Dhamelia Parth Mukeshbhai, Mokariya Dipak R, Anand Jaspreet Singh, Futela Pragyat, Murawska Baptista Aleksandra, Singla Abhinav
Department of Internal Medicine, Maulana Azad Medical College and Lok Nayak Hospital, New Delhi, India.
Department of Internal Medicine, MetroHealth/Case Western Reserve University, Cleveland, OH, USA.
Am J Case Rep. 2025 Sep 13;26:e948917. doi: 10.12659/AJCR.948917.
BACKGROUND Guillain-Barre syndrome (GBS) is a rare disorder arising due to immune-mediated damage to the peripheral nervous system. It most commonly occurs as a sequela of respiratory or gastrointestinal infections; however, in rare instances, cases may arise after snakebite envenomation. Several variants of GBS have been identified, with acute inflammatory demyelinating polyneuropathy (AIDP) being the most common, including our case. Other forms, such as acute motor axonal neuropathy (AMAN), are also more prevalent in tropical regions of Southeast Asia, as well as Central and South America. CASE REPORT A 52-year-old farmer from rural northern India presented with ascending palsy progressing for the past 3 days, along with bulbar symptoms and respiratory involvement for 1 day. He had been recently hospitalized a few weeks ago for snake-bite-associated neuroparalysis that had gradually resolved without any complications before discharge. Laboratory investigations and chest X-ray on presentation were suggestive of aspiration pneumonia, leading to initiation of empiric antibiotics. A diagnosis of AIDP variant of GBS was reached on the second day of admission, based on CSF studies showing albuminocytologic dissociation, and nerve conduction studies suggestive of axonal neuropathy in lower-limb nerves, and demyelination that was more pronounced in the lower limbs than in the upper limbs. He subsequently received a dose of IVIG, and was intubated for mixed hypoxic-hypercapnic respiratory failure. However, the worsening hemodynamic instability due to sepsis and GBS-related autonomic dysfunction, despite the antibiotic escalation and vasopressor support, eventually culminated in death. CONCLUSIONS This case underscores the importance of recognizing Guillain-Barre syndrome (GBS) as a neuroimmune sequela of snakebite envenomation, and the need for close neurological monitoring, patient and caregiver education, and physician awareness for early symptom recognition, and prompt initiation of empiric treatment to avoid delayed diagnoses and subsequent fatal complications.
吉兰-巴雷综合征（GBS）是一种罕见的疾病，由免疫介导的外周神经系统损伤引起。它最常作为呼吸道或胃肠道感染的后遗症出现；然而，在极少数情况下，也可能发生在蛇咬伤中毒之后。已确定GBS有几种变体，急性炎症性脱髓鞘性多发性神经病（AIDP）是最常见的，我们的病例即属于此类。其他形式，如急性运动轴索性神经病（AMAN），在东南亚以及中美洲和南美洲的热带地区也更为普遍。
一名来自印度北部农村的52岁农民，出现进行性上升性麻痹达3天，伴有延髓症状和呼吸受累1天。他几周前因蛇咬伤相关的神经麻痹住院，出院前病情逐渐缓解，无任何并发症。就诊时的实验室检查和胸部X线提示吸入性肺炎，遂开始经验性使用抗生素。入院第二天，根据脑脊液检查显示蛋白细胞分离，以及神经传导研究提示下肢神经轴索性神经病，且下肢脱髓鞘比上肢更明显，诊断为GBS的AIDP变体。他随后接受了一剂静脉注射免疫球蛋白，并因混合性低氧高碳酸血症呼吸衰竭而插管。然而，尽管升级了抗生素并给予血管升压药支持，但由于败血症和GBS相关的自主神经功能障碍导致的血流动力学不稳定恶化，最终导致死亡。
本病例强调了将吉兰-巴雷综合征（GBS）识别为蛇咬伤中毒的神经免疫后遗症的重要性，以及密切神经监测、患者和护理人员教育以及医生对早期症状识别的认识，以及及时开始经验性治疗以避免延迟诊断和随后的致命并发症的必要性。
