| Abstract|| |
Amoebiasis is a common infection in the tropical areas, which commonly presents to the physician as colitis or liver abscess. Invasive amoebiasis is associated with high morbidity, and its presentation in the form of cecal perforation following fulminant colitis with appendicitis and a ruptured liver abscess is an extremely rare entity. We would like to report one such rare case where the patient presented with all these three amoebic manifestations together. Their concomitant presentation is an indicator towards invasive amoebiasis and is associated with a dismal outcome despite aggressive management.
Keywords: Amoebiasis, cecal perforation, fulminant, invasive
|How to cite this article:|
Tanwar R, Jain SK. Amoebic cecal perforation following fulminant colitis with amoebic appendicitis and ruptured liver abscess: A rare presentation. Ann Trop Med Public Health 2013;6:367-8
|How to cite this URL:|
Tanwar R, Jain SK. Amoebic cecal perforation following fulminant colitis with amoebic appendicitis and ruptured liver abscess: A rare presentation. Ann Trop Med Public Health [serial online] 2013 [cited 2020 Jan 26];6:367-8. Available from: http://www.atmph.org/text.asp?2013/6/3/367/121014
| Introduction|| |
Invasive amoebic infection can present to the treating physician in various disguises, commonest being in the form of amoebic colitis and amoebic liver abscess. Simultaneous presentation as rupture of amoebic liver abscess and cecal perforation with appendicitis is extremely rare. We report one such rare case where the patient presented with a ruptured liver abscess along with fulminant colitis and a cecal perforation and an inflamed appendix.
| Case Report|| |
A 50-year-old man presented to surgical emergency with complaints of dull aching constant pain in the right side of the abdomen associated with low grade intermittent fever for 7 days. He had constipation for the past 2 days associated with generalized abdominal distension without any history of nausea vomiting or diarrhea preceding constipation. Patient was a known hypertensive controlled on medication, was a chronic smoker, and had an episode of myocardial infarction 8 years back. On examination, he had tachycardia with a pulse rate of 102 per minute and a temperature of 100°F with an APACHE 2 score of 8. There was generalized abdominal distension with guarding in the right hemiabdomen with rebound tenderness and decreased bowel sounds. Abdominal skiagram revealed multiple air fluid levels without any evidence of pneumoperitoneum on radiograph. Ultrasonography of abdomen revealed a 69 cc liver abscess in the right lobe with thickening of the caecum and ascending colon wall (9 mm) and free fluid in the right iliac fossa. Total leukocyte counts were raised (20,400/mm 3 ) and amoebic serology was positive.
Exploratory laparotomy revealed a ruptured right lobe liver abscess with a perforated gangrenous caecum involving the anterior wall, along with an inflamed turgid, edematous appendix, and enlarged mesenteric nodes noted in the small gut mesentery near ileum with 200 ml of pyoperitoneum [Figure 1]. A limited resection of ascending colon and caecum with end ileostomy was performed,and a drain was put in the ruptured amoebic liver abscess. Thorough peritoneal lavage was performed. The patient was shifted to the intensive care unit in view of postoperative hypotension due to myocardial infarction. The patient expired on 2 nd day due to the same in the intensive care unit. Histopathology revealed cecal, appendicular, and colonic ulcers with extensive liquefactive necrosis with focal perforation. Entrapped degenerated histiocytes and trophozoites were also seen with an overall impression of severe amoebic colitis.
|Figure 1: Intraoperative findings showing and inflamed and turgid appendix with gangrene and necrosis of the anterior cecal wall and base of appendix along with cecal perforation|
Click here to view
| Discussion|| |
Amoebiasis presents as a wide spectrum depicting pathologies as benign as the asymptomatic carrier state to fulminant colitis and colonic perforation.  Majority of patients can be managed medically, but a small percentage of patients require urgent exploration and resection with an associated high mortality rate. About 4%-10% of asymptomatic carriers eventually develop invasive disease.  Very uncommonly this disease takes a fulminant super-acute course due to the development of necrotizing amoebic colitis, which carries a mortality ranging from 55% to 100%.  Presentation of invasive intestinal amoebiasis can vary from fulminant colitis to mild, intermittent episodes of blood-tinged diarrhea. Occasionally, patients present with tachycardia, hypotension, and peritonitis. In this group, perforation must be considered, and urgent intervention is necessary as mortality is high. Occasionally, for unknown reasons, the disease progresses to a fulminant necrotizing colitis that may be indistinguishable from other forms of acute colitis. Aristizabal et al. reported that a mortality rate of 60% for the various operative procedures performed for presentation can vary from fulminating amebic colitis. 
Fulminant colitis which is a known variant of amoebic colitis develops rapidly and presents with features of acute abdomen and loose stools.  Various factors including male gender, increased age, signs of peritonitis and abdominal pain, leukocytosis, electrolyte disturbances, and hypoalbuminemia are associated with the development of fulminant amoebic colitis in patients who have invasive intestinal amoebiasis.  Intraoperatively the fulminating colitis presents as an inflamed, extremely friable colon, wrapped with omentum, and underlying full-thickness necrosis and perforation. The colon is so friable that it can disintegrate with any form of manipulation.  Resection of the necrotic colon is the treatment of choice.  There is a high risk of suture breakdown in tissue containing amoebae, and exteriorization of the bowel rather than repair should be the way to go.  Despite aggressive surgery, a retrospective analysis of 55 patients with fulminant amebic colitis presented a mortality rate of 89%. 
Simultaneous occurrence of Fulminant colitis, cecal perforation, appendicitis,and rupture of amoebic liver abscess is extremely rare, and such cases carry a very poor prognosis. Cecal perforation may spread to the appendix and lead to gangrenous appendicitis. Eggleston et al. documented a study of 26 patients with amoebic colonic perforation, wherein all 6 patients with concomitant liver disease died. 11 However, none of these six patients had rupture of liver abscess. Simultaneous rupture of amoebic liver abscess and colonic perforation is an indicator of extremely poor prognosis,and these patients should receive intensive medical and surgical management.
| Conclusion|| |
Invasive amoebiasis presenting with multiple stigmata is a rare entity. A diagnosis of dual amoebic pathology must be kept in mind in patients with liver abscess presenting with gut pathology. Invasive amoebiasis in such cases can present with involvement of multiple sites, and all sites of possible affliction must be screened. Patients with widespread amoebic infection require aggressive therapy with surgical resection and diversion and have an extremely poor prognosis.
| References|| |
|1.||Alavi KA. Amebiasis. Clin Colon Rectal Surg 2007;20:33-7. |
|2.|| Patterson M, Schoppe LE. The presentation of amoebiasis. Med Clin North Am 1982;66:689-705. |
|3.||Gupta SS, Singh O, Shukla S, Raj MK. Acute fulminant necrotizing amoebic colitis: A rare and fatal complication of amoebiasis: A case report. Cases J 2009;2:6557. |
|4.||Aristizábal H, Acevedo J, Botero M. Fulminant amebic colitis. World J Surg 1991;15:216-21. |
|5.||Nisheena R, Ananthamurthy A, Inchara YK. Fulminant amebic colitis: A study of six cases. Indian J Pathol Microbiol 2009;52:370-3. |
|6.|| Chuah SK, Sheen IS, Changchien CS, Chiu KW, Fan KD. Risk factors associated with fulminant amebic colitis. J Formos Med Assoc 1996;95:446-51. |
|7.||Elhence IP, Agrawal BM, Sharma BD. Amebic necrosis of bowel. Int Surg 1979;64:57-61. |
|8.||Grigsby WP. Surgical treatment of amebiasis. Surg Gynecol Obstet 1969;128:609-27. |
|9.||Takahashi T, Gamboa-Dominguez A, Gomez-Mendez TJ, Remes JM, Rembis V, Martinez-Gonzalez D, et al. Fulminant amebic colitis: Analysis of 55 cases. Dis Colon Rectum 1997;40:1362-7. |
|10.||Eggleston FC, Verghese M, Handa AK. Amoebic perforation of the bowel: Experiences with 26 cases. Br J Surg 1978;65:748-51. |
1013, Sector 15-II, Gurgaon, Haryana -122001
Source of Support: None, Conflict of Interest: None