Itagaki Hideya, Hagino Takuro
Honjoudaiichi Hospital, 110, Iwabuchishita, Yurihonnjou, Akita, 015-8567, Japan.
BMC Gastroenterol. 2019 Apr 18;19(1):58. doi: 10.1186/s12876-019-0978-0.
Vitamin K deficiency results in serious coagulation dysfunction, but hemorrhagic shock is rare. Herein, we describe a case of vitamin K deficiency and abnormality in the path of the intercostal artery, the combination of which led to hemorrhagic shock.
An 83-year-old woman was hospitalized for suspected gallstones. She developed septic shock after 4 days of hospitalization. We considered cholecystitis or cholangitis and performed abdominal ultrasonography, which revealed gallbladder enlargement, biliary sludge, and hyperplasia of the bile duct wall. Antibiotic treatment with sulbactam/ampicillin (SBT/ABPC) was initiated on day four, and percutaneous transhepatic gallbladder drainage (PTGBD) was performed on day five. The treatment was successful, but the patient developed bilateral pleural effusion because of hypoalbuminemia. We performed drainage for bilateral pleural effusion on days 13 and 17. The patient developed hypotension on day 18; blood tests showed anemia and severe coagulation dysfunction but a normal platelet count. We suspected vitamin K deficiency-induced coagulation dysfunction because of previous antibiotic treatment and restricted diet, and it led to hemorrhagic shock. Massive right hemothorax was observed by computed tomography, and urgent interventional radiology was performed. We observed no injury to the intercostal artery truncus but confirmed an abnormality in the course of the intercostal artery; therefore, we inferred that the cause of hemothorax in this case was injury to a small vessel, not truncus because of the abnormality. Because of the likelihood of rebleeding, we performed coil embolization from the seventh to the ninth intercostal artery. Because we confirmed vitamin K deficiency-induced coagulation dysfunction, we referred to the concentration of protein induced by vitamin K absence/antagonist-II (PIVKA-II), and it was found to increase by 23,000.
A combination of vitamin K deficiency and abnormality in the course of the intercostal artery led to hemorrhagic shock. When using certain antibiotics and restricting diet, it is important to measure coagulation function, even if the platelet count is normal. Further, when thoracentesis is performed, abnormalities in the course of the intercostal artery should be identified. Thoracentesis with ultrasound may prevent hemothorax.
维生素K缺乏会导致严重的凝血功能障碍,但出血性休克较为罕见。在此,我们描述一例维生素K缺乏合并肋间动脉走行异常,二者共同导致出血性休克的病例。
一名83岁女性因疑似胆结石入院。住院4天后发生感染性休克。我们考虑为胆囊炎或胆管炎并进行了腹部超声检查,结果显示胆囊增大、胆汁淤积和胆管壁增生。第4天开始使用舒巴坦/氨苄西林(SBT/ABPC)进行抗生素治疗,第5天进行了经皮经肝胆囊引流(PTGBD)。治疗取得成功,但患者因低蛋白血症出现双侧胸腔积液。我们在第13天和第17天对双侧胸腔积液进行了引流。患者在第18天出现低血压;血液检查显示贫血和严重凝血功能障碍,但血小板计数正常。由于先前的抗生素治疗和饮食受限,我们怀疑是维生素K缺乏引起的凝血功能障碍,进而导致出血性休克。计算机断层扫描显示右侧大量血胸,并进行了紧急介入放射治疗。我们未观察到肋间动脉干损伤,但证实肋间动脉走行异常;因此,我们推断该病例血胸的原因是由于走行异常导致小血管损伤,而非动脉干损伤。由于再次出血的可能性,我们对第7至第9肋间动脉进行了弹簧圈栓塞。由于我们确认是维生素K缺乏引起的凝血功能障碍,我们检测了维生素K缺乏/拮抗剂-II诱导蛋白(PIVKA-II)的浓度,发现其升高了23,000。
维生素K缺乏与肋间动脉走行异常共同导致出血性休克。在使用某些抗生素和限制饮食时,即使血小板计数正常,检测凝血功能也很重要。此外,进行胸腔穿刺时,应识别肋间动脉走行异常。超声引导下胸腔穿刺可预防血胸。