THERAPEUTIC HYPOTHERMIA AND TEMPERATURE MANAGEMENT Volume 3, Number 4, 2013 ª Mary Ann Liebert, Inc. DOI: 10.1089/ther.2013.0016
Case Report
Beau’s Lines After Cardiac Arrest Hallam M. Gugelmann, MD, MPH,1 and David F. Gaieski, MD 1,2
A 34-year-old man with uncontrolled hypertension suffered a ventricular fibrillation cardiac arrest from an obstructive left anterior descending artery occlusion. He was defibrillated more than 10 times before achieving return of spontaneous circulation. He was comatose after his arrest and was treated with therapeutic hypothermia, and a bare metal stent was placed in his obstructed coronary artery with restoration of excellent postobstruction blood flow. His postarrest course was complicated by cardiogenic shock; prolonged ventilatordependent respiratory failure requiring tracheostomy; tracheobronchitis, with cultures positive for methicillinresistant Staphylococcus aureus (MRSA); and an extended period of agitation and delirium. Thirty-four days after his arrest, his mental status started to improve rapidly. His delirium resolved, he became oriented and lucid, and he was able to be discharged to a rehabilitation facility on hospital day 41, with an excellent prognosis and close follow-up in primary care, cardiology, tracheostomy, and coumadin clinics. He returned to the emergency department 65 days later with the complaint of intermittent chest pain of 4 days’ duration. Upon physical examination he was found to have Beau’s lines on his fingernails. He was admitted to the hospital for a rule-out myocardial infarction workup, which was uneventful. He was discharged to home in good condition 2 days later.
Initial Arrest
A
34-year-old man with a medical history of uncontrolled hypertension and polysubstance abuse (cigarettes, marijuana, and alcohol) presented to a community hospital emergency department (ED) via emergency medical services (EMS) after having an out-of-hospital cardiac arrest (OHCA). Per family, he had complained of intermittent substernal chest pain for the past week, which he was treating with marijuana and acetaminophen-oxycodone. He described the pain as exacerbated by exertion. On the evening of his arrest, around 18:00, the pain worsened acutely, accompanied by diaphoresis and shortness of breath, prompting him to call EMS before losing consciousness. No bystander cardiopulmonary resuscitation attempts were made, and he had been unresponsive for an unknown period when EMS arrived 6 minutes later. An automatic external defibrillator was applied, and the patient was defibrillated once with transient return of spontaneous circulation (ROSC) before arrival at the ED. He was intubated en route and was comatose on arrival to the ED. Recurrent Arrest He was transferred to an ED bed, placed on a monitor, and ventilated by bag-valve through the endotracheal tube. Shortly after arrival, he had recurrent cardiac arrest, and the
monitor demonstrated asystole. Chest compressions were started, and a bolus of epinephrine (1 mg) was given. At the next pulse check, there was no palpable pulse and the monitor demonstrated recurrent ventricular fibrillation. He was immediately defibrillated at 200 joules, but ventricular fibrillation persisted after the defibrillation attempt. The patient underwent approximately 20 additional minutes of advanced cardiac life support, including 10 additional defibrillations, chest compressions, and boluses of epinephrine before obtaining ROSC for the second time. This time ROSC was sustained for > 20 minutes. The patient remained comatose with a Glasgow coma score (GCS) of 3. Post-ROSC electrocardiogram (EKG) did not reveal any signs of ST-segment elevation myocardial infarction. He was hypotensive and started on norepinephrine and amiodarone infusions through peripheral intravenous catheters, and then a right internal jugular central venous catheter. Therapeutic hypothermia (TH) was started, with infusion of 2 L of 4C normal saline through peripheral intravenous catheters and ice bags applied to the axillae and groins. Cooling blankets were applied underneath and over the patient, and target temperature was set for 33C. Norepinephrine was weaned off, milrinone and nitroprusside infusions were started, and a pulmonary artery catheter was inserted, which demonstrated a cardiac index of 0.75 L/min/ m2 and systemic vascular resistance of 4,638 dyn/sec/cm - 5.
1 Department of Emergency Medicine, Perelman School of Medicine at the University of Pennsylvania, and 2Department of Emergency Medicine, Center for Resuscitation Science, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.
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Chest radiography was consistent with pulmonary edema, and a repeat EKG on the morning of hospital day 2 showed anteroseptal ST-segment elevation. Transfer to an ST-elevation myocardial infarction (STEMI) center with expertise in postarrest care was arranged.
When he was discharged to a rehabilitation facility 41 days after arrest, he was completely neurologically intact with an excellent prognosis. Follow-up appointments had been arranged with primary care, cardiology, tracheostomy, and coumadin clinics.
Transfer to Cardiac Arrest Center for Ongoing Management
Subsequent Emergency Department Visit
He was transferred to our hospital for further management and admitted to the Cardiac Care Unit (CCU). On arrival to the CCU in the early afternoon, his vital signs were as follows: temperature, 32.7C; blood pressure, 120/87 mmHg; mean arterial pressure, 98 mmHg; heart rate, 91 beats per minute; respiratory rate, 16 breaths per minute, intubated, on assist control at 16 breaths per minute; tidal volume, 400 cc; FiO2, 100%; positive end-expiratory pressure (PEEP), 7.5 mmHg. An emergent transthoracic echocardiogram was performed demonstrating a left ventricular ejection fraction of 10–15% with apical akinesis. The patient was immediately transported to the cardiac catheterization lab, where he underwent cardiac catheterization, which revealed a 100% occlusion of the proximal left anterior descending coronary (LAD), diffuse left circumflex disease, and a 60% stenosis of the middle segment of the right coronary artery (RCA). A bare metal stent was deployed across the LAD occlusion with restoration of TIMI-III flow. The patient returned to the CCU for further management.
Three and a half months after his arrest, the patient presented to our ED with chest pain. He stated that he had chest pain, off and on, worse with deep inspiration and worse with rotational movements of his torso, for 4 days. His tracheostomy had been decannulated and PEG tube removed several weeks before without complications. His vital signs were stable and the electrocardiogram demonstrated no evidence of ischemia. On examination, his fingernails had deep transverse grooves in the nail plate, the most proximal of which was 8 mm distal to the eponychium. The patient consented to medical photography and several pictures were taken of his fingernails (Figs. 1 and 2). He was admitted to the cardiac intermediate care unit for further management of his chest pain. His work-up was unremarkable. He was ruled out for acute myocardial infarction, an echocardiogram showed an improved ejection fraction of 45%, and he was discharged to home 2 days later. Beau’s Lines The patient’s fingernail findings are consistent with Beau’s lines, which were first described in 1846 by the French
Postarrest Care He had a complicated postarrest course at our institution. He was treated with TH for 24 hours, being maintained within 0.5C of the target temperature of 33C for 24 hours total before he was gradually rewarmed to 36.0C. He had ongoing cardiogenic shock, treated with dobutamine and milrinone infusions; severe ventilator-dependent respiratory failure, requiring high levels of FiO2, PEEP, paralysis, and sedation to assure adequate oxygenation; and acute kidney injury. He had persistent fevers of 39C or higher for several days. Because of failure to wean, a tracheostomy tube and a percutaneous esophagogastrostomy (PEG) tube were placed on hospital day 10, and he was transferred to the medical ICU for further management. Because of ongoing agitation, he was taken back to the cardiac catheterization lab on hospital day 18 to rule out ongoing ischemia as cause of agitation. The 60% mid-RCA stenosis was found not to be flow-limiting, but he was found to have a markedly elevated left ventricular end diastolic pressure (45 mmHg) and a low systemic vascular resistance (500 dyn/sec/cm - 5). This mixed shock picture was treated with furosemide, antibiotics, and vasopressors. All cultures were negative at 72 hours, his hypotension resolved by hospital day 21, his fever defervesced, and his sedation was lightened. He developed episodes of severe agitation between hospital days 21 and 28 and treated with haloperidol, which was stopped because of prolonged QTc on EKG. Fever recurred and tracheobronchitis, with cultures positive for MRSA, was diagnosed and treated. He was continued on furosemide and started on lisinopril and carvedilol. On hospital day 34, his mental status improved considerably, with decreased agitation, increased ability to focus, and good short-term memory and concentration.
FIG. 1. Post-arrest patient’s fingernails demonstrating deep transverse grooves, known as Beau’s lines. Color images available online at www.liebertpub.com/ther
BEAU’S LINES AFTER CARDIAC ARREST
FIG. 2. Beau’s lines: Stress-induced cessation of cell division in the nail matrix. Color images available online at www.liebertpub.com/ther physician Joseph Honore´ Simone Beau. They result from a temporary cessation of cell division in the nail matrix and are typically the result of infection, trauma, chemotherapy, hypocalcemia, coronary artery occlusion, or, less frequently described, conditions resulting in peripheral ischemia, including cardiac arrest, septic shock, and vasopressor use (Patel et al., 2011; www.wikipedia.org/wiki/Beau’s_lines) They present as transverse grooves in the fingernails, paralleling the lunula (Figs. 1 and 2). A recent report describes a patient presenting with Beau’s lines on all fingernails on a follow-up visit 3 months after being hospitalized with an empyema and pyopericardium secondary to rupture of an amoebic liver abscess (Naik and Harikrishna, 2013). It is believed that human nails grow at approximately 0.1 mm/day and that, therefore, the time from the insult can be estimated by the distance the Beau’s line is from the lunula and the proximal nail fold (Naik and Harikrishna, 2013). Multiple Beau’s lines have been described in patients receiving sequential doses of chemotherapy, and the intensity of the lines reflects the intensity of the chemotherapy cycle, the severity of temporary cessation of proliferation of the nail matrix, and accompanying stressors, including neutropenic fever (Park and Li, 2010; Chang and Wu, 2013).
201 after cardiac arrest, which affects multiple organ systems (Neumar et al., 2008). PCAS is a result of ischemia and reperfusion. The syndrome has been classically described in the comatose patient presenting to the ED after OHCA, but also occurs after in-hospital cardiac arrest. For decades, clinicians sought to improve survival from cardiac arrest by increasing the percentage of patients who achieved ROSC; however, outcomes of comatose postarrest patients remained abysmal and little improvement was seen over decades. In 2003, using data from the National Registry of Cardiopulmonary Resuscitation, Peberdy and colleagues (2003) reported that only 17% of in-hospital arrests survived to discharge and that the average length of time from arrest to withdrawal of care in the patients who died was 1.5 days. For patients who survived to discharge, the average time from arrest to discharge was 13.4 days. In one sense, it appears that patients were being abandoned long before it was clear whether they could recover from their injury. In 2002, two landmark articles were published in the New England Journal of Medicine describing the treatment of PCAS with TH, lowering the core body temperature to a target range of 32–34C for 12–24 hours to modulate the complex pathophysiologic processes triggered by ischemia and reperfusion (Bernard et al., 2002; Hypothermia after Cardiac Arrest Study Group, 2002). Both studies showed significant improvements in neurologic outcomes in the patients treated with TH, and since their publication, this therapy has become standard of care and the cornerstone for treating PCAS. In their review of PCAS published in Circulation, Neumar et al. (2008) described four key components of PCAS: ‘‘(1) post-cardiac arrest brain injury, (2) post-cardiac arrest myocardial dysfunction, (3) systemic ischemia/reperfusion response, and (4) persistent precipitating pathology.’’ Strategies to minimize the damage from each component of PCAS need to be integrated into a comprehensive PCAS treatment protocol. Our case illustrates the complex course patients often follow after their cardiac arrest. Our patient was comatose postarrest, with a GCS of 3 and obvious postcardiac arrest brain injury. This was treated with TH, and after rewarmed to normothermia, he had ongoing coma, then agitation and delirium. His echocardiogram and hemodynamics demonstrated severe postcardiac arrest myocardial dysfunction, necessitating vasopressors, inotropes, and fluid infusions, transitioning to vasodilators, and after-load reduction after initial stabilization. The severity of his postarrest myocardial dysfunction was the summation of a large anterior wall infarct and global myocardial dysfunction seen after arrest. The improvement in his ejection fraction over the weeks after arrest demonstrates the reversibility of this process. He had a marked systemic ischemia/reperfusion response, with sepsis-like physiology, including fevers, tachycardia, and decreased systemic vascular resistance. His first days postarrest were complicated by persistent precipitating pathology, with cardiac catheterization demonstrating 100% occlusion of his proximal left anterior descending artery, requiring deployment of a bare metal stent to restore distal coronary blood flow. Conclusions
Postcardiac Arrest Syndrome and TH Postcardiac arrest syndrome (PCAS) is a complex pathophysiologic state occurring in patients who have had ROSC
When the patient returned to the ED, 3½ months after his cardiac arrest and the start of a 42-day hospitalization, he had graphic evidence of the profound stress surrounding his
202 arrest—deep, transverse grooves on his fingernails, 8 mm from his eponychium, remained as visible evidence of his extended period of ischemia and subsequent severe reperfusion injury. Beau’s lines are a recording of a time of stress and remain until the fingernails grow to the point where the line is at the distal nail edge and can be trimmed away. Author Disclosure Statement No competing financial interests exist.
GUGELMANN AND GAIESKI Neumar RW, Nolan JP, et al. Post-cardiac arrest syndrome. Epidemiology, pathophysiology, treatment and prognostication. Circulation 2008;118:2452–2483. Park J, Li K. Multiple Beau’s lines. N Engl J Med 2010;362:e63. Patel LM, Lambert PJ, et al. Cutaneous signs of systemic disease. Clin Dermatol 2011;29:511–522. Peberdy MA, Kaye W, et al. Cardiopulmonary resuscitation of adults in the hospital: A report of 14,720 cardiac arrests from the National Registry of Cardiopulmonary Resuscitation. Resuscitation 2003;58:297–308. www.wikipedia.org/wiki/Beau’s_lines Accessed July 23, 2013.
References Bernard SA, Gray TW, et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med 2002;346:557–563. Chang C-C, Wu C-C. Beau’s lines. Q J Med 2013;106:383. Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med 2002;346:549–556. Naik GS, Harikrishna J. Beau’s lines. Indian J Med Res 2013; 137:220.
Address correspondence to: David F. Gaieski, MD Department of Emergency Medicine Hospital of the University of Pennsylvania 34th and Spruce Streets, Ground Ravdin Philadelphia, PA 19104 E-mail: [email protected]
Case Report
Beau’s Lines After Cardiac Arrest Hallam M. Gugelmann, MD, MPH,1 and David F. Gaieski, MD 1,2
A 34-year-old man with uncontrolled hypertension suffered a ventricular fibrillation cardiac arrest from an obstructive left anterior descending artery occlusion. He was defibrillated more than 10 times before achieving return of spontaneous circulation. He was comatose after his arrest and was treated with therapeutic hypothermia, and a bare metal stent was placed in his obstructed coronary artery with restoration of excellent postobstruction blood flow. His postarrest course was complicated by cardiogenic shock; prolonged ventilatordependent respiratory failure requiring tracheostomy; tracheobronchitis, with cultures positive for methicillinresistant Staphylococcus aureus (MRSA); and an extended period of agitation and delirium. Thirty-four days after his arrest, his mental status started to improve rapidly. His delirium resolved, he became oriented and lucid, and he was able to be discharged to a rehabilitation facility on hospital day 41, with an excellent prognosis and close follow-up in primary care, cardiology, tracheostomy, and coumadin clinics. He returned to the emergency department 65 days later with the complaint of intermittent chest pain of 4 days’ duration. Upon physical examination he was found to have Beau’s lines on his fingernails. He was admitted to the hospital for a rule-out myocardial infarction workup, which was uneventful. He was discharged to home in good condition 2 days later.
Initial Arrest
A
34-year-old man with a medical history of uncontrolled hypertension and polysubstance abuse (cigarettes, marijuana, and alcohol) presented to a community hospital emergency department (ED) via emergency medical services (EMS) after having an out-of-hospital cardiac arrest (OHCA). Per family, he had complained of intermittent substernal chest pain for the past week, which he was treating with marijuana and acetaminophen-oxycodone. He described the pain as exacerbated by exertion. On the evening of his arrest, around 18:00, the pain worsened acutely, accompanied by diaphoresis and shortness of breath, prompting him to call EMS before losing consciousness. No bystander cardiopulmonary resuscitation attempts were made, and he had been unresponsive for an unknown period when EMS arrived 6 minutes later. An automatic external defibrillator was applied, and the patient was defibrillated once with transient return of spontaneous circulation (ROSC) before arrival at the ED. He was intubated en route and was comatose on arrival to the ED. Recurrent Arrest He was transferred to an ED bed, placed on a monitor, and ventilated by bag-valve through the endotracheal tube. Shortly after arrival, he had recurrent cardiac arrest, and the
monitor demonstrated asystole. Chest compressions were started, and a bolus of epinephrine (1 mg) was given. At the next pulse check, there was no palpable pulse and the monitor demonstrated recurrent ventricular fibrillation. He was immediately defibrillated at 200 joules, but ventricular fibrillation persisted after the defibrillation attempt. The patient underwent approximately 20 additional minutes of advanced cardiac life support, including 10 additional defibrillations, chest compressions, and boluses of epinephrine before obtaining ROSC for the second time. This time ROSC was sustained for > 20 minutes. The patient remained comatose with a Glasgow coma score (GCS) of 3. Post-ROSC electrocardiogram (EKG) did not reveal any signs of ST-segment elevation myocardial infarction. He was hypotensive and started on norepinephrine and amiodarone infusions through peripheral intravenous catheters, and then a right internal jugular central venous catheter. Therapeutic hypothermia (TH) was started, with infusion of 2 L of 4C normal saline through peripheral intravenous catheters and ice bags applied to the axillae and groins. Cooling blankets were applied underneath and over the patient, and target temperature was set for 33C. Norepinephrine was weaned off, milrinone and nitroprusside infusions were started, and a pulmonary artery catheter was inserted, which demonstrated a cardiac index of 0.75 L/min/ m2 and systemic vascular resistance of 4,638 dyn/sec/cm - 5.
1 Department of Emergency Medicine, Perelman School of Medicine at the University of Pennsylvania, and 2Department of Emergency Medicine, Center for Resuscitation Science, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.
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Chest radiography was consistent with pulmonary edema, and a repeat EKG on the morning of hospital day 2 showed anteroseptal ST-segment elevation. Transfer to an ST-elevation myocardial infarction (STEMI) center with expertise in postarrest care was arranged.
When he was discharged to a rehabilitation facility 41 days after arrest, he was completely neurologically intact with an excellent prognosis. Follow-up appointments had been arranged with primary care, cardiology, tracheostomy, and coumadin clinics.
Transfer to Cardiac Arrest Center for Ongoing Management
Subsequent Emergency Department Visit
He was transferred to our hospital for further management and admitted to the Cardiac Care Unit (CCU). On arrival to the CCU in the early afternoon, his vital signs were as follows: temperature, 32.7C; blood pressure, 120/87 mmHg; mean arterial pressure, 98 mmHg; heart rate, 91 beats per minute; respiratory rate, 16 breaths per minute, intubated, on assist control at 16 breaths per minute; tidal volume, 400 cc; FiO2, 100%; positive end-expiratory pressure (PEEP), 7.5 mmHg. An emergent transthoracic echocardiogram was performed demonstrating a left ventricular ejection fraction of 10–15% with apical akinesis. The patient was immediately transported to the cardiac catheterization lab, where he underwent cardiac catheterization, which revealed a 100% occlusion of the proximal left anterior descending coronary (LAD), diffuse left circumflex disease, and a 60% stenosis of the middle segment of the right coronary artery (RCA). A bare metal stent was deployed across the LAD occlusion with restoration of TIMI-III flow. The patient returned to the CCU for further management.
Three and a half months after his arrest, the patient presented to our ED with chest pain. He stated that he had chest pain, off and on, worse with deep inspiration and worse with rotational movements of his torso, for 4 days. His tracheostomy had been decannulated and PEG tube removed several weeks before without complications. His vital signs were stable and the electrocardiogram demonstrated no evidence of ischemia. On examination, his fingernails had deep transverse grooves in the nail plate, the most proximal of which was 8 mm distal to the eponychium. The patient consented to medical photography and several pictures were taken of his fingernails (Figs. 1 and 2). He was admitted to the cardiac intermediate care unit for further management of his chest pain. His work-up was unremarkable. He was ruled out for acute myocardial infarction, an echocardiogram showed an improved ejection fraction of 45%, and he was discharged to home 2 days later. Beau’s Lines The patient’s fingernail findings are consistent with Beau’s lines, which were first described in 1846 by the French
Postarrest Care He had a complicated postarrest course at our institution. He was treated with TH for 24 hours, being maintained within 0.5C of the target temperature of 33C for 24 hours total before he was gradually rewarmed to 36.0C. He had ongoing cardiogenic shock, treated with dobutamine and milrinone infusions; severe ventilator-dependent respiratory failure, requiring high levels of FiO2, PEEP, paralysis, and sedation to assure adequate oxygenation; and acute kidney injury. He had persistent fevers of 39C or higher for several days. Because of failure to wean, a tracheostomy tube and a percutaneous esophagogastrostomy (PEG) tube were placed on hospital day 10, and he was transferred to the medical ICU for further management. Because of ongoing agitation, he was taken back to the cardiac catheterization lab on hospital day 18 to rule out ongoing ischemia as cause of agitation. The 60% mid-RCA stenosis was found not to be flow-limiting, but he was found to have a markedly elevated left ventricular end diastolic pressure (45 mmHg) and a low systemic vascular resistance (500 dyn/sec/cm - 5). This mixed shock picture was treated with furosemide, antibiotics, and vasopressors. All cultures were negative at 72 hours, his hypotension resolved by hospital day 21, his fever defervesced, and his sedation was lightened. He developed episodes of severe agitation between hospital days 21 and 28 and treated with haloperidol, which was stopped because of prolonged QTc on EKG. Fever recurred and tracheobronchitis, with cultures positive for MRSA, was diagnosed and treated. He was continued on furosemide and started on lisinopril and carvedilol. On hospital day 34, his mental status improved considerably, with decreased agitation, increased ability to focus, and good short-term memory and concentration.
FIG. 1. Post-arrest patient’s fingernails demonstrating deep transverse grooves, known as Beau’s lines. Color images available online at www.liebertpub.com/ther
BEAU’S LINES AFTER CARDIAC ARREST
FIG. 2. Beau’s lines: Stress-induced cessation of cell division in the nail matrix. Color images available online at www.liebertpub.com/ther physician Joseph Honore´ Simone Beau. They result from a temporary cessation of cell division in the nail matrix and are typically the result of infection, trauma, chemotherapy, hypocalcemia, coronary artery occlusion, or, less frequently described, conditions resulting in peripheral ischemia, including cardiac arrest, septic shock, and vasopressor use (Patel et al., 2011; www.wikipedia.org/wiki/Beau’s_lines) They present as transverse grooves in the fingernails, paralleling the lunula (Figs. 1 and 2). A recent report describes a patient presenting with Beau’s lines on all fingernails on a follow-up visit 3 months after being hospitalized with an empyema and pyopericardium secondary to rupture of an amoebic liver abscess (Naik and Harikrishna, 2013). It is believed that human nails grow at approximately 0.1 mm/day and that, therefore, the time from the insult can be estimated by the distance the Beau’s line is from the lunula and the proximal nail fold (Naik and Harikrishna, 2013). Multiple Beau’s lines have been described in patients receiving sequential doses of chemotherapy, and the intensity of the lines reflects the intensity of the chemotherapy cycle, the severity of temporary cessation of proliferation of the nail matrix, and accompanying stressors, including neutropenic fever (Park and Li, 2010; Chang and Wu, 2013).
201 after cardiac arrest, which affects multiple organ systems (Neumar et al., 2008). PCAS is a result of ischemia and reperfusion. The syndrome has been classically described in the comatose patient presenting to the ED after OHCA, but also occurs after in-hospital cardiac arrest. For decades, clinicians sought to improve survival from cardiac arrest by increasing the percentage of patients who achieved ROSC; however, outcomes of comatose postarrest patients remained abysmal and little improvement was seen over decades. In 2003, using data from the National Registry of Cardiopulmonary Resuscitation, Peberdy and colleagues (2003) reported that only 17% of in-hospital arrests survived to discharge and that the average length of time from arrest to withdrawal of care in the patients who died was 1.5 days. For patients who survived to discharge, the average time from arrest to discharge was 13.4 days. In one sense, it appears that patients were being abandoned long before it was clear whether they could recover from their injury. In 2002, two landmark articles were published in the New England Journal of Medicine describing the treatment of PCAS with TH, lowering the core body temperature to a target range of 32–34C for 12–24 hours to modulate the complex pathophysiologic processes triggered by ischemia and reperfusion (Bernard et al., 2002; Hypothermia after Cardiac Arrest Study Group, 2002). Both studies showed significant improvements in neurologic outcomes in the patients treated with TH, and since their publication, this therapy has become standard of care and the cornerstone for treating PCAS. In their review of PCAS published in Circulation, Neumar et al. (2008) described four key components of PCAS: ‘‘(1) post-cardiac arrest brain injury, (2) post-cardiac arrest myocardial dysfunction, (3) systemic ischemia/reperfusion response, and (4) persistent precipitating pathology.’’ Strategies to minimize the damage from each component of PCAS need to be integrated into a comprehensive PCAS treatment protocol. Our case illustrates the complex course patients often follow after their cardiac arrest. Our patient was comatose postarrest, with a GCS of 3 and obvious postcardiac arrest brain injury. This was treated with TH, and after rewarmed to normothermia, he had ongoing coma, then agitation and delirium. His echocardiogram and hemodynamics demonstrated severe postcardiac arrest myocardial dysfunction, necessitating vasopressors, inotropes, and fluid infusions, transitioning to vasodilators, and after-load reduction after initial stabilization. The severity of his postarrest myocardial dysfunction was the summation of a large anterior wall infarct and global myocardial dysfunction seen after arrest. The improvement in his ejection fraction over the weeks after arrest demonstrates the reversibility of this process. He had a marked systemic ischemia/reperfusion response, with sepsis-like physiology, including fevers, tachycardia, and decreased systemic vascular resistance. His first days postarrest were complicated by persistent precipitating pathology, with cardiac catheterization demonstrating 100% occlusion of his proximal left anterior descending artery, requiring deployment of a bare metal stent to restore distal coronary blood flow. Conclusions
Postcardiac Arrest Syndrome and TH Postcardiac arrest syndrome (PCAS) is a complex pathophysiologic state occurring in patients who have had ROSC
When the patient returned to the ED, 3½ months after his cardiac arrest and the start of a 42-day hospitalization, he had graphic evidence of the profound stress surrounding his
202 arrest—deep, transverse grooves on his fingernails, 8 mm from his eponychium, remained as visible evidence of his extended period of ischemia and subsequent severe reperfusion injury. Beau’s lines are a recording of a time of stress and remain until the fingernails grow to the point where the line is at the distal nail edge and can be trimmed away. Author Disclosure Statement No competing financial interests exist.
GUGELMANN AND GAIESKI Neumar RW, Nolan JP, et al. Post-cardiac arrest syndrome. Epidemiology, pathophysiology, treatment and prognostication. Circulation 2008;118:2452–2483. Park J, Li K. Multiple Beau’s lines. N Engl J Med 2010;362:e63. Patel LM, Lambert PJ, et al. Cutaneous signs of systemic disease. Clin Dermatol 2011;29:511–522. Peberdy MA, Kaye W, et al. Cardiopulmonary resuscitation of adults in the hospital: A report of 14,720 cardiac arrests from the National Registry of Cardiopulmonary Resuscitation. Resuscitation 2003;58:297–308. www.wikipedia.org/wiki/Beau’s_lines Accessed July 23, 2013.
References Bernard SA, Gray TW, et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med 2002;346:557–563. Chang C-C, Wu C-C. Beau’s lines. Q J Med 2013;106:383. Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med 2002;346:549–556. Naik GS, Harikrishna J. Beau’s lines. Indian J Med Res 2013; 137:220.
Address correspondence to: David F. Gaieski, MD Department of Emergency Medicine Hospital of the University of Pennsylvania 34th and Spruce Streets, Ground Ravdin Philadelphia, PA 19104 E-mail: [email protected]
