Our case was presented with acute onset of bilateral limb weakness which was treated with the help of intravenous immunoglobulin and physiotherapy. few cases of GBS following the second dose of AstraZeneca are reported so AAI101 far and there is a need for strong and accurate diagnosis of the disease and proper post-vaccination surveillance for the evaluation of risk associated with COVID vaccines. Keywords: AstraZeneca, case report, Guillain-Barr syndrome, post-COVID-19 vaccination HIGHLIGHTS Guillain-Barr syndrome (GBS) is usually a rare disease that causes bilateral, symmetrical progressive weakness of the muscles. Reports of GBS following AstraZeneca COVID vaccination warrants the need for post-vaccination surveillance globally. Nerve conduction studies and Brightons criteria can be used to diagnose GBS. GBS can be successfully managed with Intravenous immunoglobulin therapy. Introduction AstraZeneca is usually a recombinant, nonreplicative Spike (S) glycoprotein vaccine created using chimpanzee adenovirus vector, in a genetically modified human embryonic kidney (HEK 293) cell lines, with reported efficacy AAI101 of 70.4%. after two standard doses1. Cerebral venous sinus thrombosis; thrombocytopenia, GBS, and acute transverse myelitis have been reported following the AAI101 AstraZeneca vaccine2. About 18.6 million people took the first dose and 7.24 million people have completed two standard doses in Nepal by the September of 2022. To our knowledge, there is the first case of GBS following Rabbit polyclonal to JAKMIP1 the second dose of the COVID-19 AstraZeneca vaccine from Nepal. This case report has been reported in line with the SCARE Criteria3. Case presentation Our 78-year-old male presented with the complaint of bilateral lower limb swelling, weakness, and tingling sensation of finger and toes for 4 days, following 15 days after the second dose of AstraZeneca vaccination. Weakness was acute in onset and gradually progressed to the upper limbs within a week and was associated with difficulty in sitting, standing, and walking activities. He had no history of trauma, headache, photophobia, double vision, abnormal body movements, loss of consciousness, bowel or bladder incontinence, and respiratory or gastrointestinal illness. However, there is a past history of Hashimoto thyroiditis, hypertension, diabetes mellitus, and chronic obstructive pulmonary disease, and have been taking medicines for these conditions. On examination vitals were stable (blood pressure 160/80?mm, respiratory rate 18/min, pulse rate 86?bpm, AAI101 and SpO2 96%). The Glasgow Coma Scale was recorded at 15/15 and all cranial nerves were intact. Muscle bulk was normal but the tone and power were diminished. Power of both the shoulder and elbow 3/5, left: wrist flexor 2/5, extensor 3/5, handgrip strength 50% and right: wrist flexor 2/5, extensor 2/5, handgrip strength 60%, left: hip flexor, abductor, and extensor 2/5, knee flexor and extensor 3/5, dorsal flexion, plantar flexion, and great toe 1/5, right: hip flexor abductor and AAI101 extensor 2/5, knee flexor 2/5, extensor 3/5, dorsiflexion and plantar flexion 1/5 and great toe 1/5. Sitting balance test: static was good and dynamic was fair and reflexes were preserved. The sensation was decreased on the right lower limb more than on the left lower limb to the pinprick test. Laboratory investigation showed hemoglobin (12.7?g/dl), packed cell volume (38.7%), increased C-reactive protein (66.6?mg/l), hypoalbuminemia (2.90?g/dl), aspartate aminotransferase (103?U/l), and elevated alkaline phosphatase (488?U/l). The patient was hyperkalemic (5.40?mmol/l) and his serum urea was 47?mg/dl. Also, the random blood sugar was 175?mg/dl and free T3 was 1.70?pg/ml. Cerebrospinal fluid showed adenosine deaminase 2.86?Ul, glucose 60?mg/dl, and total protein of 53?mg/dl. No significant findings around the computed tomography scan. Nerve conduction findings were consistent with acute inflammatory demyelinating polyneuropathy. Nerve conduction study tables show the electrophysiological evidence of sensorimotor axonomylenic polyneuropathy of a severe degree along with the abnormal motor, sensory, and F-wave patterns in Figures ?Figures11 and ?and2,2, respectively. Open in a separate window Physique 1 Motor nerve conduction (MNC). Open in a separate.