Journal of South Asian Federation of Obstetrics and Gynaecology

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VOLUME 13 , ISSUE 2 ( March-April, 2021 ) > List of Articles


“Double” Trouble in Postpartum State

Shasthara Paneyala, Nemichandra Siddanakatte Chandrashekaraiah, Harsha Sundaramurthy, Vimala C Colaco

Citation Information : Paneyala S, Chandrashekaraiah NS, Sundaramurthy H, Colaco VC. “Double” Trouble in Postpartum State. J South Asian Feder Obs Gynae 2021; 13 (2):138-143.

DOI: 10.5005/jp-journals-10006-1882

License: CC BY-NC 4.0

Published Online: 09-07-2021

Copyright Statement:  Copyright © 2021; The Author(s).


Background: Guillain–Barre syndrome (GBS) is a perplexing neurological disease of autoimmune etiology with an incidence of 1.2 to 1.9 cases/100,000 population. The overall incidence remains almost the same in pregnancy. Posterior reversible encephalopathy syndrome (PRES) is a clinicoradiological entity most commonly encountered in peripartum preeclampsia; however, it can also be seen in other clinical scenarios such as immunosuppressant treatment, infection/sepsis, autoimmune diseases, and during cancer chemotherapy. GBS can be considered as an independent risk factor of PRES, due to acute dysautonomia and pain. Here we report the unique case of a patient who presented to the neurology department with flaccid quadriparesis in the immediate postpartum period, was diagnosed as having GBS and initiated on treatment for the same, and subsequently developed seizures secondary to PRES. Case description: A 22-year-old patient, with no previously known comorbidities, was admitted to the obstetrics department in her 37th week of gestation in labor. The patient underwent an emergency lower segment cesarean section (LSCS) (previous LSCS in labor) with no periprocedural complications. On the next day, she developed progressive ascending quadriparesis sparing sensory and sphincters. Nerve conduction studies done showed features of GBS, and cerebrospinal fluid studies done showed albuminocytological dissociation. The patient was then initiated on plasmapheresis in the intensive care unit setting and closely monitored for any deterioration in overall neurological picture and bulbar symptoms. The patient remained stable and showed positive response to the plasmapheresis. On the morning of postpartum day 6, the patient complained of sudden painless bilateral complete loss of vision followed by an episode of generalized tonic–clonic seizures. She had labile blood pressure with reactive pupils, normal fundus, and no other long-tract signs. Magnetic resonance imaging (MRI) brain and magnetic resonance venogram were done. MRI brain done showed features suggestive of PRES. She was managed with antiepileptic drugs, blood pressure optimization, and supportive care with rapid recovery in vision in 2 days. She showed steady improvement in motor power following plasmapheresis and subsequently was managed with physiotherapy to full functional recovery. Conclusion and clinical significance: GBS in pregnancy, PRES in the postpartum female, and PRES in GBS are all unique entities with no defined incidence and only documented case reports. GBS rarely complicates pregnancies; there are few case reports of the same, the exact incidence of which is not defined. Proposed mechanisms leading to PRES in patients with GBS are dysautonomia leading to acute rise in the blood pressure, activation of sympathetic nervous system secondary to pain, and intravenous immunoglobulin usage. Review of the literature shows that previous cases of PRES in combination with GBS is a very unique finding with only a few case reports making this case distinctive. In our patient who developed GBS in the peripartum period, the probable mechanism of PRES was the labile blood pressures secondary to dysautonomia. With management of GBS, a close watch on pressures and close neurological observation of the patient made a near-complete recovery.

  1. Jyothi B, Verma H, Vaidyanathan, et al. Perioperative management of term pregnant patient with Guillian Barre syndrome. Indian J Anaesth 2012;56(4):409–411. DOI: 10.4103/0019-5049.100848.
  2. Hinchey J, Chaves C, Appignani B, et al. A reversible posterior leukoencephalopathy syndrome. N Engl J Med 1996;334(8):494–500. DOI: 10.1056/NEJM199602223340803.
  3. Liman TG, Bohner G, Heuschmann PU, et al. Clinical andradiological differences in posterior reversible encephalopathy syndrome between patients with preeclampsia-eclampsia and other predisposing diseases. Eur J Neurol 2012;19(7):935–943. DOI: 10.1111/j.1468-1331.2011.03629.x.
  4. Etxeberria A, Lonneville S, Rutgers MP, et al. Posterior reversible encephalopathy syndrome as a revealing manifestation of Guillain-Barré syndrome. Rev Neurol (Paris) 2012;168(3):283–286. DOI: 10.1016/j.neurol.2011.06.006.
  5. Brooks H, Christian AS, May AE. Pregnancy, anaesthesia and Guillain Barrésyndrome. Anaesthesia 2000;55(9):894–898. DOI: 10.1046/j.1365-2044.2000.01367.x.
  6. Lichtenfield P. Autonomic dysfunction in the Guillain-Barré syndrome. Am J Med 1971;50(6):772–780. DOI: 10.1016/0002-9343(71)90185-9.
  7. Fugate JE, Claassen DO, Cloft HJ, et al. Posterior reversible encephalopathy syndrome: associated clinical and radiologic findings. Mayo Clin Proc 2010;85(5):427–432. DOI: 10.4065/mcp.2009.0590.
  8. Bartynski WS. Posterior reversible encephalopathy syndrome, part 1: fundamental imaging and clinical features. AJNR Am J Neuroradiol 2008;29(6):1036–1042. DOI: 10.3174/ajnr.A0928.
  9. Schaefer PW, Buonanno FS, Gonzales RG, et al. Diffusion weighted imaging discriminates between cytotoxic and vasogenic edema in a patient with eclampsia. Stroke 1997;28(5):1082–1085. DOI: 10.1161/01.str.28.5.1082.
  10. Posterior reversible encephalopathy associated with the Dysautonomia of Guillain-Barré syndrome. Neurol Bull 2009;1:7–10. DOI: 10.7191/neurol_bull.2009.1001.
  11. Atypical aspects of hypertensive encephalopathy in childhood. Neuropediatrie 1979;10(2):150–157. DOI: 10.1055/s-0028-1085321.
  12. A case of Guillain-Barré syndrome accompanied by sympathetic overactivity and hypertensive encephalopathy. Acta Paediatr 1996;85(8):1006–1008. DOI: 10.1111/j.1651-2227.1996.tb14204.x.
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