Thoracic Trauma and Related Topics

Heart

In those patients still alive on arrival to hospital, the myocardium is more commonly affected by blunt rather than penetrating trauma. As with all blunt chest trauma, RTCs account for the vast majority but specific causes of injuries to the heart also include cardiopulmonary resuscitation.

Injury is usually caused by crushing or deceleration but cardiac damage can occur due to overdistension due to excessive hydrostatic pressure. This, combined with a reduced myocardial mass and anterior position, is likely to explain the increased incidence of right atrial and ventricular rupture. Injuries can range from asymptomatic contusions and arrhythmias, to coronary artery injury, regional wall motion abnormalities, pericardial tears, papillary rupture and valve dysfunction, with the most severe septal and free-wall rupture seen as perimortal findings. Acute imaging with CT may only show a pericardial effusion or haemopericardium—suggested by a high attenuation effusion ( Fig. 10.1 ). It may be possible to demonstrate a focal area of hypo-enhancement of myocardium, representing contusion, but this may not be appreciated on non–cardiac-gated studies. The major differential is myocardial infarction and clinical features, with electrocardiograph (ECG) and biochemical markers similar for both entities. Given a suitable history of trauma and hypotension, cardiac contusion should be suspected, particularly with evidence of mediastinal injuries or sternal fracture. Cardiac-gated CT can be performed once the patient is stable and this can demonstrate presence or absence of coronary artery occlusion.

Pericardial injury is usually associated with increased pericardial fluid, with even small effusions well demonstrated on CT. Pneumopericardium is an important sign of pericardial injury and differentiated from pneumothorax by its extent limited to the reflections at the roots of the great vessels.

Cardiac herniation is referred to as luxation and this can be associated with torsion of the great vessels and represents the most important, if rare, complication of pericardial injury ( Fig. 10.2 ).

Sudden increases in endocardial pressure can result in traumatic papillary muscle, chordae tendinae and mitral valve leaflet tears. Increased intra-aortic pressure can cause injury to the aortic valve, with consequent aortic regurgitation. These valvular injuries may present immediately or after several years.

Acute Traumatic Aortic Injury (ATAI)

Traumatic rupture or disruption to the thoracic area more frequently affects males, predominantly young men between 30 and 40 years of age. Most cases of acute traumatic aortic injury (ATAI), around 80%, occur as a result of RTCs. ATAI is present in 0.5–2% of all non-fatal RTCs and accounts for 10–20% of all high-speed deceleration fatalities. It is a serious condition with considerable morbidity and mortality, with or without treatment. The percentage of ATAI in deaths at the site of the accident is assessed at 80% to 90%. Death in hospital without appropriate treatment is 30% within 6 hours and 40% to 50% within 24 hours. Following treatment, the mortality rate is still high, varying from 5% to 28% depending on the technique used and the extent of the associated lesions. However, with modern therapeutic techniques, particularly endovascular repair, it may only be around 5%–10%. For these reasons it is essential to make an extremely quick, precise and reliable diagnosis for rapid and effective treatment of the patient.

Most ATAI cases seen on imaging are located at the aortic isthmus, around 2 cm distal to the origin of the left subclavian artery. Other sites, such as the aortic root (5% of clinical cases) and distal aorta (1% of clinical cases), are seen more frequently in post-mortem series due to the high mortality in injury at such sites. An aortic root disruption, for example, may lead to rapid death due to exsanguination, pericardial haemorrhage and tamponade, or myocardial infarction. The isthmic preponderance is thought to be related to multiple factors, including relative tethering at this site by the ligamentum arteriosum. Tethering is also thought to contribute to injuries at the aortic root and where the aorta crosses the diaphragm.

The mechanism of injury is thought to be multifactorial. A major factor is thought to be the relative movement of the heart and the relatively mobile aorta arch relative to the more tethered descending aorta. ‘Osseous pinch’ is a term used to describe the mechanical compression of the aortic arch and branch vessels between the thoracic spine and the sternoclavicular junction. Increased intravascular pressure within the aorta, also known as the ‘water hammer’ effect, as a direct result of compression, has been suggested to cause injuries at the isthmus and root.

Injuries may be divided into transections and non–full thickness tears, the latter being more commonly seen in survivors, as transections result in rapid exsanguination. Tears commonly involve the intima and media, leaving the adventitia intact but with overall weakening of the aorta and at risk of subsequent rupture and pseudoaneurysm.

The CXR signs are related to the associated mediastinal haematoma and include: mediastinal widening, with a ratio of >25% of the chest width being a useful guide; blurring of the contours of the aortic arch and loss of definition of the aortopulmonary window; left apical pleural fluid; deviation of the trachea or nasogastric (NG) tube; and widening of the paratracheal stripe and paravertebral contours ( Fig. 10.3 ). However, given the relatively poor negative predictive value of the chest x-ray, upon which 7% of ATAI may be occult, any abnormality—in the presence of a likely history—should be further investigated, usually with contrast-enhanced MDCT. This is particularly because ATAI only rarely occurs in isolation. MDCT has a sensitivity and specificity of around 98% for ATAI and is generally considered the gold standard and first-line investigation. Direct CT signs of ATAI include intimal flaps, pseudoaneurysms and contained ruptures, an abnormal aortic contour and a sudden change in aortic calibre (pseudocoarctation) ( Fig. 10.4 ). True traumatic dissection is less common but is seen.

The presence of a mediastinal haematoma in the presence of well-defined aortic borders should be assumed to represent non-aortic bleeding from small mediastinal veins. Haematoma immediately adjacent to the aorta, without evidence of other aortic injury, should be assumed to be due to occult intimal injury and should be followed up with further imaging depending on the patient's status. The term ‘minimal aortic injury’ has been used to describe these lesions and those of intramural haematoma and intimal thrombus. The Society for Vascular Surgery grading system is useful, ranging from: I, the mildest, including minimal aortic injuries; II, intimal flaps, without alteration to the external aortic contour; III, pseudoaneurysm; and IV, uncontained external disruption, including genuine rupture.

Whilst grade I acute aortic injuries can be managed conservatively, repeat CT aortography, magnetic resonance (MR) aortography or transoesophageal ultrasound is required over the subsequent few days and weeks for grade II injuries, with early intervention (e.g. endovascular repair) for those grade II injuries with any sign of progression. Some centres advocate a more cautious approach to grade II injuries but patients with grade III injuries benefit from early/emergent intervention. The role of diagnostic catheter angiography in these cases is limited in the acute setting, as it is estimated that 50% of these injuries are not detected via this technique. Some centres advocate the use of intravascular ultrasound for these indeterminate abnormalities, particularly as a problem-solving adjunct to CT. Hybrid approaches to complex injuries can be undertaken if the patient is stable, incorporating both open surgical carotid conduit creation and endovascular treatment of arch and descending aortic injuries.

In all CT studies for possible aortic injury, multiplanar reformat (MPR) review should be performed, as the signs are often subtle and difficult to appreciate on axial imaging. Further difficulties arise from cardiac motion, particularly affecting the ascending aorta, which can falsely suggest intimal flap formation, and from anatomical variants such as a ‘ductus diverticulum’ at the site where traumatic injury is most commonly seen at the aortic isthmus. Most centres would not require a subsequent catheter aortogram before surgical treatment and this would now be performed only as part of endovascular repair. Secondary CT can aid assessment, particularly if an unenhanced ECG-gated acquisition is included before the ECG-gated angiographic data acquisition to demonstrate intramural haematoma (which can be relatively occult due to similarities in attenuation to the contrast-enhanced aortic lumen).

Mediastinum

Pneumomediastinum occurs in up to 10% of cases of blunt chest trauma, most commonly as a result of alveolar rupture, either due to trauma or positive-pressure ventilation, with peribronchovascular tracking of the air into the mediastinum. Rarely, pneumomediastinum may occur as a result of tracheobronchial or oesophageal disruption. Findings on chest x-ray are of a lucency outlining the mediastinum and its structures, often extending into the neck. These features are better demonstrated with CT ( Fig. 10.5 ).

Tracheobronchial injury is seen in up to 2% of blunt chest trauma, mainly bronchial, right-sided and within 2.5 cm of the carina, and is associated with an overall mortality of approximately 30%. The proposed mechanism is of increased intrathoracic pressure against a closed glottis. Direct signs are of tracheobronchial disruption, with surrounding extra-luminal gas. Indirect signs are of pneumomediastinum and pneumothorax, which is classically resistant to treatment with a chest drain. The ‘fallen lung sign’, where the lung parenchyma is displaced dependently, indicates a complete rupture of the main bronchus (usually the right) ( Fig. 10.6 ).

Traumatic oesophageal rupture is mostly iatrogenic in origin and may provide only indirect evidence of its presence, via pneumomediastinum and a left-sided pleural effusion. The use of oral water-soluble contrast agent will reveal the presence and site of rupture on either CT or fluoroscopic examination in over 90% of cases, allowing for prompt treatment to avoid the development of mediastinitis, which is associated with greatly increased mortality.

Pleura

Pneumothorax occurs in 30% of all chest trauma and although it may be caused by increased intrathoracic pressure, causing alveolar rupture into the pleural space, it is most commonly caused by either a foreign object or fractured ribs lacerating the pleural surfaces. A tension pneumothorax occurs when there is a ‘flutter valve’, allowing unidirectional flow of air into the pleural space, resulting in an increasing volume and pressure of pleural gas. This can result in displacement of mediastinal structures, leading to cardiovascular compromise, which is a clinical emergency. Features on imaging reflect this displacement and can be identified on ‘scout’ views before formal CT.

The phenomenon of the occult pneumothorax arises from the inherent difficulties of interpreting the supine chest radiograph, where the pleural gas accumulates in the unfamiliar, anteromedial aspect of the pleural cavity. One study demonstrated an occult pneumothorax rate of 55%. Signs on the supine CXR include a deep costophrenic sulcus, hyperlucency over the hemidiaphragm and an abnormally well-defined mediastinal or cardiac border ( Fig. 10.7 ).

CT has a sensitivity and specificity for pneumothorax of almost 100%, with the only diagnostic difficulty arising from differentiating pneumomediastinum from medial pneumothorax, when identification of the mediastinal septation is key. Communication across the chest wall, the pleural space and the extra-corporeal space can lead to a specific type of pneumothorax, colloquially referred to as a ‘sucking chest wound’. This arises from the flutter-valve effect occurring through the chest wall. On CT, this type of injury can be suggested by the presence of a large pneumothorax that is resistant to chest drain insertion and evidence of a chest wall defect or large penetrating wound.

Haemothorax can be found in approximately 50% of all cases of chest trauma, with the haemorrhagic source ranging from ribs, intercostal vessels, lung parenchyma, great vessels or heart and pericardium. Arterial haemothorax can accumulate rapidly and cause both lung collapse and haemodynamic compromise. The supine chest x-ray may only show increased opacification of the affected hemithorax or a subtle lamellar effusion. On CT, haemorrhage can be identified by its increased attenuation (greater than 30 Hounsfield units (HU)) compared to water and may even demonstrate layering of blood products. Careful inspection of the great vessels, branch vessels and pericardium should be performed in the presence of a haemothorax.

Chylous pleural effusions usually occur secondary to penetrating injury and thoracic surgery. Features on imaging are evidence of penetrating trauma in the region of the thoracic duct and a pleural effusion. The exact site of injury can be demonstrated with selective puncture of the thoracic duct (and subsequent therapeutic coiling) by interventional radiology.

Lung Parenchyma

The most common parenchymal injury (up to 70%) is pulmonary contusion and occurs primarily at sites of change in tissue density, such as adjacent to the thoracic spine, ribs or heart. There is often a delay of up to 6 hours before the contusion may become apparent on a CXR, although immediate detection is possible with CT. Consolidation should become maximal before 24 hours and resolve within 3–10 days. Opacification that appears after 24 hours or fails to resolve as expected may be related to infection, aspiration, fat embolism or acute respiratory distress syndrome (ARDS).

Pulmonary laceration is a more severe injury, which results from compression, shearing or penetration. The lung tissue undergoes elastic recoil, creating a space that can fill with air, creating a pneumatocele, or with blood, creating a pulmonary haematoma. Both are more clearly demonstrated on CT and may initially be occult on the CXR caused by surrounding contusion ( Fig. 10.8 ).

Lung herniation is a rare consequence of chest trauma, where lung parenchyma herniates through a defect in the chest wall, such as in multiple comminuted rib fractures. Generally, it can be treated conservatively but its diagnosis is important because the volume of herniated tissue can increase with positive-pressure ventilation ( Fig. 10.9 ).

The term ‘blast lung’ describes a condition seen in survivors of near-proximity explosions in which there is an acute lung injury (ALI) causing alveolar rupture and haemorrhage that may manifest itself as large air embolism or pulmonary oedema/haemorrhage. The classic blast lung characteristics are those of hypoxia, respiratory distress and haemoptysis, radiologically apparent as bilateral diffuse pulmonary infiltrates, often in a ‘butterfly’ pattern on CXR. Delayed lung injury may have a similar picture to ARDS, but it is thought that any lung injury should be apparent within 2 hours and delayed deterioration is rare. The pleura and mediastinum may be disrupted and contain air or blood and the chest wall and spine may be injured by blast debris fragments.

Chest Wall

Rib fractures are common in chest trauma, occurring in approximately 50% of patients, but approximately half of these are likely to remain unidentified on the CXR, which is caused by superimposition and tangential orientation. Solitary rib fractures are not of direct acute concern but can be indicative of further occult injury. Of more concern are multiple fractures in two contiguous ribs, creating a section of chest wall that can move in a paradoxical manner in relation to the surrounding chest wall. This ‘flail’ segment is associated with hypoventilation of the underlying lung, likely parenchymal contusion, increased mortality and increased likelihood of requiring surgical treatment, which has been shown to reduce associated morbidity and mortality. Rib fractures may be associated with haemothorax or more localised extra-pleural haematoma. Elderly patients represent an important subset in whom the risk of thoracic trauma is magnified. There is an increased incidence of rib and vertebral body compression fractures with worse outcome due to reduced reserve related to natural ageing and co-morbidities. There is also an increased risk of side effects from investigations and standard treatments.

Injuries to the most superior three ribs are associated with severe trauma and, specifically, injury to the brachial plexus, subclavian vessels, trachea and spine. Scapular fractures serve as a similar indirect marker of severe trauma. Injuries to the inferior four ribs are associated with visceral injuries to the upper abdomen—left-sided being splenic lesions and right-sided being hepatic lesions.

Rib fractures in children are relatively rare and, therefore, the possibility of non-accidental injury should be considered, particularly if the posterior aspects are involved. Children and adolescents demonstrate a greater elasticity in their ribs and, subsequently, may have more severe internal thoracic injuries in the absence of rib fractures.

Sternal fractures are associated with increased cardiac and ascending aortic injury, and sternoclavicular joint dislocations, particularly the less common posterior dislocation, are associated with injury and compression of the brachiocephalic vessels.

Spinal fractures are not only of consequence to the spinal canal and surrounding neural structures, where 62% will be associated with a neurological deficit, but are also an indicator of severe trauma. Spinal fractures are commonly occult on plain radiographs and, if suspected, CT should be performed to assess further.

Diaphragm

The diaphragm can be injured by both penetrating and blunt trauma, particularly abdominal blunt trauma, due to a sudden increase in intra-abdominal pressure. This usually leads to a radial tear in the weaker, posterolateral tendinous insertion. Left-sided tears are more commonly seen on imaging and in surgical practice and this was thought to be due to a ‘protective’ effect of the liver. However, autopsy series have shown an almost equal incidence of right and left sided tears and it may be that in clinical practice many right sided tears remain radiologically and clinically occult.

Penetrating defects are generally associated with upper abdominal or chest wall injuries and are suggested by these injury patterns and the likely trajectories. Up to 70% of diaphragmatic ruptures are missed on initial assessment and prompt surgical repair is essential to avoid subsequent bowel herniation, strangulation and rupture, with an estimated 30% mortality from delayed diagnosis.

Chest radiographic signs may be delayed in appearance but include loss of clarity of the diaphragm, herniation of abdominal contents into the chest and displacement of the mediastinum away from the affected side ( Fig. 10.10 ). Key features of diaphragmatic rupture on CT are discontinuity of the diaphragm, best demonstrated on sagittal and coronal MPR; herniation of viscera or bowel into the thorax, often accompanied by a narrowing at the site of defect, which is known as the hourglass or collar sign; and the dependent viscera sign, where abdominal viscera appear to lie in a more dependent location, due to the absence of support from the ruptured diaphragm ( Fig. 10.11 ). In indeterminate cases in the stable patient, MRI can be useful: a respiratory-gated T ₁ sequence can show the diaphragm as a hypointense structure and herniated abdominal fat as high signal.

Although transabdominal ultrasound has been shown to be able to diagnose diaphragmatic rupture, its use has not gained acceptance, possibly due to the difficulties associated with concomitant injuries and dressings and operator dependency.