Shrestha Amardeep, Soriano Sheryll Mae, Song Mingchen, Chihara Shingo
Department of Internal Medicine, Division of General Internal Medicine, Illinois, United States of America.
Division of Pulmonary and Critical Care Medicine, Illinois, United States of America.
Int J Crit Illn Inj Sci. 2014 Jul;4(3):266-70. doi: 10.4103/2229-5151.141487.
The emergence of multi-drug-resistant gram negative bacillary infections has regained popularity of ancient drugs such as polymyxins. We report a case of acute respiratory failure induced by use of intravenous colistimethate, which is one of the forms of polymyxin. The patient is a 31 year old female with paraplegia due to spina bifida who underwent excisional debridement of large lumbosacral decubitus ulcer with osteomyelitis infected with pan-resistant Pseudomonas aeruginosa and MRSA. Six days after initiation of intravenous colistimethate and vancomycin, she developed acute respiratory failure requiring mechanical ventilation. Pan-culture was negative including a chest radiograph. V/Q scan showed low probability for pulmonary embolism. Echocardiogram showed normal right ventricle with no strain or pulmonary hypertension. Colistimethate was discontinued. Within 24 hours, she was extubated. In the early years after introduction of polymyxin, there were several reports of acute respiratory paralysis. The mechanism is thought to be noncompetitive myoneuronal presynaptic blockade of acetylcholine release. Though a direct causal relationship for respiratory failure is often difficult to establish in current era with multiple co morbidities, the timeframe of apnea, acuity of onset as well as rapid recovery in our case clearly point out the causal relationship. In addition, our patient also developed acute renal failure, presumably due to colistimethate induced nephrotoxicity, a possible contributing factor for her acute respiratory failure. In summary, colistimethate can induce acute neurotoxicity including respiratory muscular weakness and acute respiratory failure. Clinicians should consider its toxicity in the differential diagnosis of acute respiratory failure especially in critically ill patients.
多重耐药革兰氏阴性杆菌感染的出现使多粘菌素等古老药物再度受到关注。我们报告一例因使用多粘菌素的一种形式——静脉注射粘菌素甲磺酸钠引发急性呼吸衰竭的病例。患者为一名31岁女性,因脊柱裂导致截瘫,接受了腰骶部巨大褥疮溃疡切除清创术,该溃疡合并骨髓炎,感染了泛耐药铜绿假单胞菌和耐甲氧西林金黄色葡萄球菌。在开始静脉注射粘菌素甲磺酸钠和万古霉素6天后,她出现急性呼吸衰竭,需要机械通气。全面培养结果为阴性,包括胸部X光片。通气/灌注扫描显示肺栓塞可能性低。超声心动图显示右心室正常,无应变或肺动脉高压。停用了粘菌素甲磺酸钠。24小时内,她拔除了气管插管。在多粘菌素引入后的早期,有几例急性呼吸麻痹的报告。其机制被认为是乙酰胆碱释放的非竞争性肌神经突触前阻滞。尽管在当前这个存在多种合并症的时代,往往难以确定呼吸衰竭的直接因果关系,但我们病例中的呼吸暂停时间、发病的急性程度以及快速恢复情况明确指出了因果关系。此外,我们的患者还出现了急性肾衰竭,可能是由于粘菌素甲磺酸钠诱发的肾毒性,这也是她急性呼吸衰竭的一个可能促成因素。总之,粘菌素甲磺酸钠可诱发急性神经毒性,包括呼吸肌无力和急性呼吸衰竭。临床医生在急性呼吸衰竭的鉴别诊断中,尤其是在重症患者中,应考虑其毒性。