Bilateral brachial plexus injury following acute carbon monoxide poisoning.

IF 2.9 3区 医学 Q2 Medicine BMC Pharmacology & Toxicology Pub Date : 2013-12-07 DOI:10.1186/2050-6511-14-61
Mounia Rahmani, Halima Belaidi, Maria Benabdeljlil, Wafa Bouchhab, Nadia El Jazouli, Asmae El Brini, Saadia Aidi, Reda M Ouazzani, Mustapha El Alaoui Faris
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引用次数: 2

Abstract

Background: Carbon monoxide (CO) intoxication is a leading cause of severe neuropsychological impairments. Peripheral nerve injury has rarely been reported. It consists usually in a demyelinating polyneuropathy or mononeuropathy affecting mainly the lower limbs. Isolated involvement of both upper extremities has been described in only 4 patients related to root damage. We report the first case of bilateral brachial plexus injury following CO poisoning and review all previous CO-induced neuropathy described in literature.

Case presentation: After being unconscious for three hours, a 42 years old man experienced bilateral brachial weakness associated with edema of the face and the upper limbs. Neurological examination showed a brachial diplegia, distal vibratory, thermic and algic hypoesthesia, deep tendon areflexia in upper limbs. There was no sensory or motor deficit in lower extremities. No cognitive disturbances were detected. Creatine kinase was elevated. Electroneuromyogram patterns were compatible with the diagnosis of bilateral C5 D1 brachial axonal plexus injury predominant on the left side. Clinical course after hyperbaric oxygen therapy was marked by a complete recovery of neurological disorders.

Conclusion: Peripheral neuropathy is an unusual complication of CO intoxication. Bilateral brachial plexus impairment is exceptional. Various mechanisms have been implicated including nerve compression secondary to rhabdomyolysis, nerve ischemia due to hypoxia and direct nerve toxicity of carbon monoxide. Prognosis is commonly excellent without any sequelae.

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急性一氧化碳中毒后双侧臂丛损伤。
背景:一氧化碳中毒是导致严重神经心理障碍的主要原因。周围神经损伤鲜有报道。它通常包括脱髓鞘性多神经病变或单神经病变,主要影响下肢。孤立性上肢受累仅在4例与牙根损伤相关的患者中被描述。我们报告第一例双侧臂丛神经损伤后一氧化碳中毒和回顾所有以前的一氧化碳引起的神经病变在文献中描述。病例介绍:一名42岁男子在失去知觉3小时后,出现双侧臂膀无力,并伴有面部和上肢水肿。神经学检查显示肱二瘫,远端振动,热感和痛觉减退,上肢深腱反射。下肢无感觉或运动障碍。未发现认知障碍。肌酸激酶升高。神经肌电图与双侧C5 D1臂轴突丛损伤的诊断一致,以左侧为主。高压氧治疗后的临床过程以神经系统疾病的完全恢复为标志。结论:周围神经病变是一氧化碳中毒的罕见并发症。双侧臂丛损伤是例外。多种机制包括横纹肌溶解引起的神经压迫、缺氧引起的神经缺血和一氧化碳的直接神经毒性。预后通常很好,无任何后遗症。
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来源期刊
BMC Pharmacology & Toxicology
BMC Pharmacology & Toxicology PHARMACOLOGY & PHARMACY-TOXICOLOGY
CiteScore
4.40
自引率
0.00%
发文量
0
审稿时长
12 weeks
期刊介绍: BMC Pharmacology and Toxicology is an open access, peer-reviewed journal that considers articles on all aspects of chemically defined therapeutic and toxic agents. The journal welcomes submissions from all fields of experimental and clinical pharmacology including clinical trials and toxicology.
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