DIARRHEA/ HYPERDEFACATION
Diarrhea refers to an increase in the frequency or a decrease in the consistency of stool as compared to a patient’s normal bowel habits. A 24-hour stool volume in excess of 200 grams is consistent with a diagnosis of diarrhea. Diarrhea may be classified as acute or chronic (lasting less than or longer than 4 weeks, respectively). Diarrhea may further be classified as osmotic, secretory, exudative, or dysmotile. Medication side effect or abuse may manifest as diarrhea, or diarrhea may result from antibiotic induced Clostridium difficile infection. Diarrhea may be a symptom of an underlying disease such as hyperthyroidism, carcinoid syndrome, diabetes mellitus, inflammatory bowel disease (Crohn’s disease or ulcerative colitis), ischemic bowel, gastrinoma or vipoma. Diarrhea may also be the result of enteric bacterial, viral, or parasitic infections. Viral agents are the most common cause of acute diarrhea in the United States.
The history should first address if symptoms are acute (less than 4 weeks duration) or chronic (symptoms greater than 4 weeks), and then further questioning may help reveal a possible etiology. Patients should be questioned regarding recent travel, antibiotic use, fever, dietary inducers (lactose, sucrose, fructose, fatty foods), medication ingestion, hematochezia, the presence of mucoid stools, abdominal pain, weight loss, relationship to any recent meals (incubation periods for foodborne illnesses can range from 12 to 36 hours and in the case of E. coli O157:H7-2 to 5 days), meal partners with similar symptoms, and lifestyle habits in regards to possible HIV infection.
The physical exam should first evaluate for signs of dehydration, which if found should promptly be corrected. Further evaluation should check for bowel sounds, abdominal pain or the presence of peritoneal signs (rebound tenderness) which would necessitate immediate abdominal radiography to evaluate for the possibility of perforation. The diagnosis of Crohn’s disease should be entertained when the physical exam reveals the presence of a tender mass in the right lower quadrant especially when the history reveals the presence of mucoid stools. Rectal examination with guiac testing should always be a part of the physical exam. Anal fissures or fistulas should raise the possibility of Crohn’s disease. Further clues in the physical examination include the presence of dermatitis herpetiformis (celiac disease), arthritis (inflammatory bowel disease) or pyoderma gangrenosum (inflammatory bowel disease).
Acute diarrhea is usually infectious in etiology, and because of its usually self-limited course, requires only reassurance and counseling on maintaining hydration. Hydration should be via electrolyte solutions such as Infalyte, Rehydralyte, and Pedialyte or with a homemade solution (¾ teaspoon salt, 1 teaspoon baking powder, 4 tablespoons sugar, 1 cup orange juice, and 1 liter water). During oral rehydration avoid using caffeine and lactose-containing products. Severe dehydration may require intravenous fluids.
When symptoms are persistent or severe, further evaluation with stool studies may be required. The presence of fecal leukocyte, lactoferrin, or blood is consistent with an inflammatory pathogen: enteroinvasive E coli, Shigella, Salmonella, Yersinia, Clostridium difficile, or Campylobacter. Inflammatory pathogens which do not cause fecal blood or leukocytes include: Rotavirus or Norwalk virus. When there are fecal leukocytes and stool cultures are negative for bacterial pathogens, inflammatory bowel disease (Crohn’s disease or ulcerative colitis), ischemic colitis, or radiation enteritis should be considered as likely etiologies; however, infection can not completely be excluded by negative stool cultures as some laboratories only screen for Salmonella, Shigella, and Campylobacter when performing routine stool cultures. Specific cultures must be requested if infection with Vibrio, Yersinia, or E. coli O157:H7 is suspected. E. coli O157:H7 infection may also be diagnosed by finding Shigalike toxin in stool extracts or in E. coli culture broth filtrates. Parasitic etiologies (Giardia lamblia, Cryptosporidium, Entameoba histolytica) do not manifest with fecal leukocytes. When the history is compatible with traveler’s diarrhea, empiric therapy with ciprofloxacin (500 mg BID X 3-5 days), trimethoprim/sulfamethoxazole DS (one tablet BID for 5 days), or bismuth subsalicylate (30 mL or 2 tablets every 30 minutes for 8 total doses) may be employed. In fact, patient’s who are about to embark on a trip to an endemic area are often given a supply of either of these therapies to take with them and use when they develop symptoms. However, empiric antibiotics may worsen disease, and are actually contraindicated with certain infections such as E coli O157:H7 (may cause hemolytic uremic syndrome) and Salmonella species (antibiotics may prolong the carrier state or lead to resistance). Other infectious etiologies include Listeria monocytogenes, Vibrio vulnificus (may cause fatal septicemia in patients with underlying liver disease), Vibrio cholerae, and Vibrio parahaemolyticus. The differential in immunocompromised patients with diarrhea includes: HIV enteropathy, Cryptosporidium, Microsposida, Isospora belli, Giardia lamblia, Strongyloides stercoralis, Entamoeba histolytica, cytomegalovirus, herpes simplex virus, Epstein-Barr virus, Mycobacterium avium-intracellulare, and Mycobacterium tuberculosis. When an infectious etiology is suspected, abstain from prescribing antimotility agents.
Chronic diarrhea (symptoms lasting greater than 4 weeks) should always warrant an investigation if symptoms persist after the patient follows a lactose-free diet for several days. The reason for the trial of dietary restrictions is that a secondary lactase deficiency may occur after an acute episode of diarrhea and result in prolongation of diarrhea symptoms. If lactose intolerance proves not to be the underlying etiology, the list of other possible etiologies is extensive. Patients with long standing poorly controlled diabetes mellitus often manifest diarrhea as a result of an autonomic neuropathy. Initial testing for diarrhea may include: stool for fecal leukocytes (IBD, ischemic colitis, radiation colitis, neoplasms, invasive bacterial disease), three separate stools for ova and parasites, stool for giardia antigen, C. difficile toxin assay, stool pH (if less than 5.3 is consistent with carbohydrate intolerance whereas values greater than 5.6 exclude the diagnosis), 24-hour stool weight in grams, a 72-hour stool collection to measure for fecal fat while the patient is on a diet of 75-100 grams fat/day (steatorrhea is present if >14 grams stool fat/24 hours), plain abdominal radiography (evaluate for obstruction, perforation, or pancreatic calcifications), CBC, ESR (elevated with inflammatory etiologies especially IBD), TSH (hyperthyroidism), electrolytes (hypokalemia with gastrinoma, vipoma, or villous adenomas), urinary 5-hydroxyindoleacetic acid (carcinoid syndrome), and a serum osmolality plus fecal sodium and potassium values to calculate the stool osmotic gap. The stool osmotic gap is then calculated via the following equation:
Stool osmotic gap= serum osmolality- [2x (fecal Na+ + fecal K+)]
A stool osmotic gap less than 40 is consistent with a secretory etiology, and a gap greater than 40 is consistent with osmotic diarrhea. Another method to distinguish between these two types of diarrhea is to place the patient on a fast. While fasting, patients with osmotic diarrhea will have a dramatic decrease in symptoms whereas patients with secretory diarrhea will not experience any change in their stool volume.
Further testing may include: upper gastrointestinal barium studies, enteroclysis, barium enemas, esophagoduodenoscopy, and colonoscopy. If celiac disease is suspected, antiendomysial, antigliadin or antireticulin antibodies will help establish the diagnosis. Diagnostic considerations at this point would include: laxative abuse (early history taking should have addressed this but patients may still deny this habit despite direct questioning), decreased ileum or right colon secondary to prior surgery (again should have been addressed during the history), irritable bowel syndrome, or toxin induced (heavy metals, organophosphates, food poisoning, ethanol). Melanosis coli noted on sigmoidoscopic exam of the rectum is consistent with a diagnosis of laxative abuse. Sigmoidoscopy should be performed on all patients without a clear diagnosis after the initial stool and serum evaluations have been performed.
Therapy for diarrhea is to determine and treat the underlying etiology. However, some useful therapies include bulk forming agents (polycarbosil, kaolin, psyllium or methylcellulose which may increase stool consistency or bind bacterial toxins), loperamide (Imodium), diphenoxylate with atropine (Lomotil), bismuth subsalicylate, and cholestyramine (binds bile salts and is useful in diarrhea which develops after ileal resections). Bismuth subsalicylate (150 mg 2-4 tablets Q 30 minutes for 8 doses) is an effective therapy. Symptomatic therapy should be avoided in cases where infectious diarrhea or inflammatory bowel disease is the potential etiology. Octreotide (Sandostatin) may be effective in cases of diarrhea secondary to carcinoid syndrome, neuroendocrine tumors, short bowel syndrome, and some cases of AIDS related diarrhea. Diabetes mellitus associated diarrhea may respond to treatment with clonidine or cyclic antibiotic therapy with tetracycline, amoxicillin, or metronidazole. Proton pump inhibitor therapy may prove useful in treating diarrhea associated with Zollinger-Ellison syndrome or systemic mastocytosis. Indomethacin therapy should be employed for diarrhea associated with medullary carcinoma of the thyroid, villous adenomas, or AIDS enteropathy. C. difficile-associated diarrhea may be treated with oral metronidazole (500 mg TID or 250 mg QID) or vancomycin (500 mg QID) for a total of 10 days. In cases of C. difficile infection with associated megacolon or ileus, intravenous metronidazole (500 mg Q 8 hours) is effective. If oral therapy is not an option, the above mentioned intravenous metronidazole or vancomycin via rectal enema or intestinal catheter are appropriate potential therapies.