Clinical Evaluation and Treatment of Mesenteric Vascular Disease

Chapter 27 Clinical Evaluation and Treatment of Mesenteric Vascular Disease


Clinical evaluation of possible mesenteric ischemia begins with a careful history and physical examination and—above all—an appropriate index of suspicion for the diagnosis. The major etiologies of mesenteric ischemia include mesenteric venous thrombosis (MVT), acute mesenteric ischemia, nonocclusive mesenteric ischemia (NOMI), and chronic mesenteric ischemia (CMI). These differ in their underlying pathologies and the clinical settings in which they occur, but there may be significant overlap in their clinical presentation. The most crucial point is to understand the variety of clinical settings in which intestinal ischemia can occur and to include mesenteric ischemia in the differential diagnosis of patients presenting with abdominal pain. The goal is to achieve a diagnosis prior to the onset of bowel infarction. Without consideration of intestinal ischemia, the appropriate diagnostic evaluation is unlikely to be obtained, resulting in needless additional morbidity and mortality.

Acute Occlusive Mesenteric Ischemia

Signs and symptoms

Acute occlusive mesenteric ischemia is caused by embolism to the superior mesenteric artery (SMA) or acute thrombotic occlusion of an atherosclerotic SMA. Mortality exceeds 60%.1

Thrombotic occlusion of the SMA carries a worse prognosis than embolism to the SMA because with thrombotic occlusion, the SMA occludes proximal to the middle colic artery and interrupts arterial flow to the entire small intestine. Emboli, which usually originate from the heart, typically lodge in the SMA distal to the origin of the middle colic artery, thereby maintaining some perfusion to the small intestine via the middle colic and jejunal artery branches.

Abdominal pain is the most common presenting symptom in patients with occlusive acute mesenteric ischemia, and physical findings can range from nonspecific tenderness to an acute abdomen. Distention, rigidity, and rebound tenderness occur, particularly when the diagnosis of acute mesenteric ischemia is delayed. The classic presentation is sudden onset of acute abdominal pain out of proportion to the physical findings. This reflects profound intestinal ischemia without associated bowel perforation and peritonitis. Vomiting, fever, and diarrhea are present in one third of patients with acute mesenteric ischemia. Patients with embolism tend to present with an acute onset of abdominal pain, whereas patients with thrombosis of a stenotic SMA may have a more delayed presentation.

Laboratory values are typically nonspecific. The majority of patients will have moderate to marked leukocytosis, but about 10% of patients will have a normal white blood cell (WBC) count. Elevated serum amylase and metabolic acidosis may occur in patients with necrotic bowel, but an absence of these findings does not exclude bowel necrosis.

Radiological diagnosis

Ultrasound has a limited role in diagnosing acute occlusive mesenteric ischemia. Duplex ultrasonography in the setting of an acute abdomen is limited by abdominal distention, excessive bowel gas, and patient discomfort.

An abdominal computed tomography (CT) scan is often obtained during evaluation of a patient with abdominal pain. In addition to finding other abdominal pathologies causing abdominal pain, CT scans can detect late findings of acute mesenteric ischemia with a sensitivity of 90%, including bowel luminal dilation, bowel wall thickening, submucosal edema or hemorrhage, pneumatosis intestinalis, and portal venous gas.2 These findings are associated with some degree of intestinal infarction. Emboli tend to lodge distally, and thus the sensitivity of CT scanning in detecting mesenteric arterial embolic occlusion is low and ranges from 37% to 80%3 (Fig. 27-1). In patients with early ischemia, there may be minimal findings on CT scans. These patients benefit most from early diagnosis and definitive mesenteric revascularization before the onset of intestinal infarction. Therefore, a high index of suspicion and thorough physical examination is of the utmost importance in this population of patients.

Mesenteric angiography remains the gold standard for diagnosing vascular lesions associated with acute mesenteric ischemia, but its use is predicated on clinical judgment. In a patient with obvious peritoneal findings and suspected necrotic bowel, as evidenced by hypotension and acidosis, an urgent exploratory laparotomy is required to resect necrotic bowel and perform revascularization. In this emergent situation, preparation and performance of a mesenteric angiogram may delay definitive operative treatment and increase mortality.

In patients without peritoneal findings but clinically suspected to have mesenteric ischemia, angiography can be performed to make the definitive diagnosis and plan additional therapy. Abrupt occlusion of the SMA distal to the origin of the middle colic artery is typically seen in patients with an embolus (Figs. 27-2 through 27-4), whereas patients with thrombotic occlusion of a chronically stenotic SMA show signs of occlusion beginning at its origin from the aorta.

Chronic Mesenteric Ischemia

Radiological diagnosis

Duplex Ultrasonography

Duplex ultrasonography can serve as a valuable noninvasive screening test for splanchnic artery stenosis and for follow-up in patients with mesenteric artery reconstructions. Despite the accuracy of duplex detection of mesenteric artery stenoses, an appropriate history and physical examination and angiographic confirmation of high-grade stenoses or occlusion of the splanchnic vessels are still required for the diagnosis of CMI. Duplex examination of the mesenteric arteries can be technically difficult and should be performed by vascular technologists with extensive experience in abdominal ultrasound techniques.

In healthy individuals, fasting blood flow velocity waveforms differ between the SMA and the CA. Arterial waveforms reflect end-organ vascular resistance. The liver and spleen have relatively high constant metabolic requirements and are therefore low-resistance organs. As a result, CA waveforms are generally biphasic with a peak systolic component, no reversal of end-systolic flow, and a relatively high end-diastolic velocity (EDV). The normal fasting SMA velocity waveform is triphasic, reflecting the high vascular resistance of the intestinal tract at rest (Figs. 27-8 and 27-9). There is a peak systolic component, often an end-systolic reverse flow component, and a minimal diastolic flow component.

Changes in Doppler-derived arterial waveforms in response to feeding are different in the CA and SMA. Because the liver and spleen have fixed metabolic demands, there is no significant change in CA velocity waveform after eating. Blood flow in the SMA, however, increases markedly after a meal, reflecting a marked decrease in intestinal arterial resistance. Waveform changes in the SMA postprandially include a near doubling of systolic velocity, tripling of the EDV, and loss of end-systolic reversal of blood flow. In addition, there is a small but detectable increase in the diameter of the SMA postprandially. The diameter of the SMA has been shown to be 0.60 ± 0.09 cm in the fasting state and 0.67 ± 0.09 cm after a meal. These changes are maximal at 45 minutes after ingestion of a test meal5 and are dependent on the composition of the meal ingested. Mixed composition meals produce the greatest flow increase in the SMA when compared with equal caloric meals composed solely of fat, glucose, or protein.6

Detection of Splanchnic Arterial Stenosis

Duplex ultrasound can detect hemodynamically significant stenoses in splanchnic vessels. In 1986, investigators at the University of Washington found that flow velocities in stenotic SMAs and CAs were significantly increased when compared with normal SMAs and CAs.7 Quantitative criteria for splanchnic artery stenosis were first developed and validated at Oregon Health & Science University.8

In a blinded prospective study of 100 patients who underwent mesenteric artery duplex scanning and lateral aortography, a peak systolic velocity (PSV) in the SMA of 275 cm/s or more indicated 70% or greater SMA stenosis with a sensitivity of 92%, specificity of 96%, positive predictive value of 80%, negative predictive value of 99%, and accuracy of 96%9 (Fig. 27-10). In the same study, a PSV of 200 cm/s or higher identified 70% or greater angiographic CA stenosis with a sensitivity of 87%, specificity of 80%, positive predictive value of 63%, negative predictive value of 94%, and accuracy of 82% (Fig. 27-11).

Other duplex criteria for mesenteric artery stenoses are also in use. An SMA EDV greater than 45 cm/s correlates with 50% or greater SMA stenosis with 92% specificity and 100% sensitivity. A CA EDV of 55 cm/s or higher predicts 50% or greater CA stenosis with 93% sensitivity, 100% specificity, and 95% accuracy.10,11

Postprandial mesenteric duplex scanning has been used as an adjunct to fasting duplex scanning to aide in the diagnosis of mesenteric artery stenoses.12 In patients with less than 70% SMA stenosis, postprandial SMA PSV increases by more than 20% over baseline velocity. The percent increase in SMA PSV is less in patients with 70% or greater SMA stenosis. Specificity for the combination of fasting SMA PSV and postprandial PSV, however, is marginally improved over that provided by a fasting duplex scan alone. Therefore, although theoretically attractive, postprandial duplex scanning offers no significant improvement over fasting mesenteric duplex scanning; its routine use as part of ultrasound assessment of mesenteric artery stenosis is unnecessary. Postprandial examinations are occasionally useful in technically difficult ultrasound studies in that if there is a postprandial response, the insonated vessel can be confirmed as being the SMA.

Duplex ultrasonography is best used as an initial screening study to evaluate for visceral artery stenosis in patients with chronic abdominal pain that may be consistent with CMI. Angiography is required to establish a definitive diagnosis of mesenteric artery stenosis.

Computed Tomography

Standard CT imaging can be of some value in mesenteric artery stenosis evaluation (also see Chapter 14). Currently, however, no studies have compared the accuracy of spiral CT with angiography in assessing visceral artery stenoses. Computed tomography angiography can detect but not precisely quantify proximal stenosis of the CA and SMA, and it is limited by lower resolution and bowel motion artifact in its ability to detect lesions involving more distal branches.13 Computed tomography scans are often obtained to evaluate abdominal pain. Findings suggestive of mesenteric artery stenosis include calcification at the origin of the CA and SMA and lack of contrast enhancement within the vessel lumen (Fig. 27-12).

Magnetic Resonance Imaging

Development of fast breath-hold three-dimensional gadolinium-enhanced magnetic resonance angiography (3D Gd-enhanced MRA) has improved the ability of MRA to detect proximal splanchnic artery lesions (also see Chapter 13). Magnetic resonance angiography is limited in its ability to image more distal visceral branches because of limited spatial resolution, peristaltic and respiratory motion, and chemical shift changes between the vessels and fat. The accuracy of 3D Gd-enhanced MRA in detecting visceral artery stenosis has been well studied. Overall sensitivity and specificity for detecting 75% or greater stenosis or occlusion of the CA, SMA, or inferior mesenteric artery (IMA) were 100% and 95%, respectively.14

In addition to providing anatomical details, magnetic resonance (MR) technology can quantify arterial flow using the phase-contrast magnetic resonance imaging (MRI) technique, which provides information about the presence, magnitude, and direction of blood flow and has been studied in patients with CMI.15 Fasting and postprandial flow in the SMA have been compared in patients with documented atherosclerotic disease and normal volunteers. Mean fasting SMA blood flow has been shown to be higher in atherosclerotic patients than in normal individuals. This difference can be used to evaluate for CMI. The addition of MR oximetry technology, where increased oxygen extraction after a meal is seen in those with significant mesenteric vessel atherosclerosis, is promising with regard to diagnosing CMI.15 Further validation studies correlating the degree of change in mesenteric blood flow and oxygenation with angiographic percentage of stenosis will be necessary before phase-contrast MRI and MR oximetry are universally adopted as routine noninvasive diagnostic methods for patients with CMI.


Chronic and Acute Mesenteric Occlusive Disease

The available literature includes no randomized or controlled clinical trials of surgical intervention for treatment of mesenteric ischemia, and none are likely to be performed. Published clinical reports include varied recommendations for treatment, and many do not include descriptions of operative methods. Others describe technically demanding procedures requiring extensive dissections in difficult areas.16,17 Only recently has objective determination of postoperative graft patency been included in clinical series.18,19 For all these reasons, there is no current consensus regarding the surgical details of treatment for intestinal ischemia.

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Jul 1, 2016 | Posted by in CARDIOLOGY | Comments Off on Clinical Evaluation and Treatment of Mesenteric Vascular Disease

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