SMV thrombosis with long segment jejunal infarction
Severe abdominal pain.
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Thrombosis of superior mesenteric vein and several smaller branches. Nonocclusive thrombus in the main portal vein.
Mesenteric congestion. Small ascites.
Dilated proximal small bowel, which transitions into a segment of hypoenhancing, thick-walled small bowel in the lower abdomen. Following this segment distally, there is gradual return of enhancement starting with the mucosa, and gradual resolution of submucosal edema.
Preoperative Diagnosis: Necrotic bowel, portal vein thrombosis, SMV thrombosis
Postoperative Diagnosis: Same
1) Exploratory Laparotomy
2) Small bowel resection
3) Temporary abdominal closure
1) 48 cm necrotic bowel in proximal jejunum resected with adjacent mesenteric hematoma
2) Significant venous hypertension secondary to portal vein thrombosis
3) Mesenteric congestion with bowel edema
4) Hemorrhagic ascites
...A midline abdominal incision was made and carried down to the level of the fascia with bovie electrocautery. The fascia was incised and upon gaining entrance to abdomen, the patient was found to have significant hemorrhagic ascites. The small bowel was eviscerated and run from the ligament of Treitz to terminal ileum. There was a 48cm segment of grossly necrotic, thickened bowel with associated mesenteric congestion and a large mesenteric hematoma. This area of bowel was not viable so the decision was made to segmentally resect it. The bowel was divided with a GIA stapler and the mesentery taken with a ligasure using a double burn technique. Despite this, the cut edge of the mesentery continued to ooze secondary to venous hypertension from the patient's known portal vein and SMV thrombosis. As a result, the cut edge was oversewn with a running, locking 3-0 prolene suture. The bowel was once again run and noted to be dilated, and injected proximal to our small bowel resection. No additional areas of compromised bowel were identified. The patient was noted to have thickened congested mesentery. At this point, the decision was made to proceed with a temporary abdominal closure with abthera. The abthera was cut to size and placed at 125mmHg intermittent suction. The patient was transported, intubated, in critical condition to the ICU on pressors.
It is uncommon for SMV thrombosis to result in such a large segment of intestinal necrosis (arterial thrombosis is more likely).
This patient had a remote history of pulmonary embolism, suggesting hypercoagulable state as the cause of thrombosis. The thrombosis likely developed rapidly given the acute presentation and lack of significant collaterals. There appears to be thrombosis of the distal venous branches (venous arcades and venae rectae), which is associated with higher risk of infarct. The patient also had a history of hypertension, which perhaps contributed to elevated arterial pressures resulting in more rapid progression of edema, hemorrhage, ischemia, infarction and necrosis.
The most important sign of ischemia is wall thickening. The near complete lack of enhancement of a long segment of bowel indicates infarction, with gradual return of enhancement and resolution of wall thickening distally.