English

Abstract

Guillain-Barre syndrome is an immune mediated acute demyelinating polyradiculopathy, linked to various infectious agent. GBS has a very low incidence during pregnancy, estimated population incidence ranged from 0.62 to 2.66 cases per 100,000 person-years across all age groups.1 It is usually preceded by a bacterial or viral infection. Infections like CMV, EB, HIV-1, Hepatitis virus and campylobacter jejuni has been implicated as etiologic agents. Most common infectious agent associated with GBS is campylobacter jejuni.2 GBS classically presents with pain, numbness, paraesthesia, or weakness of the limbs, areflexia. Ascending paralysis with weakness beginning in the feet and migrating towards the trunk is the most typical symptoms. Life threatening complications particularly occurs if there is involvement of respiratory muscles. Increased incidence of respiratory complications is mostly due to gravid uterus. However, GBS is more common in the third trimester and the first 2 weeks of postpartum. 3 GBS is known to worsen in postpartum period due to an increase in delayed type IV of hypersensitivity response. Delayed diagnosis is common in pregnancy or immediate postpartum period because the initial nonspecific symptoms may mimic changes in pregnancy. GBS in pregnancy associated with high maternal mortality. A third of pregnant women required ventilator support with a mortality rate of 13 %.4 Diagnosis is based on the clinical presentation, laboratory and electrophysical investigations. Nerve conduction studies and EMG show an evolving multifocal demyelinating polyneuropathy. Management of GBS in pregnancy is a multidisciplinary approach. IVIG injection in high dose or plasmapheresis is beneficial if given within 1 to 2 weeks of motor syndrome.3 Maternal GBS is not an indication for caesarean section and operative delivery should be reserved for obstetrics indications only. A 25 years old, primigravida patient was relatively alright 9 days back, when she started complaining of weakness in right hand it was acute in onset and progressing gradually with time. The next day patient started having difficulty in standing up. On 29 / 07 / 2019 she was unable to move all four limbs. Patient was taken to private hospital where she was investigated. Her NCV was suggestive of severe acute onset polyneuropathy. She received IVIG at private hospital where her tracheostomy was done. She was brought by relatives to Indira Gandhi Government Medical College, Nagpur on 04 / 08 / 2019. On examination her general condition was not satisfactory, afebrile, pulse rate was 120/min, BP was 110 / 80 mm Hg, RBS 186 mg %. On CNS examination she was conscious oriented with time, place and person, bilateral planters absent, DTR absent, Power in all four limbs was zero.