Acute Mesenteric Ischemia

Etiology

Embolic patients commonly have a positive medical history of cardiovascular diseases, including recent myocardial infarction, congestive heart failure, and atrial fibrillation. Causes include peripheral arterial emboli, cardiac emboli, and a ruptured or dislodged atheromatous plaque after surgery.[4][5][6] The typical thrombotic patient experiences a history of postprandial abdominal pain, leading to food avoidance and weight loss. Causes include atheromatous vascular disease (eg, atherosclerosis, aortic aneurysm, aortic dissection) and decreased cardiac output due to a secondary cause (eg, dehydration, myocardial infarction, congestive heart failure).

The NOMI patient is typically critically ill, presents with several severe comorbidities, and is hemodynamically unstable. Causes include drugs that reduce blood flow (eg, vasopressors and ergotamines), hypotension from severe medical conditions (eg, myocardial infarction, sepsis, CHF, and renal disease), and patients who have recently undergone major surgery (eg, cardiac and abdominal surgery). NOMI accounts for approximately 20% of AMI cases but is associated with the highest mortality due to its insidious onset, diagnostic complexity, limited therapeutic window, and frequent association with multisystem organ dysfunction.[7][8][9]

Epidemiology

AMI is an uncommon but highly morbid condition, with an estimated prevalence of approximately 1 per 1,000 hospital admissions. Among all cases, arterial embolism accounts for 40% to 50%, arterial thrombosis for 25% to 30%, and NOMI for approximately 20%. AMI most frequently affects older adults, with a higher incidence observed in women and in patients with significant underlying comorbidities.

Pathophysiology

An acute mesenteric arterial embolism is often cardiogenic in origin and primarily affects the superior mesenteric artery (SMA). Preceding events include atrial tachyarrhythmia, congestive heart failure, myocardial ischemia or infarction, cardiomyopathy, and ventricular aneurysm, which results in thrombus formation that later embolizes to cause ischemia. Patients with acute mesenteric arterial thrombosis commonly have a preexisting atherosclerotic disease. Vasospasm in the SMA often accompanies NOMI secondary to cardiac failure, peripheral hypoxemia, or reperfusion injury. 

Toxicokinetics

In rare instances, vasopressors (eg, cocaine and norepinephrine) and ergotamines may cause NOMI. These agents cause vasoconstriction and reduced blood flow in the mesentery, which may result in bowel ischemia.

History and Physical

AMI patients typically present with abdominal pain that does not correlate with physical exam findings. Abdominal tenderness to palpation occurs when the entire bowel wall is involved, which is a later presentation as necrosis begins. Patients with an embolic disease typically have a history of bowel emptying violently, followed by severe pain. The syndrome rapidly advances to ischemia and necrosis because collateral blood flow is limited.

Thrombosis may take days or weeks to progress, with abdominal pain gradually worsening. Patients also may have a combination of diarrhea, distention, bloody stool, and, most importantly, a history of postprandial pain, suggesting chronic mesenteric ischemia. NOMI progresses slowly, and the associated abdominal pain is not localized and varies in severity and consistency. These patients are critically ill (eg, septic shock, cardiac disease, and respiratory failure), hypotensive, and usually on vasopressor agents.

Evaluation

Laboratory values and biomarkers for AMI are nonspecific and lack diagnostic power. Elevated D-lactate and lactate dehydrogenase are seen in late-stage AMI. Computed tomography (CT) angiography is the preferred method for imaging all types of AMI (see Image. CT Angiogram of the Superior Mesenteric Artery. Sensitivities for CT range from 96% to 100%, and specificities from 89% to 94%. While standard CT angiography provides adequate visualization of the visceral vasculature, a biphasic CT angiography protocol, comprising both arterial and delayed phases, offers improved sensitivity by capturing dynamic perfusion of the portal venous system and bowel wall.

Several nonvascular findings on CT imaging can herald AMI. One of these is pneumatosis intestinalis, which is the presence of gas dissecting through the layers of the bowel wall. Pneumatosis intestinalis may extend into the mesenteric venous system and eventually into the portal vein. This can be seen in 6% to 43% of cases; therefore, its presence warrants a detailed clinical examination. Other findings include changes in bowel wall thickness, which is found in 26% to 96% of AMI cases. Luminal dilatation and bowel air-fluid levels are more often seen in arterial AMI.[10] 

Catheter-directed angiography has fallen out of favor during the initial stages of AMI diagnosis because the added surgical stress is a burden on an already critically ill patient when used in conjunction with endovascular interventions to treat AMI. Plain abdominal radiography, duplex ultrasonography, and magnetic resonance angiography have narrow indications in diagnosing AMI.

Treatment / Management

Medical Interventions

Initial medical treatment focuses on fluid resuscitation and correcting electrolyte imbalances. Avoid vasopressors and alpha-adrenergic agents, which may cause vasospasm. If vasopressor support is essential to optimize cardiac output, agents with minimal adverse effects on splanchnic perfusion, eg, low-dose dopamine, dobutamine, or milrinone, are preferred. Broad-spectrum antibiotics should be given before surgery to avoid abdominal sepsis if the necrotic bowel is resected.[11][12][13](B3)

Surgical Interventions

Early surgical exploration is required to assess the level of ischemia and spread of necrosis. Revascularization of the bowel is the primary goal of surgery, and excision of necrotic bowel is necessary. After revascularization, the bowel should be assessed for viability, including checking pulses with continuous-wave Doppler, peristalsis, and normal color. Depending on the type and location of the vessel occlusion, open or endovascular surgical interventions are indicated for the treatment of occlusive mesenteric arterial ischemia.

Bowel resection occurs in 53% of second-look surgeries and 31% during exploratory surgery at the first attempt to revascularize. The difficulty of assessing the extent of necrosis of the bowel warrants a second-look surgery 12 to 48 hours after revascularization. Revascularization options during open surgery include methods, eg, retrograde open mesenteric stenting, wherein the SMA is surgically exposed, and a soft anterior arterial wall segment is punctured, facilitating placement of a stent. The arteriotomy is closed either with interrupted transverse sutures or a patch. One can also consider a traditional SMA embolectomy as well if the embolus is large and organized.[14]

Endovascular Interventions

In patients without peritonitis, endovascular options can be considered. One of them is endovascular aspiration thrombectomy (EVT), in which the SMA is catheterized, and the thrombus is aspirated using a vacuum. Several passes may occur until the clot is sufficiently removed. Risks of this approach include distal propagation of the thrombus into smaller peripheral branches within the mesentery. Closely monitoring the patient is essential to detect clinical deterioration following thrombus aspiration promptly.[15]

As NOMI is secondary to vasospasm rather than occlusion, treatment is medically focused and relies upon reversing the underlying cause of the low-flow state. Catheter-directed papaverine (a phosphodiesterase inhibitor) delivered via a side-hole catheter or thrombolysis catheter is an interventional option.[16][17]

Differential Diagnosis

The early identification of AMI is paramount to reducing the likelihood of debilitating morbidity and high mortality. AMI has a vague presentation, and a high index of suspicion is necessary to diagnose suspected patients because of the life-threatening potential of the disease. Findings of abdominal pain out of proportion to a physical exam and cardiovascular risk factors that predispose a patient to embolism and peripheral thrombosis should alert the clinician to consider AMI. Diseases to consider in the differential diagnosis are those that cause acute abdominal pain and are therefore variable in presentation. These include acute colitis, ruptured abdominal aortic aneurysm, bowel obstruction, diabetic ketoacidosis, gastrointestinal perforation, and malignancy.

Prognosis

The prognosis of AMI is poor, with patients experiencing high morbidity and mortality rates. While a downward trend in mortality rates has occurred since the 1960s, AMI mortality remains high, at 60% to 80%. The specific AMI classification affects the likelihood of mortality, with acute embolism having a better prognosis, followed by NOMI and acute thrombosis. Factors associated with mortality include advanced age, bowel resection during second-look surgery, metabolic acidosis, renal insufficiency, and symptom duration.

A study by Gupta et al found a 30-day morbidity rate of 56%. Major postoperative 30-day complications included ventilator use over 48 hours, septic shock, pneumonia, and sepsis. Follow-up surgical interventions were common, with 30% of patients revisiting the surgical department within 30 days and 14% having a hospital stay longer than 30 days. 

Complications

AMI can lead to significant portions of the small bowel that are nonviable and need to be resected during laparotomy. Depending on how much bowel is resected, patients can end up having short bowel syndrome along with intestinal failure. Short bowel syndrome can significantly diminish quality of life and worsen morbidity. The creation of ostomies during these operations can also lead to difficult-to-manage fluid losses and electrolyte imbalances.[18]