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Complete neurological recovery following delayed initiation of hypothermia in a victim of warm water near-drowning
Resuscitation (2006) 68, 421—423
CASE REPORT
Complete neurological recovery following delayed initiation of hypothermia in a victim of warm water near-drowning夽 Joseph Varon a,∗, Paul E. Marik b a
The University of Texas Health Science Center, St. Luke’s Episcopal Hospital, 2219 Dorrington Street, Houston, TX 77030, USA b Division of Pulmonary and Critical Care Medicine, Thomas Jefferson University, Philadelphia, PA, USA Received 13 May 2005 ; received in revised form 19 July 2005; accepted 19 July 2005 KEYWORDS Warm water drowning; Neurological recovery; Hypothermia; Cardiac arrest
Summary Induced hypothermia has been demonstrated to improve outcome following cardiac arrest and is now widely endorsed. However, the optimal method of cooling and the identification of patients most likely to benefit from this therapy remains to be determined. We report a patient in whom there was a long delay in return of spontaneous circulation (at least 45 min) and the initiation of induced hypothermia (12 h) who made an almost complete neurological recovery following cardiac arrest from warm-water near-drowning. © 2005 Elsevier Ireland Ltd. All rights reserved.
Introduction Induced hypothermia has been used in the operating room since the early 1950s for patients undergoing cardiac and neurosurgery. The use of induced hypothermia after cardiac arrest in humans in modern medicine was first reported in 1957 by Benson et al.1 They cooled four patients (to 30—33 ◦ C) after in-hospital cardiac arrest for
夽 A Spanish translated version of the summary of this article appears as appendix in the online version at 10.1016/j. resuscitation.2005.07.020. ∗ Corresponding author. Tel.: +1 713 669 1670; fax: +1 713 839 1467. E-mail address: [email protected] (J. Varon).
periods of 24—72 h. All four patients recovered. Interest in the use of mild to moderate induced hypothermia (32—34 ◦ C) following cardiac arrest was spurred by the pioneering work of the late Dr. Peter Safar. Dr. Safar and his group demonstrated improved neurological recovery in dogs when hypothermia was induced shortly after the restoration of spontaneous circulation.2—4 In 1997, Bernard and associates from Australia reported improved outcome in 22 survivors of out-of-hospital cardiac arrest who were cooled to 33 ◦ C for 12 h.5 Following two landmark randomized-controlled studies published in 2002, in which moderate hypothermia was demonstrated to improve the outcome in patients with coma after resuscitation from out-ofhospital cardiac arrest,6,7 this intervention is now endorsed by the International Liaison Committee
0300-9572/$ — see front matter © 2005 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.resuscitation.2005.07.020
422 on Resuscitation (ILCOR).8 Indeed, the ILCOR recommends the use of induced mild hypothermia in comatose survivors of out-of-hospital cardiac arrest caused by ventricular fibrillation. However, what remains unclear at this time is the best method of cooling and the optimal duration of cooling. Furthermore, the identification of patients most likely to benefit from this therapy has yet to be determined. We report a patient in whom there was a long delay in return of spontaneous circulation (ROSC) and the initiation of induced hypothermia who made an almost complete neurological recovery following cardiac arrest from warm water drowning.
Case report A previously healthy 53 year-old gentleman was pulled out of the waters of the Mexican Riviera during the month of December 2004 (average water temperature 23 ◦ C). He had gone swimming with his two young children who found him underwater. The length of time the patient was underwater was unknown. He was pulled out of the water by his two children who began resuscitation manoeuvers. A vacationing heath care provider saw the children and immediately assisted them. The patient was pulseless, cyanotic and had no spontaneous respirations. Cardiopulmonary resuscitation continued for approximately 20 min until emergency response professionals arrived at the beach. The patient was placed on a stretcher, chest compressions continued and the patient transported to a local clinic where he underwent tracheal intubation and advanced cardiac life support was begun. Attempts at electrical defibrillation for ventricular fibrillation (VF) were unsuccessful. Approximately 35—45 min after being pulled from the water, the patient achieved a ROSC. Arrangements were made to transfer the patient via fixed wing air ambulance to Houston, TX. However, it took over 11 h from the time of the incident until the time the patient presented to our facility. According to the aircraft medical crew, the patient had no spontaneous respirations, systolic blood pressure remained above 80 mmHg and the monitor showed sinus tachycardia. In addition, the patient had several tonic-clonic seizures and intermittent myoclonus. On our initial examination, approximately 11.5 h after the incident, the blood pressure was 110/70 mmHg, heart rate 88 min−1 and rectal temperature was 37.8 ◦ C. He was being ventilated on assist-control mode with a tidal volume of 700 cm3 , rate of 12 breaths/min and an inspired oxygen concentration of 100%.
J. Varon, P.E. Marik The patient had not received any narcotics or neuromuscular blockers and lacked corneal, pupillary and gag reflexes. The Glasgow Coma Scale was 3. Multiple ecchymotic lesions and abrasions were found on the extremities as well as abrasions. An emergency computed tomography of brain and cervical spine revealed mild-to-moderate cerebral oedema without any bone abnormalities or intracranial bleeding. A 12-lead electrocardiogram and cardiac enzymes revealed no evidence of acute myocardial ischaemia. An electroencephalogram was grossly abnormal and consistent with global ischaemia. Twelve hours after the incident, therapeutic hypothermia was started. Ice packs were applied to the groins and axilla and cooling blankets were placed on top and under the patient. The cooling blankets were set to automatic mode to maintain the patient’s bladder temperature at 32 ◦ C for a total of 72 h. He received no sedatives or neuromuscular blocking agents due to his significant neurological impairment and concern about failing to recognize improvement or deterioration. During the 72 h of hypothermia, the patient developed acute respiratory distress syndrome (ARDS), acute renal failure (with a three-fold normal elevation in serum creatinine) and a mild coagulopathy. He was ventilated with a lung protective strategy with the PaCO2 kept between 4.6 and 5.3 kPa (35—40 mmHg) and the arterial oxygen saturation above 95%. He did not require renal replacement therapy. During hypothermia, the patient did not shiver. After the period of therapeutic hypothermia, controlled rewarming to the target temperature of 37 ◦ C was achieved over 12 h on the fourth day of hospitalization. By the fifth hospital day, the patient had a corneal reflex, a pupillary reflex and was beginning to move his head. On day 6, to our surprise, the patient woke up. He indicated that he was unable to move his lower extremities and was taken as an emergency for a cervical spine magnetic resonance imaging that revealed a C3—C6 cervical spine contusion. Neurosurgical decompression followed. The patient required a temporary tracheotomy. He was subsequently weaned from mechanical ventilation and his renal function returned to normal. Other than minor motor abnormalities related to his cervical injury, a complete neurological examination revealed no abnormalities. Neuropsychometric testing revealed normal function. The patient was discharged to a rehabilitation facility 3 weeks after arrival at our institution. Three months after the incident, the patient is now living at home and has slowly resumed his regular activities.
Delayed hypothermia and near-drowning
Discussion The prognosis of patients who remain unconscious after resuscitation from out-of-hospital cardiac arrest is poor. It is believed that part of the anoxic neurological injury occurs after the return of spontaneous circulation (ROSC), the so called ‘‘reperfusion injury’’. The reperfusion injury is thought to be due to the generation of oxygen free radicals and inflammatory mediators. In addition, increased calcium influx into the cells initiates biochemical cascades leading to cell injury. Hypothermia induced before, during and after an anoxic cerebral insult has been demonstrated to protect the brain from the reperfusion injury.2—4 The mechanism(s) by which hypothermia is protective is unclear. There is evidence that induced hypothermia has maximum benefit when it is applied immediately after ROSC. In a study by Kuboyama using a dog model, the benefit of induced hypothermia was diminished if induction of hypothermia was delayed by 15 min after ROSC, although a decrease in the neurological injury as determined by histological assessment of cerebral tissue samples was still observed in the delayed-hypothermia group.9 In the study reported by the Hypothermia after Cardiac Arrest Study Group the interval between the time of collapse to initiation of cooling was 105 min, with an interquartile range of 61—192 min.6 We believe that the 12 h delay prior to the initiation of hypothermia as occurred in our case, represents the longest time delay with a good recovery reported to date. What makes this case even more remarkable is the long time until ROSC was obtained (at least 45 min). In the reports by the Hypothermia after Cardiac Arrest Study Group and by Bernard et al. the time after collapse to ROSC averaged 22 and 26 min, respectively.6,7 The optimal duration of induced hypothermia after anoxic neurological injury is unknown. In the reports by the Hypothermia after Cardiac Arrest Study Group and by Bernard et al. the duration of induced hypothermia was 24 and 12 h,
423 respectively.6,7 Due to the long time before ROSC and the delay in the initiation of hypothermic we decided to cool our patient for 72 h. It is not clear if this longer duration of hypothermia contributed to the favourable outcome in this case. In conclusion, this case suggests that induced hypothermia should be considered in of out-ofhospital cardiac arrest regardless of the initial rhythm, and the time to ROSC, even when there is a delay of up to 12 h in commencing this therapeutic technique.
References 1. Benson DW, Williams GR, Spencer FC. The use of hypothermia after cardiac arrest. Anesth Analg 1958;38:423—8. 2. Leonov Y, Sterz F, Safar P, Radovsky A, Oku K, Tisherman S, et al. Mild cerebral hypothermia during and after cardiac arrest improves neurologic outcome in dogs. J Cereb Blood Flow Metab 1990;10:57—70. 3. Sterz F, Safar P, Tisherman S, Radovsky A, Kuboyama K, Oku K. Mild hypothermic cardiopulmonary resuscitation improves outcome after prolonged cardiac arrest in dogs. Crit Care Med 1991;19:379—89. 4. Weinrauch V, Safar P, Tisherman S, Kuboyama K, Radovsky A. Beneficial effect of mild hypothermia and detrimental effect of deep hypothermia after cardiac arrest in dogs. Stroke 1992;23:1454—62. 5. Bernard SA, Jones BM, Horne MK. Clinical trial of induced hypothermia in comatose survivors of out-of-hospital cardiac arrest. Ann Emerg Med 1997;30:146—53. 6. Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med 2002;346:549—56. 7. Bernard SA, Gray TW, Buist MD, Jones BM, Silvester W, Gutteridge G, et al. Treatment of comatose survivors of out-ofhospital cardiac arrest with induced hypothermia. N Engl J Med 2002;346:557—63. 8. Nolan JP, Morley PT, Vanden Hoek TL, Hickey RW, Kloeck WG, Billi J, et al. Therapeutic hypothermia after cardiac arrest: an advisory statement by the advanced life support task force of the International Liaison Committee on Resuscitation. Circulation 2003;108:118—21. 9. Kuboyama K, Safar P, Radovsky A, Tisherman SA, Stezoski SW, Alexander H. Delay in cooling negates the beneficial effect of mild resuscitative cerebral hypothermia after cardiac arrest in dogs: a prospective, randomized study. Crit Care Med 1993;21:1348—58.
CASE REPORT
Complete neurological recovery following delayed initiation of hypothermia in a victim of warm water near-drowning夽 Joseph Varon a,∗, Paul E. Marik b a
The University of Texas Health Science Center, St. Luke’s Episcopal Hospital, 2219 Dorrington Street, Houston, TX 77030, USA b Division of Pulmonary and Critical Care Medicine, Thomas Jefferson University, Philadelphia, PA, USA Received 13 May 2005 ; received in revised form 19 July 2005; accepted 19 July 2005 KEYWORDS Warm water drowning; Neurological recovery; Hypothermia; Cardiac arrest
Summary Induced hypothermia has been demonstrated to improve outcome following cardiac arrest and is now widely endorsed. However, the optimal method of cooling and the identification of patients most likely to benefit from this therapy remains to be determined. We report a patient in whom there was a long delay in return of spontaneous circulation (at least 45 min) and the initiation of induced hypothermia (12 h) who made an almost complete neurological recovery following cardiac arrest from warm-water near-drowning. © 2005 Elsevier Ireland Ltd. All rights reserved.
Introduction Induced hypothermia has been used in the operating room since the early 1950s for patients undergoing cardiac and neurosurgery. The use of induced hypothermia after cardiac arrest in humans in modern medicine was first reported in 1957 by Benson et al.1 They cooled four patients (to 30—33 ◦ C) after in-hospital cardiac arrest for
夽 A Spanish translated version of the summary of this article appears as appendix in the online version at 10.1016/j. resuscitation.2005.07.020. ∗ Corresponding author. Tel.: +1 713 669 1670; fax: +1 713 839 1467. E-mail address: [email protected] (J. Varon).
periods of 24—72 h. All four patients recovered. Interest in the use of mild to moderate induced hypothermia (32—34 ◦ C) following cardiac arrest was spurred by the pioneering work of the late Dr. Peter Safar. Dr. Safar and his group demonstrated improved neurological recovery in dogs when hypothermia was induced shortly after the restoration of spontaneous circulation.2—4 In 1997, Bernard and associates from Australia reported improved outcome in 22 survivors of out-of-hospital cardiac arrest who were cooled to 33 ◦ C for 12 h.5 Following two landmark randomized-controlled studies published in 2002, in which moderate hypothermia was demonstrated to improve the outcome in patients with coma after resuscitation from out-ofhospital cardiac arrest,6,7 this intervention is now endorsed by the International Liaison Committee
0300-9572/$ — see front matter © 2005 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.resuscitation.2005.07.020
422 on Resuscitation (ILCOR).8 Indeed, the ILCOR recommends the use of induced mild hypothermia in comatose survivors of out-of-hospital cardiac arrest caused by ventricular fibrillation. However, what remains unclear at this time is the best method of cooling and the optimal duration of cooling. Furthermore, the identification of patients most likely to benefit from this therapy has yet to be determined. We report a patient in whom there was a long delay in return of spontaneous circulation (ROSC) and the initiation of induced hypothermia who made an almost complete neurological recovery following cardiac arrest from warm water drowning.
Case report A previously healthy 53 year-old gentleman was pulled out of the waters of the Mexican Riviera during the month of December 2004 (average water temperature 23 ◦ C). He had gone swimming with his two young children who found him underwater. The length of time the patient was underwater was unknown. He was pulled out of the water by his two children who began resuscitation manoeuvers. A vacationing heath care provider saw the children and immediately assisted them. The patient was pulseless, cyanotic and had no spontaneous respirations. Cardiopulmonary resuscitation continued for approximately 20 min until emergency response professionals arrived at the beach. The patient was placed on a stretcher, chest compressions continued and the patient transported to a local clinic where he underwent tracheal intubation and advanced cardiac life support was begun. Attempts at electrical defibrillation for ventricular fibrillation (VF) were unsuccessful. Approximately 35—45 min after being pulled from the water, the patient achieved a ROSC. Arrangements were made to transfer the patient via fixed wing air ambulance to Houston, TX. However, it took over 11 h from the time of the incident until the time the patient presented to our facility. According to the aircraft medical crew, the patient had no spontaneous respirations, systolic blood pressure remained above 80 mmHg and the monitor showed sinus tachycardia. In addition, the patient had several tonic-clonic seizures and intermittent myoclonus. On our initial examination, approximately 11.5 h after the incident, the blood pressure was 110/70 mmHg, heart rate 88 min−1 and rectal temperature was 37.8 ◦ C. He was being ventilated on assist-control mode with a tidal volume of 700 cm3 , rate of 12 breaths/min and an inspired oxygen concentration of 100%.
J. Varon, P.E. Marik The patient had not received any narcotics or neuromuscular blockers and lacked corneal, pupillary and gag reflexes. The Glasgow Coma Scale was 3. Multiple ecchymotic lesions and abrasions were found on the extremities as well as abrasions. An emergency computed tomography of brain and cervical spine revealed mild-to-moderate cerebral oedema without any bone abnormalities or intracranial bleeding. A 12-lead electrocardiogram and cardiac enzymes revealed no evidence of acute myocardial ischaemia. An electroencephalogram was grossly abnormal and consistent with global ischaemia. Twelve hours after the incident, therapeutic hypothermia was started. Ice packs were applied to the groins and axilla and cooling blankets were placed on top and under the patient. The cooling blankets were set to automatic mode to maintain the patient’s bladder temperature at 32 ◦ C for a total of 72 h. He received no sedatives or neuromuscular blocking agents due to his significant neurological impairment and concern about failing to recognize improvement or deterioration. During the 72 h of hypothermia, the patient developed acute respiratory distress syndrome (ARDS), acute renal failure (with a three-fold normal elevation in serum creatinine) and a mild coagulopathy. He was ventilated with a lung protective strategy with the PaCO2 kept between 4.6 and 5.3 kPa (35—40 mmHg) and the arterial oxygen saturation above 95%. He did not require renal replacement therapy. During hypothermia, the patient did not shiver. After the period of therapeutic hypothermia, controlled rewarming to the target temperature of 37 ◦ C was achieved over 12 h on the fourth day of hospitalization. By the fifth hospital day, the patient had a corneal reflex, a pupillary reflex and was beginning to move his head. On day 6, to our surprise, the patient woke up. He indicated that he was unable to move his lower extremities and was taken as an emergency for a cervical spine magnetic resonance imaging that revealed a C3—C6 cervical spine contusion. Neurosurgical decompression followed. The patient required a temporary tracheotomy. He was subsequently weaned from mechanical ventilation and his renal function returned to normal. Other than minor motor abnormalities related to his cervical injury, a complete neurological examination revealed no abnormalities. Neuropsychometric testing revealed normal function. The patient was discharged to a rehabilitation facility 3 weeks after arrival at our institution. Three months after the incident, the patient is now living at home and has slowly resumed his regular activities.
Delayed hypothermia and near-drowning
Discussion The prognosis of patients who remain unconscious after resuscitation from out-of-hospital cardiac arrest is poor. It is believed that part of the anoxic neurological injury occurs after the return of spontaneous circulation (ROSC), the so called ‘‘reperfusion injury’’. The reperfusion injury is thought to be due to the generation of oxygen free radicals and inflammatory mediators. In addition, increased calcium influx into the cells initiates biochemical cascades leading to cell injury. Hypothermia induced before, during and after an anoxic cerebral insult has been demonstrated to protect the brain from the reperfusion injury.2—4 The mechanism(s) by which hypothermia is protective is unclear. There is evidence that induced hypothermia has maximum benefit when it is applied immediately after ROSC. In a study by Kuboyama using a dog model, the benefit of induced hypothermia was diminished if induction of hypothermia was delayed by 15 min after ROSC, although a decrease in the neurological injury as determined by histological assessment of cerebral tissue samples was still observed in the delayed-hypothermia group.9 In the study reported by the Hypothermia after Cardiac Arrest Study Group the interval between the time of collapse to initiation of cooling was 105 min, with an interquartile range of 61—192 min.6 We believe that the 12 h delay prior to the initiation of hypothermia as occurred in our case, represents the longest time delay with a good recovery reported to date. What makes this case even more remarkable is the long time until ROSC was obtained (at least 45 min). In the reports by the Hypothermia after Cardiac Arrest Study Group and by Bernard et al. the time after collapse to ROSC averaged 22 and 26 min, respectively.6,7 The optimal duration of induced hypothermia after anoxic neurological injury is unknown. In the reports by the Hypothermia after Cardiac Arrest Study Group and by Bernard et al. the duration of induced hypothermia was 24 and 12 h,
423 respectively.6,7 Due to the long time before ROSC and the delay in the initiation of hypothermic we decided to cool our patient for 72 h. It is not clear if this longer duration of hypothermia contributed to the favourable outcome in this case. In conclusion, this case suggests that induced hypothermia should be considered in of out-ofhospital cardiac arrest regardless of the initial rhythm, and the time to ROSC, even when there is a delay of up to 12 h in commencing this therapeutic technique.
References 1. Benson DW, Williams GR, Spencer FC. The use of hypothermia after cardiac arrest. Anesth Analg 1958;38:423—8. 2. Leonov Y, Sterz F, Safar P, Radovsky A, Oku K, Tisherman S, et al. Mild cerebral hypothermia during and after cardiac arrest improves neurologic outcome in dogs. J Cereb Blood Flow Metab 1990;10:57—70. 3. Sterz F, Safar P, Tisherman S, Radovsky A, Kuboyama K, Oku K. Mild hypothermic cardiopulmonary resuscitation improves outcome after prolonged cardiac arrest in dogs. Crit Care Med 1991;19:379—89. 4. Weinrauch V, Safar P, Tisherman S, Kuboyama K, Radovsky A. Beneficial effect of mild hypothermia and detrimental effect of deep hypothermia after cardiac arrest in dogs. Stroke 1992;23:1454—62. 5. Bernard SA, Jones BM, Horne MK. Clinical trial of induced hypothermia in comatose survivors of out-of-hospital cardiac arrest. Ann Emerg Med 1997;30:146—53. 6. Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med 2002;346:549—56. 7. Bernard SA, Gray TW, Buist MD, Jones BM, Silvester W, Gutteridge G, et al. Treatment of comatose survivors of out-ofhospital cardiac arrest with induced hypothermia. N Engl J Med 2002;346:557—63. 8. Nolan JP, Morley PT, Vanden Hoek TL, Hickey RW, Kloeck WG, Billi J, et al. Therapeutic hypothermia after cardiac arrest: an advisory statement by the advanced life support task force of the International Liaison Committee on Resuscitation. Circulation 2003;108:118—21. 9. Kuboyama K, Safar P, Radovsky A, Tisherman SA, Stezoski SW, Alexander H. Delay in cooling negates the beneficial effect of mild resuscitative cerebral hypothermia after cardiac arrest in dogs: a prospective, randomized study. Crit Care Med 1993;21:1348—58.