The Dangerous Miss: Recognizing Acute Mesenteric Ischemia


80% of acute mesenteric ischemia cases result in mortality because of missed diagnosis. Here’s how to recognize the signs.

The shift has just started, and your view of the waiting room reveals several patients with abdominal pain who checked in within twenty minutes of each other. The first patient is a 32 year-old female who presents with one week of worsening abdominal pain, which is non-localized. She has no medical problems, takes only oral contraceptives, and has a family history of venous thromboembolism. Her physical exam is normal, including vital signs, but she continues to complain of severe pain. You order a CBC, liver function panel, basic metabolic panel, urinalysis, and urine pregnancy test, while also ordering medications for nausea and pain. Your second patient is a 53 year-old male presenting with abdominal pain that worsens with eating and lasts several hours. He has no desire to eat due to worsening pain with food. He has a history of hypertension, peripheral vascular disease (PVD), chronic tobacco use, and diabetes. His exam is normal with no tenderness to palpation.

Most physicians know the classic story of mesenteric ischemia, such as the 77 year-old male with a history of coronary disease, atrial fibrillation, coronary bypass, and hypertension who presents with severe abdominal pain but normal physical exam. However, acute mesenteric ischemia (AMI) does not always present so classically, and missing the diagnosis is associated with mortality rates approaching 80% [1]. The wide variety of presentations and symptoms of this disease creates a diagnostic challenge [2].

Abdominal vascular catastrophes are uncommon but can be fatal. Acute mesenteric ischemia (AMI) is one abdominal catastrophe of great interest to emergency physicians in that rapid diagnosis and initiation of treatment can prevent mortality and reduce long-term morbidity. The often quoted “Time is bowel” is a sentiment that speaks to the danger of this disease and need for diagnosis [3].

The annual incidence of this disease is 0.09-0.2% per year and ~1% of acute abdomen hospitalizations, but this rarity is offset with a 60-80% mortality within the first 24 hours especially if the disease is missed [4,5]. With the population around the world growing older, this incidence is increasing. Unfortunately this disease presents with a variety of nonspecific symptoms that overlap with other diseases, creating challenges even for the most astute clinician.

The Classic Types
There are four types of AMI, which include arterial embolism (AE), arterial thrombosis (AT), venous thrombosis, and non-occlusive (NOMI). Originally it’s thought arterial embolism is most common, but now studies demonstrate approximately equal rates of arterial thrombosis and embolism (40%) [6]. The four etiologies are shown in table 1 (below), with symptoms, presentation, risk factors, incidence, and mortality.

MissTable1Click image to enlarge

Clinical Presentation
As shown in Table 1, symptoms and presentations are nonspecific, which can provide a false sense of security. The symptoms and presentation vary based on the type and etiology of the disease [1,3,7]. The typical presentation is an elderly patient (median age 74 years) with multiple comorbidities who presents with “pain out of proportion” to exam, meaning the patient is experiencing intense pain, while there is little to no tenderness on palpation [1,3,7]. Risk factors including peripheral arterial disease (27%), coronary artery disease (46%), diabetes, and hypertension are common, but not always present [8-10].

Pain is the most consistent symptom, which begins with cramping, periumbilical pain due to small bowel ischemia, which evolves into tenderness to palpation with transmural ischemia of the bowel wall. If necrosis occurs, diffuse peritonitis and sepsis may result [7,11,12]. This is due to infarction of all bowel layers, causing diffuse pain to palpation. However, peritonitis is reported in only 16% of patients with necrotic bowel [13].

Other early symptoms including vomiting, diarrhea, distension, and bloody stool are common, but not always present. The early vomiting and diarrhea are due to bowel ischemia, causing “gut-emptying.” Bowel sounds are not helpful in ruling in or out the disease [14] and several studies have demonstrated that abnormal mental status can also be associated with presentation [7,11,12]. Presentation truly varies based on the etiology and type of AMI [1,4,7]. These findings including acute abdominal pain, pain out of proportion, peritoneal signs, guaiac-positive stool, heart failure, and atrial fibrillation possess a wide range of sensitivities and are frequently absent [1,7,15]. This wide variety of presentations and large variability in range of performance characteristics of the history and physical examination underlines the diagnostic challenge. Presentation and exam are challenging, as one study demonstrates the disease is suspected in only 22% of patients [7]! The key to diagnosis is evaluating risk factors such as critical illness, comorbidities (hypertension, diabetes, PAD), dialysis, VTE history and considering this disease in the differential. Pain out of proportion, seen in necrotizing fasciitis and compartment syndrome, must be considered a red flag and trigger the physician to consider deadly diagnoses. The patient with minimal tenderness on palpation but severe, intense pain requires consideration for AMI.

MissTable2When considering the disease, what tests can assist in diagnosis? Laboratory tests include white blood cell count (WBC), pH, D-dimer, lactate, and urine intestinal fatty acid binding protein (I-FABP). Many providers rely on these tests to enhance diagnosis. However, this is a pitfall. Approximately 75% of patients will have a WBC greater than 15,000 cells/mm3 [13]. However, this does not differentiate AMI from other diagnoses, and 25% of cases do not have an elevation! Metabolic acidosis is not always present, and metabolic alkalosis can present early if vomiting is a predominant symptom [5]. The D-dimer is sensitive at 96%, but as usual, it is not specific. Providers also rely on elevated lactate for diagnosis. However, this test is not always elevated. Early in the disease process, lactate is normal as it travels through the portal venous system to the liver, where it is converted into glucose. As gut ischemia increases, the liver is unable to keep up with converting lactate into glucose, and lactate spills over into the blood [1,7,15]. A newer test includes urine I-FABP, with a sensitivity of 90% and specificity of 89% in one study. However, these findings have not been validated, and the vast majority of EDs do not have access to this test [5,16]. A summary of laboratory test sensitivity and specificity is demonstrated in Table 2.

With the large range of symptoms and no gold standard laboratory test, imaging is required. With today’s imaging, CT angiography of the abdomen and pelvis with IV contrast is most commonly used [21-23]. Sensitivity of the new multidetector row technology CT angiography (MDRCT) is 95%, with specificity of 95% in one meta-analysis [7]. However, this test can miss 5% of patients. MDRCT angiography identifies mucosal ischemia and small perfusion defects missed with traditional angiography.

Abdominal plain films are normal in 25% of cases, and the classic thumb printing, pneumatosis, free air, portal venous gas are only present with transmural ischemia and bowel necrosis (40%). Do not rely on a normal xray to rule out disease [12,17]. Ultrasound (US) can detect greater than 50% stenosis in chronic mesenteric ischemia, but its use in AMI is limited due to distended bowel. However, this test may reveal signs of obstruction [1,18]. Magnetic resonance angiography (MRA) lacks CT resolution, overestimates degree of stenosis, and takes longer to obtain [19]. Angiography was the gold standard imaging modality, but now its primary use is for patients whose CT is not conclusive. Angiography does play a role in treatment as catheter-based therapy and vasodilation treatment are cornerstones of management, especially in those patients deemed too risky for open surgical techniques [1,5,19]. In addition, patients who undergo successful revascularization procedures may still require intra-arterial vasodilators to treat associated vasospasm [1,5,20].

Laparoscopy can be used if the prior tests are unrevealing. Studies have shown that the mean time between admission and diagnostic laparoscopy (10.2 hours) was significantly shorter in patients who underwent successful revascularization and in those who survived with or without developing short bowel syndrome [24].

Anatomy and Pathogenesis
The abdominal aorta provides three branches to the intestines, shown in Figure 1 (below). The first branch is the celiac artery, which provides blood to the distal esophagus to second portion of duodenum. AMI is rare to this area due to short, wide artery and collateral flow. The second branch is the superior mesenteric artery, which perfuses the duodenum to distal transverse colon. This artery is most commonly affected in embolism with a 45° angle take-off. Finally, the inferior mesenteric artery perfuses the transverse colon to rectum. It is rarely the sole vessel involved in MI. Collateral circulation from the CA or IMA generally allows sufficient perfusion in reduced SMA occlusion states, such as NOMI or thrombotic mesenteric ischemia. However, occlusion of a single vessel, usually in the setting of embolus, can result in marked ischemia [1,4,12,25].


Bowel wall innervation explains the presentation and symptoms of affected patients. In early disease stages, the mucosal layer becomes ischemic, as it’s the furthest from vascular supply. The pain will be visceral in nature. Eventually, the muscularis and serosal layers become ischemic, leading to peritoneal irritation and guarding with rigidity. At this point, the pain is “in proportion” to the exam. However, there can be a deceptive pain-free interval of 3-6 hours caused by a decline in intramural pain receptors from hypoperfusion. The patient may present with intense pain with minimal findings, which then improves. Once transmural infarction occurs, pain will recur [3,4,12]. Translocation of bacteria from the lumen of the intestine follows infarction [1,3,4,7].

The key to management is initiation of treatment while diagnostic evaluation is underway. Optimal treatment requires a multidisciplinary approach: general surgery, vascular surgery, and interventional radiology. Surgical intervention that can be initiated in less than six hours from symptom onset adds significant increase in survival [1,4,26,27]. Three principles guide the surgical management of thromboembolic AMI: SMA revascularization, assessment of intestinal viability, and resection of necrotic bowel. Surgeons can utilize open or endovascular repair. If peritonitis is present, this obviates the need for further testing if you are considering AMI. Instead, speak with surgery about your findings and concern for transmural infarction.

What can emergency physicians do besides calling for help? Aggressive fluid resuscitation, electrolyte management, and broad-spectrum antibiotics are needed early in the course [28]. Avoid oral intake, which can exacerbate ischemia. Patients may require 10-20 L of IV fluids within the first 24 hours due to extensive capillary leakage and third spacing. Begin anticoagulation in consultation with the treating surgeon, usually with unfractionated heparin [4,14,19,29]. Vasospasm is common and can be treated with intra-arterial papaverine infusion, but this requires angiography [28]. Another option is the vasodilator prostaglandin E1 (PGE1) which is administered intravenously [30].

Mortality was 80% as reported in 1999, but true mortality varies based on cause [1,31]. As discussed previously, early diagnosis saves lives. Beaulieu and colleagues showed a 70% mortality if time to diagnosis was more than 24 hours versus a 14% mortality if less than 12 hours [10,24]. Complications following treatment of AMI, such as respiratory failure, multi-organ system failure, sepsis, and short gut syndrome, affect 35% to 79% of patients [8,32]. These patients will require intensive care monitoring due to the high propensity of complications.

Let’s go back to our two patients: the 32 year-old female with worsening abdominal pain and 53 year-old male with “food fear,” both with minimal to no tenderness on exam but severe pain. You have given both patients IV pain and nausea medication, but their pain has continued. You order a CT angiography for both. The radiologist calls back with the results, and he has done you a huge favor by speaking with the interventional radiologist and the general surgeon on call. The 32 year-old female has mesenteric venous thrombosis of the superior mesenteric vein extending into the splenic vein. The 53 year-old male has diffuse mesenteric vascular thrombotic disease involving the origins of the superior mesenteric and inferior mesenteric arteries. You speak with the general surgeon while ordering broad-spectrum antibiotics and IV fluids. The surgeon will contact the ICU physician, and he will be calling his operative nurse as well.

In summary, AMI has four etiologies: AE, AT, venous thrombosis, and NOMI. AE and AT have equal incidences, approximately 40%. No history or physical examination finding can definitively diagnose the condition, but a wide variety of presentations occur, which creates the diagnostic challenge. Pain out of proportion and gut emptying may occur early in the disease, with minimal tenderness on exam. Once transmural infarction occurs, peritoneal findings and tenderness to palpation may occur. Be suspicious of pain out of proportion and scrutinize risk factors (critically ill, PVD, CAD, ESRD, dialysis, and hypercoagulable states). Remember, CT angiography is the best imaging modality. Laboratory findings do not have sufficient sensitivity and specificity for ruling out or in the disease. Lactate may not be elevated early in the disease course, and 25% of the time no elevated WBC will be found. Treatment requires surgery and interventional radiology consultation, IV antibiotics, IV fluids, and anticoagulation. Ultimately, the physician at the bedside is the best diagnostic tool.


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Brit Long, MD is an EM Chief Resident at San Antonio Uniformed Services Health Education Consortium.

Alex Koyfman, MD is a Clinical Assistant Professor of Emergency Medicine at UT Southwestern Medical Center and an Attending Physician at Parkland Memorial Hospital. He is also Editor-in-Chief for emDocs.


  1. Unfortunately my life partner was killed by NOMI. The doctors did not heed my warning that something needed to be done now…they let her die a slow and very miserable death until she finally coded almost 20 hours later…at that point the sepsis was starting to shut down her organs…they resected 6 inches of dead small intestine and we waited 24 hours at which time the surgeon went back in and her entire bowel including the large bowel was dead. The surgeon gave me the news and when I looked him in the eye he told me she would have died no matter what…I couldn’t believe it. She was taken off the machines an hour later and her heart slowly stopped beating. My life is forever changed from this dreaded disease. This is what defensive medicine does to surgeons and now I have to live with the question, could she have been saved if diagnosed early and properly treated? I agree it’s a tough diagnosis…but think about the ones who are left behind to ponder questions of how and why and the grief of losing the most precious person to you. Still debating weather or not to sue the 2 surgeons responsible for her care. They know they made mistakes all along the way…I need to get her medical records to find out how bad this really is…

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