Nonocclusive Mesenteric Ischemia H.S. Bassiouny Acute mesenteric ischemia and intestinal gangrene can result from arterial embolization, arterial or venous thrombosis, or nonocclusive mesenteric ischemia (NOMI). NOMI is a condition characterized by primary splanchnic vasoconstriction of a patent arterial tree and is commonly associated with low cardiac output and flow states. Paradoxically, NOMI has also been reported following successful mesenteric revascularization. Intestinal gangrene in association with heart failure was first described by Ende in 1958, and subsequent reports attributed NOMI as a cause of approximately 20% of cases of acute mesenteric ischemia, with mortality rates up to 70%. Risk factors for NOMI include suboptimal cardiopulmonary bypass, shock states, and the use of vasoconstrictive agents (e.g., digoxin, α-adrenergic agents, vasopressin), some of which are obsolete in current clinical practice. The prevalence of NOMI appears to be declining. This is likely attributed to advances in critical care, emergence of novel vasoactive drugs, accurate assessment of cardiac preload and afterload, and a higher index of clinical suspicion for this disease entity. Undiagnosed NOMI and failure to relieve splanchnic arterial vasospasm is invariably fatal. Pathophysiology NOMI was initially described as a postmortem small intestinal gangrene in patients without evidence of arterial or venous occlusive disease. Such observations formed the basis for the hypothesis that heart failure, peripheral hypoxemia, paradoxical splanchnic vasospasm, and reperfusion injury could all contribute to its development. Mesenteric vasospasm, usually in the superior mesenteric artery (SMA) distribution, is a sine qua non of NOMI. It can result from excessive sympathetic activity during cardiogenic shock or hypovolemia, and it represents a homeostatic mechanism that attempts to maintain cardiac and cerebral perfusion at the expense of blood flow to the visceral and peripheral organs. Vasopressin and angiotensin are the likely neurohormonal mediators of this process. In experimental models, angiotensin-converting enzyme (ACE) inhibitors appear to prevent NOMI and are more effective than α-adrenergic agonists. The intestinal circulation possesses extensive protective mechanisms to preserve oxygen delivery to tissues. Over a wide range of blood pressure, intestinal blood flow can be maintained as a result of an autoregulatory response mediated by local and systemic factors leading to arteriolar smooth muscle relaxation and vasodilation. Below a critical pressure of 40 mm Hg, oxygen consumption declines and ischemia ensues. Intestinal ischemia begins at the mucosal villus tip and over hours extends to the remainder of the mucosa, submucosa, and muscularis. Although intestinal autoregulation can initially offset reductions in blood flow, this adaptive response is self-limited, lasting for only several hours. Vasospasm ensues and can persist even after optimal blood flow is restored and the initiating event is corrected. The exact mechanism of persistence of vasospasm is unknown, but it plays an important role in the development and maintenance of occlusive and nonocclusive mesenteric ischemia as well as reperfusion phenomena complicating mesenteric revascularization. Digitalis, now rarely prescribed, has historically been associated with the development of NOMI. In early series of patients, digitalis use was noted in a majority of patients with this diagnosis. Digoxin preparations have been shown to induce experimental in vitro and in vivo vascular smooth muscle contraction. In the current era, vasoactive medications such as epinephrine, norepinephrine, and vasopressin have also been associated with the development of NOMI. Studies of reperfusion injury after mesenteric ischemia can further delineate mechanisms relevant to NOMI. As a consequence of restoration of oxygenated blood flow to hypoxic tissues, release of reactive oxygen species can result in significant cellular membrane injury, increased capillary permeability, and connective tissue degradation. Subsequent failure of intestinal autoregulation and paradoxical vasoconstriction can ensue, resulting in tissue injury. The degree of ischemia–reperfusion injury appears to be related to the frequency as well as duration of ischemic episodes. Clark and Gewertz demonstrated that two 15-minute periods of low flow followed by reperfusion resulted in more severe histologic injury than a singe 30-minute period of ischemia. NOMI results in an analogous scenario, where hypoperfusion may be partial and occasionally repetitive. Episodic reperfusion is thought to prime the ischemic tissue with leukocytes that are attracted to and produce reactive oxygen species. This concept is further supported by studies demonstrating attenuation of ischemia–reperfusion injury by reperfusion with leukopenic blood or blockade of endothelial cell surface receptors for leukocyte adherence. Reports of NOMI following elective mesenteric revascularization have associated this syndrome with reperfusion phenomena, further supporting reperfusion injury in the pathogenesis of NOMI. Clinical Presentation The clinical diagnosis of NOMI requires a high index of suspicion in elderly patients with any of the following risk factors: acute myocardial infarction with shock; congestive heart failure; arrhythmia; hypovolemia related to burns, sepsis, trauma, pancreatitis, or hemorrhage; and the administration of splanchnic vasoconstrictors such as α-adrenergic agents, vasopressin, or digitalis. Studies have indicated that NOMI also occurs at an increased rate in hemodialysis patients and may be associated with hypoperfusion occurring during dialysis. Early diagnosis of NOMI and treatment before intestinal infarction develops is the most important variable determining survival. Abdominal pain out of proportion to physical findings is characteristic of acute mesenteric ischemia, but this symptom is absent in 20% to 25% of cases of NOMI. When present, the pain is usually severe, but it may be variable in intensity, character, and location. The pain can become severe and constant as ischemia persists. The symptoms and signs may be unreliable because many patients are critically ill, ventilated, and obtunded. In the absence of pain, symptoms of unexplained abdominal distention and gastrointestinal bleeding may be the earliest signs of ischemia. Fever, diarrhea, nausea and vomiting, and diminished bowel sounds are other common but nonspecific manifestations. Diffuse or localized abdominal tenderness, rebound, and rigidity are ominous signs heralding transmural infarction and peritonitis. Occasional patients may present with shock or sepsis of unknown etiology. Only gold members can continue reading. Log In or Register to continue Share this:Click to share on Twitter (Opens in new window)Click to share on Facebook (Opens in new window) Related Related posts: Technical Aspects of Percutaneous Carotid Angioplasty and Stenting for Arteriosclerotic Disease In-Situ Treatment of Aortic Graft Infection with Prosthetic Grafts and Allografts Treatment of Acute Upper Extremity Venous Occlusion Intraoperative Assessment of the Technical Adequacy of Carotid Endarterectomy Stay updated, free articles. Join our Telegram channel Join Tags: Current Therapy in Vascular and Endovascular Surgery Jul 15, 2018 | Posted by admin in CARDIOLOGY | Comments Off on Nonocclusive Mesenteric Ischemia Full access? Get Clinical Tree
Nonocclusive Mesenteric Ischemia H.S. Bassiouny Acute mesenteric ischemia and intestinal gangrene can result from arterial embolization, arterial or venous thrombosis, or nonocclusive mesenteric ischemia (NOMI). NOMI is a condition characterized by primary splanchnic vasoconstriction of a patent arterial tree and is commonly associated with low cardiac output and flow states. Paradoxically, NOMI has also been reported following successful mesenteric revascularization. Intestinal gangrene in association with heart failure was first described by Ende in 1958, and subsequent reports attributed NOMI as a cause of approximately 20% of cases of acute mesenteric ischemia, with mortality rates up to 70%. Risk factors for NOMI include suboptimal cardiopulmonary bypass, shock states, and the use of vasoconstrictive agents (e.g., digoxin, α-adrenergic agents, vasopressin), some of which are obsolete in current clinical practice. The prevalence of NOMI appears to be declining. This is likely attributed to advances in critical care, emergence of novel vasoactive drugs, accurate assessment of cardiac preload and afterload, and a higher index of clinical suspicion for this disease entity. Undiagnosed NOMI and failure to relieve splanchnic arterial vasospasm is invariably fatal. Pathophysiology NOMI was initially described as a postmortem small intestinal gangrene in patients without evidence of arterial or venous occlusive disease. Such observations formed the basis for the hypothesis that heart failure, peripheral hypoxemia, paradoxical splanchnic vasospasm, and reperfusion injury could all contribute to its development. Mesenteric vasospasm, usually in the superior mesenteric artery (SMA) distribution, is a sine qua non of NOMI. It can result from excessive sympathetic activity during cardiogenic shock or hypovolemia, and it represents a homeostatic mechanism that attempts to maintain cardiac and cerebral perfusion at the expense of blood flow to the visceral and peripheral organs. Vasopressin and angiotensin are the likely neurohormonal mediators of this process. In experimental models, angiotensin-converting enzyme (ACE) inhibitors appear to prevent NOMI and are more effective than α-adrenergic agonists. The intestinal circulation possesses extensive protective mechanisms to preserve oxygen delivery to tissues. Over a wide range of blood pressure, intestinal blood flow can be maintained as a result of an autoregulatory response mediated by local and systemic factors leading to arteriolar smooth muscle relaxation and vasodilation. Below a critical pressure of 40 mm Hg, oxygen consumption declines and ischemia ensues. Intestinal ischemia begins at the mucosal villus tip and over hours extends to the remainder of the mucosa, submucosa, and muscularis. Although intestinal autoregulation can initially offset reductions in blood flow, this adaptive response is self-limited, lasting for only several hours. Vasospasm ensues and can persist even after optimal blood flow is restored and the initiating event is corrected. The exact mechanism of persistence of vasospasm is unknown, but it plays an important role in the development and maintenance of occlusive and nonocclusive mesenteric ischemia as well as reperfusion phenomena complicating mesenteric revascularization. Digitalis, now rarely prescribed, has historically been associated with the development of NOMI. In early series of patients, digitalis use was noted in a majority of patients with this diagnosis. Digoxin preparations have been shown to induce experimental in vitro and in vivo vascular smooth muscle contraction. In the current era, vasoactive medications such as epinephrine, norepinephrine, and vasopressin have also been associated with the development of NOMI. Studies of reperfusion injury after mesenteric ischemia can further delineate mechanisms relevant to NOMI. As a consequence of restoration of oxygenated blood flow to hypoxic tissues, release of reactive oxygen species can result in significant cellular membrane injury, increased capillary permeability, and connective tissue degradation. Subsequent failure of intestinal autoregulation and paradoxical vasoconstriction can ensue, resulting in tissue injury. The degree of ischemia–reperfusion injury appears to be related to the frequency as well as duration of ischemic episodes. Clark and Gewertz demonstrated that two 15-minute periods of low flow followed by reperfusion resulted in more severe histologic injury than a singe 30-minute period of ischemia. NOMI results in an analogous scenario, where hypoperfusion may be partial and occasionally repetitive. Episodic reperfusion is thought to prime the ischemic tissue with leukocytes that are attracted to and produce reactive oxygen species. This concept is further supported by studies demonstrating attenuation of ischemia–reperfusion injury by reperfusion with leukopenic blood or blockade of endothelial cell surface receptors for leukocyte adherence. Reports of NOMI following elective mesenteric revascularization have associated this syndrome with reperfusion phenomena, further supporting reperfusion injury in the pathogenesis of NOMI. Clinical Presentation The clinical diagnosis of NOMI requires a high index of suspicion in elderly patients with any of the following risk factors: acute myocardial infarction with shock; congestive heart failure; arrhythmia; hypovolemia related to burns, sepsis, trauma, pancreatitis, or hemorrhage; and the administration of splanchnic vasoconstrictors such as α-adrenergic agents, vasopressin, or digitalis. Studies have indicated that NOMI also occurs at an increased rate in hemodialysis patients and may be associated with hypoperfusion occurring during dialysis. Early diagnosis of NOMI and treatment before intestinal infarction develops is the most important variable determining survival. Abdominal pain out of proportion to physical findings is characteristic of acute mesenteric ischemia, but this symptom is absent in 20% to 25% of cases of NOMI. When present, the pain is usually severe, but it may be variable in intensity, character, and location. The pain can become severe and constant as ischemia persists. The symptoms and signs may be unreliable because many patients are critically ill, ventilated, and obtunded. In the absence of pain, symptoms of unexplained abdominal distention and gastrointestinal bleeding may be the earliest signs of ischemia. Fever, diarrhea, nausea and vomiting, and diminished bowel sounds are other common but nonspecific manifestations. Diffuse or localized abdominal tenderness, rebound, and rigidity are ominous signs heralding transmural infarction and peritonitis. Occasional patients may present with shock or sepsis of unknown etiology. Only gold members can continue reading. Log In or Register to continue Share this:Click to share on Twitter (Opens in new window)Click to share on Facebook (Opens in new window) Related Related posts: Technical Aspects of Percutaneous Carotid Angioplasty and Stenting for Arteriosclerotic Disease In-Situ Treatment of Aortic Graft Infection with Prosthetic Grafts and Allografts Treatment of Acute Upper Extremity Venous Occlusion Intraoperative Assessment of the Technical Adequacy of Carotid Endarterectomy Stay updated, free articles. Join our Telegram channel Join
