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Intrapulmonary haemorrhage and derailed coagulation: case report A 68-year-old man developed intrapulmonary haemorrhage and derailed coagulation following accidental overdose of dabigatranetexilate. Additionally, anticoagulant therapy with aspirin was considered to have contributed to derailed coagulation and intrapulmonary haemorrhage. The man, who had multiple comorbidities, such as pulmonary embolism, chronic aortic dissection type-Stanford B, ischaemic cardiomyopathy with high-grade restricted left ventricular function, had a history of a cerebral insult, treatment for chronic obstructive pulmonary disease GOLD stage IIA due to fibrosing, nicotine-induced pulmonary emphysema. Also, he had undergone right-sided hemicolectomy due to colon cancer. He presented to the emergency with an image of an abdominal emergency, anuric renal failure over multiple days and a persistent, non-productive cough. Since 2018, he had been receiving anticoagulation with dabigatran-etexilate 150mg and aspirin [ASA; acetylsalicylic acid] 100mg twice daily [routes not stated], and he had been regularly taking the medications. A CT of the chest and abdomen revealed condensation throughout the right upper and dorsal left upper lobe, with possible alveolar haemorrhage and pulmonary infiltrates. Also, an image of a small-bowel blockage in the lower abdomen was observed. Therefore, the man was admitted to the intensive care for further treatment of acute renal failure, intestinal disorder, pneumonia and a derailed coagulation status. On admission, he received oxygen for respiratory compensation through a nasogastric tube. Laboratory parameters showed increased leukocytes, CRP, procalcitonin, creatinine, urea, potassium, INR, PTT, and lactate and decreased prothrombin. He started receiving piperacillin/tazobactam and clarithromycin. The abdominal symptoms reversed rapidly with the conservative treatment, and he underwent a gastrointestinal passage procedure on the following day, during which an oral contrast medium demonstrated an image of the subileus with preserved passage. He was further treated for renal failure and pneumonia under adequate anticoagulant therapy. Thrombo-elastography (TEG) and platelet mapping was started. In the kaolinactivated CK test of the TEG (for functional analysis of the intrinsic coagulation pathway), a marked prolongation of the initial R-time to delayed formation of a stable coagulation clot was noted, and the platelet mapping revealed a nearly total aspirin effect on the derailed coagulation status. Before the insertion of a central venous and a Shaldon catheter, he received the first dose of idarucizumab. Subsequent TEG revealed that the R-time was halved along with fast formation of a stable clot, which was considered as 50% antagonist score. However, he developed relevant haemoptysis on the following night. Therefore, he received idarucizumab and erythrocytes [red blood cell concentrates] transfusion, and the symptoms decreased subsequently. On the day 2 in intensive care, he underwent discontinuous ha