Problem 5

Devin Alexander
405160054
Lower GI tract disorder
Adult
Proctitis
 Proctitis
Definition • Proctitis is inflammation of the rectal mucosa.
• Proctitis can be short term (acute) or long term (chronic).
• Proctitis involves an inflammatory change of the rectum (within 15
cm of the dentate line).
• Proctitis is similar to proctosigmoiditis but is not necessarily
associated with proximal extension of disease into the colon and
usually does not evolve into ulcerative colitis.
Etiology • Medical treatment side effects: antibiotics, radiation therapy
• STDs: gonorrhea, chlamydia, lymphogranuloma venereum, herpes
virus
• Autoimmune disease of the colon: Chron’s disease & ulcerative colitis
• Celiac disease
• Chemicals
• Rectal instrumentation
• Trauma to the anorectal area
• Idiopathic
Pathophysi• Proctitis involves mucosal cell loss, acute inflammation of the lamina
-ology propria, eosinophilic crypt abscess, and endothelial edema of the
arterioles.
• These may improve or in turn progress with subsequent fibrosis of
connective tissue and endarteritis of the arterioles, resulting in rectal
tissue ischemia and leading to mucosal friability, bleeding, ulcers,
strictures, and fistula formation.
Symptoms: • Feeling of rectal fullness
General • Anal and rectal pain
• Diarrhea, usually frequent, small amounts
• Frequent or continuous urge to have a bowel movement
• Pain in the lower left abdomen
• Passing mucus through the rectum
• Rectal bleeding
Symptoms: • Pruritus
Infectious • Rectal and anal pain (may become severe)
• Avoidance of defecation due to pain
• Most common causes - Neisseria gonorrhoeae, Chlamydia
trachomatis,herpes simplex virus (HSV) types 1 and 2
• Indolent and extensive HSV types 1 and 2 infections: Symptoms may
include the following: tenesmus, rectal pain, discharge, and
hematochezia.
Symptoms: • Early symptoms include tenesmus and diarrhea that resolve shortly
Radiation- after the radiation treatment period.
induced • Later symptoms of proctitis (occurring months to years after the
completion of radiation therapy) include tenesmus, bleeding, low-
volume diarrhea, and rectal pain.
• Symptoms of radiation-induced proctitis are associated with low-
grade obstruction or fistulous tracts into adjacent organs.
Symptoms: • Passage of blood and mucus per rectum
Idiopathic • Tenesmus
• Occasionally, passage of loose stool, with or without lower
abdominal pain or rectal cramping
Diagnosis : • A complete blood count (CBC) is performed to evaluate for
Laboratory leukocytosis, if an infectious etiology, or severity of anemia due to
blood loss.
• C-reactive protein level is elevated in patients with extensive
pancolitis but is frequently normal in patients with only distal disease.
• Cultures of rectal swabs help diagnose gonorrhea or chlamydia.
• Cultures of vesicular fluid or cytologic scrapings aid in the diagnosis
of HSV.
• Serum Venereal Disease Research Laboratory (VDRL) test and dark
field examination of scrapings from the base of the chancre reveals
spirochetes and confirms the diagnosis of syphilis.
• Stool specimen for C difficile toxin.
Treatment • Sitz baths, antispasmodic medications, stool softeners, low residue
diet (may provide relief)
• Steroid enemas or suppositories for ulcerative proctitis canasa 1 g
enema or suppository daily for a month
• Ceftriaxone and doxycycline for gonorrheal proctitis
• Acyclovir for herpetic proctitis
• Tetracycline or doxycycline for chlamydial proctitis
• Shigella proctitis is usually self-limiting but may require, under
certain circumstances, prolonged (2-4 wk) antibiotic treatment with
ampicillin, tetracycline, ciprofloxacin, or trimethoprim and
sulfamethoxazole (TMP-SMZ).
• Yersinia proctitis is usually self-limiting, but, if systemic bacteremia
occurs, treat with intravenous antibiotics such as tetracycline or
ceftriaxone.
• Campylobacter proctitis is a self-limiting disease; treatment is aimed
at symptomatic relief.
• Metronidazole (Flagyl) or iodoquinol for amebiasis proctitis
• Metronidazole (Flagyl) or oral vancomycin for C difficile proctitis
• Radiation proctitis treatment may include the following: sucralfate
alone or with rectal prednisolone enemas, short-chain fatty acid
enemas, or pentosan polysulfate.
Prognosis • Failure rates as high as 35% have been reported following treatment
of rectal gonorrhea; symptoms frequently recur.
• Most surgeons favor a diverting colostomy for medically intractable
proctitis or proctectomy.
Complica- • Chronic ulcerative colitis
tions • Fistula formation
• Abscess
• Treatment failure
• Perforation
 Diverticulosis
https://www.ncbi.nlm.nih.gov/books/NBK430771/
 Definition & etiology
• is a clinical condition in which multiple sac-like protrusions (diverticula)
develop along the gastrointestinal tract
• E/:
1. the exact cause of these abnormalities is unknown
2. peristalsis abnormalities (e.g., intestinal spasms)
3. intestinal dyskinesia, or high segmental intraluminal pressures
 Risk factor
• diet low in fiber and high in red meat
• obesity or a larger waist circumference
• Smokers
• Medications associated with an increased risk of diverticular bleeding
(NSAIDS, steroid)
 Pathophysiology
• Diverticula occur in weaker portions of the colonic
wall where the vasa recta infiltrate the circular
muscular layer
• mucosa and submucosa herniating through a defect
or weakness in the muscularis layer, covered
externally only by serosa
• colonic motility (e.g., intestinal spasms or
dyskinesis) resulting in exaggerated segmental
muscle contractions, elevated intraluminal pressures,
and separation of the colonic lumen into chambers
• Connective tissue disorders may additionally predispose an individual to the
formation of colonic diverticula
• Diverticula are prone to bleeding due to the proximity of the vasa recta to the
intestinal lumen as a result of herniation of the mucosa and submucosa through the
muscularis layer.
• diverticula formation  the vasa recta become separated from the intestinal lumen by
a layer of mucosa alone  exposed to a greater amount of injury  results in
eccentric intimal thickening, thinning of the media, and ultimately segmental
weaknesses along these arteries which predispose the vasa recta to rupture and
bleeding into the intestinal lumen
 Diagnostic approach
• Sign & symptons
1. Most of them asimptomatic
2. unexplained abdominal pain or cramping
3. alterations in bowel habits
4. blood in the stool. Any bleeding associated with diverticulosis is painless.
5. A diagnosis of diverticulosis is suspected when a patient presents with a
history of painless rectal bleeding or unexplained abdominal pain or cramping,
or alterations in bowel function.
• Work up
1. confirmed by colonoscopy or an x-ray following a barium enema
2. if presents with extreme abdominal pain  the choice is typically a CT
of the abdomen to avoid the risk of intestinal rupture in the setting of
intestinal infection or inflammation.
3. Colonoscopy  identify source of bleeding
 Treatment
• aimed at reducing intestinal spasms which may be achieved by increasing
fiber and fluids in the diet.
• Most bleeding associated with diverticulosis is self-limiting and does not
require intervention
• some cases  endoscopic, radiologic, or surgical intervention may be
required to stop persistent bleeding
• case of a giant diverticulum, with an increased risk of infection and rupture,
surgery is more likely to be considered.
 Medical nutrition therapy
• Recommended intakes of dietary fiber (from foods) = 25 g/day for adult
females; 38 g/day for males
• Adequate fluid intake 2-3 L should accompany high-fiber intake
• Pts w/ acute flare of diverticulitis:
• Low residue diet, elemental diet
• Complicated cases: total parenteral nutrition required initially  gradual return to high-
fiber diet
• High fat  discomfort  low fat diet
 Complications
1. rectal bleeding called diverticular bleeding
2. diverticular infection, called diverticulitis
• Divetticulitis :
1. An abscess, which occurs when pus collects in the pouch.
2. An abnormal passageway (fistula) between sections of bowel or the
bowel and bladder.
 Prevention
• Exercise regularly
• Eat more fiber
• Drink plenty of fluids
IBS
 Irritable Bowel Syndrome (IBS)
Definition • Functional gastrointestinal disorders characterized by pain in
abdomen and changes in bowel movement pattern
Epidemiolo • Incidence 1-2% of population/year
gy • More prevalence in Americans and Europeans
• Lower prevalence in Asians, Africans and Hispanics
• In Western countries, occurance in females 2-3x > males
• Usually symptoms begin before the age of 35
Etiology • Motility disorders (delayed or accelerated)
(unsure) • Enteric infection: colonic muscle hyperreactivity and immunologic
alterations of the colon and small bowel may persist after
gastroenteritis
• Emotions
• Overgrowth of small intestinal bacteria
• Food sensivity
Pathophysi • Myoelectric activity changes
ology • → slower wave frequency or late peaking → delayed meal transport
→ constipation
• → increased wave frequency → accelerated meal transport →
diarrhea
• Infectious enteritis (based on the duration, young age, and types of
pathogens – usually Giardia lamblia) → increased number of
mucosal lymphocytes and enteroendocrine cells → enteroendocrine
cells secrete high level of serotonin → increased colonic secretion →
diarrhea
Clicinal Altered bowel habits → constipation or diarrhea or both
Manifestatio • Constipation: hard stools, painful or infrequent defecation
n • Diarrhea: small volumes of loose stool, urgency or frequent
defecation
• Postprandial urgency
Abdominal pain
• Pain frequently is diffuse without radiation
• Common sites of pain is in left lower quadrant
• Acute episodes of sharp pain are often
• Meals may precipitate pain
• Defecation commonly improves pain
Additional symptoms
• Dyspepsia, heartburn
• Nausea, vomiting
• Sexual dysfunction (poor libido)
• Urinary frequency and urgency have been noted
• Worsening of symptoms in the perimenstrual period
• Comorbid fibromyalgia
• Stressor-related symptoms
Classifica- IBS with constipation (IBS-C)
tion • hard or lumpy stools at least 25 percent of the time
• loose or watery stools less than 25 percent of the time
IBS with diarrhea (IBS-D)
• loose or watery stools at least 25 percent of the time
• hard or lumpy stools less than 25 percent of the time
Mixed IBS (IBS-M)
• hard or lumpy stools at least 25 percent of the time
• loose or watery stools at least 25 percent of the time
Unsubtyped IBS (IBS-U)
• hard or lumpy stools less than 25 percent of the time
• loose or watery stools less than 25 percent of the time
Diagnosis : • Checks for abdominal bloating
Physical • Changes of bowel sound
• Checking for tenderness or pain
Diagnosis • CBC: to screen for anemia, inflammation, and infection is indicated
(Other) • Stool examination: parasites (consider obtaining specimens for 
Giardia antigen), enteric pathogens, leukocytes, Clostridium
difficile toxin
• Colonoscopy
• Barium enema
• Xray
Treatment • Anticholinergic
• Antidiarrhea
• Antibiotic (rifaximin)
• Laxatives
Diet • Eat more fibers to improve constipation
• Avoid foods high in fat
• Avoid some milk products
• Avoid drinks with alcohol or caffeine
• Avoid drinks with large amounts of artificial sweeteners
• Avoid beans, cabbage, and other foods that may cause gas
 Hemorroid

http://www.mayoclinic.org/diseases-
conditions/hemorrhoids/symptoms-causes/dxc-20249175
 Hemorrhoid
Definition • Swollen blood vessels in the lower rectum
Type External hemorrhoids
• Arise from the inferior hemorrhoidal venous plexus below the
mucocutaneous junction
• Covered by squamous epithelium
Internal hemorrhoids
• Arise from the superior hemorrhoidal venous above the mucocutaneus
junction, or dentate line, anorectum
• Covered by rectal mucosa
http://emedicine.medscape.com/article/775407-overview#a8
http://treatmenthemorrhoid.com/classification/
Epidemiolo • Worldwide : symptomatic hemorrhoids 4,4% in the general
gy population
• External hemorrhoids: young and middle-aged
• Peak: 45-65 years
Etiology • Decreased venous return
• Straining and constipation
• Pregnancy
• Portal hypertension and anorectal varices
• Lack of erect posture
• Familial tendency
• Higher socioeconomic status
• Chronic diarrhea
• Colon malignancy
• Hepatic disease
• Obesity
• Elevated anal resting pressure
• Spinal cord injury
• Loss of rectal muscle tone
• Rectal surgery
• Episiotomy
• Anal intercourse
• Inflammatory bowel disease
Pathophysi • Histologically, hemorrhoids consist of three important parts: the
ology lining (rectal mucosa or squamous epithelium), stroma (blood
vessels, smooth muscle, supporting connecting tissue), and anchoring
connective tissue which secures hemorrhoids to the sphincter
apparatus.
• Age or other aggravating factors - supporting connective tissue
deteriorates, hemorrhoids to bulge and descend symptoms
• Chronic constipation, diarrhea, pregnancy, or pelvic tumors -
chronically or recurrently increase pelvic venous pressure - increase
incidence of hemorrhoids
• In some individuals, the internal anal sphincter becomes hypertrophic
and the anal outlet becomes functionally narrowed.
• During straining, the fecal bolus acts as an obturator in forcing the
hemorrhoidal cushions to descend through the hypertrophic sphincter,
enlarge, and become symptomatic.
Symptoms • Rectal Bleeding
• Bright red blood in stool
• Pain during bowel movements
• Anal Itching
• Rectal Prolapse
• Thrombus
Diagnosis : Inspection
Physical • Perianal region (thrombosis or excoriation)
• Strain down: tissue prolapse
Digital rectal examination
• Position: left lateral decubitus with the patient’s knee flexed toward
the chest
• Indurated or ulcerated areas
• Masses, tenderness, mucoid discharge or blood, rectal tone.
• Palpate the prostate in all men
Diagnosis : External findings:
Physical • Redundant tissue
• Skin tags from old thrombosed external hemorrhoids
• Fissures
• Fistulas
• Signs of infection or abscess formation
• Rectal or hemorrhoidal prolapse, appearing as a bluish, tender
perianal mass
Internal hemorrhoids (soft vascular structure) usually not palpable
unless thrombosed.
Test • Stool Guaiac (FOBT)
• Sigmoidoscopy
• Anaoscopy
• proctoscopy
 ANOSCOPY
PROTOSCOPY

SIGMOIDOSCOPY
Treatment – drugs improve defecation: fiber supplement
Pharmacology (psilium, isphagula), laxans, sodium dioctyl
sulfosucsina
– symptomatic medications: anusol, boraginol,
corticosteroids
– medication to stop the bleeding: psilium, citrus
bioflavanoids, diosmin and hesperidin mixture
– cure and prevention hemorrhoid attack: ardium
– minimal invasive: hemorrhoids sclerotherapy,
ligation hemorrhoids, hemorrhoids treatment with
laser therapy
Non - –improvement of lifestyle, eating and drinking
pharmacology patterns, the pattern / way of defecation (diet, fluids,
additional fiber, changes in bowel behavior)
Yamada’s Textbook of Gastroenterology. 6th ed. Blackwell Publishing; 2016.
Prognosis • The recurrence rate with nonsurgical techniques is 10-50% over a 5-
year period, whereas that of surgical hemorrhoidectomy is less than
5%.
Prevention • Drink water
• Eat fibers
• Anal hygiene
Ca colorectal
 Colorectal Cancer
Epidemiolo • Cancer of the large bowel is second only to lung cancer as a cause of
gy cancer death in the United States: 136,830 new cases occurred in
2014, and 50,310 deaths were due to colorectal cancer.
• The incidence rate has decreased significantly during the past 25
years, likely due to enhanced and more compliantly followed
screening practices.
• Similarly, mortality rates in the United States have decreased by
approximately 25%, resulting largely from earlier detection and
improved treatment.
Etiology Diet
• Animal fats : ingestion of animal fats found in red meats and
processed meat leads to an increased proportion of anaerobes in the
gut microflora, resulting in the conversion of normal bile acids into
carcinogens. Diets high in animal (but not vegetable) fats are also
associated with high serum cholesterol, which is also associated with
enhanced risk for the development of colorectal adenomas and
carcinomas.
Etiology • Insulin resistance: obese persons develop insulin resistance with
increased circulating levels of insulin, leading to higher circulating
concentrations of insulin-like growth factor type I (IGF-I). This
growth factor appears to stimulate proliferation of the intestinal
mucosa.
Hereditary Syndrome
Harrison’s principles of internal
medicine. 19th ed
Pathophysi A number of molecular changes are noted in adenomatous polyps and
-ology colorectal cancers that are thought to reflect a multistep process in the
evolution of normal colonic mucosa to life-threatening invasive
carcinoma:
• Point mutations in the K-ras protooncogene
• Hypomethylation of DNA, leading to gene activation
• Loss of DNA (allelic loss) at the site of a tumor-suppressor gene (the
adenomatous polyposis coli [APC] gene) on the long arm of
chromosome 5 (5q21)
• Allelic loss at the site of a tumor-suppressor gene located on
chromosome 18q (the deleted in colorectal cancer [DCC] gene)
• Thus, the altered proliferative pattern of the colonic mucosa, which
results in progression to a polyp and then to carcinoma, may involve
the mutational activation of an oncogene followed by and coupled
with the loss of genes that normally suppress tumorigenesis.
• It remains uncertain whether the genetic aberrations always occur in a
defined order. Based on this model, however, cancer is believed to
develop only in those polyps in which most (if not all) of these
mutational events take place.
Harrison’s principles of internal
medicine. 19th ed
Symptoms • Change in bowel habit: increase/decrease of defecation frequency or
a change in stool consistency. Alternating diarrhea and constipation is
highly suspicious of cancer.
• Blood per rectum: varies in quantity depending on degree of tumor
ulceration and/or vascularity. The blood will be bright red and more
likely streaked on the outside of the stool if the tumor arises in the
rectum or sigmoid, or dark red and mixed in with the stool if the
tumor arises more proximally in the colon.
• Mucus per rectum: likely to be noticed with distal lesions,
particularly those of a mucinous variety.
• Tenesmus: a frequent urge to defecate but leading to the passage of a
little stool on each occasion and lack of the feeling of complete rectal
emptying. This is usually seen in rectal tumors, particularly if bulky
or invading deeply.
• Obstructive symptoms: can manifest as intermittent colicky
abdominal pain. They are more common in tumors of the descending
colon where the feces are more solid compared with right colon
tumors where the stool is more liquid.
• Chronic bleeding: leads to iron deficiency and in turn anemia. It is a
particular feature of right-sided colonic tumors, which have few
associated gastrointestinal symptoms
Diagnosis • Digital examination of the rectum/vagina
• Proctoscopy and sigmoidoscopy
• Double contrast barium enema
• Flexible sigmoidoscopy
• Colonoscopy
• CT
• Endorectal ultrasound /magnetic resonance imaging (MRI)
Harrison’s principles of internal
medicine. 19th ed
Yamada’s textbook of
gastroenterology. 6th ed.
Vol. 2
 Perianal Abscess

http://emedicine.medscape.com/article/19197
5-overview
 Perianal Abscess
• Originates from an infection arising in the cryptoglandular epithelium
lining the anal canal.
• The internal anal sphincter is believed to serve normally as a barrier to
infection passing from the gut lumen to the deep perirectal tissues.
• This barrier can be breached through the crypts of Morgagni, which
can penetrate through the internal sphincter into the intersphincteric
space.
Etiology aerobic and anaerobic bacteria has to be responsible for abscess
formation
The anaerobes most commonly implicated are:
• Bacteroides fragilis
• Peptostreptococcus
• Prevotella
• Fusobacterium
• Porphyromonas
• Clostridium
The aerobes most commonly implicated are:
• Staphylococcus aureus, Streptococcus, and Escherichia coli.
Approximately 10%
• Crohn disease
• Trauma
• Immunodeficiency resulting from HIV infection or malignancy (both
hematologic and anorectal cancer)
• Tuberculosis
• Radiation therapy
• Inflammatory bowel disease
• Appendicitis (a rare cause of supralevator abscesses)
Epidemiolo • Approximately 30% of patients with anorectal abscesses report a
gy previous history of similar abscesses that either resolved
spontaneously or required surgical intervention.

• The peak incidence of anorectal abscesses is in the third and fourth

decades of life.

• These abscesses are also quite common in infants

• Male-to-female predominance of 2:1 to 3:1

Pathophysi • Perirectal abscesses and fistulas represent anorectal disorders arising
ology predominantly (~90% of cases) from the obstruction of anal
crypts,possibly involving increased sphincter tone. 
• Infection of the now static glandular secretions results in suppuration
and abscess formation within the anal gland.
• Typically, the abscess forms initially in the intersphincteric space and
then spreads along adjacent potential spaces.
Sign and • A small, erythematous, well-defined, fluctuant, subcutaneous mass
symptom near the anal orifice.

Diagnosis • Rectal toucher

• USG
• CT scan
• MRI
• Wound cultures should be collected in all patients in whom incision
and drainage is performed
Treatment • Incision and drainage

• concomitant use of antibiotics may be warranted in patients with conditions

such as the following [1] :
• Systemic inflammatory response or sepsis
• Extensive cellulitis
• Diabetes
• Immunosuppression
• Heart valve abnormalities or prostheses
Complicatio • Fistula formation
n • Bacteremia and sepsis, including seeding of the infection to other
areas by hematogenous spread
• Fecal incontinence
• Malignancy
Inflammatory Bowel
Disease (IBD)
LI 11

http://www.colorectalcentre.co.uk/inflammatory-bowel-
disease.html
 Inflammatory Bowel Disease (IBD)
Crohn’s disease Ulcerative colitis
• Epidemiology:
Sex More in males More in females

Existing cases per 100.000 • 26 to 199 cases per • 37 to 246 cases per
population 100,000 persons 100,000 persons
• 201 per 100,000 adults • 238 per 100,000 adults

https://www.cdc.gov/ibd/ibd-epidemiology.htm
Definition
Ulcerative Colitis
• A disease characterized by remitting and relapsing inflammation
limited to mucosa and submucosa of the large intestine
Etiology • Genetics: abnormalities of humoral and cell-mediated immunity
and/or generalized enhanced reactivity against commensal intestinal
bacteria
• Immune reaction: serum and mucosal autoantibodies against intestinal
epithelial cells
• NSAID
• Stress
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(12)60150-0/fulltext
Pathophysi Epithelial barrier:
ology • Separating the intestinal bacteria from the layers below including the
APC (as the first line defence and synthesize antimicrobial peptides)
• Damage of the epithelial or disruption of tight junction → increased
intake of microflora antigens → inflammation due to recognition on
microflora
Commensal microflora:
• Increased number → inflammation
Clicinal • Rectal bleeding
Manifestatio • Diarrhoea
n • Urgency
• Tenesmus (cramping rectal pain)
• Abdominal pain
• Fever (severe cases)
• Extraintestinal manifestations: uveitis, pyoderma gangrenosum,
pleuritis, erythema nodosum, ankylosing spondylitis, and
spondyloarthropathies
Classifica- Montreal classification of extent and severity of ulcerative colitis
tion • E1 (proctitis): inflammation limited to the rectum
• E2 (left-sided; distal): inflammation limited to the splenic flexure
• E3 (pancolitis): inflammation extends to the proximal splenic flexure
• S0 (remission): no symptoms
• S1 (mild): four or less stools per day (with or without blood), absence
of systemic symptoms, normal inflammatory markers
• S2 (moderate): four stools per day, minimum signs of systemic
symptoms
• S3 (severe): six or more bloods per day, pulse rate of ≥90 beats per
min, temperature ≥37·5°C, haemoglobin concentration <105 g/L,
erythrocyte sedimentation rate ≥30 mm/h
Diagnosis : Complete blood cell (CBC) count
Laboratory • Anemia (hemoglobin <14 g/dL in males and <12 g/dL in females)
• Thrombocytosis (platelet count >350,000/µL)
Comprehensive metabolic panel
• Hypoalbuminemia (albumin <3.5 g/dL)
• Hypokalemia (potassium <3.5 mEq/L)
• Hypomagnesemia (magnesium <1.5 mg/dL)
Inflammatory markers
• Elevation of the erythrocyte sedimentation rate and C-reactive protein
level (>100 mg/L)
Stool assays
• These include evaluation of fecal leukocytes, ova and parasite
studies, culture for bacterial pathogens, and Clostridium difficile titer.
Serologic: Perinuclear antineutrophil cytoplasmic antibody (p-ANCA)
usually positive
Diagnosis : • Loss of vascular pattern
Endoscopic • Erythema
Finding • Granularity
• Friability
• Erosions
• Ulcerations
• Spontaneous bleeding
Biopsy • Distortion of crypt architecture
• Crypt abscesses
• Lamina propria cellular infiltrate (plasma cells, eosinophils,
lymphocytes)
• Shortening of the crypts
• Mucin depletion
• Lymphoid aggregates
• Erosion or ulceration
Yamada’s Textbook of Gastroenterology. 6th ed. Blackwell
Publishing; 2016.
Yamada’s Textbook of Gastroenterology. 6th ed. Blackwell Publishing; 2016.
 Treatment
http://www.thelancet.com/j
ournals/lancet/article/PIIS0
140-6736(12)60150-
0/fulltext

(A) Mild to moderate ulcerative

colitis. (B) Severe ulcerative
colitis. †Carefully selected
patients at specialist
centres.*Dependent on the
severity of symptoms and how
quickly remission needs to be
induced
Treatment Surgery is needed if:
• Colitis does not respond to complete medical therapy
• Changes in the lining of the colon that can lead to cancer
• Severe problems, such as rupture of the colon, severe bleeding, or
toxic megacolon
Diet • Eat small amounts of food throughout the day.
• Drink plenty of water (drink small amounts throughout the day).
• Avoid high-fiber foods (bran, beans, nuts, seeds, and popcorn).
• Avoid fatty, greasy or fried foods and sauces (butter, margarine, and
heavy cream).
• Limit milk products if you are lactose intolerant. Dairy products are a
good source of protein and calcium.
Complica- • Colon narrowing or blockage
tion • Episodes of severe bleeding
• Severe infections
• Sudden widening (dilation) of the large intestine within 1 to a few
days
• Tears or holes (perforation) in the colon
• Osteoporosis
• Problems maintaining a healthy weight
• Slow growth and development in children
Definition
Crohn’s Disease
• An idiopathic, chronic inflammatory process that can affect any part
of the gastrointestinal tract from the mouth to the anus
Etiology • Immune system
• Genetics
• Smoking
• NSAID
Clicinal • SS: based on the affected area
Manifestatio • Diarrhea
n • Fever
• Fatigue
• Abdominal pain and cramping
• Mouth sores
• Reduced appetite and weight loss
• Perianal abscess or fistula
• Gastrointestinal hemorrhage
• Nausea, vomitting
• Growth failure in pediatric patients
• Extraintestinal manifestation: eye inflammation, arthritis, ankylosing
spondylosis, pyoderma gangrenosum, erythema nodosum

Yamada’s Textbook of Gastroenterology. 6th ed. Blackwell Publishing;

2016.
Diagnosis : • CBC
Laboratory • Electrolyte analysis
• Inflammatory markers
• Stool studies
• Serologic:
• Antibodies to the yeast Saccharomyces cerevisiae
• Escherichia coli anti-ompC (outer membrane porin C)
Treatment • Antidiarrheal agents: loperamide (2-4 mg), diphenoxylate with
atropine (1 tablet), and tincture of opium (8-15 drops). May be
administered up to 4 times daily (should not be given to patients with
active colitis, because of the risk of developing toxic megacolon)
• Bile acid sequestrants (since patient can’t absorb bile acid normally):
cholestyramine (2-4 g) and colestipol (5 g 2 or 3 times daily before
meals).
• Abdominal cramps: propantheline (30 mg before meals and at
bedtime), dicyclomine (10-20 mg), or hyoscyamine (0.125 mg)
• Infliximab is effective in patients who have refractory perianal and
enterocutaneous fistulae. Current clinical practice is to give it 5
mg/kg by intravenous (IV) infusion at 0 weeks, 2 weeks, and 6
weeks, followed by maintenance IV infusions every 8 weeks
Treatment Surgery is needed if:
• Persistent symptoms despite high-dose corticosteroid therapy
• Treatment-related complications, including intra-abdominal abscesses
• Medically intractable fistulae
• Fibrotic strictures with obstructive symptoms
• Toxic megacolon
• Intractable hemorrhage
• Perforation
• Cancer
Diet • Avoiding carbonated drinks
• Avoiding popcorn, vegetable skins, nuts, and other high-fiber foods
• Drinking more liquids
• Eating smaller meals more often
• Keeping a food diary to help identify foods that cause problems
• High calorie
• Lactose free
• Low fat
• Low salt
Yamada’s Textbook of Gastroenterology. 6th ed. Blackwell Publishing; 2016.
Anal fissure
 Anal Fissure
Definition • A longitudinal tear or defect in the skin of the anal canal distal to the
dentate line
• 90% located in the posterior midline.
• 10% located in the anterior midline.

https://myhealth.alberta.ca www.epharmapedia.com
Epidemiolo • Anal fissures affect males and females equally; however, an anterior
gy fissure is more likely to develop in women (25%) than in men (8%).
Etiology • Primer (trauma) : hard stools, prolonged diarrhoea, vaginal delivery,
repetitive injury or penetration.
• Secondary(non-trauma) : inflammatory bowel disease (e.g. Crohn’s
disease), granulomatous diseases (e.g. tuberculosis, sarcoidosis),
infections (e.g. HIV/AIDS, syphilis) or malignancy.
• Acute injury leads to local pain and spasm of the internal anal
sphincter. This spasm and the resulting high resting anal sphincter
pressure leads to reduced blood flow and ischaemia, and poor
healing.
Schlichtemeier, Steven, and Alexander Engel. “Anal Fissure.” Australian Prescriber 39.1
(2016): 14–17. PMC. Web. 12 Sept. 2017.
Clicinal • Severe tearing pain with the passage of faeces often with a small
Manifestatio amount of bright red blood on the stool or toilet paper.
n • The ideal examining : the patient lie comfortably in a lateral position
and then gently part the buttocks to look first at the posterior midline.
• Acute fissura : a fresh laceration.
• Chronic fissure : has raised edges exposing the internal anal sphincter
muscle fibres underneath. accompanied by an external skin tag
(sentinel pile) at the distal end of the fissure and a hypertrophied anal
papilla at the proximal end .(difficult to see on physical examination)
Schlichtemeier, Steven, and Alexander Engel. “Anal Fissure.” Australian Prescriber 39.1
(2016): 14–17. PMC. Web. 12 Sept. 2017.
http://emedicine.medscape.com https://en.wikipedia.org/wiki/Anal_fissure
Differential • Haemorrhoid
Diagnosis • Anal fistula or solitary rectal ulcer
Treatment • The goals of management : break the cycle of anal sphincter spasm
allowing improved blood flow to the fissured area so that healing can
occur.
• 50% of patients with acute anal fissures will heal with conservative
measures alone involving only increased fibre intake (e.g. psyllium)
and warm bathing of the perineum (sitz baths).It is hypothesised that
warm baths lead to relaxation of the internal anal sphincter via a
somatoanal reflex.
• Topical ointment & cream
• The preparations used in clinical practice contain glyceryl
trinitrate( or a calcium channel blocker(Diltiazem ,Nifedipine)
Treatment : • Surgery is considered for patients not responding to conservative
Surgical measures.
• The gold standard surgical operation for anal fissure is lateral
internal sphincterotomy
• Lateral Internal Sphincterotomy : The purpose of the operation is to
cut the hypertrophied internal sphincter, thereby releasing tension and
allowing the fissure to heal. (healing rate of approximately 95%)
• Spinchter dilatation is a controlled anal stretch or dilatation under
general anesthetic. It is performed because one of the causative
factors for anal fissure is thought to be a tight internal anal sphincter
Prognosis • Approximately half of uncomplicated fissures resolve in 2-4 weeks
with supportive care. Fissures that heal with conservative treatment
can recur, depending on the type of treatment the patient has
undergone (ranging from 16% to more than 50%). Chronic anal
fissures frequently require surgical treatment.
• Surgical treatment of anal fissures is associated with some degree of
incontinence in approximately 14% of patients. 
Complicati- • Constipation or fecal impaction may occur. The pain from an anal
on fissure can be so overwhelming that it discourages people from
defecating. Acute fissures can become chronic, and sentinel pile can
result. A permanent skin tag can result, and fistulas may form.
Amoebiasis
 Dysentery (Amebiasis)
• Amebiasis is caused by Entamoeba histolytica.

http://emedicine.medscape.com/
article/212029-overview
Etiology • Amebiasis is a parasitic infection caused by the protozoal organism E
histolytica.
• E histolytica is transmitted primarily through the fecal-oral route.
• Infective cysts can be found in fecally contaminated food and water
supplies and contaminated hands of food handlers.
• Sexual transmission is possible, especially in the setting of oral-anal
practices (anilingus).
• Poor nutrition, through its effect on immunity, has been found to be a
risk factor for amebiasis
http://emedicine.medscape.com/
article/212029-overview
https://
www.cdc.gov/dpdx/amebiasis/inde
x.html
Pathophysi • Disease may be caused by only a small number of cysts, but the
ology processes of encystation and excystation are poorly understood.
• The adherence of trophozoites to colonic epithelial cells seems to be
mediated by a galactose/N -acetylgalactosamine (GAL/GalNAc)–
specific lectin.
• A mucosal immunoglobulin A (IgA) response against this lectin can
result in fewer recurrent infections.
• Both lytic and apoptotic pathways have been described. Cytolysis can
be undertaken by amebapores, a family of peptides capable of
forming pores in lipid bilayers.
• Furthermore, in animal models of liver abscess, trophozoites induced
apoptosis via a non-Fas and non–tumor necrosis factor (TNF)-α1
receptor pathway.
• Cysteine proteinases have been directly implicated in invasion and
inflammation of the gut and may amplify interleukin (IL)-1–mediated
inflammation by mimicking the action of human IL-1–converting
enzyme, cleaving IL-1 precursor to its active form.
• Epithelial cells also produce various inflammatory mediators,
including IL-1β, IL-8, and cyclooxygenase (COX)-2, leading to the
attraction of neutrophils and macrophages.
Clicinal • Amebic colitis is gradual in onset, with symptoms presenting over 1-
Manifestatio 2 weeks; this pattern distinguishes this condition from bacterial
n dysentery.
• Diarrhea is the most common symptom.
• Patients with amebic colitis typically present with cramping
abdominal pain, watery or bloody diarrhea, and weight loss or
anorexia.
• Fever is noted in 10-30% of patients.
• Intestinal amebiasis may mimic acute appendicitis.
• Rectal bleeding without diarrhea can occur, especially in children.
Diagnosis : • Patients with acute amebic colitis may have lower quadrant
Physical abdominal tenderness (12-85% of cases).
• Fever is noted in only a minority of patients (10-30%).
• Weight loss occurs in 40%.
• Dehydration is uncommon.
• Occult blood is nearly always present in stools (70-100%).
Diagnosis : • Findings from basic blood tests may include the following:
Laboratory • Leukocytosis without eosinophilia (80% of patients)
• Elevated alkaline phosphatase level (80%)
• Elevated transaminase levels
• Mildly elevated bilirubin level
• Reduced albumin level
• Mild anemia
• Elevated erythrocyte sedimentation rate (ESR)
• Other laboratory studies employed for diagnosis include microscopy,
culture, serologic testing, and polymerase chain reaction (PCR) assay.
Differential • Abdominal Abscess
Diagnosis • Campylobacter Infections
• Cholecystitis
• Diverticulitis
• Echinococcosis
• Escherichia coli Infections
• Hepatitis A
• Hepatocellular Adenoma
• Inflammatory Bowel Disease
• Ischemic Colitis Imaging
• Pyogenic Hepatic Abscesses
• Salmonella Shigellosis
Treatment: Metronidazole
Antibiotic • Adult : 500-750 mg PO q8hr for 5-10 days
• Child : 35-50 mg/kg PO divided q8hr for 10 days
Tinidazole
• Adult : 2 g/day PO for 3 days
• Child : < 3 years safety and efficacy not established, >3 Years 50
mg/kg/day PO for 3 days; 2 g maximum
Prognosis Amebic infections can lead to significant morbidity while causing
variable mortality. In terms of protozoan-associated mortality, amebiasis
is second only to malaria. The severity of amebiasis is increased in the
following groups:
• Children, especially neonates
• Pregnant and postpartum women
• Those using corticosteroids
• Those with malignancies
• Malnourished individuals
Complicati- • Fulminant or necrotizing colitis
on • Toxic megacolon
• Ameboma
• Rectovaginal fistula
Prevention • Avoid drinking contaminated water; use bottled water while traveling
if possible
• If local water is to be drunk, purify it by (a) boiling it for more than 1
minute, (b) using 0.22 µm filtration, or (c) iodinating it with
tetraglycine hydroperiodide
• Avoid eating raw fruits and salads, which are difficult to sterilize; eat
only cooked food or self-peeled fruits if possible
• Wash uncooked vegetables and soak them in acetic acid or vinegar
for 10-15 minutes
Food intolerance
• difficulty digesting certain
foods and having an
unpleasant physical reaction
to them.
• causes symptoms, such as
bloating and stomach pain,
which usually come on a few
hours after consuming the
food
 Etiology
• Absence of an enzyme
1. Lactose intolerant  do not have enough lactase. If lactose remains in the
digestive tract, it can cause spasm, stomachache, bloating, diarrhea, and gas.
The common cause of food intolerance
• Chemical  caffeine, tea, chocolate
• Salicylates in many foods  flavor additives (artificial enchances, artificial
color), plant-sourced foods, including the majority of fruits and vegetables,
spices, herbs, tea
 Sign & sympton
• Bloating
• Spasm
• Stomachache
• Diarrheae
• Tummy pain
• Usually come on a few hours after eating the food
• Only results in symptoms if eat reasonable amounts of the food (unlike an
allergy, where just traces can trigger a reaction)
 Work up & treatment
• For work up  no tests for food intolerances. The only way to know if
you have one is to monitor your symptoms and the food you eat.
• Treatment
1. stop eating the food for a while,
2. Then reintroduce small quantities while monitoring how much you can
eat without symptoms coming on
 Prolapse Anal

http://emedicine.medscape.com/article/2026460-
overview#a8
 Prolapse Anal
• Rectal prolapse occurs when a mucosal or full-thickness layer of
rectal tissue protrudes through the anal orifice.
• Problems with fecal incontinence, constipation, and rectal ulceration
are common.
Etiology a number of associated abnormalities have been found. As many as 50%
of prolapse cases are caused by chronic straining with defecation and
constipation.

In children, rectal prolapse is probably related to the vertical orientation

of the rectum, the mobility of the sigmoid colon, the relative weakness of
the pelvic floor muscle, mucosa that is poorly fixed to submucosa, and
redundant rectal mucosa.
Epidemiolo • Peaks in occurrence are noted in the fourth and seventh decades of
gy life, and most patients (80-90%) are women

• Pediatric patients usually are affected when younger than 3 years

• Male-to-female ratio is 1:6

Risk factors • Pregnancy
• Previous surgery
• Diarrhea
• Benign prostatic hypertrophy
• Chronic obstructive pulmonary disease (COPD)
• Cystic fibrosis
• Pertussis (whooping cough)
• Pelvic floor dysfunction
• Parasitic infections – Amebiasis,
• Schistosomiasis
• spinal tumors

Sign and Physical signs of rectal prolapse include the following:

symptom
• Protruding rectal mucosa
• Thick concentric mucosal ring
• Sulcus noted between anal canal and rectum
• Solitary rectal ulcer (10-25%)
• Decreased anal sphincter tone
Differential • Hemorrhoids
Diagnosis • Intussusception
• Proctitis
Treatment Non-operative Management
• A prolapsed rectum can be reduced with gentle digital pressure
• Contributing factors, such as constipation and diarrhea, should be
addressed and eliminated if possible.
Surgery
Complicati- • Constipation
on • Bowel injury
• Altered bladder and sexual function
Child
Anal atresia
 Anal Atresia
• Imperforate anus
• spectrum of anorectal abnormalities = from a membranous separation to complete absence of the anus
• Incidence of anal atresia 1/5000 live births
• Freq associated w/ other congenital abnr:
VACTERL (vertebral anomalies, anal atresia, cardiac malformations, trach e oesophageal fistula, renal anomalies,
radial aplasia, limb anomalies)
• May have fistulous tracts w:
• Urethra
• Vagina
• Perineum
• Rarely bladder
Pathology
• Clinically there is no anal opening
• It can be broadly be classified:
• high (supralevator)
• low (infralevator)
depending on location of the atretic portion
• Obvious on routine examination of neonate
• Anus ✗ patent
• Diagnosis is missed & neonate is fed  signs of distal bowel
obstruction dev
• Urine should be filtered & examined for meconium = indicates
fistula to urinary tract
 Diagnosis & Treatment
• Plain x-rays & fistulograms w/ neonate in lateral prone
position  define lvl of lesion
• Cutaneous fistula generally indicates low atresia  definitive
repair: perineal approach possible
• ✗ fistula exist = high lesion is likely
• Neonates w/ fistula & low lesion ✓ undergo primary repair
• Neonates w/ high lesion = temporary colostomy; definitive
repair deferred until infant is older & structures  larger

Cochran WJ. Anal Atresia. MSD: 2013. available from: http://www.msdmanuals.com/professional/pediatrics/congenital-

gastrointestinal-anomalies/anal-atresia
Radiographic Features
• Abdominal radiographs
• Variable depends on site of atresia (high or
low), level of impaction w/ meconium &
physiological effects: straining
Marked gaseous distension of the
large bowel, particularly of the
• Show multiple dilated bowel loops w/ absence rectosigmoid. Features here are of a
of rectal gas distal large bowel obstruction.

• Invertogram
• Coin/metal piece placed over expected anus &
baby turned upside down (~3 minutes)
• Distance of gas bubble in rectum from metal
piece is noted:
• >2 cm  high type
• <2 cm  low type
prone lateral view is performed to
demonstrate the position of the most
distal portion of the large bowel and
therefore determine whether it is a
high or low anal atresia.
 • Fluoroscopy: contrast study
• Detect recto-urinary, recto-vaginal, rectoperineal
fistula
• Fistula considered low if below pubooccygeal line
(PCL); high fistula above PCL

• Ultrasound
• Anus seen as echogenic spot at lvl of perineum 
absent in atresia
• Show bowel dilation
• Infracoccygeal or transperineal approach 
differentiation b/w high or low subtype

Complication
• Meconium peritonitis
Cystourethrogram study reveals
• Sterile chemical peritonitis due to intra-uterine bowel rectal pouch which is in
continuation with the urethra
perforation & spillage of fetal meconium to fetal giving rise to recto-urethral
peritoneal cavity fistula. The newborn also has
partial sacral agenesis.
Knipe H, Jones J. Anal Atresia. Available from: http://radiopaedia.org/articles/anal-atresia
 Hirschsprung Disease
(Congenital Aganglionic Megacolon)
• Developmental disorder (neurocristopathy) of enteric nervous system
• Absence of ganglion cells in submucosal & myenteric plexus
• Most common cause of Lower intestinal obstruction in neonates
• Overall incidence: 1/5000 live births
• Male female ratio = 4:1 (short segment); 1:1 (longer segment) involved
• Prematurity = uncommon
•  in familial incidence in long segment disease
• May be associated w/ congenital defects syndromes:
• Down, Goldberg-Shprintzen, Smith-Lemli-Opitz, cartilage-hair hypoplasia,
Congenital hypoventilation (Ondine’s curse)
& urogenital & CV abnormalities
• Seen in association w/:
• Microcephaly
• Mental retardation
• Abnr facies
• Autism
• Cleft palate
• Hydrocephalus
• Micrognathia
Pathology
• Result of absence of ganglion cells in bowel wall
• Extending proximal & continuously from anus  variable distance
• Absence of neural innervation = consequence of an arrest of
neuroblast migration from prox  distal bowel
• W/out myenteric & submucosal plexus = inadequate relaxation of
bowel wall & hypertonicity  intestinal obstruction
• Genetic defects have been identified in multiple genes that encode
proteins of:
• RET signaling pathway (RET, GDNF, and NTN)
• involved in the endothelin (EDN) type B receptor pathway
(EDNRB, EDN3, and EVE-1)
• Syndromic forms of Hirschsprung disease have been associated with
the L1CAM, SOX10, and ZFHX1B (formerly SIP1) genes.
• The aganglionic segment:
• limited to the rectosigmoid = 80% of
patients.
• 10% to 15% of patients = long-segment
dilation of bowel (megacolon) proximal to the
disease affected region of narrowing at the lower left
center in sigmoid colon. Mucosal damage and
• proximal to the sigmoid colon secondary infection may follow.
http://library.med.utah.edu/WebPath/PEDHTML/PED048.html

• Total bowel aganglionosis is rare;

accounts for approximately 5% of cases.
• Histologically:
• absence of Meissner & Auerbach plexus
• hypertrophied nerve bundles w/  [] of
acetylcholinesterase b/w muscular layers
and in submucosa.
Clinical Manifestation:
• Usually diagnosed in the neonatal period:
• a distended abdomen
• failure to pass meconium, and/or bilious emesis or aspirates with
feeding intolerance.
healthy full-term infants = meconium is passed within 48 hr of
birth
• Hirschsprung disease = suspected in any full-term infant (the disease
is unusual in preterm infants) with delayed passage of stool.
• Failure to thrive; hypoproteinemia ✗ common presentation 
Hirschsprung disease recognized early in the course of the illness
• Breast-fed infants might not suffer disease as severe as formula-fed
infants
Failu dilatation Intral  blood
of the flow &
umina
re to proximal deteriora
bowel & l tion of
pass abdomina
l press the
mucosal
stool distention ure  barrier
Enterocolit associated
prolif is diarrhea,

Sta eratio
n of
(Clostridiu
m difficile,
Staphyloco
abdominal
tenderness,
sepsis and

sis
ccus signs of
bacter aureus, bowel
anaerobes, obstruction
ia coliforms) .

Early recognition of Hirschsprung disease before the onset of

enterocolitis is essential in reducing morbidity and mortality.
• In neonates: Differentiate Hirschsprung disease from:
• meconium plug syndrome
• meconium ileus
• intestinal atresia
• In older patients: Currarino triad must be considered
• Anorectal malformations
• ectopic anus, anal stenosis, imperforate anus)
• Sacral bone anomalies
• hypoplasia, poor segmentation
• Presacral anomaly
• anterior meningoceles, teratoma, cyst
Diagnosis:

• Rectal suction biopsy = gold standard for diagnosing

Hirschsprung disease
• Biopsy material: contain an adequate # of submucosa to evaluate for the
presence of ganglion cells

• Avoid obtaining biopsies in the normal area of hypoganglionosis: suction

rectal biopsy should be obtained no closer than 2 cm above the dentate
line

• Specimen should be stained for acetylcholinesterase to facilitate

interpretation.

• Findings: large # of hypertrophied nerve bundles stain (+) for

acetylcholinesterase w/ absence of ganglion cells
• Anorectal manometry
• measures the pressure of the internal anal sphincter while a balloon is
distended in the rectum.
• Normal patients:
• rectal distention initiates relaxation of the internal anal sphincter in
response to rectal distention with a balloon
• Hirschsprung disease:
• the internal anal sphincter fails to relax in response to rectal distention.
• Technically difficult to perform in young infants
• A normal response in the course of manometric evaluation precludes a
diagnosis of Hirschsprung disease
• Equivocal or paradoxical response requires a repeat motility or rectal
biopsy.
• An unprepared contrast enema
• ✓ Diagnosis in children older than 1 mo = proximal
ganglionic segment ✗ significantly dilated in the 1st few
weeks of life
• Classic findings: abrupt narrow transition zone between the
normal dilated proximal colon & a smaller-caliber
obstructed distal aganglionic segment.
• Rectal diameter = or << than the sigmoid colon 
Hirschsprung disease.
Performed without preparation: prevent transient dilatation of
the aganglionic segment.
• 24 hour delayed films = showing retained contrast
• If significant barium is still present in the colon = 
suspicion of Hirschsprung disease
• even if a transition zone is not identified
 Hirschsprung disease

• Barium enema examination

• determining the extent of
aganglionosis before surgery
• evaluating other diseases that
manifest as lower bowel
obstruction in a neonate

• Full-thickness rectal Functional megacolon

biopsies can be performed

at the time of surgery to
confirm the diagnosis and
level of involvement.
 Treatment
• Diagnosis established  definitive treatment = operative intervention
• Pull-through procedure
• Removal of diseased mucosa + resection + anastomosis
• 3 basic surgical options:
1. Swenson
• Excise aganglionic segment
• anastomose the normal proximal bowel to the rectum 1- 2 cm above the dentate line
2. Duhamel
• Neorectum: bringing down normally innervated bowel behind the aganglionic rectum
• anterior aganglionic ½ = normal sensation and a posterior ganglionic ½ = normal
propulsion.
3. Soave
• Tripping the mucosa from the aganglionic rectum
• Bringing normally innervated colon through the residual muscular cuff  bypassing
the abnormal bowel from within
Advances in techniques have led to successful laparoscopic single-stage
endorectal pull-through procedures = treatment of choice.
 TYPES OF HIRSCHSPRUNG DISEASE
Ultrashort-segment
• Internal sphincter achalasia
(aganglionic segment is limited to the
internal sphincter)
• Symptoms similar to those of children
with functional constipation
• Ganglion cells ✓ on rectal suction
biopsy, but the anorectal manometry is
abnormal  failure of relaxation of the
internal anal sphincter in response to
rectal distention
• Current treatment (still controversial):
• anal botulism injection  relax the anal
sphincter
• Anorectal myectomy (surgical excision
of part of a muscle) if indicated
Long-segment
• Involving the entire colon
• at times, part of the small bowel
presents a difficult problem
• Anorectal manometry & rectal suction
biopsy = findings of Hirschsprung disease
• Radiologic studies are difficult to interpret
 a colonic transition zone ✗ identified
• The extent of aganglionosis can be
determined accurately by biopsy at the
time of laparotomy
• Entire colon is aganglionic, + length of
terminal ileum  ileal-anal anastomosis
treatment of choice,
• preserving part of the aganglionic colon to
facilitate water absorption (helps the stools
to become firm)
PROGNOSIS
• Surgically treated Hirschsprung disease is generally
satisfactory; the great majority of patients achieve fecal
continence.
• Long-term postoperative problems:
• constipation
• recurrent enterocolitis
• stricture
• prolapse
• perianal abscesses
• fecal soiling
• Some children require myectomy or a redo pull-through procedure.
Physiology of
defecation
 LARGE INTESTINE
• Consist of: colon, rectum, cecum, appendix
• Cecum: forms blind-end pouch at ileocecal valve
• Appendix: fingerlike projection: lymphoid tissue
• Colon: not coiled, 3 straight parts
• End part: S shaped: sigmoid  straightened  rectum
• Primarily a drying & storage organ
COLON
• Main function of colon: absorption of H2O, Na+, minerals
• Receives ~500 mL chyme from SI/day
• Consist of: indigestible food residues (cellulose), unabsorbed biliary components,
remaining fluid
• Main motility: haustral contraction initiated by autonom rhythmicity of colon SMC
(~30 min b/w contraction)
 • MASS MOVEMENT
• 3-4x/day after meals

 motility during drive feces 1/3 – Distal part of LI,

contraction of
ascending & transverse ¾ length of colon materials stored
colon simultaneously in few seconds until defecation

Food enters stomach; Triggers mass

stimulate gastrin & movement in colon
extrinsic autonomic (GASTROCOLIC
nerves REFLEX)

New foods enters

Urge to defecate
DT

Reflexes initiated to
Make way for
move content further
incoming new foods
along down tract

Defecation reflex
(distention of rectum
Rectum
 receptor in rectal
 Circumstances are Tightening of external
unfavorable sphincter

Inhibit defecation;
despite the reflex

• During inactivity, both anal sphincters remain

contracted to ensure fecal continence
• Possible causes for delayed
Distended rectal wall
• Defecation: defecation:
Urge 
gradually
• Assistedrelaxes
by voluntary straining movements: – Ignoring urge to defecate
• Contraction of abdominal muscles –  colon motility: aging, emotion, low
• Forcible expiration against closed glottis bulk diet
•  Intraabdominal pressure
– Obstruction of fecal movement due to
• Constipation: tumor or colonic spasm
Next mass movement
• Defecation delayed too long
– Impairment
propels more feces to of defecation reflex
• >H2O # absorbed from feces  dry & hard
rectum (injury of nerve pathway)
 INTESTINAL GASES
• Flatus – gas, primarily driven by 2 sources:
• Swallowed air
• (500 mL air during meal)
• Gas produced by bacterial fermentation in colon
• Presence of gas percolating through luminal contents  gurgling sound (borborygmi)
• Eructation (burping) removes most of swallowed air from stomach, some passes to
intestine
• Little # of gas present in SI absorbed or passes on to colon + bacterial products from
undigested KH  expelled through anus
• Abdominal contraction  pressure against contracted anal sphincter  ΔP forces air
out at  velocity through slit like opening  edge of anal opening vibrates  low