|ECR 2019 / C-3257|
|A pictorial review and guide of the ischemic bowel|
Findings and procedure details
MDCT protocols should be optimized for an angiographic study and assessment of the Intestines / mesentery / abdominal viscus:
In this context, triphasic CT involves the acquisition of scans in the pre-contrast, arterial and venous phases.
The use of oral contrast is not recommended in patients with AMI. The transit time for oral contrast through the bowel will delay definitive treatment in AMI and the associated vomiting and adynamic ileus limit the useful passage of oral contrast material.
Intravenous contrast medium:
IV rapid injection of 120 ml nonionic contrast material, smart prep is used to obtain an optimal arterial phase with a region of interest (ROI) drawn over the proximal aorta and scanning of the abdomen and pelvis is obtained once a 150 HU threshold is reached. Then porto venous phase ( 60 sec ) is obtained.
- From the diaphragm through the symphysis pubis
Include heart and thoracic aorta if suspicion of emboli
- Thin collimation: 2,5 mm ( 4B ) 0.75 mm ( 16 B ) and 0.6 mm ( 64 B )
•3D imaging and images reviews: multiplanar, maximum intensity projection and volume rendered techniques
- Sagittal projection : origin and proximal portion of mesenteric branches ++
- Volume rendered techniques / MIP coronal and coronal oblique: distal branches ++
- MIP: small bowel loops and colon ++
Key CT key diagnostic findings:
Direct signs: direct visualization of the thrombus (thrombosis, emboli)
Occlusive emboli can be readily detected within the lumen leading to abrupt cessation of contrast material flow within vessel lumen (fig3,4). Additionally, no or few collaterals are seen secondary to acute nature of the pathology.
In AMI secondary to mesenteric arterial thrombosis, thrombus is generally seen relatively hypodense just adjacent to an atherosclerotic lesion, and there can be collaterals since the pathology is almost always insidious.
Mesenteric venous thrombus is seen as a focal rounded hypoattenuating lesion with a peripheral contrast enhancement; thickness of enhancement around the venous thrombus depends on the degree of obstruction (partial or total) (fig 7,8,9,10).
Indirect signs: vary according to the state of the ischemia. Abnormalities of the bowel wall:
- Thickening of the bowel wall
Although it is not a specific finding, bowel wall thickness is the most common CT finding in acute bowel ischaemia (fig11).
In AMI, the bowel wall may be thickened or thinned, depending on the aetiological mechanism. In cases of bowel ischaemia caused by occlusions of mesenteric veins, bowel wall thickening is more pronounced than in cases caused exclusively by occlusions of mesenteric arteries. This is caused by haemorrhage, oedema and/or superimposed infection, which results in bowel wall thickening of up to 15 mm of the small and large intestines.
In cases of arterial occlusion or transmural infarction, bowel wall can be as thin as paper due to the ischemic insult on muscle and nerve tissues
- Dilated fluid-filled bowel loops
Bowel dilatation may result from interruption of intestinal peristalsis as a reflex to ischaemic injury or from irreversible and transmural ischaemic damage to the bowel wall.
- Abnormal enhancement of the bowel wall:
An ischaemic bowel segment may manifest with a hypoattenuating or spontaneous hyperattenuating bowel wall.
On unenhanced CT images, hypoattenuation of the bowel wall indicates bowel wall oedema, which is more typical in cases of acute bowel ischaemia caused by mesenteric venous occlusions. Otherwise, under these circumstances, hyperattenuation of the thickened bowel wall could also be seen because of intramural haemorrhage and haemorrhagic infarction.
On contrast-enhanced CT images, a highly specific although not sensitive finding for AMI is absent or substantially diminished bowel mural enhancement and has been termed “pale ischaemia”. Alternatively, in the postreperfusion period after arterial injury, hyperenhancement of the bowel is present much like “shock bowel”.
In cases of mesenteric venous occlusion, the vascular engorgement and oedema of the bowel wall in turn lead to leakage of extravascular fluid into the bowel wall and mesentery. The resultant oedematous bowel may have a “halo” or “target” appearance due to mild mucosal enhancement, submucosal and muscularis propria nonenhancement, and mild serosal/subserosal enhancement.
The pneumatosis (PI) can interest: the bowel wall, the adjacent structures (sub serous or mesentery), the porto-mesenteric veins (fig12):
Although pneumatosis is not a specific finding of intestinal ischaemia, which may occur in a wide range of non-emergent benign scenarios, when found, bowel ischaemia must be excluded first and foremost.
PI with porto-mesenteric venous gas correlates strongly with trans mural bowel infarction.
Adjacent Omental abnormalities:
- Omental edema
- Blurring of vessels contour (venous thrombosis)
- Pneumoperitoneum: the presence of gas within the peritoneal cavity suggests perforation and peritonitis, which are high-mortality complications of infarction.
- Associated ischemia of abdominal viscus (emboli): spleen, kidney, liver