THERAPEUTIC HYPOTHERMIA AND TEMPERATURE MANAGEMENT Volume 1, Number 1, 2011 ª Mary Ann Liebert, Inc. DOI: 10.1089/ther.2010.0008
Case Reports
Giant Osborn Waves Seen in a Patient with Hypothermia Associated with Status Epilepticus-Induced Diffuse Cerebral Injury Aarti Sarwal,1 Christopher R. Newey,2 and Venu Menon3
This is a case of a patient with hypothermia associated with status epilepticus-induced diffuse cerebral injury, with electrocardiogram showing Osborn waves. The electrocardiogram changes resolved as the patient became normothermic.
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limits on admission. Initial electrocardiogram (EKG) performed after intubation and prior to magnetic resonance imaging did not show any significant abnormality (Fig. 2). Midazolam and propofol were started for seizure control. Over the next few hours, she developed hypothermia to 33.8C and was noticed to have giant Osborn waves on the EKG (Fig. 3). Basic metabolic profile and magnesium were noted to be normal. pH on the arterial blood gas was 7.36 and serial troponin values were 0.02. Warming blankets were used for gradual warming to 37C. EEG monitoring showed severe encephalopathy with burst suppression pattern. None of the antiepileptic or sedative agents was changed. Repeat EKG
ur patient was a 67-year-old woman with metastatic breast cancer who presented to the emergency room with new speech deficits and right-sided weakness. She developed convulsive status epilepticus with right frontal origin on electroencephalogram, leading to intubation and initiation of antiepileptic medications. Head computed tomography scan showed acute ischemic infarct in the left sylvian area. Magnetic resonance imaging of head within the next few hours confirmed changes compatible with diffuse anoxic injury attributed to ongoing nonconvulsive status epilepticus in addition to a left sylvian fissure and cerebellar transcortical infarct (Fig. 1). Her vitals were noted to be within normal
FIG. 1. Magnetic resonance imaging of brain. T2 sequence showed hyperintensity in anterior left sylvian fissure, suspicious for nonhemorrhagic infarct (A). Diffuse restricted diffusion throughout gray matter involving entire brain and also deep gray matter and cortex is seen and compatible with changes of diffuse anoxic injury (B).
1
Cleveland Clinic, Neurocritical Care, Cerebrovascular Center, Cleveland, Ohio. Cleveland Clinic, Department of Adult Neurology, Neurologic Institute, Cleveland, Ohio. Cleveland Clinic, Department of Cardiovascular Medicine, Adult Neurology, Neurologic Institute, Cleveland, Ohio.
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FIG. 2. Twelve-lead electrocardiogram obtained at body temperature 37C.
FIG. 3. Twelve-lead electrocardiogram obtained at body temperature 33.8C showing giant Osborn waves (arrow).
showed resolution of the changes. Her hospital course was complicated by bleeding, thrombocytopenia, pneumonia, and sequelae of diffuse anoxic encephalopathy. Because of overall grim prognosis, her family requested comfort care measures and the patient expired with family by bedside. Osborn waves or J waves of hypothermia were first described by Thomashewsky in 1938 (Gusak et al., 1995), although Osborn’s name is associated with them after he described J waves in 1953 in experimental hypothermia in dog models (Osborn, 1953). The pathogenesis of these waves is unclear though thought to be related to the effect of hypothermia on depolarization and repolarization by slowing ion fluxes. Other EKG abnormalities seen in hypothermia include sinus bradycardia, prolonged PR, QRS, or QT interval (Patel et al., 1994). Some associated conditions reported to have Osborn waves even in normothermia include hypercalcemia, Brugada syndrome, cerebral injury, subarachnoidal hemorrhage, myocardial ischemia, and sepsis. J waves are not prognostic indicators when they are present, unlike atrial fibrillation, which incurs survival disadvantage (Mareedu et al.,
2008). Fatal ventricular fibrillation or asystole can occur when core body temperature is below 28C (Mareedu et al., 2008). Hypothermia in our patient was thought to be related to use of midazolam and propofol or autonomic failure associated with diffuse cerebral injury, because the first EKG was unremarkable at the time of ongoing status epilepticus. Disclosure Statement All authors have no financial disclosures to report. Author Contribution A.S., C.R.N., and V.M. equally contributed to the writing of the case and formatting the images. References Gussak I, Bjerregaard P, Egan T, Chaitman B. ECG phenomenon called the J wave. J Electrocardiol 1995;28:49–58.
OSBORN WAVES SEEN IN HYPOTHERMIA Mareedu RK, Grandhe NP, Gangineni S, Quinn DL. Classic EKG changes of hypothermia. Clin Med Res 2008;6:107– 108. Osborn JJ. Experimental hypothermia; respiratory and blood pH changes in relation to cardiac function. Am J Physiol 1953;175: 389–398. Patel A, Getsos JP, Moussa G, Damato AN. The Osborn wave of hypothermia in normothermic patients. Clin Cardiol 1994;17:273–276.
55 Address correspondence to: Aarti Sarwal, M.D. Cleveland Clinic Neurocritical Care Cerebrovascular Center 9500 Euclid Avenue Cleveland, OH 44195 E-mail: [email protected]
Case Reports
Giant Osborn Waves Seen in a Patient with Hypothermia Associated with Status Epilepticus-Induced Diffuse Cerebral Injury Aarti Sarwal,1 Christopher R. Newey,2 and Venu Menon3
This is a case of a patient with hypothermia associated with status epilepticus-induced diffuse cerebral injury, with electrocardiogram showing Osborn waves. The electrocardiogram changes resolved as the patient became normothermic.
O
limits on admission. Initial electrocardiogram (EKG) performed after intubation and prior to magnetic resonance imaging did not show any significant abnormality (Fig. 2). Midazolam and propofol were started for seizure control. Over the next few hours, she developed hypothermia to 33.8C and was noticed to have giant Osborn waves on the EKG (Fig. 3). Basic metabolic profile and magnesium were noted to be normal. pH on the arterial blood gas was 7.36 and serial troponin values were 0.02. Warming blankets were used for gradual warming to 37C. EEG monitoring showed severe encephalopathy with burst suppression pattern. None of the antiepileptic or sedative agents was changed. Repeat EKG
ur patient was a 67-year-old woman with metastatic breast cancer who presented to the emergency room with new speech deficits and right-sided weakness. She developed convulsive status epilepticus with right frontal origin on electroencephalogram, leading to intubation and initiation of antiepileptic medications. Head computed tomography scan showed acute ischemic infarct in the left sylvian area. Magnetic resonance imaging of head within the next few hours confirmed changes compatible with diffuse anoxic injury attributed to ongoing nonconvulsive status epilepticus in addition to a left sylvian fissure and cerebellar transcortical infarct (Fig. 1). Her vitals were noted to be within normal
FIG. 1. Magnetic resonance imaging of brain. T2 sequence showed hyperintensity in anterior left sylvian fissure, suspicious for nonhemorrhagic infarct (A). Diffuse restricted diffusion throughout gray matter involving entire brain and also deep gray matter and cortex is seen and compatible with changes of diffuse anoxic injury (B).
1
Cleveland Clinic, Neurocritical Care, Cerebrovascular Center, Cleveland, Ohio. Cleveland Clinic, Department of Adult Neurology, Neurologic Institute, Cleveland, Ohio. Cleveland Clinic, Department of Cardiovascular Medicine, Adult Neurology, Neurologic Institute, Cleveland, Ohio.
2 3
53
54
SARWAL ET AL.
FIG. 2. Twelve-lead electrocardiogram obtained at body temperature 37C.
FIG. 3. Twelve-lead electrocardiogram obtained at body temperature 33.8C showing giant Osborn waves (arrow).
showed resolution of the changes. Her hospital course was complicated by bleeding, thrombocytopenia, pneumonia, and sequelae of diffuse anoxic encephalopathy. Because of overall grim prognosis, her family requested comfort care measures and the patient expired with family by bedside. Osborn waves or J waves of hypothermia were first described by Thomashewsky in 1938 (Gusak et al., 1995), although Osborn’s name is associated with them after he described J waves in 1953 in experimental hypothermia in dog models (Osborn, 1953). The pathogenesis of these waves is unclear though thought to be related to the effect of hypothermia on depolarization and repolarization by slowing ion fluxes. Other EKG abnormalities seen in hypothermia include sinus bradycardia, prolonged PR, QRS, or QT interval (Patel et al., 1994). Some associated conditions reported to have Osborn waves even in normothermia include hypercalcemia, Brugada syndrome, cerebral injury, subarachnoidal hemorrhage, myocardial ischemia, and sepsis. J waves are not prognostic indicators when they are present, unlike atrial fibrillation, which incurs survival disadvantage (Mareedu et al.,
2008). Fatal ventricular fibrillation or asystole can occur when core body temperature is below 28C (Mareedu et al., 2008). Hypothermia in our patient was thought to be related to use of midazolam and propofol or autonomic failure associated with diffuse cerebral injury, because the first EKG was unremarkable at the time of ongoing status epilepticus. Disclosure Statement All authors have no financial disclosures to report. Author Contribution A.S., C.R.N., and V.M. equally contributed to the writing of the case and formatting the images. References Gussak I, Bjerregaard P, Egan T, Chaitman B. ECG phenomenon called the J wave. J Electrocardiol 1995;28:49–58.
OSBORN WAVES SEEN IN HYPOTHERMIA Mareedu RK, Grandhe NP, Gangineni S, Quinn DL. Classic EKG changes of hypothermia. Clin Med Res 2008;6:107– 108. Osborn JJ. Experimental hypothermia; respiratory and blood pH changes in relation to cardiac function. Am J Physiol 1953;175: 389–398. Patel A, Getsos JP, Moussa G, Damato AN. The Osborn wave of hypothermia in normothermic patients. Clin Cardiol 1994;17:273–276.
55 Address correspondence to: Aarti Sarwal, M.D. Cleveland Clinic Neurocritical Care Cerebrovascular Center 9500 Euclid Avenue Cleveland, OH 44195 E-mail: [email protected]
