Blunt cerebrovascular injuries (BCVIs) to the extracranial carotid and vertebral arteries, which are thought to result from neck hyperflexion, hyperextension, or rotational mechanisms, occur in about 1 % of hospitalized trauma patients and are associated with increased risk of potentially devastating ischemic strokes, both on admission and within days of injury. Classic studies have shown that certain injury patterns, including traumatic brain injury, complex skull fractures, facial or mandibular fractures, cervical spine fractures, neck soft-tissue injuries, and thoracic or thoracic vascular injuries, are associated with BCVIs and can be used as criteria for screening with CT angiography and/or digital subtraction angiography [14–16]. However, it is estimated that 30 % of patients with BCVIs do not meet any of these screening criteria, and some investigators advocate for more liberal screening, even based on suspicious mechanism alone [17]. Surgeons caring for patients with major thoracic trauma should ensure that their patients have been screened for BCVI, and started on prophylactic antiplatelet or anticoagulant therapy as soon as the risks of stroke (thought to be 21 % in untreated patients) [18] begin to outweigh the risks of anticoagulation-associated hemorrhage.

Blunt thoracic aortic injury (BTAI) is most often caused by rapid deceleration, from motor vehicle or motorcycle crashes. Other common mechanisms include fall from height more than 5 m, crush between two objects, and ejection from a vehicle. Only 20 % of patients with BTAI will survive to the hospital. The injury usually occurs on the descending thoracic aorta, just distal to the takeoff of the left subclavian artery. The diagnosis can be suspected on CXR, with suggestive signs like widened mediastinum, apical cap, loss of aortic knob, or a depressed left main stem bronchus (Fig. 10.2). However, these signs may not be obvious on a supine anteroposterior CXR and are not specific to BTAI. As discussed above, the trauma surgeon should have a low threshold for performing a CT scan in patients with serious mechanism and/or suspicious findings on CXR. Helical CT angiography is the gold standard for diagnosing these injuries. If equivocal, a formal angiogram can be performed. The treatment of BTAI has drastically evolved over the course of the past decades. Two large prospective studies from the American Association for the Surgery of Trauma have redefined the optimal management of this injury [19, 20]. They have shown, first, that delayed repair improves outcomes and, second, that the endovascular stent graft technique has less morbidity and mortality than conventional open repair. A recent study reports 0 % 30-day mortality, no conversion to open repair, and a re-intervention rate of 5.8 % at 3 years with the endovascular approach [21]. In patients with multiple rib fractures and BTAI, priority should be given to patient resuscitation, blood pressure control, and semi-urgent endovascular repair. Rib plating should only be done once the aortic injury has been repaired.

Patients sustaining motor vehicle crashes, motorcycle crashes, and high-level falls (≥20 feet), as well as pedestrians that are hit by cars, and certainly all patients with significant chest wall trauma, are at risk of blunt cardiac injury (BCI). The clinical manifestations of BCI can be structural, from trauma to the structural elements of the heart, or electrical, from injuries to the heart’s electrical conduction system. From a structural standpoint, injuries include transmural rupture (which is usually fatal at the scene), valvular rupture causing acute heart failure and necessitating valve repair or replacement, coronary artery dissection necessitating immediate revascularization procedures, and intramural hematomas, which often resolve with simple expectant management. Electrical disturbances seen in BCI include commotio cordis, a trauma-induced conduction abnormality that is rapidly fatal in the vast majority of cases, as well as atrial and ventricular dysrhythmias and bundle branch block, which often require pharmacological control, cardioversion, or pacing, depending on their severity and hemodynamic effects [22].

BCIs are uncommon, but are of extreme clinical significance. Surgeons caring for patients with significant chest wall trauma should ensure that the possibility of BCI has been considered and ruled out or adequately addressed. A 12-lead ECG (an essential part of the diagnostic workup of chest trauma patients), when normal, has a 95 % negative predictive value for BCI [23], which increases to 100 % when combined with a normal cardiac troponin I [24]. Patients with new ECG abnormalities or troponin elevations require admission to monitored settings and may need additional investigation with echocardiography or cardiac catheterization, depending on the nature of the abnormalities and their hemodynamic status (Fig. 10.3). Such patients can still undergo urgent procedures, provided that their cardiac function can be monitored and optimized.

Blunt esophageal injury is very rare, estimated to be present in 0.1 % of trauma admissions [25], possibly because the esophagus is protected between the aorta and vertebral column in the posterior mediastinum. Blunt esophageal injuries are caused by an increased pressure in the lumen against a closed upper or lower esophageal sphincter, usually secondary to a blow to the epigastrium [26]. A less common cause of esophageal injury in blunt mechanisms is impalement by an adjacent thoracic vertebral osteophyte fracture. Although rare, esophageal injuries cause significant morbidity, especially if diagnosed late. A combination of clinical evaluation (odynophagia, chest pain, hematemesis, sepsis) and multiple imaging modalities is recommended for diagnosis: CXR, CT, water-soluble and barium esophagogram, and esophagoscopy [27]. Pneumomediastinum on CT should prompt consideration of investigation for esophageal trauma, if the clinical circumstances are suggestive. A thoracic esophageal injury should be approached with a posterolateral right or left thoracotomy, depending on the site of perforation. These cases are usually heavily contaminated and the repair is at high risk of dehiscence. If associated rib fractures are present, rib plating should be discouraged because of the high risk of hardware infection.

Respiratory failure in blunt chest trauma results from a combination of injury to the lung parenchyma (pulmonary contusion (PC)) and disruption of the chest wall (flail chest (FC)). Therapeutic efforts are therefore directed at the consequences of both types of injury.

PC is characterized by parenchymal hemorrhage, inflammation, and occlusion of alveoli with blood and pulmonary edema (Fig. 10.4) [28, 29]. Blood or fluid-filled alveoli are unable to participate in gas exchange, and blood shunting past these alveoli will remain deoxygenated. Large lung contusions create large shunt fractions and worse hypoxemia. The extent of pulmonary contusion correlates closely with the severity of hypoxemic respiratory failure, the risk of pneumonia, and the duration of mechanical ventilation. In the long term, patients with PC can develop fibrotic changes in the lung that correlate with worse pulmonary function.

Supportive care with supplemental oxygen, adequate analgesia (including thoracic epidural analgesia) [30], chest physiotherapy, and the judicious use of intravenous fluids helps the hypoxemic effects of PC resolve in most cases. Positive pressure ventilation with positive end-expiratory pressure (PEEP) reduces shunt fraction and improves rib fracture apposition. However, invasive mechanical ventilation is associated with significant complications and high cost. In recent years, the practice of intubating all patients with significant pulmonary contusion has given way to the more selective use of intubation and mechanical ventilation as a safety net for PC patients who develop respiratory failure despite aggressive supportive care. In recent years, well-designed studies have shown that the liberal use of noninvasive modes of positive pressure ventilation, such as continuous positive airway pressure (CPAP), is effective in reducing atelectasis, pneumonia, respiratory failure, and the need for invasive mechanical ventilation [29]. A multidisciplinary approach to PC, which includes the use of noninvasive positive pressure ventilation as needed, along with bronchial hygiene, chest physiotherapy, early mobilization, and conscientious pain control has been shown to drastically reduce the need for invasive mechanical ventilation [31]. When a flail chest is present, rib fracture fixation may be an important adjunct in a multidisciplinary strategy, although the indications and timing of the intervention should be tailored to the specific injury patterns and clinical circumstances.