OUTLINE I. Physiology of Diarrhea
II. Diarrhea III. Acute Diarrhea IV. Chronic Diarrhea
V. Constipation
Source: Dr. Sandejas’ ppt, Harisson’s Textbook of Medicine BOLD – emphasized by lecturer in his PPT
I. PHYSIOLOGY OF DIARRHEA
A. Neural Control• Intrinsic and Extrinsic innervations which modulate motor and secretory functions
B. Intestinal Fluid Absorption and Secretion
• Large capacitance and functional reserve can partially compensate for excess fluid delivery to the colon caused intestinal absorptive or secretory disorders
C. Small-Intestinal Motility
• Migrating Motor Complex (MMC) clears non-digestible residue from the small intestine during fasting
• Irregular mixing contractions occur in the small intestine after ingestion
D. Ileocolonic Storage and Salvage
• Allows time for salvage of fluids, electrolytes and nutrients • Diarrhea or constipation may result from alteration in the
reservoir function of the proximal colon or the propulsive function of the left colon
E. Colonic Motility and Tone
• Increased frequency of High Amplitude Propagated Contractions (HAPCs) may result in diarrhea or urgency • Colonic Tone is an important cofactor in the colon's
capacitance (volume accommodation) and sensation F. Colonic Motility After Meal Ingestion
• Colonic phasic and tonic contractility is mediated initially by the vagus nerve in response to mechanical distention of the stomach and at least in part by hormones, e.g., gastrin and serotonin.
G. Defecation
• Tonic contraction of the puborectalis muscle (a sling around the rectoanal junction) is important to maintain continence • During defecation, sacral parasympathetic nerves relax the
puborectalis, facilitating the straightening of the rectoanal angle
II. DEFINITION OF DIARRHEA
• loosely defined as passage of abnormally liquid or unformed stools at an increased frequency
• For adults on a typical Western diet, stool weight >200 g/d can generally be considered diarrheal
• May be further defined according to the DURATION: o Acute if < 2 weeks
o Persistent if 2-4 weeks o Chronic if > 4 weeks
• 2 Conditions to Differentiate from Diarrhea (usually stool weight <200 g/d)
o Pseudodiarrhea, or the frequent passage of small volumes of stool, is often associated with rectal urgency and accompanies IBS or proctitis.
o Fecal incontinence is the involuntary discharge of rectal contents and is most often caused by neuromuscular disorders or structural anorectal problems
Diarrhea and urgency, especially if severe, may aggravate or cause incontinence
o Pseudodiarrhea and fecal incontinence occur at
prevalence rates comparable to or higher than that of chronic diarrhea
• Overflow diarrhea may occur in nursing home patients due to fecal impaction that is readily detectable by rectal examination.
•
Careful history and physical examination generally allow these conditions to be discriminated from true diarrheaIII.
ACUTE DIARRHEA
• Infectious agents - > 90% of cases of acute diarrhea o often accompanied by vomiting, fever, and
abdominal pain. • Other causes - the remaining 10%
o Medications o Toxic ingestions o Ischemia o other conditions CAUSES OF DIARRHEA A. Infectious Agents
• 90% of cases of acute diarrhea
• often accompanied by vomiting, fever, and abdominal pain • Most are acquired by fecal-oral transmission
o ingestion of food or water contaminated with pathogens from human or animal feces. • In the immunocompetent person, the resident fecal
microflora, containing >500 taxonomically distinct species
o rarely the source of diarrhea
o may actually play a role in suppressing the growth of ingested pathogens.
• Disturbances of flora by antibiotics can lead to diarrhea o by reducing the digestive function
o by allowing the overgrowth of pathogens, such as
Clostridium difficile
• Acute infection / injury occurs when the ingested agent
overwhelms the host's mucosal immune and nonimmune
defenses (gastric acid, digestive enzymes, mucus,
peristalsis & suppressive resident flora)
• Established clinical associations with specific enteropathogens may offer diagnostic clues.
HIGH RISK GROUPS
• Travelers
o Nearly 40% of tourists to endemic regions of Latin America, Africa, and Asia develop so-called traveler's diarrhea
Causes: enterotoxigenic E. coli or
enteroaggregative E. coli as well as to Campylobacter, Shigella, Aeromonas, norovirus, Coronavirus and Salmonella
o Visitors to Russia may have increased risk of
Giardia-associated diarrhea
o Visitors to Nepal may acquire Cyclospora
o Campers, backpackers, and swimmers in wilderness areas may become infected with Giardia
o Cruise ships may be affected by outbreaks of gastroenteritis caused by agents such as Norwalk
virus
• Consumers of certain foods
o Diarrhea closely following food consumption at a picnic, banquet, or restaurant may suggest infection with Salmonella, Campylobacter, or Shigella from chicken
o Enterohemorrhagic E. coli (O157:H7) from
undercooked hamburger o Bacillus cereus from fried rice
o Staphylococcus aureus or Salmonella from
mayonnaise or creams
Page 1 of 7
Dr. Sandejas |December 3, 2013
2nd
2013-2014
o Salmonella from eggs, vibrio species, Salmonella, or acute hepatitis A from seafood,
especially if raw. • Immunodeficient persons
o 1o immunodeficiency (e.g., IgA deficiency & chronic
granulomatous disease)
o 2o immunodeficiency states (e.g., AIDS, senescence,
pharmacologic suppression) o AIDS patients
Common enteric pathogens often cause a
more severe & protracted diarrheal illness
Agents transmitted venereally per rectum (e.g., Neisseria gonorrhoeae,
Treponema pallidum, Chlamydia) may
contribute to proctocolitis. o Persons with hemochromatosis
prone to invasive enteric infections with
Vibrio species and Yersinia infections
and should avoid raw fish. o Opportunistic infections
Mycobacterium species, certain viruses
(cytomegalovirus, adenovirus, and
herpes simplex) and protozoa
(Cryptosporidium, Isospora belli,
Microsporida, and Blastocystis hominis) may also play a role
• Daycare attendees and their family members o Shigella
o Giardia o Cryptosporidium o Rotavirus • Institutionalized persons
o Infectious diarrhea is one of the most frequent
categories of nosocomial infections in many hospitals and long-term care facilities
o the causes are a variety of microorganisms but most commonly C. difficile
o
CLINICAL PRESENTATION
• Toxin Producers (ingestion of pre-formed toxins and
enterotoxin producing bacteria
o Profuse watery diarrhea 2o to small bowel
hypersecretion occurs
o Diarrhea associated with marked vomiting and
minimal or no fever may occur abruptly within a
few hours after ingestion • Enteroadherent pathogens
o Profuse watery diarrhea 2o to small bowel
hypersecretion occurs o Vomiting is usually less
o Abdominal cramping or bloating is greater
o Fever is higher
• Cytotoxin-producing & Invasive microorganisms
o Usually produce high fever and abdominal pain • Invasive bacteria & Entamoeba histolytica
o often cause bloody diarrhea (referred to as dysentery)
o Yersinia invades the terminal ileal and proximal
colon mucosa and may cause especially severe abdominal pain with tenderness mimicking acute appendicitis
SYSTEMIC MANIFESTATIONS ASSOCIATED WITH INFECTIOUS DIARRHEA
• Reiter's syndrome
o Salmonella, Campylobacter, Shigella, Yersinia Arthritis
Urethritis Conjunctivitis
• Enterohemorrhagic E. coli (O157:H7) & Shigella can lead to
the hemolytic-uremic syndrome high mortality rate B. Medications
• Side effects are probably the most common noninfectious
cause of acute diarrhea
• Etiology may be suggested by a temporal association between use and symptom onset.
o Examples: Antibiotics Cardiac antidysrhythmics Antihypertensives NSAIDs Antidepressants Chemotherapeutic agents Bronchodilators Antacids Laxatives C. Toxins • Organophosphate insecticides
• Amanita and other mushrooms
• Arsenic
• Preformed environmental toxins in seafood such as Ciguatera (foodborne illness from eating certain reef fish whose flesh is contaminated with toxins originally produced by
dinoflagellates) such as Gambierdiscus toxicus which live in tropical and subtropical waters and scombroid (foodborne illness that results from eating spoiled, decayed fish) D. Ischemia
• Ischemia or nonocclusive or nonocclusive ischemic colitis o typically occurs in persons >50 years
o
presents as acute lower abdominal pain preceding watery
bloody diarrheao generally results in acute inflammatory changes in the sigmoid or left colon while sparing the rectum.
APPROACH TO PATIENT
Figure 1. Algorithm for the management of acute diarrhea
severity and duration and on various host factors
• Most episodes of acute diarrhea are mild and self-limited
o
does not justify the cost and potential morbidity of diagnostic or pharmacologic interventions
ex.) Colonoscopy for acute diarrhea • Indications for evaluationo Profuse diarrhea with dehydration o Grossly bloody stools
o Fever 38.5° C
o Duration > 48 h without improvement o Recent antibiotic use
o New community outbreaks
o Diarrhea w/ severe abdominal pain in patients >50 years, and elderly (70 years) or
immunocompromised patients.
• In some cases of moderately severe febrile diarrhea associated with fecal leukocytes or with gross blood
o a diagnostic evaluation might be avoided o empirical antibiotic trial may be considered
• Microbiologic analysis of the stool is the cornerstone of
diagnosis in those suspected of severe acute infectious diarrhea is
• Workup includes:
o cultures for bacterial & viral pathogens
o Direct inspection for ova & parasites
o Immunoassays
for certain bacterial toxins (C. difficile) for viral antigens (rotavirus)
for protozoal antigens (Giardia, E. histolytica)
• Persistent diarrhea is commonly due to Giardia
• Additional causative organisms for persistent diarrhea include: o C. difficile
o E. histolytica
o Cryptosporidium
o Campylobacter
• If stool studies are unrevealing
o Flexible sigmoidoscopy with biopsies
o Upper endoscopy with duodenal aspirates and biopsies
• In patients with uncharacterized persistent diarrhea o Flexible sigmoidoscopy: exclude IBD o Colonoscopy: initial approach in patients with
suspected non-infectious acute diarrhea due to
ischemic colitis, diverticulitis or partial bowel obstruction
o Abdominal CT scanning (or other imaging approaches)
TREATMENT
• Fluid replacement alone may suffice for mild cases • Oral sugar-electrolyte solutions (sport drinks or designed
formulations) should be instituted promptly with severe
diarrhea to limit dehydration
• Profoundly dehydrated patients, esp. infants & elderly pts, require IV rehydration.
•
In moderately severe nonfebrile and nonbloody diarrhea
antimotility & antisecretory agents (e.g. loperamide)• Such agents should be avoided with febrile dysentery, which may be exacerbated or prolonged by them.
•
Bismuth subsalicylate may reduce symptoms of vomiting & diarrhea but should NOT be used to treatimmunocompromised patients w/renal impairment
riskof bismuth encephalopathy.
• Judicious use of antibiotics is appropriate in selected
instances of acute diarrhea and may reduce its severity and duration
• In moderate to severely ill patients with febrile dysentery
empiric treatment without diagnostic evaluation using a quinolone is an option
o Ciprofloxacin (500 mg bid for 3–5 d).
• Empirical treatment for suspected Giardiasis o Metronidazole 250 mg QID for 7 days
• Selection of antibiotics and dosage regimens are otherwise dictated by
o specific pathogens
o geographic patterns of resistance and conditions found
• Antibiotic coverage is indicated whether or not a causative
organism is found
o Immunocompromised patients
o Patients with mechanical heart valves o Patients with recent vascular grafts
o Elderly
• Antibiotic prophylaxis is indicated if
o patients traveling to high-risk countries in whom the likelihood or seriousness of acquired diarrhea would be especially high,
o includes:
Immunocompromised patients patients with IBD
patients with hemochromatosis patients with gastric achlorhydria. • Ciprofloxacin (invasive disease) or Rifaximin (uncomplicated
traveler’s disease) may reduce bacterial diarrhea in travelers by 90%
• During an outbreak of diarrheal illness
o alert the public health authorities promptly o may reduce the ultimate size of the affected
population.
IV.
CHRONIC DIARRHEA
• Diarrhea lasting > 4 weeks warrants evaluation to exclude serious underlying pathology (e.g. diarrhea due to colon cancer)
• Most causes are non-infectious, in contrast to acute diarrhea
• Classification by pathophysiologic mechanism facilitates a rational approach to management
A. Secretory
• due to derangements in fluid and electrolyte transport across the enterocolonic mucosa
• characterized by watery, large-volume fecal outputs that are
typically painless & persist with fasting
• No malabsorbed solute stool osmolality is accounted for by normal endogenous electrolytes with no fecal osmotic gap • Causes:
o Side effects from regular ingestion of drugs and toxins
Habitual use of stimulant laxatives: senna,
cascara, bisacodyl, ricinoleic acid (castor oil)-seen in long term use
Chronic ethanol consumption enterocyte injury with impaired Na+ &
Fecal Osmotic Gap
A lot of ingested substances have osmotic potential. If a solute cannot be absorbed, it will promote the flow of water from inside the GI tract into the lumen. More fluid drawn into the GI tract will aggravate the diarrhea
In secretory diarrhea: there is NO ingestion = no malabsorbed
Enteropathic Circulation of Bile
Bile is reabsorbed in the ileum. Absent ileum = Bile NOT reabsorbed Bile acids have an osmotic effect. Consequently, water gets drawn into the GI tractDiarrhea
water absorption
Chronic ingestion of certain toxins (arsenic)
Persistent bacterial infections may be associated with a secretory-type diarrhea o Bowel Resection, Mucosal Disease, or Enterocolic
Fistula
Inadequate surface for reabsorption of
secreted fluids and electrolytes due to a shorter bowel.
Tends to worsen with eating- peristalsis occurs which aggravates the diarrhea In Crohn's ileitis or resection of <100 cm
of terminal ileum, dihydroxy bile acids may escape absorption stimulate colonic secretion cholorrheic diarrhea) Idiopathic secretory diarrhea, in which
bile acids are functionally malabsorbed from a normal-appearing terminal ileum.
Partial bowel obstruction, ostomy stricture, or fecal impaction mayparadoxically lead to increased fecal output due to fluid hypersecretion o Hormones (Sir said this part will most likely NOT
come out in the exam except GASTRINOMA) Metastatic g.i. carcinoid tumors or,
rarely, 1o bronchial carcinoids may produce watery diarrhea alone or as part of the carcinoid syndrome
Release of potent intestinal
secretagogues (serotonin, histamine,
prostaglandins & various kinins)
diarrhea
Gastrinoma (neuroendocrine tumors) diarrhea occurs in up to 1/3 of cases.
Low pH pancreatic enzyme inactivation fat maldigestion diarrhea
The Watery Diarrhea Hypokalemia Achlorhydria (WDHA syndrome) (pancreatic cholera) 2o non-cell
pancreatic adenoma (VIPoma) Massive secretory diarrhea with stool
volumes >3 L/day
Medullary carcinoma of the thyroid may
present with watery diarrhea caused by calcitonin, other secretory peptides, or prostaglandins
o Congenital Defects in Ion Absorption
Defects in specific carriers associated with ion absorption cause watery
diarrhea from birth
Congenital chloridorrhea: defective
Cl/HCO3– exchange with alkalosis and
defective Na+/H+ exchange with acidosis
Addison's disease: may be associated
with watery diarrhea and skin hyperpigmentation.
B. Osmotic
• Ingestion of poorly absorbable osmotically active solutes which draws fluid into the lumen and overwhelms the reabsorptive capacity of the colon
• Fecal water output increases in proportion to such a solute load
• Ceases with fasting or with discontinuation of the causative
agent • Causes: o Osmotic Laxatives Magnesium-containing antacids Health supplements Laxatives
may induce osmotic diarrhea typified by a stool osmotic gap (>50 mosmol/L) serum osmolarity - typically 290
mosmol/kg
measurement of fecal osmolarity is no longer recommended
o Carbohydrate Malabsorption
acquired or congenital defects in brush-border disaccharidases and other enzymes leads to osmotic diarrhea with a low pH
One of the most common causes of
chronic diarrhea in adults is lactase
deficiency
Most patients avoid milk products without requiring treatment with enzyme suppl. Sorbitol (sweeteners), Lactulose, or
Fructose are frequently malabsorbed
diarrhea C. Steatorrheal
• Greasy, foul-smelling, difficult-to-flush diarrhea associated with weight loss & nutritional deficiencies due to concomitant malabsorption of amino acids and vitamins
• Fat Malabsorption
• Osmotic effects of fatty acids increased fecal output • Steatorrhea is defined as stool fat > 7 grams of stool fat/day D. Inflammatory
• Accompanied by pain, fever, bleeding or other manifestations of inflammation
• Mechanisms: 1. Exudation 2. Fat malabsorption
3. Disruption of fluid/electrolyte absorption
4. Hypersecretion or hypermotility from release of cytokines and other inflammatory mediators
• On stool analysis: presence of leukocytes or
leukocyte-derived proteins (calprotectin)
• With severe inflammation, exudative protein loss can lead to
anasarca
1. Anasarca: Edema all over! (Dr. Sandejas, 2013)
• Any middle-aged or older person with chronic inflammatory-type diarrhea, especially with blood
o Must exclude a colorectal tumor E. Dysmotility
• Rapid transit may accompany many diarrheas as a 2o
phenomenon
• Primary dysmotility is an unusual etiology of true diarrhea • Stool features often suggest a secretory diarrhea, but mild
steatorrhea of up to 14 g of fat per day can be produced by maldigestion from rapid transit alone.
• Hyperthyroidism, carcinoid syndrome, and certain drugs (e.g., prostaglandins, prokinetic agents) may produce hypermotility with resultant diarrhea.
• Primary visceral neuromyopathies or idiopathic acquired
intestinal pseudoobstruction may lead to stasis with
secondary bacterial overgrowth causing diarrhea.
• Diabetic diarrhea may occur in part because of intestinal
dysmotility.
• The exceedingly common irritable bowel syndrome (10% point prevalence, 1–2% per year incidence) is characterized by disturbed intestinal and colonic motor and sensory responses to various stimuli.
• Symptoms of stool frequency typically cease at night, alternate with periods of constipation, are accompanied by abdominal
Lactase Deficiency
GI tract no longer is able to break down lactose. As a result, bacteria end up breaking down the milk products
pain relieved with defecation, and rarely result in weight loss or true diarrhea.
F. Factitial
• Accounts for up to 15% of unexplained diarrheas referred to tertiary care centers.
• Munchausen syndrome
o Patients who resort to deception or self-injury for secondary gain (e.g. Those who drink lactacyd to BE
SICK, “para maawa sa kanila”, attention towards them)
• Eating disorders, some patients covertly self-administer
laxatives alone or in combination with other medications or surreptitiously add water or urine to stool sent for analysis. • Contamination of the stool with water or urine is suggested by
very low or high stool osmolarity, respectively
• Typically women with histories of psychiatric illness and disproportionately from careers in health care
• Patients may benefit from psychiatric counseling when they acknowledge their behavior.
• Hypotension and hypokalemia are common co-presenting features.
TREATMENT
Figure 2. Initial Management based on symptoms or features
Figure 3. Evaluations based on findings from a limited age appropriate screen for organic disease
Treatment of chronic diarrhea depends on the specific etiology o Curative
Surgical resection of colorectal cancer Antibiotic administration for Whipple’s disease Discontinuation of a drug
o Suppressive
Elimination of dietary lactose for lactase deficiency Elimination of gluten for celiac sprue
Use of glucocorticoids or other anti inflammatory agents for idiopathic IBDs
Use of cholestyramine for ileal bile acid malabsorption Proton pump inhibitors (e.g. Omeprazole) to suppress
the gastric hypersecretion of gastrinomas o Empirical
When specific cause of mechanism of chronic diarrhea evades diagnosis
• Mild opiates (e.g. diphenoxylate or loperamide) for mild or moderate watery diarrhea
• Codeine or tincture of opium for more severe diarrhea
• Clonidine for control of diabetic diarrhea
• Replacement of fat-soluble vitamins may also be necessary in patients with chronic steatorrhea
• For all patients with chronic diarrhea o Fluid and electrolyte repletion
o Replacement of fat-soluble vitamins may also be necessary in patients with chronic steatorrhea
V. CONSTIPATION
• Chronic constipation generally results from inadequate fiber or fluid intake or from disordered colonic transit or anorectal function
• Patients with Severe/ Intractable Constipations includes: o those who do not benefit from simple measures o those who require long-term treatment with potent
laxatives
o those with attendant risk of developing laxative abuse •
Sir said this part will most likely NOT come out in the exam
Measurement of Colonic Transit
• Radiopaque marker transit: markers are ingested: an abdominal flat film taken 5 days later should indicate passage of 80% of the markers out of the colon without the use of laxatives or enemas.
• Radioscintigraphy with delayed-release capsule:- contains radiolabeled particles to noninvasively characterize normal, accelerated, or delayed colonic function over 24–48 h with low radiation exposure.
Anorectal and Pelvic Floor Tests
• Straining: During DRE, have the patient strain to expel the index finger. Motion of the puborectalis posteriorly during straining indicates proper coordination of the pelvic floor muscles.
• Balloon expulsion test: A balloon-tipped urinary catheter is placed and inflated with 50 mL of water. Normally, a patient can expel it while seated on a toilet or in the left lateral decubitus position.
• Anorectal manometry: in patients with severe constipation, an excessively high resting (>80 mmHg) or squeeze anal sphincter tone may be found suggesting anismus (anal sphincter spasm). • Defecography: barium enema reveals "soft
abnormalities” i.e. rectoanal angle, anatomic defects of the rectum like internal mucosal prolapse, and enteroceles or rectoceles.
Figure 4. Causes of Constipation
APPROACH TO PATIENT
Figure 5. Approach to Patient with Constipation
• History:
o Evaluate the patient's symptoms
o Confirm if patient is indeed constipated based on frequency (e.g. < than 3 bowel
movements/week) consistency (lumpy/hard) excessive straining prolonged defecation time
need to support the perineum or digitate the anorectum.
o In >90% of cases, no underlying cause (e.g., cancer, depression, or hypothyroidism)
o Constipation responds to ample hydration, exercise, and supplementation of dietary fiber (15–25 g/d) o Evaluate the diet & medication history and any
psychosocial issues
• P.E. and a rectal examination
o exclude fecal impaction and most of the important diseases that present with constipation
o high anal sphincter tone may indicate features
suggesting an evacuation disorder
o (+) Weight loss, rectal bleeding, or anemia with constipation in pxs >40 years
o flexible sigmoidoscopy + barium enema colonoscopy
Colonoscopy allows for biopsy of lesions, polypectomy, or dilatation of strictures o Barium enema
less costly
identifies colonic dilatation,mucosal lesions or strictures
o Melanosis coli indicates abuse of anthraquinone laxatives such as cascara or senna
o Megacolon or cathartic colon may also be detected by colonic radiographs
o Serum Ca++, K+, and TSH levels will identify rare
patients with metabolic disorders.
o If constipation doesn’t not respond to fiber alone use an osmotic laxative
Lactulose Sorbitol
Polyethylene glycol
o After breakfast, a distraction-free 15–20 min on the toilet without straining is encouraged
o (+) weakness of the pelvic floor or injury to the pudendal nerve obstructed defecation from descending perineum syndrome several years later o Patients with severe or intractable constipation
require long-term treatment with potent laxatives (with the attendant risk of developing laxative abuse syndrome) should have further investigation
TREATMENT
• Once cause of constipation is known treatment decision • Slow-transit constipation aggressive medical / surgical
treatment
• Anismus or pelvic floor dysfunction biofeedback management
have such a physiologic disorder o 50% with colonic transit delay o 50% with evacuation disorder
• Patients with spinal cord injuries or other neurologic disorders require a dedicated bowel regime that often includes
o rectal stimulation o enema therapy o laxative therapy
• Patients with slow-transit constipation o Bulk laxatives: FIBER o Osmotic laxatives: PSYLLIUM
o Prokinetic agents: MILK OF MAGNESIA
o Secretory & stimulant laxatives: POLYETHYLENE
GLYCOL, LUBIPROSTONE, BISACODYL
• Newer treatment aimed at enhancing motility and secretion o constipation-predominant IBS in females or severe
constipation • Surgical Treatment
o Laparoscopic colectomy w/ ileorectostomyfor treatment failures with documented slow-transit constipation (unassociated with obstructed
defecation) , not an option if with continued evidence of an evacuation disorder/generalized GI dysmotility
The decision to resort to surgery is facilitated in the presence of megacolon and megarectum
o The complications after surgery include small-bowel obstruction (11%) and fecal soiling
o Frequency of defecation is
3–8 per day (first year post op) 1–3 per day (second year post op) • Patients with combined evacuation & transit / motility disorder
o Pelvic floor retraining (biofeedback and muscle relaxation)
o Psychological counseling
o Dietetic advice
• if colonic transit studies do not normalize & symptoms are intractable colectomy or ileorectosomy
• Patients with pelvic floor dysfunction alone
o Biofeedback training has a 70–80% success rate
measured by the acquisition of comfortable stool habits
o Surgical management (internal anal sphincter or puborectalis muscle division) minimal success abandoned.
