Hyperacute onset of Guillain Barre Syndrome in the immediate postpartum period following Caesarean section under spinal anaesthesia.

Abstract

Sir, Guillain–Barre syndrome (GBS) is an acute flaccid paralysis syndrome with an incidence of 1.2–1.9 cases/100,000 population and the incidence remains almost the same in pregnancy. However, in pregnancy it may be associated with increased maternal morbidity and mortality.[1] There are reports of safe use of regional anaesthesia in pregnancy with GBS,[2] and also where GBS worsened in the postoperative period after regional anaesthesia.[3] We describe a patient with the hyperacute onset and rapidly progressive neuropathy leading to quadriplegia and respiratory failure following spinal anaesthesia for caesarean section. A 22-year-old primipara of 36 weeks gestation underwent an emergency caesarean section under spinal anaesthesia for foetal distress with 2.5 cc of 0.5% hyperbaric bupivacaine. There was history of diarrhoea, mild fever, tingling sensation, and numbness of all four limbs without any obvious neurological deficits one week earlier. There was failure of return of muscle power in the lower limbs following the surgery and the weakness progressed rapidly within 12 h in all the four limbs, associated with difficulty in breathing. She was intubated and shifted to the neuromedical Intensive Care Unit of our hospital. She was quadriplegic and areflexic with no signs of meningitis or raised intracranial pressure. Bifacial weakness was present, but bowel and bladder functions were normal. Cerebrospinal fluid examination showed albumino-cytological dissociation (nil cells with proteins at 98 mg/dl). Nerve conduction study revealed absent F waves with inexcitable median, ulnar and superficial peroneal nerves, and a decrease in velocity and amplitude of sensory nerves. Based on the clinical presentation and above findings, a diagnosis of acute motor-sensory axonal neuropathy type of GBS was made. Possibilities of transverse myelitis, lumbar epidural haematoma, and poliomyelitis were ruled out on the basis of the absence of hyperreflexia, presence of quadriplegia and symmetrical weakness, respectively. A tracheostomy was performed and 65 days later, she was weaned off from the ventilator and the tracheostomy closed. She was wheelchair bound at discharge (muscle power in upper limbs 3/5 and lower limbs 1/5). The power improved after 1½ years to 5/5 in the upper limbs and 3/5 in lower limbs, and she was able to walk with support. Recently, Mangar et al.[4] reported acute precipitation of GBS after epidural analgesia. The patient's recent vaginal infection and probable chorioamnionitis during labour may have served as triggering agent via molecular mimicry. The authors concluded that no direct link between neuraxial anaesthesia and GBS could be confirmed. Wiertlewski et al.[3] reported worsening of neurological symptoms after epidural anaesthesia in a patient with GBS and the authors attributed immunological changes associated with pregnancy and anaesthetic toxicity as possible causes. In two-thirds of patients, GBS is associated with prodromal infections in the form of flu or gastroenteritis, triggering an abnormal immune response to axolemmal or Schwann cell antigens, damaging the peripheral nerves. In our patient, there was a positive history of diarrhoea a week before surgery. Therefore, we postulate that a possible aberrant immune reaction due to infection, associated with changes in immune system due to the stress of surgery[5] or nerve damage through a possibly exaggerated neural response to the local anaesthetic agent[3] may have complexly interacted to accelerate the profound muscle weakness and hastened progression to full-fledged GBS. The possibility of an association between regional anaesthesia and the associated hastening of symptoms of GBS requires further understanding and research as seen from the present and previous reports. ACKNOWLEDGMENTS Source of funding Nil. Conflicts of interest There are no conflicts of interest.