Last updated: March 13, 2019
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Pseudomembranous ColitisIn the past ten years, the incidence of pseudomembranous colitis climbed up.

At present pseudomembranous colitis is among the major and expensive healthcare problem across the globe. In 2004, the number of cases of pseudomembranous colitis in England is estimated to be 45,000 cases. This rise in the number of cases of pseudomembranous colitis is attributed to the intensive utilization of antibiotics to treat various infections. Most of the cases that manifested the symptoms of this disease condition are linked to hospitals but community incidences also occurs (“Pseudomembranous Colitis,” 2007a).Pseudomembranous colitis is a disease condition characterized by inflammation of the colon due to prior utilization of antibiotics. The intake antibiotics destroyed the intestinal flora by killing the “good” bacteria.

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The loss of the “good” bacteria led to the proliferation of the harmful types of bacteria. The bacterial specie that frequently proliferates causing the colitis is Clostridium difficile. Other terms for Pseudomembranous colitis are: antibiotic associated colitis, Clostridium difficile associated diarrhea (CDAD); and necrotizing colitis. The incidence of Pseudomembranous colitis is higher in adults compared to children and infants. This disease has grave clinical manifestations and is often a critical condition(“Pseudomembranous colitis,” 2006).

The forms of this disease vary from colonization without symptoms and severe fulminant colitis that needs to be surgically removed. The first description of pseudomembranous colitis was in 1893 wherein “diphtheritic colitis” was observed in an autopsy of a patient that died due to severe diarrhea. The pathogenesis of this disease was then believed to be either viral infection or mucosal ischemia. The recognition that inflammation in pseudomembranous colitis is due to the toxin produced cytopathic alteration of the tissue-culture cells(“Pseudomembranous Colitis,” 2007a).Many antibiotics can cause pseudomembranous colitis but those that are broad spectrum and with activity against enteric bacteria are the often cause of this condition. Drugs for tuberculosis therapy like ethambutol and isoniazid also sometimes cause pseudomembranous colitis(Jung, 2007). In children, the antibiotics that frequently are associated with the development of pseudomembranous colitis are cephalosporins, ampicillin, and clindamycin. This disease condition seldom occurs in infants younger than 1 year because the titer of their maternal antibodies between day old and one year old children is still high(“Pseudomembranous colitis,” 2007b).

Pseudomembranous colitis has the following clinical manifestations: abdominal pain, diarrhea, decreased in leukocyte number (leukocytosis), and fever. Diarrhea as a clinical sign usually is observed after 5 to 10 days of antibiotic intake(Jung, 2007). The characteristic of the diarrhea in pseudomembranous colitis can be blood tinged, with foul smell, and watery stools excretion up to 20 times a day.

The complications of this disease condition consist of: ileus, sepsis, megacolon, ascites, dehydration, hypovolumia, hypoalbuminemia, and perforation(Peralta, 2008). Dehydration manifest into the following signs: dry mouth, glassy eyes appearance, fast pulse, drying of the skin, confusion, excessive tiredness, and sunken fontanelles in infants(“Pseudomembranous colitis,” 2007b). Toxic megacolon is an infrequent clinical manifestation of pseudomembranous colitis but the mortality rate among those who develop megacolon can reach up to 30%. In immunosupressed and geriatric patients, the mortality rate due to this disease condition can reach up to 25% of the cases(“Pseudomembranous Colitis,” 2007a).The predisposing factors for the development of pseudomembranous colitis include: prior utilization of antibiotics specifically penicillins, clindamycin, and second or third generation cephalosporins; increased length of hospitalization; number of antibiotics taken; the length of antibiotic therapy; increasing age; suppressed immune system; presence of other gastrointestinal problems; and sever underlying disease. Involvement of genetics as a predisposing factor of the disease is still not known(Peralta, 2008).

The major bacteria that serve as the causative agent of pseudomembranous colitis are the Clostridium difficile. This bacterial specie is gram positive and unaerobic. This microorganism produces exotoxins classified into enterotoxin A and cytotoxin B. Approximately, toxin B is a thousand more potent that toxin A. The mechanism of transmission of C. difficile can be through direct contact with contaminated equipment and carrier of this disease(“Clostridium difficile infection,”). Ten to fifteen percent of the antibiotic related occurrence of diarrhea and almost the entire incidence of pseudomembranous colitis are caused by C.

difficile(“Pseudomembranous Colitis,” 2007a).The lesion in pseudomembranous demonstrates the existence of white to yellow plaques that consist inflammatory exudates in the mucosal surface of the colon. The composition of the pseudomembrane includes epidermal debris, fibrinoid material, and leukocytes. The inflammatory cells infiltrate the lamina propria aside from infiltrating the mucosa of the colonic intestine also. The characteristic lesion of pseudomembranous colitis usually occurs in the sigmoid colon and the rectum but it can also assault the ascending colon (Jung, 2007).Diagnosis of pseudomembranous colitis can be done with the utilization of computed tomography (CT scan). The usual finding observed through the CT scan in pseudomembranous colitis cases is the existence of mural thickening of the colon.

This imaging technique does not only facilitate the diagnosis of this disease condition but also can be utilized in the evaluation of the extent of the pseudomembranous colitis lesion. Thus, CT scan is recommended to be utilized as the primary imaging technique for the diagnosis of severe cases of pseudomembranous colitis(Kawamoto, 1999). The sensitivity of CT scan in 98% while colonoscopy is 100%(Berman, 2008).The confirmation of diagnosis of pseudomembranous colitis is through the bacterial isolation of Clostridium difficile bacteria or isolation from stools of the cytotoxins produced by C. difficile. The pseudomembrane present in the mucosal surface of the colon in pseudomembranous colitis cases can be visualized with through colonoscopy and sigmoidoscopy(Jung, 2007). Other techniques that can be used for diagnosis of pseudomembranous colitis are: cell cytotoxin test and enzyme immunoassay.

The differential diagnosis of pseudomembranous colitis include: diverticular disease; ulcerative colitis; acute abdomen due to pathology; and other enteric infections such as cholera, amoebiasis, salmonellosis, and shigellosis(“Pseudomembranous Colitis,” 2007a).The primary medical intervention for pseudomembranous colitis is ending the patient’s intake of the antibiotic that has caused the disease condition. The antibiotics are then substituted with other drugs that will not destroy the normal colonic flora. Examples of substitute drugs are: ciprofloxacin and levofloxacin. Other drugs used as therapy of pseudomembranous colitis are: rifampicin, vancomycin, and metronidazole. The primary drug used to treat pseudomembranous colitis is metronidazole. The therapy with metronidazole is thrice a day oral intake of 500 mg tablet or four times a day intake of 250 mg tablet for the duration of 10 days.

Vancomycin is only utilized as a therapy of pseudomembranous colitis cases that does not respond to metronidazole due to the high possibility of bacterial resistance build up with vancomycin. Twenty to twenty-five percent of the pseudomembranous colitis cases recur after the ending of the antibiotic therapy. The relapses though still respond to metronidazole if the therapy is repeated after the relapse(Jung, 2007).Patients with pseudomembranous colitis that does not respond to medical therapy such those with fulminant and toxic forms of this disease need to undergo surgical intervention. The surgery is indicated in pseudomembranous colitis patients that do not respond to drug therapy after 48 to 72 hours of administration(Kawamoto, 1999). The surgical procedure in the severe cases of pseudomembranous colitis is subtotal colectomy.Symptomatic treatment of the clinical manifestations of pseudomembranous colitis is also necessary to promote the recovery of the patient. Diarrhea which is a clinical sign of this disease condition result into dehydration thus electrolyte solutions and fluids should be administered intravenously.

The absence of complication will have a good outcome but the relapse occurs in 20% of the cases(“Pseudomembranous colitis,” 2007b).The prevention of pseudomembranous colitis can be instituted through appropriate treatment of oral antibiotics to be prescribed and lowering the length of the antibiotic administration. The goal of antibiotic therapy is to kill the bacteria that cause pseudo membranous colitis and not harming the individual due to the treatment regimen.

Pseudomembranous colitis is a life-threatening disease that can be prevented thus appropriate precautionary measures should be observed. The utilization of antibiotics needs to be properly regulated to prevent the occurrence of pseudomembranous colitis.   ReferencesBerman, L. C., Tobias ; Fitzgerald, Tamara N. ; Bell, Robert L. ; Duffy, Andrew J.

; Longo, Walter E. ; and Roberts, Kurt E. (2008). Defining Surgical Therapy for Pseudomembranous Colitis with Toxic Mega colon. Journal of Clinical Gastroenterology42(5).Clostridium difficile infection. WD, from http://www., S.

-W. J., Seong-Woo ; Do, Byung-Hun ; Kim, Sang-Gi ; Ha, Seung-Soo ; Cho, Chang-Min ; Tak, Won-Young ; Kweon, Young-Oh; Kim, Sung-Kook ; Choi, Yong-Hwan ; and Cha, Seung-Ick (2007). Clinical Aspects of Rifampicin-associated Pseudomembranous Colitis. Journal of Clinical Gastroenterology, 41(1), 38-40.Kawamoto, S. H.

, Karen M.; and Fishman, Elliot K. (1999). Pseudomembranous Colitis: Can CT Predict Which Patients Will Need Surgical Intervention? Journal of Computer Assisted Tomography, 23(1), 79-85.Peralta, R.

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