Clay Cothren Burlew and Ernest E. Moore
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. This chapter reviews these features 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 decade, 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
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.”12 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 (i.e., clinical death). Patients with “no vital signs” have no palpable blood pressure, but demonstrate electrical activity, respiratory effort, or pupillary reactivity.
PHYSIOLOGIC RATIONALE FOR EDT
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).13 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.14Initially, increased pericardial pressure restricts ventricular diastolic filling and reduces subendocardial blood flow.15 Cardiac output under these conditions is maintained by compensatory tachycardia, increased systemic vascular resistance, and elevated central pressure (i.e., 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 (e.g., 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.16,17 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).
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.18 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.19,20 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.21 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 2-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.22,23 Canine studies have shown that the left ventricular stroke-work index and myocardial contractility increase in response to thoracic aortic occlusion during hypovolemic shock.24 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.25
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.26,27 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.30–32 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. Typically, 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.33–35 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 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.
CLINICAL RESULTS FOLLOWING EDT
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.37–39 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.38A 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.43 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 varies 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.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 (i.e., blood pressure, respiratory effort, cardiac electrical activity, and pupillary activity).
TABLE 14-1 Outcome Following Emergency Department Thoracotomy in Adults
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 , 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).45 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, or (3) manifest asystole without pericardial tamponade. We recognize, however, that there will invariably be exceptions to the recorded literature.28,41,46,47
TABLE 14-2 Current Indications and Contraindications for Emergency Department Thoracotomy
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.48–52 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 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.
TABLE 14-3 Outcome Following Emergency Department Thoracotomy in Children
In sum, overall analysis of the available literature indicates that the success of EDT approximates 35% in the patient arriving in shock with a penetrating cardiac wound, and 15% for all penetrating wounds. Patients undergoing CPR upon arrival to the ED should be stratified based upon injury and transport time to determine the utility of EDT. Conversely, patient outcome is relatively poor when EDT is done for blunt trauma; 2% survival in patients in shock and less than 1% survival with no vital signs.
INDICATIONS FOR EDT
Based on our 26 successive years of EDT prospective analysis10 and the recent WTA multicenter trial,45 we propose current indications for EDT (Table 14-2). Clearly, the specific application of these guidelines must include consideration of the patient’s age, preexisting disease, signs of life, and mechanism of injury, as well as logistic issues such as the proximity of the ED to the OR, and qualified personnel. Our current decision algorithm for resuscitation of the moribund trauma patient and use of EDT was formulated and implemented as a key clinical pathway in the ED (Fig. 14-1). At the scene, patients in extremis without electrical cardiac activity are declared dead. Patients in extremis but with electrical cardiac activity are intubated, supported with cardiac compression, and rapidly transported to the ED.
FIGURE 14-1 Algorithm directing the use of EDT in the multiply injured trauma patient.
On arrival to the ED, the time from initiation of CPR is recorded; blunt trauma patients with greater than 10 minutes of prehospital CPR and no signs of life are declared, whereas penetrating trauma patients with greater than 15 minutes of prehospital CPR and no signs of life are pronounced. Patients within the time guidelines or those with signs of life trigger ongoing resuscitation and EDT. After performing a generous left anterior thoracotomy and subsequent pericardotomy, the patient’s intrinsic cardiac activity is evaluated. Patients in asystole without associated cardiac tamponade are declared. Patient’s with a cardiac wound, tamponade, and associated asystole are aggressively treated; the cardiac wound is repaired first followed by manual cardiac compressions and intracardiac injection of epinephrine. Following several minutes of such treatment and volume resuscitation, one should reassess salvageability, typically defined as the patient’s ability to generate a SBP >70 mm Hg.
Patient’s with an intrinsic rhythm following EDT should be treated according to underlying pathology. Those with tamponade should undergo cardiac repair, either in the trauma bay or in the OR (see Chapter 26). Control of intrathoracic hemorrhage may entail hilar cross-clamping, digital occlusion of the direct injury, or even packing of the apices for subclavian injuries. Treatment of bronchovenous air embolism includes cross-clamping of the hilum, putting the patient in Trendelenberg’s position, aspirating the left ventricle and aortic root, and massaging the coronaries. Finally, aortic cross-clamping is performed to decrease the required effective circulating volume, for either thoracic or abdominal sources of hemorrhage, and facilitate resuscitation. In all of these scenarios, reassessment of the patient following intervention and aggressive resuscitation efforts is performed, with the goal systolic pressure of 70 mm Hg used to define salvageability.
TECHNICAL DETAILS OF EDT
The optimal benefit of EDT is achieved by a surgeon experienced in the management of intrathoracic injuries. The emergency physician, however, should not hesitate to perform the procedure in the moribund patient with a penetrating chest wound when thoracotomy is the only means of salvage. The technical skills needed to perform the procedure include the ability to perform a rapid thoracotomy, pericardiotomy, cardiorrhaphy, and thoracic aortic cross-clamping; familiarity with vascular repair techniques and control of the pulmonary hilum are advantageous. Once life-threatening intrathoracic injuries are controlled or temporized, the major challenge is restoring the patient’s hemodynamic integrity and minimizing vital organ reperfusion injury.
A left anterolateral thoracotomy incision is preferred for EDT. Advantages of this incision in the critically injured patient include (a) rapid access with simple instruments, (b) the ability to perform this procedure on a patient in the supine position, and (c) easy extension into the right hemithorax, a clamshell thoracotomy, for exposure of both pleural spaces and anterior and posterior mediastinal structures. The key resuscitative maneuvers of EDT, namely, pericardiotomy, open cardiac massage, and thoracic aortic cross-clamping are readily accomplished via this approach. The initial execution of a clamshell thoracotomy should be done in hypotensive patients with penetrating wounds to the right chest. This provides immediate, direct access to a right-sided pulmonary or vascular injury while still allowing access to the pericardium from the left side for open cardiac massage. Clamshell thoracotomy may also be considered in patients with presumed air embolism, providing access to the cardiac chambers for aspiration, coronary vessels for massage, and bilateral lungs for obliteration of the source.
Preparation for EDT should be performed well ahead of the patient’s arrival. Set-up should include a 10-blade scalpel, Finochietto’s chest retractor, toothed forceps, curved Mayo’s scissors, Satin-sky’s vascular clamps (large and small), long needle holder, Lebsche’s knife and mallet, and internal defibrillator paddles. Sterile suction, skin stapler, and access to a variety of sutures should be available (specifically 2-0 prolene on a CT-1 needle, 2-0 silk ties, and teflon pledgets). Upon patient arrival and determination of the need for EDT, the patient’s left arm should be placed above the head to provide unimpeded access to the left chest. The anterolateral thoracotomy is initiated with an incision at the level of the fifth intercostal space (Fig. 14-2). Clinically, this level for incision corresponds to the inferior border of the pectoralis major muscle, just below the patient’s nipple. In women, the breast should be retracted superiorly to gain access to this interspace, and the incision is made at the inframammary fold. The incision should start on the right side of the sternum; if sternal transection is required, this saves the time-consuming step of performing an additional skin incision. As the initial incision is carried transversely across the chest, and one passes beneath the nipple, a gentle curve in the incision toward the patient’s axilla rather than direct extension to the bed should be performed; this curvature in the skin correlates with the natural curvature of the rib cage. The skin, subcutaneous fat, and chest wall musculature are incised with a knife to expose the ribs and associated intercostal space. Intercostal muscles and the parietal pleura are then divided in one layer either with curved Mayo scissors or sharply with the scalpel; the intercostal muscle should be divided along the superior margin of the rib to avoid the intercostal neurovascular bundle. Chest wall bleeding is minimal in these patients and should not be a concern at this point in the resuscitation. Once the incision is completed and the chest entered, a standard Finochietto’s rib retractor is inserted, with the handle directed inferiorly toward the axilla (Fig. 14-2). Placement of the handle toward the bed rather than the sternum allows extension of the left thoracotomy into a clamshell thoracotomy with crossing of the sternum without replacing the rib retractor.
FIGURE 14-2 (A) and (B) The thoracotomy incision is performed through the fourth or fifth intercostal space; the incision should start to the right of the sternum, and begin curving into the axilla at the level of the left nipple. The Finochietto’s rib retractor is placed with the handle directed inferiorly toward the bed.
If the left anterolateral thoracotomy does not provide adequate exposure, several techniques may be employed. The sternum can be transected for additional exposure with a Lebsche’s knife; care must be taken to hold the Lebsche’s knife firmly against the underside of the sternum when using the mallet to forcefully transect the sternum, or the tip of the instrument may deviate and result in an iatrogenic cardiac injury. If the sternum is divided transversely, the internal mammary vessels must be ligated when perfusion is restored; this may be performed using either a figure of eight suture with 2-0 silk or by clamping the vessel with a tonsil and individually ligating it with a 2-0 silk tie (Fig. 14-3). A concomitant right anterolateral thoracotomy produces a “clamshell” or “butterfly” incision, and achieves wide exposure to both pleural cavities and anterior and posterior mediastinal structures (Fig. 14-4). Once the right pleural space is opened, the rib retractor should be moved to more of a midline position to enhance separation of the chest wall for maximal exposure. When visualization of penetrating wounds in the aortic arch or major branches is needed, the superior sternum is additionally split in the midline.
FIGURE 14-3 (A) and (B) Transverse division of the sternum requires individual ligation of the internal mammary arteries.
FIGURE 14-4 (A) and (B) A bilateral anterolateral (“clamshell”) thoracotomy provides access to both thoracic cavities including the pulmonary hila, heart, and proximal great vessels.
Pericardiotomy and Cardiac Hemorrhage Control
The pericardium is incised widely, starting at the cardiac apex and extending toward the sternal notch, anterior and parallel to the phrenic nerve (Fig. 14-5). If the pericardium is not tense with blood it may be picked up at the apex with toothed forceps and sharply opened with scissors. If tense pericardial tamponade exists, a knife or the sharp point of a scissors is often required to initiate the pericardiotomy incision. Blood and blood clots should be completely evacuated from the pericardium. The heart should be delivered from the pericardium by placing the right hand through the pericardial incision, encircling the left side of the heart and pulling it into the left chest. This effectively places the left side of the pericardium behind the heart allowing access to the cardiac chambers for repair of cardiac wounds and access for effective open cardiac massage.
FIGURE 14-5 (A) and (B) Pericardiotomy is done with toothed pickups and curved Mayo scissors; the incision begins at the cardiac apex, anterior to the phrenic nerve, and extends on the anterior surface of the heart toward the great vessels.
Prompt hemorrhage control is paramount for a cardiac injury. In the beating heart, cardiac bleeding sites should be controlled immediately with digital pressure on the surface of the ventricle and partially occluding vascular clamps on the atrium or great vessels. Efforts at definitive cardiorrhaphy may be delayed until initial resuscitative measures have been completed. In the nonbeating heart, cardiac repair is done prior to defibrillation and cardiac massage. Cardiac wounds in the thin walled right ventricle are best repaired with 3-0 nonabsorbable running or horizontal mattress sutures. Buttressing the suture repair with Teflon pledgets is ideal for the thinner right ventricle, but not essential. When suturing a ventricular laceration, care must be taken not to incorporate a coronary vessel into the repair. In these instances, vertical mattress sutures should be used to exclude the coronary and prevent cardiac ischemia. In the more muscular left ventricle, control of bleeding can occasionally be achieved with a skin-stapling device if the wound is a linear stabwound whose edges coapt in diastole. Low-pressure venous, atrial, and atrial appendage lacerations can be repaired with simple running or pursestring sutures. Posterior cardiac wounds may be particularly treacherous when they require elevation of the heart for their exposure; closure of these wounds is best accomplished in the OR with optimal lighting and equipment. For a destructive wound of the ventricle, or for inaccessible posterior wounds, temporary inflow occlusion of the superior and inferior vena cava may be employed to facilitate repair (see Chapter 26). BioGlue may be used as a hemostatic agent in such cases. Use of a Foley catheter for temporary occlusion of cardiac injuries has been suggested; in our experience this may inadvertently extend the injury due to traction forces.
Advanced Cardiac Life Support Interventions Including Cardiac Massage
The restoration of organ and tissue perfusion may be facilitated by a number of interventions.53 First, a perfusing cardiac rhythm must be established. Early defibrillation for ventricular fibrillation or pulseless ventricular tachycardia has proven benefit, and evidence supports the use of amiodarone (with lidocaine as an alternative) following epinephrine in patients refractory to defibrillation. Magnesium may be beneficial for torsades de pointes; other dysrhythmias should be treated according to current guidelines.53 Internal defibrillation may also be required, with similar indications as closed-chest CPR. Familiarity with the internal cardiac paddles and appropriate charging dosages in joules is required (Fig. 14-6). In the event of cardiac arrest, bimanual internal massage of the heart should be instituted promptly (Fig. 14-7). We prefer to do this with a hinged clapping motion of the hands, with the wrists apposed, sequentially closing from palms to fingers. The ventricular compression should proceed from the cardiac apex to the base of the heart. The two-handed technique is strongly recommended, as the one-handed massage technique poses the risk of myocardial perforation with the thumb.
FIGURE 14-6 (A) and (B) Internal paddles for defibrillation are positioned on the anterior and posterior aspects of the heart.
FIGURE 14-7 (A) and (B) Open cardiac massage is performed with a two-handed hinged technique; the clapping motion sequentially closes the hands from palms to fingers.
Pharmocologic adjuncts to increase coronary and cerebral perfusion pressure may be needed. The first agent in resuscitation at this juncture is intracardiac epinephrine. Epinephrine should be administered using a specialized syringe, which resembles a spinal needle, directly into the left ventricle. Typically, the heart is lifted up slightly to expose the more posterior left ventricle, and care is taken to avoid the circumflex coronary during injection. Although epinephrine continues to be advocated during resuscitation, there is a growing body of data suggesting that vasopressin may be superior to epinephrine in augmenting cerebral perfusion and other vital organ blood flow.54Administration of calcium, while theoretically deleterious during reperfusion injury, increases cardiac contractility, and may be helpful in the setting of hypocalcemia produced by massive transfusion. Although metabolic acidosis is common following EDT and resuscitation, the mainstay of therapy is provision of adequate alveolar ventilation and restoration of tissue perfusion. Sodium bicarbonate therapy has not been proven beneficial in facilitating defibrillation, restoring spontaneous circulation, or improving survival. It may be warranted following protracted arrest or resuscitation, because catecholamine receptors may be sensitized.
Thoracic Aortic Occlusion and Pulmonary Hilar Control
Following thoracotomy and pericardiotomy with evaluation of the heart, the descending thoracic aorta should be occluded to maximize coronary perfusion if hypotension (SBP < 70 mm Hg) persists. We prefer to cross-clamp the thoracic aorta inferior to the left pulmonary hilum (Fig. 14-8). Exposure of this area is best provided by elevating the left lung anteriorly and superiorly. Although some advocate taking down the inferior pulmonary ligament to better mobilize the lung, this is unnecessary and risks injury to the inferior pulmonary vein. Dissection of the thoracic aorta is optimally performed under direct vision by incising the mediastinal pleura and bluntly separating the aorta from the esophagus anteriorly and from the prevertebral fascia posteriorly. Care should be taken in dissecting the aorta, and completely encircling it may avulse thoracic and other small vascular branches. Alternatively, if excessive hemorrhage limits direct visualization, which is the more realistic clinical scenario, blunt dissection with one’s thumb and fingertips can be done to isolate the descending aorta. Once identified and isolated, the thoracic aorta is occluded with a large Satinsky or DeBakey’s vascular clamp. If the aorta cannot be easily isolated from the surrounding tissue, digitally occlude the aorta against the spine to affect aortic occlusion. Although occlusion of the thoracic aorta is typically performed after pericardiotomy, this may be the first maneuver upon entry into the chest in patients sustaining extrathoracic injury and associated major blood loss.
FIGURE 14-8 (A) and (B) Aortic cross-clamp is applied with the left lung retracted superiorly, below the inferior pulmonary ligament, just above the diaphragm. The flaccid aorta is identified as the first structure encountered on top of the spine when approached from the left chest.
Control of the pulmonary hilum has two indications. First, if coronary or systemic air embolism is present, further embolism is prevented by placing a vascular clamp across the pulmonary hilum (Fig. 14-9). Associated maneuvers such as vigorous cardiac massage to move air through the coronary arteries and needle aspiration of air from the left ventricular apex and the aortic root are also performed (Fig. 14-10). Second, if the patient has a pulmonary hilar injury or marked hemorrhage from the lung parenchyma, control of the hilum may prevent exsanguination. Hilar control can be performed by a Satinsky’s clamp, the pulmonary hilar twist, or temporarily with digital control (see Chapter 26).
FIGURE 14-9 (A) and (B) A Satinsky clamp is used to clamp the pulmonary hilum for hemorrhage control or to prevent further bronchovenous air embolism.
FIGURE 14-10 In cases of bronchovenous air embolism, sequential sites of aspiration include the left ventricle (1), the aortic root (2), and the right coronary artery (3).
COMPLICATIONS AND CONSEQUENCES OF EDT
Technical complications of EDT involve virtually every intrathoracic structure. The list of such misadventures included lacerations of the heart, coronary arteries, aorta, phrenic nerves, esophagus, and lungs, as well as avulsion of aortic branches to components of the mediastinum. Previous thoracotomy virtually assures technical problems from the presence of dense pleural adhesions and is therefore a relative contraindication to EDT. Additional postoperative morbidity among ultimate survivors of EDT includes recurrent chest bleeding; infection of the pericardium, pleural spaces, sternum, and chest wall; and postpericardiotomy syndrome.
Importantly, there is a finite risk to the health care providers and trauma team performing an EDT.55 The use of EDT by necessity involves the rapid use of sharp surgical instruments and exposure to the patient’s blood. Even during elective procedures in the OR, the contact rate of patient’s blood with the surgeon’s skin can be as high as 50%, and the contact rate of patients’ blood with health care workers’ blood as high as 60%. The overall seroprevalence rate of human immunodeficiency virus (HIV) among patients admitted to the ED for trauma is around 4%, but is much higher among the subgroup of patients most likely to require an EDT, for example, 14% of penetrating trauma victims and nearly 30% of intravenous drug abusers. Caplan et al.56 found that 26% of acutely injured patients had evidence of exposure to HIV (4%), hepatitis B (20%), or hepatitis C virus (14%); there was no difference in the incidence comparing blunt to penetrating trauma. Thus, the likelihood of a health care worker sustaining exposure to HIV or hepatitis in the ED is substantial. The risk of contagion from exposures to HIV and other blood-borne pathogens can be minimized by the use of appropriate barrier precautions and the selective use of EDT.
Hemodynamic and Metabolic Consequences of Aortic Cross-Clamping
Aortic cross-clamping may be life saving during acute resuscitation, but there is a finite cost to the patient. Occlusion of the aorta results in an increase in blood pressure, but there is an associated 90% reduction in femoral artery SBP; in addition, abdominal visceral blood flow decreases to 2–8% of baseline values.31,32 Therefore, cross-clamping magnifies the metabolic cost of shock by reducing local blood flow to abdominal viscera even further. This results in tissue acidosis and increased oxygen debt, and may ultimately contribute to postischemic multiple organ failure.32 Additionally, return of aortic flow may not result in normalization of flow to vital organs; in animal models, blood flow to the kidneys remained at 50% of baseline despite a normal cardiac output. The metabolic penalty of aortic cross-clamping becomes exponential when the normothermia occlusion time exceeds 30 minutes, both in trauma and in elective thoracic aortic procedures.57–59 Hypoxia of distal organs, white blood cells, and endothelium induces the elaboration, expression, and activation of inflammatory cell adhesion molecules and inflammatory mediators; this systemic inflammatory response syndrome has been linked to impaired pulmonary function and multiple organ failure60 (see Chapter 61). Consequently, the aortic clamp should be removed as soon as effective cardiac function and adequate systemic arterial pressure have been achieved.
Removal of aortic occlusion may result in further hemodynamic sequelae.61 Besides the abrupt reperfusion of the ischemic distal torso and washout of metabolic products and inflammatory mediators associated with aortic declamping, there are direct effects on the cardiopulmonary system. The return of large volumes of blood from the ischemic extremities, with its lower pH, elevated lactate, and other mediators may exert a cardiodepressant activity on myocardial contractility.62 Overzealous volume loading during aortic occlusion may also result in left ventricular strain, acute atrial and ventricular dilatation and, consequently, precipitous cardiac failure.32 Following release of aortic occlusion there is impaired left ventricular function, systemic oxygen utilization, and coronary perfusion pressure in the postresuscitation period.61,63 The transient fall in coronary perfusion may not be clinically relevant in patients with efficient coronary autoregulation; however, in patients with coronary disease or underlying myocardial hypertrophy, this increase in cardiac work may result in clinically critical ischemia.63
OPTIMIZING OXYGEN TRANSPORT FOLLOWING EDT
Following EDT, patients are frequently in a tenuous physiologic state. The combination of direct cardiac injury, ischemic myocardial insult, myocardial depressants, and pulmonary hypertension adversely impact postinjury cardiac function (see Chapter 56). Additionally, aortic occlusion induces profound anaerobic metabolism, secondary lactic academia, and release of other reperfusion-induced mediators. Consequently, once vital signs return, the resuscitation priorities shift to optimizing cardiac function and maximizing oxygen delivery to the tissues. The ultimate goal of resuscitation is adequately tissue oxygen delivery and cellular oxygen consumption (see Chapter 55). Circulating blood volume status is maintained at the optimal level of cardiac filling in order to optimize cardiac contractility, and the oxygen-carrying capacity of the blood is maximized by keeping the hemoglobin above 7–10 g/dL. If these measures fail to meet resuscitative goals64 (e.g., oxygen delivery ≥500 mL/min/,2 resolution of base deficit, or clearance of serum lactate), inotropic agents are added to enhance myocardial function.
As clinicians faced with increasing scrutiny over appropriation of resources, it is critical to identify the patient who has permanent neurologic disability or death. Resuscitative efforts should not be abandoned prematurely in the potentially salvageable patient but field assessment of salvageability is unreliable.41,65–67 Our clinical pathway attempts to optimize resource utilization, but outcomes must continue to be evaluated, searching for more definitive predictors of neurologic outcome. For example, markers of brain metabolic activity such as increased serum neuron–specific enolase activity appear to have prognostic significance for irreversible brain damage.68 The use of more advanced monitoring devices in the ED, together with further elucidation of the characteristics of irreversible shock, may permit a more physiologic prediction of outcome for these critically injured patients in the future.
Temporary Physiologic Hibernation
A potential adjunct in the care of traumatic arrest is the timely application of hypothermia. Recent randomized studies suggest the use of hypothermia for central nervous system protection after nontraumatic cardiac arrest.69,70 In these studies, patients randomized to a period of mild-to-moderate hypothermia (32–34°C) after cardiac arrest had improved neurologic outcomes compared to those kept normothermic. This favorable effect was presumably due to a decrease in cerebral metabolic demand during hypothermia. In addition, hypothermia may reduce oxygen radical generation and inflammatory mediator production. By extension, then, if an injured patient in transport could be cooled to a minimal metabolic rate (i.e., suspended animation), one can posit that transfer to definitive care might be possible.71,72Application of this principle to the multiply injured or bleeding patient, however, is problematic. Rapid cooling is not currently practical in the field, and there are legitimate concerns about the adverse effects of hypothermia on immune function and effective clot formation. Overall, while some73 preclinical work supports the application of hypothermia after resuscitation from hemorrhage, other investigators have reached the opposite conclusion.74
Temporary Mechanical Cardiac Support
The concept of temporary mechanical cardiac support for the failing heart following injury is intuitively attractive. Unfortunately, experience with the intra-aortic balloon pump in this scenario has been unrewarding. The advent of centrifugal pumps (Bio-Medicus Pump; Bio-Medicus, Inc., Minneapolis, MN), that allow partial cardiac bypass without systemic anticoagulation, offers another potential means for increasing salvage of the moribund patient. Centrifugal pumps have become the standard approach to the torn descending thoracic aorta in the patient with associated myocardial contusion (see Chapter 26).75,76 The adjunctive use of extracorporeal membrane oxygenation may also play a critical role in supporting the patient with massive injuries or early multiple organ failure.77 Finally, hypothermia circulatory arrest may find utility in a broad spectrum of patients with injuries that are considered “irreparable.”78,79
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