Multimodality Diagnosis of Mesenteric Ischemia

This protocol will be helpful for making an early diagnosis and treatment of mesenteric ischemia before developing broad necrosis. Non-invasive method without an exposure of irradiation, or need of contrast media. It may be also useful for diagnosing non-obstructive mesenteric ischemia, as well as strangulated hernias.

Emergency medicine, intensive care medicine, gastroenterology, digestive surgery, and so on. It may be difficult for beginners to manipulate the T probe in the stomach. Experienced anesthesiologists may help them because this technique is based on comprehension of images related to the probe manipulations.

Begin by visualizing the descending aorta on the short axis and advancing the probe into the stomach while maintaining the aorta image in view. Rotate the probe counterclockwise with slight anti flexion of the probe tip for continuous contact with the esophageal wall. Switch to color doppler mode for easy identification of visceral branches through flow signals.

Ensure the celiac artery orifice appears at the 12 o'clock position of the abdominal aorta. Advance the probe one inch further, positioning the superior mesenteric artery or SMA at the 12 to two o'clock position. Rotate the scanning plane to 90 degrees to visualize the long axis view of the aorta and visceral branches.

Use a convex or sector probe with a frequency range of two to five megahertz for optimal visualization and assessment of the intestine through the abdominal wall. Position the probe on the abdominal wall near the navel to visualize the intestine. Locate an acoustic window between the intestinal gas.

Then place the probe vertically above the naval level to assess the SMA flow. Locate the SMA originating from the abdominal aorta and running caudally within a short distance. Inject 2.5 milligrams of ICG dissolved in 10 milliliters of distilled water into the central venous line.

Follow the injection with a 10 milliliter saline flush. Visualize the perfused ICG in the mesenteric artery and the intestinal tissue. Use a suitable sensor to measure the relative oxygen saturation for the targeted tissue depth.

Observe the regional oxygen saturation value displayed, which updates every five seconds. The representative TEE findings of three cases of bowel necrosis caused by acute aortic dissection are shown. In one case, the true lumen in the SMA was severely compressed.

In the case of aortic-type malperfusion, the SMA had no detectable flow while the celiac artery exhibited a strong flow signal. In a different case, both arteries experienced malperfusion resulting in no blood flow at the respective locations. The abdominal ultrasound revealed diminished or absent peristalsis and intestinal dilation.

Portal vein thrombosis was observed, characterized by a lack of blood flow in the left branch of the portal vein, leading to the umbilical portion, as well as an enlarged extra hepatic portal vein with a flow signal defect. In a case involving salvaged intestine associated with acute aortic dissection, the blood flow in the SMA was weak. However, an increased flow with a reverse direction into the distal portion from the branch artery was observed.

During laparotomy, the intestine displayed a slightly pale appearance and diminished peristalsis. Following revascularization, both color and movement showed improvement. Upon arterial clamping, relative oxygen saturation dropped to less than 60%in many cases, but recovered after re-perfusion.

Post-surgery, relative oxygen saturation stayed more than 60%with no necrosis. Vein clamping slightly reduced the relative oxygen saturation and significantly elevated the hemoglobin index. During surgery, the perfusion status of a patient can change rapidly and unpredictably.

Therefore, it is essential to conduct timely assessments to ensure that the patient's condition is closely monitored and any necessary interventions are taken promptly.