American Journal of Emergency Medicine 33 (2015) 600.e5–600.e7
Contents lists available at ScienceDirect
American Journal of Emergency Medicine journal homepage: www.elsevier.com/locate/ajem
Case Report
Resuscitative thoracotomy for nontraumatic pericardial tamponade: case reports and review of the literature☆,☆☆,★ Abstract Nontraumatic cardiac tamponade is a life-threatening process, and pericardiocentesis is the established treatment designed to relieve tamponade physiology during a cardiac arrest. We report 2 cases, where after traditional resuscitation including serial pericardiocentesis failed, a resuscitative thoracotomy was performed. Cardiac tamponade is a life-threatening condition that results from an accumulation of fluid, blood, pus, clots, or gas in the pericardial space leading to compression of the heart and limitations in cardiac output [1]. In nontraumatic cases, pericardiocentesis is the established modality of treatment and has been shown to be effective in a majority of patients [2]; however, there are circumstances where the procedure fails to correct tamponade physiology. We present 2 cases of pulseless electrical activity arrest secondary to cardiac tamponade; the first being secondary to an inflammatory effusion and the second to a malignant effusion. The patients were managed with resuscitative thoracotomy after traditional resuscitation using advanced cardiac life support algorithms, and serial pericardiocenteses proved unsuccessful. Case #1: A 58-year-old woman presented to a tertiary, academic emergency department with a chief complaint of dyspnea and generalized weakness. The patient had presented 2 days earlier to the same emergency department with left-sided chest pain and dyspnea but then left against medical advice after a chest x-ray (Fig. 1). On the second presentation, the patient had an initial blood pressure of 127/84 mm Hg, heart rate of 107 beats per minute, respiratory rate of 18 breaths per minute, an oxygen saturation of 99% on room air, and a temperature of 97.4°F. Medical history included paroxysmal atrial fibrillation, hypertension, and a right middle cerebral artery aneurysm repair 8 years prior. On physical examination, the patient appeared to be in no acute distress. Lung fields were clear to auscultation, heart sounds were regular and audible, her abdomen was soft and nontender, and the extremities had no significant edema. Approximately 90 minutes into her emergency department stay, the patient was directly observed by staff to abruptly collapse secondary to a PEA arrest. Chest compressions were initiated; an endotracheal tube was secured; and epinephrine, atropine, calcium, bicarbonate, and normal saline were administered without return of spontaneous circulation (ROSC). The prior chest x-ray obtained before arrest was notable for cardiomegaly (Fig. 1), and an intraarrest bedside echocardiography showed pericardial tamponade. Ultrasound☆ Funding: None. ☆☆ Previously presented: No. ★ Conflicts of interest: All authors have no conflicts of interest.
0735-6757/© 2014 Elsevier Inc. All rights reserved.
guided pericardiocentesis was performed using an 18-gauge spinal needle that yielded 20 cm 3 of dark clotted blood. The patient was then noted to be in ventricular fibrillation and was defibrillated; however, the patient did not have return of spontaneous circulation. The code continued, and 4 subsequent pericardiocenteses were performed yielding 5 to 20 cm 3 of blood. In total, approximately 60 cm 3 of fluid was aspirated; however, repeated attempts were limited by clotting, and the patient remained in a PEA arrest with visible cardiac contractility on bedside ultrasound. During the code, a surgical consultation was obtained. An emergent left-sided anterolateral thoracotomy was performed. Upon incision of the pericardium, a large amount of tense bloody fluid was released, and the patient regained cardiac activity and peripheral pulses. Twenty-eight minutes elapsed from initial PEA arrest to completion of the thoracotomy and ROSC. Of significance, the patient was noted to have inflammatory adhesions in the pericardial sack. Upon further exploration in the operating room, the patient was found to have multiple sources of slowly oozing blood without any lesion that required ligation. The patient had a 6-week hospital stay complicated by pneumonia and a prolonged ventilator wean. During the course of her care, her antinuclear antibody returned strongly positive, and the etiology of the tamponade was attributed to systemic lupus erythematous. The patient was discharged to a long-term care facility. Approximately 5 months after initial presentation, the patient had recovered to her baseline state of health and was neurologically intact. Case #2: A 65-year-old woman was admitted to a community, level 2 trauma center with a diagnosis of chest pain. The patient had a medical history that included lymphoma, congestive heart failure, hypothyroidism, and thrombocytopenia. Several hours after admission, the patient had agonal breathing that progressed to a PEA arrest. Cardiopulmonary resuscitation (CPR) was initiated, and the patient's airway was secured. During the cardiac arrest, the patient received epinephrine, atropine, calcium, bicarbonate, and a normal saline bolus without return of spontaneous circulation. A simultaneous review of the record noted that a prior computed tomography of the chest (Fig. 2) showed a large pericardial effusion. Laboratory data revealed a white blood cell count of 82 000 and platelets of 32 000. An echocardiogram was immediately obtained which showed a massive pericardial effusion. An ultrasoundguided percardiocentesis with an 18-gauge spinal needle was performed, yielding 50 to 60 cm 3 of serous fluid. Cardiac motion was observed to improve marginally with the fluid removal; however, the patient did not regain pulses. A repeat pericardiocentesis was performed yielding 60 cm 3 of additional fluid. The echo showed no significant reduction in the size of the effusion, and ROSC was not achieved.
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K.A. Corl et al. / American Journal of Emergency Medicine 33 (2015) 600.e5–600.e7
Fig. 1. A chest x-ray taken 2 years prior and on the day of presentation showing significant cardiomegaly.
Given the lack of response to aspiration, an emergent left-sided anterolateral thoracotomy was performed. Upon dissecting through the intracostal muscles, the distended pericardium was incised, as parts of it were adherent to the chest wall. An estimated 500 cm 3 of serosanguineous fluid was released, and after a brief period of cardiac massage, the patient regained spontaneous circulation. The time elapsed between the initial PEA arrest and completion of thoracotomy was 29 minutes. The cardiothoracic surgeon was consulted, and the patient was further resuscitated with blood transfusions, vasopressors, and normal saline, while the operating team was assembled. Operative exploration showed fibrinous matter inside the pericardium without active bleeding consistent with a malignant effusion. The patient survived the initial arrest and operation; however, at 48 hours postoperatively, she remained on multiple vasopressors in the cardiothoracic intensive care unit. At this time, resuscitative efforts were withdrawn per family request, and the patient died.
Fig. 2. A computed tomography of the chest showing a massive pericardial effusion on the day of admission.
Resuscitative thoracotomy is widely accepted and recommend as a treatment modality for patients with penetrating and, under some circumstances, blunt traumatic arrest [3]. A large meta-analysis reviewing 25 years of trauma data with 4620 patients showed a combined survival rate of 7.4%. Among the subset, where the location of major injury was cardiac, the rate increases to 19.4% [4]. Open chest cardiac massage was a common and accepted practice for nontraumatic arrest during the first half of the 20th century [5]. In 1953, Stephenson et al [6] presented a case series of 1200 arrests managed with open chest cardiac massage; 28% of the patients survived to discharge with a favorable neurologic outcome. The practice became less popular in 1960 when Jude et al [7] showed that closed chest compressions were an effective alternative. Since this time, the research has been limited to a handful of clinical trials, case reports, and animal models. Research in canine models provides the most substantial supportive evidence for the use of open chest CPR (OCCPR). Bircher et al [8] showed that when the dogs received 30 minutes of OCCPR before defibrillation, nearly all survived with a favorable neurologic outcome, compared with standard CPR, where nearly all died or had a poor neurologic outcome. Because OCCPR is a deviation from what is currently accepted to be standard care, most human studies are limited to patients who have failed standard CPR or have had prolonged resuscitations. A clear criticism of this data is that the opportunity to intervene when the physiologic conditions may be amenable to OCCPR is missed. This was substantiated in a canine study that showed if OCCPR was initiated within the first 20 minutes of untreated ventricular fibrillation, all animals were resuscitated, compared with poor long-term survival in a 20 to 40-minute window and 100% mortality after 40 minutes [9]. Contemporary data from human clinical trials are limited. A 1995 study that enrolled 10 patients who failed standard CPR (average arrest time, 54 minutes) showed that the mean coronary perfusion pressures were 4.5 times higher in patients receiving OCCPR [10]. Notably, this study had 3 OCCPR survivors who were initially considered to be unsalvageable. A subsequent study underscored the limitations of using OCCPR as a rescue therapy, where there was 100% mortality associated with prolonged delays in initiation of the resuscitative efforts [11]. More recently, there are case reports documenting successful resuscitative thoracotomies for medical arrests, all secondary to cardiac tamponade physiology. One report documents a patient who 24 days after admission to a trauma service developed constrictive pericarditis leading to a PEA arrest who regained ROSC with
K.A. Corl et al. / American Journal of Emergency Medicine 33 (2015) 600.e5–600.e7
thoracotomy after pericardiocentesis failed [12]. Two subsequent reports describe tamponade refractory to pericardiocentesis secondary to a type-A aortic dissection [13] and as a complication of cardiac ablation [14]. Both patients were managed successfully with resuscitative thoracotomy. We present 2 cases, where patients in PEA arrest secondary to tamponade, who failed serial pericardiocentesis, were managed with a resuscitative thoracotomy. Both patients survived the initial PEA arrest and subsequent operative management; however, only the first patient survived until discharge. Although pericardiocentesis remains the firstline treatment for nontraumatic PEA arrest secondary to tamponade, we believe that these cases support the use of resuscitative thoracotomy in select cases that are refractory to standard care. Moreover, these cases and a review of the literature suggest that if thoracotomy and OCCPR are to be viable options, these must be initiated early in the resuscitation effort. A preplanned and coordinated effort between the emergency department and surgical service is necessary to obtain optimal outcomes.
Keith A. Corl, MD, FACEP Department of Critical Care Medicine The Warren Alpert Medical School of Brown University Rhode Island Hospital, Providence RI Corresponding author. Department of Critical Care 593 Eddy St, Providence RI 02903 Tel.: +1 401 793 4501 E-mail address: [email protected] Wade N. Sears, MD, FACEP Fremont Emergency Medicine Services and ACES Sunrise Hospital, Las Vegas NV Shea C. Gregg, MD Section of Trauma, Burns, and Surgical Critical Care Bridgeport Hospital, Bridgeport CT
600.e7
David G. Lindquist, MD, FACEP Department of Emergency Medicine The Warren Alpert Medical School of Brown University Rhode Island Hospital, Providence RI
http://dx.doi.org/10.1016/j.ajem.2014.09.015
References [1] Spodick D. Acute cardiac tamponade. N Engl J Med 2003;349:684–90. [2] Tsang T, Barnes M, Hayes S, Freeman W, Dearani J, Butler S, et al. Clinical and echocardiographic characteristics of significant pericardial effusions following cardiothoracic surgery and outcomes of echo-guided pericardiocentesis for management: Mayo Clinic experience 1979-1998. Chest 1999;116:322–31. [3] Advanced trauma life support (ATLS®): the ninth edition. J Trauma Acute Care Surg 2013;74(5):1363–6. [4] Rhee PM, Acosta Jose, Bridgeman Amy. Survival after emergency department thoracotomy: review of published data from the past 25 years. J Am Coll Surg 2000;190: 288–98. [5] Vallejo-Manzur F, Varon J, Fromm Jr R, Baskett P. Moritz Schiff and the history of open-chest cardiac massage. Resuscitation 2002;53:3–5. [6] Stephenson H, Reid C, Hinton J. Some common denominators in 1200 cases of cardiac arrest. Ann Surg 1953;137:1–44. [7] Jude J, Kouwenhoven W, Knickerbocker G. Closed-chest cardiac massage. JAMA 1960;173:1064–7. [8] Bircher N, Safar P. Cerebral preservation during cardiopulmonary resuscitation. Crit Care Med 1985;13:185–90. [9] Kern K, Sanders A, Janas W, Nelson J, Badylak S, Babbs C, et al. Limitations of openchest cardiac massage after prolonged, untreated cardiac arrest in dogs. Ann Emerg Med 1991;20:761–7. [10] Boczar M, Howard M, Rivers E, Martin G, Horst H, Lewandowski C, et al. A technique revised: hemodynamic comparison of closed-and open chest-cardiac massage during human cardiopulmonary resuscitation. Crit Care Med 1995;23:498–503. [11] Geehr E, Auerbach P. Open-chest cardiac massage for victims of medical cardiac arrest. Ann Emerg Med 1985;178:498. [12] Schweitzer J, Nirula R, Romero J. Successful emergent thoracotomy for pericardial tamponade caused by late constrictive pericarditis after trauma. J Trauma 2001; 50(5):945–8. [13] Keiko T, Yanagawa Y, Isoda S. A successful treatment of cardiac tamponade due to an aortic dissection using open-chest massage. Am J Emerg Med 2012;30(4):634.e1–2. [14] Wyatt T, Haug E. Modified emergency department thoracotomy for postablation cardiac tamponade. Ann Emerg Med 2012;59(4):265–7.
Contents lists available at ScienceDirect
American Journal of Emergency Medicine journal homepage: www.elsevier.com/locate/ajem
Case Report
Resuscitative thoracotomy for nontraumatic pericardial tamponade: case reports and review of the literature☆,☆☆,★ Abstract Nontraumatic cardiac tamponade is a life-threatening process, and pericardiocentesis is the established treatment designed to relieve tamponade physiology during a cardiac arrest. We report 2 cases, where after traditional resuscitation including serial pericardiocentesis failed, a resuscitative thoracotomy was performed. Cardiac tamponade is a life-threatening condition that results from an accumulation of fluid, blood, pus, clots, or gas in the pericardial space leading to compression of the heart and limitations in cardiac output [1]. In nontraumatic cases, pericardiocentesis is the established modality of treatment and has been shown to be effective in a majority of patients [2]; however, there are circumstances where the procedure fails to correct tamponade physiology. We present 2 cases of pulseless electrical activity arrest secondary to cardiac tamponade; the first being secondary to an inflammatory effusion and the second to a malignant effusion. The patients were managed with resuscitative thoracotomy after traditional resuscitation using advanced cardiac life support algorithms, and serial pericardiocenteses proved unsuccessful. Case #1: A 58-year-old woman presented to a tertiary, academic emergency department with a chief complaint of dyspnea and generalized weakness. The patient had presented 2 days earlier to the same emergency department with left-sided chest pain and dyspnea but then left against medical advice after a chest x-ray (Fig. 1). On the second presentation, the patient had an initial blood pressure of 127/84 mm Hg, heart rate of 107 beats per minute, respiratory rate of 18 breaths per minute, an oxygen saturation of 99% on room air, and a temperature of 97.4°F. Medical history included paroxysmal atrial fibrillation, hypertension, and a right middle cerebral artery aneurysm repair 8 years prior. On physical examination, the patient appeared to be in no acute distress. Lung fields were clear to auscultation, heart sounds were regular and audible, her abdomen was soft and nontender, and the extremities had no significant edema. Approximately 90 minutes into her emergency department stay, the patient was directly observed by staff to abruptly collapse secondary to a PEA arrest. Chest compressions were initiated; an endotracheal tube was secured; and epinephrine, atropine, calcium, bicarbonate, and normal saline were administered without return of spontaneous circulation (ROSC). The prior chest x-ray obtained before arrest was notable for cardiomegaly (Fig. 1), and an intraarrest bedside echocardiography showed pericardial tamponade. Ultrasound☆ Funding: None. ☆☆ Previously presented: No. ★ Conflicts of interest: All authors have no conflicts of interest.
0735-6757/© 2014 Elsevier Inc. All rights reserved.
guided pericardiocentesis was performed using an 18-gauge spinal needle that yielded 20 cm 3 of dark clotted blood. The patient was then noted to be in ventricular fibrillation and was defibrillated; however, the patient did not have return of spontaneous circulation. The code continued, and 4 subsequent pericardiocenteses were performed yielding 5 to 20 cm 3 of blood. In total, approximately 60 cm 3 of fluid was aspirated; however, repeated attempts were limited by clotting, and the patient remained in a PEA arrest with visible cardiac contractility on bedside ultrasound. During the code, a surgical consultation was obtained. An emergent left-sided anterolateral thoracotomy was performed. Upon incision of the pericardium, a large amount of tense bloody fluid was released, and the patient regained cardiac activity and peripheral pulses. Twenty-eight minutes elapsed from initial PEA arrest to completion of the thoracotomy and ROSC. Of significance, the patient was noted to have inflammatory adhesions in the pericardial sack. Upon further exploration in the operating room, the patient was found to have multiple sources of slowly oozing blood without any lesion that required ligation. The patient had a 6-week hospital stay complicated by pneumonia and a prolonged ventilator wean. During the course of her care, her antinuclear antibody returned strongly positive, and the etiology of the tamponade was attributed to systemic lupus erythematous. The patient was discharged to a long-term care facility. Approximately 5 months after initial presentation, the patient had recovered to her baseline state of health and was neurologically intact. Case #2: A 65-year-old woman was admitted to a community, level 2 trauma center with a diagnosis of chest pain. The patient had a medical history that included lymphoma, congestive heart failure, hypothyroidism, and thrombocytopenia. Several hours after admission, the patient had agonal breathing that progressed to a PEA arrest. Cardiopulmonary resuscitation (CPR) was initiated, and the patient's airway was secured. During the cardiac arrest, the patient received epinephrine, atropine, calcium, bicarbonate, and a normal saline bolus without return of spontaneous circulation. A simultaneous review of the record noted that a prior computed tomography of the chest (Fig. 2) showed a large pericardial effusion. Laboratory data revealed a white blood cell count of 82 000 and platelets of 32 000. An echocardiogram was immediately obtained which showed a massive pericardial effusion. An ultrasoundguided percardiocentesis with an 18-gauge spinal needle was performed, yielding 50 to 60 cm 3 of serous fluid. Cardiac motion was observed to improve marginally with the fluid removal; however, the patient did not regain pulses. A repeat pericardiocentesis was performed yielding 60 cm 3 of additional fluid. The echo showed no significant reduction in the size of the effusion, and ROSC was not achieved.
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K.A. Corl et al. / American Journal of Emergency Medicine 33 (2015) 600.e5–600.e7
Fig. 1. A chest x-ray taken 2 years prior and on the day of presentation showing significant cardiomegaly.
Given the lack of response to aspiration, an emergent left-sided anterolateral thoracotomy was performed. Upon dissecting through the intracostal muscles, the distended pericardium was incised, as parts of it were adherent to the chest wall. An estimated 500 cm 3 of serosanguineous fluid was released, and after a brief period of cardiac massage, the patient regained spontaneous circulation. The time elapsed between the initial PEA arrest and completion of thoracotomy was 29 minutes. The cardiothoracic surgeon was consulted, and the patient was further resuscitated with blood transfusions, vasopressors, and normal saline, while the operating team was assembled. Operative exploration showed fibrinous matter inside the pericardium without active bleeding consistent with a malignant effusion. The patient survived the initial arrest and operation; however, at 48 hours postoperatively, she remained on multiple vasopressors in the cardiothoracic intensive care unit. At this time, resuscitative efforts were withdrawn per family request, and the patient died.
Fig. 2. A computed tomography of the chest showing a massive pericardial effusion on the day of admission.
Resuscitative thoracotomy is widely accepted and recommend as a treatment modality for patients with penetrating and, under some circumstances, blunt traumatic arrest [3]. A large meta-analysis reviewing 25 years of trauma data with 4620 patients showed a combined survival rate of 7.4%. Among the subset, where the location of major injury was cardiac, the rate increases to 19.4% [4]. Open chest cardiac massage was a common and accepted practice for nontraumatic arrest during the first half of the 20th century [5]. In 1953, Stephenson et al [6] presented a case series of 1200 arrests managed with open chest cardiac massage; 28% of the patients survived to discharge with a favorable neurologic outcome. The practice became less popular in 1960 when Jude et al [7] showed that closed chest compressions were an effective alternative. Since this time, the research has been limited to a handful of clinical trials, case reports, and animal models. Research in canine models provides the most substantial supportive evidence for the use of open chest CPR (OCCPR). Bircher et al [8] showed that when the dogs received 30 minutes of OCCPR before defibrillation, nearly all survived with a favorable neurologic outcome, compared with standard CPR, where nearly all died or had a poor neurologic outcome. Because OCCPR is a deviation from what is currently accepted to be standard care, most human studies are limited to patients who have failed standard CPR or have had prolonged resuscitations. A clear criticism of this data is that the opportunity to intervene when the physiologic conditions may be amenable to OCCPR is missed. This was substantiated in a canine study that showed if OCCPR was initiated within the first 20 minutes of untreated ventricular fibrillation, all animals were resuscitated, compared with poor long-term survival in a 20 to 40-minute window and 100% mortality after 40 minutes [9]. Contemporary data from human clinical trials are limited. A 1995 study that enrolled 10 patients who failed standard CPR (average arrest time, 54 minutes) showed that the mean coronary perfusion pressures were 4.5 times higher in patients receiving OCCPR [10]. Notably, this study had 3 OCCPR survivors who were initially considered to be unsalvageable. A subsequent study underscored the limitations of using OCCPR as a rescue therapy, where there was 100% mortality associated with prolonged delays in initiation of the resuscitative efforts [11]. More recently, there are case reports documenting successful resuscitative thoracotomies for medical arrests, all secondary to cardiac tamponade physiology. One report documents a patient who 24 days after admission to a trauma service developed constrictive pericarditis leading to a PEA arrest who regained ROSC with
K.A. Corl et al. / American Journal of Emergency Medicine 33 (2015) 600.e5–600.e7
thoracotomy after pericardiocentesis failed [12]. Two subsequent reports describe tamponade refractory to pericardiocentesis secondary to a type-A aortic dissection [13] and as a complication of cardiac ablation [14]. Both patients were managed successfully with resuscitative thoracotomy. We present 2 cases, where patients in PEA arrest secondary to tamponade, who failed serial pericardiocentesis, were managed with a resuscitative thoracotomy. Both patients survived the initial PEA arrest and subsequent operative management; however, only the first patient survived until discharge. Although pericardiocentesis remains the firstline treatment for nontraumatic PEA arrest secondary to tamponade, we believe that these cases support the use of resuscitative thoracotomy in select cases that are refractory to standard care. Moreover, these cases and a review of the literature suggest that if thoracotomy and OCCPR are to be viable options, these must be initiated early in the resuscitation effort. A preplanned and coordinated effort between the emergency department and surgical service is necessary to obtain optimal outcomes.
Keith A. Corl, MD, FACEP Department of Critical Care Medicine The Warren Alpert Medical School of Brown University Rhode Island Hospital, Providence RI Corresponding author. Department of Critical Care 593 Eddy St, Providence RI 02903 Tel.: +1 401 793 4501 E-mail address: [email protected] Wade N. Sears, MD, FACEP Fremont Emergency Medicine Services and ACES Sunrise Hospital, Las Vegas NV Shea C. Gregg, MD Section of Trauma, Burns, and Surgical Critical Care Bridgeport Hospital, Bridgeport CT
600.e7
David G. Lindquist, MD, FACEP Department of Emergency Medicine The Warren Alpert Medical School of Brown University Rhode Island Hospital, Providence RI
http://dx.doi.org/10.1016/j.ajem.2014.09.015
References [1] Spodick D. Acute cardiac tamponade. N Engl J Med 2003;349:684–90. [2] Tsang T, Barnes M, Hayes S, Freeman W, Dearani J, Butler S, et al. Clinical and echocardiographic characteristics of significant pericardial effusions following cardiothoracic surgery and outcomes of echo-guided pericardiocentesis for management: Mayo Clinic experience 1979-1998. Chest 1999;116:322–31. [3] Advanced trauma life support (ATLS®): the ninth edition. J Trauma Acute Care Surg 2013;74(5):1363–6. [4] Rhee PM, Acosta Jose, Bridgeman Amy. Survival after emergency department thoracotomy: review of published data from the past 25 years. J Am Coll Surg 2000;190: 288–98. [5] Vallejo-Manzur F, Varon J, Fromm Jr R, Baskett P. Moritz Schiff and the history of open-chest cardiac massage. Resuscitation 2002;53:3–5. [6] Stephenson H, Reid C, Hinton J. Some common denominators in 1200 cases of cardiac arrest. Ann Surg 1953;137:1–44. [7] Jude J, Kouwenhoven W, Knickerbocker G. Closed-chest cardiac massage. JAMA 1960;173:1064–7. [8] Bircher N, Safar P. Cerebral preservation during cardiopulmonary resuscitation. Crit Care Med 1985;13:185–90. [9] Kern K, Sanders A, Janas W, Nelson J, Badylak S, Babbs C, et al. Limitations of openchest cardiac massage after prolonged, untreated cardiac arrest in dogs. Ann Emerg Med 1991;20:761–7. [10] Boczar M, Howard M, Rivers E, Martin G, Horst H, Lewandowski C, et al. A technique revised: hemodynamic comparison of closed-and open chest-cardiac massage during human cardiopulmonary resuscitation. Crit Care Med 1995;23:498–503. [11] Geehr E, Auerbach P. Open-chest cardiac massage for victims of medical cardiac arrest. Ann Emerg Med 1985;178:498. [12] Schweitzer J, Nirula R, Romero J. Successful emergent thoracotomy for pericardial tamponade caused by late constrictive pericarditis after trauma. J Trauma 2001; 50(5):945–8. [13] Keiko T, Yanagawa Y, Isoda S. A successful treatment of cardiac tamponade due to an aortic dissection using open-chest massage. Am J Emerg Med 2012;30(4):634.e1–2. [14] Wyatt T, Haug E. Modified emergency department thoracotomy for postablation cardiac tamponade. Ann Emerg Med 2012;59(4):265–7.
