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HEALTH > TIMES HEALTH GUIDE > E > ENTERITIS

Enteritis

Overview

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Causes Symptoms Exams and Tests Treatment Outlook (Prognosis) Possible Complications When to Contact a Medical Professional Prevention References

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Gastritis Colitis Abdominal Pain Fever Dehydration Salmonella Enterocolitis Shigellosis Staph Aureus Food Poisoning Campylobacter Enteritis Bacterial Gastroenteritis Radiation Enteritis Crohn's Disease

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Enteritis is inflammation of the small intestine.

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Back to TopCauses
Enteritis is usually caused by eating or drinking substances that are contaminated with bacteria or viruses. The germs settle in the small intestine and cause inflammation and swelling, which may lead to abdominal pain, cramping, diarrhea, fever, and dehydration. Enteritis may also be caused by:

An autoimmune condition such as Crohn's disease Certain drugs, including ibuprofen, naproxen sodium, and cocaine Damage from radiation therapy

The inflammation can also involve the stomach (gastritis) and large intestine (colitis). Risk factors include recent family illness with intestinal symptoms, recent travel, or exposure to untreated or contaminated water. Types of enteritis include:

Bacterial gastroenteritis Campylobacter enteritis E. coli enteritis Food poisoning Radiation enteritis Salmonella enteritis Shigella enteritis Staph aureus food poisoning

Back to TopSymptoms
The symptoms may begin hours to days after you become infected. Symptoms may include:

Abdominal pain Diarrhea - acute and severe Loss of appetite Vomiting - rare

Back to TopExams and Tests

A stool culture may be done to determine the specific type of infection, however, this test may not always identify the bacteria causing the illness.

Back to TopTreatment
Mild cases usually need no treatment. Antidiarrheal medication may delay the organism from leaving the digestive tract, and therefore may not be recommended. Rehydration with electrolyte solutions may be necessary if dehydration occurs. Persons with diarrhea (especially young children) who are unable to drink fluids because of nausea may need medical care and fluids through a vein ( intravenous fluids) . If you take diuretics and develop diarrhea, you may need to stop taking the diuretic during the acute episode. Do not stop taking any medicine unless told to do so by your health care provider.

Back to TopOutlook (Prognosis)

Symptoms usually go away without treatment in a few days.

Back to TopPossible Complications

Dehydration Prolonged diarrhea

Note: The diarrhea can cause rapid and extreme dehydration in babies.

Back to TopWhen to Contact a Medical Professional

Call for an appointment with your health care provider if:

Dehydration develops Diarrhea does not go away in 3 to 4 days You have a fever over 101 degrees Fahrenheit There is blood in the stools

Back to TopPrevention

Always wash hands after using the toilet and before eating or preparing food or drink. You may also clean your hands with a 60% alcohol based product. Avoid drinking from unknown sources, such as streams and outdoor wells, without boiling the water first. Use only clean utensils for eating or handling foods, especially when handling eggs and poultry. Cook food completely and properly. Store food appropriately in coolers.

Back to TopReferences
DuPont HL. Approach to the patient with suspected enteric infection. In: Goldman L, Ausiello D, eds. Cecil Medicine . 23rd ed. Philadelphia, Pa: Saunders Elsevier; 2007:chap 305. Steiner TS, Guerrant RL. Principles and syndromes of enteric infection. In: Mandell GL, Bennett JE, Dolin R, eds. Principles and Practice of Infectious Diseases . 7th ed. Philadelphia, Pa: Elsevier Churchill Livingstone; 2009:chap 93. Craig SA, Zich DK. Gastroenteritis. In: Marx JA, ed. Rosens Emergency Medicine: Concepts and Clinical Practice . 7th ed. Philadelphia, Pa: Mosby Elsevier; 2009:chap 92.

More Information on This Topic News & Features

Review Date: 4/12/2010 Reviewed By: Linda J. Vorvick, MD, Medical Director, MEDEX Northwest Division of Physician Assistant Studies, University of Washington, School of Medicine; George F Longstreth, MD, Department of Gastroenterology, Kaiser Permanente Medical Care Program, San Diego, California. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc.

A.D.A.M., Inc. is accredited by URAC, also known as the American Accreditation HealthCare Commission (www.urac.org). URAC's accreditation program is an independent audit to verify that A.D.A.M. follows rigorous standards of quality and accountability. A.D.A.M. is among the first to achieve this important distinction for online health information and services. Learn more about A.D.A.M.'s editorial policy, editorial process and privacy policy. A.D.A.M. is also a founding member of Hi-Ethics and subscribes to the principles of the Health on the Net Foundation (www.hon.ch).

A.D.A.M. Copyright The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. A licensed medical professional should be consulted for diagnosis and treatment of any and all medical conditions. Call 911 for all medical emergencies. Links to other sites are

provided for information only -- they do not constitute endorsements of those other sites. 1997- 2008 A.D.A.M., Inc. Any duplication or distribution of the information contained herein is strictly prohibited.

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ENTERITIES
Introduction

Inflammatory bowel disease encompasses two idiopathic, chronic, inflammatory diseases: Crohns disease and ulcerative colitis. Crohns disease and ulcerative colitis are disorders of unknown cause, involving genetic and immunological influence on the gastrointestinal tracts ability to distinguish foreign from selfantigens. They share many overlapping epidemiological, clinical, and therapeutic characteristics. In some patients it is not possible to distinguish which form of inflammatory bowel disease is present (Figure 2).

Figure 1. Location of the colon in the body.

Figure 2. Inflammatory bowel disease subsets.

There are, however, important pathological and clinical differences that distinguish these inflammatory disease processes. Clinically, Crohn's disease tends to present

more frequently with abdominal pain and perianal disease, whereas ulcerative colitis is more often characterized by gastrointestinal bleeding. Cobblestoning mucosa and aphthous or linear ulcers characterize the endoscopic appearance of Crohns disease. Ulcerative colitis presents with diffuse continuous involvement of the mucosa. Radiographic studies of patients with Crohns disease characteristically show fistulae, asymmetry, and ileal involvement. In contrast, radiographic studies of patients with ulcerative colitis show continuous disease without fistulizing or ileal disease. Pathologically, Crohn's disease features mucosal discontinuity, transmural involvement, and granulomas, whereas ulcerative colitis does not. Crypt abscesses and granulomas are present only in Crohn's disease. Figure 3 compares the anatomic distribution of Crohns disease and ulcerative colitis.

Figure 3. Anatomic distribution of Crohns disease and ulcerative colitis.

Crohn's disease is a form of inflammatory bowel disease. The term Crohn's disease has replaced older terms, which included regional enteritis, regional or terminal ileitis, and granulomatous colitis. Although the terminal ileum and the right colon are the most commonly involved sites, a similar pathological and clinical disorder can affect any part of the gastrointestinal tract, from the mouth to the perianal area. Only one third of patients with Crohns disease have granulomatous inflammation. The broad term Crohns disease does not imply any one cause, site, or pathological response. Crohns is a chronic illness that requires expensive medications, often hospitalization and/or surgery, and results in a heavy social and economic toll.

Figure 4. Comparison of the appearance of normal, Crohns, and ulcerative colitis mucosa; gross (top); histological (center); endoscopic (bottom).

The geographic distribution of Crohn's disease historically suggested a north-south gradient of incidence; however, more recent investigations have reported increased prevalence in temperate regions of North America, South Africa, and Australia. Urban areas have a higher incidence of disease than rural populations, and ethnic minorities (south Asians in the United Kingdom, blacks in South Africa, Bedouin Arabs in Israel) are at lower risk. Jews originating from middle Europe (Ashkenazi Jews) and those individuals of Scandinavian descent are at increased risk (Figure 5).

Figure 5. Geographic distribution of Crohns disease.

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General Info

What is Crohn's Disease? Crohns disease is a chronic inflammatory disease of the gastrointestinal tract. Inflammation extends all the way through the intestinal wall from mucosa to serosa. Like ulcerative colitis, Crohns disease is a relapsing and remitting disease. Initially only a small segment of the gastrointestinal tract may be involved, but Crohns disease has the potential to progress extensively.

Although surgical resection of inflamed segments may temporarily arrest symptoms, subsequent inflammation is likely to recur. Resection is not curative in Crohns disease, which is in contrast to ulcerative colitis, where colectomy eliminates the illness. This illness usually appears early in life; about one-sixth of patients present before the age of 15 and often with severe disease. The average age at diagnosis is 27 years. The cause of Crohns disease is unknown, although strong genetic influences are suggested by the occurrence of this disease in families, with a higher incidence in Jews than in the general population. Genetic influences are more prominent in the younger onset subgroup of patients than those who present after the age of 40. In one-third of patients with Crohns disease, the gross pathologic changes are limited to the terminal part of the ileum. About 40% of patients have ileocolitis, involvement of the distal ileum and proximal colon. About 5% have ileojejunitis, in which there is either continuous involvement throughout the small bowel, or more commonly, several sharply demarcated skip areas separated by normal bowel, sparing the terminal ileum. As many as one-third of young patients with Crohn's disease have subtle microscopic and macroscopic ulceration of the gastric antrum and the duodenum. In these cases, the lesions are not often symptomatic. Up to 20% of patients have involvement limited to the colon (Figure 6).

Figure 6. Anatomic distribution of Crohns disease.

The colonic lesions are often segmental and sometimes spare the rectum; this helps to distinguish them from ulcerative colitis, which always involves the rectum and is continuous rather than segmental. Crohn's disease is also more likely than ulcerative colitis to cause fistula, benign fibrous strictures, and perianal disease. Despite these differences, in about 10% of patients with chronic inflammatory bowel disease confined to the colon both macroscopically and microscopically, the diagnosis must be classified as indeterminate. This distinction becomes important when the clinician is considering surgery. Ulcerative colitis can be cured by total colectomy, and disease does not recur in an ileoanal pouch. However, patients with Crohn's disease can have troublesome recurrences in the ileum. Alternatively, segmental resections of the colon can be helpful in patients with Crohns disease. Most patients with Crohn's disease have focal mucosal inflammation seen endoscopically and aphthous ulcers visible macroscopically scattered throughout extensive portions of an otherwise normal bowel. The widespread microscopic disease may partially account for the high rate of recurrence (50% at 5I0 years) after surgical resection of all gross disease. With time, the inflammation extends through most layers of the bowel. In contrast, ulcerative colitis usually remains within the mucosa; in only a few patients does colitis go on to perforate.

Noncaseating granulomas are found in 3050% of resected bowel sections from patients with Crohn's disease. These are usually considered diagnostic, since granulomas are rare in ulcerative colitis. The pathologic findings in Crohn's disease correlate with three distinct disease courses. The inflammatory type affects 30% of patients, remains localized to the mucosa and submucosa, and causes diarrhea and pain from acute partial obstruction. Fistulizing or perforating disease affects 20% of patients who have ileitis. Aggressive transmural inflammation leads to intra-abdominal fistulae from the diseased bowel wall to another bowel loop, or to a nearby organ like the urinary bladder. Some patients suffer free bowel perforation early in the disease.

Figure 7. Types of Crohns disease; A, stenosing; B, inflammatory; C, fistulizing; D, radiographic image of fistula.

Stenosing or stricturing disease characterizes the third course. About 50% of patients with ileitis follow this route. Early in the course of Crohn's disease in the small bowel, patients seem to develop muscle hypertrophy followed by collagen (scar) deposition. After about 78 years of ileal disease, patients develop a fixed, scarred obstruction that causes painful cramping and requires surgical management. Most patients go to surgery 810 years after the onset of disease or after a previous resection for obstruction. This obstructive process seems to be caused by inflammatory cytokines that are not inhibited by corticosteroids, anti-inflammatory salicylates, or immunomodulator drugs. In the bowels effort to decompress the obstructed segment, fistula can develop through fissures in the thickened bowel

wall in the proximal part of a stenotic area, causing secondary fistula or even perforation.

Symptoms Crohns disease usually begins in the teens and twenties; however, ones-sixth of patients present before age 15. More than 90% of patients have symptoms before the age of 40. Patients most often present with abdominal cramps, diarrhea, delayed growth (in prepubescent patients), weight loss, fever, anemia, a right lower quadrant abdominal mass (if a complication has developed in the ileal area), or perianal fistula. Typically, patients with ileitis or ileocolitis have an insidious onset and a long course before they receive a specific diagnosis. The average duration of symptoms before diagnosis and initiation of therapy used to be 22 years, but this lag time has been shortened with better imaging techniques such as ultrasonography and computed tomography (CT), and a higher index of suspicion for Crohns disease.

Crohns disease can have several patterns of involvement: jejunoileitis, ileitis, ileocolitis and colitis. Each subtype has a distinct clinical presentation and typical course. Patients with inflammation of the jejunum and ileum often present with cramping abdominal pain after meals and eventually develop diarrhea. These patients, many of whom are teenagers or young adults, may have prominent extraintestinal manifestations including arthritis, fever, skin lesions, and delayed growth. Ileitis causes discomfort 12 hours after meals. Patients lose weight because they eat less to avoid discomfort. The inflammation in the ileum can extend transmurally into adjacent structures as tracks or fistulae, or can cause perforation of abscesses adjacent to the bowel. This form of Crohns disease is known as fistulizing or perforating. It has the worst prognosis of all the forms and often requires surgical resection after three or four years. Other patients with ileitis develop intestinal obstruction 810 years after the onset of disease because muscle hypertrophy and fibrosis narrow the lumen of the bowel. This form of Crohns disease is known as stricturing or stenosing. Crohns disease in the colon causes diarrhea and may be difficult to distinguish from ulcerative colitis. The clinical picture of Crohns disease depends on the areas of the bowel that are involved. Patients with ileal involvement may notice a gradual decrease in their sense of well-being, with vague cramping abdominal pain 12 hours after meals. This discomfort, caused by partial obstruction and inflammation of the bowel lumen, may be localized to the periumbilical area, or more commonly, to the right lower quadrant. Because of anorexia, nausea, or the fear of abdominal cramps, patients eat less and invariably lose weight. Most patients with small-bowel Crohns disease have an increase in the number of bowel movements, although rarely more than five per day, with soft and unformed stools. About 80% of patients with ileal disease have diarrhea.

Crohns disease is associated with extraintestinal manifestations that may be more problematic than the bowel disease. Colitic arthritis is a migratory arthritis that affects knees, ankles, hips, wrists, and elbows that may accompany Crohns disease (although it is uncommon when Crohns is confined to the small intestine). Often, joint pain, swelling, and stiffness parallel the course of the bowel disease. Successful treatment of the bowel disease results in improvement in the arthritic symptoms. Pericholangitis, usually associated with primary sclerosing cholangitis (PSC), is the most common hepatic complication of inflammatory bowel disease. PSC is demonstrable by endoscopic retrograde cholangiopancreatography (ERCP) or hepatic magnetic resonance imaging (MRI). Pericholangitis is characterized by inflammation of the portal tracts with lymphocyte and eosinophil infiltrates. Degenerative changes in the bile ductules are also characteristic. Kidney stones (calcium oxalate stones) are seen in patients with small-intestine Crohns disease. Inflammation from the bowel can result in urinary tract complications. Occlusion of the ureters, leading to obstruction and hydronephrosis, usually involves the right ureter in Crohns patients. Fistula can form between inflamed bowel and the urinary bladder leading to infection (Figure 8).

Figure 8. Extraintestinal manifestations of Crohns disease.