Download nonocclusive mesenteric ischemia

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 involves 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 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. 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.
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. 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. 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, 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, his clinical condition worsened quickly within 24 h of
admission, and diffuse abdominal distension and muscle guarding became prominent.
Therefore, mild abdominal signs on initial presentation do not rule out a diagnosis of
NOMI.8
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 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 was 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 diagnoses 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.
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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: The histopathology ( hematoxylin and eosin x 100 magnifications ) of
terminal ileum mucosa reveals multiple areas of hemorrhage and tissue necrosis.
Figure 3: Histopathology section ( hematoxylin and eosin x 140 magnifications ) of
mesenteric vessels shows non-occluded artery.