Version May 2024
INTRODUCTION — Spontaneous mesenteric artery dissection can occur because of instrumentation or as a spontaneous event. It can occur in conjunction with aortic dissection or in isolation. The focus of this review is spontaneous, isolated dissection of the mesenteric arteries, particularly of the superior mesenteric artery but also of the celiac axis; isolated inferior mesenteric artery dissection is rarely reported.
Acute aortic dissection is discussed separately. (See "Overview of acute aortic dissection and other acute aortic syndromes" and "Clinical features and diagnosis of acute aortic dissection" and "Management of acute type B aortic dissection".)
MESENTERIC VASCULAR ANATOMY — Spontaneous mesenteric artery dissection has a predilection for the superior mesenteric artery and also occurs in the celiac artery, though rarely in the inferior mesenteric artery. Combined superior mesenteric and celiac artery dissection can also occur. Interestingly, reports of celiac artery spontaneous mesenteric artery dissection indicate increasing frequency, which has been attributed to the increasing use of axial imaging for diagnosis [1].
Celiac axis — The celiac axis originates from the abdominal aorta at the level of the 12th thoracic vertebrae and provides blood flow to the structures arising from the primitive foregut (figure 1). The 10th primitive ventral segmental artery gives rise to the celiac axis [2]. The celiac axis is short, with its takeoff perpendicular to the aorta and perhaps slightly caudal. Most commonly, after a short course, the celiac axis branches to provide left gastric, hepatic, and splenic arteries; however, the pattern of branching can be highly variable.
Superior mesenteric artery — The superior mesenteric artery (SMA) originates from the abdominal aorta and provides arterial inflow to the structures of the midgut (figure 2). The SMA typically develops out of the 13th primitive ventral segmental artery; however, many aberrations can occur during development, resulting in a range of anomalies [2]. The origin of the SMA is located just below the origin of the celiac axis at the level of the first lumbar vertebrae. From its origin, the SMA courses anteriorly with varying degrees of angulation from the aorta for a distance of approximately 2 cm, after which it turns inferiorly, coursing along a similar axis to the aorta. Within this portion, the SMA has an outer wall and an inner wall, which has a bearing on the pathophysiology of SMA dissection. (See 'Etiologic factors' below.)
The SMA continues inferiorly, passing behind the splenic vein and pancreas but anterior to the duodenum. It is normally positioned anterior to the left renal vein (figure 3). The first branch arising from the SMA is typically the inferior pancreaticoduodenal artery (figure 4). The next branch is typically the middle colic artery. Thereafter, the SMA gives rise to multiple jejunal branches and then to right colic and ileocolic branches, which provide terminal branches that supply the intestines.
Collateral circulation — The SMA has collateral connections to the celiac axis and inferior mesenteric artery (IMA) (figure 5). The celiac axis pathway to the SMA is via the inferior pancreaticoduodenal artery and, in some individuals, via a persistent embryonic connection known as the arc of Bühler. The middle colic branch of the SMA connects to the IMA via the marginal artery of Drummond and via the meandering mesenteric artery, which is also known as the arc of Riolan [3,4].
DEFINITION AND PATHOPHYSIOLOGY — The arterial wall is composed of three layers. From lumen to exterior, these are the intima, media, and adventitia; the media is the thickest layer with the most number of and frequently separated layers. Vascular dissection refers to the phenomenon that occurs when a focal tear in the intima exposes the deeper layers of the artery and forcibly separates these layers [5].
Separation occurs longitudinally and circumferentially and is variable in extent, ranging from a short, focal intimal flap to a lengthy lesion that creates a true lumen and a false lumen. By definition, the true lumen of the artery is surrounded by all three vessel layers [6]. The dissection can remain focal or can progress to obliterate the true lumen or weaken the arterial wall, leading to arterial rupture [5]. The extent of the dissection (circumferential, longitudinal) and severity of lumen compromise determine the nature of the clinical manifestations. (See 'Clinical features' below.)
Manifestations of mesenteric artery dissection are most commonly related to lumen reduction with varying degrees of intestinal ischemia. Lumen reduction is caused by pressurization of the false lumen leading to compression of the true lumen. If flow is occurring through the false lumen, then flow in the true lumen is proportionately reduced with increasing impingement. However, multiple communications can occur between the true and false lumens, thereby allowing flow through the false lumen to contribute to distal perfusion. As the dissection propagates distally, branch vessels can also become compressed, leading to local ischemia and infarction despite minimal compromise of the main vessel [7].
Etiologic factors — Blood pressure, along with other factors (eg, flow vectors, mural defects) within the artery, contribute to the initiation and propagation of mesenteric artery dissection [8].
●Fluid pressure – The occurrence of the intimal tear and progression of the dissection are mediated by the presence of forces that overwhelm the tensile and adhesive strength of the arterial wall. With spontaneous mesenteric artery dissection, this force is produced in part by intra-arterial blood pressure. However, it should be noted that only a minority of patients with mesenteric artery dissection are hypertensive [9].
●Flow vectors – Dissection of the superior mesenteric artery (SMA) has been observed to begin on its anterior surface along the convex outer curvature just beyond its takeoff as it turns inferiorly. With the assistance of computer models, increased hemodynamic forces are consistently shown within this segment of the SMA [10,11]. One author has suggested that greater aortomesenteric angle is an important etiologic factor for SMA dissection. This seems plausible given the larger the angle, the more force being delivered through flow vectors into the arterial wall [12]. Similar conditions are present within the descending thoracic aorta occurring along the greater curvature of the aortic arch just distal to the takeoff of the subclavian artery, which may contribute to thoracic aortic dissection [13]. However, with SMA dissection, hypertension and histologic abnormalities are less frequently encountered, and thus this hemodynamic condition is regarded by some as the primary etiologic component. On the other hand, similar descriptions have not been offered for occurrence of dissection occurring in the celiac axis.
●Wall strength – Limited histologic evaluation is available for specimens of SMA dissection. Unlike aortic dissection, where wall abnormalities related to atherosclerosis, cystic medial necrosis, or connective tissue disorders have been associated with aortic dissection, no such abnormalities are commonly identified with mesenteric artery dissection. Myxoid degeneration of the dissected arterial has been reported in cases of SMA dissection [14]. In addition, another entity segmental arterial mediolysis known to affect the celiac and SMA has been associated with increased rates of dissection for these vessels as well as progression of dissection; follow-up imaging in these patients is encouraged [15].
EPIDEMIOLOGY AND RISK FACTORS — The true incidence of mesenteric artery dissection is unknown. One review identified 450 cases of spontaneous mesenteric artery dissection affecting the celiac artery in 200 and superior mesenteric artery in 250 [16]. With the increasing use of cross-sectional abdominal imaging, the incidence is likely to increase.
Patients tend to be in the fifth and sixth decades of life. Males are much more commonly affected than females [14,17-21]. In a systematic review, the majority of reported case series were from China, Japan, and Korea [19].
Typical risk factors for atherosclerosis (eg, hypertension, smoking, hypercholesterolemia) are usually absent [9]. Smoking and hypertension appear to have some correlation, though these are absent in the majority of cases.
CLINICAL FEATURES
Asymptomatic — Some cases may come to clinical attention due to an incidental finding of mesenteric dissection on computed tomography (CT) of the abdomen performed for reasons not related to the dissection, although this is thought to occur in a minority of patients. Asymptomatic patients represent a small group of patients with superior mesenteric artery (SMA) dissection, but the numbers may be increasing as axial imaging is increasingly being used to evaluate patients with suspected abdominal pathology.
Asymptomatic patients are more likely to present with low-grade dissection (ie, grade I) (see 'Classification' below) compared with symptomatic patients. In addition, asymptomatic patients are more often treated with observation alone and discharged home than patients with symptoms or complications [16]. (See 'Initial medical therapy and monitoring' below.)
Symptomatic — Symptoms and signs are directly related to the effects of the dissection (ie, pain from tissue separation, local hematoma, inflammation) or are from malperfusion leading to intestinal ischemia. Patients typically present with their first episode and will not report having similar episodes in the past [14].
Nearly all patients with symptomatic SMA dissection will present with abdominal, flank, and/or back pain. The prevalence of the SMA component in spontaneous mesenteric artery dissection appears higher in symptomatic than in asymptomatic patients, likely related to findings of longer affected vessel length and greater maximum percentage of stenosis when compared with asymptomatic patients [22]. Associated symptoms such as nausea, vomiting, and diarrhea may also be present but are often absent. Patients with celiac artery dissection present similarly, and differentiating between these is not possible without imaging. (See 'Vascular imaging' below.)
The pain is typically sudden in onset, severe in intensity, and located in the epigastric or periumbilical regions. It is not alleviated or aggravated by eating. Pain can be attributed to dissection alone without the occurrence of ischemia. However, pain that is characterized as out of proportion to the physical exam is suggestive of intestinal ischemia. The degree of pain has been correlated to both the extent of the dissection as well as the resulting ischemia.
Physical examination — While performing the survey, the clinician should note the patient's comfort level. Patients with mesenteric artery dissection are uncomfortable appearing and cannot remain still for very long. Findings on physical examination are minimal, at least initially. (See "Acute mesenteric arterial occlusion", section on 'Presentation and evaluation'.)
Laboratories — Routine laboratory studies are typically obtained for patients presenting with abdominal pain, including complete blood count, chemistry panel, liver function tests, amylase tests, lipase tests, lactate tests, and urinary analysis. However, these are nonspecific. Much of the laboratory examination will be completely normal in patients with mesenteric dissection, particularly early on, but laboratories are useful for ruling out other potential etiologies for abdominal pain, and certain abnormalities (eg, elevated lactate, elevated white blood count, elevated liver function tests) may suggest the occurrence of complications, such as intestinal ischemia or perforation [23]. (See "Evaluation of the adult with abdominal pain", section on 'Initial workup' and "Overview of intestinal ischemia in adults", section on 'Laboratory studies'.)
DIAGNOSIS — A specific diagnosis of mesenteric arterial dissection is often not initially suspected based on the clinical presentation, given the rarity of the condition. In less severe pain presentations, the diagnosis can be elusive, often resulting in a diagnostic delay, which increases the potential for the development of complications and medical deterioration of the patient. For patients suspected of having a vascular cause for abdominal pain, determining the specific etiology relies on advanced vascular imaging.
Vascular imaging — For patients who have undergone cross-sectional abdominal imaging (with or without intravenous contrast), the dissected portion of the vessel may be apparent depending upon the resolution of the scan. If another etiology for abdominal pain is not identified, we suggest high-resolution multislice computed tomographic (CT) angiography. In most centers, CT angiography is readily available and can be performed in most patients with minimal risk. However, in a subset of patients with allergy or renal dysfunction, the intravenous contrast load may be less desirable. Magnetic resonance (MR) angiography is an alternative.
CT angiography is highly sensitive for identifying intimal flaps of clinical significance and differentiating arterial dissection from atherosclerotic thrombotic occlusion or embolic occlusion. The anatomic findings for various vascular lesions have characteristic anatomic locations (first branch of the superior mesenteric artery [SMA] for embolism, atherosclerotic lesions at the origin of the SMA for thrombotic occlusion). (See "Overview of intestinal ischemia in adults" and "Acute mesenteric arterial occlusion", section on 'Presentation and evaluation'.)
The extent and severity of SMA or celiac artery dissection range from a small intimal flap to lengthy artery occlusion. CT angiography also shows the collateral flow around the dissected vessel, which can be important for anticipating the severity of clinical manifestations [24,25]. (See 'Classification' below.)
Catheter-based arteriography can also establish a diagnosis of SMA or celiac artery dissection and has the added advantage of providing hemodynamic information and potentially providing treatment. However, it is invasive and generally does not provide much information regarding nonvascular etiologies contained within the differential diagnosis. Thus, arteriography is generally reserved for patients shown to have mesenteric artery dissection and who have concerning radiographic features (eg, large intimal flap, lumen compromise, risk for rupture) that require additional diagnostic information or that may be considered for endovascular treatment. It may also be indicated in those who fail to improve in response to medical therapy. (See 'Treatment' below.)
Duplex ultrasonography can also be used to evaluate the mesenteric arteries but is highly operator dependent and often requires other confirmatory imaging [26]. However, at institutions that perform mesenteric ultrasonography routinely and with consistently good results, the examination can be incorporated into the diagnostic algorithm. A combination of duplex ultrasound and contrast-enhanced ultrasound may possibly be used in place of CT angiography for the surveillance of SMA dissection [27]. (See 'Follow-up and surveillance' below.)
Classification — A classification scheme has been proposed based upon the angiographic appearance and correlates with the clinical course (figure 6) [11].
●Type I lesions do not result in compromised distal flow. They represent lesions in which an intimal tear has occurred but the resulting dissection merely forms a septum that separates flow in the true lumen from flow in the false lumen, both of which contribute to uncompromised distal flow.
●Type II lesions result in compromised flow. These lesions occur when flow beyond the proximal tear between the true and false lumens is separated by the septum and there are no communications distally. Flow can persist into a false lumen but will continue to compromise flow in the true lumen, leading to decreased distal flow and ischemia. In addition, branch vessels in the region of dissection are at risk for compromise leading to local ischemia in the distribution of the affected branch.
●Type III lesions result in complete occlusion and cessation of flow through the dissected segment of artery. The distal flow depends completely on collateral pathways that reconstitute beyond the occlusion [11,14]. (See 'Collateral circulation' above.)
DIFFERENTIAL DIAGNOSIS — The differential diagnosis of mesenteric artery dissection as a cause of abdominal pain includes nonvascular and vascular etiologies. (See "Causes of abdominal pain in adults" and "Evaluation of the adult with abdominal pain", section on 'Initial workup'.)
The suddenness and severity of the abdominal pain combined with minimal initial physical findings provide a clue that suggests a vascular rather than another more typical etiology for abdominal pain, although this alone is not helpful in distinguishing mesenteric artery dissection from other vascular etiologies of intestinal ischemia. However, such a presentation in a younger patient without risk factors for embolism, nonocclusive ischemia, or thrombotic mesenteric occlusion may point toward mesenteric dissection, particularly among individuals who are Asian. Like patients with other etiologies of acute abdominal vascular syndromes, vascular imaging will demonstrate the anatomic problem. (See "Overview of intestinal ischemia in adults", section on 'Diagnosis' and 'Vascular imaging' above.)
TREATMENT — Spontaneous mesenteric artery dissection is an uncommon disease entity with a risk of mesenteric ischemia. Nonetheless, most patients with asymptomatic or symptomatic dissection can be treated medically, with only a small minority requiring emergency surgery. Patients have good long-term survival and symptom relief regardless of the type of treatment.
Endovascular treatment demonstrates higher rates of complete remodeling; however, medical therapy has been shown to have significantly shorter hospital stays, lower hospital costs, and similar cumulative rates of symptom relief. Open surgery for spontaneous mesenteric artery dissection is uncommonly needed and is associated with longer hospital stay and more complications but similar mortality compared with endovascular therapy. Thus, medical treatment remains the main strategy for uncomplicated symptomatic superior mesenteric artery dissection. Most patients who either fail medical therapy or present with bowel ischemia will be treated initially via an endovascular approach. Sakamoto type II inferior mesenteric artery dissection is a risk factor for incomplete superior mesenteric artery remodelling [28]. Open surgery is reserved for patients with the most severe complications or in those who do not have the anatomy to undergo an endovascular approach [28,29].
Initial medical therapy and monitoring — A majority of patients with spontaneous celiac artery and/or superior mesenteric artery (SMA) dissection will not require operative intervention [30-34]. For symptomatic patients not requiring immediate abdominal exploration, medical therapy should be initiated as soon as the diagnosis of SMA or celiac artery dissection is confirmed to prevent vessel thrombosis and to reduce the likelihood of progression [14]. Asymptomatic patients may also be considered for treatment. Treatment includes antithrombotic therapy, controlling blood pressure, and treatment of pain. (See 'Antithrombotic therapy' below and 'Blood pressure lowering' below and 'Pain control' below.)
In addition to specific treatment for mesenteric artery dissection, management includes bowel rest, fluid resuscitation, correction of electrolyte abnormalities, and possibly broad-spectrum antibiotics. Supplemental parenteral nutrition may be needed if the period of bowel rest required becomes prolonged. (See "Overview of intestinal ischemia in adults", section on 'Initial management'.)
Patients should undergo serial examination and follow-up imaging typically after 48 hours but prior to discharge. The majority of patients with symptomatic mesenteric artery dissection will be successfully managed with medical therapy. Failure of medical management occurs in 10 to 45 percent, with higher rates correlating with more severe or complex dissection (figure 6) [11] (see 'Classification' above). Combined celiac axis and SMA involvement has a higher failure rate, presumed to be due to compromised collateral flow between the two vessels [18]. Patients who fail to improve clinically or who worsen either clinically or radiographically should be considered for intervention [35]. (See 'Intervention' below.)
Antithrombotic therapy — The best strategy for treating spontaneous mesenteric artery or celiac artery dissection is not well defined; however, preventing thrombosis using antiplatelet therapy or anticoagulation appears to be beneficial. We place patients on aspirin and heparin initially. Once pain has resolved, we repeat imaging and, if there is any residual abnormality, the patient is transitioned to oral Vitamin K antagonist (eg, warfarin). If the artery shows interval remodeling, we maintain the patient on antiplatelet therapy alone with aspirin. However, others have suggested anticoagulation with vitamin K antagonists for one year as a standard regimen [36].
Blood pressure lowering — Medications to lower blood pressure and control heart rate are prescribed in a manner similar to the treatment of aortic dissection. Although hypertension is not commonly present in patients with mesenteric artery dissection, it is thought that local increased hemodynamic forces at least contribute to the pathophysiology. (See 'Definition and pathophysiology' above.)
Beta blockade followed by alpha blockade, if needed, appears to be the best strategy. Beta blockade is initiated to achieve the lowest allowable heart rate while avoiding symptomatic bradycardia. If pain and hypertension persist, an alpha blocker can be added to the regimen to achieve normotensive target. Our target blood pressure is 100 to 120 mmHg. Caution should be taken not to lower blood pressure to a point where intestinal perfusion becomes compromised. (See "Overview of acute aortic dissection and other acute aortic syndromes", section on 'Acute medical management'.)
Pain control — It is important to adequately control pain as this can contribute to hypertension, which in turn worsens pain in a positive feedback loop. We use short-acting intravenous agents that have minimal histamine release (eg, fentanyl). (See "Approach to the management of acute pain in adults".)
Intervention — Emergency intervention is warranted in patients for whom there is a concern for rupture and hemorrhage. Expeditious abdominal exploration is also indicated for patients who present initially with severe bowel ischemia (eg, peritonitis, free air) and for those patients who fail to improve or develop signs of worsening intestinal ischemia with initial medical management [37]. (See 'Initial medical therapy and monitoring' above.)
For patients with compromised distal perfusion and those with refractory pain but without signs of severe intestinal ischemia, the goal of intervention is to correct the arterial abnormality and restore distal perfusion prior to loss of bowel viability. This can be accomplished using an open surgical or endovascular approach or a combination of both. The approach depends upon the extent and location of the dissection [38]. Certainly, patients with potential loss of bowel viability should be considered for an open surgical approach. Vascular intervention will also be required for patients who develop mesenteric artery aneurysm (typically late aneurysm formation; diameter ≥2 cm) to prevent future rupture [10,39]. (See 'Aneurysm formation' below and "Treatment of visceral artery aneurysm and pseudoaneurysm".)
Although more invasive, early success rates for open surgical revascularization are similar to those of endovascular therapy, with both approaches having increased mortality for patients with symptomatic dissection who fail medical therapy [14,38]. However, the long-term patency for surgical revascularization appears superior. Therefore, each patient should be assessed individually on the basis of patient risk, anatomy, and status of disease to select the most appropriate form of therapy [21,40].
Open approach — An open surgical approach allows complete assessment of the bowel, which is not possible with an endovascular approach alone; however, when an open approach is deemed necessary (eg, emergency exploration for hemorrhage, free air), endovascular revascularization may still be possible using open, retrograde vascular access. Alternatively, laparoscopy can be used to inspect the bowel, and, if no issues are identified, an endovascular approach may be used. Laparotomy, rather than laparoscopy, may be safer and more expedient for evaluating the viscera in the face of grossly dilated bowel.
The extent and severity of intestinal ischemia, including the appearance of the abdominal contents (color, distention), peristalsis, arterial pulsations in the mesenteric arcades, and bleeding from cut surfaces, should be assessed. Areas of the intestine that are clearly nonviable (ie, full-thickness ischemia with dilated, dark, paralyzed bowel (picture 1)) and areas of impending or gross perforation should be quickly resected using a stapler to contain or prevent gross spillage.
Whether to restore distal perfusion depends on the perfusion of the remaining bowel at the time of abdominal exploration. Bowel of questionable viability that peristalses even a little should be left intact until after perfusion is restored, after which bowel viability should be reassessed. Instillation of fluorescein may aid with determining the level of bowel perfusion (picture 2).
Open surgical reconstruction is the best option for managing long SMA lesions and possibly occlusions that involve multiple branch vessels. One option is excision of the intimal flap with patch angioplasty. It is important to resect all of the septum proximally and achieve a satisfactory distal endpoint. Inability to address all of the proximal pathology will mandate surgical bypass. Vein conduit is preferred in most circumstances [21,40].
Surgical exposure depends on the vessel affected and extent of the arterial dissection.
●The celiac axis can be approached though an upper midline laparotomy. The left lobe of the liver is mobilized and retracted to the right. The lesser omentum is divided, allowing for retraction of the esophagus and stomach to the left. The aorta is palpated, and the overlying crural fibers are divided until the aorta is exposed. Dissection along the aorta inferiorly will intersect the takeoff of the celiac axis. Further dissection along the celiac axis itself will lead to the branch vessels [41].
●The first few centimeters of the SMA (picture 3) are best exposed via a medial visceral rotation either through a transabdominal or retroperitoneal approach. More distal exposure is limited by the pancreas and duodenum through this approach. Exposure of the SMA beyond the pancreas is best performed using an anterior approach. The omentum and transverse colon are retracted cephalad while the small bowel is moved to the right of the abdomen. The SMA is located at the base of the small bowel mesentery as it crosses the duodenum. Taking down the ligament of Treitz further facilitates exposure. The artery is positioned to the left and posterior in relation to the superior mesenteric vein [41].
Endovascular approach — Endovascular treatment is generally used for focal, proximal lesions without significant branch involvement, but it can be used for more extensive lesions in patients who are not felt to be good operative candidates. Endovascular stent placement is the most commonly used technique to reestablish lumen patency. Treatment may also be needed to address arterial vasospasm or thrombus. Direct infusion of papaverine has been reported with favorable results as an adjunct; however, experience with thrombolysis has produced marginal results [42].
It is unclear whether bare metal or covered stents should be used for the initial dissection, but, in the presence of mesenteric aneurysm, covered stent placement is required. (See "Treatment of visceral artery aneurysm and pseudoaneurysm".)
FOLLOW-UP AND SURVEILLANCE — Short-term imaging assessment during the initial episode and long-term imaging surveillance to observe for aneurysmal changes are warranted in patients with spontaneous mesenteric artery or celiac artery dissection [14,43].
The vessel undergoes remodeling, typically within the first 12 months (image 1). The arterial lesions resolve on follow-up computed tomography (CT) angiography in approximately 10 to 30 percent of medically treated patients while rarely experiencing progression of dissection [10,14,35]. In one study of 26 patients, improvement or complete resolution occurred in 8 patients [10]. In another review of 58 patients with superior mesenteric artery (SMA) dissection, complete resolution of radiographic findings occurred in 15 percent of patients [14]. Type I lesions were most stable, with a majority remaining without change. Type II and type III lesions ironically demonstrated the highest likelihood for achieving complete remodeling; however, rates were still low at 20 percent.
Aneurysm formation — Aneurysm formation and even arterial rupture are known delayed complications of SMA dissection [7,14,18,24,44-49]. This should not come as a surprise, as the primary pathophysiology involves the loss of arterial mural integrity.
Arterial dilation occurs in up to 25 percent of cases of SMA involvement and possibly at even higher rates for celiac artery involvement, given the proportionally higher rate of intervention for aneurysm [14,18].
Arterial dilation can also occur following interventions such as the open surgical technique of intimectomy and patch angioplasty as well as endovascular stent placement [14,18].
The treatment of celiac artery or SMA aneurysm is reviewed in detail separately. (See "Treatment of visceral artery aneurysm and pseudoaneurysm".)
MORTALITY — The main cause of death among patients with spontaneous superior mesenteric artery (SMA) or celiac artery dissection is intestinal gangrene and its consequences. Mortality for all patients who present with spontaneous SMA dissection is overall low (<1 percent) [14,35]. However, in a review of 58 patients, the mortality rate for those who required intervention due to failure of medical management was 18 percent [14].
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Intestinal ischemia".)
SUMMARY AND RECOMMENDATIONS
●Vascular dissection refers to the phenomenon that occurs when a focal tear in the intima exposes the deeper layers of the artery and forcibly separates these layers. Spontaneous mesenteric dissection has a predilection for the superior mesenteric artery (SMA) and also occurs in the celiac artery, but rarely in the inferior mesenteric artery. Combined SMA and celiac artery dissection can also occur. (See 'Definition and pathophysiology' above.)
●Mesenteric artery dissection is rare. Risk factors include male sex and older age. Risk factors for atherosclerosis are usually absent. Although blood pressure likely plays a role in the pathogenesis, only a minority of patients with mesenteric artery dissection are hypertensive. (See 'Epidemiology and risk factors' above.)
●Nearly all patients with SMA or celiac artery dissection will present with abdominal pain; asymptomatic presentations are rare. The severity and suddenness of abdominal pain in the face of minimal abdominal findings suggests a vascular rather than another etiology for abdominal pain. Such a presentation in a younger patient without risk factors for other vascular etiologies of intestinal ischemia (eg, embolism, nonocclusive ischemia, thrombotic mesenteric occlusion) may point to mesenteric dissection, particularly among patients who are Asian. (See 'Clinical features' above and 'Diagnosis' above and 'Differential diagnosis' above.)
●Computed tomographic (CT) angiography is highly sensitive for identifying intimal flaps of clinical significance and for differentiating arterial dissection from embolic or atherosclerosis-related thrombotic occlusion. CT angiography also shows the collateral flow around the dissected vessel, which can be important for anticipating the clinical course. A classification scheme of the extent of SMA dissection based upon the angiographic appearance also correlates with the clinical course. (See 'Diagnosis' above and 'Classification' above.)
●For patients with confirmed spontaneous mesenteric or celiac artery dissection without severe intestinal ischemia necessitating abdominal exploration, we suggest initial medical therapy, rather than any form of vascular intervention (Grade 2C). The aim of medical therapy is to prevent vessel thrombosis and to reduce the likelihood of progression. The majority of patients with mesenteric artery dissection can be successfully managed medically, which includes antithrombotic therapy, blood pressure lowering, and treatment of pain. Patients should undergo serial examination, with follow-up imaging typically after 48 hours but prior to discharge. (See 'Initial medical therapy and monitoring' above.)
●Failure of medical management occurs in 10 to 45 percent of patients. Higher failure rates are seen with combined celiac and SMA involvement, presumably because of a loss of collateral flow between the two vessels. Patients who develop signs of worsening intestinal ischemia with initial medical management also require abdominal exploration to evaluate the bowel and resect nonviable segments. Whether to restore distal perfusion depends on the perfusion of the remaining bowel at the time of exploration. (See 'Intervention' above.)
●The aim of vascular intervention is to restore distal perfusion prior to loss of bowel viability. This can be accomplished using an open surgical or endovascular approach, or a combination of both. (See 'Open approach' above and 'Endovascular approach' above.)
•Endovascular treatment is used primarily for focal proximal lesions without significant branch involvement; however, more extensive lesions can be treated in patients who are not felt to be good operative candidates. Endovascular stent placement is the most commonly used technique to reestablish lumen patency.
•Open surgical reconstruction is the best option for managing long lesions and possibly occlusions that involve multiple branch vessels. Open surgery includes excision of the intimal flap with patch angioplasty, or mesenteric bypass.
●Long-term imaging is warranted to monitor for resolution or aneurysm formation, which may occur at a higher rate with celiac involvement. (See 'Follow-up and surveillance' above.)
●Mortality for all patients who present with spontaneous SMA dissection is overall low (<1 percent). The main cause of death is intestinal gangrene and its consequences. (See 'Mortality' above.)
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