx,
transfer to paediatric surgery centre. Ovserve? Passage of meconium through
fistula/GUT.
Surgical (neonatal): Severe: primary diverting colostomy. Low: cutback
anoplasty/limited PSARP. Rectovestibular fistula dilation.
Surgical (definite): Posterior sagittal anorectoplasty (PSARP) with separate

colostomy closure.
Post surgical bowel management programmes inducidng enemas, laxatives and
dietary advice.
Complicaitons
Most common dunctional disorder is constipation. Urinary and fecal
incontinence may occur due to poorly developed spinal outflow.
Prognosis
Generally good, Low ARM has less complications than high.
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Acute appendicitis
Definition
Acute inflammation of the vermiform appendix
Aetiology
Obstruction of appendiceal lumen by faecolith  contraction  muscle decrease
venous drain and arterial supply  fail to relax  necrosis  peritonitis.
Related to poor fibre intake, increased fecal viscosity, and bowel transit time.
Epidemiology
Most common cause of acute abdomen in children, 4/1k children. Usually >5y.
History
Large variation in clinical picture, Classically colic pain from umbilicus to RIF.
Constant with peritoneal inflammation and more with movement. Anorexia,
vomiting, constipation and diahrrea. Fever (low grade)
Examination
General: tachycardia, pyrexia, not moving
Abdominal exam: rebound tenderness, guarding with palpation in RIF
(McBurney’s point). Rosving’s sign (RIF pain reproduced with palpation of LIF).
There may be pain in breathing and coughing.
Rectal exam: should only be preformed by most senior doctor, only if diagnosis
in doubt. Tenderness against anterior abdominal wall.
Investigation
General: clinical diagnosis
Bloods: increased WCC, CRP/ESR, U&E if vomiting.
Utine: MCS if UTI is DDx.
Radiology: plain XR may show dilated loops of bowel proximal to appendix. Not
necessary to preform.
Management
Traditional open surgical approach (Lanz incision) or laprescopically. Washout
essential if complicated by perforation.
Conservative: with confirmed appendiceal abscess that responds to IV abx.
Interval appendicectomy offered.
Complications
Perforation very common in children <3, but very uncommon in children >10.
Abscess formation, wound infection, abdominal abscess, low fertility in girls if
complicated, obstructions, adhesions.
Prognosis
Usually excellent.
.
Coeliac disease
Definition
A lifelong luten induced enteropathy of the small bowel resulting in
malabsorption and inflammation, which resolves completely upon gluten
withdrawal
Aetiology
Sensitivity to the a-gliadin component of gluten protein. Immunological reaction
to this component leads to mucosal damage.
Associated with HLA DQ2 or DQ8.
Pathology: Macro - subtotal villous atrophy of proximal SI, flattened mucosa.
Micro – inflammatory infiltrate, crypt hyperplasia, atrophy.
Epidemiology
1% positive in the UK.
History
Classic history of constipation, abdominal pain, weight loss, failure to thrive,
steatorrhea, fatigue, irritability.
Examination
Many children will have no abnormal findings.
General: miserable, pale, anaemic, irritable, clubbing, uttock wating, pot belly
appearance, distension, delayed puberty.
Dermatitis herpetiformis: causing itchy blisters on elbows, knees, face, buttocks.
Investigation
Serological testing offered in any individual with AI thyroid disease, dermatitis
herpetiformis, IBS, T1DM and first degree relatives.
Serology: check IgA level as 2% will be deficient. Abx directed against tTga, or
anti EMA antibodies.
Bloods: low Hb, high MCV (B12 def) low Ca and albumin if severe.
Jejunal biopsy: gold standard for diagnosis, shows subtotal villous atrophy and
crypt hyperplasia.
Gluten challenge can confirm.
Management
Prevention: breastfeeding while weaning onto wheat may be protective.
Nutritional advice: complete avoidance required. Strict diet. Iron supplements.
Complications
Osteoporosis, higher chance of leukemia, secondary lactose intolerane due to
damage to brush border, bacterial overgrowth, social morbidity, decreased
fertility, weight gain after dx.
Prognosis
With adherence to diet, fine.
.
Constipation
Definition
Delay or difficulty in defecation, for over two weeks or enough to cause
considerable distress.
Aetiology
Functional: 90-95%. Due to vicious cycle of retention, pain on defecation, more
retention.  retention leads to pain, and eventually leads to decreased sensory
input. Chronic retention then also leads to dilation of rectum, muscle weakness,
and reabsorption of more water from stools leading to harder and harder stool.
Slow transit constipation STC: poor prognosis, refractory to medical
management.
Nutritional: coeliac, CMPA, intolerance, low fibre diet.
Organic (rare) due to GI abnormalities: Hirschprungs, neuromuscular disease,
spinal disease, anal atresia or abnormalities, hypothyroidism, cerebral palsy.
Epidemiology
Very common – 3-5% and 35% gastro clinic presentations.
History
Pain, difficulty passing stool, may have diahrrea.
Take history of diet, social setting, stress factors, birth. Delayed meconium
passing (>24h) is common in Hirschprungs.
Examination
General: abdominal distension and pain, presence of stool.
DRE: location of anus, tone, anal wink, presence of stools in passage, presence of
anal fussires, fistulae etc.
Investigation
Radiology not helpful
Anorectal manometry: to measure pressures in bowel and anus
Radionuclear transit scintiography: to identify causes of slow colonic transit.
Management
General: evacuation of stools, education of emptying, regular routine.
Medical: lidocaine gel if fissure, dietary changes, exercise etc
Hurschprungs: ENdorectal pullthrough, with placement antegrade continence
enema.
Other: ?transcutanous electrical stimulation
Complications
Fecal overload, encopresis, peritonitis, overflow incontinence, behavioral
difficulty.
Prognosis
50% recoverin 1y and 65% in 2y. REMainder require laxative therapy.
.
Cow’s milk protein allergy (CMPA)

Definition
Immune hypersentivitiy reaction to cows milk.
Aetiology
Related to parental atopy. Reaction to cows milk proteins, either whey or casein
(80%). Children often also suffer from atopic eczema and other allergies.
Epidemiology
2.5% at 1y.
History / Examination
Symptoms within the first five weeks of introducing cow’s milk. Divided into
immediate IgE, Mixed IgE and non IgE, and Delayed Non IgE
 Immediate IgE (1h)
o Skin – flush, itch, urticarial, angioedema
o Resp: wheeze, angioedema, cough, bronchospasm
o CVS: tachycardia and hypotension
o GI: vomiting, diahrrea, abdominal pain
o Pathophysiology: exposure to food in a sensitized individual leads
to mass degranulation of PG/LKT from Mast cells, activated by IgE
cross binding.
 Mixed IgE and Non IgE (2-12h)
o Skin: atopic eczema
o GI: eosinophilic oesophagitis (leading to reflux, food aversion,
dysphagia) proctolitis (bloody stools in otherwise well child)
 Delayed non IgE (12+h)
o GI: food protein induced enterocolitis, FPIES – presents with
vomiting and possibly diahrrea, shock and metabolic acidosis.
Failure to thrive, constipation.
o Pathology: food protein taken up by APCs, presented to T cells. Th2
interact with B cells and produce allergic cytokines leading to
inflammation
Investigation
IgE mediated: skin prick tests and specific IgE (95% positive) Gold standard is a
double blind, placebo food trial.
Non IgE mediated: no good diagnostic criteria other than exclusion trials. Blood
may show signs of malabsorption (low Hb, low Alb).
Management
Prevention: breastfeeding up until 4 months can be protective, especially in
families with atopy. Maternal avoidance of dairy may be required. If no
breastfeeding, hypoallergenic formulas essential.
Avoidance: all mammalian dairy products. Replace cows milk with either
extensively hydrolised formulas EHF, or with Amino acid formulas. If those still
cause problem, rice/soya/pea milk may be given fortified with calcium.
NB: soya milk has high cross allergenicity in children therefore often not an
option.
Reintroduction: may be attempted in children who can tolerate traces of milk
over 6-12m.
Complications
Anaphylaxis risk, failure to thrive, malabsorption, electrolyte disturbances from
vomiting, existence of other allergies and therefore asthma.
Prognosis
IgE mediated, 1/3 resolve by 2y, ½ by 3, and 2/3 by 4. Non IgE, 90% by 3y.
High risk of eczema developing, and allergic asthma / rhinitis.
.
Exomphalos and gastroschisis

Definition
Congenital anterior wall defects resulting in herniation of abdominal viscera.
Aetiology
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.
Epidemiology
Exo: 3/10k, Gastrosch: 5/10k.
Associations:
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.
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.
Investigation
USS: screening antenatally
Amniocentesis: if associated with chromosomal abnormalities.
Management
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.
Complications
Adhesions, SBS, syndrome related cmx, volvulus antenatally.
Prognosis
Good with antenatal diagnosis, and appropriate surgical management.
.
Encopresis (fecal soiling)

Definition
Voluntary or involuntary passing of faeces in places and moments when
inappropriate, in a child of age at which fecal control is expected (>4y).
Aetiology
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.
Epidemiology
3/100 children, reduces with age.
History
Detialed history of encopresis, neonatal and birth, social history important too.
Examination
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).
Investigation
Anorectal manometry: to measure defecation dynamics, exclusion of ultra short
Hirschprings.
Radionuclear transit scintiography: identifies slow colonic transit.
Management
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.
Complications
Low self esteem, psychological, fall behind in school.
Prognosis
Depends on cause, unusual to persist after teenage years.
.
Food allergy
Definition
Immune mediated hypersensitivity reaction to food proteins.
Aetiology
Associated with parental atopy and atopic eczema, allergy, allergic rhinitis.
Epidemiology
6-8% of children. 90% are caused by the big eight: cows milk, peanuts, sesame,
kiwi, eggs, wheat, fish, soybean, shellfish, nuts.
History/ Examination
See CMPA.
Investigation
See CMPA.
Management
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.
Complications
Anaphylaxis.
Prognosis
Children often grow out of all, apart form nut/peanut allergies and shellfish.
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Functional abdominal pain (FAP)

Definition
Abdominal pain of enough severity to interfere with daily activities but with no
proven underlying pathological disease.
Aetiology
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.
Epidemiology
4-25% of school children.
History/Examination
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).
Investigation
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.
Management
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.
Complications
Psychological, school missing, family dynamics.
Prognosis
Self limiting, resolves in most.
.
Gastroenteritis
Definition
Inflammation of the GI tract secondary to acute infection by enteropathogen
Aetiology
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.
History
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.
Examination
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.
Investigation
General: monitor vitals and temperature.
Blood: FBC, WCC, LFT.
Stool MCS
Management
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.
Complications
Dehydartion, post gastroenteritis syndrome, acute renal failure, severe
dehydration.
Prognosis
Developing countries: 5 million children <5 die per year
Developed countries: very low <1% mortality.
.
Gastro oesophageal reflux disease

Definition
Abnormal retrograde flow of gastric contents through LOS into oesophagus.
Aetiology
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.
Epidemiology
1/3k infants. GORD over-diagnosed due to difficulty to differentiate.
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
Investigation
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.
Management
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.
Complications
Fail to thrive, Sandifer syndrome (dystonig head and neck movements).
Oesophagitis, peptic stricture, Barrett oesophagus.
Aspiration pneumonia
Prognosis
60% resolve by 6month.
Hernia: Congenital diaphragmatic hernia (CDH)

Definition
Congenital defects in the formation of the diaphragm which results in the
protrusion of abdominal contents into the thoracic cabity.
Aetiology
More common unilateral though may be bilateral. L>R. Bowel or intraabdominal
viscera may be herniated. Common for liver and spleen to be herniated, with
associated abnormal hepatic vasculatures. Associated with pulmonary tree
abnormalities, surfactant defificney and vasculature changes (hypoplastic lung)
 Posterolateral Bochdalek heriaL 90%, left sided, posterolateral
 Morgagni hernia 3%, right sided anterolateral
 Congenital hiatus hernia: rare, stomach through the esophageal hiatus.
Associated w/ cardiac abnormalities, affected siblings, PPH, CRA, malrotation of
bowel.
Epidemiology
1/2k infants.
History/Examination
Hx of polyhydramnios, cyanosis, respiratory distress as a neonate. Bochdalek
hernia: poor air entry on L and shift in cardiac sounds to the right of the chest.
Smaller defects present later as wheezy child or recurrent chest infection.
Investigation
Karyotype if appropriate, chromosomal studies
Radiology: CXR with placing of orogastric tube to aid gastric positioning. Cardiac
echo for associated abnormalities.
Management
Medical: NGT to decompress, respiratory support via ETT and mechanical
ventilation (avoid high peak inspiratory pressures) Avoid bag/mask. UAC/UVC
with monitoring of ABG. Surfactant administration after intubation. ?NO therapy
and ECMO.
Surgical: if stabilized, open subcostal approach or thoracoscopic/laproscopic
approach. Depends on position of hernia and surgeon. Surgical technique
involves careful reduction of herniated contents, definition of the posterior rim
and repair with non absorbable sutures.
Complications
Pulmonary hypoplasia, malrotation, volvulis, perforations, renal hypertrophy
Prognosis
Mortality 25-60%. Associated with degree of pulmonary hypoplasia.
Hernia: Inguinal hernias (IH)

Definition
Abnormal protrusion of abdominal structures through the inguinal canal and
into the inguinal region or scrotum.
Aetiology
Testicle develops retriperitoneally and then descends into the processus
vaginalis under the control of hormones and gubernaculum. The processus
vaginalis closes after development but rmains patent in some chinden (PPV)
allowing the passage of boewl (IH) or fluid (hydrocele) into the canal. In females,
the gubernaculum becomes the ovarian ligament and round ligament, with a PPV
it etends into the labium and becomes the canal of Nuck. Hernia is most
commonly ileum (male) or ovary (female).
Assoc w/ preterm, low BW, FHx, undescended testes, gastroschisis/exomphalos,
Ehlers Danlos, CF, CT disorders and anything increasing IAP.
Epidemiology
5% ful term and 30% premature infants. RHS 60%. Bilateral 15%.
History/Examination
Infant: inguinoscrotal swelling ,First presentation with incarceration. Unable to
palpate cord superiorly (Differentiate hydrocele) Reducible unless incarcerated.
Non transluminable.
Child: supine and standing position, expansile cough impulse
Incarceration: pain, tender non reducible scrotal mass, erythema, vomiting,
abdominal distension
DDX: torsion, hydrocele, retractile testes, indescended, femoral hernia,
lymphadenopathy.
Investigation
USS rarely needed to diagnose.
Management
General: herniotomy preformed, Hernia sac located, separated form vas deferens
and testicular vessels, transected and ligated. Can be laproscopic with placement
of intraperitoneal purse string for closure.
Neonate with reducible hernia: elective repair. Infant: elective repair.
Incarceration: manual reduction under sedation (IV morphine) with repair
within 48h.
Complications
Inguinal hernia: incarceration (50% within 1y). Henioromy recurrence 1%.
Prognosis excellent with surgical repair.
Hirschsprung disease
Definition
Aganglionosis of the enteric (Auerbach) and submucoasl (Meissner) plexus.
Results in functional obstruction.
Aetiology
General: affects anus and variable distance of bowel proximally from it. Classified
according to distal bowel affected (ultra short, short, long, total colonic, total
intestinal).
EmbryologyL failure of neural crest derived ganglion cells to migrate from
proximal to distal bowel during development, leading to lack of PSNS nerves. SNS
only in affected bowel leads to hyerptonicity and lack of secretion/ relaxation in
response to distension. This leads to stool stasis and narrow lumen.
Pathlogy: increased number of acetylcholinesterase stained nerve endings, and
hypertrophied nerve trunks in lamina propria or muscolaris propria.
Epidemiology
1/5k live births, 20% neonatal obstruction.
History
NN:
 Failure to pass meconium <24h.
 Acute intestinal obstruction, distension, poor feeding
 Life threatening enterocolitis
Infantile:
 Chronic obdurate constipation with abdominal distension, No soiling.
 Intermittend abdominal pain and fever during episodes
 Failure to thrive
Examination
Depends on age of presentation. Typically abdominal distension with dilated
bowel. PR exam leads to sudden explosive gush of stool as examination bypasses
aganglionic segment, Septic signs if infected
Investigation
Bloods: high WCC and CRP if infected. Blood cultures. venous gas.
Radiology: AXR shows dilated bowel, exclude atresia as DDX, Gastrogriffin enema
may show transition zone.
Suciton rectal biopsy: taken at 2, 3, 4 cm from anal margin. Full thickness biopsy
under GA required if insufficient sample with SRB
Anorectal manometry: older children with consitpaiton.
Management
Initial: managed with BS ABx, NGT decompress, rectal washouts. ? colostomy
Surgical: pull through preformed (3-6/12). Can be preformed with laproscopic
assistance, take biopsies for investigation of segment length
Complications
Enterocolitis, encopresis, constipation, incontinence,
Prognosis
Poor if not adequately managed. Enterocolitis mortality 50% if not treated.
Postoperatively good outcome but majority will retain intestinal problems.
.
Inflammatory bowel disease

Definition
Inflammatory chronic idiopathic condition of the bowel encompassing two
related but distinct syndromes: UC and CD.
Aetiology
Unknown, thought to be genetic and environmental factors. Genetic component
CD>UC. Smoking increases risk of CD but decreases risk of UC.
UC: Diffuse mucosal inflammation of rectum extending proximally, variable
length. Subdivision into distal, and extensive diseases.
CD: Patchy transmural inflammation characterized by skip lesions. Defined by
anatomical location or pattern of disease (inflammatory, fistulaitng or
structuring). Montreal classification.
Intermediate colitis (IC) 10% of children unclassifiable.
Epidemiology
Fhx , smoking, 5/100k. 60% CD, 30% UC, 10% IC. Usual diagnosis teenager or
late child.
History/Examination
General: UC has remission and exacerbations, skin manifestations rare, typically
bloating, diahrrea and pain. CD is more heterogenous and non specific, triad of
diahrrea/abdominal pain/weight loss.
Abdo pain C>U, Diahrrea U>C, rectal bleed U>C, wt loss C>U, lethargy C>U.
Signs o/e: anal fistulae, apthrous ulcers in mouth, clubbing, delayed puberty,
perianal abscesses, erythema nodosum or rash, liver disease, toxic megacolon.
Investigation
General: ESPHGAN IBD workup is consensus protocol
Bloods: low Hb, high ESR/CRP, low B12/folate. LFT (may need ERCP/USS if
abnormal due to PSC risk).
Specific: limited use of pANCA with UC, ASCA with CD, low sensitivity.
Microbiology: stool sample, C diff toxins.
Radiology: AXR strictures fistulae, small bowel follow through, Tc white cell stain
Endoscopy: eileocolonoscopy and upper GI endoscopy with histology of multiple
biopsies from all segments.
Management
CD: Exclusive enteral liquid nutrition, corticosteroids, Abx (perianal abscess),
aminosalycilates (mesalazine/sulphalazine), budesonide, IV steroids. Second
line: azathriopine, parenteral nutrition. Third line: infliximab and surgery
(strictures or fistulae). Remission maintenance requires AZA/6MCP.
UC: Induction of remission requires ASA/SLZ if mild and corticosteroids if

severe. Maintenance: ASA/MSLZ. Surgery with acute toxic megacolon required.
Complications
UC: toxic megacolon, perforation, CRC, PSC
CD: Megaloblastic anaemia, gallstones, perianal disease, strictures, obstruction.
Prognosis
Good with early detection and treatment, mortality highest in 2y post diagnosis.
.
Intussusception
Definition
Invagination or telescoping of part of the intestine (instussuscepian) into
another part of the intestine (intussusceptum).
Aetiology
90% idiopathic. 10% identified lead point – Peyers patches after a viral illness,
lymph nodes, Meckels diverticulum, adhesions from recent surgery, appendix
stump. Related to HSP and FAP.
Most common site of invagination is the terminal ileum into the caecum.
Mesenteric constriction  VR obstruction  engorgement  press out arterial
supply  more contraction due to acidosis  engorgement and odema –a>
intestinal infarction
Epidemiology
4/1k. 60%<1y, very rare over 2y.
History/Examination
Triad of symptoms: vomiting, colic pain, and PR bleeding.
Vomiting is non bilious and then becomes bilious once total obstruction occurs.
Pain episodes are severe with leg pulling etc. Redcurrant jelly stools.
Investigation
Bloods (CRP, UE, FBC, GS).
AXR: dilated bowel before site, crescent sign (curvilinear mass on the right, in
transverse colon before hepatic flexure).
USS: confirmatory investigation  donut or target sign.
Management
Urgent care: IV access, fluid resusc, NGT, IV Abx, confirmation with USS.
Therapeutic enemaL air, water or contrast enema for reduction. Three attempts
then stopped due to risk of perforation.
Surgical: if therapeutic enema fails (in long standing IS) laproscopic or open
technique, Right lower transverse incision.
Complications
Prolonged can lead to shick, perforation, peritonitis.
Prognosis
Highest recurrence risk in the first 24h.
.
Lactose intolerance
Definition
Inability to metabolise lactose due to lactase deficiency.
Aetiology
Congenital: AR condition
Primary: natural non persistence of enzymes after birth, mainly in Asian
population.
Secondary: damage to brush border following gastroenteritis.
NOT the same thing as CMPA. Disaccharide enxymes normally at brush border,
break down lactose into glucose and galactose. 50% activity required for
effective metabolism.
Epidemiology
Congenital is extremely rare, primary in 5% of children.
History/Examination
Gi Hx: loose stools, frothy and explosive, bloating, cramping, flatus. II: ask about
gastroenteritis recently.
Congenital: infantile diahrrea and failure to thrive.
Primary: GI symptoms increase with age due to progressive loss. Wide variety in
amount of lactose expressed.
Investigation
Hydrogen breath test: detects H2 in breath 3-6 hours after ingestion of lactose.
Stools for reducing substances: acidic as have undigested sugars.
Jejunal biopsy: rarely needed, differentiate from coeliac.
Management
Lactose is only in mammalian milk. Congenital require lifelong absolute
abstinence from milk. Beware of Ca supplementation in replacement products.
Primary: low lactose diet can be tolerated.
SecondaryL complete avoidance for 4-6w to allow mucosal regeneration
Complications
Malabsorption, failure to thrive, Ca deficiency if on different milk for Tx.
Prognosis
Congenital is a lifelong condition. Primary is variable depending on level of
residual lactase. Secondary is transient.
.
Liver disease, Chronic

Definition
Chronic disease of hepatic cells, leading to decrease in overall liver function.
Aetiology
Chronic active hepatitis:
 AI disease of parenchyma (AIH) or biliary tree (PSC) ( inflammatory
infiltrate with hepatocellular necrosis)
 Viral: HBV, HCV. ( death of hepatocytes at interface between
parenchyma and CT, with lymphocyte infiltration)
 DrugsL NSAID, Abx, AEDs, paracetamol.
Wilsons disease: hepatolenticular degeneration due to Cu deposits in brain, liver,
kidney and cornea. (AR gene 13 mutation with low serum ceruloplasmin/
defective bile excretion of Cu).
Cystic fibrosis.
Epidemiology
FHx, Hx of infection. HBV: 5% infected in world. The younger the infection the
higher the rates to chronic conversion. HCV infection in 1% worldwide, cirrhosis
interval 10-15y. AI hepatitis 0.1/100k. Wilsons 1/30k.
History/ Examination
Acute or insidious presentation
General fever, malaise, failure to thrive, loss of fat and muscle bulk.
GI: distended abdomen, scrotal swelling, dilated abdominal vein (portal HTN)
AI hepatitis: skin rash, lupus, arthritis, AIHA. Nephritis.
Wilson: KF ring >7y, neuro features >12y parkinonian.
Investigation
HBV/HCV serology and surface antigen screen
AI hepatitis anti SMA Ab, IgG levels (IgG >20mg/l), ANA in PSC, liver/kidney
microsomal antibodies.
Wilson disease: gene 13 mutaiton, low serum ceruloplasmin/copper. High
urinary copper and hepatic copper.
Management
HBV: immunize at risk, support, aIFN.
HCV: aIFN.
AI hepatitis 90% respond to prednisolone/AZA
Wilson: Penicillamine (reduces hepatic/CNS copper), Zn (reduces Cu
absorption), pyroxidone (prevents peripheral neuropathy) ? think of transplant
Complications
End stage liver disease, coagulation and electrolyte disturbances.
Prognosis
Depends on underlying pathology. Px improved with adequate tx of underlying
condition. AI has best prognosis.
Hepatitis, Acute
Definition
Acute failure of hepatic cells to maintain normal function.
Aetiology
Damage to hepatocytes caused by:
 InfectionL acute HepA/HepB, EBV
 DrugsL paracetamol, isoniazid, halothane, Amanita phalloides.
 Reye syndrome aspirin in patients<14y, associated with acute non
inflammatory encephalopathy associated with liver damage (especially if
with varicella). Shows microvescicular infiltration of the liver on
pathology.
Epidemiology
Uncommon in children, EBV in adolescents.
History/Examination
General: jaundice, encephalopathy, coagulopathy, hypoglycaemia, other
electrolyte disturbances.
Encephalopathy: drowsy, alternating irritability and drowsiness. Older may have
hx of aggression and being difficult.
Investigation
Blood: high BR, deranged clotting, high LFT, high NH4, glucose check
ABG: may have metabolic acidosis or alkalosis
Viral serology: hep EBV
CT.MRI brain to exclude encephalopathy
Management
Tx complications, including:
 Hypoglycaemia: dextrose infusion
 Sepsis: IV BSAbx
 Coagulaton defects: FFP and H2 blockers/PPI to prevent gastric bleed. Vit
K to be avoided unless necessary.
 Verebral odema: Hyperosmolar therapy
 Liver transplant with worsening clinical and biochemical profile.
Complications
Cerebral odema, haemorrage from gastritis, sepsis, pancreatitis
Prognosis
High mortality though uncommon. Poor signs include shrinking in size, rising BR
with falling transaminases, coagulation defects, progression to encephalopathy
and coma. Patients in coma have 70% morality if no transplant. .
Malrotation of the intestine

Definition
Failure of normal embryological rotation of the SI around the SMA during
development, predisposing to obstruction, volvulus and ischaemia.
Aetiology
Normal rotation around SMA in three stages – Stage I herniation, Stage II return
to abdomen with 270 counterclockwise rotation, stage III fixation.
Non rotation: midgut only rotates 180
Incomplete rotation: duodenal loop lacks 90 and caecocolic loop 180 of normal
270 rotation.
Epidemiology
1/500, Common PM finding.
History
Acute modgut volvulusL presents <1y, SO bilious vomiting, abdominal
distension, severe pain.
Chroning midgut volvulus: recurrent abdo pain, malabsorption, Between
episodes, normal.
Acute DD obstruction presents with forceful vomiting, abdominal distension,
gastric waves, Compression or kinking of duodenum by Ladd bands.
Chronic DD obstruction Presents in infancy with bilious vomiting, intermittent
abdominal pain.
Examination
Acute obstruction tachycardia, distension, tinkling bowel sounds.
Infarction/necrosisL shock (high HR, pallor, high CRT, low responsiveness(
pyrexia and acute peritonitis signs.
Investigation
Bloods: high WCC, low Hb if bleeding, UW, Acidosis with high lactate can be
present if vessel obstruction present.
AXR: Variable appearance with dilated loops of bowel or gasless abdominal field.
UGI contrast: if patient stable, preformed on all infants with bilious vomiting.
Corkscrew appearance with volvulus or DJ flexure to the right of midline with
malrotations (normal is on the left)
Management
Preoperative: correct fluid and electrolyte imbalance, BSAbx, NG tube insertion,
?UGI if stable.
Ladd procedure: reduction of volvulus, division of mesenteric bands, placement

of small bowel on right and large bowel on left, and appendicectomy. Transverse
supraumbilical incision.
Complications
Strangulaiton and necrosis, perforation, peritonitis, septic shock. Loss of small
bowel leading to SBS.
Prognosis
Good with prompt surgical management. Pgx dependson bowel preservation
extent.
.
Meckel’s diverticulum
Definition
Outpouching of the ileum along the antimesenteric border, containing
heterotopic tissue of the stomach (acid secreting parietal cells) pancreas or
normal intestinal mucosa.
Aetiology
GeneralL partial or incomplete involution of the vitelline duct
(omphalomesenteric duct) during embryogenesis. True diverticulum containing
all three layers of intestinal wall and its own blood supply.
Rule of 2: 2% population, 2 inches, 2 feet form ileocecal valve, 2% symptomatic,
2 types of ectopic tissue, commonly aged 2 and males 2:1.
Epidemiology a/a
History/Examination
Most children asymptomatic.
Intermittent painless rectal bleeding due to acid production and its ulcerating
effect on the gastrointestinal mucosa downstream.
May have anaemia, intussusception, and may have acute meckels diverticulitis
presenting identically to acute appendicitis.
Investigation
Bloods for anaemia, Stool sample for occult blood/MCS
Tc99 scan – binds to gastric mucosa, will show ectopic tissue with pre scan
suppression with H2 antagonist. Sensitivity 50-90% so only helpful with positive
diagnosis.
Management
General: if incidental finding in asymptomatic patient, not recommended to be
removed, even if seen on appendicectomy.
Surgical: if symptomatic, ileal resection (not only diverticulotomy as tissue may
extend beyond diverticulum). May be done laproscopically through umbilicus.
Complications
Anastomotic complications (stricture, leak) with surgical intervention. May
sometimes contain sarcomas or adenocarcinomas.
Prognosis
Excellent with surgical treatment.
Mesenteric adenitis
Definition
Mesenteric lymph node inflammation associated with systemic illness and
abdominal symptoms
Aetiology
Acute or chronic. Infection causes enlargement of lymph nodes and possibly
odematous mesentery, with suppuration. Involved nodes may be intraabdomina,
retroperitoneal, ileocolic vascular distribution common.
Caused by viruses (URTI) bacterial (GAS, Yrs, Hel J, Camp j, Salm Shig)
Common DD for acute appendicitis. With URTI and tonsillitis.
Pathology: MACRO LN enlarged and soft, mesenteric odema. MICRO non specific
hyperplasia, necrotic changes if suppurative.
Epidemiology
All ages, incidence unknown
History
Dx of exclusion. Most common finding at negative appendicectomy. Recent Hx of
URTI, corysa, GI infection.
Examination
General: may be identical to AA. Cervical lymphadenopathy. High pyrexia, vague
abdominal signs.
Specific: peritoneal irritation may be present  guarding on percussion and
tenderness
Investigation
Bloods: high WCC, ESR, CRP.
USS of RIF: May confirm Dx with visualization of enlarged nodes OR appendix
inflamed (non compressive tubular structure in RIF). With MA nodes are in
clusters of >5 and are >1cm in diameter.
CT scan: rarely preformed or needed, but excellent positive predictor.
Management
All should be admitted to be observed for acute appendicitis. MA is self limiting.
Complications
None
Prognosis
Benign.
Necrotising enterocolitis NEC

Definition
Severe gastrointestinal disease characterized by massive epithelial destruction
leading to intestinal barrier failure.
Aetiology
Unknown, likely multifactorial. Hypothesis: immature intestinal battier and
mucosal immune system  bacterial translocation and epithelial inflammation.
Localised injury leads to increased infiltration in that area leading to more
infection and more inflammation  further damage.
Eventually, intestinal necrosis and sepsis.
Bell’s classification I (suspect, non septic signs) II (definite, blood investigation
and XR changes), III (advanced shock, peritonitis or pneumoperitoneum)
Associated with prematurity, low BW, formula feeding, stress, bacterial
colonization. UVA/C insertion, CHD, maternal cocaine nuse, RDS.
Epidemiology
0.5% births.
History/Examination
Stage I: temperature instability, bradycardia, aopnea, lethargy, poor feeding,
bilious aspirates, GI bleeding, ileus on XR.
StageII: + metabolic acidosis, thrombocytopenia, GI bleeding, tender abdomen,
wall erythema, mass, AXR signs
Stage III: + shock, marked peritonitis, abdominal distension, neutropenia, DIC,
ionotropic support, pneumoperitoneum on AXR.
Investigation
Bloods: depend on stage, but usually low Hb, high WCC, metabolic acidosis and
electrolyte imbalances
AXR: Football sign of air collecting in anterior abdomen when supine, may see
fxed dialted loops of bowel, outlined falciform ligament, pneumoperitoneum.
USS: operator dependent, may see intramural gas.
Management
Conservative: Stages I/II, NBM, IV feed and fluids, NGT decompression, IV Abx,
Blood/platelet transfusion and electrolyte monitoring.
Surgical: failure of conservative management, Laparotomy via supraumbilical
transverse incision with resection of necrosed bowel and formation of
stoma/mucous fistula.
Complications
Stricture, fistula, recurrence, short gut syndrome, malabsorption, TPN associated
cholethiasis.
Prognosis
20-40% of NEC require surgery. Mortality 50%.
.
Neonatal jaundice
Definition
Excess bilirubin leading to yellow discoloration of skin and sclera.
Aetiology
Unconjugated (pre hepatic)
 Physiological
o Unstable fetal Hb: high turnover
o Defective BR metabolism: low hepatic metabolism in neonates.
o Defective excretion: underdeveloped gut flora.
o Breast milk jaundice: 2nd week to 3rd month, due to UPDGR
inhibition
 Pathological
o Haemolytic
 AIHA
 HDN
 Hereditary spherocytosis, G6PD
 Congenital infection, bacterial sepsis.
o Non-haemolytic
 High Hb load: haemorrage or polycythaemia
 Galactosaemia and hypothyroidism
Conjugated (hepatic / post hepatic)
 Neonatal hepatitis: TPN related, congenital infection, a1ATD, CF.
 Bile duct obstruction: biliary atresia, coledochal cyst
Epidemiology
50% of neonates to different degrees.
History
General: May be asymptomatic (phys) or unwell (poor feeding, vomiting, fevers
confusion, seizures, behavioral etc)
Age of onset: <24h pathological, >24h probably physiological, >2/52 breast milk
Examination
Clinical jaundice starts at BR level 80-120 umol/l. Look in sclera.
Investigation
Early(<24h): FBc, film, maternal/infant ABO, maternal TORCH screen, DAT
>24h: Blood + film, examine
Persistent (>2wk) Total serum BR and conj/unconj fraction. Then bloods or USS.
Conjugated: requires urgent investigation, USS biliary tree of biopsy isotope
scanning.
Management
General: tx cause if present.
Tx jaundice: prevent bilirubin encephalopathy (kernicterus)
Phototherapy: Place neuonate under 450nm wavelength lights on warm bed.
Converts stereoisomer rendering it soluble and leading to renal excretion.
Exchange transfusion: if intensive phototherapy fails, or extreme cases. Must
have hearing screening.
Complications
BR has neurotoxic effects: seizures, cerebral palsy, sensorineural deafness, LDs.
Prognosis
Good if physiological, spontaneous resolvement.
.
Oesophageal atresia / trachea esophageal fistulae

Definition
Congenital malformation of the oesophagus leading to loss of continuity in the
lumen, leading to an upper or lower oesophageal pouch. TOFs are abnormal
communication between oesophagus and trachea and are related to OA.
Aetiology
General: Aetiology unclear. Spritx classification involves judgement of
presence/absence of cardiac abnormalities and low BW extent.
Classification:
 Proximal OA with distal/proximal TOF (or both)
 Isolated OA
 H type TOF without OA
Associated with VACTERL (vertebral, anorectal, cardiac, tracheal, oesophageal,
renal, limb) / CHARGE (coloboma, heart defects, atresia choanal, retarded G&D,
genital hypoplasia, ear deformities). SCHISIS (Exhomphalos, cleft lip and palate,
genital hypoplasia). Potter syndrome (bilateral renal agenesis) and Trisomy 18.
Epidemiology
1/4500.
History
Prenatal: polyhydramnios due to intestinal obstruction. Small or absent stomach
bubble in scan.
Postnatal: all infants with hx of polyhydramnios should have NG tube passed at
birth. May present with coughing and choking at first feed.
Examination
Abdominal distension in TOF, or scaphoid abdomen. Examine other anomalies.
Investigation
Plain XR: CXR confirms dx with coiled NGT in upper pouch. Distal bowel gas
shows distal TOF.
Specific: ECHO for other abnormalities.
Management
Initial: immediate transfer to neonatal surgical centre. Head up and prone,
preventing regurgitation. Suciton and irrigation to upper pouch. NBM.
Surgical: (short gap) Single stage correction with anastomosis of upper and
lower ends with TOF ligation. Chest drain may be left at anastomotic site.
Surgical (long gap): Placement of Peg and ligation of TOF then allow child
growth. Secondary surgery with oesophageal replacement with gastric
transposition. Thoracotomy or thoracoscopic.
Complications
Surgical: anastomosis leak, dysmotility, GORD, strictures, recurrence of fistula.
Tracheomalacia, failure to thrive and other complicaitons too.
Prognosis
Survival rates 90%. RF are low BW, and other abnormalities. Long gap OA
require the most operations.
.
Pyloric stenosis
Definition
Hypertrophy and hyperplasia of the pyloric sphincter muscle leading to gastric
outflow obstruction. AKA HPF.
Aetiology
Multifactorial – genetic and environmental. May be due to deficiency of NOS
containing neurons at pylorus, abnormal innervation, hypergastrinaemia,
hyperacidity.
Due to hypertrophy or hyperplasia of the clls in the circular/longitudinal muscle
wall muscles in gastric pylorus.
Epidemiology
1-500 live births.
History
Presents at 2-6/52, with progressive non bilious projectile vomiting after
prolonged feeds, which can be projectile. May have coffeeground vomiting from
Mallory Weiss tear.
Persistently hungry after vomit, constipated, failure to thrive.
Examination
Systemic: weight loss, dehydration, CRT high , low skin turgor, sunken fontanelle,
low urine output.
GI: visible peristalsis from left to right LUQ during feed, Palpation of pyloris feels
like olive mass and aided by use of test feed.
Investigation
Bloods: ABG shows classic: low K, metabolic alkalosis, hypochloraemia.
USS abdomen used to aid diagnois. Pyloric muscle parameter of >4mm
Management
Preoperative: electrolyte imbalance correction.
Operation: Ramstedt pyloromyotomy – longitudinal incision through serosa with
splitting of sphincter muscle. Can be supraumbilical incision or laporoscopic.
Complications
Recurrence uncommon, <1% morbidity.
Prognosis
Post operative vomiting common but settles in 25h. .
Small bowel atresia

Definition
Congenital malformation in the GI tract (duodenum, JJ etc) leading to absence or
closure of a part of the lumen.
Aetiology
DD atresia: Duodenum ends in blind pouch past Ampulla of Vater. Type I:
duodenal web or wind sock. Type II: complete obstruction with fibrous cord
between prox/dist pouches. Type III: complete gap.
JJ or IL atresia: Type I membranous, Type II (intact mesentery but cord between
pouches) type III (mesenteric defect with gap between pouches), Type IV
(Multiple JJ atresia.
General: Cause unknown.
Epidemiology
DD 1/ 5k , JJ 1 /2 K
History/Examination
Depends on level and extent. USS dx before birth. NNU admission at birth, AXR.
Vomiting may be seen, may be bile stained or non bilious depending on atresia
site.
Investigation
AXR: dilated bowel loops, double bubble (absent/reduced gas post obstruction).
Contrast studies may be warranted. Examine for other potential malformations.
Management
General: NGT and stabilize. IV fluids and feeds. Explore other anomalies.
Surgical: transverse supraumbilical incisions, primary anastomosis between
pouch ends,
Complications
Aspiration, anastomotic complications, stenosis or leak, abnormal peristalsis in
proximal bowel, SBS.
Prognosis
Mortality related to severity of associated abnormalities, not this one itself.
Dependent on prematurity.
.
Template condition
Definition
Aetiology
Epidemiology
History
Examination
Investigation
Management
Complications
Prognosis
.

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MAA Paediatrics - Gastroenterology

Anorectal malformations (ARM)

Surgical (definite): Posterior sagittal anorectoplasty (PSARP) with separate

Cow’s milk protein allergy (CMPA)

Exomphalos and gastroschisis

Surgical: prompt assessment to make diagnosis and ensure bowel is not

Encopresis (fecal soiling)

Functional abdominal pain (FAP)

Dietary modifications: no evidence.

Oral rehydration therapy (ORT) with ESPGHAN

Gastro oesophageal reflux disease

Hernia: Congenital diaphragmatic hernia (CDH)

Hernia: Inguinal hernias (IH)

Inflammatory bowel disease

UC: Induction of remission requires ASA/SLZ if mild and corticosteroids if

Liver disease, Chronic

Malrotation of the intestine

Ladd procedure: reduction of volvulus, division of mesenteric bands, placement

Necrotising enterocolitis NEC

Oesophageal atresia / trachea esophageal fistulae

Small bowel atresia

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