Acute diarrhea in adults

World Gastroenterology Organization Practice Guidelines
Acute diarrhea in adults
Review team <author names to be supplied> Contents
1 Definition
Acute diarrhea is defined as an abnormally frequent discharge of semisolid or fluid fecal matter from the bowel, lasting less than 14 days.
2 Pathogenesis
The causes of acute diarrhea can be grouped under four main headings: bacterial, viral, parasitic, and noninfectious causes. Diarrhea can be viewed as an increase in the quantity of water and electrolytes in the feces, leading to frequent production of unformed stool. It is an impaired balance between resorption and secretion in the intestinal wall that leads to the increased wateriness of the feces. Often, this involves noninvasive microorganisms that are especially active in the intestine, causing watery diarrhea with no fever (or low fever). These microorganisms lead to diarrhea through a variety of interactions with the intestinal mucosa. Enterotoxic Escherichia coli and Vibrio cholerae do not spread beyond the intestinal lumen; they cause diarrhea without any invasion of the intestinal epithelium by producing enterotoxins, which in turn induce fluid secretion. Some microorganisms damage the resorption surface of the microvilli, which in turn can lead to a disaccharidase deficiency — as happens in Giardia lamblia infection, for example. Other microorganisms are invasive and penetrate the intestinal epithelium, resulting in an inflammatory disorder. The best-known example of this is Shigella infection.
Campylobacter and Salmonella can also invade the intestinal mucosa (Table 1).
Table 1 Major
Bacteria
Parasites
3 Possible risk situations and high-risk groups for
infectious diarrhea
— Developing nations, tropical areas — Peace corps and voluntary workers — Campers (ground water) • Unusual food or eating circumstances — Seafood and shellfish, especially raw • Homosexuals, sex workers, intravenous drug users, risk of human — Gay bowel syndrome — Acquired immune deficiency syndrome 4 Diagnosis and differential diagnosis (Table 2)
• History taking • Physical examination Table 2 Epidemiologic clues to infectious diarrhea
Water (including foods washed
Vibrio cholerae, Norwalk agent, Giardia organisms and Salmonella, Campylobacter, and Shigella spp. Vibrio cholerae, V. parahaemolyticus, and V. vulnificus; Salmonella spp.; tapeworm and Anisakis Staphylococcus and Clostridium food poisoning; Salmonella, Campylobacter, Cryptosporidium and Giardia spp. Animal-to-person (pets and
Most enteric bacteria, viruses, and parasites Person-to-person (including
Shigella, Campylobacter, Cryptosporidium and Giardia spp.; viruses; Clostridium difficile Giardia and Cryptosporidium spp. E. coli of various types; Salmonella, Shigella, Campylobacter, Giardia, and Cryptosporidium spp.; Entamoeba histolytica The blood–fever matrix
One important factor should be ascertained immediately: is there dehydration? There are two possible conditions in acute diarrhea — diarrhea with fever and blood; or diarrhea without fever and without blood (Table 3).
Table 3 Correlations between the pathophysiology and symptoms of
infectious diarrhea
Toxin-producing
Cytotoxin-producing
Enteroadherent
Giardia organisms, cryptosporidiosis, helminths Invasive organisms
Salmonella, Campylobacter, Shigella species, enteroinvasive E. coli, Entamoeba histolytica Rehydration
• Stress doing nothing, but always manage any dehydration. • Serious dehydration possible in the aged. • Use oral rehydration solution (ORS) (also when there is vomiting). • Isotonic intravenous saline solution only if there is serious weight loss (> 8–10%) • Fasting is not necessary; eat small amounts often • No foods containing lactose (milk!) or caffeine (these aggravate the diarrhea) Nonspecific antidiarrhetics
• Use loperamide for symptomatic treatment. The use of loperamide when the patient is febrile (> 38.5°) or dysenteric, or has fecal leukocytes, is controversial. Antimicrobial therapy (Table 4)
• Bacterial causes, such as persistent Shigella, Salmonella, or Campylobacter infections, also in immunocompromised patients and patients with acquire immune deficiency syndrome (AIDS), and especially in: — Patients with impaired resistance or sepsis — Patients with artificial prostheses • In other circumstances, physicians should be reluctant to prescribe antimicrobials, especially in immunocompetent individuals, in order not to increase the prevalence of antimicrobial resistance. Table 4 Antimicrobial therapy (oral; adult dosages)
Ciprofloxacin 500 mg b.i.d.; 10 days (1st choice) Amoxicillin 750 mg q.i.d.; 14 days (alternative 1) Co-trimoxazole 960 mg b.i.d.; 14 days (alternative 2) Ciprofloxacin 500 mg b.i.d.; 10 days (1st choice) Amoxicillin 750 mg q.i.d.; 14 days (alternative 1) Co-trimoxazole 960 mg b.i.d.; 14 days (alternative 2) Campylobacter (serious and persistent Doxycycline 200 mg 1st day; then 100 mg 1dd; 4 days Co-trimoxazole 960 mg b.i.d.; 5 days (alternative 1) Ciprofloxacin 500 mg b.i.d.; 5 days (alternative 2) Tinidazole 2 g 1 × d; 3 days (1st choice) Metronidazole 750 mg t.i.d.; 5 days (alternative 1; this is followed by diloxanide furoate 500 mg t.i.d.; 10 days) Ciprofloxacin 1 g once only Vibramycin 300 mg once only Albendazole 400 mg 1 × d; 3 days Ivermectin 150–200 µg/kg once only Tiabendazole 25 mg/kg b.i.d.; 2 days (max. 1500 mg per dose) Paromomycin 500–1000 mg t.i.d.; 14 days status. If the patient is immunocompromised with persistent diarrhea: Metronidazole 500 mg t.i.d.; 7–10 days (if Usually spontaneous recovery after stopping Vancomycin 125 mg q.i.d.; 7–10 days (alternative) N.B.: multiresistant Salmonella typhi and other multiresistant microorganisms are common, especially in developing countries. Treatment with amoxicillin and co-trimoxazole is not effective in many parts of the world. The duration of antimicrobial therapy is variously indicated in the literature, and longer periods are often suggested. Clostridium difficile is resistant to metronidazole in some 30% of cases. 5 Treatment approaches using the blood–fever matrix
Diarrhea with fever and with blood
General observations. Diarrhea as a result of invasive microorganisms; location
often in the colon; frequent low-volume bloody diarrhea, often preceded by watery
diarrhea.
Pathogens
• Shigella spp. (bacillary dysentery, shigellosis) • Campylobacter jejuni • Salmonella spp; Aeromonas hydrophila; Vibrio parahaemolyticus; Plesiomonas Diagnosis
• Clinical differentiation is difficult, especially versus noninfectious idiopathic • Many leukocytes are present in feces (invasive pathogens). • Fecal culture for Salmonella, Shigella, Campylobacter, Yersinia/ • Thick blood smear for malaria. Treatment
• In case of serious and persistent infection, antibiotics should always be used; one should beware of multiresistance of Shigella spp. (see antimicrobial therapy,
Table 4).
Diarrhea without fever and without blood
General observations
• Noninvasive pathogens (voluminous watery feces; no fecal leukocytes); often • Most frequent presentation in traveler’s diarrhea (85% of cases) • In the case of cholera: rice water–like feces, often vomiting; if travelers observe hygiene, then the chance of contracting this infection is very low. Pathogens
• Enterotoxic E. coli (ETEC); the most frequent cause of traveler’s diarrhea • Giardia lamblia • Preformed exotoxin from Staphylococcus aureus, food poisoning; also by Bacillus cereus, Clostridium perfringens (type A); diarrhea produced by this toxin is characterized by a short, 6-hour incubation period. — Vibrio parahaemolyticus (when fish and shellfish are not kept adequately refrigerated) — Vibrio cholerae: cholera — Toxic substances in food (heavy metals—e.g., tin preservatives, nitrites, pesticides, histamines in fish); mushrooms Cryptosporidium, Isospora belli (in immunodeficient HIV-positive patients, although it can also occur in healthy individuals). Diagnosis
• No leukocytes in feces • Fecal culture (very low yield in watery diarrhea; ETEC not in routine laboratory • Parasitological examination of feces (fresh feces); often several repeated examinations are required to establish the presence of Giardia. Treatment
• Prevent or correct dehydration (if necessary using ORS). • Spontaneous recovery. If this does not ensue, see under antimicrobial therapy, above (Table 4).
6 References
American Gastroenterological Association. American Gastroenterological Association medical position statement: guidelines for the evaluation and management of chronic diarrhea. Gastroenterology 1999;116:1461–3 (PMID: 10348831). DuPont HL. Guidelines on acute infectious diarrhea in adults. The Practice Parameters Committee of the American College of Gastroenterology. Am J Gastroenterology 1997;92:1962–75 (PMID: 9362174). Thielman NM, Guerrant RL. Clinical practice. Acute infectious diarrhea. N Engl J Med 2004;350:38– Wingate D, Phillips SF, Lewis SJ, Malagelada JR, Speelman P, Steffen R, et al. Guidelines for adults on self-medication for the treatment of acute diarrhoea. Aliment Pharmacol Ther 2001;15:773–82 (PMID: 11380315). 7 Links to useful web sites
• The American College of Gastroenterology (ACG): • The Practice Parameters Committee of the ACG has published practice guidelines on diarrhea: http://www.acg.gi.org/physicians/clinicalupdates.asp#guidelines • The American Gastroenterological Association (AGA) has published a medical position statement on “Guidelines for the Evaluation and Management of Chronic Diarrhea” in Gastroenterology 1999;116:1461–3 (full text available at: http://www2.us.elsevierhealth.com/inst/serve?action=searchDB&searchDBfor=art&artType=fullfree&id=a0069901461a) • The World Health Organization provides information on diarrheal diseases at: 8 Queries and feedback
The Practice Guidelines Committee welcomes any comments and queries that readers may have. Do you feel we have neglected some aspects of the topic? Do you think that some procedures are associated with extra risk? Tell us about your own experience. You are welcome to click on the link below and let us know your views. <mailto:omge@worldgastroenterology.org>

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