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Year : 2017  |  Volume : 10  |  Issue : 5  |  Page : 1350-1353
Ruptured amoebic liver abscess with perforated amoebic typhlitis: A rare entity

Department of Surgery, Maulana Azad Medical College, New Delhi, India

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Date of Web Publication6-Nov-2017


Background: Amoebic liver abscess (ALA) is the most frequent extra intestinal manifestation of Entamoeba histolytica infection. Rupture of ALA is an important cause of morbidity and mortality mainly in developing countries. In invasive amoebiasis, the trophozoites penetrate the intestinal mucosa causing amoebic colitis. Simultaneous amoebic cecal perforation and ALA rupture is a rare complication of invasive amoebiasis with a high rate of mortality which mainly occurs in malnourished patients. We report 4 rare cases of amoebic cecal perforation with ruptured liver abscess. Cases Patients and Methods: 4 unusual cases of ruptured ALA associated with perforated cecum which were operated at Department of Surgery, Maulana Azad Medical College from June 2016 to May 2017 are reported along with relevant review of literature. Results: Three patients were male and 1 was female. The mean age was 35.5 years. All cases had generalized peritonitis. Two patients had a single abscess in the right lobe, 1 had an abscess in both lobes of liver and 1 had multiple abscesses. Liver abscess in all 4 cases were amoebic as amoebic serology of pus was positive in all cases. At presentation, all 4 cases had clinical signs of generalized peritonitis. Ultrasonography for collection in peritoneal cavity showed moderate free fluid in with internal echoes suggestive of pyoperitoneum. Two patients had free air under the diaphragm. All 4 patients underwent resuscitation and then taken up for surgery. Exploratory laparotomy was done which showed pyoperitoneum. One patient had sealed perforation in the cecum, 2 had a perforation in cecum, and 1 had multiple perforations in cecum and ascending colon. Limited resection was done in 3 cases and right hemicolectomy in 1 case who had multiple perforations in cecum and ascending colon, in all 4 cases, exteriorization of bowel was done. Postoperatively, 1 patient died of respiratory failure due to bilateral pneumonia. Conclusion: Ruptured ALA along with perforation of cecum is a rare condition presenting as acute abdomen with high mortality. Surgical intervention is mandatory in all these cases.

Keywords: Amoebic cecal perforation, amoebic liver abscess, exploratory laparotomy

How to cite this article:
Nishanth S, Jain SK, Singh CB, Bains L. Ruptured amoebic liver abscess with perforated amoebic typhlitis: A rare entity. Ann Trop Med Public Health 2017;10:1350-3

How to cite this URL:
Nishanth S, Jain SK, Singh CB, Bains L. Ruptured amoebic liver abscess with perforated amoebic typhlitis: A rare entity. Ann Trop Med Public Health [serial online] 2017 [cited 2020 Sep 25];10:1350-3. Available from:

   Introduction Top

Amoebiasis is a parasitic infection caused by the protozoon, Entamoeba histolytica, that infects 10% of the world's population, resulting in 100,000 deaths/year.[1] The colon and liver are the principal organs affected in amoebiasis. The parasite exists in two forms: a motile form called the trophozoite, and a cyst form, responsible for human transmission of the infection. The trophozoite inhabits the colon where it produces lesions of amoebic colitis. Invasion of the colonic mucosa leads to dissemination of the organism to extracolonic sites, predominantly the liver. Infection by E. histolytica causes a spectrum of intestinal illnesses as asymptomatic infection, symptomatic noninvasive infection, acute proctocolitis (dysentery), and fulminant colitis with perforation.

The most common complications of amoebic liver abscess (ALA) arise from rupture of the abscess into surrounding organs or anatomical spaces. Communication occurs in the peritoneum, viscera, and large vessels on one side of the diaphragm and the pleura, bronchi, lungs, and pericardium on the other side.

Invasive intestinal amoebiasis presenting as cecal perforation is a rare entity. It is associated with high mortality and dismal outcome.[2] Ruptured liver abscess with invasive intestinal amoebiasis is even rarer.

   Patients and Methods Top

Patients presenting to Surgery emergency of Lok Nayak Hospital from May 2016 to June 2017 diagnosed to have liver abscess with clinical signs of generalized peritonitis were evaluated. Ultrasound of all patients showed liver abscess with breech in liver parenchyma with mild to moderate free fluid in the abdomen. A review of these data was performed to document the clinical presentation, etiology, diagnostic work-up, treatment, morbidity, and mortality. Four out 24 such patients were found to have ruptured liver abscess with cecal perforation. Amoebic serology was positive in all 4 patients. Of 4 patients, 3 were male and 1 female. Mean age was 39.5 years. Procedure to be done was decided based on intra-operative findings. From May 2016 to June 2017, we have operated 24 cases of ruptured liver abscess of which 4 patients had cecal perforation along with ruptured liver abscess.

   Results Top

All patients presented with generalised abdominal pain, fever, and distension of abdomen. Clinically, all these patients had frank signs of peritonitis. Two out of four patients had free air under the diaphragm. All these patients were malnourished with body mass index of <18. In all these patients, serum albumin was <3 g%.

Intraoperatively, [Table 1] all 4 patients had cecal perforation of which in 1 patient it was a sealed perforation and in 1 multiple perforations in cecum and ascending colon were present [Figure 1] and [Figure 2].
Table 1: Case summary

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Figure 1: Intraoperative finding showing caecal perforation

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Figure 2: Intraoperative finding showing perforation in ascending colon

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Three patients underwent limited resection, and right hemicolectomy was done in one patient who had multiple perforations in the cecum and ascending colon. Exteriorization of bowel was done in all patients. The drain was placed in liver abscess cavity in all patients. Resected specimen in two patients showed multiple flask-shaped ulcers with yellowish plaques. Microscopically, numerous amoebic trophozoites were present in the necrotic debris of the colon ulcers in all cases [Figure 3].
Figure 3: Histopathology of cecum showing degenerated trophozoites and areas of necrosis

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Postoperatively, two patients had wound infection which was managed conservatively with antibiotics. All patients were given intravenous Metronidazole along with a broad-spectrum antibiotic. One patient developed bilateral pneumonia and subsequently respiratory failure and expired.

   Discussion Top

ALA is a common presentation of infection by E. histolytica, however, carries high morbidity and mortality. It is the most common extra intestinal form of invasive amoebiasis. Indeed, an estimated 100,000 people succumb to ALA each year.[3] Trophozoites that successfully penetrate the colonic mucosal barrier cause invasive disease enter the portal system and travel to the liver. Amoebic colitis and ALA rarely occur simultaneously, and the colonic lesions are usually silent; direct extension to the liver and lymphatic spread do not occur. The cecum is the most common site of amoebic colitis, and the right lobe of the liver is more commonly affected because of drainage of the right portal branch from the right side of the colon.

The condition usually starts as diffuse amoebic hepatitis; liver cells undergo liquefactive necrosis, starting in the center and spreading peripherally to produce a cavity full of blood and liquefied liver tissue resembling anchovy sauce; it has no odor and is sterile. The fluid itself is free from any amoebae, which may be found at the expanding edge of the abscess cavity with little inflammation. Amoebae are known to lyse neutrophils, and the release of neutrophilic mediators may promote hepatocyte death and extension of the abscess. Secondary bacterial infection may occur spontaneously, altering the color, odor, and consistency of the pus. Lack of fibrotic response by the surrounding tissue with centrifugal extension results in extension of the abscess to the Glisson capsule, which is resistant to the amoebae. Generally, ALAs are solitary, large, and located in the right liver. Left lobe abscesses are less common, but because of the smaller volume of the left liver, abscesses in this location are more prone to rupture the capsule.

Amoebic serology is highly sensitive and specific in the differentiation between pyogenic and amoebic hepatic abscess. Enzyme immunoassay (EIA) is simple, rapid, inexpensive, and more sensitive, and it has now largely replaced indirect hemagglutination test and counter immunoelectrophoresis.[4] EIA detects antibodies specific for E. histolytica in approximately 95% of patients with extra intestinal amoebiasis, 70% with active intestinal infection, and 10% who are asymptomatic cyst passers.

Primary surgical therapy is indicated in patients with intraperitoneal rupture, in which complete exploration and lavage of the abdomen are indicated.[5] In some other patients, surgery may be indicated for the treatment of complications of the percutaneous drainage, such as bleeding or intraperitoneal leakage of pus. Patients with an underlying pathology that needs surgical resolution can undergo treatment for the liver abscess during the same operation, such as cases of acute cholecystitis presenting with an adjacent abscess. Large, multiloculated abscesses containing thick pus are more prone to not respond to percutaneous treatment. In these patients, complete evacuation and removal of necrotic tissue and debris may be more easily achieved surgically.[6]

Peritonitis with amoebiasis is due to rupture of an ALA in 78% of patients and perforated or necrotizing amoebic colitis in the other 22%. Spontaneous rupture of ALA with colon may occur in 2.7%–17% of cases.[7],[8],[9]

Fulminant colitis which is a known variant of amoebic colitis develops rapidly and presents with features of acute abdomen and loose stools.[10] 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.[11] 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.[12] Resection of the necrotic colon is the treatment of choice.[13] 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.

   Conclusion Top

Simultaneous occurrence of Fulminant colitis, cecal perforation and rupture of ALA 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.[14] Simultaneous rupture of ALA and colonic perforation is an indicator of extremely poor prognosis, and these patients should receive intensive medical and surgical management.

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Conflicts of interest

There are no conflicts of interest.

   References Top

Reed SL. Amebiasis: An update. Clin Infect Dis 1992;14:385-93.  Back to cited text no. 1
Chen HT, Hsu YH, Chang YZ. Fulminant Amebic Colitis: Recommended Treatment to Improve Survival. Journal of Thoracic Medicine 2004;16:1-8.  Back to cited text no. 2
Santi-Rocca J, Rigothier MC, Guillén N. Host-microbe interactions and defense mechanisms in the development of amoebic liver abscesses. Clin Microbiol Rev 2009;22:65-75.  Back to cited text no. 3
Restrepo MI, Restrepo Z, Elsa Villareal CL, Aguirre A, Restrepo M. Diagnostic tests for amoebic liver abscess: Comparison of enzyme-linked immunosorbent assay (ELISA) and counterimmunoelectrophoresis (CIE). Rev Soc Bras Med Trop 1996;29:27-32.  Back to cited text no. 4
Siu WT, Chan WC, Hou SM, Li MK. Laparoscopic management of ruptured pyogenic liver abscess. Surg Laparosc Endosc 1997;7:426-8.  Back to cited text no. 5
Hope WW, Vrochides DV, Newcomb WL, Mayo-Smith WW, Iannitti DA. Optimal treatment of hepatic abscess. Am Surg 2008;74:178-82.  Back to cited text no. 6
Kimura K, Stoopen M, Reeder MM, Moncada R. Amebiasis: Modern diagnostic imaging with pathological and clinical correlation. Semin Roentgenol 1997;32:250-75.  Back to cited text no. 7
Radin DR, Ralls PW, Colletti PM, Halls JM. CT of amebic liver abscess. AJR Am J Roentgenol 1988;150:1297-301.  Back to cited text no. 8
Viana RL. Selective arteriography in the diagnosis and evaluation of amebic abscess of the liver. Dig Dis Sci 1975;20:632-8.  Back to cited text no. 9
Nisheena R, Ananthamurthy A, Inchara YK. Fulminant amebic colitis: A study of six cases. Indian J Pathol Microbiol 2009;52:370-3.  Back to cited text no. 10
[PUBMED]  [Full text]  
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.  Back to cited text no. 11
Elhence IP, Agrawal BM, Sharma BD. Amebic necrosis of bowel. Int Surg 1979;64:57-61.  Back to cited text no. 12
Grigsby WP. Surgical treatment of amebiasis. Surg Gynecol Obstet 1969;128:609-27.  Back to cited text no. 13
Eggleston FC, Verghese M, Handa AK. Amoebic perforation of the bowel: Experiences with 26 cases. Br J Surg 1978;65:748-51.  Back to cited text no. 14

Correspondence Address:
S Nishanth
Department of Surgery, Maulana Azad Medical College, New Delhi - 110 002
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ATMPH.ATMPH_319_17

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