- Email: [email protected]
Mild hypothermia induction after cardiac arrest using water-circulating cooling device
730
Correspondence
score on the first day, did not show any temporal difference. To the best of our knowledge, there are no studies on the possible relationship between temporal patterns of stroke and outcome. The question whether circadian rhythms may influence the clinical outcome of cardiovascular events is still being debated. On 1 hand, acute myocardial infarctions seem to be not only more frequent, but also more severe during morning hours [12]. In contrast, no differences have been found for aortic dissections [13]. As for site of lesion, similar to that reported for ischemic stroke [14], the circadian variation is quite independent of the cerebral vessel affected. As for underlying risk factors, hypertension is known to be 1 of the most important risk conditions for stroke. Nonetheless, as previously seen for other hypertension-related diseases, for example, stroke and aortic dissection [12,15,16], it is interesting that the circadian biphasic peak of SAH is independent of the presence/absence of hypertension. Because arterial blood pressure fluctuates over 24 hours after a circadian rhythm characterized by a main peak in the morning shortly after awakening and a trough during night, it is possible that this circadian variation per se (and not strictly the condition of hypertension) and particularly the morning surge [10,17,18], together with endogenous rhythmic changes in coagulation/fibrinolysis factors, may play a crucial role in determining the onset of SAH. In conclusion, time of presentation cannot help in discriminating between ischemic stroke, intracranial hemorrhage, and SAH, conditions that exhibit identical temporal patterns of onset [19]. Thus, high level of alertness, clinical findings, and correct use of current diagnostic modalities remain crucial for early diagnosis and treatment.
Acknowledgment This study was supported, in part, by a scientific grant bFinanziament per ricerca localeQ from the University of Ferrara, Italy. Arturo Chieregato MD Fernanda Tagliaferri MD Francesco Cocciolo MD Department of Anesthesiology and Intensive Care Hospital of Cesena 47023 Cesena, Italy Benedetta Boari MD Massimo Gallerani MD Department of Internal Medicine Hospital of Ferrara 44100 Ferrara, Italy Roberto Manfredini MD Department of Clinical and Experimental Medicine Section of Clinica Medica and Vascular Diseases Center University of Ferrara 44100 Ferrara, Italy E-mail address: [email protected] doi:10.1016/j.ajem.2006.11.048
References [1] Mark DG, Pines JM. The detection of nontraumatic subarachnoid hemorrhage: still a diagnostic challenge. Am J Emerg Med 2006;24:859 - 63. [2] Muller JE, Stone PH, Turi ZG, et al. Circadian variation in the frequency of onset of acute myocardial infarction. N Engl J Med 1985;313:1315 - 22. [3] Muller JE, Ludmer PL, Willich SN, et al. Circadian variation in the incidence of sudden cardiac death. Circulation 1987;75:131 - 8. [4] Gallerani M, Manfredini R, Ricci L, et al. Sudden death from pulmonary thromboembolism: chronobiological aspects. Eur Heart J 1992;13:661 - 5. [5] Marler JR, Price TR, Clarck GL, et al. Morning increase in onset of ischemic stroke. Stroke 1989;20:864 - 70. [6] Gallerani M, Manfredini R, Ricci L, et al. Chronobiological aspects of acute cerebrovascular diseases. Acta Neurol Scand 1993;87:482 - 7. [7] Gallerani M, Trapella G, Manfredini R, et al. Acute intracerebral haemorrhage: circadian and circannual patterns of onset. Acta Neurol Scand 1994;89:280 - 6. [8] Manfredini R, Gallerani M, Portaluppi F, et al. Chronobiological patterns of onset of acute cerebrovascular diseases. Thromb Res 1997;88:451 - 63. [9] Mojo`n A, Ferna`ndez JR, Hermida RC. Chronolab: an interactive software package for chronobiologic time series analysis written for the Macintosh computer. Chronobiol Int 1992;9:403 - 12. [10] Portaluppi F, Manfredini R, Fersini C. From a static to a dynamic concept of risk: the circadian epidemiology of cardiovascular events. Chronobiol Int 1999;16:33 - 49. [11] Dubinsky I, Penello D. Can specific patient variables be used to predict outcome of intracranial hemorrhage? Am J Emerg Med 2002;20:26 - 9. [12] Casetta I, Granieri E, Fallica E, et al. Patient demographic and clinical features and circadian variation in onset of ischemic stroke. Arch Neurol 2002;59:48 - 53. [13] Manfredini R, Boari B, Bressan S, et al. Influence of circadian rhythm on mortality after myocardial infarction: data from a prospective cohort of emergency calls. Am J Emerg Med 2004;22:555 - 9. [14] Mehta RH, Manfredini R, Bossone E, et al. Does circadian and seasonal variation in the occurrence of acute aortic dissection influence inhospital mortality outcomes? Chronobiol Int 2005;22:343 - 51. [15] Casetta I, Granieri E, Portaluppi F, et al. Circadian variability in hemorrhagic stroke. JAMA 2002;287:1266 - 7. [16] Mehta HR, Manfredini R, Hassan F, et al. Chronobiological patterns of acute aortic dissection. Circulation 2002;106:1110 - 5. [17] Manfredini R, Gallerani M, Portaluppi F, et al. Relationships of the circadian rhythms of thrombotic, ischemic, hemorrhagic, and arrhythmic events to blood pressure rhythms. Ann N Y Acad Sci 1996;783:141 - 58. [18] Kario K, Pickering TG, Umeda Y, et al. Morning surge in blood pressure as a predictor of silent and clinical cerebrovascular disease in elderly hypertensives: a prospective study. Circulation 2003;18: 1401 - 6. [19] Manfredini R, Boari B, Smolensky MH, et al. Circadian variation in stroke onset: identical temporal pattern in ischemic and hemorrhagic events. Chronobiol Int 2005;22:417 - 53.
Mild hypothermia induction after cardiac arrest using water-circulating cooling device To the Editor, Out-of-hospital sudden cardiac arrest is common, occurring in approximately 1 in 2000 adults per year [1]. For
Correspondence patients who are successfully resuscitated and transported to hospital, anoxic neurologic injury remains a major problem. It has been demonstrated that postarrest cooling may improve survival and neurologic outcomes when the initial cardiac rhythm is ventricular fibrillation [2]. In fact, the use of therapeutic hypothermia (32-348C for 12-24 hours) for comatose survivors of cardiac arrest has been endorsed by the American Heart Association and the International Liaison Committee on Resuscitation [3]. Although a variety of techniques such as endovascular catheters, cool intravascular fluid, and cardiopulmonary bypass have been used to therapeutically lower core body temperature, what remains unclear at this time is the best method of cooling and the optimal duration of cooling. Unintentional overcooling is common with some techniques such as cool intravascular fluid or the use of ice packs [4]. Nowadays, the maintenance of hypothermia can be facilitated with new technology as surface cooling devices with temperature feedback controls that automatically control the set temperature and avoid unintentional overcooling [5]. We report an elderly patient in whom hypothermia was rapidly induced with water-circulating cooling device, and an almost complete neurological recovery was observed. A 77-year-old man with a history of hypertension, previously replacement of aortic valve, and a right coronary artery bypass was admitted to our intensive care unit (ICU) after cardiac arrest. He had collapsed while walking. The emergency service arrived within 5 minutes. The initial cardiac rhythm was ventricular fibrillation. Estimated time to return to spontaneous circulation was 20 minutes. The patient arrived in the hospital 50 minutes after collapse and was immediately admitted in the ICU. Thirty minutes after ICU admission, he was unconscious with a Glasgow coma score of 5. Hypothermia was induced by the Artic Sun 2000 cooling system (Medivance, Louisville, Colo), and the goal temperature was obtained 105 minutes after induction. He was ventilated mechanically and sedated with fentanyl and midazolam. Shivering was controlled by cisatracurium continuous infusion. Body temperature was monitored continuously with a Foley catheter. Hypothermia was maintained for 24 hours at 338C, and rewarming to the target temperature of 378C was achieved over 12 hours. The use of dobutamine at 20 lg kg 1 min 1 was necessary to maintain a good blood pressure. Three days after admission, the patient developed acute renal failure (with a 4-fold normal elevation in serum creatinine). No electrolyte imbalances or coagulopathies were observed. No overcooling was observed in any moment. On day 7, his renal function returned to normal. He was extubated on day 6 after admission and discharged from the ICU on day 10 without neurological sequelae. Despite the general consensus that hypothermia could benefit a subset of patients who have restoration of spontaneous circulation but remain comatose, it is used
731 in only a minority of patients [6]. A number of barriers exist to implementation of therapeutic hypothermia. Like many treatments for patients in cardiac arrest, hypothermia requires a well-coordinated team effort that crosses many medical specialties. A hypothermia protocol and order set could guide physicians how best to institute cooling and rewarming procedures, as well as monitoring for complications. Although therapeutic hypothermia for cardiac arrest survivors has been shown to improve neurologically intact survival, optimal methods to ensure controlled induction and maintenance of cooling are not clearly established. Careful monitoring of temperature is important during use of therapeutic hypothermia because unintentional overcooling below 328C may place the patient at risk for serious complications as arrhythmias, infection, and coagulopathy. In a recent study, the prevalence of overcooling (b328C) in postarrest survivors receiving primarily noninvasive cooling lasting for more than 1 hour was 62% [4]. A variety of techniques such as surface cooling, endovascular catheters, cooling caps/helmets, cool intravascular fluid, and cardiopulmonary bypass have been used to therapeutically lower core body temperature in either clinical or experimental settings [7]. Moreover, the effectiveness of mild hypothermia could be improved if initiated as soon as possible after return of spontaneous circulation [8]. Cooling with water-circulating cooling device is fast and safe. Clinicians should work to institute protocols for mild hypothermia treatment for such patients as a part of their critical care treatment. Eduardo Min˜ambres MD, PhD Alejandro Gonza´lez-Castro MD Elsa Ots MD Maria Angeles Ballesteros MD Borja Suberviola MD Fernando Ortı´z-Melo´n MD Intensive Care Service Hospital Universitario Marque´s de Valdecilla 39008 Santander, Spain E-mail address: [email protected] doi:10.1016/j.ajem.2006.12.014
References [1] Zheng ZJ, Croft JB, Giles WH, et al. Sudden death in the United States, 1989-1998. Circulation 2001;104:2158 - 63. [2] Bernard SA, Gray TW, Buist MD, et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med 2002;346:557 - 63. [3] 2005 International Consensus on Cardiopulmonary Resuscitation (CPR) and Emergency Cardiovascular Care (ECC) Science with Treatment Recommendations. Circulation 2005;112(Suppl):III-1-III-136. [4] Merchant RM, Abella BS, Peberdy MA, et al. Therapeutic hypothermia after cardiac arrest: unintentional overcooling is common using ice
732 packs and conventional cooling blankets. Crit Care Med 2006; 34(Suppl):S490 - 4. [5] Mayer SA, Kowalski RG, Presciutti M, et al. Clinical trial of a novel surface cooling system for fever control in neurocritical care patients. Crit Care Med 2004;32:2508 - 15. [6] Abella BS, Rhee JW, Huang KN, et al. Induced hypothermia is underused after resuscitation from cardiac arrest: a current practice survey. Resuscitation 2005;64:181 - 6.
Correspondence [7] Bernard S, Buist M, Monteiro O, et al. Induced hypothermia using large volume, ice-cold intravenous fluid in comatose survivors of outof-hospital cardiac arrest: a preliminary report. Resuscitation 2003;56:9 - 13. [8] Kliegel A, Losert H, Sterz F, et al. Cold simple intravenous infusions preceding special endovascular cooling for faster induction of mild hypothermia after cardiac arrest—a feasibility study. Resuscitation 2005;64:347 - 51.
Correspondence
score on the first day, did not show any temporal difference. To the best of our knowledge, there are no studies on the possible relationship between temporal patterns of stroke and outcome. The question whether circadian rhythms may influence the clinical outcome of cardiovascular events is still being debated. On 1 hand, acute myocardial infarctions seem to be not only more frequent, but also more severe during morning hours [12]. In contrast, no differences have been found for aortic dissections [13]. As for site of lesion, similar to that reported for ischemic stroke [14], the circadian variation is quite independent of the cerebral vessel affected. As for underlying risk factors, hypertension is known to be 1 of the most important risk conditions for stroke. Nonetheless, as previously seen for other hypertension-related diseases, for example, stroke and aortic dissection [12,15,16], it is interesting that the circadian biphasic peak of SAH is independent of the presence/absence of hypertension. Because arterial blood pressure fluctuates over 24 hours after a circadian rhythm characterized by a main peak in the morning shortly after awakening and a trough during night, it is possible that this circadian variation per se (and not strictly the condition of hypertension) and particularly the morning surge [10,17,18], together with endogenous rhythmic changes in coagulation/fibrinolysis factors, may play a crucial role in determining the onset of SAH. In conclusion, time of presentation cannot help in discriminating between ischemic stroke, intracranial hemorrhage, and SAH, conditions that exhibit identical temporal patterns of onset [19]. Thus, high level of alertness, clinical findings, and correct use of current diagnostic modalities remain crucial for early diagnosis and treatment.
Acknowledgment This study was supported, in part, by a scientific grant bFinanziament per ricerca localeQ from the University of Ferrara, Italy. Arturo Chieregato MD Fernanda Tagliaferri MD Francesco Cocciolo MD Department of Anesthesiology and Intensive Care Hospital of Cesena 47023 Cesena, Italy Benedetta Boari MD Massimo Gallerani MD Department of Internal Medicine Hospital of Ferrara 44100 Ferrara, Italy Roberto Manfredini MD Department of Clinical and Experimental Medicine Section of Clinica Medica and Vascular Diseases Center University of Ferrara 44100 Ferrara, Italy E-mail address: [email protected] doi:10.1016/j.ajem.2006.11.048
References [1] Mark DG, Pines JM. The detection of nontraumatic subarachnoid hemorrhage: still a diagnostic challenge. Am J Emerg Med 2006;24:859 - 63. [2] Muller JE, Stone PH, Turi ZG, et al. Circadian variation in the frequency of onset of acute myocardial infarction. N Engl J Med 1985;313:1315 - 22. [3] Muller JE, Ludmer PL, Willich SN, et al. Circadian variation in the incidence of sudden cardiac death. Circulation 1987;75:131 - 8. [4] Gallerani M, Manfredini R, Ricci L, et al. Sudden death from pulmonary thromboembolism: chronobiological aspects. Eur Heart J 1992;13:661 - 5. [5] Marler JR, Price TR, Clarck GL, et al. Morning increase in onset of ischemic stroke. Stroke 1989;20:864 - 70. [6] Gallerani M, Manfredini R, Ricci L, et al. Chronobiological aspects of acute cerebrovascular diseases. Acta Neurol Scand 1993;87:482 - 7. [7] Gallerani M, Trapella G, Manfredini R, et al. Acute intracerebral haemorrhage: circadian and circannual patterns of onset. Acta Neurol Scand 1994;89:280 - 6. [8] Manfredini R, Gallerani M, Portaluppi F, et al. Chronobiological patterns of onset of acute cerebrovascular diseases. Thromb Res 1997;88:451 - 63. [9] Mojo`n A, Ferna`ndez JR, Hermida RC. Chronolab: an interactive software package for chronobiologic time series analysis written for the Macintosh computer. Chronobiol Int 1992;9:403 - 12. [10] Portaluppi F, Manfredini R, Fersini C. From a static to a dynamic concept of risk: the circadian epidemiology of cardiovascular events. Chronobiol Int 1999;16:33 - 49. [11] Dubinsky I, Penello D. Can specific patient variables be used to predict outcome of intracranial hemorrhage? Am J Emerg Med 2002;20:26 - 9. [12] Casetta I, Granieri E, Fallica E, et al. Patient demographic and clinical features and circadian variation in onset of ischemic stroke. Arch Neurol 2002;59:48 - 53. [13] Manfredini R, Boari B, Bressan S, et al. Influence of circadian rhythm on mortality after myocardial infarction: data from a prospective cohort of emergency calls. Am J Emerg Med 2004;22:555 - 9. [14] Mehta RH, Manfredini R, Bossone E, et al. Does circadian and seasonal variation in the occurrence of acute aortic dissection influence inhospital mortality outcomes? Chronobiol Int 2005;22:343 - 51. [15] Casetta I, Granieri E, Portaluppi F, et al. Circadian variability in hemorrhagic stroke. JAMA 2002;287:1266 - 7. [16] Mehta HR, Manfredini R, Hassan F, et al. Chronobiological patterns of acute aortic dissection. Circulation 2002;106:1110 - 5. [17] Manfredini R, Gallerani M, Portaluppi F, et al. Relationships of the circadian rhythms of thrombotic, ischemic, hemorrhagic, and arrhythmic events to blood pressure rhythms. Ann N Y Acad Sci 1996;783:141 - 58. [18] Kario K, Pickering TG, Umeda Y, et al. Morning surge in blood pressure as a predictor of silent and clinical cerebrovascular disease in elderly hypertensives: a prospective study. Circulation 2003;18: 1401 - 6. [19] Manfredini R, Boari B, Smolensky MH, et al. Circadian variation in stroke onset: identical temporal pattern in ischemic and hemorrhagic events. Chronobiol Int 2005;22:417 - 53.
Mild hypothermia induction after cardiac arrest using water-circulating cooling device To the Editor, Out-of-hospital sudden cardiac arrest is common, occurring in approximately 1 in 2000 adults per year [1]. For
Correspondence patients who are successfully resuscitated and transported to hospital, anoxic neurologic injury remains a major problem. It has been demonstrated that postarrest cooling may improve survival and neurologic outcomes when the initial cardiac rhythm is ventricular fibrillation [2]. In fact, the use of therapeutic hypothermia (32-348C for 12-24 hours) for comatose survivors of cardiac arrest has been endorsed by the American Heart Association and the International Liaison Committee on Resuscitation [3]. Although a variety of techniques such as endovascular catheters, cool intravascular fluid, and cardiopulmonary bypass have been used to therapeutically lower core body temperature, what remains unclear at this time is the best method of cooling and the optimal duration of cooling. Unintentional overcooling is common with some techniques such as cool intravascular fluid or the use of ice packs [4]. Nowadays, the maintenance of hypothermia can be facilitated with new technology as surface cooling devices with temperature feedback controls that automatically control the set temperature and avoid unintentional overcooling [5]. We report an elderly patient in whom hypothermia was rapidly induced with water-circulating cooling device, and an almost complete neurological recovery was observed. A 77-year-old man with a history of hypertension, previously replacement of aortic valve, and a right coronary artery bypass was admitted to our intensive care unit (ICU) after cardiac arrest. He had collapsed while walking. The emergency service arrived within 5 minutes. The initial cardiac rhythm was ventricular fibrillation. Estimated time to return to spontaneous circulation was 20 minutes. The patient arrived in the hospital 50 minutes after collapse and was immediately admitted in the ICU. Thirty minutes after ICU admission, he was unconscious with a Glasgow coma score of 5. Hypothermia was induced by the Artic Sun 2000 cooling system (Medivance, Louisville, Colo), and the goal temperature was obtained 105 minutes after induction. He was ventilated mechanically and sedated with fentanyl and midazolam. Shivering was controlled by cisatracurium continuous infusion. Body temperature was monitored continuously with a Foley catheter. Hypothermia was maintained for 24 hours at 338C, and rewarming to the target temperature of 378C was achieved over 12 hours. The use of dobutamine at 20 lg kg 1 min 1 was necessary to maintain a good blood pressure. Three days after admission, the patient developed acute renal failure (with a 4-fold normal elevation in serum creatinine). No electrolyte imbalances or coagulopathies were observed. No overcooling was observed in any moment. On day 7, his renal function returned to normal. He was extubated on day 6 after admission and discharged from the ICU on day 10 without neurological sequelae. Despite the general consensus that hypothermia could benefit a subset of patients who have restoration of spontaneous circulation but remain comatose, it is used
731 in only a minority of patients [6]. A number of barriers exist to implementation of therapeutic hypothermia. Like many treatments for patients in cardiac arrest, hypothermia requires a well-coordinated team effort that crosses many medical specialties. A hypothermia protocol and order set could guide physicians how best to institute cooling and rewarming procedures, as well as monitoring for complications. Although therapeutic hypothermia for cardiac arrest survivors has been shown to improve neurologically intact survival, optimal methods to ensure controlled induction and maintenance of cooling are not clearly established. Careful monitoring of temperature is important during use of therapeutic hypothermia because unintentional overcooling below 328C may place the patient at risk for serious complications as arrhythmias, infection, and coagulopathy. In a recent study, the prevalence of overcooling (b328C) in postarrest survivors receiving primarily noninvasive cooling lasting for more than 1 hour was 62% [4]. A variety of techniques such as surface cooling, endovascular catheters, cooling caps/helmets, cool intravascular fluid, and cardiopulmonary bypass have been used to therapeutically lower core body temperature in either clinical or experimental settings [7]. Moreover, the effectiveness of mild hypothermia could be improved if initiated as soon as possible after return of spontaneous circulation [8]. Cooling with water-circulating cooling device is fast and safe. Clinicians should work to institute protocols for mild hypothermia treatment for such patients as a part of their critical care treatment. Eduardo Min˜ambres MD, PhD Alejandro Gonza´lez-Castro MD Elsa Ots MD Maria Angeles Ballesteros MD Borja Suberviola MD Fernando Ortı´z-Melo´n MD Intensive Care Service Hospital Universitario Marque´s de Valdecilla 39008 Santander, Spain E-mail address: [email protected] doi:10.1016/j.ajem.2006.12.014
References [1] Zheng ZJ, Croft JB, Giles WH, et al. Sudden death in the United States, 1989-1998. Circulation 2001;104:2158 - 63. [2] Bernard SA, Gray TW, Buist MD, et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med 2002;346:557 - 63. [3] 2005 International Consensus on Cardiopulmonary Resuscitation (CPR) and Emergency Cardiovascular Care (ECC) Science with Treatment Recommendations. Circulation 2005;112(Suppl):III-1-III-136. [4] Merchant RM, Abella BS, Peberdy MA, et al. Therapeutic hypothermia after cardiac arrest: unintentional overcooling is common using ice
732 packs and conventional cooling blankets. Crit Care Med 2006; 34(Suppl):S490 - 4. [5] Mayer SA, Kowalski RG, Presciutti M, et al. Clinical trial of a novel surface cooling system for fever control in neurocritical care patients. Crit Care Med 2004;32:2508 - 15. [6] Abella BS, Rhee JW, Huang KN, et al. Induced hypothermia is underused after resuscitation from cardiac arrest: a current practice survey. Resuscitation 2005;64:181 - 6.
Correspondence [7] Bernard S, Buist M, Monteiro O, et al. Induced hypothermia using large volume, ice-cold intravenous fluid in comatose survivors of outof-hospital cardiac arrest: a preliminary report. Resuscitation 2003;56:9 - 13. [8] Kliegel A, Losert H, Sterz F, et al. Cold simple intravenous infusions preceding special endovascular cooling for faster induction of mild hypothermia after cardiac arrest—a feasibility study. Resuscitation 2005;64:347 - 51.