The number of patients arriving at hospitals in extremis, rather than expiring in the prehospital setting, has increased due to the maturation of regionalized trauma systems (see Chapter 4). Salvage of individuals with imminent cardiac arrest or those already undergoing cardiopulmonary resuscitation (CPR) often requires immediate thoracotomy as an integral component of their initial resuscitation in the emergency department (ED). The optimal application of emergency department thoracotomy (EDT) requires a thorough understanding of its physiologic objectives, technical maneuvers, and the cardiovascular and metabolic consequences. Although, resuscitative endovascular balloon occlusion of the aorta (REBOA) has been advocated as a resuscitation maneuver that should replace EDT, there is no objective data to substantiate this proposal and we believe its clear role at this moment is for unstable pelvic fractures with advanced hemorrhagic shock (see Chapter 35). This chapter reviews the features of EDT and highlights the specific clinical indications, all of which are essential for the appropriate use of this potentially life-saving yet costly procedure.

Emergent thoracotomy came into use for the treatment of heart wounds and anesthesia-induced cardiac arrest in the late 1800s and early 1900s.¹ The concept of a thoracotomy as a resuscitative measure began with Schiff’s promulgation of open cardiac massage in 1874.¹ Block first suggested the potential application of this technique for penetrating chest wounds and heart lacerations in 1882.² Following use of the technique in animal models, the first successful suture repair of a cardiac wound in a human was performed at the turn of the century.³ Subsequently, Igelsbrud described the successful resuscitation of a patient sustaining cardiac arrest during a surgical procedure using emergent thoracotomy with open cardiac massage.¹ The utility of the emergent thoracotomy was beginning to be tested in a wide range of clinical scenarios in the early 1900s.

With improvement in patient resuscitation and an ongoing evaluation of patient outcomes, the indications for emergent thoracotomy shifted. Initially, cardiovascular collapse from medical causes was the most common reason for thoracotomy in the early 1900s. The demonstrated efficacy of closed-chest compression by Kouwenhoven et al.⁴ in 1960 and the introduction of external defibrillation in 1965 by Zoll et al.⁵ virtually eliminated the practice of open-chest resuscitation for medical cardiac arrest. Indications for emergent thoracotomy following trauma also became more limited. In 1943, Blalock and Ravitch advocated the use of pericardiocentesis rather than thoracotomy as the preferred treatment for postinjury cardiac tamponade.⁶ In the late 1960s, however, refinements in cardiothoracic surgical techniques reestablished the role of immediate thoracotomy for salvaging patients with life-threatening chest wounds.⁷ The use of temporary thoracic aortic occlusion in patients with exsanguinating abdominal hemorrhage further expanded the indications for emergent thoracotomy.^8,9 In the past two decades, critical analyses of patient outcomes following postinjury EDT has tempered the unbridled enthusiasm for this technique, allowing a more selective approach with clearly defined indications.^{10,11,12,13,14,15}

The literature addressing EDT appears confusing, likely due to widely varying terminology. As a result, there is a lack of agreement among physicians regarding the specific indications for EDT as well as the definition of “signs of life.”¹⁶ In this chapter, EDT refers to a thoracotomy performed in the ED for patients arriving in extremis. At times, the term EDT is used interchangeably with the term resuscitative thoracotomy; however, this should not be confused with a thoracotomy that is performed in the operating room (OR) or intensive care unit (ICU) within hours after injury for delayed physiologic deterioration. The value of an indication for EDT for acute resuscitation may also be confusing because of the variety of indices used to characterize the patient’s physiologic status prior to thoracotomy. Because there have been a wide range of indications for which EDT has been performed in different trauma centers, comparisons in the literature are difficult. The authors define “no signs of life” as no detectable blood pressure, respiratory or motor effort, cardiac electrical activity, or pupillary activity (ie, clinical death). Patients with “no vital signs” have no palpable blood pressure, but demonstrate electrical activity, respiratory effort, or pupillary reactivity.

The primary objectives of EDT are to (a) release pericardial tamponade, (b) control cardiac hemorrhage, (c) control intrathoracic bleeding, (d) evacuate massive air embolism, (e) perform open cardiac massage, and (f) temporarily occlude the descending thoracic aorta. Combined, these objectives attempt to address the primary issue of cardiovascular collapse from mechanical sources or extreme hypovolemia.

Release Pericardial Tamponade and Control Cardiac Hemorrhage

The highest survival rate following EDT is in patients with penetrating cardiac wounds, especially when associated with pericardial tamponade.⁷ Early recognition of cardiac tamponade, prompt pericardial decompression, and control of cardiac hemorrhage are the key components to successful EDT and patient survival following penetrating wounds to the heart (see Chapter 26).¹⁷ The egress of blood from the injured heart, regardless of mechanism, results in tamponade physiology. Rising intrapericardial pressure produces abnormalities in hemodynamic and cardiac perfusion that can be divided into three phases.¹⁸ Initially, increased pericardial pressure restricts ventricular diastolic filling and reduces subendocardial blood flow.¹⁹ Cardiac output under these conditions is maintained by compensatory tachycardia, increased systemic vascular resistance, and elevated central pressure (ie, ventricular filling pressure). In the intermediate phase of tamponade, rising pericardial pressure further compromises diastolic filling, stroke volume, and coronary perfusion, resulting in diminished cardiac output. Although, blood pressure may be maintained deceptively well, subtle signs of shock (eg, anxiety, diaphoresis, and pallor) become evident. During the final phase of tamponade, compensatory mechanisms fail as the intrapericardial pressure approaches the ventricular filling pressure. Cardiac arrest ensues as profound coronary hypoperfusion occurs.

The classic description of clinical findings, Beck’s triad, is rarely observed in the ED; therefore, a high index of suspicion in the at-risk patient sustaining penetrating torso trauma is crucial, with prompt intervention essential. In the first two phases of cardiac tamponade, patients may be aggressively managed with definitive airway control, volume resuscitation to increase preload, and pericardiocentesis. The patient in the third phase of tamponade, with profound hypotension (systolic blood pressure [SBP] < 60 mm Hg), should undergo EDT rather than pericardiocentesis as the management for evacuation of pericardial blood. Following release of tamponade, the source of tamponade can be directly controlled with appropriate interventions based on the underlying injury (see Technical Details of EDT).²⁰

Control Intrathoracic Hemorrhage

Life-threatening intrathoracic hemorrhage occurs in less than 5% of patients following penetrating injury presenting to the ED, and in even lower percentage of patients sustaining blunt trauma.²¹ The most common injuries include penetrating wounds to the pulmonary hilum and great vessels; less commonly seen are torn descending thoracic aortic injuries with frank rupture or penetrating cardiac wounds exsanguinating into the thorax through a traumatic pericardial window. There is a high mortality rate in injuries to the pulmonary or thoracic great-vessel lacerations due to the lack of hemorrhage containment by adjacent tissue tamponade or vessel spasm (see Chapters 25 and 26). Either hemithorax can rapidly accommodate more than half of a patient’s total blood volume before overt physical signs of hemorrhagic shock occur. Therefore, a high clinical suspicion is warranted in patients with penetrating torso trauma, particularly in those with hemodynamic decompensation. Patients with exsanguinating wounds require EDT with rapid control of the source of hemorrhage if they are to be salvaged.

Perform Open Cardiac Massage

External chest compression provides approximately 20–25% of baseline cardiac output, with 10–20% of normal cerebral perfusion.²² This degree of vital organ perfusion can provide reasonable salvage rates for 15 minutes, but few normothermic patients survive 30 minutes of closed-chest compression. Moreover, in models of inadequate intravascular volume (hypovolemic shock) or restricted ventricular filling (pericardial tamponade), external chest compression fails to augment arterial pressure or provide adequate systemic perfusion; the associated low diastolic volume and pressure result in inadequate coronary perfusion.²³ Therefore, closed cardiac massage is ineffective for postinjury cardiopulmonary arrest. The only potential to salvage the injured patient with ineffective circulatory status is immediate EDT.

Achieve Thoracic Aortic Cross-Clamping

The rationale for temporary thoracic aortic occlusion in the patient with massive hemorrhage is two fold. First, in patients with hemorrhagic shock, aortic cross-clamping redistributes the patient’s limited blood volume to the myocardium and brain.⁹ Second, patients sustaining intra-abdominal injury may benefit from aortic cross-clamping due to reduction in subdiaphragmatic blood loss.⁸ Temporary thoracic aortic occlusion augments aortic diastolic and carotid SBP, enhancing coronary as well as cerebral perfusion.²⁴ Canine studies have shown that the left ventricular stroke-work index and myocardial contractility increase in response to thoracic aortic occlusion during hypovolemic shock.²⁵ These improvements in myocardial function occur without an increase in the pulmonary capillary wedge pressure or a significant change in systemic vascular resistance. Thus, improved coronary perfusion resulting from an increased aortic diastolic pressure presumably accounts for the observed enhancement in contractility.²⁶

These experimental observations suggest that temporary aortic occlusion is valuable in patients with either shock due to nonthoracic trauma or continued shock following the repair of cardiac or other exsanguinating wounds. Indeed, occlusion of the descending thoracic aorta appears to increase the return of spontaneous circulation following CPR.²⁷ Reports of successful resuscitation using EDT in patients in hemorrhagic shock and even sustaining cardiac arrest following extremity and cervical injuries exist.²⁸ In these situations, EDT may be a temporizing measure until the patient’s circulating blood volume can be replaced by blood product transfusion. However, once the patient’s blood volume has been restored, the aortic cross-clamp should be removed. Thoracic cross-clamping in the normovolemic patient may be deleterious because of increased myocardial oxygen demands resulting from the increased systemic vascular resistance.²⁹ Careful application of this technique is warranted as there is substantial metabolic cost and a finite risk of paraplegia associated with the procedure.^30,31,32 However, in carefully selected patients, aortic cross-clamping may effectively redistribute the patient’s blood volume until external replacement and control of the hemorrhagic source is possible. Complete removal of the aortic cross-clamp or replacement of the clamp below the renal vessel should be performed within 30 minutes; the gut’s tolerance to normothermic ischemia is 30–45 minutes.

Evacuate Bronchovenous Air Embolism

Bronchovenous air embolism can be a subtle entity following thoracic trauma, and is likely to be much more common than is recognized.^33,34,35 The clinical scenario typically involves a patient sustaining penetrating chest injury who precipitously develops profound hypotension or cardiac arrest following endotracheal intubation and positive-pressure ventilation. Traumatic alveolovenous communications produce air emboli that migrate to the coronary arterial systems; any impedance in coronary blood flow causes global myocardial ischemia and resultant shock. The production of air emboli is enhanced by the underlying physiology—there is relatively low intrinsic pulmonary venous pressure due to associated intrathoracic blood loss and high bronchoalveolar pressure from assisted positive-pressure ventilation. This combination increases the gradient for air transfer across bronchovenous channels.³⁶ Although, more often observed in penetrating trauma, a similar process may occur in patients with blunt lacerations of the lung parenchyma (see Chapter 25).

Immediate thoracotomy with pulmonary hilar cross-clamping prevents further propagation of pulmonary venous air embolism. Thoracotomy with opening of the pericardium also provides access to the cardiac ventricles; with the patient in the Trendelenburg’s position (done to trap to air in the apex of the left ventricle), needle aspiration is performed to remove air from the cardiac chambers. Additionally, vigorous cardiac massage may promote dissolution of air already present in the coronary arteries.³⁵ Aspiration of the aortic root is done to alleviate any accumulated air pocket, and direct needle aspiration of the right coronary artery may be attempted.

The value of EDT in resuscitation of the patient in profound shock but not yet dead is unquestionable. Its indiscriminate use, however, renders it a low-yield and high-cost procedure.^14,37,38,39 In the past three decades there has been a significant clinical shift in the performance of EDT, from a nearly obligatory procedure before declaring any trauma patient to very few patients undergoing EDT. During this swing of the pendulum, several groups have attempted to elucidate the clinical guidelines for EDT. In 1979, we conducted a critical analysis of 146 consecutive patients undergoing EDT and suggested a selected approach to its use in the moribund trauma patient, based on consideration of the following variables: (1) location and mechanism of injury, (2) signs of life at the scene and on admission to the ED, (3) cardiac electrical activity at thoracotomy, and (4) SBP response to thoracic aortic cross-clamping.³⁹

To validate these clinical guidelines, we established a prospective study in which these data were carefully documented in all patients at the time of thoracotomy. In 1982, the first 400 patients were analyzed.³⁸ A more recent review has summarized the data on 868 patients who have undergone EDT at the Denver Health Medical Center.⁴⁰ Of these, 676 (78%) were dead in the ED, 128 (15%) died in the OR, and 23 (3%) succumbed to multiple organ failure in the surgical ICU. Ultimately, 41 (5%) patients survived, and 34 recovered fully without neurologic sequelae. Although, this yield may seem low, it is important to emphasize that thoracotomy was done on virtually every trauma patient delivered to the ED. In fact, 624 (72%) were without vital signs in the field, and 708 patients (82%) had no vital signs at the time of presentation to the ED. In contrast, it is equally important to stress that patients without signs of life at the scene but who responded favorably to resuscitation were excluded from this analysis because they did not require EDT; these patients remind the practitioner that prehospital clinical assessments may not always be reliable in triaging these severely injured patients. Indeed, the authors have salvaged a number of individuals sustaining blunt and penetrating trauma who were assessed to have no signs of life at the scene of injury.

The survival rate and percentage of neurologic impairment following EDT vary considerably, due to the heterogeneity of patient populations reported in the literature. As previously discussed, critical determinants of survival include the mechanism and location of injury and the patient’s physiologic condition at the time of thoracotomy.^41,42,43 We have attempted to elucidate the impact of these factors in ascertaining the success rate of EDT by collating data from a number of clinical series reporting on 50 or more patients (Table 14-1). Unfortunately, inconsistencies in patient stratification and a paucity of clinical details limit objective analysis of these data. Although, some reviews provide a specific breakdown of the injury mechanism and clinical status of patients presenting to the ED, others combine all injury mechanisms. We believe it is crucial to stratify patients according to the location and mechanism of injury as well as the status of signs of life (ie, blood pressure, respiratory effort, cardiac electrical activity, and pupillary activity).

The data summarized to date confirm that EDT has the highest survival rate following isolated cardiac injury (Table 14-1). An average of 35% of adult patients presenting in shock, defined as an SBP <70 mm Hg, and 20% without vital signs were salvaged after isolated penetrating injury to the heart if EDT was performed. In contrast, only 1–3% of blunt trauma patients undergoing EDT survive, regardless of clinical status on presentation. Following penetrating torso injuries, 14% of patients requiring EDT are salvaged if they are hypotensive with detectable vital signs, whereas 8% of those who have no vital signs but have signs of life at presentation, and 1% of those without signs of life are salvaged. These findings are reiterated by a recent report incorporating all patients undergoing EDT for either blunt or penetrating mechanism from 24 separate studies⁴²; survival rates for patients undergoing EDT for penetrating injuries was 8.8% and 1.4% for blunt mechanisms. Additionally, more patients survive EDT for isolated cardiac wounds (19.4%) followed by stab wounds (16.8%) and gunshot wounds (4.3%).

Although, there is a clear role for EDT in the patient presenting in shock but with measurable vital signs, there is disagreement about its use in the patient population undergoing CPR prior to arrival in the ED. Although, there have been multiple reports with low survival rates and dismal outcomes following prehospital CPR, termination of resuscitation in the field should not be performed in all patients.⁴⁴ Our most recent evaluation, spanning 26 years of experience, indicates EDT does play a significant role in the critically injured patient undergoing prehospital CPR.¹⁰ The majority of patients arriving in extremis who survived to discharge sustained a stab wound to the torso, consistent with previous reports. Additionally, over 80% of patients were neurologically intact at discharge. In this study, clear guidelines for the use of EDT as a resuscitative measure to ensure that all potentially salvageable patients were proposed. EDT should be performed for blunt trauma and penetrating non-torso trauma with CPR less than 5 minutes, and in penetrating torso trauma if less than 15 minutes of CPR.¹⁰

To further define the limits of EDT, a prospective, multicenter trial was performed by the Western Trauma Association (WTA).¹² The WTA data substantiate that injury mechanism alone is not a discriminator of futility. Specifically, with the exception of an overtly devastating head injury, blunt trauma does not prohibit meaningful survival, even with requirements for CPR. This multicenter experience suggests current indications for EDT (Table 14-2). Specifically, EDT is unlikely to yield productive survival when patients: (1) sustain blunt trauma and require >10 minutes of prehospital CPR, (2) have penetrating wounds and undergo >15 minutes of prehospital CPR, (3) have isolated extremity trauma with >5 minutes or prehospital CPR, or (4) manifest asystole without pericardial tamponade. We recognize, however, that there will invariably be exceptions to the recorded literature.^28,41,45,46

Emerging data indicate the clinical results in the pediatric population mirror that of the adult experience (Table 14-3). One might expect that children would have a more favorable outcome compared to adults, due to improved results following head injury (see Chapter 43); however, this has not been borne out in multiple studies.^{47,48,49,50,51,52,53} Beaver et al. reported no survivors among 27 patients, from 15 months to 14 years of age, undergoing postinjury EDT at Johns Hopkins Hospital.⁴⁹ Powell et al., at the South Alabama Medical Center, described an overall survival of 20% (3 of 15 patients) in patients ranging from 4 to 18 years.⁵² A review using the National Trauma Data Bank (NTDB) of all pediatric blunt trauma patients with no sign of life in the field identified a 1.3% survival rate for those undergoing EDT.⁵³ In a study at Denver Health Medical Center, encompassing an 11-year experience with 689 consecutive EDT, we identified 83 patients (12%) who were under 18 years old.⁵⁰ Survival by injury mechanism was 9% (1 of 11) for stab wounds, 4% (1 of 25) for gunshot wounds, and 2% (1 of 47 patients) for blunt trauma. Among 69 patients presenting to the ED without vital signs, only 1 patient (1%) survived (with a stab wound). This contrasted to a salvage of 2 (14%) among 14 patients with vital signs. The outcome in blunt trauma, the predominant mechanism of lethal injury in children, was disappointing, with only 2% salvage, and no survivors when vital signs were absent. Thus, as in adults, outcome following EDT in the pediatric population is largely determined by injury mechanism and physiologic status on presentation to the ED.