Diarrhea Constipation

November 10, 2017 | Author: Dia Dimayuga | Category: Constipation, Diarrhea, Rectum, Gastroenterology, Clinical Medicine
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4. 5: Diarrhea and Constipation


Dr. Sandejas |December 3, 2013


OUTLINE I. Physiology of Diarrhea II. Diarrhea III. Acute Diarrhea IV. 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 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

V. Constipation

Source: Dr. Sandejas’ ppt, Harisson’s Textbook of Medicine BOLD – emphasized by lecturer in his PPT



Neural Control •


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

Colonic Motility and Tone • •


Migrating Motor Complex (MMC) clears non-digestible residue from the small intestine during fasting Irregular mixing contractions occur in the small intestine after ingestion

Ileocolonic Storage and Salvage • •


Large capacitance and functional reserve can partially compensate for excess fluid delivery to the colon caused intestinal absorptive or secretory disorders

Small-Intestinal Motility •


Intestinal Fluid Absorption and Secretion •


Intrinsic and Extrinsic innervations which modulate motor and secretory functions

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

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 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 Delgado M., Desabelle, Dimayacyac, Dimayuga, Dingco, Dizon

Delas Peñas, Delgado G., Delgado M., Desabelle, Dimayacyac, Dimayuga, Dingco, Dizon

SUBJECT Med 4.5 o

Salmonella from eggs, vibrio species, Salmonella, or acute hepatitis A from seafood, especially if raw.

the hemolytic-uremic syndrome  high mortality rate


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



Toxins • • • •


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 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)

Ischemia •

Ischemia or nonocclusive or nonocclusive ischemic colitis o typically occurs in persons >50 years o presents as acute lower abdominal pain preceding o

watery  bloody diarrhea generally results in acute inflammatory changes in the sigmoid or left colon while sparing the rectum.


Figure 1. Algorithm for the management of acute diarrhea •

The decision to evaluate acute diarrhea depends on its

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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

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 tractDiarrhea

 ex.) Colonoscopy for acute diarrhea Indications for evaluation o 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)

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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 treat immunocompromised patients w/renal impairment risk of bismuth encephalopathy. Judicious use of antibiotics is appropriate in selected instances of acute diarrhea and may reduce its severity and duration

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.


• •


In moderate to severely ill patients with febrile dysentery



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

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

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+ &

• •

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SUBJECT Med 4.5 water absorption Chronic ingestion of certain toxins (arsenic)  Persistent bacterial infections may be associated with a secretory-type diarrhea 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 50 mosmol/L)  serum osmolarity - typically 290 mosmol/kg  measurement of fecal osmolarity is no longer recommended Carbohydrate Malabsorption  acquired or congenital defects in brushborder disaccharidases and other enzymes  leads to osmotic diarrhea with a low pH  One of the most common causes of  


Lactase Deficiency GI tract no longer is able to break down lactose. As a result, bacteria end up breaking down the milk products




Partial bowel obstruction, ostomy stricture, or fecal impaction may paradoxically lead to increased fecal output due to fluid hypersecretion 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 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.

 


Steatorrheal •

Inflammatory •

• • •

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

Accompanied by pain, fever, bleeding or other manifestations of inflammation

• 1. 2. 3. 4. • • •


Mechanisms: Exudation Fat malabsorption Disruption of fluid/electrolyte absorption Hypersecretion or hypermotility from release of cytokines and other inflammatory mediators On stool analysis: presence of leukocytes or leukocytederived 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 inflammatorytype diarrhea, especially with blood o Must exclude a colorectal tumor

Dysmotility • • • •

Osmotic •

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

• • •


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

• • •

Rapid transit may accompany many diarrheas as a 2 o 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

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SUBJECT Med 4.5 pain relieved with defecation, and rarely result in weight loss or true diarrhea.


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

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.



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


Replacement of fat-soluble vitamins may also be necessary in patients with chronic steatorrhea

Chronic constipation generally results from inadequate fiber or fluid intake or from disordered colonic transit or anorectal function

Patients with Severe/ Intractable Constipations includes:

Figure 2. Initial Management based on symptoms or features


o o o

those who do not benefit from simple measures those who require long-term treatment with potent laxatives those with attendant risk of developing laxative abuse


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

Suppressive 

Elimination of dietary lactose for lactase deficiency

Elimination of gluten for celiac sprue

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SUBJECT Med 4.5 Figure 4. Causes of Constipation o




o o o o

o o o

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 5. Approach to Patient with Constipation • History: Evaluate the patient's symptoms 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 o

suggesting an evacuation disorder (+) Weight loss, rectal bleeding, or anemia with constipation in pxs >40 years  flexible sigmoidoscopy + barium enema colonoscopy  Colonoscopy allows for biopsy of lesions, polypectomy, or dilatation of strictures Barium enema  less costly  identifies colonic dilatation,mucosal lesions or strictures Melanosis coli  indicates abuse of anthraquinone laxatives such as cascara or senna Megacolon or cathartic colon may also be detected by colonic radiographs Serum Ca++, K+, and TSH levels will identify rare patients with metabolic disorders. If constipation doesn’t not respond to fiber alone  use an osmotic laxative  Lactulose  Sorbitol  Polyethylene glycol After breakfast, a distraction-free 15–20 min on the toilet without straining is encouraged (+) weakness of the pelvic floor or injury to the pudendal nerve  obstructed defecation from descending perineum syndrome several years later 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



high anal sphincter tone may indicate features

Once cause of constipation is known  treatment decision

Slow-transit constipation aggressive medical / surgical treatment

Anismus or pelvic floor dysfunction biofeedback management

Only ~60% of patients with severe constipation are found to

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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.

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