key: cord-0689241-zoml62wz authors: English, William; Banerjee, Saswata title: Coagulopathy and mesenteric ischaemia in severe SARS‐CoV‐2 infection date: 2020-07-13 journal: ANZ J Surg DOI: 10.1111/ans.16151 sha: cd2ca678553b16a5121a93ab8fa1baad09072566 doc_id: 689241 cord_uid: zoml62wz nan We read with interest the recently published literature detailing coronavirus disease 2019 (COVID-19) and thrombotic complications. 1 Patients with COVID-19 can develop coagulopathy, 2 which is related to poor outcomes. 3, 4 We describe a case of mesenteric thrombosis presenting as a late complication of severe COVID-19. A 40-year-old man presented with COVID-19 symptomssevere dyspnoea, fever and cough. His medical history is relevant for obesity. Initial laboratory tests demonstrated a normal leucocyte and lymphocyte count (8.6 and 1.7 × 10 9 /L, respectively), a raised D-dimer of 13.75 mg/L (reference range 0-0.5 mg/L), which rose to >35 mg/L after 48 h, and a raised ferritin of 633 μg/L (reference range 30-400 μg/L). Chest radiograph demonstrated features of severe acute respiratory syndrome coronavirus 2 infection and polymerase chain reaction was positive. He deteriorated over 24 h requiring intubation and ventilation. After 9 days in the critical care unit, he developed abdominal distension, increasing inotrope requirements, rising blood lactate and haemodynamic instability. A computed tomography pulmonary angiogram of the abdomen and pelvis with contrast was performed, which demonstrated hypoperfusion of the distal small bowel with intramural gas (Fig. 1) . Clotting studies were deranged: prothrombin time 17.1 (reference range 9-13 s), thrombin time 46.0 (reference range 13-17 s), activated partial thromboplastin time 44.9 (reference range 20-33 s) and fibrinogen 5.48 (reference range 1.5-4 g/L). Over 24 h, platelet count dropped from 516 to 124 (reference range 150-400 × 10 9 /L). He was receiving unfractionated heparin as anticoagulation (5000 U three times daily). The patient underwent emergency damage control laparotomy; ischaemic distal small bowel was resected. Given the haemodynamic instability, a laparostomy was performed. After 48 h, he returned to theatre for abdominal wall closure and stoma formation, which was uneventful. We add further evidence that there can be significant coagulopathy with severe acute respiratory syndrome coronavirus 2 infection, which can lead to arterial thrombi. Clinicians should investigate these patients thoroughly for thrombotic complications of COVID-19. Acute aorto-iliac and mesenteric arterial thromboses as presenting features of COVID-19 Coagulopathy and antiphospholipid antibodies in patients with Covid-19 Abnormal coagulation parameters are associated with poor prognosis in patients with novel coronavirus pneumonia Disseminated intravascular coagulation in patients with 2019-nCoV pneumonia