Working Diagnosis:
Mesenteric Ischemia secondary to Superior Mesenteric Vein Thrombosis

Treatment:
Due to clinical deterioration, the patient underwent an emergent exploratory laparotomy and removal of 80 cm of small bowel. He was transferred to the ICU intubated with an open abdomen and wound vacuum in place. The next day, he underwent re-anastomosis. His postoperative course was uncomplicated. His initial hypercoagulable work-up was negative. He was discharged on oral apixaban. Final communication and hand-off were completed to his primary care physician.

Outcome:
He followed up with general surgery and had his Jackson Pratt drain removed 1 week following hospital discharge. He followed strict physical limitations for one month including no strenuous physical exertion, running, jumping, sit-ups, push-ups, or pulling/lifting greater than 20 pounds.
Two months following his surgery, he is exercising daily without restrictions and has no plan to restart testosterone or growth hormone use.

Author's Comments:
Performance enhancing drugs, including testosterone, are widely used to increase muscle mass, improve performance, and enhance appearance. Although controversial, some studies associate use of exogenous testosterone with hypercoagulability.
Several theories have been proposed, including platelet activation and increased erythropoiesis. In this case, the patient's only risk factors for venous thromboembolism were elevated BMI and androgen use.
Prolonged and consistent use of exogenous testosterone may have been the sole trigger for a thrombotic event, however he may have had a provoking event or an underlying predisposition despite a normal initial work-up.

Editor's Comments:
Key Educational Elements. Mesenteric venous thrombosis (MVT) is most often attributed to components of Virchow’s triad (stagnated blood flow, hypercoagulability, and vascular inflammation) and results in 80% of cases (secondary MVT). However, approximately 20% are idiopathic and considered primary MVT occurring in the absence of any identifiable predisposing factor. Hypercoagulability may be due to inherited disease (Factor V Leiden, prothrombin mutation, protein S deficiency, protein C deficiency, antithrombin deficiency, and antiphospholipid syndrome) or be acquired due to malignancies, hematologic disorders, and oral contraceptives. Alterations in the blood flow can occur with portal hypertension, pancreatitis, inflammatory bowel disease, sepsis, and trauma. MVT may also occur after ligation of the splenic vein for a splenectomy or ligation of the portal vein or the SMV as part of damage control surgery for severe penetrating abdominal injuries. The mechanism responsible for ischemia is a massive influx of fluid into the bowel wall and lumen resulting in systemic hypovolemia and hemoconcentration. The consequent bowel edema and decreased outflow of blood secondary to venous thrombosis impede the inflow of arterial blood, and this leads to bowel ischemia. Acute mesenteric ischemia is commonly considered a disease of the older population, (typical age of onset being older than 60 years) but it also affects the younger population, especially in those with atrial fibrillation or other risk factors such as oral contraceptive use or hypercoagulable states. In the younger population, symptoms may be present longer than in more typical cases of AMI, for more than 30 days. Infarction from MVT is rarely observed with isolated SMV thrombosis, unless collateral flow in the peripheral arcades or vasa recta is compromised and fluid sequestration and bowel wall edema are more pronounced than in arterial occlusion, sparing the colon because of better collateral circulation.

Elements critical to the educational value. There is no overall sex preference for AMI but men might be at higher risk for occlusive arterial disease because they have a higher incidence of atherosclerosis. Conversely, women who are taking oral contraceptives or are pregnant are at higher risk for MVT. Causes of MVT in over 80% of patients with MVT are found to have predisposing conditions such as hypercoagulability from protein C and S deficiency, antithrombin III deficiency, dysfibrinogenemia, abnormal plasminogen, polycythemia vera (most common), thrombocytosis, sickle cell disease, factor V Leiden mutation, pregnancy, and oral contraceptive use. Other causes include a tumor causing venous compression or hypercoagulability (paraneoplastic syndrome), infection (appendicitis, diverticulitis, or abscess), venous congestion from cirrhosis (portal hypertension) and venous trauma from accidents or surgery. Patients need to be educated regarding short-bowel syndrome and its side effects.

Take Home Points. Severe abdominal pain out of proportion to physical examination findings should be assumed to be acute mesenteric ischemia (AMI) until disproven. AMI can be due to mesenteric arterial emboli, mesenteric arterial thrombosis, non-obstructive mesenteric ischemia (NOMI) or mesenteric venous thrombosis. There are no laboratory studies that accurately identify the presence or absence of ischemic or necrotic bowel, although elevated lactate, and D-dimer may assist in the diagnosis.

References:
1. Bala M, Kashuk J, Moore EE, Kluger Y, Biffl W, Gomes CA, et al. Acute mesenteric ischemia: guidelines of the World Society of Emergency Surgery. World J Emerg Surg. 2017. 12:38.
2. Clair DG, Beach JM. Mesenteric Ischemia. N Engl J Med. 2016;374:959–968.
3. Chat V Dang, MD; Mark Su, MD, MPH, FACEP, FACMT; Daniel K Nishijima, MD, MAS and Chief Editor: John Geibel, MD, MSc, DSc, AGAF. Acute Mesenteric Ischemia Clinical Presentation. Access Medscape June 23, 2022. https://emedicine.medscape.com/article/189146-clinicalb3.

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