Previous articleTable of Contents Next article

Year : 2008  |  Volume : 2  |  Issue : 2  |  Page : 67-73

Perioperative care of the child with guillain-barre syndrome

Department of Anesthesiology, Professor of Anesthesiology and Pediatrics, University of Missouri., USA

Correspondence Address:
J D Tobias
Department of Anesthesiology, Professor of Anesthesiology and Pediatrics, University of Missouri, Columbia, MO
Login to access the Email id

Source of Support: None, Conflict of Interest: None

Rights and PermissionsRights and Permissions
Date of Web Publication18-Jul-2009


The authors present 2 pediatric patients with acute Guillain-Barre syndrome (GBS) who required anesthetic care: one for diagnostic testing and another during a laparoscopic procedure to evaluate a possible intra­abdominal process. Given the multi-system involvement of the disease, several concerns may arise in the perioperative period. Of primary concern is the potential for respiratory failure related either to upper airway control or skeletal muscle weakness. These issues may be made more problematic by aspiration risks and issues of a potential "full stomach" related to autonomic dysfunction and poor gastrointestinal (GI) motility. Autonomic involvement with cardiovascular dysfunction may manifest as abnormalities in the control of heart rate, systemic vascular resistance, and blood pressure. The potential perioperative implications of the disorder are discussed and its pathophysiology presented.

How to cite this article:
Gipson C, Tobias J D. Perioperative care of the child with guillain-barre syndrome. Saudi J Anaesth 2008;2:67-73

How to cite this URL:
Gipson C, Tobias J D. Perioperative care of the child with guillain-barre syndrome. Saudi J Anaesth [serial online] 2008 [cited 2023 Feb 2];2:67-73. Available from:

   Introduction Top

GBS IS AN EVOLVING POLYRADICULOPATHY, which typically presents as an ascending, symmetric, motor paralysis frequently accompanied by sensory and autonomic dysfunction. In severe cases, the disease may progress to involve cranial and bulbar nerves with respiratory muscle paralysis leading to respiratory failure. Autonomic instability is commonly present and may result in GI symptoms, urinary retention, and cardiovascular involvement manifested as blood pressure lability, tachycardia, bradycardia, arrhythmias and an abnormal response to vasoactive medications. [1],[2],[3] The multi-system involvement of GBS can have a significant impact on the perioperative care of such patients. We present 2 pediatric patients with acute GBS. One required anesthetic care for radiological imaging while the second patient was brought to the operating room for a laparoscopic procedure to evaluate a possible co-existing acute intra-abdominal process. The potential perioperative implications of the disorder are discussed and its pathophysiology presented.

   Case Reports Top

Review of these cases and their presentation in this format was approved the Institutional Review Board of the University of Missouri.

Patient #1:

3.5 yr-old, 28 kg African American male presented to his primary care physician with a 1­week history of weakness, slurred speech, and an inability to walk. A tentative diagnosis of cerebellar ataxia was made and the patient was referred to the pediatric neurology service at our institution for further evaluation and treatment. Prior to this acute illness, the child had been healthy, except for the complaint of minor rhinorrhea, diarrhea, and low­grade temperature for one week prior to the onset of his recent symptoms. The following day, the symptoms continued to progress to the point that the patient was bedridden and had difficulty grasping objects. The patient had also developed a tremor, complained of pain in his legs, and was more irritable. The anesthesia service was consulted to provide care during a magnetic resonance imaging (MRI) scan and the performance of a lumbar puncture to aid in the diagnostic evaluation. The preoperative evaluation revealed stable vital signs with (BP 105/56 mmHg, HR 92 beats/minute, RR 24 breaths/minute and a room air oxygen saturation of 96%). Physical examination revealed an acutely ill appearing child. He had 2/5 motor strength in his upper and lower extremities with decreased deep tendon reflexes (DTR's). He was not cooperative with negative inspiratory force (NIF) or forced vital capacity (FVC) measurements. Past medical history was negative for previous hospitalizations, current medication use, allergies or previous surgical procedures. The patient was held nil per os for 4 hr. Premedication included famotidine (0.5 mg/kg) and metoclopramide (0.1 mg/kg). There were difficulties with obtaining intravenous access and the IV had infiltrated 60 min prior to the procedure. The child was transported to the operating room and following the application of routine monitors, anesthesia was induced with sevoflurane in 100% oxygen with the application of cricoid pressure. Following anesthetic induction, intravenous access was obtained and the trachea intubated under deep sevoflurane anesthesia. Anesthesia was maintained with 2% sevoflurane in air and oxygen with spontaneous ventilation during the procedure. The patient's vital signs remained stable throughout the procedure. After MRI scan, a lumbar puncture was performed. Following this, the patient's trachea was extubated and he was transported to the post-anesthesia care unit (PACU). The remainder of his post-anesthetic course was unremarkable. Based on the results of the lumbar puncture, the diagnosis of GB was confirmed and he was treated with intravenous gamma globulin. His motor weakness did not progress and there was a gradual resolution of his symptoms over the next 14 days. He was discharged home on hospital day 16 with minimal residual weakness in all 4 extremities.

Patient #2:

A previously health 6 yr-old, 36 kg boy was admitted to the pediatric ICU with a presumptive diagnosis of GB following a 2-day history o f progressive motor weakness starting in his lower extremities. He had also developed urinary retention which required placement of a Foley catheter. On hospital day 3, he complained of abdominal pain with rebound tenderness, vomiting, and an elevated white blood cell count (26,000/mm 3 ). A laparoscopy was planned to rule out appendicitis. Physical examination revealed an acutely ill appearing child. He had 2/5 motor strength in his lower extremities, 3/5 in the upper extremities, and decreased deep tendon reflexes (DTR's). The NIF was -40 cmH20 and the FVC was 30 mL/kg. Past medical history was negative for previous hospitalizations, current medication use, allergies or previous surgical procedures. The patient had been placed nil per os that morning when he developed abdominal pain (6 hr earlier). Premedication included famotidine (0.5 mg/kg) and metoclopramide (0.1 mg/kg). The child was transported to the operating room. Twenty mL/kg of lactated Ringers was administered prior to anesthetic induction. Following the application of routine monitors, a rapid sequence induction with cricoid pressure was performed following the intravenous administration of glycopyrrolate (5 µg/kg), lidocaine (1 mg/kg), propofol (2 mg/kg), and remifentanil (2 µg/kg). Sixty seconds after the IV medications, the trachea was intubated without difficulty. The first BP following anesthetic induction was 58/32 mmHg. Phenylephrine (1 µg/kg) was administered and the BP returned to 82/46 mmHg. Maintenance of anesthesia consisted of propofol (50-125 µg/kg/min) titrated to maintain the bispectral index at 40-60 and remifentanil (0.1-0.4 µg/kg/min). Laparoscopy confirmed the diagnosis of appendicitis and a laparoscopic appendectomy was performed. During peritoneal insufflation, there was an episode of bradycardia (HR 42 beats/min) and hypotension (BP 64/32 mmHg) which responded to release of the intra-abdominal pressure and the administration of atropine (10 µg/kg). Following the surgical procedure, the patient's trachea was extubated and he was transported to PACU. His postoperative course was unremarkable. His motor weakness did not progress further and there was a gradual resolution of his symptoms over the next 21 days. He was discharged home on hospital day 28 with minimal residual weakness in all 4 extremities.

   Discussion Top

GBS is a spectrum of diseases of rapidly evolving polyradiculopathies, which typically present as an ascending, symmetric motor paralysis with associated sensory and autonomic dysfunction. [4],[5],[6] It was first described by the French neurologist Landry in 1859. [7] Guillain, Barre, and Strohl further characterized the disease process and identified the characteristic findings in the cerebrospinal fluid. It is the most common acute paralytic illness with an incidence of 1-2 cases per 100,000 per year. GBS typically follows a triggering event such as an infection with a viral agent or other pathogen (C. jejuni, CMV, Epstein­Barr, Mycoplasma pneumonia), following immunizations such as rabies or swine flu, or following some traumatic event including a surgical procedure. [6] ,[8] In many cases, no specific triggering event or etiology is identified. [6] ,[8] The inciting events are postulated to trigger an antibody response with a resultant multifocal demyelination and secondary axonal degeneration. Although the exact mechanism of this process has not been definitively determined, there is a growing body of evidence suggesting that the pathogenesis involves an immune response directed against glycolipids similar to gangliosides naturally found in the nervous system. The estimated incidence of GBS varies from 1-3 per 100,000 up to 4 in 10,000 people worldwide each year. [4] ,[6] Treatment is primarily supportive with up to one-third of patients requiring assisted ventilation. [9] Both plasmapheresis and the administration of intravenous gamma globulin have been shown to shorten the course and hasten recovery with more recent evidence favoring the use of immunoglobulin. [10],[11],[12],[13]

Although the majority of patients do not require anesthetic care during the acute phase of GBS, radiological investigations such as MR imaging may be required to rule out other conditions in the differential diagnosis. In the pediatric-aged patient, deep sedation or general anesthesia may be required to successfully complete such imaging. As demonstrated by our second patient, co-morbid, yet unrelated, diseases may arise which require surgical intervention and anesthetic care. Additionally, GBS may develop following a surgical procedure or patients may experience an exacerbation of the disease following a surgical procedure, well after they have become asymptomatic and are thought to be fully recovered. [14] Given the potential for multi­system involvement with GBS, there are several end-organ issues which may impact on the perioperative care of these patients. Two separate issues may impact on the perioperative respiratory function of patients with GBS including upper airway issues related to bulbar involvement as well as primary intercostal and diaphragmatic weakness. Upper cranial nerve involvement with bulbar dysfunction may predispose these patients to perioperative aspiration or respiratory failure due to upper airway obstruction. Although generally reported in the later stages of the disease process as the disease ascends from the lower spinal cord, bulbar involvement may occur early in the disease and may even be the presenting symptom of acute GBS. Involvement of the cranial nerves may lead to dysphasia and laryngeal paralysis with an increased risk of aspiration and upper airway obstruction which may also lead to respiratory failure. [17] Involvement of cranial nerves occurs in 50-75% of patients. Although involvement of cranial nerve VII is most common, dysfunction of all cranial nerves except for I, II and VIII has been described. The potential for predominantly bulbar involvement is illustrated by several variants of acute GBS. Miller­Fisher syndrome, the most common variant, includes the clinical triad of opthalmoplegia, ataxia, and areflexia. [18] The pharyngeal-cervical-brachial variant may present initially with bulbar signs and one case report describes its misdiagnosis as epiglottitis. [19] Similarly, upper airway obstruction with stridor, initially thought to be related to airway pathology, has also been reported as the presenting symptom of GBS. [20]

Perioperative respiratory dysfunction may also result from intercostal and diaphragmatic muscle paralysis and weakness. Respiratory failure remains the leading cause of death as well as accounting for prolonged morbidity with the resultant dependency on mechanical ventilation resulting in prolonged hospital stays. [8] ,[21] The progression of respiratory failure can be monitored by following serial bedside forced vital capacity (FVC) measurements with values less than 1.5 liters (in adults) indicative of impending respiratory failure and the need for [22],[23] ventilatory assitance.Residual deficiencies in ventilatory function may persist for prolonged periods following apparent recovery from GBS. [24] Given these concerns and the potential impact of the residual effects of anesthetic agents on both bulbar and respiratory function, we would suggest the use of short-acting anesthetic agents whenever feasible. In our patients, we chose to use short-acting inhalational agents (sevoflurane), intravenous agents (propofol), and opioids (remifentanil). Given the potential for perioperative airway obstruction or respiratory failure, ongoing monitoring of postoperative respiratory function is suggested. Although MR imaging is frequently accomplished with " conscious sedation" and not necessarily general anesthesia, given the potential for respiratory failure and aspiration with loss of protective airway reflexes, we felt that general anesthesia with endotracheal intubation was the safest option. In patients with respiratory insufficiency following anesthetic care, options include not only conventional mechanical ventilation via an endotracheal tube, but also non-invasive ventilatory techniques such as continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BiPAP). [4] However, non-invasive ventilatory support may be relatively contraindicated in patients with poor airway control who are at risk for aspiration. Concerns regarding respiratory function and airway protective reflexes may be compounded by aspiration risk due to altered GI motility related to autonomic dysfunction. The latter may be related primarily to the disease process with impaired gastric emptying/GI motility and compounded by an intra-abdominal process as was present in our second patient. Given these concerns, we chose to administer GI prophylaxis (metoclopramide and an H 2 -antagonist) and apply cricoid pressure during anesthetic induction. Another issue of significant concern related to airway management and the perioperative care of patients with acute GBS is the decision whether to use a neuromuscular blocking agent (NMBA) as well as which NMBA to use. Given the potential for altered responses to NMBA, we chose to avoid their use in our 2 patients by performing endotracheal intubation under deep sevoflurane anesthesia in the first patient and using a combination of propofol and remifentanil in the second patient. Successful intubation with various combinations of remifentanil and propofol has been reported in both the adult and the pediatric literature. [25],[26],[27] Batra et al. reported that propofol (3 mg/kg) and remifentanil (3 µ/kg) could be used to allow for endotracheal intubation within 90 seconds without the use of a NMBA in children ranging in age from 5 to 10 years. [25] Similar efficacy has been reported in a cohort of adult patients when using propofol (2 mg/kg) and remifentanil (3 µg/kg). [26]

Given the potential for hemodynamic lability in our patient with acute GBS, we chose to use only 2 µg/kg of remifentanil as the study of Batra et al, included only ASA 1 and 2 patients.

If the use of a non-depolarizing NMBA is indicated, we would suggest the use of short acting agent. Although mivacurium has been shown to be effective in patients with underlying muscle weakness [28] , it is no longer commercially available. We would therefore recommend the use of small, incremental doses of an intermediate acting agent with ongoing monitoring of neuromuscular function when NMBA's are needed. Both hypersensitivity and resistance to non-depolarizing NMBA's have been described in acute GBS. [29] ,[30] as well as other demyelinating polyradiculopathies. [23] The variability in response to NMBA's is dependent on the time course of the disease process. Fiacchino et al. reported variable response to vecuronium during two separate procedures in the same patient. [30] Using peripheral monitoring of the neuromuscular junction, they noted resistance to the effects of 7 mg of vecuronium (low intensity block with rapid recovery). Seventeen days later, there was increased sensitivity to 6.5 mg of vecuronium (increase in the degree and duration of the block). Increased sensitivity may result from the loss of motor units and/or to pre/postsynaptic acetylcholine (Ach) receptor channel blockade by antibodies. [6] Alternatively, early in the disease, there may be a resistance to NMBA's due to a denervation effect with increased number of ACH receptors, which is gradually replaced by " reinnervation-induced hypersensitivity". [30] In addition to the potential for exaggerated responses to NMBA's, various other medications (antibiotics, anti-arrhythmic agents, anticonvulsants, calcium channel blockers, et al), which may be used in the perioperative period, may have effects at the neuromuscular junction. [31],[32],[33] Although these effects are generally of limited clinical significance, they may cause profound weakness or potentiate the effects of NMBA's in patients with diseases of the neuromuscular junction. Therefore, their impact should be considered in the perioperative care of patients with acute GBS. It would appear that depolarizing neuromuscular blocking agents such as succinylcholine should be avoided in patients with GBS. There are anecdotal reports of rhabdomyolysis, hyperkalemia, and cardiac arrest following its administration to patients with GBS, sometimes well after the resolution of symptoms. [6] ,[31] ,[32] As many as 67% of patients with GBS manifest clinical evidence of autonomic dysfunction. [1] Involvement may include visceral afferent fibers of the autonomic nervous system, efferent fibers of the sympathetic or parasympathetic nervous system, or a combination of both. [37] The degree of autonomic dysfunction does not necessarily correlate with the extent of motor involvement. [37] ,[38] Involvement of the parasympathetic or sympathetic nervous may predominate, manifesting as abnormalities in the control of heart rate, systemic vascular resistance, and blood pressure. [2] ,[38],[39],[40],[41],[42] Arrhythmias and even sudden cardiac arrest may occur. [42],[43],[44] Hypotension is the most common cardiovascular manifestation of autonomic nervous system involvement. [38] Typical perioperative events leading to hypotension such as blood loss, positive pressure ventilation, and positional changes which are unrelated to the disease process, may be exacerbated by poor autonomic control and lack of normal compensatory mechanims. [8] Cardiovascular collapse has been reported following the administration of barbiturates and phenothiazines in patients with GBS, thereby emphasizing the need to avoid medications with negative effects on cardiovascular function. [45] Autonomic dysfunction may also manifest as the abnormal release of catecholamines in response to intraoperative stimuli such as endotracheal intubation or surgical incision or may occur without provocation secondary to brain stem dysfunction. [8] ,[38] The autonomic dysfunction may thus result in wide variations in blood pressure with periods of both hypertension and hypotension. [37] ,[38] ,[41] Although we noted no significant exaggeration of the hemodynamic effects of inhalational anesthetic agents in our 2 patients, our second developed hypotension following intravenous induction with propofol (2 mg/kg) and remifentanil (2 µg/kg) despite pre-induction volume loading with 20 mL/kg of isotonic crystalloid. Invasive hemodynamic monitoring may be indicated in patients manifesting significant autonomic involvement or during surgical procedures in which alterations in hemodynamic status are anticipated. Gradual changes in parameters that may affect blood pressure such as positive pressure ventilation or patient positioning may minimize their impact on cardiovascular function. [8] ,[17] Hypotensive episodes can typically be managed with volume expansion or use of direct acting adrenergic agents. However, there may be increased sensitivity to vasoactive medications due to denervation supersensitivity. [37] ,[38] Various arrhythmias have been observed in patients with GBS including nodal tachycardia, atrial fibrillation, paroxysmal atrial tachycardia, ventricular tachycardia, ST segment elevation or depression, flat or inverted T-waves, prolonged -T intervals, axis deviation, and conduction blocks. [37],[39],[43] Brady-arrhythmias occur in up to 50% o f patients with severe GBS. [37] Dunlop et al. reported 2 patients who developed severe sinus bradycardia during endotracheal suctioning that resulted in asystole and death of one of the patients. [42] The propensity for brady-arrhythmias have led some authors to recommend insertion of a demand pacemaker in patients with severe GBS if cardiac monitoring reveals bradycardia or other rhythms originating from locations other than the sinus node. [5] ,[44] It is postulated that these rhythm effects are primarily related to imbalances of the autonomic nervous system; however, autopsy findings have demonstrated a toxic myocarditis in fatal GBA with areas of focal, perivascular, lymphocytic infiltration of the myocardium. [1] ,[43]

A final issue in the perioperative care of patients with acute GBS is the choice of modality for perioperative analgesia. In the absence of surgical trauma, pain is commonly present as the disease process affects not only motor, but also sensory neurons. Autonomic dysfunction and opioids may have synergistic effects on GI motility leading to a high incidence of ileus. [4] ,[38] ,[45] Carbamazepine and gabapentin may serve as successful adjuncts to pain control in this population and decrease opioid requirements. [46],[47],[48] Gabapentin has been shown to be superior to carbamazepine in decreasing pain associated with GBS. [46] When compared with carbamazepine, patients receiving gabapentin had decreased pain scores and decreased fentanyl requirements. Despite the theoretical concern o f exacerbating the disease process [49],[50],[51] , regional anesthesia has been administered to patients with acute GBS without untoward effects as the primary anesthetic, for postoperative pain management, or to treat acute pain issues primarily related to the disease process. Anecdotal experience suggests increased sensitivity to neuraxial anesthesia due to axonal conduction abnormalities. [53] An additional concern with the use of neuraxial anesthesia is the potential for exaggerated hemodynamic changes related to the associated autonomic dysfunction.

In patients with acute GBS, anesthetic care may be required during radiological imaging such as MR imaging to rule out other conditions in the differential diagnosis or when co-morbid diseases arise which require surgical intervention and anesthetic care. Also of concern to the anesthesia provider is that GBS may develop following a surgical procedure or patients may experience an exacerbation of the disease following surgery, even when they are thought to be fully recovered. Given the multi-system involvement of the disease, several concerns may arise in the perioperative period. Of primary concern is the potential for respiratory failure related either to upper airway control or skeletal muscle weakness. These issues may be made more problematic by aspiration risks and issues of a potential " full stomach" related to autonomic dysfunction and poor GI motility. Autonomic involvement with cardiovascular dysfunction may manifest as abnormalities in the control of heart rate, systemic vascular resistance, and blood pressure.

   References Top

1.Singh NK, Jaiswal AK, Misra S, Srivastava PK. Assessment of autonomic dysfunction in Guillain-Barre syndrome and its prognostic implications. Acta Neurol Scand 1987;75:101-105.  Back to cited text no. 1  [PUBMED]  
2.Panegyres PK, Mastaglia FL. Guillain-Barre syndrome with involvement of central and autonomic nervous systems. Med J Austral 1989;150:655-659.  Back to cited text no. 2  [PUBMED]  
3.Yamamoto K, Sobue G, Iwase S, et al. Skin sympathetic nerve activity in Guillain-Barre syndrome: a microneurographic study. J Neurol Neurosurg Psych 1997;63:537-540.  Back to cited text no. 3    
4.Newswanger DL, Warren CR. Guillain-Barre Syndrome. Am Fam Phy 2004;69:2405-2410.  Back to cited text no. 4    
5.Winer JB. Treatment of Guillain-Barre syndrome. Q J Med 2002;95:717-721.   Back to cited text no. 5    
6.Naguib M, Flood P, McArdle JJ, Brenner HR. Advances in neurobiology of the neuromuscular junction: Implications for the anesthesiologist. Anesthesiol 2002; 96: 202-231.  Back to cited text no. 6    
7.Landry O. Note sur la paralysie ascendate aigue. GaxHebd Med 1859;6:472-473.  Back to cited text no. 7    
8.Plaugher ME. Emergent exploratory laparotomy for a patient with recent Guillain-Barre recurrence: A case report. JANA 1994;62:437-440.  Back to cited text no. 8    
9.Hahn AF. Guillain-Barre syndrome. Lancet 1998;352:635­641.   Back to cited text no. 9  [PUBMED]  [FULLTEXT]
10.Hughes RAC. Plasma exchange for Guillain-Barre syndrome. Br Med J 1995;291:615-616.  Back to cited text no. 10    
11.Ropper AH. The Guillain-Barre syndrome. New Engl J Med 1992;326:1130-1136.  Back to cited text no. 11  [PUBMED]  
12.Rajah A. The use of high dose intravenous immunoglobulins in GBS. Anaesthesia 1992;47:220-222.  Back to cited text no. 12  [PUBMED]  
13.Plasma exchange/Sandoglobulin Guillain-Barre syndrome trial group. Randomized trial of plasma exchange, intravenous immunoglobulin and combined treatments in Guillain-Barre syndrome. Lancet 1997;349:225-230.  Back to cited text no. 13    
14.Parobeck V, Burnham S, Laukhuf GA. An unusual nursing challenge: Guillain-Barre syndrome following cranial surgery. J Neurosci Nurs 1992;24:251-255.  Back to cited text no. 14  [PUBMED]  
15.Renlund DG, Hanley DF, Traill TA. Guillain-Barre syndrome following coronary artery bypass surgery. Am Heart J 1987;113:844-845.  Back to cited text no. 15  [PUBMED]  
16.Shuert GT, Gamble JW. Guillain-Barre syndrome after mandibular surgery: report of two cases. J Oral Surg 1972;30:913-915.  Back to cited text no. 16  [PUBMED]  
17.Desmeules H, Fournier L, Sirois GH. The Guillain-Barre syndrome: role of the anesthetist in the treatment of cardiovascular and respiratory complications. Can Anaesth Soc J 1972;19:290-298.  Back to cited text no. 17  [PUBMED]  
18.Rodriguez Uranga JJ, Delgado Lopez F, Franco Macias E, et al. Miller Fisher syndrome : clinical features, associated infections, and clinical course in 8 cases. Medicina Clinica 2004;122:223-226.  Back to cited text no. 18    
19.MacLennan SC, Fahey MC, Lawson JA. Pharyngeal­cervical-brachial variant Guillain-Barre syndrome in a child. J Child Neurol 2004;19:626-627.  Back to cited text no. 19  [PUBMED]  
20.Larsen A, Tobias JD. Landry-Guillain-Barre syndrome presenting with symptoms of upper airway obstruction. Pediatr Emerg Care 1994;10:347-348.  Back to cited text no. 20  [PUBMED]  
21.Ramesh VJ, Umamaheswara GS. Weaning from mechanical ventilation in a neurologic disease: an unusual application for tracheal gas insufflation. Anesthesiol 2002;97:515-517.  Back to cited text no. 21    
22.Hund EF, Borel CO, Cornblath DR, et al. Intensive care management of Guillain-Barre syndrome. Crit Care Med 1993;21:433-446.  Back to cited text no. 22  [PUBMED]  
23.Gracey DR, McMichan JC, Divertie MB, et al. Respiratory failure in Guillain-Barre syndrome: A six year experience. Mayo Clin Proc 1982;57:742-746.  Back to cited text no. 23  [PUBMED]  
24.Silbert KS, Sladen RN. Impaired ventilatory capacity after recovery from Guillain-Barre syndrome. J Clin Anesth 1994; 6: 133-138.  Back to cited text no. 24    
25.Batra YK, AL Qattan AR, Ali SS, et al. Dosing study of remifentanil and propofol for tracheal intubation without use of muscle relaxants. Pediatr Anesth 2004;14:452-456.  Back to cited text no. 25    
26.Stevens JB, Wheatley L. Tracheal intubation in ambulatory surgery patients: using remifentanil and propofol without muscle relaxants. Anesth Analg 1998;86:45-49.  Back to cited text no. 26  [PUBMED]  [FULLTEXT]
27.Durmus M, Ender G, Kadir BA, et al. Remifentanil with thiopental for tracheal intubation without muscle relaxants. Anesth Analg 2003;96:1336-1339.  Back to cited text no. 27  [PUBMED]  [FULLTEXT]
28.Tobias JD, Atwood R. Mivacurium in children with Duchenne muscular dystrophy. Paeditr Anaesth 1994;4:57­60.  Back to cited text no. 28    
29.Hara K, Minami K, Takamoto K, et al. The prolonged effect of a muscle relaxant in a patient with chronic inflammatory demyelinating polyradiculoneuropathy. Anesth Analg 2000;90:224-226.  Back to cited text no. 29    
30.Fiacchino F, Gemma M, Bricchi M, et al. Hypo-and hypersensitivity to vecuronium in a patient with Guillain­Barre syndrome. Anesth Analg 1994;78:187-189.  Back to cited text no. 30  [PUBMED]  [FULLTEXT]
31.Ostergaard D, Engbaek J, Viby-Mogensen J. Adverse reactions and interactions of the neuromuscular blocking drugs. Med Toxicol Adverse Drug Exp 1989;4:351-368.  Back to cited text no. 31  [PUBMED]  
32.Cammu G. Interactions of neuromuscular blocking drugs. Acta Anaesthesiol Belg 2001;52:357-363.  Back to cited text no. 32  [PUBMED]  
33.Feldman S, Karalliedde L. Drug interactions with neuromuscular blockers. Drug Safety 1996;15:261-273.  Back to cited text no. 33  [PUBMED]  
34.Feldman JM. Cardiac arrest after succinylcholine administration in a pregnant patient recovered from Guillain-Barre syndrome. Anesthesiology 1990;72:942­944.  Back to cited text no. 34  [PUBMED]  
35.Hawker F. Rhabdomyolytic renal failure and suxamethonium. Anesth Intens Care 1985;13:208-209.  Back to cited text no. 35    
36.Dalman JE, Verchagen WI. Cardiac arrest in Guillain-Barre syndrome after the use of suxamethonium. Acta Neurol Belg 1994;94:259-261.  Back to cited text no. 36    
37.Zochodne DW. Autonomic involvement in Guillain-Barre syndrome: a review. Muscle Nerve 1994;17:1145-1155.  Back to cited text no. 37  [PUBMED]  
38.Lichtenfeld P. Autonomic dysfunction in the Guillain-Barre Syndrome. The Amer J Med 1971;50:772-780.  Back to cited text no. 38    
39.McLeod JG, Tuck RR. Disorders of the autonomic nervous system: Part 1. Pathophysiology and clinical features. Ann Neurol 1987;21:419-430.  Back to cited text no. 39    
40.Hickory JE, Wilcox JW. Cardiopulmonary arrest as a complication of Guillain-Barre syndrome in a postsurgical patient. J Oral Surgery 1978;36:549-550.  Back to cited text no. 40    
41.Ropper AH, Wijdicks EF. Blood pressure fluctuations in the dysautonomia of Guillain-Barre syndrome. Arch Neurol 1990;47:706-708.  Back to cited text no. 41  [PUBMED]  [FULLTEXT]
42.Dunlop RJ, Davidson JN, Orpin MJ, et al. Arrhythmias and Guillain-Barre syndrome. NZ Med J 1987;100:139-141.  Back to cited text no. 42    
43.Greenland P, Griggs RC. Arrhythmic complications in the Guillain-Barre syndrome. Arch Intern Med 1980;140:1053­1055.  Back to cited text no. 43    
44.Emmons PR, Blume WT, DuShane JW. Cardiac monitoring and demand pacemaker in Guillain-Barre syndrome. Arch Neurol 1975;32:59-61.  Back to cited text no. 44    
45.Perel A, Reches A, Davidson JT. Anesthesia in the Guillain-Barre syndrome. Anaesthesia 1977;32:257-260.  Back to cited text no. 45    
46.Tripathi M, Kaushik S. Carbamazepine for pain management in Guillain-Barre syndrome patients in the intensive care unit. Crit Care Med 2000;28:655-658.  Back to cited text no. 46    
47.Pandey CK, Bose N, Garg G, et al. Gabapentin for the treatment of pain in Guillain-Barre syndrome: a double­ blinded, placebo-controlled, crossover study. Anesth Analg 2002;95:1719-1723.  Back to cited text no. 47    
48.Pandey CK, Raza M, Ranjanet R, et al. The comparative evaluation of gabapentin and carbamazepine for pain management in Guillain-Barre syndrome patients in the intensive care unit. Anesth Analg 2005;101:220-225.  Back to cited text no. 48    
49.Wiertlewski S, Magot A, Drapier S, et al. Worsening of neurologic symptoms after epidural anesthesia for labor ina Guillain-Barre patient. Anesth Analg 2004;98:825-827.  Back to cited text no. 49    
50.Bamberger PD, Thys DM. Guillain-Barre syndrome in a patient with pancreatic cancer after an epidural-general anesthetic. Anesth Analg 2005;100:1197-1199.  Back to cited text no. 50    
51.Steiner I, Argov Z, Cahan C, et al. Guillain-Barre syndrome after epidural anesthesia: direct nerve root damage may trigger disease. Neurology 1985;35:1473-1475.  Back to cited text no. 51    
52.Connelly M, Shagrin J, Warfield C. Epidural opioids for the management of pain in a patient with the Guillain-Barre syndrome. Anesthesiol 1990;72:381-383.  Back to cited text no. 52    
53.McGrady EM. Management of labour and delivery in a patient with Guillain-Barre syndrome. Anaesthesia 1987;42: 899-891.  Back to cited text no. 53    


Previous article Next article
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

  IN THIS Article
    Case Reports

 Article Access Statistics
    PDF Downloaded387    
    Comments [Add]    

Recommend this journal