Acute vascular insufficiency of intestines (AVI) is a rare cause of severe abdominal pain contributing to 0.09% to 2% of admissions in surgical emergency. Despite its rarity, it needs early recognition because of its high mortality of 40% to 80% requiring timely diagnosis and prompt intervention. Occlusion of mesenteric vessels by arterial embolism (50%) or thrombosis (15% to 25%) and venous thrombosis (5%) are the predominant underlying causes. However, AVI may be nonocclusive in 20% to 30% of the patients. 1,2 Normally intestinal ischemia is prevented by its high perfusion through celiac mesenteric artery, superior mesenteric artery/inferior mesenteric artery, and a parallel system of venous drainage. 3 Therefore, bowel ischemia can occur only when blood supply is markedly reduced to 75% or more leading to a continuum of intestinal necrosis, perforation, infarction, or gangrene stimulating a severe inflammatory response that may be fatal. 4 Recently, activation of Janus kinase/transducer signaling pathway is proposed as an underlying mechanism for mesenteric ischemia. 5 Bowel ischemia is of interest to the clinical hematologist because of its association with thromboembolism. Hematologists are frequently consulted for anticoagulating patients having AVI with or without concomitant bleeding risks. It is important for the hematologists to know the pathophysiology of bowel ischemia, rationale of anticoagulation, preferred anticoagulants, and the selection of patients for thrombophilia screening. This study was conducted to evaluate the clinicopathological spectrum and outcome of thrombosis in acute mesenteric ischemia at