==== Front J Anaesthesiol Clin PharmacolJ Anaesthesiol Clin PharmacolJOACPJournal of Anaesthesiology, Clinical Pharmacology0970-91852231-2730Medknow Publications & Media Pvt Ltd India JOACP-34-26610.4103/0970-9185.173385Letters to EditorAnticoagulant-induced subdural hemorrhage in a patient with Guillain-Barré syndrome: An anesthetic challenge Rayadurg Vivek Ramesh Venkatapura J Department of Neuroanaesthesia, National Institute of Mental Health and Neurosciences, Bengaluru, Karnataka, IndiaAddress for correspondence: Dr. Vivek Rayadurg, Department of Neuroanaesthesia, National Institute of Mental Health and Neurosciences, Bengaluru, Karnataka, India. E-mail: rayadurg.vivek@gmail.comApr-Jun 2018 34 2 266 267 Copyright: © 2018 Journal of Anaesthesiology Clinical Pharmacology2018This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms. ==== Body Madam, Guillain-Barré syndrome (GBS) is characterized by acute, progressive motor weakness, areflexia, and ascending paralysis.[1] Literature describing the perioperative anesthetic management and associated complications in these patients is lacking. We report the successful anesthetic management of a GBS patient with anticoagulant induced posterior-fossa subdural hemorrhage (SDH). A 54-year-old, approximately 70 kg male presented with headache, drowsiness, and vomiting. He was diagnosed with GBS 3 months ago; was bed-ridden since then and was on warfarin 3 mg/day for deep venous thrombosis prophylaxis. There was no history of respiratory compromise requiring respiratory support. He was hemodynamically stable; Glasgow Coma Score (GCS) was 15/15; power was grade 1/5 in all the limbs. Investigations revealed hemoglobin of 8.6 g/dL and INR 3.84. Computed tomography of the brain revealed acute posterior-fossa SDH [Figure 1] with hydrocephalus [Figure 2]. Chest X-ray showed left ventricular hypertrophy and patchy opacities [Figure 3]. Figure 1 Non-contrast computed tomography brain showing posterior fossa subdural hemorrhage Figure 2 Non-contrast computed tomography brain showing hydrocephalus Figure 3 Chest X-ray AP view Warfarin was stopped and vitamin K 10 mg administered intravenously (i.v). Transfusion of six units of fresh frozen plasma (FFP) was planned, but due to minor transfusion reactions (itching and erythematous rashes) during transfusion of the fourth unit, transfusion was discontinued. Pheniramine 22.75 mg, and Dexamethasone 8 mg administered. Repeat INR was 1.41. Patient was taken up for emergency posterior fossa craniotomy and evacuation of SDH in the prone position plus insertion of ventriculoperitoneal shunt in the supine position. Anesthesia was induced with fentanyl 150 μg and propofol 150 mg. Lignocaine 100 mg was given i.v. to suppress the response to laryngoscopy. After spraying vocal cords with lignocaine, without neuromuscular blockade, trachea was intubated with flexometallic cuffed endotracheal tube. Monitoring included an electrocardiogram, SpO2, ET CO2, invasive blood pressure (BP), respiratory gas analysis, temperature, and urine output. Anesthesia was maintained with oxygen, air, sevoflurane, and intermittent fentanyl. Neuromuscular blocking agents (NMBAs) were not administered. Significant hypotension occurred thrice — after induction, after prone positioning, and once intraoperatively — which responded to mephentermine boluses. Total blood loss of 500 ml was replaced with two units packed red cells and two units FFP. At the end of surgery, once the patient was awake and breathing spontaneously, he was extubated. GCS in the post anesthesia care unit was 15/15. Therapies available for emergency reversal of warfarin are FFP, recombinant factor VIIa (rFVIIa), and prothrombin complex concentrates (PCCs) administered with vitamin K. Although the recommendation is to treat with a mixture of PCCs and rFVIIa,[2] in view of their inavailability on the emergent basis, FFP transfusion, and i.v. vitamin K administration was advocated and found effective. Perioperative events such as laryngoscopy and intubation, blood loss, positive pressure ventilation, and positional changes may cause wide fluctuations in BP, exacerbated due to autonomic dysfunction, emphasizing the need for invasive BP monitoring. Succinylcholine is contraindicated in GBS, due to the risk of potentially fatal hyperkalemia.[3] Nondepolarizing NMBAs may result in prolonged neuromuscular block and postoperative mechanical or assisted ventilation may be required.[4] In view of the possibility of prolonged neuromuscular blockade and the need for immediate postoperative neurological assessment, NMBAs were completely avoided. However, wherever possible neuromuscular monitor is indicated. Although GBS patients should be investigated for pulmonary dysfunction because of the risk of asymptomatic impaired lung function,[5] assessment could not be done due to the emergent nature of the surgery. Because there was no history of respiratory distress or previous ventilatory support, and because we avoided NMBAs, we could safely extubate the patient. ==== Refs 1 van Doorn PA Ruts L Jacobs BC Clinical features, pathogenesis, and treatment of Guillain-Barré syndrome Lancet Neurol 2008 7 939 50 18848313 2 Zareh M Davis A Henderson S Treatment of warfarin-associated intracerebral haemorrhage: Literature review and expert opinion West J Emerg Med 2011 12 386 92 22224125 3 Martyn JA Richtsfeld M Succinylcholine-induced hyperkalemia in acquired pathologic states: Etiologic factors and molecular mechanisms Anesthesiology 2006 104 158 69 16394702 4 Brooks H Christian AS May AE Pregnancy, anaesthesia and Guillain Barré syndrome Anaesthesia 2000 55 894 8 10947755 5 Hines RL Marschall KE Stoelting's Anaesthesia and Co-existing Disease 2012 6th ed Philadelphia Elsevier Saunders 269 70