January 2010
Case study: 44 y/o previously healthy female, no significant medical history, no medications, presents to the emergency room with nausea, vomiting and blood diarrhea
Figure 1a
Figure 1b
Figure 1: Axial (a) and coronal (b) abdominal CT shows thickened descending colon walls with mild surrounding inflammation.
Figure 2a
Figure 2b
Figure 2: Axial (a) and coronal (s) CT shows filling defects in the right and left (arrowheads in ‘A’) and main (arrow in ‘B’) portal vein branches, representing thrombus.
Diagnosis:
Ulcerative colitis complicated by acute portal vein thrombosis.
Discussion:
Ulcerative colitis is an inflammatory bowel disease (IBD) which is characterized by inflammation which predominantly involves the colonic mucosa and sometimes the submucosa and deeper layers of the bowel wall. In the active stages of the disease, the mucosa is erythematous, hemmorhagic, and granular in appearance. In its chronic phase, the colon may become fibrotic, narrowed, and shortened. In acute disease involving only the mucosa, the CT findings may be minimal, showing slight bowel wall thickening. In more severe cases, where the submucosa or muscularis is involved, bowel wall thickening and inflammation may be more pronounced. In more chronic forms, fat is deposited in the submucosa, giving a “target” appearance to the bowel wall.
The etiology of ulcerative colitis is controversial, and multiple factors may be involved. Some theories include: environmental exposures, diet, immune dysfunction, and genetic factors.
Venous thrombosis is an uncommon, but recognized complication of inflammatory bowel disease. The incidence of thromboembolic complications of inflammatory bowel disease range from 1-8%. Deep vein thrombosis with or without pulmonary emboli are more common vascular events, although other veins, such as the portal and mesenteric veins, can be involved.
The cause of increased thromboembolic events in IBD is uncertain, and factors such as fibrinogen levels, activated protein C resistance, hyperhomocysteinemia, nutritional deficiencies such as vitamin B6, B12, and folic acid have all been investigated. It has been theorized that bowel inflammation itself can activate the coagulation cascade.
At the time of this writing, the patient is being evaluated for presumed ulcerative colitis complicated by portal vein thrombosis.
Teaching Point:
While radiologists should always evaluate the mesenteric, portal and all venous systems when interpreting abdominopelvic CT, they should be particularly attentive to these areas in patients with inflammatory bowel disease.
