Literature DB >> 26664217

Mesenteric ischemia masquerading as refractory peritonitis in continuous ambulatory peritoneal dialysis patients.

K Vishwakarma1, U Anandh2.   

Abstract

We report two cases of mesenteric ischemia in patients on long term peritoneal dialysis both of which were associated with poor outcomes. Both were diabetic and on peritoneal dialysis for a long time. On evaluation of refractory peritonitis we found evidence of non occlusive mesenteric ischemia. Despite adequate treatment both succumbed to their illness. Abdominal pathology, especially mesenteric ischemia leading to gut infarction, should be considered in patients with refractory peritonitis.

Entities:  

Keywords:  Ischemia; mesenteric; nonocclusive; peritonitis

Year:  2015        PMID: 26664217      PMCID: PMC4663779          DOI: 10.4103/0971-4065.160332

Source DB:  PubMed          Journal:  Indian J Nephrol        ISSN: 0971-4065


Introduction

Peritonitis is a common complication in patients on continuous ambulatory peritoneal dialysis (CAPD). In certain cases, the peritonitis episode becomes difficult to treat. In such patients, underlying gut pathology can contribute. We present two cases of underlying mesenteric ischemia responsible for refractory peritonitis.

Case Reports

Case 1

A 62-year-old lady, a known case of diabetes mellitus, hypertension, dyslipidemia, and chronic kidney disease (CKD), was admitted with abdominal pain, vomiting and loose stools of 7 days duration. For the last 6 years, she has been on CAPD, and her dialysis has been largely uneventful. She had similar symptoms about 4 weeks ago which was diagnosed as peritonitis and was treated with IP cephalosporin, aminoglycoside, and vancomycin. Her cultures were negative. She showed gradual improvement and her antibiotics were stopped after 14 days of therapy. After 48 hours, she started having abdominal pain, vomiting, and diarrhea. She was restarted on intravenous (IV) antibiotics (meropenem and amikacin). As she did not show any improvement, she was referred to us, and she was subsequently admitted in our hospital. At admission, she was afebrile and her vitals were stable. Her systemic examination revealed a soft abdomen with no evidence of exit site or tunnel infection. Her laboratory investigations are shown in Table 1. The peritoneal fluid count came as 3233 cells/mm3 with 85% neutrophilic predominance. The peritoneal fluid culture was negative. Acid fast bacilli (AFB) were not seen on ZN stain, and a mycobacterial culture was asked for. A relapse of CAPD-associated peritonitis was diagnosed, and IV Vancomycin was added. Tenckhoff catheter removal was planned for the next day.
Table 1

Laboratory investigations of patients

Laboratory investigations of patients Early next day, she showed hemodynamic deterioration and her peritoneal dialysis catheter was removed on the same day. Her postoperative course was satisfactory, and she was switched to hemodialysis. However, on fourth postoperative day, she deteriorated again. A computed tomography (CT) scan of the abdomen was done which revealed dilated, thin and fuzzy appearing wall of a segment of the jejunal loop with air in the parietal wall. The adjacent mesentery showed fat stranding suggestive of mesenteric ischemia. An exploratory laparotomy revealed extensive infarction of the gut extending from jejunum to transverse colon [Figure 1]. No vascular occlusive lesion was found and arterial pulsations were appreciated by the operating surgeon. No resection was attempted because of extensive gut involvement.
Figure 1

Exploratory laparatomy showing extensive infarction of the gut

Exploratory laparatomy showing extensive infarction of the gut

Case 2

A 70-year-old male, known case of diabetes mellitus, hypertension, CKD stage 5 on CAPD for last 5 years, was admitted with low-grade fever, vomiting, and drowsiness. On evaluation, he was febrile and icteric. He was in altered sensorium with no obvious deficit. His abdominal examination revealed a distended tender abdomen. His initial laboratory investigations are given in Table 1. A diagnosis of CAPD peritonitis with sepsis was made, and he was started on antibiotics. His peritoneal fluid assay showed evidence of culture negative peritonitis. Despite the treatment, he showed minimal improvement. After 2 days, he developed hypotension and breathlessness. His blood culture sent on admission showed growth of Enterococcus faecium. He was intubated, ventilated and started on meropenem and tigecycline. A CT scan of the abdomen was done, which showed diffuse thickening of small bowel loop predominantly in the jejunum with thumb printing appearance [Figure 2]. There was no enhancement of the jejunal loops on contrast administration suggestive of ischemic bowel disease. Celiac and superior mesenteric arteries appeared small in caliber along with diffuse atherosclerotic changes in CT angiography. There was no evidence of thrombotic occlusion of the artery. Peripheral nonenhancing areas were seen in spleen suggestive of splenic infarcts. These changes progressively worsened on repeat scan and patient rapidly deteriorated. He was managed conservatively keeping in view of his poor general condition and advanced comorbidities, and he expired after 2 days.
Figure 2

Computed tomography scan of the abdomen showing thumbprinting suggestive of mesenteric ischemia

Computed tomography scan of the abdomen showing thumbprinting suggestive of mesenteric ischemia

Discussion

The two cases illustrate the presence of bowel ischemia in patients on long-term CAPD. These patients presented to the hospital with episodes of peritonitis that were difficult to treat. They had nonocclusive mesenteric ischemia as the underlying cause of peritonitis which was missed on initial evaluation. Both had poor outcome. Nonocclusive mesenteric ischemia (NOMI) was described 1958[1] as one of the diseases that affect the vasculature of the intestine. It may be called as “intestinal gangrene in the presence of a patent arterial tree.” The pathology is well-described in hemodialysis. The dialysis population, and in particular hemodialysis patients, are especially prone to mesenteric ischemia.[2] Besides the traditional risk factors, CKD patients are more prone for vascular calcification[3] and increasing risk of ischemia because of the use of erythropoietin.[45] Erythropoietin has also direct vasopressor effect on mesenteric blood vessels.[6] Despite its definite association in hemodialysis, NOMI has been surprisingly rarely reported in association with PD. The higher incidence of diabetes mellitus in PD patients with vascular disease actually predisposes this group of patients to underlying chronic mesenteric ischemia. This ischemic compromise becomes critical during a peritonitis episode when there is an increased metabolic demand. It is also worthwhile to note that there is an increased incidence of transmigration of gut bacteria across the ischemic intestinal wall which again predisposes these patients to an increased risk of peritonitis. Hypotension is the leading precipitating cause and the mechanisms being the inappropriate use of dialysate resulting in excessive fluid removal, diuretics, and very low salt intake. The clinical presentation in such patients remain similar to that of peritonitis and thus pose a difficult challenge needing a high index of suspicion for diagnosis.[7] There have been a few case reports in the past where the presence of peritonitis masked the underlying pathology. Korzets et al. reported one such case where the patient was thought to suffer from an episode of peritonitis and mesenteric ischemia was suspected only when the CT scan showed pneumatosis coli of the right colon. Laparotomy revealed extensive necrosis of the ascending and transverse colon. A total colectomy and ileorectal anastomosis were performed. The patient died on the 17th day following surgery.[8] Thus, NOMI can masquerade as refractory peritonitis as in above cases and needs a high index of clinical suspicion. The mortality remains high in view of the presence of underlying comorbidities, delayed diagnosis and subsequent delay in treatment.
  8 in total

1.  Infarction of the bowel in cardiac failure.

Authors:  N ENDE
Journal:  N Engl J Med       Date:  1958-05-01       Impact factor: 91.245

Review 2.  Nonocclusive mesenteric infarction in continuous ambulatory peritoneal dialysis.

Authors:  Z Korzets; S Ben-Chitrit; J Bernheim
Journal:  Nephron       Date:  1996       Impact factor: 2.847

3.  Non-occlusive mesenteric infarction in dialysis patients: the importance of prevention and early intervention.

Authors:  M Zeier; M Wiesel; M Rambausek; E Ritz
Journal:  Nephrol Dial Transplant       Date:  1995       Impact factor: 5.992

Review 4.  Current theories of pathogenesis and treatment of nonocclusive mesenteric ischemia.

Authors:  M G Wilcox; T J Howard; L A Plaskon; J L Unthank; J A Madura
Journal:  Dig Dis Sci       Date:  1995-04       Impact factor: 3.199

5.  Unexpected nonocclusive mesenteric infarction during continuous ambulatory peritoneal dialysis.

Authors:  R G Appel
Journal:  Am J Nephrol       Date:  1994       Impact factor: 3.754

6.  Direct vasopressor effect of recombinant human erythropoietin on renal resistance vessels.

Authors:  S Heidenreich; K H Rahn; W Zidek
Journal:  Kidney Int       Date:  1991-02       Impact factor: 10.612

Review 7.  Nonocclusive mesenteric ischemia: a lethal complication in peritoneal dialysis patients.

Authors:  Fotios Archodovassilis; Emmanuel E Lagoudiannakis; Dimitrios Konstantinos Tsekouras; Konstantinos Vlachos; Konstantinos Albanopoulos; Konstantinos Fillis; Andreas Manouras; John Bramis
Journal:  Perit Dial Int       Date:  2007 Mar-Apr       Impact factor: 1.756

8.  Nonocclusive mesenteric ischemia remains a diagnostic dilemma.

Authors:  T J Howard; L A Plaskon; E A Wiebke; M G Wilcox; J A Madura
Journal:  Am J Surg       Date:  1996-04       Impact factor: 2.565

  8 in total

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