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Title Page Case Report NONOCCLUSIVE MESENTERIC ISCHEMIA IN A CHRONIC HEMODIALYSIS PATIENT Yung-Hsin Huang1, Hsin-Chang Lin1, Chih-Jen Wu1,2,3 , Chi-Yuan Tzen4, Han-Hsiang Chen1,2,5 Division of Nephrology, Department of Internal Medicine, Mackay Memorial Hospital, Taipei, Taiwan1 Mackay Medicine, Nursing and Management College, Taipei, Taiwan2 Graduate Institute of Medical Science, Taipei Medical University, Taipei, Taiwan3 Department of Pathology, Mackay Memorial Hospital, Taipei, Taiwan4 National Taipei College of Nursing, Taipei, Taiwan5 Correspondence and reprint requests to: Dr. Han-Hsiang Chen Division of Nephrology, Department of Internal Medicine, Mackay Memorial Hospital. No. 92, Section 2, Chung Shan North Road, Taipei, Taiwan. Tel:+886-2-25433535 Fax:+886-2-25433642 E-mail: [email protected] Running title : NOMI in HD patient Title Page (中文) Case Report 長期血液透析病患之非阻塞性腸繫膜缺血症 黃永新 1, 林信昌 1, 吳志仁 1,2,3 , 曾岐元 4 , 陳漢湘 1,2,5 馬偕紀念醫院,腎臟內科 1 馬偕醫護管理專科學校 2 台北醫學大學醫學研究所 3 馬偕紀念醫院,病理科 4 國立台北護理學院 5 抽印本索取及聯絡地址: 陳漢湘醫師 台北市中山區中山北路二段 92 號 電話 : (02) 25433535 傳真 : (02) 25433642 電子郵件信箱: [email protected] NONOCCLUSIVE MESENTERIC ISCHEMIA IN A CHRONIC HEMODIALYSIS PATIENT Abstract Nonocclusive mesenteric ischemia (NOMI) is characterized by progressive intestinal ischemia and infarction despite having a patent artery. The high mortality rate of NOMI is due to delayed diagnosis and treatment initiation. In the general population, old age and cardiac disease are known as risk factors for this complication. However, NOMI occurs at an increased frequency in chronic hemodialysis (HD) patients because they usually have predisposing risks of intensive ultrafiltration and intradialytic hypotension. Other conditions of acute intravascular volume depletion, such as profound diarrhea or vomiting, also mirror the same risks for NOMI. We present a case of NOMI after acute severe diarrhea in a chronic HD patient without previous obvious intradialytic hypotension. Timely anticipation of NOMI as one of a number of differential diagnoses of nonspecific abdominal symptoms in HD patients is of utmost importance for survival in this fatal syndrome. Key words: Nonocclusive mesenteric ischemia, Hemodialysis, Intradialytic hypotension ABSTRACT (中文) 長期血液透析病患之非阻塞性腸繫膜缺血症 非阻塞性腸繫膜缺血症的特點是雖然動脈是通暢的,但腸子卻有進行性的缺血甚 至梗塞的變化。它的高致死率是與延誤診斷及治療有關。在一般人中,老年人和 有心臟病史是高危險群。在長期血液透析患者,易有脫水過渡和透析中低血壓的 情形,會使它的發生率增加。此外,急性血管內水份大量流失例如嚴重腹瀉或嘔 吐也可同樣視為是危險因子。我們提出一位無發生透析中低血壓的長期血液透析 患者, 以嚴重腹瀉後併發非阻塞性腸繫膜缺血症。對血液透析患者而言,只是一 般腹部症狀以表現,非阻塞性腸繫膜缺血症仍應即時列為鑑別診斷之一,才能提 高這種致命性疾病的存活率。 關鍵詞 : 非阻塞性腸繫膜缺血症,血液透析,透析中低血壓 Introduction Nonocclusive mesenteric ischemia (NOMI) has been defined as one of the diseases that involve the vasculature of the intestine, resulting in intestinal gangrene despite the presence of a patent artery. Occlusive causes of mesenteric ischemia account for about 80% of all cases and include acute mesenteric arterial thrombosis, embolism, mesenteric venous thrombosis, or strangulated bowel obstruction.1 In most patients with NOMI, mesenteric vasoconstriction/vasospasm contributes to the development of this complication in response to circulatory collapse caused by hypotension, acute heart failure, or use of vasoconstrictor drugs.2 Chronic hemodialysis (HD) patients are predisposed to NOMI due to intradialytic hypotension resulting from intensive ultrafiltration.2 Other conditions independent of HD causing rapid intravascular volume depletion and subsequent hypovolemia, such as acute severe diarrhea, vomiting, and fever, can also precipitate NOMI.3,4 The overall mortality due to NOMI is very high—approximately 50%—5if there is any delay in diagnosis or treatment initiation for this dangerous complication. We report a case of NOMI after acute severe diarrhea in a chronic HD patient. Case report A 57-year-old man, a chronic smoker of 30 pack-years and an ex-drinker, was rushed to the emergency department (ED) in a state of drowsy consciousness. He had experienced watery diarrhea several times over a period of 2 days and had vomited twice, with vague abdominal pain and fever, over the time course of 1 day. His medical history included end-stage renal failure (ESRD) of unknown etiology, and he had received regular hemodialysis (HD) three times a week for 5 years and hypertension treatment for 1 year. He also had a history of gastric ulcer and pancytopenia due to alcohol abuse. His usual medications included amlodipine (5 mg) once per day, folic acid, vitamin B complex, and a calcium-based phosphate binder with meals three times per day. The patient did not exhibit any obvious intradialytic hypotension previously or during the last HD session according to HD records. His usual intradialytic systolic blood pressure was around 125–145 mmHg. After the last HD session, he and his younger brother drank a home-made cocktail fruit juice at a friend’s house and both experienced severe watery diarrhea since that night. But, the condition of healthy younger brother got improved by initial treatment of ED and was discharged later. On examination, the patient’s initial supine blood pressure was 95/32 mmHg, his temperature was 37.5 °C, his pulse rate was 117/min, and his respiratory rate was 22/min and tachypnic, but with clear breath sounds in both lungs. Abdominal examination revealed increased bowel sounds and mild tenderness of both lower quadrants without rebound tenderness or muscle guarding. Laboratory findings included a white blood cell count of 3900/μL; bands, 16%; hemoglobin, 14.7 g/dL; platelets, 99000/μL; blood urea, 41 mg/dL; creatinine, 8.6 mg/dL; and an aspartate amino-transferase (AST) level of 214 IU/L. An arterial blood gas analysis showed severe metabolic acidosis with respiratory compensation. A plain X-ray of the abdomen was nonsignificant. Despite an initial 1 h of resuscitation effort, his condition worsened to hypotension of 73/25 mmHg and acute respiratory failure, and he was admitted to the intensive care unit (ICU) for unknown sepsis with shock. Aggressive resuscitation including empirical antibiotics with cefepime 1 gram q24 h and teicoplanin 6 mg per kilogram q12 h three loading doses and maintainance q72 h doses were given. Hypotension with shock, drowsy consciousness, and diarrhea subsided within 6 h after admission, but intermittent fever and abdominal symptoms persisted. The patient demonstrated progressive abdominal distension, tenderness of the right lower quadrant, and muscle guarding. Follow-up laboratory findings showed a white blood cell count of 4100/μL; bands, 31%; procalcitonin, 402 ng/mL; and a lactate dehydrogenase (LDH) of 5303 IU/L. Metronidazole 250 mg q6 h was added to current regimen for better coverage of anaerobic bacteria. Computed tomography (CT) of the abdomen disclosed wall thickening and edematous change of distal ileum loops that were indicative of ischemic bowel (Figure 1). Consequently, an emergent laparotomy with surgical resection of a 10.5-cm necrotic segment of the terminal ileum was performed 48 h after admission. The pathology found multiple areas of hemorrhage and tissue necrosis, which were most prominent in the mucosa (Figure 2). The visible mesenteric artery was nonoccluded (Figure 3) and did not show evidence of thrombosis or embolism. These findings were compatible with NOMI. Two sets of preantibiotic blood cultures and all stool cultures did not grow bacteria. After his stay in the ICU, he was discharged 1 month later. Discussion Although NOMI comprises about 20% of all cases of mesenteric ischemia,1 it is notorious for its high mortality rate due to delays in diagnosis or misdiagnosis. In the majority of patients actually dying from NOMI, intestinal infarction is rarely suspected, even at the time of the patient’s death.6 Nevertheless, NOMI is increasingly recognized as a lethal complication in the dialysis population owing to the escalating number of elderly ESRD patients with atherosclerotic cardiovascular disease who are chronically dialyzed. The estimated incidence of NOMI in the HD population is up to 1.9% per patient-year, in contrast to a 0.2% value for the non-HD group.5 The dialysis population is susceptible to development of NOMI because they share many predisposing factors, including advanced age, widespread atherosclerosis, diabetes mellitus, long-standing hypertension, and the use of drugs causing mesenteric vasoconstriction.3 Other causes of mesenteric vasospasms are dehydration, septicemia, various forms of shock, and hypotension after a major operation.7 In addition, prolonged exposure to calcium-based phosphate binders and high-dose vitamin D analogues in dialysis patients can result in calcification of their arteries.3 Our patient had underlying hypertension, was a chronic smoker, and had undergone a long duration of HD, and these conditions may have predisposed him to develop nondistensible and calcified vessels. Hypotension, especially repeated episodes, is the most important and immediate precipitating factor for NOMI, particularly in HD patients, as they need to remove large volumes of intravascular fluid, resulting in relative hypovolemia.8 Previous studies2,3 have shown that all NOMI patients experienced severe hypotension before onset of abdominal pain. Although our patient did not suffer any obvious hypotension during previous HD sessions, he did suffer from severe diarrhea after his last round of HD. This would aggravate the already decreased intravascular fluid volume typically seen during the immediate postregular HD period. The subsequent hemoconcentration, which was evident by the patient’s high hemoglobin level of 14.7 g/dL compared with the previous month’s value of 10.7, might have led to hypoperfusion in splanchnic vessels. Moreover, sepsis with hypotension on arrival to ED might be another inciting factor for already vulnerable mesenteric circulation, increasing vasospasm and resulting in NOMI. Clinical presentation of NOMI is variable and is dependent on the severity and presence of collateral circulation or lack thereof.8 Most often, abdominal pain begins in the right iliac fossa8,9,10 because the right colon, which is supplied by the superior mesenteric vessel, is more vulnerable to ischemic insult than is the left colon, which has collateral circulation due to the Drummond artery.11 Pain is followed by abdominal guarding, and previous studies have described a high incidence of abdominal guarding upon presentation.2,3,8 Pain is often accompanied by fever, leukocytosis, and metabolic acidosis. Unexplained abdominal distension and/or gastrointestinal bleeding may be the earliest signs of impending bowel infarction if pain is not relevant initially.8 Our patient, after an uneventful HD session, experienced severe watery diarrhea at home followed by pain in the bilateral iliac fossae, which later shifted to the right lower quadrant. Although the patient presented with a nonsurgical abdomen to the ED, his symptoms of fever, drowsy consciousness and relative hypotension all had pointed out a clinical sepsis syndrome might have been happening to him at the outset. Then, his clinical condition worsened quickly within 24 h of admission, and diffuse abdominal distension and muscle guarding became prominent. Therefore, another possible disease course was that there might be enterocolitis induced sepsis process first happened in our patient before appearance of NOMI symptoms. Nonspecific laboratory clues for early suspicion of NOMI include unexplained leukocytosis and/or lactic acidosis and rising LDH.3 Positive findings on plain abdominal X-rays are found in only 20–60% of cases and indicate a late stage of the course.12 Our patient’s initial plain film was not informative. Angiography can exclude occlusive causes but is usually of little help for diagnosis of mesenteric vasospasm.4 Enema abdominal CT scan findings of thickening fatty tissues around the involved bowel segment, together with gas in the edematous bowel wall, could lead to early diagnosis and initiate timely surgical treatment.8 The CT finding in our patient was highly suggestive for small bowel ischemia. Concerning therapy, it is important to correct any underlying cause of shock first, with aggressive resuscitation before any diagnostic or therapeutic tests are performed. Our patient’s hypovolemic shock was recovered after resuscitation within 6 h of admission, but bowel ischemia may be persisted because the onset of ischemia may have been much earlier since he had already experienced severe diarrhea for 2 days. If peritoneal signs are present or ischemia time exceeds 12 h, surgical resection is the treatment of choice.2 Methods of NOMI prevention include control of predisposing factors, such as prevention of intradialytic hypotension by avoidance of rapid ultrafiltration.4 When an HD patient encounters an episode of acute intravascular volume depletion in the form of severe diarrhea or vomiting, an appropriate strategy might be to initiate volume repletion first, before HD, and then to start HD without ultrafiltration. In conclusion, NOMI should be considered as a differential diagnosis for abdominal pain in HD patients if there have been hypotensive episodes during treatment or if other conditions of acute intravascular volume depletion, such as profound diarrhea or vomiting, are evident. Early diagnosis of predisposed patients is the cornerstone of survival of this fatal disorder in chronic HD patients. References 1. Montgomery RA, Venbrux AC, Bulkley GB: Mesenteric vascular insufficiency. Prob Surg 1997; 34:941–1028. 2. John AS, Tuerff SD, Kerstein MD: Nonocclusive mesenteric infarction in hemodialysis patients. J Am Coll Surg 2000; 190:84-88. 3. Ori Y, Chagnac A, Schwartz A, Herman M, Weinstein T, Zevin D, et al: Non-occlusive mesenteric ischemia in chronically dialyzed patients: a disease with multiple risk factors. Nephron Clin Pract 2005; 101:c87–93. 4. Zeier M, Wiessel M, Rambausek, Ritz E: Non-oclusive mesenteric infarction in dialysis patients: the importance of prevention and early intervention. Nephrol Dial Transplant 1995; 10: 771-773. 5. Archodovassilis F, Lagoudiannakis EE, Tsekouras DK, Vlachos K, Albanopoulos K, et al: Nonocclusive mesenteric ischemia: a lethal complication in peritoneal dialysis patients. Perit Dial Int 2007; 27:136–141. 6. Acosta S, Ogren M, Sternby NH, Bergqvist D, Bjorck M: Fatal nonocclusive mesenteric ischaemia: populationbased incidence and risk factors. J Intern Med 2006; 259: 305–313. 7. Trompeter M, Brazda T, Remy CT, Vestring T, Reimer P: Nonocclusive mesenteric ischemia: etiology, diagnosis, and interventional therapy. Eur Radiol 2002; 12:1179–1187. 8. Bassilios N, Menoyo V, Berger A, Mamzer MF, Daniel F, Cluzel P, et al: Mesenteric ischaemia in haemodialysis patients: a case/control study. Nephrol Dial Transplant 2003;18:911–917. 9. Charra B, Cuche J, Ruffet M, Terrat JC, Beurlet J, Labrosse H, et al: Segmental necrosis of ascending colon in haemodialysis patients. Nephrol Dial Transplant 1995; 10:2281-2285. 10. Brener ZZ, Bergman M, Ohm HK, Winchester JF: Acute non-occlusive mesenteric ischemia of the small bowel in a patient started on hemodialysis: a case report. Cases J 2008;1(1):217-220. 11. Landreneau RJ, Fry WJ: The right colon as a target organ of non occlusive mesenteric ischemia. Arch Surg 1990; 125:591-594. 12. Howard TJ, Plaskon LA, Wiebke EA, Wilcox MG, Madura JA: Nonocclusive mesenteric ischemia remains a diagnostic dilemma. Am J Surg 1996; 171:405–408. Figures Figure 1: Abdominal computed tomogram (CT) shows bowel wall thickening and edematous change of distal ileum loops (arrows), indicative of ischemic bowel. Figure 2: Histopathology slide ( hematoxylin and eosin x 100 magnifications ) of terminal ileum mucosa reveals multiple areas of hemorrhage (arrows) and tissue necrosis (arrowheads). Figure 3: Histopathology section ( hematoxylin and eosin x 40 magnifications ) shows the nonoccluded mesenteric artery ( left ) and congestion within the lumen of vessels.