Acute mesenteric ischemia: updated guidelines of the World Society of Emergency Surgery

Acute mesenteric arterial embolism

Half of cases of AMI are due to acute SMA embolism [2, 3]. Mesenteric emboli can originate from the left atrium (e.g., atrial fibrillation), left ventricle (e.g., left ventricular dysfunction with poor ejection fraction), or cardiac valves (e.g., endocarditis). Occasionally emboli are generated from an atherosclerotic aorta. Emboli typically lodge at points of normal anatomic artery narrowing. The SMA is particularly vulnerable because of its relatively large diameter and low takeoff angle from the aorta. The majority of emboli lodge 3–10 cm distal to the origin of the SMA, thus sparing the proximal jejunum and colon. More than 20% of SMA emboli are associated with concurrent emboli to another arterial bed including the spleen and kidney [25].

Acute mesenteric arterial thrombosis

Thrombosis of the SMA (approximately 25% of cases) is usually associated with pre-existing chronic atherosclerotic disease leading to stenosis. Many of these patients have a history consistent with chronic mesenteric ischemia (CMI), including postprandial pain, weight loss, or “food fear.” A detailed medical history is important when evaluating a patient suspected to have AMI. Thrombosis usually occurs at the origin of visceral arteries. An underlying plaque in the SMA usually progresses eventually to a critical stenosis resulting in collateral beds. Accordingly, symptomatic SMA thrombosis most often accompanies celiac occlusion [26]. SMA thrombosis may also occur due to vasculitis, mesenteric dissection, or mycotic aneurysm. Involvement of the ileocolic artery will result in necrosis of the proximal colon.

Acute non-occlusive mesenteric ischemia

NOMI occurs in approximately 20% of cases, and is usually a consequence of SMA vasoconstriction associated with low splanchnic blood flow [27]. The compromised SMA blood flow also affects the proximal colon due to involvement of the ileocolic artery. Patients with NOMI typically suffer from severe coexisting illness, commonly cardiac failure which may be precipitated by sepsis. Hypovolemia and the use of vasoconstrictive agents may precipitate NOMI.

Mesenteric venous thrombosis

Mesenteric venous thrombosis (MVT) accounts for less than 10% of cases of mesenteric infarction. Thrombosis is attributed to a combination of Virchow’s triad; stagnant blood flow, hypercoagulability, and endothelial damage. In young patients, 36% of MVT occurs without an obvious cause [28]. An inflammatory process around the superior mesenteric vein (SMV) due to acute pancreatitis or inflammatory bowel disease may cause thrombosis. Surgical trauma such as splenectomy or bariatric surgery may also provoke SMV thrombosis. Hypercoagulability may be due to inherited disease such as Factor V Leiden, prothrombin mutation, protein S deficiency, protein C deficiency, antithrombin deficiency, and antiphospholipid syndrome. Additionally, recent work suggests that fibrinolysis shutdown (resistance to tissue plasminogen activator—tPA) is a significant risk factor for hypercoagulability [29]. Thrombophilia may also be acquired due to malignancies, hematologic disorders, and oral contraceptives [30].

Recent trends: prevalence, pathophysiology

The prevalence of AMI has changed in recent decades. The prevalence of acute mesenteric occlusion among patients with an acute abdomen may vary from 17.7% in emergency laparotomy and 31.0% in laparotomy for elderly non-trauma patients [31].

Mesenteric arterial embolism decreased to 25% of cases [3, 32]. Mesenteric arterial thrombosis was the second most common cause of mesenteric ischemia, which historically accounted for 20–35% and recently increased to 40% [32]. NOMI accounts for 25% of cases [3], which is also increasing, compared to the historical cohort, because of increased number of critically ill patients and overall improvement of intensive care. Although the mechanism is still unknown, heart failure, renal failure, cardiac surgery using cardiopulmonary bypass, and the use of catecholamine are reported as risk factors [33].

The etiology of AMI has changed over the years with increasing percentages of acute arterial thrombosis due to atherosclerosis which may in part be explained by modern anticoagulant therapy used for the treatment of atrial fibrillation.

The incidence of AMI increases exponentially with age. In patients aged 75 years or older, AMI is a more prevalent cause of acute abdomen than appendicitis [1]. The incidence of AMI in an 80-year-old is roughly tenfold that of a 60-year-old patient [34].

Abdominal compartment syndrome with very high intraabdominal pressure may cause bowel ischemia that is complicated with ischemia–reperfusion injury when decompression laparotomy is performed [35].

AMI has been described in patients with coronavirus disease (COVID -19), probably related to large vessel thromboembolic events as well as to small vessel thrombosis linked to hypercoagulability and fibrinolysis shutdown [36].

1.

Severe abdominal pain out of proportion to physical examination findings should be assumed to be AMI until disproven. (Strong recommendation based on low-quality evidence 1C)

The key to early diagnosis is a high level of clinical suspicion.

The clinical scenario of a patient complaining of excruciating abdominal pain with an unrevealing abdominal examination is classic for early AMI [37]. The reason for the pain being disproportionate to the clinical findings is that ischemia starts from the mucosa toward the serosa. That is why initially there is severe pain without clinical findings.

If the physical examination demonstrates signs of peritonitis, there is likely irreversible intestinal ischemia with bowel necrosis. In a study on AMI, 95% of patients presented with abdominal pain, 44% with nausea, 35% with vomiting, 35% with diarrhea, and 16% with blood per rectum [38]. Approximately, one-third of patients present with the triad of abdominal pain, fever, and hemoccult-positive stool. Other patients, particularly those with delayed diagnosis, may present in extremis with septic shock. Clinical signs of peritonitis may be subtle. Accordingly, one must have a high index of suspicion, because such findings are predictive of intestinal infarction.

The classic presentation of AMI, i.e., “severe, poorly localized abdominal pain that is out of proportion to the physical examination,” is becoming less common, while the “acute on chronic” presentations of mesenteric ischemia are more typical, and probably underdiagnosed [39]. Patients presenting with symptomatic chronic mesenteric ischemia are at high risk of developing in-hospital AMI.

Severe COVID-19 infection and AMI have a poor prognosis, delay in diagnosis, and intervention [40,41,42]. AMI should be suspected in patients with COVID-19 who present with nausea, vomiting, diarrhea, abdominal pain, and abdominal distension because of hypercoagulability and hypoperfusion. Blood tests will not aid in the diagnosis of AMI, though essential in patient management. CTA is the diagnostic modality of AMI along with clinical correlation.

2.

Clinical scenario and risk factors differentiate AMI as mesenteric arterial emboli, mesenteric arterial thrombosis, NOMI, or mesenteric venous thrombosis. (Weak recommendation based on low-quality evidence 1C)

Types of AMI

A careful medical history is important because distinct clinical scenarios are associated with the pathophysiological form of AMI [43]. Patients with mesenteric arterial thrombosis often have a history of chronic postprandial abdominal pain, progressive weight loss, and previous revascularization procedures for mesenteric arterial occlusion. Patients with NOMI have pain that is generally more diffuse and episodic associated with poor cardiac performance. These patients are more likely to have suffered from cardiac failure, and recent surgery. Several other smaller cohorts also reported hemodialysis as a risk factor of NOMI [44, 45]. Furthermore, NOMI represents a cause of secondary worsening in septic shock, particularly in septic patients treated with high-dose vasoactive drugs.

Patients with MVT present with a mixture of nausea, vomiting, diarrhea, and abdominal cramping. Gastrointestinal bleeding occurs in 10% [46].

Nearly 50% of patients presenting with embolic AMI have atrial fibrillation, and approximately one-third of patients have a prior history of arterial embolus with preexisted peripheral vascular disease [38].

Risk factors for specific phenotypes of AMI are presented in Table 1..

3.

Plain X-ray is not recommended in evaluating patients for intestinal ischemia. (Strong recommendation based on moderate-quality evidence 1B)

Table 1 Risk factors for specific types of AMI

A radiograph is usually the initial test ordered in patients with acute abdominal pain but has a limited role in the diagnosis of mesenteric ischemia, especially in the early setting. A negative radiograph does not exclude mesenteric ischemia [47]. Plain radiography only becomes positive when bowel infarction has developed and intestinal perforation manifests as free intraperitoneal air.

4.

There are no laboratory parameters that are sufficiently accurate to conclusively identify the presence or absence of ischemic or necrotic bowel, although elevated l-lactate, leukocytosis, and D-dimer may assist. (Weak recommendation based on moderate-quality evidence 2B)

Although laboratory results are not definitive, they may help to corroborate clinical suspicion. More than 90% of patients will have an abnormally elevated leukocyte count [48]. The second most commonly encountered abnormal finding is metabolic acidosis with elevated lactate level, which occurs in 88% [49].

Patients may present with lactic acidosis due to dehydration and decreased oral intake. Thus, differentiation of early ischemia versus irreversible bowel injury based upon the lactate level alone is not reliable unless accompanied by other clinical evidence. Elevated serum lactate levels > 2 mmol/l is associated with irreversible intestinal ischemia hazard ratio: 4.1 (95% CI: 1.4–11.5; p < 0.01) in case of AMI [50].

It should be emphasized that the presence of lactic acidosis in combination with abdominal pain when the patient may not otherwise appear clinically ill should lead to consideration of early CTA.

Based on the current literature, no accurate biomarkers have been identified to diagnose AMI [51, 52]. D-dimer has been reported to be an independent risk factor for intestinal ischemia [52], reflecting ongoing clot formation and endogenous degradation via fibrinolysis. No patient presenting with a normal D-dimer had intestinal ischemia and D-dimer > 0.9 mg/L had a specificity, sensitivity, and accuracy of 82%, 60%, and 79%, respectively [53]. Thus, D-dimer may be useful in the early assessment.

Elevated amylase has been reported in roughly a half of patients with AMI. [54] This is important to note to as patient may be misdiagnosed as having acute pancreatitis, and delay in critical interventions could impact survival outcomes.

Other biomarkers reported to be of use in the diagnosis of AMI include intestinal fatty acid-binding protein (I-FABP), serum alpha-glutathione S-transferase (alpha-GST), and cobalt–albumin binding assay (CABA) [55, 56]. A cross-sectional diagnostic study of 129 patients admitted for acute abdominal pain found that the three most promising circulating biomarkers for AMI—citrulline, I-FABP, and d-lactate—were neither sensitive nor specific enough for the differential diagnosis of AMI [57].

These results, however, contrast with other published reports [56, 58]. This could be explained by selection bias (established severe AMI cases were included) leading to an overestimated performance of the studied biomarkers.

5.

Computed tomography angiography (CTA) should be performed without delay in any patient with suspicion for AMI. (Strong recommendation based on high-quality evidence 1A)

Delay in diagnosis is the dominant factor that accounts for high mortality rates of 30–70% despite increased knowledge of this entity [59, 60]. Every 6 h of delay in diagnosis (actually—delay in CTA) doubles mortality [61]. The multidetector CTA has replaced formal angiography as the diagnostic study of choice. Volume rendering is now a semiautomatic workflow component of many CT machines. These can aid remote communities with less experienced staff.

In the presence of advanced AMI, the CTA findings reflect irreversible ischemia (intestinal dilatation and thickness, reduction or absence of visceral enhancement, pneumatosis intestinalis, and portal venous gas, especially the combination of all) and free intraperitoneal air [62].

Comprehensive biphasic CTA includes the following important steps:

(a)

Pre-contrast scans to detect vascular calcification, hyper-attenuating intravascular thrombus, and intramural hemorrhage.

(b)

Arterial and venous phases to demonstrate thrombus in the mesenteric arteries and veins, abnormal enhancement of the bowel wall, and the presence of embolism or infarction of other organs.

(c)

Multiplanar reconstructions (MPR) to assess the origin of the mesenteric arteries [63].

The oral contrast is not indicated and even harmful. CTA should be performed despite the presence of acute kidney injury, as the consequences of delayed or missed diagnosis are far more detrimental for patients than exposure to the iodinated contrast agent. A recent study found that in 27 of 28 patients (96.4%) MDCT correctly diagnosed AMI (specificity of 97.9%) [27, 64]. A sensitivity of 93%, specificity of 100%, and positive and negative predictive values of 100% and 94%, respectively, were achieved [65, 66].

Six radiological findings (bowel loop dilatation, pneumatosis intestinalis, SMV thrombosis, free intraperitoneal fluid, portal vein thrombosis, and splenic vein thrombosis) were found to be predictors of bowel necrosis in patients with AMI [67]. The clinical significance of pneumatosis intestinalis as a single radiological finding remains the challenge. In a biggest multicentral retrospective study, 60% of patients had benign disease [68].

In NOMI, CTA may demonstrate bowel ischemia and free fluid in the face of patent mesenteric vessels. In MVT, the most common positive radiological finding on venous phase CTA is thrombus in the superior mesenteric vein described as the target sign [69].

Associated findings that suggest MVT include bowel wall thickening, pneumatosis, splenomegaly, and ascites [69]. Portal or mesenteric venous gas strongly suggests the presence of bowel infarction.

Diagnostic angiography can differentiate occlusive, embolic, and thrombotic from non-occlusive AMI.

Duplex ultrasonography has a limited role in this entity, but may be helpful if obtained early in chronic cases [47]. It could be useful to monitor the bowel’s peristalsis or the amount of free peritoneal fluid especially in NOMI.

MRA is an established technique in the evaluation of the mesenteric arterial and venous vasculature in patients with suspected AMI. It has been well accepted for chronic mesenteric ischemia cases and functional assessment of bowel insufficiency as a result of SMA pathology [70]. Nevertheless, its use is limited in the emergency setting.

6.

Non-occlusive mesenteric ischemia (NOMI) should be suspected in critically ill patients with abdominal pain or distension requiring vasopressor support and evidence of multiorgan dysfunction. (Weak recommendation based on low-quality evidence 2C)

Clinical examination and routine laboratory tests are of only little value in reaching an early and reliable diagnosis of NOMI. Unexplained abdominal distension or gastrointestinal bleeding may be the only signs of acute intestinal ischemia in NOMI and may be undetectable in sedated patients in the ICU in approximately 25% of cases [71, 72]. Patients surviving cardiopulmonary resuscitation who develop bacteremia and diarrhea should be suspected of having NOMI, regardless of presence or absence of abdominal pain. Right-sided abdominal pain associated with the passage of maroon or bright red blood in the stool is highly suggestive of NOMI.

Gastrointestinal perfusion is often impaired early in critical illnesses, major surgery, or trauma, all of which are characterized by increased demands on the circulation to maintain tissue oxygen delivery [73].

Most of the symptoms listed in this section are often not clinically apparent in a critically ill and ventilated patients. Accordingly, any negative changes in a patient's physiology, including new onset of organ failure, increase in vasoactive support, and nutrition intolerance, should raise the suspicion of AMI.

Experimental and observational studies suggest that the use of vasopressors such as norepinephrine and epinephrine might result in impaired mucosal perfusion [74, 75]. Other pharmacological agents such as vasopressin and digoxin [76] as well as acute profound hypovolemia could also worsen ischemia.

Lastly, the role of enteral nutrition in critically ill patients on development of intestinal ischemia is controversial. In general, enteral and parenteral nutrition is complementary to meet patient’s daily caloric requirements. In the recent randomized controlled trial “NUTRIREA 2” [77], enteral nutrition was compared to parenteral nutrition: Mortality did not differ between the two groups, but a significantly higher rate of bowel ischemia was reported in the enteral group.

7.

When the diagnosis of AMI is made, fluid resuscitation should commence immediately to enhance visceral perfusion. Electrolyte abnormalities should be corrected, and nasogastric decompression initiated. (Strong recommendation based on moderate-quality evidence 1B)

Fluid resuscitation with crystalloid and blood products is essential for the management of the patient with suspected AMI. Preoperative resuscitation is important to prevent cardiovascular collapse on induction of anesthesia. To guide effective resuscitation, early hemodynamic monitoring should be implemented [78]. Assessment of electrolyte levels and acid–base status should be performed. This is especially true in patients with AMI, where severe metabolic acidosis and hyperkalemia may result from underlying bowel infarction and reperfusion [79]. Vasopressors should be used with caution. Dobutamine, low-dose dopamine, and milrinone to improve cardiac function have been shown to have less impact on mesenteric blood flow [80, 81]. The fluid volume requirement in these patients may be high, due to extensive capillary leakage, but the infusion of large volume of crystalloid should be utilized carefully to optimize bowel perfusion [82]. The goals of therapy should address physiologic levels of oxygen delivery with continued monitoring of lactate level as an indication of perfusion improvement. Supra-physiologic level of oxygen delivery was suggested in the past which is not supported by the current evidence [83].

8.

Broad-spectrum antibiotics should be immediately administered. (Strong recommendation based on moderate-quality evidence 1C)

The high risk of infection among patients with AMI outweighs the risks of acquired antibiotic resistance, and therefore, broad-spectrum antibiotics should be administered early in the course of treatment [84]. Intestinal ischemia leads to early loss of the mucosal barrier, which facilitates bacterial translocation and the risk of septic complications. Antibiotic therapy should be administered for at least 4 days in immunocompetent stable patients with consideration given to a longer duration of therapy for signs of ongoing infection [85]. As soon as possible, antibiotic regimen should be tailored according to the microbial isolation. Prolonged course of empiric antibiotics, if clinically deemed necessary, should be guided in accordance with local antibiotic stewardship team.

9.

Prompt laparoscopy/laparotomy should be done for patients with an overt peritonitis. (Strong recommendation based on low-quality evidence 1C)

When physical findings suggestive of an acute intraabdominal catastrophe are present, bowel infarction has already occurred, and the chance of survival in this patient population with significant associated comorbidity is reduced dramatically. Peritonitis secondary to bowel necrosis mandates surgery without delay.

The goal of surgical intervention for AMI includes:

1)

Re-establishment of the blood supply to the ischemic bowel.

2)

Resection of all non-viable regions.

3)

Preservation of all viable bowel.

Intestinal viability is the most important factor influencing outcome in patients with AMI. Non-viable intestine, if unrecognized, results in multisystem organ dysfunction and ultimately death. Prompt laparotomy allows for direct assessment of bowel viability.

Emergency laparotomy

After initial resuscitation, midline laparotomy should be performed, followed by the assessment of all areas of the intestine with decisions for resection of all frankly necrotic areas. The SMA is easily palpated by placing fingers behind the root of the mesentery. The SMA is identified as a firm tubular structure, which may have or not a palpable pulse. Otherwise, the SMA can also be reached by following the middle colic artery where it enters the SMA at the mesentery. Direct sharp dissection, exposing the artery from its surrounding mesenteric tissue, is required for proper exposure to perform revascularization. In cases where there is diagnostic uncertainty, arteriogram is the study of choice. It can be done intraoperatively especially in hybrid suites. Intraoperative duplex is a simple, rapid, repeatable, and often definitive alternative diagnostic modality.

Re-establishment of the blood supply to the ischemic bowel

Revascularization when relevant has an essential role in the multidisciplinary approach to AMI. As an example, among the 104 patients who did not undergo revascularization, 64 (62%) died within 30 days compared to 36 out of 85 (42%) patients who were re-vascularized (p = 0.01) [86].

Different techniques of blood flow restoration are used depending on the AMI pathophysiology. Embolectomy and angioplasty are a well-established definitive treatment for SMA emboli. On the other hand, thrombosis of the SMA at the origin of the aorta (a common pathology in diffuse atherosclerosis) will require a bypass procedure. Bypass may be performed in either an antegrade fashion from the supraceliac aorta or retrograde fashion from the infrarenal aorta or common iliac arteries. Single-vessel revascularization (SMA) is usually sufficient in the acute setting. However, it increases the magnitude of the procedure and may require prosthetics in the presence of contaminated field. Nowadays endovascular procedures reduce the requirement for surgical bypasses. Thus, multidisciplinary collaborative approach including specialists from multiple disciplines is integral for good clinical outcomes.

Temporary SMA shunting may spare considerable bowel. For patients in extremis, or where the necessary technical skillset is not available, temporary SMA shunting should be considered.

Neither NOMI nor MVT typically requires vascular repair. Full-dose anticoagulation should be initiated on all patients prior to the surgical procedure. Unfractionated heparin is effective and easy to manage, especially in patients with acute kidney failure.

Intraoperative bowel viability assessment

There are limited intraoperative tools to help surgeons in decision making regarding bowel viability, especially in circumstances in which the bowel appears to be “dusky” or threatened but not clearly ischemic. In this case, a temporary abdominal closure via a negative pressure wound therapy device or temporary dressing (custom made with plastic sheets, gauzes, and drains) is convenient in order to provide an opportunity for a second-look surgery. Clear documentation of bowel length is crucial in every operation note.

In addition to traditional surgical inspection of the bowel, available techniques of intraoperative assessment of bowel viability rely on bowel oxygenation, myoelectric activity, and perfusion. The intraoperative absence of any one of these criteria is a sufficient predictor of bowel non-viability.

Many surgeons use their hands and eyes to look for the presence or absence of peristalsis or mesenteric pulsation to evaluate whether blood flow is adequate.

Doppler ultrasonography (DUS) is a safe and noninvasive technique to measure blood flow and is popular for its easiness of use and relatively low cost [87].

Flowmetry with fluorescein dye is currently part of the accepted standard of clinical care for intraoperative assessment of bowel viability. Fluorescein can therefore be used to visualize perfusion in open laparotomies using a Woods Lamp or laparoscopically using an endoscope with appropriate filters [88, 89].

Indocyanine Green (ICG) is a near-infrared (NIR) fluorophore with an emission peak of 832 nm in whole blood [90]. It has been used in the same way as fluorescein, but primarily in the elective surgical setting [

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