Funayama Toru, Tsukanishi Toshinori, Noguchi Hiroshi, Tatsumura Masaki, Yamazaki Masashi
Orthopaedic Surgery, Faculty of Medicine, University of Tsukuba, Tsukuba, JPN.
Orthopaedic Surgery, Tokyo Medical University Ibaraki Medical Center, Ami, JPN.
Cureus. 2022 Feb 26;14(2):e22618. doi: 10.7759/cureus.22618. eCollection 2022 Feb.
Congenital antithrombin (AT) III deficiency has a high incidence of deep vein thrombosis and pulmonary embolism due to reduced anticoagulation. In this study, we report a case of a patient who experienced cardiac arrest due to pulmonary embolism after emergency posterior spinal fusion for acute paraplesia due to a metastatic spinal tumor associated with AT III deficiency. A 49-year-old man with a history of familial AT III deficiency visited our hospital due to difficulty in walking caused by a progressive paralysis of the lower limbs. Clinical examination revealed multiple bone metastases due to prostate cancer and spinal cord compression caused by a pathological fracture of the T1 vertebral body. He had low AT III activity levels and high D-dimer levels. The following day, he underwent posterior spinal decompression and fusion. However, he had pulmonary embolism with cardiac arrest three days after surgery. He recovered without sequelae after emergency thrombectomy following resuscitation. Patients with AT III deficiency who cannot walk due to a metastatic spinal tumor inevitably develop deep vein thrombosis and pulmonary embolism. To avoid lethal pulmonary embolism, preventing deep vein thrombosis should be prioritized before surgery, even in the presence of acute progressive paraplegia.
先天性抗凝血酶(AT)III缺乏症由于抗凝作用减弱,深静脉血栓形成和肺栓塞的发生率较高。在本研究中,我们报告了一例患者,该患者因转移性脊柱肿瘤伴AT III缺乏症导致急性截瘫,在急诊后路脊柱融合术后因肺栓塞发生心脏骤停。一名有家族性AT III缺乏症病史的49岁男性因下肢进行性麻痹导致行走困难前来我院就诊。临床检查发现前列腺癌导致多处骨转移以及T1椎体病理性骨折引起脊髓受压。他的AT III活性水平较低,D-二聚体水平较高。第二天,他接受了后路脊柱减压融合术。然而,术后三天他发生了伴有心脏骤停的肺栓塞。复苏后经急诊血栓切除术,他康复且无后遗症。因转移性脊柱肿瘤而无法行走的AT III缺乏症患者不可避免地会发生深静脉血栓形成和肺栓塞。为避免致命的肺栓塞,即使存在急性进行性截瘫,术前也应优先预防深静脉血栓形成。