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The Identification and Treatment of Toxic Megacolon Secondary To Toxic Megacolon Secondary to Pseudomembranous Colitis The Identification and TreatmentofToxic Megacolon Secondary to Pseudomembranous Colitis Megan M. Earhart, MSN, RN Toxic megacolon is an infrequently occurring, potentially life-threatening complication of pseudomembranous colitis. Although toxic megacolon may be considered rare, incidence is expected to increase because of the rapidly increased prevalence of pseudomembranous colitis. This article discusses the pathophysiology, clinical manifestation, diagnosis, treatment, and prognosis for toxic megacolon secondary to pseudomembranous colitis. Critical care nurses should be aware of the disease to intervene early and increase the chance of the patient’s survival. Keywords: Inflammatory bowel disease, Gastrointestinal disease, Pseudomembranous colitis, Toxic megacolon [DIMENS CRIT CARE NURS. 2008;27(6):249/254] CASE STUDY and was treated with Neosynephrine (Hospira, Inc., Lake A 49-year-old African American man with a history of Forest, IL) and Xigris (Eli Lilly and Co., Indianapolis, IN) hypertension, type 2 diabetes mellitus, and glaucoma was before seeking surgical treatment of toxic megacolon. The treated with chemotherapeutic agents for a new diagnosis patient underwent a subtotal colectomy and permanent of acute myelogenous leukemia. After he developed ileostomy for an edematous, thickened, and hemorrhagic neutropenia from the chemotherapy, Ambisome (Astellas right colon up to the splenic flexure and sigmoid colon. Parm US, Inc., Deerfield, IL), Cefepime (Bristol-Myers Squibb Company, Princeton, NJ), Zyvox (Pfizer Inc., New INTRODUCTION York, NY), Valtrex (GlaxoSmithKline, Philadelphia, PA), Toxic megacolon is an infrequently occurring, potentially and Flagyl (Pfizer Inc., New York, NY) were administered life-threatening complication of pseudomembranous colitis. for repeated fevers and diarrhea, although all blood The first documented case of toxic megacolon secondary to cultures had been negative. The patient further developed pseudomembranous colitis was reported in 1968.1 Toxic renal failure, diarrhea with a positive Clostridium difficile megacolon is a disease characterized by segmental or total toxin, abdominal pain, and distention. A computed colonicdistentionofgreaterthan6cminthepresenceof tomography (CT) scan of the abdomen showed a acute colitis and signs of systemic toxicity.2 Toxic mega- thickened right colon. The patient developed hypotension colon is present when 3 of the 4 following criteria are November/December 2008 249 Copyright @ 2008 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. Toxic Megacolon Secondary to Pseudomembranous Colitis met: (1) temperature greater than 101.5-F, (2) heart rheal or anticholinergic drugs.2 Toxic megacolon has been rate more than 120 beats/min, (3) leukocyte count more seen in patients as a consequence of Crohn disease, Kaposi than 10,500/2L with a left shift, and (4) anemia with sarcoma, cytomegalovirus, human immunodeficiency virus a hemoglobin or hematocrit level of less than 60% of (HIV), acquired immunodeficiency syndrome (AIDS), is- normal.3 One of the following 4 signs must also exist: (1) chemic colitis, Cryptosporidium, Salmonella, Shigella, hypotension, (2) electrolyte imbalances, (3) mental status Yersinia, Campylobacter, Entameba,andC difficile.2 Che- changes, and/or (4) dehydration.3 Most cases of toxic motherapy and colonoscopy have been reported as pos- megacolon occur in individuals with inflammatory bowel sible risk factors, whereas graft-versus-host disease and disease, but there has been a significant increase in the radiation therapy have not been reported to induce toxic number of cases associated with pseudomembranous megacolon2 (see Table 1). colitis.2 Colonic distention is also seen in patients with Hirschsprung disease, idiopathic megacolon, and intestinal PATHOPHYSIOLOGY pseudo-obstruction (Ogilvie syndrome) and is associated A variety of pathogenic mechanisms most likely contribute with postoperative complications, stroke, and spinal cord to the development of toxic megacolon. One of the most injury. Because these presentations lack systemic toxicity, important contributing factors in the development of toxic they are different from toxic megacolon.4 megacolon is the progression of the inflammation beyond the submucosa into the muscularis, and serosa.4 Severe in- Incidence flammation and damage to the colonic wall are necessary The incidence of toxic megacolon in pseudomembranous for the development of toxic megacolon.2 As acute inflam- colitis is reported at 0.4% to 3%, but it is challenging to mation progresses in the colon, neural injury occurs in the determine from the literature because it has not been bowel wall, resulting in both dysmotility and dilation.4 regularly reported. It affects all ages and both sexes, and Inflammation in the colon disrupts the normal absorptive the incidence is expected to increase in proportion owing function, leading to water, sodium, and potassium to be to the rapidly increasing prevalence of pseudomembra- trapped in the lumen of the colon. Hypokalemia and other nous colitis.2 The increase in use of broad-spectrum electrolyte abnormalities further decrease the bowel’s abil- antibiotics may lead to a doubling of the overall inci- ity to contract.2 The barrier mechanism of the colon is lost, dence of pseudomembranous colitis.2 which allows for the absorption of toxins, microbes, and Critical care nurses must be aware of the signs and toxic wastes causing systemic toxicity.2 The systemic symptoms of toxic megacolon and be prepared to assess for symptoms associated with toxic megacolon are not directly potential complications. Acute colitis is often resistant to therapy, and the signs and symptoms can be present for a TABLE 1 Toxic Megacolon Risk Factors week before the onset of distention. Diarrhea, malaise, ab- dominal pain, and distention are the most common com- Pseudomembranous colitis plaints in patients presenting with infectious colitis and toxic Discontinuation of 5-aminosalicylate agents or steroids 5 megacolon. It is essential that the patient with toxic mega- Barium enemas colon secondary to pseudomembranous colitis be diagnosed Drugs that slow colonic motility, such as rapidly and correctly to decrease morbidity and mortality. Narcotics It is essential that the patient with Antidiarrheal drugs toxic megacolon secondary to Anticholinergic drugs pseudomembranous colitis be Crohn disease diagnosed rapidly and correctly to Kaposi sarcoma decrease morbidity and mortality. Cytomegalovirus Human immunodeficiency virus (HIV) Acquired immunodeficiency syndrome (AIDS) Risk Factors Ischemic colitis In addition to pseudomembranous colitis as an underlying Cryptosporidium, Salmonella, Shigella, Yersinia, Campylobacter, factor, additional risk factors for the occurrence of toxic Entameba, and Clostridium difficile megacolon include (1) discontinuation of 5-aminosalicylate Chemotherapy agents or steroids, (2) barium enemas, and (3) medications Colonoscopy that slow colonic motility, such as narcotics and antidiar- 250 Dimensions of Critical Care Nursing Vol. 27 / No. 6 Copyright @ 2008 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. Toxic Megacolon Secondary to Pseudomembranous Colitis related to bacteremia, colonic perforation, or ischemia films revealing a dilated colon (see Table 2). Toxic but to toxic-induced inflammatory mediators such as megacolon should be considered in all patients present- interleukin-8, macrophage-inflammatory protein-2, sub- ing with abdominal distention and acute or chronic stance P, and tumor necrosis factor !,releasedinthecolon.6 diarrhea.5 The best-accepted clinical criteria for diag- It has been postulated that nitric oxide, a known in- nosing toxic megacolon uses any 3 of the 4 following hibitor of smooth muscle tone, may also be involved in the criteria: (1) temperature greater than 101.5-F, (2) heart pathogenesis of toxic megacolon. Nitric oxide is generated rate greater than 120 beats/min, (3) white blood cell in the macrophages and smooth muscle cells of the inflamed count greater than 10.5 Â 109/L, or (4) anemia. Patients colon.5 It is an important nonadrenergic, noncholinergic should also have one of the following: (1) dehydration, neurotransmitter in the intestines.2 One group of research- (2) mental changes, (3) electrolyte disturbances, or (4) ers found higher levels of nitric oxide synthase in colonic hypotension.3 muscles of patients with toxic megacolon than in those Abdominal radiographs should be obtained in the with uncomplicated colitis.7 Nitric oxide is a marker of left lateral decubitus and supine positions.4 The radio- increased inflammation, so it is uncertain if its production logical diagnosis is made when transverse colon or is directly involved in the pathogenesis of toxic megacolon. ascending colon are greater than 6 cm dilated.2 Plain Medications that disrupt gastric motility act as films often show a loss of haustrations in patients with possible triggers for toxic megacolon.4 Antidiarrheal pseudomembranous colitis.1 It is recommended that medications including loperamide, diphenoxylate with abdominal CT be obtained because it is useful in deter- atropine, and opiates, as well as anticholinergics and mining the etiology of toxic megacolon.2 Computed antidepressants all have the ability to slow peristalsis and lead to dilation.4 Barium enemas and colonoscopy can cause further dilation, leading to impaired blood TABLE 2
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