Doppler Ultrasound of the Mesenteric Vasculature

Anatomy

A thorough understanding of the anatomy of the mesenteric circulation provides a foundation for the interpretation of the sonographic examination. The mesenteric arterial circulation is comprised of the celiac, superior mesenteric, and inferior mesenteric arteries ( Fig. 26.1 ), all of which arise from the abdominal aorta. The abdominal aorta is a continuation of the thoracic aorta and extends from the aortic hiatus of the diaphragm to the aortic bifurcation. The average male abdominal aorta measures approximately 13 cm in length, up to 27 mm in anteroposterior diameter in its proximal portion, and tapers down to 13 mm in anteroposterior diameter at the level of the bifurcation. The celiac artery is the first major branch of the abdominal aorta and arises from the ventral surface of the aorta at the level of the T12 and L1 vertebral bodies. It courses anteroinferiorly before branching into the common hepatic, splenic, and left gastric arteries. The celiac artery supplies blood to the solid visceral organs (liver, pancreas, and spleen), the stomach, and proximal small bowel. The SMA originates approximately 1 cm inferior to the celiac artery, at the L1 vertebral level, and supplies blood to the bowel from the duodenum to the splenic flexure. The IMA is the smallest mesenteric vessel and originates from the left anterolateral aspect of the abdominal aorta, approximately 4 cm above the aortic bifurcation at the L4 vertebral level. It supplies the descending and rectosigmoid colon. Note that both the right and left renal arteries arise from the lateral aspects of the abdominal aorta between the SMA and the IMA. The mesenteric arteries may have variant anatomy in approximately 20% of the population, which may lead to misinterpretation of Doppler examination findings. The most common variant is a replaced right hepatic artery, in which the right hepatic artery originates from the SMA rather than the common hepatic artery (a branch of the celiac artery). This anomaly is seen in up to 17% of the general population. On gray-scale and color Doppler imaging, the replaced right hepatic artery may be seen arising from the SMA and coursing into the liver ( Fig. 26.2 ). On pulsed Doppler interrogation, the examiner may observe a low-resistance blood flow pattern in the SMA, a feature that is more characteristic of the celiac artery. Other common anatomic variants include an anomalous common hepatic artery that originates from the SMA (2% to 3% of cases) or from the aorta (1% to 2% of cases); and a common origin of the celiac artery and the SMA, termed the celiacomesenteric artery, which originates from the abdominal aorta and is seen in less than 1% of the population ( Fig. 26.3 ).

A rich collateral network exists between the mesenteric arteries via the mesenteric arcades and the marginal artery of Drummond, which ensures continuous perfusion of the organs that these vessels supply. Additional vascular protection is provided from communicating pathways between the three mesenteric arteries. For example, communication between the celiac artery and the SMA occurs by way of the gastroduodenal artery (also known as the pancreatoduodenal arcade; Fig. 26.4 ). The superior and inferior mesenteric arteries are connected by the arc of Riolan and the marginal artery of Drummond. The arc of Riolan, also known as the “meandering mesenteric artery” connects the middle colic artery, a branch of the SMA, with the left colic artery, a branch of the IMA ( Fig. 26.5 ). The marginal artery of Drummond represents a continuous arterial arcade along the inner margin of the colon, formed by anastomoses of the terminal branches of the SMA (ileocolic, right colic, and middle colic arteries) and IMA (left colic and sigmoid arteries) ( Fig. 26.6 ). Additional anastomoses exist between the IMA and branches of the internal iliac arteries, specifically via the superior rectal artery (a distal continuation of the IMA), the middle rectal artery (a branch of the internal iliac artery), and the inferior rectal artery (a branch of the internal pudendal artery) ( Fig. 26.7 ).

Given this extensive collateral circulation, patients may remain asymptomatic despite the presence of underlying mesenteric arterial disease. Mesenteric stenosis or occlusion of a single vessel may not produce symptoms in the setting of a patent collateral network. In general, severe compromise (≥70% stenosis or occlusion) of at least two of the three mesenteric arteries is required for symptoms of mesenteric ischemia to be present. This “two-vessel rule” holds in most patients and is utilized clinically for the diagnosis of chronic mesenteric ischemia.

Physiology

Normal blood flow patterns differ between the celiac artery and the mesenteric arteries ( Fig. 26.8 ). The celiac artery supplies blood to the low-resistance vascular beds of the liver and spleen. The waveforms of the celiac artery and its branches demonstrate a low-resistance pattern with high end-diastolic velocities seen on pulsed Doppler imaging ( Fig. 26.9 ). This low-resistance flow pattern is because of the continuous forward flow of blood during both systole and diastole necessary to meet the high oxygen demands of the liver and spleen. The low-resistance blood flow pattern in the celiac artery is independent of food intake; therefore there is no significant change in peak systolic or end-diastolic velocities in the celiac artery following a meal.

The superior and inferior mesenteric arteries supply the high-resistance vascular beds of the small intestine and colon. Pulsed Doppler evaluation reveals high-impedance flow with low diastolic velocities in the fasting state ( Fig. 26.10A ). This is because of the relative vasoconstriction of the mesenteric branch vessels before a meal, when the bowel is empty and quiescent. After a meal, however, there is an increase in mesenteric arterial blood flow in order to assist digestion. This is accomplished by vasodilatation of the mesenteric branches, which in turn allows for increased blood flow to the intestines (see Fig. 26.10B ). Moneta and colleagues showed that both peak systolic and end-diastolic velocities increase after a meal, with at least doubling of the end-diastolic velocity (EDV) in the SMA after eating. They found the greatest increases in blood flow velocity following meals that included fat, carbohydrate, and protein, and concluded that providing a patient with a mixed meal could be used as a provocative test to assess the reactivity of the mesenteric circulation. The presence of increased flow velocities after a meal infers the patency of splanchnic blood supply in their studies.

Although duplex ultrasound examinations of the mesenteric arteries may be performed before and after a meal to identify physiologic changes in blood flow, there appears to be significant variability in the response to food. Healy and associates found that postprandial duplex studies were not dependable and did not improve diagnostic accuracy in their series of patients. Because of the inconsistency and unreliability of the preprandial and postprandial examination results, this technique has fallen out of favor and is not commonly utilized in clinical practice.

Natural history of bowel ischemia

Mesenteric ischemia is an uncommon disorder that is associated with high mortality and morbidity, with mortality rates ranging between 30% and 90%. Factors that are related to the high mortality include insidious onset of symptoms, age at presentation greater than 60 years, and delay in diagnosis. Most cases of mesenteric ischemia are attributable to an acute event such as embolization or thrombosis of an artery or vein, which leads to decreased blood supply to the splanchnic vasculature. Mesenteric ischemia can be classified into acute and chronic forms, with chronic mesenteric ischemia accounting for less than 5% of all cases.

Acute mesenteric ischemia

Acute mesenteric ischemia is a life-threatening condition with reported mortality rates ranging from 59% to 93%. It is estimated that approximately 33% of cases of acute mesenteric ischemia are caused by arterial embolism, 33% are caused by arterial thrombosis, between 20% and 30% are caused by nonocclusive ischemia (hypotension), and the few remaining cases are caused by venous thrombosis.

Acute Arterial Occlusive Disease.

Acute arterial occlusive disease is caused by embolus, thrombosis, dissection, or external compression of a vessel. Doppler sonography is generally less useful in this situation because of the rapid time course of the disease and necessity for emergent intervention. Computed tomography (CT) angiography is the examination of choice. Duplex Doppler ultrasound may demonstrate acute thrombosis of a mesenteric artery as an echogenic focus within the lumen of a mildly dilated artery. High-resistance waveforms may be detected just proximal to the level of occlusion, and tardus-parvus waveforms may be seen distal to the site of occlusion ( Fig. 26.11 ). The treatment of choice depends on the size and location of the thrombus. Anticoagulation with thrombolytics and continuous papaverine infusion is considered acceptable in the case of a small thrombus that is located within a proximal vessel, prior to the branching of collateral arteries. A large thrombus that is located distal to branching collaterals is typically treated with embolectomy and/or resection, particularly in the setting of positive peritoneal findings ( Fig. 26.12 ).

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