Guillain-Barre Syndrome Secondary to SARS-CoV-2

D. Chaudhary, D. Norton
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引用次数: 1

Abstract

Guillain-Barre Syndrome (GBS) is an acute autoimmune disorder that is provoked by a preceding infection. It is characterized by progressive, ascending, symmetrical muscle weakness accompanied by hyporeflexia or areflexia. We describe two cases of GBS associated with COVID-19. 36-year-old Hispanic female presented ten days after diagnosis of COVID-19 with symptoms of headache, bilateral leg and facial weakness, and facial paresthesias for five days. Within 24 hours of admission, she developed areflexia and progressive bulbar and appendicular weakness. Nerve conduction study and electromyography were consistent with demyelinating form of GBS. Due to difficulty with clearing oral secretions, patient was intubated two times during the hospitalization. 79-year-old Caucasian female presented with progressive weakness, weight loss and fevers. She was diagnosed with COVID-19 on the day of admission. She had paralysis of all four extremities with dysphagia and required intubation. She was extubated and re-intubated two more times due to worsening hypoxia and stridor which led to placement of a tracheostomy tube. Both our patients developed features of dysautonomia, including hypotension and tachycardia. Severe respiratory muscle weakness and dysphagia led to recurrent intubations. Their CT head and MRI brains were negative for facial nerve enhancement. Lumbar punctures in both revealed albuminocytologic dissociation. Plasma exchange was initiated in both females immediately after first intubation for total duration of five days. Upon outpatient follow up, they had significant improvement in motor function. Common precipitants of GBS are Campylobacter jejuni, EBV, CMV, HIV and Zika virus. Clearly, GBS is an infrequent complication of COVID-19. It is possible that SARS-CoV-2 evokes an immune response against peripheral nerve components leading to acute polyneuropathy of heterogenous presentation. Typically, demyelinating and axonal forms of GBS have been described. However, in our cases, both had demyelinating features including symmetric weakness with predominant bulbar symptoms of dysphagia and dysphonia. These cases highlight that GBS is a potential neurological complication of COVID-19 that physicians must be aware of. Thorough daily neurological exam is critical, and early recognition of GBS symptoms may prompt regular evaluation of negative inspiratory force and vital capacity. This may lead to early initiation of intravenous immunoglobulin (IVIG) or plasma exchange leading to improvement in motor symptoms thus avoiding ventilatory support. Plasma exchange should be considered as a first line treatment in COVID-19 patients since high concentrations of IVIG can lead to increased blood viscosity in these patients who are already at increased risk for thrombotic complications.
继发于SARS-CoV-2的格林-巴利综合征
格林-巴利综合征(GBS)是一种由先前感染引起的急性自身免疫性疾病。它的特征是进行性、上升性、对称性肌肉无力,并伴有反射不足或反射不足。我们描述了两例与COVID-19相关的GBS病例。36岁西班牙裔女性,确诊后10天出现头痛、双侧腿和面部无力,面部感觉异常5天。入院24小时内,患者出现反射性屈曲和进行性球尾无力。神经传导和肌电图与脱髓鞘型GBS一致。因口腔分泌物清除困难,住院期间两次插管。79岁白人女性,表现为进行性虚弱,体重减轻和发烧。她在入院当天被诊断出患有COVID-19。她四肢瘫痪,伴有吞咽困难,需要插管。由于缺氧和喘鸣加重,她拔管并重新插管两次,导致放置气管造口管。我们的两名患者都出现了自主神经异常的特征,包括低血压和心动过速。严重的呼吸肌无力和吞咽困难导致反复插管。他们的头部CT和脑部MRI显示面部神经增强为阴性。腰椎穿刺均显示白蛋白细胞分离。两名女性在首次插管后立即开始血浆置换,总共持续5天。在门诊随访中,他们的运动功能有了显著的改善。GBS的常见沉淀物有空肠弯曲杆菌、EBV、CMV、HIV和寨卡病毒。显然,GBS是COVID-19的罕见并发症。SARS-CoV-2可能引起对周围神经成分的免疫反应,导致急性异质性多发性神经病。典型的,脱髓鞘和轴突形式的GBS已被描述。然而,在我们的病例中,两人都有脱髓鞘特征,包括对称无力,主要是吞咽困难和发音困难的球症状。这些病例突出表明,GBS是COVID-19的潜在神经系统并发症,医生必须意识到这一点。每日彻底的神经系统检查至关重要,早期识别GBS症状可能促使定期评估负吸气力和肺活量。这可能导致早期开始静脉注射免疫球蛋白(IVIG)或血浆置换,从而改善运动症状,从而避免呼吸支持。应考虑将血浆置换作为COVID-19患者的一线治疗,因为高浓度IVIG可导致这些患者血液粘度增加,而这些患者已经处于血栓性并发症的高风险中。
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