THE DIGESTIVE SYSTEM

Maria Victoria M. Villarica MD

OLFU College of Medicine
Department of Pediatrics
Pediatric Module on the Digestive System

Grading system: Written examination

A. quizzes - 5 long quiz (25 items) 40%
B. shifting exam 60%
class standing: 100%
Textbook: Nelson Textbook of Pediatrics 19th ed.
by: Kleigman, Stanton, St. Geme, Schor, Behrman
Course Outline:
Mouth
Esophagus
GIT
Anus and Rectum
Liver
Gallbladder
Pancreas
Normal Digestive Phenomena
GI function varies with maturity
Toungue is thrust upward and outward backwards
1 month old sweet and salty
Complimentary feeds 6 mos.
Burping encouraged to prevent gastric distention
Major Symptoms and Signs
of Digestive Tract Disorders
Dysphagia
difficulty in swallowing; odynophagia; globus
Oropharyngeal dysphagia transfer (mouth to esophagus)
due to neurologic and muscular disorders aspiration
Esophageal dysphagia neuromuscular disorders
(achalasia, collagen disorders) or mechanical obstruction
(intrinsic: stricture, web, tumor: extrinsic: compression
from vascular rings, mediastinal lesions or vertebral
abnormalities)
Vomiting :
reflex process; bile-stained 2nd part of the duodenum
Highly coordinated reflex process preceded by salivation and involuntary
retching; medulla and direct: afferent innervations and indirect: CTZ and higher
CNS centers
Cyclic vomiting: syndrome with numerous episodes of vomiting interspersed with
well intervals; criteria (at least 2): 5 attacks in any interval or minimum of 3 in
6mos; occurs 1 hr to 10 days and occurs 1 week apart; > 4x/hr at > 1hr; return to
baseline; not associated with another disorder; age onset: 2-5yrs old; precipitants
(stress, infection); theories
Differential diagnosis GI abnormalities, CNS disorders, metabolic-endocrine
disorders, nephrolithiasis, etc
Laboratory evaluation based on history and PE: endoscopy, GI radiography,
brain MRI, metabolic studies (lactate, organic acids, ammonia)
Management hydration and antiemetics (ondansetron); prophylactic meds
(cyproheptadine, propanolol, amitriptyline, phenobarbital); lifestyle changes
Potential complications metabolic, nutritional, Mallory-Weiss tear, esophagitis,
aspiration, shock, pneumomediastinum/pneumothorax, petechiae/retinal hgges
 Regurgitation effortless movement of stomach contents
into the esophagus and mouth; LES
Rumination - to chew
Anorexia prolonged lack of appetite; hypothalamus
Diarrhea excessive loss of fluid and electrolytes in the
stool; acute (>10ml/kg/day in infants and >200ml/kg/day
in older children) lasts <14 days; chronic or persistent
lasts >14 days
Diarrhea
SI absorbs 10-11L/day of water; voluminous diarrhea
LI absorbs 0.5L/day of water; lower-volume diarrhea
Mechanisms of diarrhea:
a. secretory - absorption, secretion, electrolyte transport (
cholera toxin, etc); large volume; persists with fasting; normal
osmolality, <100mOs/kg ion gap
b. osmotic maldigestion; transport defects, ingestion of
unabsorbable substances (lactose def., etc); lesser volume; stops
with fasting; acidic, high osmolality, >100mOs/kg ion gap
c. motility disorders rapid (IBS, thyrotoxicosis) or delayed (pseudo-
obstruction, blind loop); lesser volume
d. decreased surface area (osmotic, motility) Short bowel
syndrome, rotavirus,celiac disease
e. mucosal invasion Salmonella,Shigella; Amoeba, Yersinia,
Campylobacter; blood and WBC; inflammation, colonic
reabsorption, motility
Constipation
relative definition; depends on stool consistency,
frequency and difficulty in passing stool
defects on filling or emptying the rectum; causes (non-
organic and organic)
Neonatal period: Hirschsprung disease, intestinal pseudo-
obstruction, hypothyroidism
Defective rectal filling: ineffective colonic peristalsis
colonic stasis (excessive drying lessens the sensitivity)
Defect in emptying: failure of defecation reflex (lesions in
rectal muscle, sacral spinal cord or abdominal and pelvic
muscles)
Involuntary encopresis
Generates ANXIETY
 Abdominal pain skin and muscle A fibers sharp,
localized pain; C fibers viscera, peritoneum, muscle
dull, poorly localized pain; visceral pain (dull, aching;
dermatome), somatic pain (inflammed viscus) and
referred pain (extraintestinal locations)
Gastorintestinal hemorrhage hematemesis (esophagus,
stomach, duodenum); hematochezia (distal bleeding site
or above distal ileum); melena (blackened stools-
duodenum or above distal ileum)
Abdominal distention ascites fluid in the peritoneal
cavity
jaundice
Abdominal Pain
Acute and Chronic
Visceral Pain: radiation of pain is helpful
a. epigastrium liver, pancreas (back), biliary tree (right
scapula), stomach, upper bowel
b. umbilicus distal small bowel, cecum, appendix,
proximal colon
c. suprapubic distal large bowel, urinary tract (inguinal
area, same side), pelvic organs, transverse colon
Somatic Pain peritonitis: rigidity, involuntary muscle
guarding, rebound tenderness, cutaneous hyperesthesia
Referred Pain parietal pleura in pneumonia
Gastrointestinal Hemorrhage
Erosive damage to the mucosa most common cause
Others: variceal bleeding, prolapse gastropathy, Mallory-
Weiss lesion
Diagnostics: EGD (esophagogastroduodenoscopy);
colonoscopy; tagged RBC scan; guaiac test (blue color)
Complications: iron-deficiency anemia, hypotension,
tachycardia; breakdown products: bilirubin
Oral Cavity: Teeth
Dental laminae (mesenchyme)/ectoderm 12 wk fetal
life; 20 primary teeth
Eruption: primary dentition: mandibular: central incisor
at 6 mos; maxillary: central incisor at 7 mos.;
permanent dentition: mandibular: central incisor and 1st
molar at 6-7 yrs; maxillary: 1st molar at 6-7 yrs.
Anomalies: anodontia; supernumerary teeth
Radiographic examination
Anomalies Associated with Tooth Development
Twinning 2 teeth are joined together
Germination division of 1 tooth gem to form a bifid crown
Fusion joining of incompletely developed teeth due to crowding, pressure or
trauma
Concrescence attachment of root of adjacent teeth by an excessive deposit of
cementum

Macrodontia/Microdontia/Peg-shaped laterals
Amelogenesis imperfecta hereditary; enamel
defects, grooves and pits; abrasion
Dentinogenesis imperfecta hereditary; bluish-
opalescent sheen on poorly calcified dentin
 Anomalies in tooth development due to illness,
malnutrition, premature birth or birth trauma:
Hypocalcification opaque, white patches or horizontal line on the tooth
Hypoplasia more severe; pitting or areas devoid of enamel

Fluorosis inconspicuous white, lacy patches on the enamel

to severe brownish discoloration and hypoplasia;
>0.05mg/kg/day fluoride or >2.0ppm (water, toothpaste,
flouride rx)
Discolored teeth black (neonatal hyperbil); red-brown
(prophyria); brown-yellow (tetracycline)
Natal teeth at birth; mandibular central incisors;
associated with cleft palate, Pierre-Robin synd., etc
Neonatal teeth erupt 1st month of life;
Riga-Fede disease tip of tongue is amputated/lacerated
Cleft Lip
Hypoplasia of the mesenchymal layer, resulting to failure of
the medial nasal and maxillary process to join
M>F
Causes: maternal drug exposure, a syndrome malformation
complex or genetic factors (IRF6 gene)
Unilateral (L>R) or bilateral and can involve the alveolar ridge
FEEDING plastic obturator; soft, artificial nipples
Surgery: 3 mos. of age; Millard rotation-advancement
technique; revised at 4-5 yrs. of age
Cleft Palate
Failure of the palatal shelves to approximate or fuse
Isolated (midline); associated with cleft lip
FEEDING plastic obturator; soft, artificial nipples
Surgery: Timing is individualized (width, adequacy of
existing palatal segments, morphology of surrounding
areas, neuromuscular function of soft palate and
pharyngeal walls); GOALS: union of cleft segments,
intelligible and pleasant speech, reduction of nasal
regurgitation and avoidance of injury to the growing
maxilla; < 1 yr. of age; prosthetics (missing teeth);
speech therapy
Sequelae:
Cleft Lip:
Misarticulation and velopharyngeal dysfunction (cleft
lip and palate) (p,b,d,t,h,y or s,sh,ch or cats,boats,
sisters)
Cleft Palate:
Recurrent otitis media and subsequent hearing loss
Displacement of maxillary arches and malposition of
the teeth (orthodontic correction)
Misarticulation and velopharyngeal dysfunction (cleft
lip and palate) (p,b,d,t,h,y or s,sh,ch or cats,boats,
sisters)
Post-operative Management:
Gentle aspiration of the nasopharynx minimizes
atelectasis or pneumonia
Maintenance of a clean suture line and avoidance of
tension on the sutures
Infant is fed with a mead-Johnson bottle
Arms are restrained
Fluid or semifluid diet X 3 weeks
Velopharyngeal Dysfunction
Speech disturbance
Hypernasal speech; p.b,d,t,h,v,f,s; inability to whistle,
gargle, blow out a candle or inflate a balloon; loss of
liquid through the nose when drinking; otitis media;
hearing loss
Radiographic studies (true lateral view); nasoendoscopy
Surgery: pharyngoplasty (retropositioning of palate)
Dental caries
Interrelationship between tooth surface, dietary carbohydrates and
specific oral bacteria (Strep. mutans, lactobacilli)
Reduces pH of dental plaque demineralization cavitation
Sucrose (most cariogenic sugar); by-product: glucan (polymer that
enables bacteria to adhere to tooth structures)
< 3yrs old: requires restraint, sedation or general anesthesia
Prevention: screening < 3yrs. By pedia; flouride (1ppm); daily
brushing; avoid fruit juice (<6oz/day); dental sealant
Periodontal Diseases
Gingivitis
Periodontitis (inflammation of the periodontal ligament
resulting in loss of alveolar bone)
Teething: excessive salivation, low-grade fever,
irritability; give oral analgesics, ice rings
Dental Trauma
Concussion - gentle hitting of tooth with an instrument
Sublaxation horizontal and/or vertical mobility
Intrusion pushed up into the socket
Extrusion displacement of tooth from socket; reduction
and fixation
Avulsion replant within 20mins after injury
Endodontic therapy
Common Lesions of the Oral Soft Tissues

Oropharyngeal Candidiasis C. albicans; neonates;

white plaques covering all or part of the
oropharyngeal mucosa; lesions inflamed and has
pinpoint hemorrhages; KOH smears; management:
0.2% chlorhexidine solution and systemic antifungals
Aphthous ulcers canker sore; allergic or
immunologic reactions, emotional stress, genetics,
soft tissue injury; well circumscribed ulcerative
lesions with a white necrotic base surrounded by a
red halo; lasts 10-14 days; heals without scarring;
management: benzocaine and topical lidocaine;
tetracycline use (caution)
candidiasis
cheilitis
 Herpetic gingivostomatitis erythematous gingiva, mucosal
hemorrhages and clusters of small vesicles; mucocutaneous
margin and perioral skin with fever, lymphadenopathy and
difficulty of eating and drinking
Bohn nodules remnants of mucosal gland tissue; disappears
Dental lamina cysts epithelial remnants of dental lamina;
disappears
Parulis gum boil
Cheilitis dryness of the lips, cracking, scaling, burning
sensation; contact sensitivity, vit def, weakened immune
system, fungal/bacterial infection
Ankyloglossia tongue-tie; short lingual frenulum; interferes
with speech and feeding; spontaneous or may require surgery
Geographic tongue and Fissured tongue
END OF 1ST SESSION
Esophagus
Hollow, muscular tube that conveys
ingested material from the mouth into the
stomach
Esophageal atresia with TEF
Esophageal atresia most common (esophagus); 50%
associated with TEF
Presentation: frothing and bubbling at the mouth
and nose; episode of coughing, cyanosis and
respiratory distress
Sequelae: aspiration pneumonitis
Diagnosis:inability to pass a NGT/OGT; maternal
polyhydramnios; plain Xray: coiled feeding tube or
air-distended stomach or scaphoid abdomen
 Management: > maintain patent airway
> prevent aspiration of secretions
> surgical ligation and end-to-end anastomosis of the
esophagus
> ET intubation is C/I
> If surgery cannot be done, a primary closure can be
delayed by temporizing with fistula ligation and
gastrostomy tube placement
> If gap is > 3-4cm, primary repair cannot be done
Outcome: post-op: anastomotic leak, refistulization,
anastomotic stricture; reactive airway disease from
GERD
Obstructing and Motility Disorders of the
Esophagus compress
Obstructing lesions produce dysphagia to solids earlier
than liquids
Diagnosis: radiographic studies
Extrinsic causes: esophageal duplication cysts: leads to
respiratory distress because of compression of airways;
mediastinal or subcarinal lymph nodes; vascular
anomalies (dysphagia lusoria: subclavian artery or aortic
arch)
Intrinsic causes: peptic stricture; Schatzki ring (thin
bands at squamocolumnar junction); congenital
webs/ring; cricopharyngeal achalasia; eosinophilic
esophagitis
Dysmotility
Cricopharyngeal achalasia (UES) failure to relax
Cricopharyngeal incoordination (chalasia) full relaxation
of UES
Diagnosis: manometry; videofluoroscopic evaluation of
swallowing
Cricopharyngeal spasm Arnold-Chiari malformation;
due cranial decompression; may lead to Zenker
diverticulum
Dysmotility (LES)
Achalasia loss of LES relaxation and loss of
esophageal peristalsis
Causes: degenerative autoimmune and infections
Manifestations: regurgitation and dysphagia (solids and liquids) with
respiratory symptoms, esophagitis
Chest xray: air-fluid level in dilated esophagus
Barium fluoroscopy: birds beak
Manometry most sensitive diagnostic test; high LES pressure and low
amplitude esophageal body contractions
Treatment: Pneumatic dilatation (initial tx of choice) and surgical
(Heller) myotomy; Ca-channel blockers and PDE-inhibitors;
endoscopic injection of Botulinum toxin
Achalasia (birds beak)
Hiatal Hernia
Herniation of the stomach through the esophageal
hiatus; type 1 or sliding hernia:gastroesophageal
junction slides into the thorax ; type 2: paraesophageal
or the stomach fundus next to the esophagus; type 3
GERD problem
Symptoms: fullness after eating and upper abdominal
pain
Management: medical (GERD) and correction of hernia at
fundoplication
Hiatal hernia
GERD
Most common esophageal disorders in children (all ages)
Retrograde movement of gastric contents across the LES into
the esophagus; physiologic vs pathologic
Antireflux barriers: LES + crura of the diaphragm at
gastroesophageal junction
Manifestations: esophagitis (irritability, arching, choking,
gagging, feeding aversion, failure to thrive); respiratory
symptoms
Diagnostics: manometry, Barium radiographic studies,
extended esophageal pH monitoring, endoscopy, multichannel
intraluminal impedance, laryngotracheobroncoscopy
GERD
Management: dietary measures (feeding technique, thickened
formulas + 1 tbsp rice cereal/oz , hypoallergenic diet); weight
reduction; positioning (seated is avoided, supine to left side, is
recommended); prone and upright carried position
Drugs: antacids, H2RA, PPI (most potent antireflux drug),
prokinetic (metoclopramide (tardive dyskinesia), betanechol,
erythromycin; baclofen (centrally-acting GABA agonist
Surgery : fundoplication (radiofrequency therapy Stretta
procedure)
Complications: esophagitis: stricture, Barrett esophagus
(metaplastic transformation: squamous to columnar);
nutritional, respiratory presentations
Stomach
Embryology: starts at 4th week AOG; completed by 8th
week AOG
Foregut (esophagus, stomach, duodenum), midgut
(jejunum, ileum, large bowel until mid-transverse
colon), hindgut (remainder of the colon and anal canal)
Hypertrophic Pyloric Stenosis
M>F; with blood types B and O; familial; not present at birth;
associated with Apert syndrome, Zellweger syndrome, trisomy 18,
etc; erythromycin use
Manifestations: nonbilous vomiting (initial symptom); progressive
vomiting (3 week old) leading to hypochloremic metabolic alkalosis;
hyperbilirubinemia (icteropyloric syndrome) most common clinical
association
Diagnosis: palpation of an olive-shaped, firm, movable, -2cm mass
from the left side and located above and to the right of the umbilicus
in the midepigastrium beneath the live edge
Imaging studies: UTZ and contrast studies (string sign elongated
pyloric channel; shoulder sign bulge of the pyloric muscle into the
antrum; double-tract sign- parallel streaks of barium in narrowed
channel
 Differential diagnosis: GERD, hiatal hernia, inborn errors
of metabolism, adrenal insufficiency, AGE, duodenal
stenosis
Treatment: preoperative treatment: nasoduodenal
feedings; correcting fluid, acid-base and electrolyte;
vomiting stops when the stomach is empty
Surgery: pyloromyotomy (Ramstedt procedure); feeding
can be initiated 12-24 hrs after surgery; for incomplete
pyloromyotomy, endoscopic balloon dilatation is done
Congenital Gastric Outlet Obstruction
results from pyloric atresia and antral webs ; uncommon;
nonbilious vomiting, feeding difficulties and abdominal distention
on 1st day of life
associated with polyhydramnios, LBW and epidermolysis bullosa
UGIS show pyloric dimple; endoscopy
treatment is correction of dehydration and hypochloremic alkalosis;
surgical or endoscopic repair once stable
Peptic Ulcer in Children
Inflammation due to an imbalance between
cytoprotective and cytotoxic factors in the stomach
and duodenum; gastritis and ulcerations
Endoscopy
Peptic ulcers: deep mucosal lesions that disrupts
the muscularis mucosa of the gastric and duodenal
wall; lesser curvature of the stomach
Primary: H.pylori (serologic assay; C-urea breath
test and stool antigen test
Secondary: stress from sepsis, shock, drugs
Peptic Ulcer:
Clinical manifestation: epigastric pain; periumbilical;
dull or aching; hematemesis or melena
Diagnosis: esophagogastroduodenoscopy
Management: H. pylori gastritis: Amoxicillin (50mkd X
14days) + Clarithromycin (15mkd X 14days) + PPI (1mkd
X 1 mo.) or Amoxicillin + Metronidazole (20mkd X
14days) + PPI (1mo.) or Clarithromycin + Metronidazole +
PPI
Antisecretory therapy: H2RAs, PPI; cytoprotective
agents
END OF 2ND SESSION
Intestinal Obstruction
Partial or complete; simple or strangulating (leads to bowel infarction
and perforation); polyhydramnios
Intrinsic inherent abnormalities of intestinal innervation, mucus
production or tubular anatomy; atresia or stenosis
Extrinsic compression of bowels by vessels, organs or cysts
Classic presentation: vomiting, abdominal distention and obstipation
High: large volume, frequent bilious vomiting with little or no
distention; intermittent pain; obstipation
Low/distal: marked distention with vomiting (feculent); obstipation
Plain radiographs (upright and cross-table lateral views); contrast
studies (since colonic haustra are not fully developed)
Stabilize patient (fluid resuscitation); surgery
Malrotation
Inadequate mesenteric attachment of the intestines to
the posterior abdominal wall, leaving the bowel
vulnerable to volvulus or intestinal twisting (5th week to
12th week AOG)
Accompanied by congenital adhesions (Ladd bands)
1st week of life: bilious emesis; malabsorption and
protein-losing enteropathy
Volvulus
Life-threatening complication of malrotation
Small bowel twists around the superior mesenteric artery
Contrast studies confirms diagnosis; UTZ; xray show gasless
abdomen or duodenal obstruction with a double-bubble sign
UGIS gold standard in evaluation; malposition of the
Ligament of Treitz, corkscrew appearance of the small bowel
and duodenal obstruction with birds beak appearance
Surgery
Volvulus (double bubble sign)
Meckel Diverticulum
Remnant of the embryonic yolk sac, or the omphalomesenteric
duct (provides nutrition until the placenta is established) or
vitelline duct
5th 7th week, duct attenuates and separates from the
intestine
Most common GI anomaly; lead point in intussusception;
intraperitoneal bands
Outpouching of the ileum along the antimesenteric border 50-
75 cm from the ileocecal valve
Manifestations: 1st 2nd yr of life; painless rectal bleeding
(lined by ectopic mucosa); stool brick or currant jelly
colored; anemia
Meckel Diverticulum
Diagnosis: Meckel radionuclide scan (technetium-99m
pertechnetate (plain xray and routine barium studies are
of no value)
Diverticulitis
Surgical excision
Congenital Aganglionic Megacolon (Hirschsprung
Disease)
Developmental disorder (neurocristopathy) of the
enteric nervous system; absence of ganglion cells in the
submucosal and myenteric plexus (arrest of neuroblast
migration from the proximal to the distal bowel)
Results to inadequate relaxation of the bowel wall and
bowel wall hypertonicity, leading to intestinal
obstruction
Most common cause of lower intestinal obstruction in
neonates; M>F
Congenital Aganglionic Megacolon (Hirschsprung
Disease)
Neonatal period: distended abdomen, failure to pass meconium,
bilious emesis or aspirates with feeding intolerance; Differentials:
meconium plug/ileus, intestinal atresia
Older child: constipation, ribbon-like stools; consider Currarino
triad: anorectal malformations, sacral bone and presacral
anomalies
Failure to pass stool dilatation of the proximal bowel distention
intraluminal pressure blood flow deterioration of
mucosal barrier stasis and proliferation of bacteria (C. difficile,
S. aureus, anaerobes, coliforms)diarrhea, abdominal tenderness,
sepsis and signs of bowel obstruction
Congenital Aganglionic Megacolon (Hirschsprung
Disease)
Diagnosis: rectal suction biopsy (gold standard); submucosa; 2
cm above the dentate line; anorectal manometry (failure to
relax of the internal anal sphincter); > 1 month old,
unprepared contrast enema (barium)
Treatment of choice: laparoscopic single-stage endorectal
pull-through procedure
Other operative interventions: 1. Swenson (excise aganglioninc
segment and anastomose); 2. Duhamel (create a neorectum);
3. Soave (endorectal pull-through (stripping the mucosa from
the aganglionic rectum and bringing normally innervated colon
through the muscular cuff)
Post-op problems: constipation, recurrent enterocolitis,
stricture, prolapse, perianal abscess, fecal soiling
Intussusception
A portion of the alimentary tract is telescoped into an adjacent segment;
ileocolic>cecocolic > ileoileal
Intussusceptum: upper portion of the bowel; invanginates
Intussuscipiens: lower portion;pulls its mesentery
Most common cause of obstruction in 3mos 6 yrs
Most common abdominal surgery in < 2yrs; M>F
Cause: idiopathic (90%); resp. adenovirus type C
Risk factors: GI infection (swelling of Peyer patches), lymphoid nodular
hyperplasia (mucosal prolapse of the ileum into the colon); lead points:
Meckel diverticulum, intestinal polyp, neurofibroma, intestinal duplication
cyst, hemangioma, lymphoma; cystic fibrosis
Intussusception
Clinical manifestations: sudden onset of paroxysmal
colicky pain; recurs; straining efforts with legs and knees
flexed and loud cries; weak and LETHARGIC
Triad: pain, palpable sausage-shaped abdominal mass,
bloody or currant-jelly stool
Diagnosis: UTZ ; air, hydrostatic (saline), water soluble
contrast media coiled-spring sign
Treatment: radiologic hydrostatic reduction under
fluoroscopic or ultrasonic guidance; or resection with
end-to-end anastomosis (ileoileal); fatal if untreated
Inflammatoy Bowel Disease
Represent idiopathic chronic intestinal inflammation
Onset: preadolescent/adolescent to young adulthood
Genetic and Environmental influences
Genes: NOD2 (1st IBD gene identified); IBD-5 risk
haplotype
Pathogenesis: abnormality in intestinal mucosal
immunoregulation abnormal rsponse to customary
enteric Ags or a normal response to a yet to-be identified
microbe activation of mediators in inflammation
tissue destruction and remodelling with fibrosis
Crohns disease and Ulcerative colitis
Ulcerative Colitis
Involves the colon (rectum and extends proximally)
Ulcerative protitis and pancolitis
Clinical manifestations: blood, mucus, pus in the stools;
diarrhea, tenesmus, urgency, crampy abdominal pain,
nocturnal BM
Extraintestinal sumptom: pyodermal gangrenosum,
ankylosing spondylitis, Fe-deficiency anemia
Fulminant colitis
Differential diagnosis: dietary protein intolerance;
infectious colitis, H-S purpura
Colon Ca - mucosal dysplasia
 Diagnosis: endoscopy and histologic findings
a. flexible sigmoidoscopy can confirm the diagnosis
b. colonoscopy extent of the disease; C/I: fulminant
colitis because of risk of toxic megacolon
c. barium enema suggestive but not diagnostic
(cut-off demarcation)
d. Fe-deficiency anemia, leukocytosis, hypoalbuminemia
e. biopsy cryptitis, crypt abscesses, separation of crypts
by inflammatory cells, mucus depletion and branching
crypts
f. radiographs loss of haustral markings in air-filled colon
(>6cm on diameter )
 Treatment: medical management N/A; control
symptoms and reduce the risk
1. aminosalicylate Sulfasalazine 50-75mkd (allergic rxn)
- Mesalamine 50mkg
- Balsalazide 110-175 mkd
2. probiotics for maintenance of remission; prevents
pouchitis
3. prednisone moderate to severe pancolitis; 1-2mkg; SE
4. Immunomodulators Azathioprine 2-2.5mkg
- 6-mercatopurine 1-1.5mkg
5. Infliximab Ab to tnf-; induction and maintenance but SE
 Surgery colectomy: intractable disease, complication of
therapy, fulminant disease unresponsive to treatment
- colectomy with endorectal pull-through (J-pouch)
- temporary ileostomy
- pouchitis bloody diarrhea, abdominal pain and low-
grade fever
TPN vs. Enteral no difference
Surveillance colonoscopy (8-10 yrs colon Ca)
Crohns disease
Inflammatory process eccentric and segmental with skip
areas; transmural
50% - ileum and colon (ileocolitis)
30% - upper GI (esophagus, stomach, duodenum)
20% - colonic disease
Onset: teenage years
Clinical manifestations: inflammatory, stricturing,
penetrating
- abdominal pain, fever, malaise, easy fatigability,
diarrhea, vomiting; growth failure; fistula formation
(enteroenteric, enterocolonic, enterovesical; hepatic
abscess, etc)
 Diagnosis:
1. upper GI contrast study choice for small bowel;
cobblestone appearance to the mucosal surface
2. endoscopy inflammatory changes (eryhtema, friability,
loss of vascular patterns), apthous ulcers, linear ulcers,
nodularity and strictures
3. radiologic evidence of stricturing or penetrating
disease
4. CBC, low serum albumin, fecal calprolectin or
lactoferrin
 Treatment: medical management
1. Mesalamine
2. Metronidazole 10-20mkd 1st line for perianal disease
3. Prednisone especially for fistulas
4. Immunomodulators azathioprine, 6-mercaptopurine
if poor response to prednisone; not helpful acutely but has
beneficial effect
-methotrexate
- tnf- Ab (Infliximab 0,1,6week infusions; do PPD
Adalimumab subcutaneous
Enteral nutrition (elemental or polymeric diets)
 Surgery: colectomy with conventional ileostomy (remove as limited
a length as possible) is performed; endorectal pullthrough is
discouraged because of recurrence
Prognosis: high morbidity, low mortality
- nutrition
- prevent osteopenia due to poor nutrition and use of corticosteroids
- complications: bowel strictures, fistulas, perianal disease,
extraabdominal or retroperitoneal abscess
- surgery is unlikely to be curative (rate of reoperation is high and
repeated surgeries lead to malabsorption due to short bowel
syndrome_
- Colonoscopy is done
End of 3rd Session