| Article Access Statistics|
| Viewed||4700 |
| Printed||99 |
| Emailed||1 |
| PDF Downloaded||111 |
| Comments ||[Add] |
| Cited by others ||2 |
Click on image for details.
|Year : 1992 | Volume
| Issue : 3 | Page : 151-2
Necrotising arteritis in amoebic colitis.
RB Deshpande, MA Bharucha, JM Modhe, RA Bhalerao
Dept of Pathology, PD Hinduja National Hospital, Mahim, Bombay, Maharashtra.,
R B Deshpande
Dept of Pathology, PD Hinduja National Hospital, Mahim, Bombay, Maharashtra.
Massive intestinal haemorrhage rarely occurs in amoebic colitis. We report a case of caecal amoebic ulcer in a 61 year old diabetic male who presented with massive lower intestinal haemorrhage requiring blood transfusion and emergency surgical intervention. Histologically, trophozoites of Entamoeba histolytica were seen invading the wall of the submucosal arteries, causing necrotising arteritis. Rupture of a necrosed artery probably caused massive haemorrhage.
Keywords: Blood Transfusion, Case Report, Dysentery, Amebic, complications,surgery,Gastrointestinal Hemorrhage, etiology,therapy,Human, Male, Middle Age, Polyarteritis Nodosa, etiology,surgery,
|How to cite this article:|
Deshpande R B, Bharucha M A, Modhe J M, Bhalerao R A. Necrotising arteritis in amoebic colitis. J Postgrad Med 1992;38:151
Massive lower intestinal haemorrhage due to intestinal amoebiasis is rare. Most of the standard textbooks do not list amoebiasis as one of the causes of massive lower intestinal haemorrhage. We report here a case with evidence of necrotising arteritis caused by aggressive amoebic invasion.
A robust 61-year-old fisherman was admitted with massive lower intestinal haemorrhage of 2 days duration. He was known to be a diabetic for three years, taking oral hypoglycaemic agents irregularly. At admission, he looked pale, disoriented, passing copious frank blood and blood clots per rectum. e haemoglobin concentration was 5.6 g/d] with a packed red cell volume of 16.7%. There was marke neutrophilic leucocytosis (total WBC count: 45,000 cells/cu mm, 85% being neutrophils). The ESR was 60mm at the end of the l st hour. The random blood sugar was 500 mg/dl and urine showed presence of sugar (2+). Ketones were absent in urine and blood. There was no proteinuria or haematuria.
Emergency mesenteric artery angiography showed active bleeding from a vasa recta in the region of the caecum. There was no narrowing or occlusion of any artery. At emergency laparotomy, an actively bleeding ulcer was seen in the caecum. The ulcer along with a rim of normal caecal mucosa was excised. Post-operatively, the intestinal bleeding stopped immediately. The diabetes was difficult to control. After a course of metronidazole, he was discharged on the 25th postoperative day.
Grossly, the excised specimen measured 3cm x 2 cm. The mucosal ulcer was irregular, 2cm in diameter, surrounded by a rim of normal mucosa. Microscopically, the uicer was partly covered by eosinophilic, powdery necrotic material. Clusters of trophozoites of Entamoeba histolytica were seen in the necrotic material with a clear halo around each trophozoite. Phagoeytosed red blood cells were seen in the cytoplasm of the tophozoites.
The inflammatory exudate in the caecal wall was intense, comprising of neutrophils, lymhocytes, macrophages, plasma cells and many eosinophils. An occasional foreign body type giant cell was also seen on the necrotic mucosa. There were no granulomas. There was necrosis of the muscle wall and the inflammatory exudate extended transmurally.
A small artery exposed on the surface of the ulcer showed necrosis of the adventitia and media, with intense inflammatory exudate similar to that surrounding the artery. Trophozoites of Entamoeba histolytica were seen invading the wall (See [Figure - 1]) There was focal rupture of the internal elastic lamina of the affected artery (See inset, [Figure - 1]). Similar but less intense inflammatory exudate was seen on the wall of an occasional vein. An occasional vein showed organised and recanalised thrombus. Trophozoites were not seen invading the walls of the affected veins.
One year after the event, the patient has been in good health and on regular insulin therapy. Even on repeated stool examinations, no evidence of amoebiasis has been found. There has also been no further episode of interstinal haemorrhage, proteinuria or hematuria.
Necrosis of blood vessels is not unusual in infectious processes, especially ulceration of the gastrointestinal tract. However, arterial destruction and massive intestinal haemorrhage have rarely been reported in amoebiasis. The probable explanation may be the low grade of invasiveness of the amoebae. In the case reported here, uncontrolled diabetes may have rendered the tissue susceptible to aggressive invasion by the amoebae resulting in rupture of the arterial wall and massive haemorrhage.
Invasion of arteries by amoebae, resulting in necrotising arteritis has been recorded before. In 1985, Luvuno et al  showed that transumural necrosis in amoebic colitis is due to thrombotic occlusion of vessels supplying that segment of the bowel. Of the 16 colonic specimens studied histologically, they saw amoebae invading the wall of the artery in 12. The occluding thrombus was inflammatory in nature, suggesting a reaction to the presence of amoebae. The illustration published by them of amoebic invasion of the arterial wall and total thrombotic occlusion of the lumen, shows features similar to those described in our case. None of their patients, however, had massive intestinal haemorrhage.
Luvuno et al did not use the term 'vasculitis' or arteritis' in their publication. In 1982 however, the same authors while commenting on the pathogenesis of toxic dilatation complicating fulminant amoebic colitis, had stated that amoebae initiate vasculitis and thrombosis, with subsequent partial or total muscle necrosis and perforation of the bowel wall . Surprisingly, there are no other studies, to the best of our knowledge, highlighting the vasculitis/arteritis in intestinal amoebiasis. Vasculitis, including necrotising arteritis, of intracranial vessels however, has been well documented in granulomatous amoebic encephalitis caused by freeliving amoebae,.
| :: References|| |
Luvuno FM, Mtshali Z, Baker LW. Toxic dilatation complicating fulminant amoebic colitis. Br J Surg 1985; 69:56-57. |
|2.||Luvuno FM, Mtshali Z, Baker LW. Vascular occlusion in the pathogenesis of complicated amoebic colitis: evidence for a hypothesis. Br J Surg 1982; 72:123-125. |
|3.||Anzil AP, Rao C, Wrzolek MA, Visvesvara GS, Sher JH, Kozlowski PB. Amebic meningoencephalitis in a patient with AIDS caused by a newly recognized opportunistic pathogen. Leptomyxid ameba. Arch pathol Lab Med 1991; 115:21-25. |
|4.||Martinez AJ, Sotelo-Avila C, Alcala H, Wilaert E. Granulomatous encephalitis, intracranial arteritis, and mycotic aneurysm due to a free-living amoeba, Acta Neuropathol (Berl) 1980; 49:7-12.
[Figure - 1]
|This article has been cited by|
||Gastrointestinal involvement in polyarteritis nodosa
| ||Ebert EC, Hagspiel KD, Nagar M, et al. |
| ||CLINICAL GASTROENTEROLOGY AND HEPATOLOGY. 2008; 6(9): 960-966 |
||Rheumatic manifestations of parasitic diseases
| ||Peng SL |
| ||SEMINARS IN ARTHRITIS AND RHEUMATISM. 2002; 31 (4): 228-247 |