Tatsumura Masaki, Kato Mikiro, Takahashi Kei, Funayama Toru
Department of Orthopaedic Surgery and Sports Medicine, Tsukuba University Hospital Mito Clinical Education and Training Center, Mito Kyodo General Hospital, Mito, JPN.
Department of Infectious Diseases, University of Tsukuba, Tsukuba, JPN.
Cureus. 2024 Jul 8;16(7):e64076. doi: 10.7759/cureus.64076. eCollection 2024 Jul.
Postoperative surgical site infection in the lumbar spine is one of the serious complications that sometimes results in death. Herein, we describe a case in which a patient was found to have coagulopathy due to vitamin K deficiency when he was transferred to a hospital for treatment for a postoperative infection of the lumbar spine. The coagulation disorder was caused by antimicrobial agents administered to the patient, who was suffering from hyponutrition. The patient was a 70-year-old man with a history of diabetes mellitus. He was diagnosed with lumbar spinal canal stenosis and underwent posterior decompression of the L2-L5 and S1 laminae at a previous hospital five months before transfer to our hospital. Four months before transfer, purulent discharge was observed from the wound, and methicillin-susceptible was detected in the wound culture. Cefazolin was administered for two weeks, resulting in initial improvement. However, one month before the transfer, the wound infection recurred, accompanied by bacteremia and a psoas abscess. He had been treated with cefazolin, levofloxacin, rifampicin, trimethoprim, and sulfamethoxazole, but the antibiotics' effects were insufficient. Upon transfer for debridement surgery due to uncontrolled infection, his coagulation parameters were as follows: prothrombin time (PT) 74.0 sec, PT-international normalized ratio (INR) 6.69, PT% 9.0, activated partial thromboplastin time (APTT) 138 sec, fibrinogen (FIB) 664 mg/dl, fibrin degradation products (FDP) 7.1 μg/ml, and protein induced by vitamin K absence-II (PIVKA-II) 34400 mAU/ml. Because we suspected vitamin K deficiency, vitamin K 40 mg was administered as a test dose, and coagulation function improved to PT 16.4 sec, PT-INR 1.30, PT% 65.2, and APTT 79 sec after four hours. The diagnosis of vitamin K deficiency was confirmed, vitamin K was administered for four days, and the coagulation status normalized five days after transfer. Debridement was performed for the left psoas abscess. Cefazolin was administered for eight weeks, and administration was completed. The coagulation abnormality did not recur due to careful attention to his nutrition. We experienced a case of coagulopathy due to vitamin K deficiency caused by antimicrobial agents administered to a hyponourished patient with a postoperative infection of the lumbar spine. The cause of vitamin K deficiency, in this case, was thought to be low nutrition, suppression of vitamin K-producing bacteria by cefazolin and rifampicin, and the use of cefazolin with a methyl-thiadiazole thiol group. It should be kept in mind that severe coagulopathy due to vitamin K deficiency caused by antimicrobial treatment with hyponutrition can occur in postoperative infections.
腰椎术后手术部位感染是一种严重并发症，有时会导致死亡。在此，我们描述一例患者，该患者因腰椎术后感染转院治疗时被发现因维生素K缺乏而出现凝血病。凝血障碍是由给予该营养不良患者的抗菌药物引起的。患者为一名70岁男性，有糖尿病病史。他被诊断为腰椎管狭窄症，并在转至我院前五个月于前一家医院接受了L2 - L5和S1椎板的后路减压术。转院四个月前，伤口出现脓性分泌物，伤口培养检测到对甲氧西林敏感的[细菌名称未给出]。给予头孢唑林治疗两周，病情初步好转。然而，转院一个月前，伤口感染复发，伴有菌血症和腰大肌脓肿。他接受了头孢唑林、左氧氟沙星、利福平、甲氧苄啶和磺胺甲恶唑的治疗，但抗生素效果不佳。因感染控制不佳转来进行清创手术时，他的凝血参数如下：凝血酶原时间（PT）74.0秒，PT国际标准化比值（INR）6.69，PT% 9.0，活化部分凝血活酶时间（APTT）138秒，纤维蛋白原（FIB）664毫克/分升，纤维蛋白降解产物（FDP）7.1微克/毫升，维生素K缺乏诱导蛋白-II（PIVKA-II）34400毫国际单位/毫升。由于我们怀疑维生素K缺乏，给予40毫克维生素K作为试验剂量，4小时后凝血功能改善为PT 16.4秒，PT-INR 1.30，PT% 65.2，APTT 79秒。维生素K缺乏的诊断得到证实，给予维生素K治疗四天，转院五天后凝血状态恢复正常。对左侧腰大肌脓肿进行了清创术。给予头孢唑林治疗八周，治疗结束。由于对其营养状况的密切关注，凝血异常未再次出现。我们遇到一例因给予营养不良的腰椎术后感染患者抗菌药物而导致维生素K缺乏引起的凝血病病例。在本例中，维生素K缺乏的原因被认为是营养不足、头孢唑林和利福平对维生素K产生菌的抑制以及使用了带有甲基噻二唑硫醇基团的头孢唑林。应牢记，在术后感染中，因营养不足导致抗菌治疗引起的维生素K缺乏所致的严重凝血病可能会发生。
