Mesenteric ischemia has 4 etiologies: arterial embolus, arterial thrombosis, venous thrombosis, and nonocclusive. No history or physical examination finding can definitively diagnose the condition. A wide variety of presentations occur. Pain out of proportion and gut emptying may occur early, with minimal tenderness. Once transmural infarction occurs, peritoneal findings and tenderness to palpation may occur. Physicians must be suspicious of pain out of proportion and scrutinize risk factors. Computed tomography angiography is the best imaging modality. Treatment requires surgery and interventional radiology consultation, intravenous antibiotics and fluids, and anticoagulation. The physician at the bedside is the best diagnostic tool.
Key points
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Mesenteric ischemia has a variety of etiologies, each with its own historical clues to assist in diagnosis.
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Early computed tomography angiography without waiting for administration of oral contrast should be pursued in suspected cases of mesenteric ischemia.
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Laboratory findings do not have sufficient sensitivity and specificity for ruling out or in the disease.
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Treatment requires surgery and interventional radiology consultation, intravenous antibiotics and fluids, and anticoagulation.
Introduction
Mesenteric ischemia is one of a few vascular abdominal catastrophes where rapid diagnosis and initiation of treatment are imperative to reduce long-term morbidity and prevent mortality. There are 4 major etiologies of acute mesenteric ischemia, namely, arterial embolus, arterial thrombosis, venous thrombosis, and nonocclusive, which are discussed in detail. The presentation of patients with mesenteric ischemia is usually nonspecific with a “benign” objective abdominal examination, which can provide a false sense of security because the late findings of this disease process (ie, absent bowel sounds, positive fecal occult blood test, focal or generalized peritonitis from visceral ischemia, elevated lactate, hypotension, fever) have not revealed themselves. In general, a high degree of clinical suspicion should be based on the combination of history, examination, laboratory results, and imaging studies to arrive to this diagnosis.
Introduction
Mesenteric ischemia is one of a few vascular abdominal catastrophes where rapid diagnosis and initiation of treatment are imperative to reduce long-term morbidity and prevent mortality. There are 4 major etiologies of acute mesenteric ischemia, namely, arterial embolus, arterial thrombosis, venous thrombosis, and nonocclusive, which are discussed in detail. The presentation of patients with mesenteric ischemia is usually nonspecific with a “benign” objective abdominal examination, which can provide a false sense of security because the late findings of this disease process (ie, absent bowel sounds, positive fecal occult blood test, focal or generalized peritonitis from visceral ischemia, elevated lactate, hypotension, fever) have not revealed themselves. In general, a high degree of clinical suspicion should be based on the combination of history, examination, laboratory results, and imaging studies to arrive to this diagnosis.
Epidemiology
Although a rare case of abdominal pain with an annual incidence of 0.09% to 0.2% per year and approximately 1% of acute abdomen hospitalizations, this is offset with a 60% to 80% mortality within the first 24 hours. With the ever-expanding geriatric population, this disease is expected to increase.
Anatomy
The abdominal aorta gives off 3 major branches to the intestines, which are the celiac artery (CA), superior mesenteric artery (SMA), and inferior mesenteric artery. The CA perfuses the foregut (distal esophagus to second portion of duodenum). Acute mesenteric ischemia of the foregut is very rare, because the CA is a short, wide artery with good collateral flow. The SMA perfuses the midgut (duodenum to distal transverse colon), which encompasses nearly the entire small bowel and two-thirds of the large bowel. This is the most common embolic site of mesenteric ischemia owing to a favorable take-off angle (approximately 45°) from the aorta. The inferior mesenteric artery perfuses the hindgut (transverse colon to rectum) and is rarely the sole vessel involved in mesenteric ischemia. Collateral circulation from the CA or inferior mesenteric artery generally allows sufficient perfusion in reduced SMA flow states, such as nonocclusive or thrombotic mesenteric ischemia.
Pathophysiology
Beside the abdominal aortic anatomy, it is important to understand how the bowel layers are affected by mesenteric ischemia starting from the inner to most outer layer (mucosa, submucosa, muscularis, and serosa). With mesenteric ischemia early on, the furthest layer (mucosa) from the blood supply is the first to become ischemic and is the reason for extreme, visceral pain. However, because the outer structures (musclaris and serosa) have not become ischemic, there is minimal irritation of the parietal peritoneum when the examiner indents down against the serosa and the external layers of the bowel. Hence, there is pain “out of proportion” to examination early in the disease process, where there is no focal localization or peritonitis. Eventually, the muscularis and serosal layers become ischemic and infarct, leading to peritoneal irritation and guarding with rigidity. At this point, the pain is “in proportion” to the examination with development of peritonitis. It is also important to consider that, between the early and late presentations mentioned, there may be a deceptive pain-free interval of 3 to 6 hours caused by a decline in intramural pain receptors from hypoperfusion.
The classic types
Mesenteric ischemia can be classified as acute versus chronic or occlusive versus nonocclusive. The following are the major 4 etiologies of acute mesenteric ischemia : Acute arterial emboli, acute arterial thrombosis, mesenteric venous thrombosis, and nonocclusive.
Acute Arterial Emboli
In the most frequent cause of mesenteric ischemia, accounting for 40% to 50% of cases, the embolus lodges in the SMA. The proximal branches of the SMA (jejunal and middle colic arteries) are usually preserved, because generally the embolus lodges 3 to 10 cm distally from the SMA takeoff, where the artery tapers. This is just after the first major branch of the SMA (the middle colic artery). As a result, the proximal small and large bowels are usually spared. Owing to poorly developed collateral circulation, the onset of symptoms in cases of embolus is usually severe and dramatic pain. When the bowel becomes ischemic, it has a propensity to empty itself, leading to vomiting or diarrhea, so-called gut emptying. This is one reason mesenteric ischemia is often misdiagnosed as gastroenteritis. Common predisposing factors include atrial fibrillation, cardiomyopathy, recent angiography, and valvular disorders, such as rheumatic valve disease.
Acute Arterial Thrombosis
Patients with long-standing atherosclerosis may experience plaque development at the origin of the SMA, a site of turbulent blood flow. This subsequent stenosis may lead to long-standing postprandial pain (“intestinal angina”) and “food fear” with resultant weight loss. These symptoms of chronic mesenteric ischemia can be seen in up to 80% of patients who develop arterial thrombosis. If the plaque ruptures acutely or the stenosis reaches a critical level, patients may present with acute pain, similar to those with arterial emboli.
Mesenteric Venous Thrombosis
This form of mesenteric ischemia is generally found in patients with an underlying hypercoagulable state, and mesenteric venous thrombosis accounts for 10% to 15% of the total cases. Patients typically present with less severe and more insidious pain than those with arterial occlusion. Patients may demonstrate weight loss, depending on the duration of symptoms. Most patients present after more than 24 hours of symptoms. In 1 study, the mean symptom duration was 5 to 14 days, with many patients experiencing pain for 1 month before diagnosis. Predisposing risk factors include malignancy, sepsis, liver disease or portal hypertension, sickle cell disease, and pancreatitis. Many patients have heritable hematologic disorders including protein C and S deficiency, antithrombin III deficiency, and factor V Leiden mutation. One-half of patients with mesenteric venous thrombosis have a personal or family history of venous thromboembolism.
Nonocclusive
This form of mesenterial ischemia occurs in 20% of patients owing to failure of autoregulation in low-flow states such as hypovolemia, potent vasopressor use, heart failure, or sepsis. The underlying ischemia from splanchnic vasoconstriction can further lead to hypotension from endogenous substances, perpetuating a vicious cycle. This accounts for the extremely high mortality rate, usually owing to the poor health of the affected population with multiple comorbidities, combined with the difficulty in treating the primary cause of diminished intestinal blood flow.
Features and presentation
Mesenteric ischemia is often described in 3 progressive phases when the pathophysiology is considered: the hyperactive phase, paralytic phase, and shock phase.
Hyperactive Phase
Severe abdominal pain out of proportion is the usual presenting symptom. Other early symptoms including emesis, diarrhea, and bloody stools are common, but not always present. Early emesis and diarrhea are due to ischemia of the innermost bowel layers leading to gut emptying and eventual bloody stools. Several studies have demonstrated that abnormal mental status may be associated with early presentation, but can also be indicative of late phase.
Paralytic Phase
As ischemia progresses, the abdominal pain becomes in proportion to the examination leading to focal, localized tenderness. Bowel motility decreases, leading to abdominal distention and absent bowel sounds. However, bowel sounds are not helpful in ruling in or out the disease.
Shock Phase
Eventual necrosis leads to leaking of fluid through the bowel wall, resulting in diffuse peritonitis. However, peritonitis is only reported in 16% of patients with necrotic bowel. Sepsis with metabolic acidosis, dehydration, hypotension, tachycardia, and confusion often occurs. The typical patient is usually elderly (median age, 74 years) with multiple risk factors presenting with sudden onset of severe abdominal pain that is out of proportion to the examination (ie, pain out of proportion), meaning intense subjective pain with no objective tenderness on palpation. Risk factors including peripheral arterial disease (27%), coronary artery disease (46%), diabetes, dialysis, venous thromboembolism, and hypertension are common, but not always present. Pain is the most consistent presenting symptom, beginning as crampy, vague periumbilical abdominal pain that evolves over time to focal, localized tenderness and peritonitis owing to transmural infarction of all bowel layers, as discussed in the Pathophysiology section.
It is important to understand that presentation varies based on the etiology and type of mesenteric ischemia. The presentation of mesenteric ischemia is typically acute severe abdominal pain with a paucity of physical examination findings. History and physical examination findings, such as acute abdominal pain, pain out of proportion, peritoneal signs, guaiac-positive stool, acute abdominal pain, heart failure, and atrial fibrillation, have a wide range of sensitivities and are frequently absent. The presentation and examination are challenging; 1 study demonstrates the disease is suspected in only 22% of patients. Therefore, clinicians should be vigilant in considering mesenteric ischemia in the differential of abdominal pain of unclear etiology. Assessing the patient’s pretest probability for disease, actively searching for known risk factors, and adding in clues based on the patient’s history and physical examination findings are important factors in the diagnostic process for wary clinicians.
Diagnosis
Laboratory Tests
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White blood cell count
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Lactate
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d -Dimer
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Urine intestinal fatty acid binding protein
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Diagnostic biomarkers are tools designed to improve clinical decision making, especially in mesenteric ischemia, where early symptoms are nonspecific, and mortality increases with delayed or missed diagnosis. Numerous laboratory abnormalities have been described in mesenteric ischemia, including elevated amylase, lactate dehydrogenase, large base deficit, hemoconcentration, leukocytosis, and high anion gap metabolic acidosis with elevated lactate (specifically d -lactate). None of these findings are sensitive or specific for mesenteric ischemia and are often late findings. Troponin I levels may be elevated, but this finding is not specific for mesenteric ischemia and has been shown to lead to delays in definitive care of these patients with inappropriate cardiology consultations.
Laboratory tests include white blood cell count, pH from venous blood gas, d -dimer, lactate, and urine intestinal fatty acid binding protein. A summary of laboratory test sensitivity and specificity is provided in Table 1 . Many physicians rely on these tests to enhance decision making and diagnosis, but this is a potential pitfall. Approximately 75% of patients will have a white blood cell count of greater than 15,000 cells/mm. However, this does not differentiate mesenteric ischemia from other diagnoses, where 25% of cases do not have an increase. Metabolic acidosis is not always present, and metabolic alkalosis can present early if vomiting is a predominant symptom. d -Dimer is 96% sensitive, but it is not specific. Physicians should not rely on lactate for diagnosis, because this test is not always increased. 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 via the Cori cycle. As gut ischemia increases, the liver is unable to keep up with converting lactate into glucose, and lactate spills over into the systemic circulation, where it eventually increases in late stages of disease. A newer test is the urine intestinal fatty acid binding protein, and this test has demonstrated a sensitivity of 90% and specificity of 89% in 1 study. However, these findings have not been validated, and the vast majority of emergency departments do not have access to this test.
Imaging
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Abdominal plain films
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Ultrasound imaging
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Computed tomography (CT) angiography of the abdomen and pelvis
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Angiography
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Laparoscopy
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