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Saudi Journal of Kidney Diseases and Transplantation
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CASE REPORT  
Year : 2016  |  Volume : 27  |  Issue : 3  |  Page : 585-589
Nonocclusive mesenteric ischemia after renal transplantation: A case report and literature review


1 Department of Urology, Mashhad University of Medical Sciences, Mashhad, Iran
2 Department of Pathology, Mashhad University of Medical Sciences, Mashhad, Iran

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Date of Web Publication13-May-2016
 

   Abstract 

Nonocclusive mesenteric ischemia (NOMI) is a very rare occurrence after renal transplantation. This disorder is difficult to diagnose and can even be fatal. We describe a 51- year-old man with end-stage renal disease who developed intestinal ischemia and infarction due to NOMI three days after deceased donor kidney transplantation, which was managed success- fully and his renal graft function was saved. To the best of our knowledge, this is one of the few cases of NOMI occurring after renal transplantation reported in the literature.

How to cite this article:
Tavakkoli M, Mahdavi-Zafarghandi R, Ghoreifi A, Khooei A. Nonocclusive mesenteric ischemia after renal transplantation: A case report and literature review. Saudi J Kidney Dis Transpl 2016;27:585-9

How to cite this URL:
Tavakkoli M, Mahdavi-Zafarghandi R, Ghoreifi A, Khooei A. Nonocclusive mesenteric ischemia after renal transplantation: A case report and literature review. Saudi J Kidney Dis Transpl [serial online] 2016 [cited 2022 Jan 16];27:585-9. Available from: https://www.sjkdt.org/text.asp?2016/27/3/585/182412

   Introduction Top


Nonocclusive mesenteric ischemia (NOMI) is a mesenteric circulatory disorder, which is defined as diffuse intestinal ischemia in the presence of a patent arterial trunk.[1]Immediate diagnosis and effective management of this condition are of great importance because missed diagnosis results in a high mortality rate.[2]However, early diagnosis is still a chal- lenging problem. A high index of clinical suspicion and urgent appropriate intervention can be curative in this condition.[3]End-stage renal disease (ESRD) is a risk factor for NOMI but only a few cases of NOMI have been reported in renal transplant recipients in the available literature.[4]The high mortality rate in this group of patients appears to be related to the effects of immunosuppressive drugs and the altered response to sepsis.[2],[4]

Herein, we report a 51-year-old man who developed intestinal ischemia and infarction due to NOMI three days after deceased donor kidney transplantation; he was managed suc- cessfully, and his renal graft function was saved.


   Case Report Top


A 51-year-old man, known case of ESRD of unknown etiology, who was medically ma- naged by hemodialysis for 60 months, under- went deceased donor kidney transplantation. His blood group was A+. He did not have any history of hypertension, vascular disease, or diabetes mellitus. The deceased donor was a 45-year-old man who was confirmed to be brain dead after a car accident. His blood group was also A+. Panel reactive antibody was 5%, and lymphocyte cross-match test was negative.

During the operation, we did not manipulate the intra-peritoneum, and the transplant was per-formed extraperitoneally in the iliac fossa. No complications including hypotension occurred perioperatively.

After kidney transplantation, vital signs including blood pressure were well controlled with about 200 mL/h urine output; the patient did not receive any vasopressors after the operation. In addition, no blood transfusion was required during or after the operation and the coagulation profile was in the normal range during the postoperative days (POD) (prothrombin time: 12 s, partial thromboplas- tin time: 30 s, and International Normalized Ratio: 1.2). The administered immunosup- pressive regimen in the postoperative period included cyclosporine, mycophenolate mofetil, and prednisolone.

On the 3rd POD, the patient complained of abdominal pain with localized guarding in the epigastric and right upper quadrant regions,

but there were no signs of tenderness or re- bound tenderness. Laboratory studies showed high white blood cell count; the urine output dropped to 50 mL/h and creatinine (Cr) level was elevated to about 3 mg/dL. There was a slight elevation in serum lactate dehydro- genase, but the aspartate and alanine trans- aminase levels were in the normal range. Emergency ultrasound imaging showed free fluid in the abdominal cavity, and a plain radiography showed air under the diaphragm [Figure 1]. Emergency laparotomy was per- formed due to vital sign instability. During surgery, ischemic necrosis of a segment of the small intestine was seen, but the inferior and superior mesenteric arteries did not have any occlusive lesions. The necrotic segment was removed and end ileostomy was performed. Histopathological evaluation revealed a nec- rotic intestine without evidence of vascular thrombosis or vasculitis [Figure 2]. The post- operative period was uneventful. One week after surgery, the stoma had turned blue, and stoma revision was performed successfully with a second operation.
Figure 1. Plain X-ray of the abdomen showing an ileus pattern with sub-diaphragmatic free air (arrow). Double J stent is visible in the right iliac fossa

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Figure 2. The histological appearance of the intestinal specimen showing transmural hemorrhagic infarction with acute inflammation, but without evidence of vascular thrombotic obstruction or vasculitis (H and E)

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The patient remained stable. Urine output was about 50-60 mL/h and serum Cr dropped to 1 mg/dL. He was discharged on the 15th POD, and the ileostomy was closed three months after the last surgery. The patient at last follow-up has maintained normal renal graft function with no gastrointestinal symptoms.


   Discussion Top


NOMI is a potentially fatal condition which often results in intestinal gangrene. It accounts often results in intestinal gangrene. It accounts for more than 10-20% of cases of acute mesenteric circulatory disorders.[1]The first cases of NOMI were reported by Ende in 1958 in three patients with heart failure.[5]

Aging of the society and a rise in the dialysis population has resulted in an increasing num- ber of NOMI cases. Today, the overall inci- dence is estimated to be approximately one case in every 5000 hospital admissions.[6]How- ever, the disease concept has not yet been fully established.[1],[2]Moreover, NOMI is difficult to diagnose and many patients may be diagnosed during laparotomy or may have died without receiving adequate treatment. High mortality rates up to 90% have been reported, which have not changed over time.[1],[4]

The primary pathogenesis of NOMI is thought to be prolonged intestinal hypoperfusion.[7]Risk factors of NOMI include atherosclerosis, diabetes mellitus, hypertension, dyslipidemia, renal failure, and long-term dialysis.[4]Mesenteric ischemia may appear more fre- quently among dialysis than nondialysis pa- tients, and in recent studies, its frequency is increasing.[8]Vaziri et al reported mesenteric ischemia in 14% of the 78 hemodialysis pa- tients who underwent autopsy.[9]In a recent study by Bender et al, the frequency was esti- mated to be as high as 1.9% per patient-year.[10]Therefore, patients with ESRD are among the highest risk populations for developing this complication; NOMI is not unique to hemo- dialysis and can occur in peritoneal dialysis patients as well.[11]On the other hand, there are few reports of NOMI in posttransplant pa- tients. The first study which reported intestinal ischemia after renal transplantation was published in 1975 by Demling et al.[12]They described an acute intestinal disorder occur- ring in seven patients soon after renal trans- plantation. Surgical manipulation did not appear to be the cause, and the mesenteric vessels were patent with no evidence of throm- bus formation or vasculitis. In their article, they did not mention the term "NOMI," but it seems that this phenomenon may have played a great role in the etiology of their cases. The authors stated that the cause appeared to be related to immunosuppressive agents, in par- ticular, high doses of corticosteroids. Tasaki et al reported a 54-year-old man who developed NOMI during the peritransplant period follo- wing ABO-incompatible living-donor kidney transplantation; he was successfully treated and his renal graft function remained unim- paired.[4]In the mentioned case, abdominal pain had appeared on the 6th POD, and emergency surgery had been performed two days later. Halldorsson et al and Königsrainer et al re-ported the possible role of cyclosporine and mycophenolate mofetil in NOMI in posttrans- plant patients, respectively.[13],[14]In our case, the patient was treated with both cyclosporine and mycophenolate mofetil after transplant, but the exact role of these drugs in the pathogenesis of NOMI is still unclear.

NOMI is more likely to occur in elderly pa- tients after cardiovascular surgery and dialysis. The presenting symptoms are variable but usually include abdominal pain, nausea, vomi- ting, and ileus. There is no specific clinical finding and laboratory parameters are of limi- ted value and hence a high index of suspicion is necessary for early diagnosis.[1]Fibrin throm- bi, the pathological hallmark of disseminated intravascular coagulation (DIC), are a nonspe- cific feature of necrosis and can be identified in both occlusive and nonocclusive ischemic bowel disease, and their presence in the intestine of NOMI therefore cannot be used to implicate DIC as the primary cause of this entity.[15]

Radiographic studies, including plain abdo- minal films or computed tomography scans, are not helpful in diagnosing NOMI. Routine abdominal radiographs may show a dilated featureless colon and "thumb-printing" signs suggestive of patchy sub-mucosal edema or hemorrhage.[16]Furthermore, Doppler ultrasound of the mesenteric vessels has little value in the acute phase of ischemic attacks.[17]Magnetic resonance imaging with gadolinium is also of little benefit in the acute phases but is better than ultrasound for visualizing the origin of the mesenteric vessels.[8]However, selective mesenteric angiography with concomitant per- fusion of papaverine hydrochloride, PGE1, and nitroglycerin has been shown to be an effective diagnostic and therapeutic proce- dure.[4]Boley et al reported narrowing of many branches of the superior mesenteric artery ("string of sausages" sign), spasm of the intes- tinal marginal artery, and poor contrast en- hancement of veins in the muscular layer as features of vasospasm associated with NOMI.[18]Although angiography appears to be the gold standard for diagnosis, it may not be feasible in the emergency status. Furthermore, the indi- cation for angiography in NOMI is not clear, especially in cases of abdominal complications following renal transplant.[19]Although angio- graphy may play a role in the management of these patients as a noninvasive procedure, laparotomy should not be delayed due to fear of intervening after transplant, particularly because missed intestinal ischemia carries a 100% mortality rate. Boley et al reported only a 20% survival rate among patients with NOMI, who had peritoneal signs and were treated initially with intra-arterial papaverine.[17]In our case, emergency laparotomy was per- formed due to vital sign instability and evi- dence of intestinal perforation according to the plain radiography. To note, progressive ische- mia is frequent in NOMI and second look surgery may be required for this reason. However, in our patient, only stoma revision was performed, and no further intervention has been required so far. Finally, a written in- formed consent was obtained from the patient to publish this case report and the performed procedures.


   Conclusion Top


NOMI after kidney transplantation is a rare occurrence but should be considered in pa- tients with abdominal symptoms besides the previously mentioned risk factors. In this way, the physician would be able to diagnose early and treat this rare but potentially fatal condi-tion.

Conflict of interest: None.

 
   References Top

1.
Mitsuyoshi A, Obama K, Shinkura N, Ito T, Zaima M. Survival in nonocclusive mesenteric ischemia: Early diagnosis by multidetector row computed tomography and early treatment with continuous intravenous high-dose prosta- glandin E(1). Ann Surg 2007;246:229-35.  Back to cited text no. 1
    
2.
Yu CC, Hsu HJ, Wu IW, et al. Factors associated with mortality from non-occlusive mesenteric ischemia in dialysis patients. Ren Fail 2009;31:802-6.  Back to cited text no. 2
    
3.
Bassiouny HS. Nonocclusive mesenteric ischemia. Surg Clin North Am 1997;77:319-26.  Back to cited text no. 3
    
4.
Tasaki M, Saito K, Nakagawa Y, et al. Successful treatment of nonocclusive mesen- teric ischemia that developed during the peri- transplant period following ABO-incompatible kidney transplantation. Clin Exp Nephrol 2010;14:199-202.  Back to cited text no. 4
    
5.
Ende N. Infarction of the bowel in cardiac failure. N Engl J Med 1958;258:879-81.  Back to cited text no. 5
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6.
Liu HL, Huang JJ, Lan RR, Wang MC, Sung JM, Hsieh RY. Ischaemic bowel disease in patients on continuous ambulatory peritoneal dialysis. Nephrol Dial Transplant 1999;14: 2032-4.  Back to cited text no. 6
    
7.
Oldenburg WA, Lau LL, Rodenberg TJ, Edmonds HJ, Burger CD. Acute mesenteric ischemia: a clinical review. Arch Intern Med 2004;164:1054-62.  Back to cited text no. 7
    
8.
Bassilios N, Menoyo V, Berger A, et al. Mesenteric ischaemia in haemodialysis pa- tients: a case/control study. Nephrol Dial Transplant 2003;18:911-7.  Back to cited text no. 8
    
9.
Vaziri ND, Dure-Smith B, Miller R, Mirahmadi MK. Pathology of gastrointestinal tract in chronic hemodialysis patients: an autopsy study of 78 cases. Am J Gastroenterol 1985; 80:608-11.  Back to cited text no. 9
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10.
Bender JS, Ratner LE, Magnuson TH, Zenilman ME. Acute abdomen in the hemo- dialysis patient population. Surgery 1995;117: 494-7.  Back to cited text no. 10
    
11.
Archodovassilis F, Lagoudiannakis EE, Tsekouras DK, et al. Nonocclusive mesenteric ischemia: a lethal complication in peritoneal dialysis patients. Perit Dial Int 2007;27:136- 41.  Back to cited text no. 11
    
12.
Demling RH, Salvatierra O Jr., Belzer FO. Intestinal necrosis and perforation after renal transplantation. Arch Surg 1975;110:251-3.   Back to cited text no. 12
    
13.
Halldorsson A, Hunter GC, Zukoski CF, Putnam CW. The possible role of cyclosporine in nonocclusive mesenteric ischemia in a renal transplant patient. Transplantation 1991;51: 1298-301.  Back to cited text no. 13
    
14.
Königsrainer A, Steurer W, Spechtenhauser B, Margreiter R, Rieger M, Waldenberger P. Nonocclusive segmental mesenteric ischemia after combined pancreas kidney transplan- tation: Mycophenolate mofetil as an etiological factor? Transplantation 2000;70:695-6.  Back to cited text no. 14
    
15.
Brandt LJ, Gomery P, Mitsudo SM, Chandler P, Boley SJ. Disseminated intravascular coagu- lation in nonocclusive mesenteric ischemia: the lack of specificity of fibrin thrombi in intes- tinal infarction. Gastroenterology 1976;71: 954-7.   Back to cited text no. 15
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16.
Gandhi SK, Hanson MM, Vernava AM, Kaminski DL, Longo WE. Ischemic colitis. Dis Colon Rectum 1996;39:88-100.  Back to cited text no. 16
    
17.
Roobottom CA, Dubbins PA. Significant disease of the celiac and superior mesenteric arteries in asymptomatic patients: predictive value of Doppler sonography. AJR Am J Roentgenol 1993;161:985-8.  Back to cited text no. 17
    
18.
Boley SJ, Sprayregan S, Siegelman SS, Veith FJ. Initial results from an agressive roent- genological and surgical approach to acute mesenteric ischemia. Surgery 1977;82:848-55.  Back to cited text no. 18
[PUBMED]    
19.
Klotz S, Vestring T, Rötker J, Schmidt C, Scheld HH, Schmid C. Diagnosis and treat- ment of nonocclusive mesenteric ischemia after open heart surgery. Ann Thorac Surg 2001;72:1583-6.  Back to cited text no. 19
    

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Correspondence Address:
Alireza Ghoreifi
Department of Urology, Mashhad University of Medical Sciences, Mashhad
Iran
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DOI: 10.4103/1319-2442.182412

PMID: 27215255

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