腰椎术后手术部位感染是严重的并发症之一,有时会导致死亡。在这里,我们描述了一例患者因腰椎术后感染被转院治疗时发现维生素K缺乏导致凝血障碍的病例.凝血障碍是由患者服用的抗菌药物引起的,患有营养不良的人。患者是一名70岁的男性,有糖尿病史。他被诊断为腰椎管狭窄症,并在前一家医院接受了L2-L5和S1椎板的后路减压,然后转移到我们医院五个月。转移前四个月,从伤口观察到脓性分泌物,在伤口培养中检测到甲氧西林敏感的金黄色葡萄球菌。给予头孢唑啉两周,导致初步改进。然而,转移前一个月,伤口感染复发,伴有菌血症和腰大肌脓肿。他曾接受过头孢唑林治疗,左氧氟沙星,利福平,甲氧苄啶,和磺胺甲恶唑,但抗生素的作用是不够的。由于不受控制的感染而转移清创手术后,他的凝血参数如下:凝血酶原时间(PT)74.0秒,PT-国际标准化比率(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)664mg/dl,纤维蛋白降解产物(FDP)7.1μg/ml,和由维生素K缺失-II(PIVKA-II)诱导的蛋白质34400mAU/ml。因为我们怀疑维生素K缺乏,维生素K40毫克作为测试剂量给药,凝血功能改善至PT16.4秒,4小时后,PT-INR1.30,PT%65.2和APTT79秒。诊断为维生素K缺乏症,服用维生素K4天,转移后五天凝血状态恢复正常。对左侧腰大肌脓肿进行清创术。给予头孢唑啉八周,行政工作已经完成。由于仔细注意他的营养,凝血异常没有复发。我们经历了一例由于维生素K缺乏而导致的凝血病,该维生素K缺乏是由向患有腰椎术后感染的低营养患者服用的抗菌剂引起的。维生素K缺乏的原因,在这种情况下,被认为是低营养,头孢唑啉和利福平抑制维生素K产生菌,以及具有甲基噻二唑硫醇基团的头孢唑啉的用途。应该记住,术后感染可能会发生由营养不足的抗菌治疗引起的维生素K缺乏引起的严重凝血病。
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 Staphylococcus aureus 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.