CHAPTER 104: TRAUMATIC HEART DISEASE

Trauma is the leading cause of death and disability among young people in the United States.^1,2,3 Thoracic injures account for 20% to 25% of deaths from trauma, and contribute to 25% to 50% of the remaining deaths. Thus, thoracic injures are a contributing factor in up to 75% of all trauma-related deaths.⁴ Cardiac and great vessel injuries are common contributors to the morbidity and mortality of severely injured patients.⁵ Causes of injury to the heart and thoracic aorta can be broadly divided into penetrating or blunt mechanisms.

Penetrating Cardiac Injuries

Penetrating injury to the heart must be suspected with any missile or knife wound to the thorax or upper abdomen. The mechanism of injury may be categorized as low, medium, or high velocity. Knife wounds are low velocity, shotgun injuries are medium velocity, and high-velocity injuries include bullet wounds caused by rifles and wounds resulting from military and civilian weapons. The amount of tissue damage is directly related to the amount of energy exchange between the penetrating object and the body part.⁴

Traumatic cardiac penetration injuries are highly lethal, at 70% to 80%. The anteriorly positioned right ventricle is most frequently injured, followed by the left ventricle, right atrium, and left atrium (Table 104–1).⁶ Other potentially injured structures include the interatrial or interventricular septum, coronary arteries, valves, subvalvular apparatus, and conduction system.⁷ Low-velocity injuries, such as stab wounds, produce damage commensurate to the structure penetrated and size of the defect. High-velocity missiles produce injury beyond the region of myocardial penetration secondary to concussive effects and are more frequently lethal.^8,9,10,11

The primary manifestations of cardiac penetration are hemorrhage and tamponade. Valve or coronary injury may, of course, produce acute valvular incompetence or myocardial infarction. Stab victims often present with tamponade when clot and surrounding pericardial fat partially seal the pericardial defect. Injuries to the left ventricle more commonly result in overt hemorrhage. Patients presenting with tamponade may have a survival advantage, with mortality as low as 8% in experienced trauma centers.⁸ Early diagnosis is critical to survival, and this is only possible with a high index of suspicion, bearing in mind that patients with potentially fatal wounds can be stable at presentation. Echocardiography can confirm the diagnosis of cardiac injury, but the lack of an effusion does not disprove injury.¹² The diagnostic gold standard, short of exploration, is a subxiphoid window.

Management of penetrating wounds to the heart depends on the stability of the patient. If the patient presents with a recent loss of vital signs or in a moribund state, a left anterior thoracotomy performed in the emergency department is potentially lifesaving. Emergent thoracotomy may salvage as many as 20% of unstable or pulseless patients who have isolated penetrating trauma to the heart, but results are less favorable with missile wounds.^13,14 Most cardiac wounds can be repaired through a left thoracotomy. Additionally, the thoracic aorta can be compressed or clamped to improve cerebral and cardiac perfusion while volume is restored. More stable patients are transported to the operating room, where a median sternotomy is the preferred approach. A sternotomy allows adequate exposure of all cardiac structures and permits rapid institution of cardiopulmonary bypass when required. Most injuries are repaired with simple pledgeted sutures using finger control to stop bleeding once identified. Coronary artery injuries are common, and the surgeon must use his or her judgment regarding coronary artery bypass versus ligation. An effort should be made to bypass large epicardial vessels, whereas smaller terminal branches or side branches can be ligated. The principal objective is to relieve tamponade and stop life-threatening hemorrhage. Further procedures, once again, require individualized surgical judgment based on the severity of the lesion and the physiologic significance on echocardiogram.

Blunt Cardiac Injury

The reported incidence of blunt cardiac trauma varies widely in the literature, but blunt injury is involved in up to 20% of all motor vehicle collision deaths.¹⁵ The Centers for Disease Control and Prevention estimates 30,000 cases of blunt cardiac injuries per year in the United States.¹⁶ Blunt cardiac injury results from either a rapid deceleration mechanism or a direct blow to the precordium; in all cases, blunt cardiac injury requires significant force, such as occurs in motor vehicle crashes, pedestrians struck by motor vehicles, falls from heights, and sports-related injuries. Severe sudden abdominal compression can acutely increase pressure and blood flow to the heart, resulting in right-sided rupture. The absence of a clear definition and rapid laboratory testing makes the diagnosis of blunt cardiac injury difficult.

Resulting injuries include cardiac contusion, valve disruption, atrial or ventricular septal defects, or frank cardiac rupture. These injuries vary by anatomic location (Table 104–2). Once again, because of its anterior position, the right ventricle is the chamber most frequently involved. Cardiac rupture is a common mechanism of death in blunt trauma, with survival after medical care being uncommon.^15,17 In patients reaching medical care with vital signs, however, a reasonable survival rate can be expected if cardiac injury is promptly recognized and operated on.¹⁸ Those surviving cardiac rupture more frequently have injuries to the right heart.¹⁹ Myocardial contusion encompasses a spectrum of injuries. In its mildest form, cardiac contusion results in mild epicardial ecchymosis without functional significance. More severe contusion can cause muscular injury, dysfunction, and infarction. The true incidence of myocardial contusion following blunt trauma is difficult to discern. It is important to note that severe myocardial injury can occur with little evidence of external chest trauma.

A high index of suspicion along with careful evaluation of mechanism should accompany all trauma patients from these accident scenarios, as a majority of patients with blunt cardiac trauma are asymptomatic. Diagnostic testing including chest x-ray, electrocardiogram (ECG), Holter monitoring, cardiac markers, transthoracic and transesophageal echocardiography, and cardiac computed tomography (CT) and magnetic resonance imaging (MRI) may be needed to make the diagnosis.⁴ All patients who have a significant mechanism of injury should have a screening ECG. Findings suggestive of cardiac contusion include nonspecific ST- and T-wave changes. Arrhythmias such as atrial fibrillation, atrial flutter, and premature ventricular complexes are also common and are usually self-limiting. Ventricular tachycardia and fibrillation are uncommon in patients surviving to the hospital. With a normal ECG in an otherwise uninjured patient, the risk of complications is low. Serial cardiac enzyme measurements are nonspecific for the diagnosis of myocardial contusion in the blunt injury patient.²⁰ In the patient who remains unstable or responds poorly to standard resuscitative efforts, echocardiography is indicated to look for regional wall-motion abnormalities or structural defects.

The American Association for the Surgery of Trauma Injury Scale for Cardiac Injuries is one way of quantifying the extent of injury (Table 104–3).

The management of myocardial contusion is often expectant, particularly in the patient who remains hemodynamically stable after treatment of concurrent injuries. Arrhythmias are treated with standard agents for rate control and suppression of ectopy as well as optimization of electrolytes. In patients with hemodynamic instability, definitive echocardiography should be obtained. In cases of severe ventricular dysfunction and low cardiac output, inotropic support is appropriate with perhaps less concern for extension of injury than with a primary ischemic event. If inotropic support does not produce satisfactory improvement, intra-aortic balloon counterpulsation should be considered.

Pericardial injury results from direct high-energy impact of acute increase in intra-abdominal pressure. The presence of absence of a sternal fracture is not diagnostic. The pericardium may rupture along the diagphragmatic or pleural surface parallel to the phrenic nerve, resulting in evisceration of the heart and/or torsion of the great vessels. Pneumopericardium, abnormal gas pattern, or displacement of the cardiac silhouette may be present. Emergency surgical intervention via sternotomy is mandatory.

Direct coronary artery injury may cause arterial thrombosis, resulting in myocardial infarction, post-myocardial infarction ventricular septal defect, cardiac failure, or malignant arrhythmias.

Valve injury following blunt trauma is uncommon. The aortic valve is most frequently involved and can result from commissural avulsion, leaflet tears, or aortic dissection, all resulting in acute aortic insufficiency.^21,22 Isolated injury of the mitral valve is less common and most frequently involves rupture of the papillary muscle or chordal apparatus. Tricuspid valve injury is more commonly reported than mitral injury perhaps because the latter is frequently fatal. Figure 104–1 shows the two-dimensional transthoracic echocardiogram in a female patient who was kicked in the anterior chest wall by her horse.²³ Tricuspid valve injury may become evident at a time remote from the injury as right heart failure develops.^24,25,26

Recently a case of traumatic left ventricular intramural dissection has been reported (Fig. 104–2).²⁷

Delayed Sequelae of Cardiac Injury

Patients sustaining significant blunt or penetrating cardiac injuries require long-term follow-up. Injuries may not be appreciated at the time of trauma. Possible late sequelae include evolving atrial or ventricular septal defects, progressive valvular incompetence, aortocardiac or aortopulmonary fistulas, coronary artery fistulas, ventricular aneurysms, and post-traumatic pericarditis.^28,29,30,31

Penetrating Injury of the Great Vessels

The great vessels of the chest include the aorta, its major branches at the arch (innominate, carotid, subclavian) and the major pulmonary arteries. The primary venous conduits include the superior and inferior vena cavae, their main tributaries (eg, azygous vein), and the pulmonary veins. The prevalence of great vessel injuries ranges from 0.3% to 10%. More than 90% of thoracic great vessel injuries are caused by penetrating trauma.^4,15

The pathophysiology of penetrating wounds to the great vessels is similar to penetrating wounds of the heart, with the extent of injury being determined by the specific structures injured and the velocity of the weapon. Cardiac tamponade may develop if the wound is below the pericardial reflection. Delayed sequelae of great vessel injury include pseudoaneurysm formation with delayed rupture and arteriovenous malformation with development of congestive heart failure.

Penetrating injuries of the great vessels have a historically high mortality. The trauma surgeon must resuscitate, diagnose, and treat the patient within minutes following admission to the trauma emergency unit. Through an emergent left thoracotomy, operative repair of thoracic aortic injuries is virtually always possible by direct aortic repair with short cross-clamp times. Only rarely is an interposition graft required, and adjunctive measures of cardiopulmonary bypass, bypass shunts, or active aortic shunts (eg, a centrifugal pump) are usually not described for penetrating injuries, but are almost exclusively used for blunt injury. Paraplegia following successful repair of penetrating aortic injuries is rare, even with prolonged aortic clamping following emergency thoracotomy.⁴

Aortic Rupture

Aortic transection is second only to closed head injury as a cause of death in blunt trauma patients, resulting in an estimated 8000 deaths in the United States annually.^32,33,34,35 It is believed that approximately 20% of patients sustaining descending aortic transections survive to reach medical care.³³ The injury mechanism involves any type of severe deceleration, most commonly a motor vehicle accident. Tears are most often encountered at the aortic isthmus just beyond the subclavian artery where the aorta is tethered by the ligamentum arteriosum.^34,35 Patients acutely surviving aortic injury have partial or complete transections contained by adventitia and surrounding structures forming a false aneurysm. Avulsion of the innominate, carotid, or subclavian arteries occurs less frequently.^36,37

Aortic transaction must be suspected based on the mechanism of injury. Patients may have multiple other injuries or have remarkably few other manifestations of severe trauma. The classic findings of a widened mediastinum, apical capping, or depression of the left mainstem bronchus may not be evident on plain films of the chest in a patient with an aortic injury. Aortography has previously been the definitive means of diagnosis, but advancements in multidetector CT have made CT angiography a more commonly used tool to identify aortic injury in major trauma centers. Transesophageal echocardiography can be performed at the bedside or in the operating room in the patient too unstable for the CT scanner. In skilled hands, this has a sensitivity similar to that of helical CT scanning.^38,39

Once a diagnosis of aortic transection from blunt aortic trauma is made, several emergent/urgent treatment options are available.⁴ Immediate repair through a left thoracotomy should be considered depending on the patient's stability and other injuries. Delayed repair is appropriate in the multiply injured patient requiring ongoing resuscitation, and this management strategy has grown in popularity. Nonoperative management is not risk free, however, with as many as 4% of patients thought to be candidates for delayed repair experiencing rupture within a week of injury in some series.^40,41 A more recent additional option is endovascular stent graft insertion in selected patients, which has yielded promising results (Fig. 104–3) when compared with traditional repair.^{42,43,44,45,46,47,48} The Society for Vascular Surgery database documented endovascular treatment for acute aortic transections. Ninety-seven percent were the result of a motor vehicle accident. Sixty symptomatic patients were treated with an aortic endograft, with an all-cause mortality of 9.1% at 30 days, and a mean operative time of 125 minutes.⁴⁹ An endovascular approach may be preferred in patients who are higher risk for open repair such as the elderly or those with significant lung or head injuries, making thoracotomy and heparinization less appealing.

I would like to thank Dr Curtis Anderson, who contributed to the previous version of this chapter in the 13th edition.