eMedicine Specialties > Emergency Medicine > Gastrointestinal

Diverticular Disease

Author: A Antoine Kazzi, MD, Chief of Service, Department of Emergency Medicine, Medical Director of the Emergency Unit, American University of Beirut
Coauthor(s): Ziad N Kazzi, MD, Assistant Professor, Director of Medical Toxicology, Department of Emergency Medicine, University of Alabama in Birmingham; Assistant Medical Director, Alabama Poison Center; Medical Toxicologist, Regional Poison Center of Birmingham
Contributor Information and Disclosures

Updated: Jun 13, 2006

Introduction

Background

Diverticular disease is a common disorder, yet it was not recognized as a pathologic entity until the mid-19th century. Diverticulitis and lower gastrointestinal (GI) bleeding secondary to diverticulosis are the main complications of clinical importance to emergency physicians.

Pathophysiology

Diverticular disease may involve any part of the GI tract. Typically acquired, diverticular disease may be congenital, such as Meckel iliac diverticulum (although this is rare). Diverticula are herniations of the mucosa and submucosa or the entire wall thickness through the muscularis, as seen in congenital diverticula. The sigmoid is the most commonly affected segment (95-98%); however, diverticular disease also can involve the descending, ascending, and transverse colon as well as the jejunum, ileum, and duodenum.

Precise etiology of this disease is unknown. High intraluminal pressure and a weak colonic wall at the sites of nutrient vessel penetration into the muscularis may lead to herniation. The condition also may be caused by abnormal colonic motility, defective muscular structure, defects in collagen consistency (ie, increased cross-linking of collagen), and aging.

Diverticulitis is an abscess or peridiverticular inflammation initiated by the rupture of a microscopic mucosal abscess into the mesentery. The infection may progress, fistulize, obstruct, or spontaneously resolve.

Acute diverticulitis results from the inspissation of fecal material in the neck of the diverticulum and resultant bacterial replication. Lower GI bleeding from diverticulosis results from rupture of the small blood vessels that are stretched while coursing over the dome of the diverticula.

Frequency

United States

Diverticular disease occurs frequently, especially among elderly patients. One third of the general population develops diverticulosis by age 45 years and two thirds by age 85 years.

Mortality/Morbidity

Mortality and morbidity are related to complications of diverticulosis, which are mainly diverticulitis and lower GI bleeding. These occur in 10-20% of patients with diverticulosis during their lifetime.

Race

  • Diverticular disease primarily is a disease of industrialized Western societies.
  • Cultural diet may influence prevalence.
  • In contrast to westerners, diverticular disease among Asians demonstrates right-sided predominance. A Japanese study conducted over 15 years has shown in their Asian population a steady increase in the incidence of right-sided diverticulitis but no increase in the incidence of its left-sided counterpart.

Sex

Male-to-female ratio is equal.

Age

  • Incidence rises with age.
  • Diverticular disease is rare in people younger than 40 years.
  • Morbidity has been traditionally reported to be worse in younger patients. However, a 1997 study by Spivak et al looking at the natural history of diverticulitis in patients younger than 45 years old found no worse course than in adults.

Clinical

History

  • Clinical historical features of inflammatory disease include the following:
    • Abdominal pain - Occurs mostly in the left lower quadrant and tends to be steady, severe, and deep
    • History of fever suggestive of diverticulitis
    • Previous episodes of dull, colicky, and diffuse abdominal pain accompanied with flatulence, distention, and change in bowel habits (diverticulosis)
    • Altered bowel habits including diarrhea, increased constipation, and tenesmus (physician may note obstipation when treating a complicating bowel obstruction)
    • Nausea and vomiting
    • Dysuria, pyuria, and urinary frequency if bladder or ureter are irritated
    • History of pneumaturia or recurrent urinary tract infections (colovesicular fistulas)
    • Feculent vaginal discharge (fistulas with the uterus or vagina)
    • Severe and generalized abdominal pain (diffuse peritonitis)
    • Back or lower extremity pain (perforation)
  • Establish history of hemorrhagic disease, including the following:
    • Lower GI bleeding from diverticulosis occurs in the form of bright red-colored or wine-colored stools.
    • Onset of bleeding typically is sudden, painless, and accompanied by an urge to defecate.
    • Amount of bleeding typically is massive and tends to stop spontaneously.
    • Ascertain a previous history of gastric or duodenal ulcers, liver disease, or GI bleeding.
    • Discomfort and pain upon defecation indicate hemorrhoids or anal fissures.
    • History of weight loss and mucus in the stools indicates inflammatory bowel disease.
    • Establish list of medications used (nonsteroidal anti-inflammatory drugs [NSAIDs], steroids) and of alcohol abuse.
    • Establish bleeding tendencies.

Physical

  • Establish localized tenderness, rebound tenderness, and/or guarding. This is essential in the clinical management of diverticular disease. Their presence indicates diverticulitis.
  • When associated with GI bleeding, tenderness is not typical of diverticular etiology; it indicates other disease processes.
  • Assess vital signs to determine hemodynamic stability and profile of presentation.
  • Low-grade fever commonly is found in diverticulitis.
  • Rectal examination identifies tenderness, establishes the color of stools, and determines the presence and extent of GI bleeding. A mass may be seen in the cul-de-sac.
  • Diffuse abdominal tenderness, rebound, absent bowel sounds, and/or high-grade fever may be elicited. These indicate possible complications of perforation and/or peritonitis.
  • Pelvic and rectal examinations establish the correct diagnosis.
  • Palpate for any mass or fullness, particularly in the left iliac fossa.
  • Abdomen may be distended and tympanic.
  • Pain may be acute and located mainly in the left lower quadrant.

Causes

  • Low-fiber diet is the highest risk factor. Common in industrialized nations, a low-fiber diet forms low-bulk stool that lead to increased segmentation of the colon during propulsion, causing increased intraluminal pressure and formation of diverticula.
  • High fat and beef diets also cause diverticular disease, probably for the same reasons as above.
  • Genetic causes exist. Asians have right-sided diverticula preponderance. In westerners, diverticula develop mostly on the left side.
  • Aging leads to change in collagen structure, such as increased cross-linking and acid solubility.
  • Colonic motility disorders are a cause.
  • Corticosteroids but not nonsteroidal anti-inflammatory therapy have recently been shown to increase the risk of diverticulitis.
  • Colonic segmentation: Nonpropulsive contractions produce isolated segments or little chambers with high pressure within.
  • Defects in colonic wall strength can cause the condition.

More on Diverticular Disease

Overview: Diverticular Disease
Differential Diagnoses & Workup: Diverticular Disease
Treatment & Medication: Diverticular Disease
Follow-up: Diverticular Disease
Multimedia: Diverticular Disease
References

References

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  2. Baron TH, Morgan DE. Endoscopic transrectal drainage of a diverticular abscess. Gastrointest Endosc. Jan 1997;45(1):84-7. [Medline].

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  15. Mpofu S, Mpofu CM, Hutchinson D, et al. Steroids, non-steroidal anti-inflammatory drugs, and sigmoid diverticular abscess perforation in rheumatic conditions. Ann Rheum Dis. May 2004;63(5):588-90. [Medline].

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Further Reading

Keywords

acute diverticulitis, diverticulosis, lower gastrointestinal bleeding, lower GI bleeding, Meckel iliac diverticulum, congenital diverticula, peridiverticular inflammation, tenesmus, recurrent urinary tract infections, colovesicular fistulas, pneumaturia, feculent vaginal discharge, low-fiber diet, high fat diets, beef diets, colonic segmentation, defects in colonic wall strength

Contributor Information and Disclosures

Author

A Antoine Kazzi, MD, Chief of Service, Department of Emergency Medicine, Medical Director of the Emergency Unit, American University of Beirut
A Antoine Kazzi, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Medical Association, California Medical Association, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Ziad N Kazzi, MD, Assistant Professor, Director of Medical Toxicology, Department of Emergency Medicine, University of Alabama in Birmingham; Assistant Medical Director, Alabama Poison Center; Medical Toxicologist, Regional Poison Center of Birmingham
Ziad N Kazzi, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Emergency Physicians, and American College of Medical Toxicology
Disclosure: Nothing to disclose.

Medical Editor

Steven A Conrad, MD, PhD, Chief, Department of Emergency Medicine; Chief, Multidisciplinary Critical Care Service, Professor, Department of Emergency and Internal Medicine, Louisiana State University Health Sciences Center
Steven A Conrad, MD, PhD is a member of the following medical societies: American College of Chest Physicians, American College of Critical Care Medicine, American College of Emergency Physicians, American College of Physicians, International Society for Heart and Lung Transplantation, Louisiana State Medical Society, Shock Society, Society for Academic Emergency Medicine, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Eugene Hardin, MD, FACEP, FAAEM, Chair and Associate Professor, Department of Emergency Medicine, Charles R Drew University of Medicine and Science; Chair, Department of Emergency Medicine, Martin Luther King, Jr/Drew Medical Center
Eugene Hardin, MD, FACEP, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and American College of Forensic Examiners
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Barry E Brenner, MD, PhD, FACEP, Program Director, Department of Emergency Medicine, University Hospitals, Case Medical Center
Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

 
 
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