Madhuri Patil1, Trupti Wankhede2
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.
