Key points are not available for this paper at this time.
This algorithm was developed by the Journal of Trauma and Acute Care Surgery Emergency General Surgery Algorithms working group,1 to guide the management of acute mesenteric ischemia (AMI) in adult patients. It is based on published peer-reviewed evidence and expert opinions of the working group and represents a safe and sensible approach that can be implemented at most centers. The algorithm (Fig. 1) is annotated with letters; the corresponding text includes rationale and citations of supporting data. This article is not a comprehensive summary of the literature, and the algorithm is not a substitute for the clinical judgment and experience of the bedside clinician; it should not be considered the “standard of care.” We recognize that there will be patient, personnel, institutional, and situational factors that may warrant or require deviation from the algorithm, and we encourage institutions to use these recommendations to formulate local protocols. The annotated algorithm is intended to (a) serve as a quick bedside reference for clinicians, (b) foster more detailed patient care protocols that will allow for prospective data collection and analysis to identify best practices, and (c) generate research projects to answer specific questions concerning decision making in the management of adults with AMI.Figure 1: Algorithm for the diagnosis and management of AMI.Acute mesenteric ischemia is a life-threatening condition that is increasing in prevalence as the population ages. Acute mesenteric ischemia includes acute mesenteric arterial embolism or thrombosis, nonocclusive mesenteric ischemia (NOMI), and mesenteric venous thrombosis (MVT). Approximately 1% of patients with acute abdomen have AMI, but among those older than 70 years, it may be as high as 10%.2 In one Finnish study, AMI was the most common etiology of acute abdominal pain in patients older than 75 years.3 Prompt clinical recognition and intervention are critical, as ischemic injury to the bowel can rapidly progress to intestinal necrosis, sepsis, multiple-organ failure, and death. The overall mortality associated with AMI exceeds 50% and doubles with every 6 hours of delay in treatment.4 The current algorithm (Fig. 1) is conceptually based on “six R's”: Recognize, Resuscitate, Reflect, Revascularize, Resect, and Reevaluate. While some acute care surgeons may manage all aspects of the treatment, in many institutions, a multidisciplinary approach is followed, which may involve general and vascular surgery, interventional radiology, and critical care specialists. RECOGNIZE A. Early diagnosis of AMI can be challenging, as the symptoms often mimic other abdominal pathologies. A complete history and physical examination will help establish the differential diagnosis. Severe poorly localized midabdominal pain is a hallmark of AMI; in the absence of peritonitis on examination, this constitutes the classic “pain out of proportion to physical findings.” The abrupt onset of pain is consistent with acute arterial occlusion, whereas NOMI or MVT may have a more insidious presentation. A history of postprandial pain, weight loss, and food fear is consistent with chronic mesenteric ischemia, which may progress to acute arterial thrombosis. Atrial fibrillation is a common underlying etiology of embolic AMI. Nonocclusive mesenteric ischemia is due to low cardiac output, vasoconstriction, or hypovolemia. It may be seen in hospitalized critically ill patients or in patients presenting to the emergency department with severe recent illness that might have led to sepsis or dehydration. Mesenteric venous thrombosis is typically seen in patients with one or more of Virchow's triad (stasis, hypercoagulability, endothelial damage), which may be associated with diseases such as pancreatitis, inflammatory bowel disease, portal hypertension, and liver disease; it may also be seen after splenectomy or bariatric surgery.2,4 B. Laboratory tests are invariably obtained in patients with acute abdominal pain, but it is important to recognize that no biomarkers are adequately sensitive or specific enough to diagnose or exclude AMI.5 A complete blood count and comprehensive chemistry panel can help identify inflammatory and metabolic disturbances. Lactate and D-dimer tests may be helpful if they are abnormal. Lactate level is often obtained in the setting of abdominal pain or sepsis and is frequently elevated in patients with AMI; lactate >2 mmol/L is associated with increased mortality. However, a normal lactate does not exclude AMI or obviate the need for diagnostic imaging in the appropriate clinical setting.2,4–7 The D-dimer has low specificity but high sensitivity, and a normal level is reassuring but cannot be completely relied upon.2,4,5 Noteworthy pitfalls in laboratory testing include the findings of elevated amylase or troponin I levels. They can both be elevated in the setting of AMI and may incorrectly lead the clinician toward a diagnosis of pancreatitis or acute coronary syndrome.2,4,8,9 C. Plain x-rays or ultrasonography have little role in diagnosing AMI. The standard for diagnosis is contrast-enhanced multidetector row computed tomographic angiography, which can diagnose and allow differentiation between intestinal ischemia subtypes. Computed tomographic angiography should be obtained without delay in patients who present with signs and symptoms highly suggestive of AMI. The optimal protocol includes nonenhanced acquisition followed by biphasic contrast-enhanced phases with a delay of 30 seconds for the arterial phase and 60 to 70 seconds for the venous phase; the optimal thickness of image acquisition is 1 to 2 mm.10 Multiplanar reconstruction and maximum intensity projection can help identify vessel thrombosis and reduced bowel wall enhancement.10 Oral contrast is discouraged, as it delays time to imaging and obscures the bowel wall.2,4,10 For patients with acute or chronic kidney disease or risk of contrast-induced nephropathy, computed tomographic angiography is still recommended, given the critical consequences of the diagnosis, to improve diagnostic accuracy and chances of survival.2,4,10 RESUSCITATE D. All patients suspected of AMI should be promptly resuscitated to reverse shock and perfuse all organs, including the gut. This includes correcting electrolytes and other metabolic disturbances. Resuscitation should be based primarily on volume loading, as essentially all vasopressors are themselves associated with AMI.11 Early assessment with echocardiography will help identify a cardiogenic component to hypoperfusion. Intestinal ischemia leads to loss of mucosal barrier function and, theoretically, bacterial translocation and sepsis. Although the evidence base is relatively sparse, broad-spectrum antibiotics are recommended for patients with AMI.2,4,12 Additionally, patients should receive nasogastric tube decompression and bowel rest to decrease intestinal metabolic demands.2,4 REFLECT E. An understanding of expected outcomes and careful consideration of patient preferences and goals of care is crucial to shared decision making in patients with AMI. Many factors are associated with “poor outcomes,” including tachycardia, respiratory distress, organ failure, creatinine >1.7, lactate >2, absent bowel wall enhancement, peritoneal effusion, and ileal or multisegment bowel involvement;13,14 American Society of Anesthesiologists score >3;15 and the need for open surgical intervention or open abdomen.16 The American Association for the Surgery of Trauma grading scale for mesenteric ischemia,17 based on the degree of intestinal ischemia, is useful in classifying disease severity. However, Sindall et al.14 were unable to correlate grades with outcomes and emphasized the fraught nature of prognostication in AMI based on presenting findings alone. Lengthy discussions about prognosis are premature and potentially counterproductive during the early (i.e., diagnosis and resuscitation) phase, as time is of the essence and the extent of vascular disease and nonsalvageable bowel may not be definitively known. However, gaining an early understanding of the patient's preferences can help to guide subsequent interventions and intraoperative decision making. Although every effort should be made to ascertain the patient's wishes and goals of care before operative intervention, this is not always possible. When confronted with extensive intestinal necrosis, the surgeon should not hesitate to seek intraoperative consultation with surrogate decision-makers or other surgeons if there is uncertainty about how to proceed. If no surrogate is available, the surgeon must make a judgment. Extensive midgut necrosis in a frail 90-year-old with multiple-organ failure is unlikely to result in survival to hospital discharge, so it is probably appropriate to close the abdomen without resection. On the other hand, a younger healthier patient who has experienced a sudden catastrophic loss of intestine may be a candidate for small bowel transplantation or may still value life even if dependent on parenteral nutrition, so resection is likely appropriate. The surgeon needs to provide medically appropriate care but not feel compelled to pursue interventions that will not benefit the patient. Involvement of hospital ethics or appropriate care committees may be necessary or helpful prior to intervention if time allows or if the patient survives the initial operation and faces a difficult ICU stay. REVASCULARIZE Early and effective revascularization can significantly reduce mortality and improve patient outcomes. In most cases, we recommend completing revascularization prior to making decisions on bowel resection; exceptions are discussed hereinafter. Acute mesenteric ischemia generally falls into one of four categories (arterial embolism, arterial thrombosis, NOMI, and MVT), the relative distribution of which depends upon the patient population being served in an individual hospital. The revascularization approach and subsequent steps depend on the type of insult and the patient's physiology. Anticoagulation should be considered at the time of diagnosis unless there is an absolute contraindication. F. Arterial embolism accounts for roughly 25% of all AMI diagnoses and has been decreasing in recent decades.4,18 The source of the embolus is typically the heart or the aorta; approximately 50% of patients have concurrent atrial fibrillation, and 33% have a history of previous emboli.19,20 Emboli typically lodge at points of normal anatomic vessel narrowing, and the superior mesenteric artery (SMA) is commonly involved because of its relatively large diameter and low takeoff angle.4 More than 20% of SMA emboli are associated with concurrent emboli, most commonly to the kidney and spleen.21 For arterial embolism, embolectomy is generally preferred.2,4,22 Thrombolytic therapy is an option, but it is not recommended as it may take hours to days to lyse clot and risks progression of bowel ischemia. Postintervention antiplatelet or anticoagulant therapy may be beneficial in the setting of small-vessel thrombosis and is recommended as long as the source of potential emboli remains.20 G. Arterial thrombosis has increased in recent decades, accounting for about 40% of all cases.4,18 The gradual formation of plaque can eventually progress to critical stenosis with thrombosis of mesenteric vessels, and patients with acute on chronic disease will often have concurrent atherosclerosis and stenosis of the celiac artery.4 Thrombosis typically occurs at the origin of the celiac trunk, SMA, and inferior mesenteric artery.2 Endovascular treatment options include thrombectomy and angioplasty with or without stenting.2,22 Compared with open techniques, endovascular revascularization is associated with lower short -and long-term mortality; however, there is no significant difference in the need for second-look laparoscopy or laparotomy.23–25 If bypass is performed, antegrade is preferred over retrograde because of a lower reintervention rate.2,26 If the patient has shock, peritonitis, or evidence of bowel necrosis on CT, then a joint procedure is recommended, including open revascularization, to reduce time to resection of necrotic intestine.15,25,27,28 H. Nonocclusive mesenteric ischemia is increasing, representing about 25% of AMI cases.4,18 If there is no evidence of necrosis on CT, the recommended treatment is resuscitation to improve organ perfusion, considering the possible use of vasodilators.2,4 Both papaverine and prostaglandin E1 are associated with decreased mortality and need for surgical intervention.2,29–31 Early exploration is not recommended; it should be reserved for circumstances that strongly suggest full-thickness necrosis and impending perforation. With improved perfusion, even very significant ischemic changes may be reversible. However, if the patient has recalcitrant shock, exploration via laparoscopy or laparotomy is necessary to exclude necrotic intestine. It may not be clear on initial evaluation if a patient's gut is dying because of systemic critical illness or vice versa; these situations warrant discussion of goals of care before intervention. I. Venous thrombosis makes up 10% of AMI cases.4,20 The first-line treatment is systemic anticoagulation and bowel rest. Pharmacologic thrombolysis and mechanical thrombectomy may be useful adjuncts in patients without signs of bowel necrosis who do not have an adequate response to anticoagulation. It may be performed via percutaneous transhepatic, transjugular, or transfemoral approaches or by direct venous cannulation intraoperatively. There are no controlled studies of these techniques, and they are considered experimental at this time.32 Similar to patients presenting with NOMI, exploration should be undertaken only in circumstances such as persistent shock, peritonitis, or evidence of full-thickness bowel necrosis or perforation on CT.2,4,15,25,27,28 RESECTION J. Timely resection of necrotic bowel is critical to eliminate the source of toxic inflammatory mediators and bacterial translocation. On the other hand, abdominal exploration should not delay revascularization if the bowel may be salvageable. The decision to do sequential versus joint procedures is based on several factors, including whether the management is shared between acute care/general surgeon and vascular surgeon/interventional radiologist or whether the procedures will all be done in a single hybrid operating room (OR) versus different sites (e.g., interventional radiology and OR). A hybrid OR is the preferred site given the ability to revascularize and explore/resect without having to move the patient.4 There are several signs of bowel necrosis on imaging. Absence of bowel wall enhancement is indicative of cessation of arterial flow and is specific for AMI.10 Paper-thin hypo-enhancing bowel wall can be an early finding, and mesenteric stranding and ill-marginated bowel wall with peritoneal effusion can be late findings.10 Bowel wall thickening, common in ischemia, is nonspecific for necrosis.6,10 Other concerning findings include vascular filling defects, ascites, portomesenteric venous gas, and pneumatosis; however, none are specific to AMI, and up to 60% of pneumatosis findings are benign.6,10,22 Necrotic bowel in the setting of peritonitis and shock necessitates immediate resection to prevent further systemic complications. Intraoperatively, surgeons should assess bowel viability through appearance and color, visible and palpable pulsation in the mesenteric arcade, peristalsis, and bleeding from cut surfaces. Adjuncts such as pulse oximetry/photoplethysmography, electromyography, Doppler ultrasonography, fluorescein flowmetry, and near-infrared imaging- for example, fluorescence angiography using indocyanine green- can all be used to evaluate the integrity of intestinal perfusion.4,13,33 To date, none of them have proven superior to clinical judgment.4,33 However, emerging data suggest that fluorescence angiography using indocyanine green may be a useful adjunct. For example, in one case series of 42 patients with mesenteric ischemia, management was changed in 40% of patients based on the fluorescence assessment.34 More research is needed in this area. If adjuncts are unavailable, it is safe to conclude that atonic bowel with bluish discoloration should be resected.2,4 It is safer to err on the side of resecting a few more centimeters to avoid anastomotic or staple line dehiscence. REEVALUATION K. After initial treatment, patients with AMI should be continuously monitored and assessed for signs of recurrent or ongoing ischemia. Our general practice is to perform a second look 12 to 24 hours after the first operation to check intestinal viability.2,4,28,35 This should allow the newly revascularized intestine time to regain perfusion and will not let necrotic intestine sit too long before resection. This structured approach can help improve the chances of favorable outcomes by systematically addressing the multifaceted aspects of AMI management. Long-term Outcomes The long-term outcomes of AMI are heavily influenced by the extent of intestinal damage, the timing of intervention, and the patient's underlying health status. For those who survive the acute phase, the prognosis varies widely.13,15,16,35,36 Patients who undergo timely revascularization and have minimal bowel necrosis may recover with preserved bowel function, although they may face ongoing challenges such as nutritional deficiencies or bowel dysfunction. In contrast, individuals who require extensive bowel resection due to irreversible ischemic damage can experience significant long-term complications, including short gut syndrome, malabsorption, and dependence on parenteral nutrition. The minimum length of small bowel sufficient to reliably process enteral nutrition is generally 50 cm with and 100 cm without an intact ileocecal valve.2 However, tolerance of enteral nutrition is also related to adaptive changes in the small bowel, the length of remaining colon, and the presence of intestinal disease/malabsorption.37 Through adaptation, the remaining small bowel will become hypertrophic with enlarged villi and increased absorptive capacity, which can take up to 1 year.2 Quality of life on home parenteral nutrition can be moderate to good, and the surgeon should not feel pressured to make an intraoperative assessment of nonsurvivability prior to having a goals of care discussion with the patient or surrogate decision-makers.2,38 Performance of a damage-control procedure with temporary abdominal closure may allow time for such discussions to occur before determining the ultimate clinical course. Survivors of AMI are at increased risk of developing chronic conditions such as chronic pain, bowel obstructions, and recurring ischemic events. After thrombotic arterial occlusion, patients should be maintained on lifelong statin and antiplatelet therapy.20 After embolic AMI, patients should receive lifelong vitamin K antagonist or oral anticoagulant drugs (i.e., direct thrombin For venous thrombosis, if the diagnosis was to a patients need anticoagulation for to 6 however, if there is proven or patients will require lifelong For a patient who mesenteric artery or if there is no of the is 1 at 6 12 and then A contrast is if recurrent symptoms or a in on is After antiplatelet therapy is To bleeding single therapy is recommended for the long the long-term for AMI is to the extent of initial the of surgical and the management of subsequent complications, making a comprehensive and multidisciplinary approach for and of
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