|Year : 2008 | Volume
| Issue : 2 | Page : 214-216
Bispectral Index Monitoring in Guillain Barre Syndrome with Dysautonomia
Deepak Sharma1, Virendra Jain2, Girija P Rath3, Parmod K Bithal4
1 Ex- Senior Resident, Department of Neuroanaesthesiology, Neurosciences Centre, All India Institute of Medical Sciences (A.I.I.M.S.), New Delhi -110029, India
2 Senior Resident, Department of Neuroanaesthesiology, Neurosciences Centre, All India Institute of Medical Sciences (A.I.I.M.S.), New Delhi -110029, India
3 Assistant Professor, Department of Neuroanaesthesiology, Neurosciences Centre, All India Institute of Medical Sciences (A.I.I.M.S.), New Delhi -110029, India
4 Professor, Department of Neuroanaesthesiology, Neurosciences Centre, All India Institute of Medical Sciences (A.I.I.M.S.), New Delhi -110029, India
|Date of Acceptance||11-Mar-2008|
|Date of Web Publication||19-Mar-2010|
Parmod K Bithal
Department of Neuroanaesthesiology, Neurosciences Centre, All India Institute of Medical Sciences, New Delhi -110029
Source of Support: None, Conflict of Interest: None
Bispectral index (BIS) is commonly used as an index of depth of anaesthesia and sedation. BIS can provide an additional benefit in detecting a critical neurological event, especially if the change of neurological status is caused by the critical illness itself. We encountered such an incident where the BIS value was decreased in a patient with Guillain Barre Syndrome, possibly due to cerebral hypoperfusion. The present report emphasises that BIS can be used not only as an indicator of cerebral ischaemia, but also as a tool to judge adequacy and efficacy of interventions targeted to restore the same.
Keywords: Bispectral index monitor; Dysautonomia; Cerebral hypoperfusion
|How to cite this article:|
Sharma D, Jain V, Rath GP, Bithal PK. Bispectral Index Monitoring in Guillain Barre Syndrome with Dysautonomia. Indian J Anaesth 2008;52:214-6
|How to cite this URL:|
Sharma D, Jain V, Rath GP, Bithal PK. Bispectral Index Monitoring in Guillain Barre Syndrome with Dysautonomia. Indian J Anaesth [serial online] 2008 [cited 2019 Dec 13];52:214-6. Available from: http://www.ijaweb.org/text.asp?2008/52/2/214/60627
| Introduction|| |
The bispectral index (BIS) of the electroencephalogram (EEG) is an empirical, statistically derived variable that provides information about the interaction of brain cortical and subcortical regions.  Since its introduction to the clinical armamentarium, BIS has gained popularity over years as an index of measure of depth of anaesthesia. It is expressed as a dimensionless number between 0 and 100, with scores of 95 or greater typically indicating conscious state.  Recently, attempts have been made to extend the use of BIS to patients in the intensive care units (ICU), where sedative drugs are used frequently.  In this setting, BIS was shown to be correlated with the depth of sedation, and was proposed as a guide to prevent over-sedation in cases, where neurological assessment is a frequent requirement.
| Case report|| |
A 36-yr-old male patient (weight 50 kg) of GuillainBarre (GB) Syndrome was admitted in our ICU with complaint of progressive difficulty in breathing. In view of impending respiratory failure, his trachea was intubated and mechanical ventilation was initiated. Intravenous immunoglobulin (IVIg) 100gm/day was given for 5 days. Monitoring parameters included ECG, SpO 2 , noninvasive blood pressure (BP), central venous pressure (CVP), and urine output. A BIS sensor was attached on the forehead of the patient, connected to a BIS monitor. Intravenous infusion of midazolam and fentanyl was started and dose titrated to keep the BIS at 70-80. Two days after initiation of IVIg therapy the patient developed fluctuations of BP and dysrrhythmias. An association of dysautonomia was confirmed with positive tests for autonomic function. As the patient developed severe and persistent hypotension, sedative medicants were withdrawn, and dopamine infusion was started to achieve a mean BP of 65-75 mmHg.
On day 4, while the patient was still on ventilatory and inotropic support, BIS was observed to be zero with suppression ratio (SR) of 100, and the EEG signal was a flat line. The patient was unresponsive and peripheral pulses were not palpable. Monitor showed absence of pulse oximetry tracing with sinus bradycardia (heart rate of 42 bpm). Cardiopulmonary resuscitation (CPR) was started, immediately. Atropine 0.6 mg followed by mephentermine 6 mg was administered, intravenously and patient was ventilated with 100% oxygen. Normal saline 500 ml was infused rapidly. Within a minute, radial pulse could be palpated; heart rate increased to 120 bpm and blood pressure was 116/54 mm Hg. Simultaneously, the BIS value increased to 58 and SR decreased to 10. Soon, the patient regained consciousness and started following verbal commands. Five minutes later, the patient was fully alert with BIS of 90. The monitoring trend revealed last BP of 96/58 mmHg, which was recorded 3 minutes before the event. It was observed that the infusion pump delivering dopamine has stopped delivering the drug, without an alarm. Dopamine infusion was restarted. Monitoring trends revealed progressive hypotension with bradycardia over last 10 minutes with progressive fall of BIS value over same time period.
Dopamine infusion was tapered off, over next two days, as the haemodynamic status improved. In view of prolonged intubation, tracheostomy was performed and he was weaned off ventilator over next 4 weeks. His muscle power gradually improved and he was discharged from the hospital after 6 weeks with intact neurological status and stable vital parameters.
| Discussion|| |
GB Syndrome or acute inflammatory polyneuropathy is characterized by ascending and areflexic motor paralysis, respiratory failure, and autonomic dysfunction.  Autonomic failure (dysautonomia) may cause profound hypotension or hypertension, urinary retention, various dysrrhythmias, and ECG changes. Some episodes of hypotension are precipitated by suctioning or other provocative vagal stimuli, but most seem to be spontaneous. Vasodepressor response mediated by medullary and sympathetic mechanism may cause severe hypotension which may even lead to loss of consciousness due to cerebral hypoperfusion.  Probably, a similar type of episode occurred in this patient. Hypotension in GB syndrome may not always be due to autonomic failure. It may occur as a result of prolonged bed rest, dehydration, positive pressure ventilation, and heavy sedation, or else because of sepsis and myocardial infarction.  As these causes were ruled out, we attribute the cause of sudden hypotension to malfunction of infusion pump of dopamine, in presence of an already existing dysautonomia.
Well known causes of low BIS value include deep anaesthesia, over-sedation, and hypothermia. In addition, low BIS values attributable to hypoxia  , cerebral hypoperfusion  and intracranial catastrophe  have been reported in anaesthetized individuals. Our observation represents reversible global cerebral hypoperfusion in a conscious patient, detected by BIS monitoring.
The patient was not administered any sedative medication at the time of the event and was on inotropic support. The fall in BIS value was associated with flat EEG tracing with simultaneous loss of consciousness and circulatory collapse. The haemodynamic recovery was associated with return of consciousness and simultaneous normalization of BIS value with normal EEG pattern. Hence, we believe, the cause of low BIS in this patient was cerebral hypoperfusion. Nevertheless, an invasive BP monitoring could have helped in early diagnosis of this untoward event.
Cerebral autoregulation is a critical homeostatic mechanism that minimizes fluctuations in cerebral blood flow (CBF) with changes in cerebral perfusion pressure (CPP) and thus, protects the brain against ischaemic and hyperaemic insults. Though there is no information available regarding the status of cerebral autoregulation in patients with autonomic dysfunction, acute ischaemia with fall in blood pressure below the critical level of 50 mm Hg is expected to cause compromise of CBF. There are no clinical studies to indicate a definite relationship between BIS and CBF or CPP. However, it has been suggested that a BIS value below 30 is an indicator of EEG suppression.  Consequently, cerebral hypoperfusion leading to EEG suppression should result in low BIS values and restoration of adequate perfusion with consequent recovery of EEG activity should lead to 'normalization' of BIS values.
The present case indicates that BIS can be used as an indicator of cerebral ischaemia in conscious patients admitted into the intensive care unit. It may be helpful not only in early detection of impending neurological catastrophic events, but also to judge the adequacy and efficacy of interventions targeted to restore the same.
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