| Abstract|| |
Gastrointestinal (GI) hemorrhage is a problem, the management of which needs the right decision at the right time and close cooperation between physicians and surgeons. We herewith report a renal transplant recipient who developed severe GI bleed and intestinal perforations seven months after renal transplantation. Despite extensive investigations, the exact cause of the problem could not be identified.
Keywords: Gastrointestinal bleeding, Intestinal perforation, Renal transplantation
|How to cite this article:|
Khattab OS, Al-Timimi SM. Massive Gastrointestinal Bleeding and Intestinal Perforation in a Renal Transplant Recipient: A Case Report. Saudi J Kidney Dis Transpl 2006;17:568-71
|How to cite this URL:|
Khattab OS, Al-Timimi SM. Massive Gastrointestinal Bleeding and Intestinal Perforation in a Renal Transplant Recipient: A Case Report. Saudi J Kidney Dis Transpl [serial online] 2006 [cited 2021 Oct 26];17:568-71. Available from: https://www.sjkdt.org/text.asp?2006/17/4/568/32497
| Introduction|| |
Gastrointestinal (GI) hemorrhage is a problem, the management of which needs the right decision at the right time and close cooperation between physicians and surgeons. Only by identifying accurately the source of bleeding, and acting quickly, will a successful outcome be achieved. There are many causes for GI bleeding and a lesion can be identified in more than 95% of the patients.  The reported incidence of intestinal perforation in renal transplant recipients ranges from 0.6 to 3.4%. Most perforations occur within the first few weeks or months after engraftment.  We herewith report a 35-yearold Iraqi male renal transplant recipient who developed severe GI bleed and intestinal perforations seven months after renal transplantation.
| Case Report|| |
A 35-year-old Iraqi male was referred to the renal transplant center at the Medical City Teaching Hospital, Baghdad, Iraq for renal transplantation. He was diagnosed to have chronic renal failure of uncertain etiology, nine months earlier. His body mass index was 23.8, he was hypertensive on medications; he was not a diabetic and there was no previous history of GI bleeding.
We created an arteriovenous fistula in his forearm and regular hemodialysis was started. He received two units of blood three months before transplantation. He underwent renal transplantation in September 2004; the donor being his wife. Following transplantation, four immunosuppressive drugs were used: Basiliximab, 20 mg, was given two hours prior to transplantation, and the dose was repeated on the fourth post-operative day. Maintenance was with azathioprine (AZA)) 1.5 mg/kg/day, cyclosporine (CyA) l0 mg/ kg/day, and corticosteroids (intravenous methylprednisolone 1 gm/day for three days, followed by oral prednisolone in a dose of 30 mg/day). The post-operative period was uneventful and he had brisk diuresis. The serum creatinine dropped from 6.4 to 1 mg/dl within 48 hours of-surgery. The patient was discharged from the hospital on the 12 th post-operative day with serum creatinine of 0.8 mg/dl. He attended the follow-up clinic regularly without any complications other than post-transplant diabetes mellitus, which was controlled with oral hypoglycemic agents.
About seven months after the transplant, he presented with an episode of fresh bleeding per rectum, continuous epigastric pain and dyspepsia. He was admitted to the hospital where he was found to have severe pallor, blood pressure was 100/60 mm Hg, pulse rate 100 beats/min and temperature was 38° Celsius. His chest, abdominal, and per rectal examination did not reveal any abnormality. At that stage, the patient was taking CyA 200 mg/day, AZA l00 mg/day, and prednisolone l0 mg/day. There was no previous history of ingesting aspirin /non-steroidal anti-inflammatory drugs (NSAIDs), change in bowel habits or any prior gastrointestinal illnesses.
Investigations done revealed hemoglobin (Hb) of 8 gm/dl, white blood count of 4800/ cu mm, platelet count of 220.000/cu mm and ESR of 120 mm in the first hour. Blood film showed normochromic normocytic anemia with lymphopenia and relative neutrophilia. The reticulocyte count was 4.7% and the prothrombin time, partial thromboplastin time, INR, and bleeding time were within normal limits. The blood urea was 41 mg/dl, serum creatinine 1.4 mg/dl and random blood sugar was 128 mg/dl. The serum electrolytes, liver function test and lipid profile were normal. Detailed viral serology was negative as were Widal and Rosebengol tests. Stool examination was normal and cultures of urine, stool and blood were negative. Abdominal ultrasonography, chest X-Ray and echocardiogram did not reveal any abnormality.
Proctoscopic examination was normal. Gastroduodenoscopy was done and multiple biopsies were taken which showed no significant pathology. Colonoscopy up to the ileocecal region showed congested mucosa; there was blood coming from the ileocecal valve. There was a solitary sessile polyp l cm in diameter in the ascending colon, which was excised. Histopathological examination revealed hyperplasia and no malignancy. Enteroscopy was then done up to 180 cm, which showed congested mucosa, abnormally elevated mucosal folds and no obvious bleeding; multiple biopsies were taken which showed mucosal congestion and no evidence of malignancy. Barium meal and follow through was normal.
Despite these investigations, we were unable to diagnose the cause or site of bleeding. During the three week period of stay in the hospital, he had four attacks of fresh bleeding per rectum, his Hb dropped to less than 4 gm/dl, his renal function remained normal, and he received 12 units of blood to maintain his Hb. The patient also received broad-spectrum antibiotics and omeprazole as well as valacyclovir for prophylaxis against cytomegalovirus. The dose of CyA was reduced to l00 mg/day, AZA was stopped, and steroids were continued. Towards the end of the third week, he developed features of acute abdomen and an emergency explorative laparotomy was performed. There were multiple big perforations, about 15 in number, involving parts of the jejunum and ileum, each about 2 cm in diameter with necrosed edges [Figure l]. The entire small intestine was friable, there was no lymphadenopathy or fecal peritonitis. Resection of 360 cm of unhealthy small intestine, mainly jejunum and part of the ileum was performed [Figure - 2], with endto-end anastomosis of the unaffected jejunum and ileum.
Post-operatively, the fever subsided; vital signs became stable, and the patient was passing about three liters urine per day. Immunosuppressive drugs were reduced to the minimum, and the serum creatinine increased to 2 mg/dl. On the fourth post-operative day, he developed fresh bleeding per rectum, which persisted resulting in death of the patient. Histopathological examination of the resected small intestine showed intense inflammation involving the mucosa, submucosa and serosa, with predominantly histiocytes mixed with neutrophils. There were no inclusion bodies, granuloma, or features suggestive of malignancy.
| Discussion|| |
There are many reasons for massive GI bleeding which include angiomata (30%), diverticulosis (17%), polyps or cancer (11%), focal ulcers (9%), upper GI lesions (11%), and presumed small bowel lesions (9%). No obvious cause or site is identified in about 6% of the cases. About 64% of the patients need intervention for control of bleeding of which 39% require therapeutic endoscopy, 24% surgery, and 1% therapeutic angiography. The diagnostic yield of visceral angiography was 14% and the complication rate was 9%.  In our patient, there was no evidence of any of the common disorders that cause GI bleed. Also, there was no evidence of systemic vasculitis and, even if that disorder had been present, it would have been effectively treated by the immunosuppressive agents that the patient was taking.
The incidence of three major acute bacterial infections, namely, shigella, campylobacter, and Salmonella More Details is increased in immunosuppressed persons.  In our patient, infection was unlikely in view of treatment with broadspectrum antibiotics including ciprofloxacin, to which these organisms are usually sensitive.
The reported incidence of intestinal perforations in renal transplant recipients ranges from 0.6 to 3.4% , in some reports and between 1.1 and 2.1% in other reports involving larger samples., Most perforations occur within few weeks or months of engraftment, the period of most intense immunosuppression. , The pathogenesis is probably related to a high incidence of diverticular disease in patients with polycystic kidneys and/or chronic renal failure.  Other risk factors include over-immunosuppression, , CMV infection,  and the transplant procedure itself.  The average mortality rate is 56.5%.  This high mortality appears to be related to the effects of immunosuppression and the associated poor response to the management of sepsis. Additionally, the immunosuppressive agents might mask the classical clinical findings, such as fever or leucocytosis, in these patients.  Pneumoperitoneum on abdominal roentgenograms is not necessarily positive in all patients. , Therefore, prompt diagnosis, aggressive surgical care consisting of resectional therapy, use of broad-spectrum antibiotics, and a reduced immunosuppressive protocol, all of which are crucial to outcome, may be delayed.
In our case, it was not possible to identify any cause for the perforations. We were unable to exclude CMV definitely, because PCR for CMV and immunohistochemical study were unavailable in our country.
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Omar S Khattab
General and Transplant Surgeon, Renal Transplant Center, Medical City, Teaching Hospital, P.O. Box: 19503 Baghdad
[Figure - 1], [Figure - 2]