Medical Journal of Dr. D.Y. Patil Vidyapeeth

: 2018  |  Volume : 11  |  Issue : 4  |  Page : 338--341

Acute fulminant necrotizing amoebic pancolitis: A lethal entity in children

Rahul Gupta1, Shahida Riyaz2, Nilima Soni2,  
1 Department of Paediatric Surgery, Kota Medical College, Kota, Rajasthan, India
2 Department of Pathology, Kota Medical College, Kota, Rajasthan, India

Correspondence Address:
Rahul Gupta
Department of Paediatric Surgery, Kota Medical College, Kota, Rajasthan


A 4-year-old boy presented in a state of septicemic shock, disoriented with peritonitis, and marked hemodynamic instability. The child was resuscitated; radiographs confirmed pneumoperitoneum. Intraoperatively, there were multiple perforations with necrotic changes in the entire colon up to the rectum, suggestive of acute fulminant necrotizing pancolitis. He was managed by total colectomy, ileostomy, with Hartman's pouch. Histopathology confirmed necrotizing amoebic pancolitis. Postoperatively, administration of metronidazole with broad-spectrum antibiotic coverage, hyperalimentation, and multiple platelet concentrates was given. The child had profound immunosuppression and expired due to multiple organ dysfunction syndrome. Acute fulminant necrotizing amoebic pancolitis is an extremely lethal entity in children.

How to cite this article:
Gupta R, Riyaz S, Soni N. Acute fulminant necrotizing amoebic pancolitis: A lethal entity in children.Med J DY Patil Vidyapeeth 2018;11:338-341

How to cite this URL:
Gupta R, Riyaz S, Soni N. Acute fulminant necrotizing amoebic pancolitis: A lethal entity in children. Med J DY Patil Vidyapeeth [serial online] 2018 [cited 2021 Jan 24 ];11:338-341
Available from:

Full Text


Invasive intestinal amoebiasis presenting as colonic perforation is a rare entity in children.[1] It is associated with high mortality rate.[2],[3] We are presenting a 4-year-old child who presented late in a state of septicemic shock with peritonitis due to multiple perforations and necrotic changes in the entire colon diagnostic of acute fulminant necrotizing amoebic pancolitis and had a dismal outcome.

 Case Report

A 4-year-old boy presented to us with severe abdominal pain, marked abdominal distension, and vomiting for the past 5 days. There was 1 month history of fever and pain abdomen (dull aching). The patient had previously received several courses of antibiotics and antispasmodics over the past few weeks. On examination, the child's general condition was very poor and had marked hemodynamic instability. He was disoriented, dehydrated, and was and in a state of shock with pulse rate of 132/min, respiratory rate of 28/min and blood pressure of 66/40 mmHg. Abdominal signs included generalized tenderness, markedly distended abdomen and absent bowel sounds suggestive of severe peritonitis. Rectal examination revealed rectum filled with foul-smelling feculent discharge with mucus. He was resuscitated and optimized with fluids, blood transfusion, and inotropic support along with administration of the third generation cephalosporin and metronidazole. Laboratory values revealed anemia (Hb – 6.2 g%), thrombocytopenia (platelets - 99,000/mm 3) and leukocytopenia (total leukocyte count-19,900/mm 3). Liver function tests revealed total bilirubin of 0.8 mg%, raised serum transaminases (3 times); hypoproteinemia (4.3 g%), and hypoalbuminemia (1.5 g%). Renal functions were normal; serum electrolytes revealed hyponatremia (Na-126 mmol/L) and hypocalcemia (6.5 mg/dL). Abdominal ultrasonography showed pneumoperitoneum, ascites with echoes and thickened bowel wall. An abdominal radiograph revealed pneumoperitoneum with free gas under both the domes of the diaphragm. Laparotomy revealed gross fecal peritonitis with along with flakes and pus. There were multiple areas of the colon that appeared frankly necrotic and markedly friable with perforations in the cecum, ascending, and transverse colon up to the rectum, suggestive of fulminant necrotizing pancolitis [Figure 1]. There was no evidence of thrombosis of the mesenteric arteries or veins. Total abdominal colectomy, ileostomy, and Hartmann's pouch procedure were performed along with thorough debridement and irrigation of the entire peritoneal cavity. The abdominal drain was placed in the pelvic cavity. Postoperatively, administration of metronidazole with broad-spectrum antibiotic coverage, blood transfusions, and peripheral intravenous infusion of 3%–5% amino acids (partial parenteral nutrition) were given in view of severe muscle wasting and cachexia. The child had prolonged paralytic ileus in the postoperative period with bilious Ryle's tube aspirate (>500 ml/24 h); abdominal drain had seropurulent output (200 ml/24 h). Dyselectrolytemia and hypocalcemia were corrected. Peritoneal washes with metronidazole through the abdominal drain were also performed. Ileostomy started functioning on the 4th postoperative day.{Figure 1}

Stool sample evaluation revealed amoebic infection. Pathologic examination confirmed multiple perforations in the entire colon [Figure 2]. Microscopic examination revealed extensive superficial necrosis of the mucosa and congested mucosal and submucosal blood vessels, multiple amoebic trophozoites in the submucosa surrounded by acute inflammation [Figure 3]. PAS staining confirmed the presence of multiple amoebic trophozoites in the submucosa [Figure 4]. There was no evidence of fungal infection in the specimen. There were deep ulcers scattered into the muscularis, multiple areas of full-thickness necrosis, and bowel wall rupture suggestive of acute fulminant necrotizing amoebic pancolitis. The mesenteric vessels were without thrombosis or emboli. The child had profound immunosuppression with falling platelet counts (9000–16,000/mm 3) for which multiple platelet transfusions were given postoperatively. However in spite of all resuscitative efforts, patient succumbed to multiple organ dysfunction syndrome (MODS) and expired on the 7th postoperative day.{Figure 2}{Figure 3}{Figure 4}


Amoebiasis is an infestation of human tissues by the pathogenic unicellular Entamoeba histolytica which exists in two forms, i.e., sporozoite (cystic) and trophozoite (vegetative).[4] Infection is acquired by swallowing the sporozoites (passed in the stools of patients or carriers) in food or contaminated by fecally soiled fingers. The trophozoites may be harmless and normally thrive only in the large bowel. They are excreted as the mature infective cyst. Immunosuppression favors invasion of amoeba through gut wall (by secreting lytic enzymes) forming typical flask-shaped ulcers. Full-thickness invasion depends on the virulence of the amoeba and the host resistance. This may result in intestinal perforation.[4] Involvement of the liver is usually hematogenous; when it manifests clinically, amoebic colitis is usually settled, though there may be hepatic amoebiasis with concurrent amoebic dysentery.[4] Thus, intestinal amoebiasis has a wide spectrum of presentation ranging from asymptomatic disease to invasive intestinal amoebiasis and extra-intestinal amoebiasis.[1],[2],[3]

Intestinal amoebiasis may present as: (i) asymptomatic colonization, (ii) acute amoebic colitis, (iii) fulminant amoebic colitis, (iv) appendicitis, and (v) amoeboma. The most lethal complication of invasive intestinal amoebiasis is known as acute fulminant colitis with perforation.[1],[2],[3] Invasive intestinal amoebiasis presents with intermittent episodes of blood-tinged diarrhea, enlarged tender liver, rectal ulceration along with acute abdomen.[2] It may mimic acute cholecystitis, ulcerative colitis, and lower intra-abdominal malignancy. There is a predilection for males. Its diagnosis is confirmed by stool examination, sigmoidoscopy and rectal biopsy, and serological tests. The routine stool examination may or may not reveal cysts and trophozoites, but fresh stool or rectal discharge obtained by sigmoidoscopy may demonstrate trophozoites, which are diagnostic.[1],[2],[3],[4] Colonoscopy shows large geographic mucosal ulcers accompanied by yellow–green pseudomembranes.

Acute fulminant necrotizing amoebic colitis

It is difficult to predict the development of fulminant necrotizing amoebic colitis in patients with intestinal amoebiasis. If a patient presents with tachycardia, hypotension, and peritonitis, perforation should be considered and urgent intervention is necessary. The risk factors are male gender, extremes of age, tropical climate, associated liver abscess, persistent abdominal pain, poor nutrition, immunocompromised state, the presence of peritonitis, pancolitis (involvement of most of the colon), hypoalbuminemia and electrolyte imbalance (hyponatremia, hypokalemia, and hypocalcemia).[1],[2] Most of the risk factors were present in our case.

Perforation is rare and usually on the right side of the colon. Single perforation is common, while multiple are also seen in one-third cases.[2],[3] Features of peritonitis may be absent in 20% of cases with colonic perforation, and radiographic evidence of pneumoperitoneum may be seen in <50% of cases.[2] This has been explained by a slow leak through an extensively diseased bowel.[5] In addition to free air, plain abdominal radiographs may show megacolon or a papery thin colon wall.[1],[2] Necrotizing amoebic colitis may be associated with ruptured liver abscess, bilateral pleural effusion and gross intra-abdominal collection. Unless early antiamoebic therapy is started and appropriate surgical intervention is performed, the mortality is very high.

Diagnosis of fulminant necrotizing amoebic colitis is either intraoperative or on histopathological evaluation.[3] The characteristic feature of the diseased colon are high predilection for the right side, wrapped with omentum and underlying full-thickness necrosis and perforation, extensively friable and disintegrates with a simple manipulation.[2],[5],[6]

Surgical options include (a) diversion and drainage, and (b) resection with stoma formation for necrotic/gangrenous bowel. The ideal management for children with acute fulminant colitis with perforation is the latter option, as in addition to removing the diseased bowel, it also eliminates the septic foci and prevents further fecal contamination.[2],[3] Primary anastomosis is not considered as there is a very high probability of anastomotic dehiscence due to the inflamed and friable bowel.[4] In our case, the whole colon was found to have extensive patchy necrosis with perforation at multiple sites (pancolitis) and thus, total colectomy was performed.[4]

Medical management with effective antiamoebic agents like metronidazole is given along with parenteral nutritional therapy. Postoperative peritoneal irrigation in amoebic peritonitis resulted in a significant reduction in mortality and morbidity, and also faster recovery in one large study.[7] Furthermore, intraoperative peritoneal washes with metronidazole in the patients with peritonitis has been found to be more beneficial as to compared to saline.[8] Thus, in the index case, mechanical cleansing of the peritoneal cavity by peritoneal washes with metronidazole through the abdominal drain were performed to remove the residual infection (flakes, pus, and necrotic material scattered all over the peritoneal cavity) and decrease the amoebic load.[7],[8]

Other postoperative complications such as wound infection, severe sepsis, and MODS (as seen in our case) have been reported. Overall mortality rate with necrotizing amoebic colitis range from 55% to 100%.[5] Mortality associated with resection was higher in one study,[9] which could be due to the severity of the disease in the cases being selected for resection.

Thuse reported three cases with fulminant necrotizing amoebic colitis; out of three, two had colonic perforation. Resection of the colon and terminal ileostomy was performed in two cases, and in the third case colostomy was performed due to extensive adhesions in the abdomen, friable, and gangrenous colon.[4] There were no survivors in his series. Lami and Moore reported the first survivor of fulminant necrotizing amoebic pancolitis among pediatric cases. The patient was a 6-year-old boy with situs abnormality and cyanotic congenital heart disease. Early colectomy, ileostomy, gastrostomy, and extensive drainage of the peritoneal cavity with the administration of metronidazole postoperatively and hyperalimentation were performed.[1]

Raj and Sarin presented a 4-year-old survivor with ileocecal perforation due to necrotizing amoebic colitis. Ileocecal resection, ileostomy and ascending colostomy was accomplished as part of the staged surgery.[3] Unfavorable outcome in our case was due to the pancolitis, delayed presentation associated with immunosuppression, sepsis, thrombocytopenia along with MODS.

Clinicians should have a high index of suspicion for invasive intestinal amoebiasis and its lethal complication of “acute fulminating necrotizing amoebic colitis” in a child presenting with acute pain abdomen with a history of dysentery. By making focused changes in the management of these patients by performing stool examination, the addition of anti-amoebic therapy along with improvement in intensive care, morbidity and mortality can be prevented.

To conclude, malnutrition, history of recurrent pain abdomen, immunocompromised state, dyselectrolytemia, the presence of peritonitis and delayed presentation in a child are associated with unfavorable outcome in acute fulminant necrotizing amoebic in children. A high index of suspicion is required for its early diagnosis.


I am sincerely thankful to faculty and residents of Department of Anaesthesia, Kota Medical College, Kota, for helping in this endeavor.

Declaration of patient consent

These authors certify that they have obtained all appropriate patient consent forms. In the form, the legal guardian has given his consent for images and other clinical information to be reported in the journal. The guardian understands that names and initials will not be published and due efforts will be made to conceal patient identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


1Lami JL, Moore TC. Colectomy for necrotizing amebic pancolitis in early childhood with survival. J Pediatr Surg 1989;24:1174-6.
2Jain BK, Garg PK, Kumar A, Mishra K, Mohanty D, Agrawal V, et al. Colonic perforation with peritonitis in amoebiasis: A tropical disease with high mortality. Trop Gastroenterol 2013;34:83-6.
3Raj P, Sarin YK. Acute fulminant necrotizing amoebic colitis leading to intestinal perforation and peritonitis. APSP J Case Rep 2015;6:10.
4Thuse MG. Fatal intestinal amoebiasis. Postgrad Med J 1979;55:548-52.
5Gupta 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.
6Tanwar 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.
7Dalvi AN, Gondhalekar RA, Upadhye AS. Post-operative irrigation in the management of amoebic peritonitis. J Postgrad Med 1987;33:61-4.
8Singh H, Agrawal M, Singh NK, Kaul RK, Ilahi I, Ahuja R. Intraoperative lavage in peritonitis: Comparison between saline and metronidazole. Int J Sci Stud 2016;4:131-4.
9Eggleston FC, Verghese M, Handa AK. Amoebic perforation of the bowel: Experiences with 26 cases. Br J Surg 1978;65:748-51.