J Neurosurg Anesthesiol
Volume 27, Number 1, January 2015
lactated ringer solution, lumber puncture (LP) was performed under sterile conditions with 25 G Quincke’s spinal needle inserted one time without trauma at the L3-4 interspace. Free flow of yellow-colored cerebrospinal fluid (CSF) appeared. The yellowish tinge of CSF made us suspicious of an undiagnosed traumatic subarachnoid hemorrhage (SAH). To confirm the same we collected 1 mL of CSF sample and sent it to the biochemistry department for spectrophotometric analysis. However, we proceeded with subarachnoid block in this patient using 2.7 mL of 0.5% hyperbaric bupivacaine (13.5 mg). Perioperative course remained uneventful. Result of spectrophotometric analysis of CSF confirmed xanthochromia, which occurs from hemoglobin catabolism and is diagnostic of SAH. A review by neurosurgeon established the diagnoses of isolated traumatic SAH. According to the literature, computed tomography (CT) scan has 95% sensitivity for diagnosing SAH and in CT-negative cases LP is carried out to visualize xanthochromia along with spectrophotometric analyses of the CSF to confirm the same.1–5 Nowadays, isolated traumatic SAH with subtle presentation is being increasingly recognized. A recent study by Quigley et al6 identified that isolated traumatic SAH in the settings of mild traumatic brain injury (GCSZ13) without other intracranial pathology are a form of benign head injury that does not warrant extensive observation and followup. Ours was one such case of benign SAH diagnosed accidently while performing neuraxial blockade. Despite suspecting the underlying pathology we proceeded with regional anesthesia as our patient was relatively asymptomatic, had no sign and symptoms of raised intracranial pressure, and had been neurologically cleared. His headache was mild in nature in contrast to characteristic severe thunderclap headache associated with SAH. To conclude, xanthochromic CSF on lumbar puncture should alert anesthesiologist about an underlying undiagnosed SAH, especially in settings of preceding trauma. Weather to proceed with neuraxial blockade in such cases must be viewed within the apr
2014 Lippincott Williams & Wilkins
propriate clinical context like signs of raised ICP, any neurologic deficits, and hemodynamic status of the patient. Tarandeep Singh, MBBS, MD, DNB Sarla Hooda, MBBS, MD Asha Anand, MBBS, DA, DNB Pooja Bihani, MBBS Department of Anesthesiology & Critical Care, Postgraduate Institute of Medical Sciences, Rohtak, Haryana, India
REFERENCES 1. Vermuelen M, Hasan D, Blijenberg BG, et al. Xanthochromia after subarachnoid haemorrhage needs no revisitation. J Neurol. 1989;52:826–828. 2. Beetham R. Spectrophotometric examination of CSF for xanthochromia (Letter Comment). Lancet. 1992;339:1492. 3. Roost KT, Pimstone NR, Diamond I, et al. The formation of cerebrospinal fluid xanthochromia after subarachnoid haemorrhage: enzymic conversion of haemoglobin to bilirubin by the arachnoid and choroid plexus. Neurology. 1972;22:973–977. 4. MacDonald A, Mendelow AD. Xanthochromia revisited: a re-evaluation of lumbar puncture and CT scanning in the diagnosis of subarachnoid haemorrhage. J Neurol Neurosurg Psychiatry. 1998;51:341–344. 5. Foot C, Staib A. How valuable is a lumber puncture in the management of patients with suspected subarachnoid hemorrhage? Emerg Med. 2001;13:326–332. 6. Quigley MR, Chew BG, Swartz CE, et al. The clinical significance of isolated traumatic subarachnoid hemorrhage. J Trauma Acute Care Surg. 2013;74:581–584.
Abnormal Bispectral Index Values Associated With the Presence of Periodic Lateralized Epileptiform Discharges To JNA Readers: We report a case in which the presence of periodic lateralized epileptiform discharges (PLEDs) in the unprocessed electroencephalogram (EEG) of a patient with acute herpes simplex encephalitis was associated with the display of an abnormally high processed bispectral index (BIS) value. Written consent was obtained from the next-ofkin of the deceased (for the publication of this report). The authors have no funding or conflicts of interest to disclose.
Correspondence
A 67-year-old man with a history of previous stroke presented to the emergency department with seizures and expressive dysphasia. A computed tomography brain scan demonstrated no focal lesions. He was admitted to the neurology ward where initial routine blood tests and lumbar puncture (LP) were unremarkable. The patient developed status epilepticus that failed to respond to maximum medical therapy, necessitating tracheal intubation and admission to the neurointensive care unit. BIS monitoring was instituted to guide sedation. Magnetic resonance imaging revealed appearances consistent with viral encephalitis. A repeat LP proved positive for herpes simplex virus. The patient had already been commenced on antimicrobials on admission including acyclovir. Sedation was stopped 3 days later to assess neurologic status, but the patient continued to be deeply comatose. Periodic high-amplitude spikes against electrophysiological silence were noted on the BIS monitor. Concurrent increase in the calculated BIS indices from near 0 to higher values (Fig. 1) seemed inconsistent with the underlying clinical picture. A formal EEG showed the presence of PLEDs in all montages with no underlying normal EEG pattern, suggestive of severe cerebral dysfunction. Despite treatment with acyclovir for 2 weeks, the patient remained comatose. The patient died soon after ventilatory support was withdrawn. PLEDs are patterns of abnormal EEG activity indicative of severe cerebral pathology and are associated with poor outcome. Etiological factors for PLEDs include viral encephalitis,1 as seen in our case. It has been suggested that the poor outcome that PLEDs confers is independent of etiology.2 The persistence of PLEDs on continuous full EEG monitoring during the process of death has been previously described.3 The phenomenon of PLEDs has not been previously reported when using BIS. In this case, the BIS monitor detected an actual clinical EEG anomaly and incorporated this anomaly into the processed value to produce an abnormally high BIS value. Although clinicians would rarely act on a BIS value in www.jnsa.com |
73
J Neurosurg Anesthesiol
Dube et al
FIGURE 1. Periodic lateralized epileptiform discharges-PLEDs (highlighted) in raw electroencephalogram (EEG) waveform with abnormally high bispectral index of 74.
isolation, this report illustrates the utility of the real-time raw EEG waveforms that can be obtained from the BIS monitor, and in this situation, prompting a formal EEG evaluation. Matthew Smith, FRCA Patrick Dobbs, FRCA George Eapen, FRCA, FFICM Sheffield Teaching Hospitals Sheffield, UK
REFERENCES 1. Hernandez-Fernandez F, Fernandez-Diaz E, Pardal-Fernandez J, et al. Periodic lateralized epileptiform discharges as manifestation of pneumococcal meningoencephalitis. Int Arch Med. 2011;4:23. 2. Pedersen G, Rasmussen S, Gyllenborg J, et al. Prognostic value of periodic electroencephalographic discharges for neurological patients with profound disturbances of consciousness. Clin Neurophysiol. 2013;124:44–51. 3. Fishman O, Legatt A. PLEDs following control of seizures and at the end of life. Clin EEG Neurosci. 2010;41:11.
left eye ball, and tinnitus in the left ear since the past 3 months. He had a history of road traffic accident for which he underwent repair of mandibular and maxillary fracture under anesthesia. The patient was diagnosed to have a left carotico-cavernous fistula (CCF) with venous drainage into ipsilateral cavernous sinus and inferior petrosal sinus and a significant steal in ipsilateral middle cerebral artery and anterior cerebral artery territories. He was scheduled for balloon occlusion of the CCF under monitored anesthesia care. In the neuroradiologic suite standard monitors were attached and femoral artery was cannulated for the procedure under local anesthetic infiltration. Two balloons were used for complete occlusion of the high-flow CCF (Fig. 1). The patient had stable hemodynamics throughout the procedure, which lasted
Volume 27, Number 1, January 2015
for 150 minutes and he received 8 mg of intravenous (IV) dexamethasone 30 minutes before completion of the procedure. The proptosis was visibly reduced after of the procedure. Ten minutes later, the patient complained of nausea and vomiting. The blood pressure, electrolytes, neurological status, and computed tomographic scan of the head were normal. Ondansetron (6 mg) was administered intravenously (IV) but without any relief to the episodes of nausea and vomiting. However, these episodes later responded to an injection of propofol 20 mg IV. The patient was then shifted to ICU for observation during which he remained asymptomatic for 4 to 5 hours. This was followed by recurrence of nausea and vomiting albeit with reduced severity. The patient received second dose of dexamethasone and ondansetron. Next morning, the computed tomography scan and fluoroscopic imaging confirmed correct position of the balloon. The patient continued to have nausea and vomiting but with each passing day, the severity and frequency was diminished and completely subsided on fifth postprocedural day. Balloon occlusion is one of the therapeutic options for CCF.1 This case is probably the first report of isolated episodes of nausea and vomiting following the procedure. Subanesthetic doses of propofol have been used to treat intractable nausea and vomiting, which was also used in our patient.2 Nakashima et al3 reported abducens nerve palsy, headache, vomiting, and convulsion in a patient with high-flow
Intractable Nausea and Vomiting Following Balloon Occlusion of Carotico-Cavernous Fistula To JNA Readers: A 19-year-old male patient weighing 60 kg presented with prominent veins on forehead, protrusion of The authors have no funding or conflicts of interest to disclose.
74 | www.jnsa.com
FIGURE 1. X-ray image showing balloon occlusion of carotico-cavernous fistula.
r
2014 Lippincott Williams & Wilkins
Volume 27, Number 1, January 2015
lactated ringer solution, lumber puncture (LP) was performed under sterile conditions with 25 G Quincke’s spinal needle inserted one time without trauma at the L3-4 interspace. Free flow of yellow-colored cerebrospinal fluid (CSF) appeared. The yellowish tinge of CSF made us suspicious of an undiagnosed traumatic subarachnoid hemorrhage (SAH). To confirm the same we collected 1 mL of CSF sample and sent it to the biochemistry department for spectrophotometric analysis. However, we proceeded with subarachnoid block in this patient using 2.7 mL of 0.5% hyperbaric bupivacaine (13.5 mg). Perioperative course remained uneventful. Result of spectrophotometric analysis of CSF confirmed xanthochromia, which occurs from hemoglobin catabolism and is diagnostic of SAH. A review by neurosurgeon established the diagnoses of isolated traumatic SAH. According to the literature, computed tomography (CT) scan has 95% sensitivity for diagnosing SAH and in CT-negative cases LP is carried out to visualize xanthochromia along with spectrophotometric analyses of the CSF to confirm the same.1–5 Nowadays, isolated traumatic SAH with subtle presentation is being increasingly recognized. A recent study by Quigley et al6 identified that isolated traumatic SAH in the settings of mild traumatic brain injury (GCSZ13) without other intracranial pathology are a form of benign head injury that does not warrant extensive observation and followup. Ours was one such case of benign SAH diagnosed accidently while performing neuraxial blockade. Despite suspecting the underlying pathology we proceeded with regional anesthesia as our patient was relatively asymptomatic, had no sign and symptoms of raised intracranial pressure, and had been neurologically cleared. His headache was mild in nature in contrast to characteristic severe thunderclap headache associated with SAH. To conclude, xanthochromic CSF on lumbar puncture should alert anesthesiologist about an underlying undiagnosed SAH, especially in settings of preceding trauma. Weather to proceed with neuraxial blockade in such cases must be viewed within the apr
2014 Lippincott Williams & Wilkins
propriate clinical context like signs of raised ICP, any neurologic deficits, and hemodynamic status of the patient. Tarandeep Singh, MBBS, MD, DNB Sarla Hooda, MBBS, MD Asha Anand, MBBS, DA, DNB Pooja Bihani, MBBS Department of Anesthesiology & Critical Care, Postgraduate Institute of Medical Sciences, Rohtak, Haryana, India
REFERENCES 1. Vermuelen M, Hasan D, Blijenberg BG, et al. Xanthochromia after subarachnoid haemorrhage needs no revisitation. J Neurol. 1989;52:826–828. 2. Beetham R. Spectrophotometric examination of CSF for xanthochromia (Letter Comment). Lancet. 1992;339:1492. 3. Roost KT, Pimstone NR, Diamond I, et al. The formation of cerebrospinal fluid xanthochromia after subarachnoid haemorrhage: enzymic conversion of haemoglobin to bilirubin by the arachnoid and choroid plexus. Neurology. 1972;22:973–977. 4. MacDonald A, Mendelow AD. Xanthochromia revisited: a re-evaluation of lumbar puncture and CT scanning in the diagnosis of subarachnoid haemorrhage. J Neurol Neurosurg Psychiatry. 1998;51:341–344. 5. Foot C, Staib A. How valuable is a lumber puncture in the management of patients with suspected subarachnoid hemorrhage? Emerg Med. 2001;13:326–332. 6. Quigley MR, Chew BG, Swartz CE, et al. The clinical significance of isolated traumatic subarachnoid hemorrhage. J Trauma Acute Care Surg. 2013;74:581–584.
Abnormal Bispectral Index Values Associated With the Presence of Periodic Lateralized Epileptiform Discharges To JNA Readers: We report a case in which the presence of periodic lateralized epileptiform discharges (PLEDs) in the unprocessed electroencephalogram (EEG) of a patient with acute herpes simplex encephalitis was associated with the display of an abnormally high processed bispectral index (BIS) value. Written consent was obtained from the next-ofkin of the deceased (for the publication of this report). The authors have no funding or conflicts of interest to disclose.
Correspondence
A 67-year-old man with a history of previous stroke presented to the emergency department with seizures and expressive dysphasia. A computed tomography brain scan demonstrated no focal lesions. He was admitted to the neurology ward where initial routine blood tests and lumbar puncture (LP) were unremarkable. The patient developed status epilepticus that failed to respond to maximum medical therapy, necessitating tracheal intubation and admission to the neurointensive care unit. BIS monitoring was instituted to guide sedation. Magnetic resonance imaging revealed appearances consistent with viral encephalitis. A repeat LP proved positive for herpes simplex virus. The patient had already been commenced on antimicrobials on admission including acyclovir. Sedation was stopped 3 days later to assess neurologic status, but the patient continued to be deeply comatose. Periodic high-amplitude spikes against electrophysiological silence were noted on the BIS monitor. Concurrent increase in the calculated BIS indices from near 0 to higher values (Fig. 1) seemed inconsistent with the underlying clinical picture. A formal EEG showed the presence of PLEDs in all montages with no underlying normal EEG pattern, suggestive of severe cerebral dysfunction. Despite treatment with acyclovir for 2 weeks, the patient remained comatose. The patient died soon after ventilatory support was withdrawn. PLEDs are patterns of abnormal EEG activity indicative of severe cerebral pathology and are associated with poor outcome. Etiological factors for PLEDs include viral encephalitis,1 as seen in our case. It has been suggested that the poor outcome that PLEDs confers is independent of etiology.2 The persistence of PLEDs on continuous full EEG monitoring during the process of death has been previously described.3 The phenomenon of PLEDs has not been previously reported when using BIS. In this case, the BIS monitor detected an actual clinical EEG anomaly and incorporated this anomaly into the processed value to produce an abnormally high BIS value. Although clinicians would rarely act on a BIS value in www.jnsa.com |
73
J Neurosurg Anesthesiol
Dube et al
FIGURE 1. Periodic lateralized epileptiform discharges-PLEDs (highlighted) in raw electroencephalogram (EEG) waveform with abnormally high bispectral index of 74.
isolation, this report illustrates the utility of the real-time raw EEG waveforms that can be obtained from the BIS monitor, and in this situation, prompting a formal EEG evaluation. Matthew Smith, FRCA Patrick Dobbs, FRCA George Eapen, FRCA, FFICM Sheffield Teaching Hospitals Sheffield, UK
REFERENCES 1. Hernandez-Fernandez F, Fernandez-Diaz E, Pardal-Fernandez J, et al. Periodic lateralized epileptiform discharges as manifestation of pneumococcal meningoencephalitis. Int Arch Med. 2011;4:23. 2. Pedersen G, Rasmussen S, Gyllenborg J, et al. Prognostic value of periodic electroencephalographic discharges for neurological patients with profound disturbances of consciousness. Clin Neurophysiol. 2013;124:44–51. 3. Fishman O, Legatt A. PLEDs following control of seizures and at the end of life. Clin EEG Neurosci. 2010;41:11.
left eye ball, and tinnitus in the left ear since the past 3 months. He had a history of road traffic accident for which he underwent repair of mandibular and maxillary fracture under anesthesia. The patient was diagnosed to have a left carotico-cavernous fistula (CCF) with venous drainage into ipsilateral cavernous sinus and inferior petrosal sinus and a significant steal in ipsilateral middle cerebral artery and anterior cerebral artery territories. He was scheduled for balloon occlusion of the CCF under monitored anesthesia care. In the neuroradiologic suite standard monitors were attached and femoral artery was cannulated for the procedure under local anesthetic infiltration. Two balloons were used for complete occlusion of the high-flow CCF (Fig. 1). The patient had stable hemodynamics throughout the procedure, which lasted
Volume 27, Number 1, January 2015
for 150 minutes and he received 8 mg of intravenous (IV) dexamethasone 30 minutes before completion of the procedure. The proptosis was visibly reduced after of the procedure. Ten minutes later, the patient complained of nausea and vomiting. The blood pressure, electrolytes, neurological status, and computed tomographic scan of the head were normal. Ondansetron (6 mg) was administered intravenously (IV) but without any relief to the episodes of nausea and vomiting. However, these episodes later responded to an injection of propofol 20 mg IV. The patient was then shifted to ICU for observation during which he remained asymptomatic for 4 to 5 hours. This was followed by recurrence of nausea and vomiting albeit with reduced severity. The patient received second dose of dexamethasone and ondansetron. Next morning, the computed tomography scan and fluoroscopic imaging confirmed correct position of the balloon. The patient continued to have nausea and vomiting but with each passing day, the severity and frequency was diminished and completely subsided on fifth postprocedural day. Balloon occlusion is one of the therapeutic options for CCF.1 This case is probably the first report of isolated episodes of nausea and vomiting following the procedure. Subanesthetic doses of propofol have been used to treat intractable nausea and vomiting, which was also used in our patient.2 Nakashima et al3 reported abducens nerve palsy, headache, vomiting, and convulsion in a patient with high-flow
Intractable Nausea and Vomiting Following Balloon Occlusion of Carotico-Cavernous Fistula To JNA Readers: A 19-year-old male patient weighing 60 kg presented with prominent veins on forehead, protrusion of The authors have no funding or conflicts of interest to disclose.
74 | www.jnsa.com
FIGURE 1. X-ray image showing balloon occlusion of carotico-cavernous fistula.
r
2014 Lippincott Williams & Wilkins
