Since December, 2019, Wuhan, China, has experienced an outbreak of COVID-19, caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Epidemiological and clinical characteristics of patients with COVID-19 have been reported but risk factors for mortality and a detailed clinical course of illness, including viral shedding, have not been well described [2].However, cases have been accumulated and the pathophysiology thereof has gradually been clarified. The most common cause of COVID-19 death is acute respiratory distress syndrome (ARDS) and the associated thrombosis of systemic organs. Acute mesenteric ischemia is a rare symptom for COVID-19 disease, so it is difficult to know the accurate occurrence thereof due to limitations in diagnostic imaging under strict disease management regulations. Studies have shown that thrombosis is associated with prognosis. The increase in D-dimer and FDP is a risk factor [3].The frequency of thrombosis by site was highest in the lower limb arteries (71%), followed by the upper limb arteries (14%), cerebral arteries (10%), and visceral arteries (4%) [4].In a report examining acute mesenteric ischemia of COVID-19 patients, small bowel ischemia (46.67%) was the most prevalent abdominal finding, followed by ischemic colitis (37.3%). Non-occlusive mesenteric ischemia (NOMI; 67.9%) indicating microvascular involvement was the most common pattern of bowel involvement. 50% of the patients receiving conservative/medical management died, highlighting high mortality without surgery [5].The mechanism of thrombosis is thought to be excessive complement system activity, inflammatory response, DIC status, vascular endothelitis, and cytokine storm [6].

There are two types of intestinal necrosis with COVID-19: those due to thrombosis; and those due to non-occlusive mesenteric ischemia. It has been reported that intestinal necrosis due to thrombosis occurs more frequently in patients who have not undergone anticoagulant therapy, with non-occlusive mesenteric ischemia occurring more frequently in severe cases. Non-occlusive mesenteric ischemia is a segmental disease that results in non-continuous intestinal blood flow obstruction in areas controlled by the main stem of the mesenteric vein, even with no organic obstructions [7]. In this case, because heparin was administered due to the patient being diagnosed with COVID-19 pneumonia, and because microvascular thrombosis was observed within the vein based on a pathological exam of the surgically removed small intestine, non-occlusive mesenteric ischemia was not the cause of the intestinal avascular necrosis. Although we were unable to confirm via CT that the blood clot causing the intestinal necrosis was from a clot in the aorta, as confirmed by CT, that had ruptured, it is possible that a microthrombus occurring in the ileum vessel caused the intestinal necrosis. If the clot in the aorta had ruptured, it is likely that many clot-derived events would have occurred in many organs, such as in the brain or lower limbs; however, this was not observed. Although we cannot completely rule out that the clot in the aorta had ruptured, we believe that the microthrombus which occurred in the ileum vessel led to a shower embolism, which in turn caused intestinal necrosis in multiple areas of the ileum, as intestinal necrosis was localized in the terminal ileal region.

The frequency of thrombosis was revealed by a Japanese domestic investigation. Among 6,202 COVID-19 inpatients, 108 cases (1.86%) of thromboembolism (24 cases of cerebral infarction, 7 cases of myocardial infarction, 41 cases of deep vein embolism, 30 cases of pulmonary thromboembolism, and 22 cases of others) were observed. In addition, the higher the severity, the higher the rate of thromboembolism [8]. Our hospital admitted a total of 1308 COVID-19 patients from February 8, 2020 to March 31, 2022. In addition to this case, we experienced 1 case of cerebral infarction, 2 cases of pulmonary thromboembolism, and 1 case of myocardial infarction. These all involved patients whose condition was classified as moderate or severe patients at the time of hospitalization. In this case, although the WBC count was always high due to the administration of steroids, CRP was not elevated due to the anti-inflammatory effect of tricizumab administration. Therefore, caution should be exercised regarding complications of serious infections in these patients. Regarding the treatment of COVID-19 thrombosis, it is stated in the < Guide to Medical Examinations for Coronavirus Disease 2019 Ver. 6 [9] > , that although the prophylactic dose of heparin has not been established, it should be a low dose (10,000 units/day). In this case, despite administering 10,000 units/day of heparin from the time of hospitalization, thromboembolism occurred; thus, the preventive effect of heparin seems to be limited. The accumulation of further evidence, such as when to switch to DOAC and when to discontinue anticoagulant therapy, is awaited.