Abstract
A 57-year-old nondiabetic male underwent related live donor renal transplantation in July 2002. The perioperative period was uneventful and the patient was discharged on triple immunosuppression with baseline creatinine of 0.9 mg/dl. In November 2002, he developed biopsy-proven acute rejection. Three doses of methylprednisolone were given. Azathioprine was switched over to mycophenolate mofetil (MMF) at 2 g/day. His baseline creatinine stabilized at 2 mg/dl. In December 2002, he was readmitted with rising creatinine (3.05 mg/dl) and renal biopsy suggestive of cyclosporine toxicity. Despite stopping cyclosporine, his creatinine stabilized at 3 mg/dl. In January 2003, the patient was admitted with generalized weakness and anorexia. MMF was reduced to 1 g/day. In the hospital, he developed headache and left infraorbital swelling. A necrotic blackened patch was noticed on left side of the hard palate. Spiral computed tomography scan of paranasal sinuses showed complete opacification of sphenoid, ethmoid, frontal, and maxillary sinuses of left side. Patient underwent Caldwell Luc’s operation. Yellowish-white necrotic material was excised and histopathological examination revealed aseptate fungal hyphae invading the vessels causing necrosis and intraluminal thrombosis. Treatment with amphotericin B was started (1 mg/kg/day). Immunosuppression was stopped. Six days after the procedure, the patient developed left-sided sixth and seventh nerve palsies. Magnetic resonance imaging of the cranium revealed fusiform basilar artery aneurysm (Figure 1).FIGURE 1.: Magnetic resonance imaging of the cranium showing big fusiform basilar artery aneurysm.Patient developed signs of peritonitis and pneumoperitoneum two weeks later. He underwent emergency laparotomy; 1 liter of seropurulent fluid was present in the peritoneal cavity. A single 1-cm perforation in the distal transverse colon, about 5 cm proximal to splenic flexure, was present. Perforation site was exteriorized as stoma. Peritoneal fluid microscopy revealed aseptate fungal hyphae and histopathology of colonic margin was consistent with mucormycosis. Patient developed septicemia with multi-organ dysfunction in the postoperative period and succumbed to his illness. Of patients developing invasive zygomycosis after solid organ transplantation, 64–76% had diabetes or augmented immunosuppression (1). The fungal infection in our patient manifested after starting mycophenolate therapy for proven acute rejection. Intracranial fungal aneurysms are extremely rare, reported less than 15 times since their first description in 1968 (2). Most of the reported cases are due to aspergillosis. Organisms of mucormycosis have a predilection for vascular invasion causing thrombosis, infarction, and necrosis of the tissue. Reported mortality of renal transplant recipients with Rhinocerebral mucormycosis is approximately 50% (3). The intradural portion of internal carotid artery is the most commonly reported site of aneurysm. Basilar artery aneurysm has not been reported in literature to the best of our knowledge. Similarly, fungal intestinal perforation is extremely rare. The few reported cases are due to aspergillosis, histoplasma capsulatum, and candidiasis. Intestinal infections are usually fatal in 2–3 weeks as a result of bowel impaction, sepsis, and hemorrhagic shock (4). Only 11 cases of gastrointestinal mucormycosis in solid organ transplantation are reported (5). To the best of our knowledge, this is the first case of gastrointestinal mucormycosis with colonic perforation. In conclusion, enhanced immunosuppression (mycophenolate) might be responsible for this rare, fulminating course of the disease, as seen in our patient. As gastrointestinal involvement is associated with very poor prognosis, early detection is crucial. Anand Sehgal M. Raghavendran Devendra Kumar Aneesh Srivastava Deepak Dubey Anant Kumar Department of Urology and Renal Transplantation Sanjay Gandhi Post Graduate Institute of Medical Sciences Lucknow, India
Published Version
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