Chest injuries

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Chapter 69 Chest injuries

IMMEDIATE MANAGEMENT

During the primary survey a rapid assessment of the respiratory, circulatory and neurological status of the patient is made (Table 69.1). Airway patency is ensured, oxygen administered by facemask and ventilation assessed. Obvious external bleeding is controlled. Two large bore intravenous cannulae are sited, blood samples taken for crossmatch, haematology and biochemistry tests, and intravenous fluids commenced. Intravenous opioid analgesia is given as repeated small boluses, titrated to effect. There are four critical chest injuries that should be sought during the primary survey for which immediate intervention may be life saving:

Table 69.1 Immediate management of chest trauma

In addition, the clinical features of flail chest should be sought as these will no longer be apparent if positive-pressure ventilation is instituted (see below). A chest radiograph is integral to the initial assessment and should be performed promptly. Subcostal ultrasonography of the heart as part of the focused assessment with sonography for trauma (FAST) should be performed with penetrating chest trauma, or if there is haemodynamic instability.3 An ECG is important in the assessment for blunt cardiac injury (see below).4

Endotracheal intubation and mechanical ventilation are indicated for the patient with a compromised airway, severe head injury, or gross hypoventilation and/or hypoxaemia not attributable to pneumothorax. Haemodynamic instability should be anticipated (Table 69.2). Emergency cricothyroidotomy or tracheostomy is only rarely required when an airway obstruction cannot be bypassed by translaryngeal intubation. A nasogastric tube (or orogastric, if facial injuries are suspected) should be inserted to decompress the stomach after endotracheal intubation.

Table 69.2 Causes of cardiovascular collapse on induction of anaesthesia and positive-pressure ventilation in chest-injured patients

PNEUMOTHORAX

Pneumothorax visible on the initial chest radiograph should be treated with insertion of an intercostal tube connected to an underwater seal drainage system (Figure 69.1). A single-bottle drainage system without suction is usually adequate. Low-pressure suction (20 cmH2O) is applied if the pneumothorax fails to fully resolve, or if there is associated haemothorax (Figure 69.2). A three-bottle system (or commercially available three-in-one system) allows more accurate control of suction (Figure 69.3). Presumptive antibiotics are not indicated.5

Tension pneumothorax results from progressive accumulation of air in the pleural space, leading to vena caval compression and cardiopulmonary decompensation. Clinically, tension pneumothorax is characterised by:

If tension pneumothorax is suspected clinically an intercostal tube should be inserted immediately, prior to the chest radiograph. Needle thoracostomy with a large bore cannula inserted into the second intercostal space in themidclavicular line may be used to drain air more rapidly for patients in extremis. However, this is rarely necessary and may puncture the lung, fail to reach the pleural space, or kink when the needle is removed from within the cannula. Whether successful or not, needle thoracostomy must be followed by formal intercostal tube drainage.

Open pneumothorax occurs when a chest wall defect allows direct communication of a pneumothorax with the exterior, usually after penetrating trauma. Tension can develop if air can enter but not exit through the defect. Treatment involves application of an occlusive, non-adherent, square dressing sealed along three edges over the wound after sterile skin preparation. This allows air to escape but not to enter through the wound, but should be followed by intercostal tube insertion at a site not immediately adjacent to the wound.

Simple pneumothorax may develop tension at any stage, especially with positive-pressure ventilation (Table 69.2). A small pneumothorax may be missed on the initial chest radiograph. In the supine position pleural air collects anteroinferiorly and is demonstrated radiologically by a deep sulcus sign or increased radiolucency of one side of the chest compared to the other (Figure 69.4).6

Occult pneumothorax is defined as visible on chest CT (or upper slices of an abdominal CT) but not plain radiograph.7 Drainage is not mandatory, but should be considered if prolonged surgery is anticipated, there is significant cardiorespiratory compromise or interhospital transport is necessary. With a conservative approach the patient should be carefully monitored for deterioration from expansion of the pneumothorax.7

Subcutaneous emphysema over the chest wall in a patient with blunt chest trauma is almost always associated with pneumothorax, but should raise suspicion of other injuries (Table 69.3). The pneumothorax may not be visible on the plain chest radiograph, either because it is obscured by the emphysema or because it has largely decompressed into subcutaneous tissues. An intercostal tube should be inserted.

Table 69.3 Causes of pneumothorax, subcutaneous emphysema and/or pneumomediastinum

If there is no associated fluid collection the chest tube can be removed once the pneumothorax is no longer visible on chest radiograph and there has been no air drained for at least 24 hours. Persistent air leak and incomplete drainage of a pneumothorax after intercostal tube insertion should prompt investigation for tracheobronchial injury. However, the depth of the tube within the pleural space and tubing connections should be checked to ensure that extraneous air is not being inadvertently entrained. Incomplete drainage with no air leak is usually due to tube malplacement.

PERICARDIAL TAMPONADE

Pericardial tamponade should be suspected in any patient with a gunshot wound to the chest or stab wound to the precordium. It occurs rarely with blunt trauma, but should be suspected if there is hypotension out of proportion to blood loss, and distended neck veins. Pulsus paradoxus may be detected in the spontaneously breathing patient. The differential diagnosis includes tension pneumothorax (most likely) and cardiogenic shock from severe blunt cardiac injury or delayed and inadequate resuscitation. Pericardial fluid can be detected with ultrasound (FAST scan).3 Cardiac structures are imaged via a subcostal view using a low-frequency transducer (3.5 MHz) to provide good tissue depth penetration. Echocardiography, or operative subxiphoid window, can be used if diagnostic uncertainty remains.

Haemodynamically unstable patients should undergo thoracotomy.8 Subxiphoid pericardiotomy can be performed in selected stable patients, but may require conversion to open thoracotomy. Needle pericardiocentesis is rarely effective in the acute setting, but may have a role in the drainage of delayed pericardial effusions following stab wounds.8

SPECIFIC INJURIES

Specific chest injuries should be systematically excluded. Imaging techniques play an important role. Choice of investigation is influenced by clinical findings. The degree of haemodynamic and respiratory instability will determine whether the patient can be moved to an imaging facility. Local availability of equipment and clinician expertise may limit the options available. Extrathoracic injuries will often determine investigation and management priorities. With the advent of rapid high-resolution CT scanners, routine chest CT has become increasing popular, particularly in patients who require abdominal or head CT.10 Endotracheal intubation and mechanical ventilation may be required to facilitate investigations (e.g. the combative trauma patient with ethanol intoxication).

BLUNT AORTIC INJURY

Blunt aortic injury usually occurs at the junction between the mobile arch and fixed descending aorta, just distal to the origin of the left subclavian artery, as a result of severe deceleration injury. Less frequently, the ascending aorta or arch vessels are injured by direct trauma. Blunt aortic injuries may be divided into:11

Most patients with blunt aortic injury die at the scene from complete aortic wall transection or associatedinjuries. Of those that reach hospital, 90% will have a significant injury.11 Clinical signs include unequal upper limb pulses, pseudocoarctation or interscapular murmur, but these are rarely detected.12 Aortic injury should be suspected if the mechanism of injury is suggestive of rapid deceleration, such as high speed (greater than 90 km/h) motor vehicle or motorcycle crashes, or a pedestrian hit by a vehicle.13

Historically, chest radiography has been the screening test (to detect mediastinal haematoma) and aortic angiography the diagnostic test for blunt aortic injury.12,14 More recently, CT and echocardiography have been introduced for screening and diagnostic purposes:15

Chest radiograph features of blunt aortic injury are caused by distortion of normal mediastinal contour by periaortic haemorrhage. A widened mediastinum (> 8 cm at the level of the aortic knuckle) is the principal finding (Table 69.4).12,16 A good quality erect chest radiograph has a high sensitivity (> 90%), but low positive predictive value for aortic injury. Historically, this has resulted in a large number of negative aortograms.12,13 Furthermore, a supine chest radiograph accentuates mediastinal width and in the acute trauma setting is often of lower quality. Measurement of left mediastinal width (> 6 cm), or left mediastinal width to mediastinal width ratio (> 0.6), may improve specificity.16
Single slice helical chest CT may demonstrate direct signs of aortic injury. However, more commonly aortic injury manifests indirectly with periaortic haematoma, and a further diagnostic test is required.13 Nevertheless, by differentiating periaortic haematoma from other types of mediastinal haematoma, and excluding other causes of an abnormal mediastinal contour, helical CT provides a useful screening test. Routine chest CT has thus been advocated for haemodynamically stable patients with a high-risk mechanism of injury, especially if other CT scans are planned.13,17Multirow detector chest CT (with more than 16 detectors) provides sufficient resolution in multiple planes for CT to be used as the sole diagnostic test. However, the diagnostic role of CT for branch vessel injuries remains undefined (Table 69.5).18
Transoesophageal echocardiography is rapid and portable, making it suitable for examination of the unstable patient (who is intubated). It provides high diagnostic accuracy for aortic injury and also allows examination for blunt cardiac injury.19,20 However, imaging of the distal aorta, proximal arch and major branches is limited. Thus, if signs of mediastinal haematoma are detected, but an aortic injury not identified, further diagnostic testing is warranted.19 It is contraindicated if an upper-airway or oesophageal injury is suspected.

Table 69.4 Chest radiograph signs of blunt aortic injury

Signs of periaortic haematoma Indirect signs
Widened mediastinum (> 8 cm) Left haemothorax
Obscured aortic knuckle Left pleural cap
Opacification of aortopulmonary window Fractured first or second ribs
Deviation of trachea, left main bronchus or nasogastric tube  
Thickened paratracheal stripe  

Table 69.5 Signs of aortic branch vessel injury

Significant aortic injury requires prompt surgical or endoluminal stent repair.21 However, this should not take priority over other life-saving operations (e.g. craniotomy or laparotomy).12 Surgical options include direct repair (clamp and sew) or techniques that maintain distal aortic perfusion.14 The latter reduce the risk of postoperative paraplegia from spinal cord ischaemia, but often require systemic heparinisation, which may exacerbate bleeding from other injuries.15 Surgery should be deferred, sometimes indefinitely, if severe associated injuries or comorbidities make the operative risk unacceptably high.12,22 In such cases endoluminal stent repair may still be feasible.21 Conservative management includes antihypertensive therapy (β-blockers ± vasodilators) and serial imaging to assess for expanding pseudoaneurysm that will require intervention. Minimal aortic injury may also be managed expectantly.11,15,20

BLUNT CARDIAC INJURY

Blunt cardiac injury results from compression of the heart between the sternum and the spine, abrupt pressure changes within cardiac chambers or deceleration shear injury. A wide spectrum of injuries has been described, but may be classified according to the clinical sequelae and need for intervention:4

All patients should have an ECG on admission (Figure 69.5). If this is normal and the patient is young, haemodynamically stable, and has no history of cardiac disease, the risk of significant injury is very low and no further cardiac evaluation is required. Other patients should be monitored for late sequelae of significant cardiac injury (arrhythmia or heart failure).4 Patients who remain haemodynamically stable, with only minor ECG changes, and who have a normal troponin level at 6–8 hours post injury, have a low risk of cardiac complications.4,23 Echocardiography is indicated for patients with hypotension unexplained by other injuries, heart failure, or persistent arrhythmias.4 Undisplaced sternal fracture does not of itself warrant cardiac evaluation.24

image

Figure 69.5 Algorithm for evaluation of patients suspected of having blunt cardiac injury (BCI).

(Modified from Schultz JM, Trunkey DD. Blunt cardiac injury. Crit Care Clin 2004; 20: 57–70.)

DIAPHRAGMATIC RUPTURE AND DIAPHRAGMATIC PARESIS

The usual mechanism of diaphragmatic rupture is gross abdominal compression from direct vehicular intrusion. The risk of rupture is higher with lateral impact collisions, but not seat belt use.28 Associated injuries are very common.28 Rupture of the left hemidiaphragm is more common, because the right hemidiaphragm is congenitally stronger and protected by the liver.

Symptoms (dyspnoea and chest pain) are non-specific. Rarely bowel sounds are audible on chest auscultation. Diagnostic chest radiograph findings are herniation of bowel into the thoracic cavity and nasogastric tube above the left hemidiaphragm. Indirect signs include an elevated or distorted diaphragmatic outline, or pleural effusion, but these may be obscured by adjacent pulmonary pathology, phrenic nerve injury or with positive-pressure ventilation.29 The low diagnostic accuracy of chest radiography often results in delayed diagnosis unless further imaging is performed. Multidetector CT has high diagnostic accuracy, but magnetic resonance imaging or video thorascopy may be required if uncertainty persists.2931 Prompt operative repair is important to prevent bowel incarceration or perforation. The choice of surgical approach (laparotomy or thoracotomy) is dictated by associated injuries.

Traumatic phrenic nerve palsy, or postoperative diaphragmatic dysfunction, may go unrecognised whilst the patient is on mandatory positive-pressure ventilation. With the transition to spontaneous ventilation, paradoxical abdominal and chest wall movement, reduced vital capacity, and difficulty weaning from ventilatory support become evident.

OESOPHAGEAL INJURY

Rupture of the oesophagus from blunt trauma is rare. Penetrating trauma usually causes injury to the cervical portion of the oesophagus. Oesophageal injury may also result from attempted endotracheal intubation or gastric tube insertion during resuscitation of the trauma patient.32 Clinical features include chest pain, dysphagia, pain on swallowing and subcutaneous emphysema (Table 69.3). Chest radiograph findings include pneumothorax and/or hydrothorax, mediastinal emphysema or widened mediastinum.26 Prompt diagnosis by oesophagoscopy or gastrograffin swallow is important. Treatment is immediate surgical repair.32 Delayed recognition or repair (more than 12 hours post injury) leads to septic shock from mediastinal contamination. Extensive irrigation and drainage are then required, but postoperative complications are common.32

PULMONARY INJURY

Pulmonary contusion is characterised by interstitial haemorrhage and oedema, with a secondary inflammatory reaction. Clinically, there is increased work of breathing, impaired gas exchange and sometimes haemoptysis. The chest radiograph demonstrates patchy interstitial infiltrates or consolidation not confined to anatomical segments. Gas exchange and radiographic findings may initially be unremarkable, with deterioration over the first 24–48 hours.2,6 CT is more sensitive at detecting contusion, and quantification of lung volume affected predicts risk of acute respiratory distress syndrome (ARDS).33 In the absence of complications (ARDS, pneumonia or aspiration), clinical and radiological recovery can be expected within 3–5 days.6,33

Treatment is supportive with humidified oxygen therapy, and encouragement of deep breathing and coughing in the spontaneously breathing patient. Non-invasive ventilation can be used in selected patients if gas exchange is poor. Intubation and mechanical ventilation are indicated for refractory hypoxaemia, or if intubation is required for non-pulmonary reasons. Routine corticosteroids are not indicated. Antibiotics should be reserved for superimposed pneumonia.2

Pulmonary laceration occurs when disruption of lung architecture, with formation of an air- or blood-filled cavity, occurs after blunt or penetrating trauma.6 On chest radiography lacerations are often initially obscured by adjacent contusion, but typically take many weeks to resolve, and may be complicated by abscess formation or bronchopleural fistula.6

BONY INJURIES

Half of all rib fractures are missed on plain chest radiography, but should be suspected if there is localised tenderness over the chest wall. Good analgesia to prevent pulmonary complications from sputum retention is essential.34 This risk may not be clinically apparent initially, but deterioration in respiratory status over the next few days should be anticipated, especially in the elderly, smokers or patients with pre-existing pulmonary disease. First and second rib fractures, scapula fracture and sternoclavicular dislocation are markers of high-energy trauma.6

Most sternal fractures occur in restrained occupants involved in frontal impact vehicular crashes. Associatedthoracolumbar spine fractures are common.24 Blunt cardiac injury should be suspected with displaced sternal fractures.24

FLAIL CHEST

Fracture of at least four consecutive ribs in two or more places results in a flail segment with paradoxical movement of the chest wall during tidal breathing (Figure 69.6).2 Associated pulmonary contusion is often present. Younger patients with no other major injuries, no pulmonary comorbidities, and good analgesia can often be managed with non-invasive ventilation or oxygen therapy alone.35 Deteriorating gas exchange and sputum retention are indications for intubation and mechanical ventilation. Prolonged ventilatory support is often not necessary in patients whose associated injuries and comorbidities are not severe. Surgical stabilisation has been advocated for severe flail to reduce the duration of ventilation.36

image

Figure 69.6 Types of flail chest.

(Modified from Wanek S, Mayberry JC. Blunt thoracic trauma: flail chest, pulmonary contusion, and blast injury. Crit Care Clin 2004; 20: 71–81.)

EXTRAPLEURAL HAEMATOMA

Traumatic extrapleural haemorrhage arises when chest wall bleeding does not enter the pleural space.37 Chest radiography shows a parietal shadow that does not cause blunting of the costophrenic angle or shift with gravity. A large haematoma should be evacuated with a chest tube or by thoracotomy.

COMPLICATIONS AND ICU MANAGEMENT

On admission to ICU, rewarming, correction of coagulopathy and ongoing fluid resuscitation are often required. Pericardial tamponade and persistent air leak should be anticipated in post-thoracotomy patients.9 A restrictive approach to fluid therapy is indicated for patients who have undergone lung surgery. However, care should be taken to ensure adequate fluid resuscitation. A judicious transfusion policy should be employed with all patients.39

As with other critically ill or injured patients, prophylactic measures against thromboembolism40 and upper gastrointestinal stress ulceration should be used. Adequate nutrition is important to ameliorate the hypermetabolic and catabolic metabolic changes, reduce the incidence of sepsis, and improve outcome. Nutrition should be instituted early, preferably via the enteral route. Nasogastric feeding may be limited by gastric stasis, in which case nasojejunal feeding is usually successful.

ANALGESIA

Adequate analgesia is essential for deep breathing and effective coughing, which, if achieved, will reduce the likelihood that endotracheal intubation is needed for less severely injured patients. Analgesia also facilitates chest physiotherapy and early mobilisation, reducing pulmonary morbidity. The choice of analgesia depends on the severity of illness and may vary over time. Options include:34

PNEUMONIA

Sepsis is the principal cause of late death after major trauma. Breach of the skin surface barrier, devitalised tissues, and the presence of invasive drains and catheters make the trauma patient especially prone to bacterial invasion. In the chest-injured patient, pulmonary contusion, emergency intubation, shock, blood transfusion and the presence of extrathoracic injuries increase the risk of nosocomial pneumonia.42

Early-onset pneumonia (within the first few days of hospitalisation) may result from aspiration at the time of injury, particularly after head injury. Common pathogens are Haemophilus influenzae, Pneumococcus and anaerobes. Late-onset nosocomial pneumonia is more likely to be due to aerobic Gram-negative bacilli and Staphylococcus aureus.

The diagnosis of pneumonia is suspected if there are new or progressive infiltrates on the chest radiograph and deterioration in respiratory status. However, new infiltrates may also be caused by pulmonary contusion, pleural fluid collections, atelectasis, aspiration and pulmonary oedema. Infection is supported by the presence of purulent sputum, new fever and leukocytosis. Confirmation depends on culture of tracheal aspirate or bronchoscopic samples.43 Antibiotic therapy should be targeted at causative organisms. Prompt empiric antibiotics should be started in unstable patients, with re-evaluation at 48–72 hours.

Preventative measures include careful hand cleansing, reduced duration of intubation and ventilation, semirecumbent position, enteral nutrition, avoidance of excessive sedation or hyperglycaemia, and avoidance of prolonged prophylactic antibiotics.43 The role of selective decontamination of the digestive tract remains controversial.

RETAINED HAEMOTHORAX AND EMPYEMA

Haemothorax that is not adequately drained within a few days becomes clotted and unable to drain via intercostal tube. The clot becomes organised and fibrosed with progressive pleural thickening (fibrothorax). This results in loss of lung volume, impaired pulmonary compliance and increased risk of empyema formation. Retained haemothorax should be evaluated by ultrasound or CT. Small haemothoraces (< 300 ml) in clinically stable patients where the pleural cavity has not been violated may be observed. However, in the presence of respiratory compromise, suspected empyema or retained haemothorax over 500 ml, further drainage is required. This should be performed within 5–7 days, before the development of fibrothorax or empyema.

If the initial chest tube is poorly positioned or blocked, a second tube may be placed through a different skin incision, preferably under ultrasound or CT guidance. In the absence of a bleeding diathesis or empyema formation, early evacuation of retained haemothorax (within a few days of the initial haemothorax) can be attempted with intrapleural administration of a thrombolytic agent. Streptokinase 250 000 units, or urokinase 100 000 units, in 100 ml saline is instilled into the intercostal tube for 4 hours each day until resolution of haemothorax with minimal further drain losses.44 Alternatively, video-assisted thoracoscopic surgery (VATS) may be used in haemodynamically stable patients who can tolerate single lung ventilation.30,31 Failure of these techniques, or empyema formation, requires formal thoracotomy ± decortication.

FAT EMBOLISM SYNDROME

Fat embolism invariably occurs in patients with long bone fractures.45 Although fat embolism syndrome (with pulmonary, neurological and cutaneous sequelae) is uncommon, oxygen desaturation occurs frequently, and may be more severe and prolonged in patients with parenchymal lung injury.46 Treatment is supportive, but early resuscitation and fracture stabilisation are important preventative measures.45 Early (< 24 hours) intramedullary nailing is the fixation method of choice, resulting in fewer orthopaedic complications than other fixation methods, and fewer pulmonary complications than delayed surgery.47 However, internal fixation may provoke further fat embolism, require a longer operative time, and result in more blood loss than external fixation.47 Thus, in severely chest-injured patients, temporary stabilisation using external fixation, with intramedullary nailing several days later, is preferred.47

PROGNOSIS

Reported mortality rates for chest-injured patients vary greatly, reflecting the severity of chest injury and associated extrathoracic injuries. Initial physiological markers that predict adverse outcome are low Glasgow Coma Scale score, hypotension and high respiratory rate. In patients with severe blunt trauma, mortality is significantly higher with bilateral than unilateral chest injuries, and depends more on the extent of parenchymal lung injury than the extent of chest wall injury.48 Older age correlates strongly with worse outcome, even though the elderly are more likely to suffer rib fractures than parenchymal lung injury.48 In the elderly, the risk of death or pneumonia increases with each additional rib fractured. In younger patients, better physiological reserve means that outcome is only significantly worsened if four or more ribs are fractured.34,49 Obese patients (BMI > 30) are likely to suffer more complications during hospitalisation than non-obese patients.50

REFERENCES

1 Kulshrestha P, Munshi I, Wait R. Profile of chest trauma in a level I trauma center. J Trauma. 2004;57:576-581.

2 Wanek S, Mayberry JC. Blunt thoracic trauma: flail chest, pulmonary contusion, and blast injury. Crit Care Clin. 2004;20:71-81.

3 Scalea TM, Rodriguez A, Chiu WC, et al. Focused Assessment with Sonography for Trauma (FAST): results from an international consensus conference. J Trauma. 1999;46:466-472.

4 Schultz JM, Trunkey DD. Blunt cardiac injury. Crit Care Clin. 2004;20:57-70.

5 Maxwell RA, Campbell DJ, Fabian TC, et al. Use of presumptive antibiotics following tube thoracostomy for traumatic hemopneumothorax in the prevention of empyema and pneumonia – a multi-center trial. J Trauma. 2004;57:742-748. discussion 748–9

6 Miller LA. Chest wall, lung, and pleural space trauma. Radiol Clin North Am. 2006;44:213-224. viii

7 Ball CG, Kirkpatrick AW, Laupland KB, et al. Incidence, risk factors, and outcomes for occult pneumothoraces in victims of major trauma. J Trauma. 2005;59:917-924. discussion 924–5

8 Hunt PA, Greaves I, Owens WA. Emergency thoracotomy in thoracic trauma – a review. Injury. 2006;37:1-19.

9 Rotondo MF, Bard MR. Damage control surgery for thoracic injuries. Injury. 2004;35:649-654.

10 Guerrero-Lopez F, Vazquez-Mata G, Alcazar-Romero PP, et al. Evaluation of the utility of computed tomography in the initial assessment of the critical care patient with chest trauma. Crit Care Med. 2000;28:1370-1375.

11 Malhotra AK, Fabian TC, Croce MA, et al. Minimal aortic injury: a lesion associated with advancing diagnostic techniques. J Trauma. 2001;51:1042-1048.

12 Nagy K, Fabian T, Rodman G, et al. Guidelines for the diagnosis and management of blunt aortic injury: an EAST Practice Management Guidelines Work Group. J Trauma. 2000;48:1128-1143.

13 Dyer DS, Moore EE, Ilke DN, et al. Thoracic aortic injury: how predictive is mechanism and is chest computed tomography a reliable screening tool? A prospective study of 1,561 patients. J Trauma. 2000;48:673-682. discussion 682–3

14 Fabian TC, Richardson JD, Croce MA, et al. Prospective study of blunt aortic injury: multicenter trial of the American Association for the Surgery of Trauma. J Trauma. 1997;42:374-380. discussion 380–3

15 Degiannis E, Boffard K. Critical decisions in trauma of the thoracic aorta. Injury. 2002;33:317-322.

16 Wong YC, Ng CJ, Wang LJ, et al. Left mediastinal width and mediastinal width ratio are better radiographic criteria than general mediastinal width for predicting blunt aortic injury. J Trauma. 2004;57:88-94.

17 Mirvis SE. Thoracic vascular injury. Radiol Clin North Am. 2006;44:181-197. vii

18 Holdgate A, Dunlop S. Review of branch aortic injuries in blunt chest trauma. Emerg Med Australas. 2005;17:49-56.

19 Cinnella G, Dambrosio M, Brienza N, et al. Transesophageal echocardiography for diagnosis of traumatic aortic injury: an appraisal of the evidence. J Trauma. 2004;57:1246-1255.

20 Vignon P, Martaille JF, Francois B, et al. Transesophageal echocardiography and therapeutic management of patients sustaining blunt aortic injuries. J Trauma. 2005;58:1150-1158.

21 Andrassy J, Weidenhagen R, Meimarakis G, et al. Stent versus open surgery for acute and chronic traumatic injury of the thoracic aorta: a single-center experience. J Trauma. 2006;60:765-771. discussion 771–2

22 Hirose H, Gill IS, Malangoni MA. Nonoperative management of traumatic aortic injury. J Trauma. 2006;60:597-601.

23 Rajan GP, Zellweger R. Cardiac troponin I as a predictor of arrhythmia and ventricular dysfunction in trauma patients with myocardial contusion. J Trauma. 2004;57:801-808. discussion 808

24 von Garrel T, Ince A, Junge A, et al. The sternal fracture: radiographic analysis of 200 fractures with special reference to concomitant injuries. J Trauma. 2004;57:837-844.

25 Kiser AC, O’Brien SM, Detterbeck FC. Blunt tracheobronchial injuries: treatment and outcomes. Ann Thorac Surg. 2001;71:2059-2065.

26 Euathrongchit J, Thoongsuwan N, Stern EJ. Nonvascular mediastinal trauma. Radiol Clin North Am. 2006;44:251-258. viii

27 Self ML, Mangram A, Berne JD, et al. Nonoperative management of severe tracheobronchial injuries with positive end-expiratory pressure and low tidal volume ventilation. J Trauma. 2005;59:1072-1075.

28 Reiff DA, McGwin GJr, Metzger J, et al. Identifying injuries and motor vehicle collision characteristics that together are suggestive of diaphragmatic rupture. J Trauma. 2002;53:1139-1145.

29 Iochum S, Ludig T, Walter F, et al. Imaging of diaphragmatic injury: a diagnostic challenge? Radiographics. 2002;22(Spec No):S103-S116. discussion S116–8

30 Carrillo EH, Richardson JD. Thoracoscopy for the acutely injured patient. Am J Surg. 2005;190:234-238.

31 Lowdermilk GA, Naunheim KS. Thoracoscopic evaluation and treatment of thoracic trauma. Surg Clin North Am. 2000;80:1535-1542.

32 Asensio JA, Chahwan S, Forno W, et al. Penetrating esophageal injuries: multicenter study of the American Association for the Surgery of Trauma. J Trauma. 2001;50:289-296.

33 Miller PR, Croce MA, Bee TK, et al. ARDS after pulmonary contusion: accurate measurement of contusion volume identifies high-risk patients. J Trauma. 2001;51:223-228. discussion 229–30

34 Simon BJ, Cushman J, Barraco R, et al. Pain management guidelines for blunt thoracic trauma. J Trauma. 2005;59:1256-1267.

35 Gunduz M, Unlugenc H, Ozalevli M, et al. A comparative study of continuous positive airway pressure (CPAP) and intermittent positive pressure ventilation (IPPV) in patients with flail chest. Emerg Med J. 2005;22:325-329.

36 Tanaka H, Yukioka T, Yamaguti Y, et al. Surgical stabilization of internal pneumatic stabilization? A prospective randomized study of management of severe flail chest patients. J Trauma. 2002;52:727-732. discussion 732

37 Rashid MA, Wikstrom T, Ortenwall P. Nomenclature, classification, and significance of traumatic extrapleural hematoma. J Trauma. 2000;49:286-290.

38 Ho AM, Ling E. Systemic air embolism after lung trauma. Anesthesiology. 1999;90:564-575.

39 Croce MA, Tolley EA, Claridge JA, et al. Transfusions result in pulmonary morbidity and death after a moderate degree of injury. J Trauma. 2005;59:19-23. discussion 24

40 Knudson MM, Ikossi DG. Venous thromboembolism after trauma. Curr Opin Crit Care. 2004;10:539-548.

41 Fan E, Needham DM, Stewart TE. Ventilatory management of acute lung injury and acute respiratory distress syndrome. JAMA. 2005;294:2889-2896.

42 Croce MA, Tolley EA, Fabian TC. A formula for prediction of posttraumatic pneumonia based on early anatomic and physiologic parameters. J Trauma. 2003;54:724-729. discussion 729–30

43 Guidelines for the management of adults with hospital-acquired, ventilator-associated, and healthcare-associated pneumonia. Am J Respir Crit Care Med. 2005;171:388-416.

44 Inci I, Ozcelik C, Ulku R, et al. Intrapleural fibrinolytic treatment of traumatic clotted hemothorax. Chest. 1998;114:160-165.

45 White T, Petrisor BA, Bhandari M. Prevention of fat embolism syndrome. Injury. 2006;37(Suppl 4):S59-S67.

46 Wong MW, Tsui HF, Yung SH, et al. Continuous pulse oximeter monitoring for inapparent hypoxemia after long bone fractures. J Trauma. 2004;56:356-362.

47 Pape HC, Giannoudis P, Krettek C. The timing of fracture treatment in polytrauma patients: relevance of damage control orthopedic surgery. Am J Surg. 2002;183:622-629.

48 Pape HC, Remmers D, Rice J, et al. Appraisal of early evaluation of blunt chest trauma: development of a standardized scoring system for initial clinical decision making. J Trauma. 2000;49:496-504.

49 Brasel KJ, Guse CE, Layde P, et al. Rib fractures: relationship with pneumonia and mortality. Crit Care Med. 2006;34:1642-1646.

50 Brown CV, Neville AL, Rhee P, et al. The impact of obesity on the outcomes of 1,153 critically injured blunt trauma patients. J Trauma. 2005;59:1048-1051. discussion 1051