Diagnostics and Scoring in Blunt Chest Trauma - Springer Link

European Journal of Trauma

Review Article

Diagnostics and Scoring in Blunt Chest Trauma Frank Hildebrand1, Martijn van Griensven1, Rajeev Garapati2, Christian Krettek1, Hans-Christoph Pape1

Abstract Background: Blunt chest trauma is frequently present in patients with multiple trauma. In polytraumatized patients thoracic injuries have significant influence on the treatment strategy, not only in the emergency room but also in the intensive care unit. They also affect the decision-making concerning fracture management. The vital role played by blunt chest trauma in the outcome after multiple injuries is highlighted by the fact that polytraumatized patients with severe thoracic trauma have a higher mortality rate than patients with the same injury severity without thoracic trauma. Diagnostics and Injury Severity: Within the broad category of thoracic trauma, there are many different types of injuries. Therefore it is crucial for the treating physician to promptly make the correct diagnosis and to quantify the severity of the injury. This will allow the selection of an appropriate treatment protocol and ensure the best possible outcome for the patient. Scoring Systems: Additionally, various treatment protocols for management can only be evaluated scientifically if the assessment of the trauma severity is standardized. Thus, a reliable CT-independent classification of the severity of thoracic trauma is essential. The “Thoracic Trauma Severity Score” (TTS) is a CT-independent classification of thoracic trauma that is reliable and can be performed quickly in the emergency room. This will allow for adequate treatment of thoracic trauma and the prevention of secondary complications. Key Words Blunt chest trauma · Multiple trauma · Diagnostics · Scoring systems Eur J Trauma 2002;28:157–67 DOI 10.1007/s00068-002-1192-1

Introduction Isolated thoracic injuries occur with a localized, blunt trauma to the chest. The majority of these cases are associated with mild injuries like thoracic bruises and rib fractures. In contrast, severe thoracic trauma (Abbreviated Injury Scale [AIS] > 3) occurs in 80–90% of patients with multiple trauma. Only 8–9% of these cases are due to penetrating trauma [1]. Blunt thoracic trauma accounts for the majority of severe chest injuries and is the second most common diagnosis, next to extremity injuries, in patients with multiple trauma [2]. The results of several studies suggest that the vast majority of isolated thoracic injuries can be treated conservatively. In younger patients, the mortality associated with this injury is 0–5%. In contrast, the mortality rate amounts to 10–15% in older patients [3–5]. Moreover, the morbidity and mortality are substantially higher in polytraumatized patients with severe thoracic trauma compared to patients with similar severity of injury without thoracic trauma [6]. This observation is based on the fact that severe thoracic trauma appears to be responsible for the posttraumatic appearance of serious respiratory insufficiency and adult respiratory distress syndrome (ARDS). Also, the occurrence of multi-organ dysfunction (MOD) and higher-infectious complications (pneumonia) is associated with these injuries [5, 7–9]. Polytrauma patients with thoracic injuries have a significant increase in the duration of ventilation (2 vs. 8 days) and intensive care unit stay (4 vs. 11 days) when compared to trauma patients without thoracic injury [2]. Moreover, thoracic injuries are associated with a mortality of nearly 40% in patients with multiple trauma and are responsible for approximately 20–25% of trauma-associated deaths. Approximately 50–75% of polytraumatized patients who died, had a thoracic injury

Department of Trauma Surgery, Hannover Medical School, Hannover, Germany, 2 Northwestern Memorial Hospital, Chicago, IL, USA. 1

Received: December 11, 2002; revision accepted: April 8, 2002

European Journal of Trauma 2002 · No. 3 © Urban & Vogel

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Hildebrand F, et al. Blunt Chest Trauma

[3–5, 8, 10–12]. The prognosis is particularly unfavorable when the triad of a difficult head trauma, a severe extremity or pelvic injury and a blunt thoracic trauma is present. The lung is the organ most frequently (80%) found to be failing, should a polytrauma patient with the above injury triad develop multiple organ failure (MOF) [13]. Blunt thoracic trauma can lead to injuries of the chest wall as well as of the lung parenchyma. Injuries to the Chest Wall Rib fractures represent the most frequent thoracic injury. They are present in approximately 60% of patients with blunt thoracic trauma and usually involve ribs IV–X. In elderly patients, even minor injuries can cause fractures, because of the low elasticity of the bone and osteoporosis. In younger patients, however, a substantial force is necessary to produce a rib fracture. Fractures of the mobile basal ribs are almost only found in cases of direct violence and are frequently associated with injuries to the liver, spleen or kidneys. Since the first two ribs provide protective envelope to the surrounding vital structures, severe thoracic injury is assumed when these two ribs are fractured. Severe lung contusion is very likely in this situation and should be anticipated. The fracture of more than three ribs is defined as a serial rib fracture. Serial rib fractures are found in onethird of all rib fractures. With an increasing number of broken ribs, the degree of chest wall instability also increases. In this context, fractures of the anterior and lateral part of the ribs have a stronger effect on the respiratory mechanics than fractures in the dorsal area. This results from the stabilizing effect of the paravertebral musculature on posterior rib fractures [14]. One of the most difficult and severe forms of chest wall injury to deal with is the flail chest. The injury is present in approximately 15% of patients with blunt thoracic trauma [15]. In a flail chest, there is an unstable motion segment as a portion of the rib is separated from the osseous chest wall due to the presence of multiple fractures. This leads to paradoxical respiratory movements of the involved segment (inward movement with inspiration and outward movement with expiration). Flail chest injuries are also frequently accompanied by pulmonary contusion [13]. The chest wall pain, associated with rib fractures, often results in decreased ventilation, which in turn can lead to a retention of secretions with formation of

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atelectasis and eventual pneumonia [16]. In case of an unstable chest, a poor unfolding of the lung leads to a decrease of tidal volume. The severity of this expansion disturbance depends, first of all, on the number of rib fractures and therefore on the extent of instability of the chest wall. In order to maintain the respiratory minute volume, an increased respiration work must be performed. As a consequence, respiratory insufficiency usually appears which leads to intubation and artificial ventilation of the patient [14, 17]. In addition to rib fractures, a fracture of the sternum with accompanying injuries (contusions of the lung and heart) can be associated with thoracic trauma [13]. Injuries to the Intrathoracic Organs and Blood Vessels Parenchymal injuries to the lung occur in the form of contusions and lacerations. Lacerations appear either from penetration of the lung parenchyma from outward (e.g., fractured ribs) or from bursting of the lung surface as a result of a high intrapulmonal pressure. With the exception of stab wounds, lacerations are always accompanied by pulmonary contusions [14]. The most frequent acute consequences of injuries to the lung parenchyma are pneumo- and hemothoraces. Also, a combination of these, a hemopneumothorax, is possible. Other causes for a pneumothorax are injuries to the tracheobronchial tree, which appear in < 2% of thoracic trauma, or outwardly open injuries to the thorax [14, 17]. A pneumothorax is present in approximately 20–30% of patients with blunt thoracic trauma. A tension pneumothorax can develop if a valve mechanism develops that leads to air inflow into the pleural cavity but prevents outflow. As a direct consequence, lung collapse occurs leading to decreased gas exchange surface and resulting hypoxia. In addition, the increased intrathoracic pressure leads to a decreased cardiac output and a reduction in blood pressure [14, 17]. It is possible for mediastinal emphysema to develop in the presence of a pneumothorax. This occurs if air reaches the mediastinal connective tissue. The forces that create a pneumothorax can also injure the trachea, esophagus, maxillofacial area, and bronchial tree. Thus, injuries to these areas must also be looked for [18]. A hemothorax is present in 40% of patients with blunt thoracic trauma and is associated with many different injuries. An associated injury to the chest wall is present in 70% of patients with hemothorax. Various



bleeding sources can contribute to hemothorax including intercostals arteries in case of rib fractures and internal mammary arteries in case of sternal fractures. Among the other sources of bleeding are lung parenchyma, hilar vessels, heart and big vessels. A massive hemothorax can be followed by hemorrhagic shock with circulatory failure. In case of an undrained massive hemothorax, a tension hemothorax may develop [17]. Incomplete drainage of a hemothorax can lead to formation of a fibrothorax. This fibrothorax may result in restrictive pulmonary disease and also, it increases the risk of pleural empyema [13]. Traumatic thoracic aortic rupture occurs in 2% of blunt chest trauma patients. Ruptures of the aorta are most commonly found after severe deceleration injuries. The complete aortic rupture is one of the most frequent causes for sudden death after trauma. Approximately 90% of aortic ruptures are still lethal at the scene of an accident. Such an injury can only be survived if the adventitia of the aorta remains intact. Injuries to other big intrathoracic vessels are present in only 1% of blunt thoracic trauma [13, 17]. With every thoracic trauma, injury to the heart must be ruled out. It is assumed that heart injuries are observed in 15–25% of all thoracic trauma [20]. In case of a sternal fracture, parasternal fractures of the first and second rib or rupture of the diaphragm, the incidence rises to 75% [21]. A myocardial contusion associated with thoracic trauma can cause structural as well as functional changes of the heart. Structural injuries include perforations of the heart muscle or of the ventricular septum and disruption of the papillary muscle or the flaps [13]. Thoracic trauma can lead to a rupture of the cardiac wall by an acute increase in intracardial pressure. The right atrium is particularly vulnerable to rupture because of the weak muscle wall. However, it is also possible for the heart to become compressed between the sternum and the spinal column. This may result in tearing of the right or left ventricle. Ruptures of the cardiac wall can appear immediately after an acute trauma or present up to 14 days after injury [13, 14]. Myocardial contusions can adversely affect the function of the heart by damaging the conduction system and causing a decrease in cardiac output. This can subsequently lead to the development of arrhythmias, such as ventricular fibrillation, or cardiogenic shock (failure of the left or right heart). These complications may also occur in a delayed fashion and lead to chronic


damages (chronic low-output syndrome, cardiac insufficiency) [13, 14, 17]. Pericardial tamponade is another injury to the heart following thoracic trauma. It usually occurs after penetrating trauma but is also present in about 1% of patients with blunt chest trauma [13, 17]. In this injury, there is epi- or intrapericardial bleeding into the fibrous pericardial pouch that quickly results in a filling impediment of the heart. This will result in a pumping failure of the heart. Besides rib fractures, contusion of the lung represents the most frequent injury caused by thoracic trauma. Multiple studies reveal that pulmonary contusion occurs in 30–50% of polytrauma patients with blunt chest injury. Pulmonary contusions are caused by direct pressure on the lung parenchyma as well as by indirect injuries like deceleration and shearing forces. While older patients frequently show rib fractures without contusions of the lung, younger patients can have substantial pulmonary contusion without an osseous injury. Therefore, the lack of rib fractures does not exclude the presence of severe lung contusion [13, 17]. In a clinical study, serious accompanying injuries were diagnosed in 25% of the patients with thoracic trauma in the absence of a bone injury [22, 23]. However, serial fractures of the ribs and flail chest were almost always accompanied by contused areas [16]. Histopathologically, focal contusions are areas with intraalveolar extravasation of blood, accompanied by perifocal edema. Lacerations of big pulmonary vessels can lead to intrapulmonary hematoma. Besides, the perifocal edema, the inflammatory and immunomodulatory reaction initiated by traumatized tissue can lead to systemic inflammatory response syndrome (SIRS) [24]. This systemic inflammatory reaction can cause damage to the uninvolved area of the lung and even the contralateral lung [22, 25, 26]. The direct and indirect injuries to the pulmonary system represent an essential promoter for the development of acute posttraumatic lung failure (ARDS) [27–29]. In this type of acute lung failure, gas exchange disturbances appear due to changes in the alveolocapillary diffusion distance. Also, pro-inflammatory mediators activate the immune system and lead to damage of the endothelial lung cells. These adverse effects on gas exchange usually begin 24–48 h after the initial trauma and can progress gradually until complete respiratory insufficiency develops [26, 30]. A lack of surfactant, which appears 16–24 h after lung contusion, plays an additional role in the develop-

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ment of respiratory insufficiency. Certainly, the severity of thoracic trauma plays an essential role in the development of such diffuse pulmonary damages, however, ARDS can also develop after seemingly mild trauma [14]. MOD is caused by the same mechanism of inflammatory reactions that causes ARDS. This SIRS damages the endothelial cells of capillary blood vessels which leads to impaired microcirculation to vital organs, eventually culminating into MOD [31, 32]. Strategy of Fracture Care in Case of Simultaneously Existing Thoracic Trauma There is a high incidence of polytrauma patients with coexisting thoracic injury and long bone fracture. Over the years, there has been much discussion about the timing and nature of fracture care in such combined injuries. The early surgical stabilization of limb fractures offers numerous advantages, such as early patient mobilization and the associated reduction of thromboembolic and infectious complications [33, 34]. Clinical studies have shown that primary fracture care leads to a reduced duration of ventilatory therapy. These studies advocate the model of “early total care” (ETC). This model of early definitive care was also thought to be of benefit in patients with thoracic trauma [35, 36]. This rule, however, seems to have only limited validity in these patients. Polytrauma patients with both thoracic injury and long bone fracture have been observed to develop pulmonary complications, especially ARDS, after the stabilization of femur fractures by intramedullary nailing. The development of ARDS is especially increased if the patient had a preexisting pulmonary impairment such as serial rib fractures, hemothorax or pulmonary contusion [37, 38]. An acute embolism of fat and bone marrow contents to the lung during intramedullary instrumentation has currently been discussed as a possible reason. In experimental studies, it has been shown that intramedullary nailing mechanically drives fat out of the bone. As thromboplastin is also released from the bone marrow, fat and blood thrombi are formed in the blood vessels [39, 40]. Eventually, these thrombi lodge into pulmonary blood vessels and impair pulmonary circulation. Additionally, granulocyte-mediated [41, 42] impaired capillary permeability leads to further damage. Just as the initial trauma can provide a “first hit” to the patient, surgical interventions can provide a “second hit” that is associated with an increase in the patient’s inflammatory reac-

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tion. The severity of this “second hit” appears to be dependent on the nature and duration of the operation. For operations on the spinal column and pelvic fractures, similar reactions have been shown [43, 44]. Giannoudis et al [45] have examined the effects of reamed versus unreamed intramedullary nailing in isolated femoral fractures and were able to show a decreased inflammatory reaction by using the unreamed technique. The results of several studies have shown that intramedullary nailing of the femur leads to a substantial intensification of lung damage. In this context, granulocyte activation plays an important role [9, 46–48]. Furthermore, it is known that systemic factors, like the cytokines tumor necrosis factor alpha (TNF-α), interleukin-(IL-)1β and IL-6, are released directly during intramedullary nailing. These cytokines directly increase the microcirculatory permeability of endothelial cells [49]. The use of an unreamed intramedullary nail, rather than a reamed one, has unambiguously shown a reduction of the increase in pulmonary artery pressure, the lung damage, and the activation of granulocytes [46]. Nevertheless, use of the unreamed procedure can also lead to systemic complications [50–53], if the patient selection for such a procedure is less critical. The use of an external fixation is the least invasive and quickest method to stabilize a long bone fracture. This leads to a minimization of the systemic inflammatory reaction and thus, decreases the amount of additional pulmonary damage caused by surgery. After the pulmonary status has been stabilized, the definitive care of the long bone fracture can take place [9, 40, 54]. A thoracic trauma can lead to a multiplicity of different diagnoses. So, in the clinical setting, different problems arise based on the complexity and severity of the injury. 1. How can an early exact diagnosis of all injuries be guaranteed? 2. How can the relevant complications be foreseen after a thoracic trauma? A prompt diagnosis of the thoracic injury leads to the best possible therapy as well as the secondary prevention of other posttraumatic damages resulting from hypoxia or shock. In addition to the proper diagnosis, a quantification of the size of the thoracic trauma is of crucial importance. There are numerous diagnostic tests that can help make the diagnosis and quantify the severity of the injury. These include:



Conventional X-Ray In the initial assessment of polytraumatized patients, the physical examination is followed by chest X-ray and abdominal sonography [55]. The chest X-ray is performed with the patient in supine position and is usually done in the anteroposterior direction. The chest X-ray is quick, easily available, and it provides a good assessment of the injury to the thoracic skeleton. The most important disadvantage of a plain chest Xray taken in the supine position is the lack of axial resolution with the absence of the second image plane. The superimposition of different structures and organs in the anteroposterior plane makes interpretation difficult resulting in a limited diagnostic value [56]. At the time of admission, the severity of pulmonary contusion is frequently underestimated by X-rays of the chest [27, 57, 58]. Marths et al [59] showed that chest X-rays revealed pulmonary contusions only in approximately one-third of the patients in whom they were present. Greene [60] demonstrated that even if a lung contusion could be demonstrated, its extent was underestimated. Computed Tomography (CT) of the Chest The deficiencies of the conventional X-rays in the diagnosis of thoracic injuries can largely be compensated for by the use of CT of the chest [56]. CT represents the most important examination method in the thoracic trauma patient. The use of a spiral CT can shorten the examination period down to a few minutes [55]. The value of thoracic CT is undisputed, but people argue about the relevance of the additional information it provides [61–67]. Marths et al [59], in their study, compared the usefulness of initial chest X-rays versus CT scan. The CT scan was shown to be superior in diagnosing pneumothorax, hemothorax, and lung parenchymal lesions (contusion/laceration). However, the additional information changed trauma treatment strategy in only 6.5% of the cases. Another study done by Guerrero-Lopez et al [68] showed that CT scans not only aided in diagnosis of thoracic injuries but also better quantified the injury severity. This was especially true for injuries of the sternum, the spinal column, and the mediastinum. In 30% of the patients, management decisions were guided by the additional information obtained on the CT scans. However, the improvement in overall outcome could not be proven and thus, the authors did not unilaterally recommend the use of an emergency thoracic CT scan in all polytrauma patients


[68]. At the other end of the spectrum, McGonigal et al [63] showed, in a retrospective study, that a CT scan of the chest resulted in therapeutic consequences in up to 70% of patients. Therefore, they recommended getting a thoracic CT scan in all high-energy polytrauma patients with an anticipated involvement of the chest. In a study on 47 patients with isolated traumatic brain injury who were on mechanical ventilation, Karaaslan et al [69] showed that a chest CT revealed the nature of the thoracic injury in 44 of the 47 patients. In 24 patients the injury was also seen on a conventional thoracic Xray. Therefore, the authors recommended a CT scan of the chest in all patients requiring artificial respiration or having a Glasgow Coma Score < 8. Ivatury & Sugarman [70] and Exadaktylos et al [71] substantiated theses findings in their prospective studies, with significant thoracic injuries found on CT scan in more than 50% of patients with normal initial chest radiograph. In 1997, a prospective study [72] has shown that a CT of the thorax in the primary diagnostics of the polytraumatized patient allows a substantially more exact diagnosis of thoracic injury. Essential additional information in comparison to conventional radiograph were obtained in up to 65% of the cases. In this study, direct therapeutic consequences were noted in 41%. On account of these results, the authors recommended that a CT scan should always be performed in case of abnormal findings on the initial chest X-ray, abnormal clinical findings, respiratory insufficiency, and high-energy thoracic trauma [72]. Looking at the results of two other studies [73, 74], contrast-enhanced spiral CT, based on its high sensitivity and negative predictive value, has a critical role in the exclusion of thoracic vessels injuries in patients with major blunt chest trauma. Potentially fatal aortic lesions were diagnosed on CT scan, despite a normal initial chest radiograph in up to 10% of patients [71]. The role of routine CT scan in blunt chest trauma is still under debate. The additional diagnostic value of this examination in the recent literature is accepted, the opinion about the effect on clinical outcome is controversial. The majority of studies, however, recommend primary routine chest CT scan in all trauma patients with multiple trauma and suspected thoracic injuries. Additionally, spiral chest CT is becoming a standard practice as an initial diagnostic procedure in most of the major trauma centers. In summary, it is feasible for thoracic CT scan to be a first-line exam in blunt chest trauma. Only in patients with severe multiple injuries, which require emergency surgery (e.g., laparotomy), time-

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consuming CT scanning should be deferred. Besides, if a patient is not admitted to a level I hospital, the method may not be available on a 24-h basis. Ultrasound Examination The examination by ultrasound offers several advantages. It is available in every hospital and can be performed without big expenditure. The required examination time is short, and the examination can be repeated at any time. Therefore, the diagnosis can be provided very quickly. This can substantially shorten the time to the initiation of therapeutic measures. Sonography is a noninvasive examination which represents no additional burden to the patient with severe multiple trauma [75]. The diagnosis of a hemothorax by ultrasound is very reliable [76, 77]. A hemothorax of 20 ml can readily be diagnosed by an experienced investigator. In a study by Röthlin et al [75], the sensitivity of sonography for the detection of intrathoracic fluid was 81% and in 3% of the cases, an associated injury to the mediastinum was diagnosed. As to the disadvantages, sonography cannot detect pneumothorax, and subcutaneous emphyema precludes accurate diagnosis by sonography [75]. In addition, the diagnosis of bone injuries is a domain of radiologic diagnostics. Therefore, sonography cannot replace the radiologic diagnostics and cannot be used as an exclusive measure in the diagnostics of thoracic trauma. In summary, it must be stated that the sonographic examination can only play a supplementary role as a possible diagnostic tool for thoracic trauma. Bronchoscopy Bronchoscopy can provide valuable additional information, both as a diagnostic and a therapeutic tool, in the management of blunt thoracic trauma. In a clinical study, bronchoscopy was of diagnostic use in 53% of the examined patients with severe multiple trauma. It was particularly useful regarding the diagnosis of damage to the tracheobronchial tree (tracheal and bronchial transections and lacerations), supraglottic injuries, aspiration, bleeding, and lung contusions [78]. The latter are diagnosed bronchoscopically by seeing the presence of petechial bleeding, submucous hemorrhage and swelling as well as intrabronchial hemorrhage [57]. Multiple studies have shown that the diagnosis of lung contusion can be made earlier by bronchoscopy than it can be made by conventional chest X-ray or blood gas analysis. Furthermore, the extent of a contusion can be determined more reliably [57, 79]. Besides the diagnos-

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tic usefulness, another advantage of bronchoscopy is its therapeutic use. Secretions, blood and aspirations from the respiratory tract can be cleared with the suction and therefore, formation of atelectasis can be prevented. Also bleeding within the respiratory tract can be coagulated. In a study by Regel et al [79], bronchopleural fistulae could be closed by means of bronchoscopy, and the risk of severe posttraumatic pneumonia could be decreased by means of bronchoalveolar lavage (BAL). In spite of the advantages mentioned, the indications for bronchoscopy in the polytrauma setting are rare (severe bleeding or tracheobronchial ruptures). Hoffmann & Gahr [80] showed that the blood gas values of polytraumatized patients were substantially worsened due to bronchoscopy. The respiratory situation of polytraumatized patients was worsened due to additional hypoxia caused by disturbances of the microcirculation associated with an increase of pulmonary vascular resistance [80]. Therefore, it is understood that bronchoscopy is not feasible as a routine procedure in the primary diagnostics of polytrauma patients, as it can intensify the respiratory insufficiency. Ventilation-Perfusion Scintigraphy In studies examining patients with isolated thoracic trauma and associated lung contusions, it could be shown that ventilation-perfusion scintigraphy was the most sensitive method for the diagnosis of functional restrictions of the lung. Because of the involved expenditure, this examination is not suitable for the diagnostic purpose in polytraumatized patients [81, 82]. Arterial Blood Gases Arterial blood gas analysis is a fairly good predictor of the current lung function. A deterioration of blood gas value as a consequence of a right-left shunt caused by pulmonary contusions is a life-threatening sign. This deterioration appears up to days earlier compared to the radiologically visible changes of the lung. In a study by Merkle & Ahrendt [81], it was proven by means of blood gas analyses that the oxygen partial pressure of polytraumatized patients with associated severe thoracic trauma was much lower at the accident scene compared to patients with multiple trauma without injuries to the chest. These results were confirmed by Helm et al [83] on the basis of peripheral oxygen saturation of blood. In cases of thoracic trauma with associated lung contusions, a deterioration of the Horovitz quotient (pO2/FiO2) is often noticed. In a clinical study, the mor-



tality was significantly higher in polytrauma patients with blunt thoracic trauma if the Horovitz quotient was below 300 mmHg at the time of admission [8]. In another study, an initial Horovitz quotient of < 250 mm Hg was found to be an independent predictor of a bad outcome in polytrauma patients [3]. On the other hand, in a series of 43 polytrauma patients with associated thoracic trauma, survivors and nonsurvivors could not be differentiated on the basis of the Horovitz quotient up to the 2nd day following the trauma. Therefore, the values on admission had no predictive value, as the pulmonary edema had not fully developed at that time [84]. Likewise, in a review of 144 patients, in ventilated patients no statistically significant difference could be found between the Horovitz quotient on admission and at discharge from the intensive care unit [1]. Erickson et al [85] and Voggenreiter et al [86] showed that the Horovitz quotient had only a minor relation to the size of lung contusion. In summary, it has to be said that the blood gas analysis alone does not reflect the overall degree of pulmonary injury. Pulmonary Arterial Pressure (PAP) In previous studies, it could be shown that the PAP, determined on admission of the polytraumatized patient with thoracic trauma, represented a good predictive value for the development of ARDS and pulmonary failure. In a series of severely injured multiple trauma patients, a PAP of > 24 mm Hg on admission adequately predicted nonsurvival [87]. The increase in PAP is caused by lung contusions and the associated vasoconstriction in the area of the damaged lung (EulerLiljestrand mechanism). However, Wagner et al [88] have shown that there are big interindividual differences with regard to the increase in PAP despite comparable pulmonary injury severity. In some patients, in spite of severe pulmonary violations, no increase in PAP was noticed. In other patients, however, it was significantly associated with the extent of pulmonary injury. Thus, the increase in PAP cannot predict the severity of the thoracic injury. Placement of a pulmonary arterial catheter in a polytrauma patient is also associated with a high risk. Additionally, the circumstances in the emergency room are often not favorable for such an undertaking. Extravascular Lung Water (EVLW) The determination of EVLW can quantify the degree of interstitial edema and represents a reliable bedside


measurement [89, 90]. For the measurement of EVLW by means of the PiCCO method, a special arterial access and a central venous access are needed. In patients with multiple trauma, who often require emergency surgery or other diagnostics, this time-consuming measuring procedure cannot be practical to use. Moreover, pulmonary edema does not develop until 2–3 days after trauma [91]; therefore, EVLW is not an adequate parameter to predict the development of pulmonary complications. Scoring Systems The review of the available diagnostic tests reveals that diagnosis and quantification of the severity of thoracic trauma are difficult. However, the early judgment of the injury pattern is vital for proper treatment of the patient. Thus, various scoring systems were developed to facilitate a reproducible classification of thoracic trauma and to assist the physician in the treatment decisions. CT-Dependent Score (Wagner & Jamieson) Wagner & Jamieson [92] used chest CT as the basis of their scoring system. In their classification, parenchymal injuries to the lung were evaluated by means of morphologic changes on the thoracic CT scan, the accident mechanism, and the localization of associated rib fractures. The authors then classified the pulmonary injury into four different categories. Wagner & Jamieson not only classified the injury but attempted to quantify the severity of injury. They did this by first separating each lobe of the lung and calculating each one’s contribution to total lung volume. Then, by using information on the CT scan, they could calculate the percentage of total lung volume that was injured. This was divided into three separate grades. The authors then showed an association between the size and type of parenchymal injuries and the need for mechanical ventilation (Figure 1). Besides the classification developed by Wagner in 1989, there is an another CT-dependent score reported in the literature [93]. CT-Independent Score (Tybursky et al) Tybursky et al [94] developed a score, which is based on the assessment of pulmonary contusions found on the conventional chest X-ray. In addition, the lung was divided bilaterally into an upper, middle and lower third. A point value between 1 and 3 was assigned to

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Grad 1 • ≥ 28% of total air space consolidated or lacerated • all patients require mechanical ventilation for pulmonary insufficiency Grad 2 • 19–27% of total air space consolidated or lacerated • 60% of these patients require mechanical ventilation for pulmonary insufficiency Grad 3 • < 19% of total air space consolidated or lacerated • no mechanical ventilation required for pulmonary insufficiency Figure 1. CT-dependent score according to Wagner & Jamieson [92].

each of these thirds. The allocation of these point values took place on account of the radiologic parenchymal changes. The total point value led to the classification in three different degrees (Table 1). The assessment was performed on patient arrival and then again 24 h later. An increase in the severity of lung contusion during this period was associated with a higher mortality and an extended duration of mechanical ventilation. Also Erickson et al [85], Shulman & Samuels [95], and Thompson et al [96] classified lung contusions in their publications. Table 1. CT-independent score according to Tybursky et al [94]. Calculation of the Pulmonary Contusion Score (PCS) • Dividing the lung fields into upper, middle and lower third • Assigning a score of 1–3 to each region on the basis of the amount of radiologic parenchymal changes Mild pulmonary contusion

Moderate pulmonary Severe pulmonary contusion contusion

PCS 1–2

PCS 3–9

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PCS 10–18

Thoracic Abbreviated Injury Scale (AIS) By means of the AIS [97], a definitive pathologicanatomic criteria-based definition of the injury severity of the chest is possible after completed diagnostics. Each separate injury is assigned to one of six fixed degrees in the AIS. It must be mentioned that the AIS is an ordinal scale which does not correlate linearly with mortality. The Injury Severity Score (ISS) is calculated by the sum of the squares of the highest AIS degrees of the three most severely injured body regions. Several severe injuries of a body region are not considered in the ISS. On account of its design, the AIS is not suitable to predict complications of a thoracic trauma. However, by calculation of the ISS, a statement about general mortality is possible [98]. Thoracic Trauma Severity Score (TTS) Pape et al [99] developed the CT-independent TTS which is suitable for the judgment of osseous and parenchymal injuries and considers physiologic parameters (Table 2). This score evaluates five different parameters (pO2/FiO2, rib fractures, pulmonary contusion, pleural involvement, and age) and assigns each one a score between 0 and 5. Then, a total score between 0 and 25 is arrived at by adding up all the individual scores. An essential advantage of the TTS is that all applied parameters can easily be ascertained in the emergency room. Therefore, an early identification of those patients with thoracic trauma, who are at high risk for complications, is possible. As the TTS does not require chest CT, it is usable in every hospital and can be calculated quickly. By using the “receiver operating characteristic (ROC) curve” it could be shown, that with a value of 0.924, the TTS is superior to all other described scores. The TTS offers a simple, reliable solution to the problem of early, CT-independent judgment of the severity of thoracic trauma. Conclusion Blunt thoracic injuries are frequently present in polytrauma patients. The presence of thoracic trauma in a polytraumatized patient significantly affects the treatment strategy in the emergency room and the intensive care unit. It also affects the timing and nature of fracture care. The prompt recognition and diagnosis of a chest injury is essential in providing adequate treatment for the patient and avoiding secondary complications. There are many different diagnostic modalities that are at a physician’s disposal to aid his/her decision-making. The diagnostic



modalities used are dependent on many factors including availability, timing, usefulness, cost, and the nature of the injury being evaluated. Also, a classification of the thoracic injury is very useful in helping the physician determine the appropriate treatment strategy. The TTS is a reliable CT-independent classification of the thoracic injury that can be quickly performed in the emergency room. The calculation of this score will assist in further treatment decisions and in turn help improve patient outcome.

Table 2. Thoracic Trauma Severity Score. A minimum value of 0 points and a maximum value of 25 points can be achieved. Grade pO2/FiO2

Rib fractures

Pulmonary contusion

Pleural involvement

Age (years)

Points

0 I II

0 1–3 3–6

None 1 lobe unilateral 1 lobe bilateral or 2 lobes unilateral

None Pneumothorax Hemothorax/ hemopneumothorax unilateral Hemothorax/ hemopneumothorax bilateral Tension pneumothorax

< 30 30–41

0 1

42–54

2

55–70

3

> 70

5

> 400 300–400 200–300

III

150–200

> 3 bilateral

< 2 lobes bilateral

IV

< 150

Flail chest

≥ 2 lobes bilateral

References 1. 2.

3.

4. 5. 6.

7.

8. 9.

10. 11. 12. 13. 14. 15. 16.

17.

Pinilla JC. Acute respiratory failure in severe blunt chest trauma. J Trauma 1982;22:221–6. Bardenheuer M, Obertacke U, Waydhas C, Nast-Kolb D. Epidemiologie des Schwerverletzten – eine prospektive Erfassung der präklinischen und klinischen Versorgung. Unfallchirurg 2000;103:355–63. Hoff SJ, Shotts SD, Eddy VA, Morris JA. Outcome of isolated pulmonary contusion in blunt trauma patients. Am Surg 1994;60:138–42. Richardson JD, Adams L, Flint LM. Selective management of flail chest and pulmonary contusion. Ann Surg 1982;196:481–7. Stellin G. Survival in trauma victims with pulmonary contusion. Am Surg 1991;57:780–4. Waydhas C, Nast-Kolb D, Trupka A, Jochum M, Schweiberer L. Die Bedeutung des traumatisch-hämorrhagischen Schocks und der Thoraxverletzung für die Prognose nach Polytrauma. Hefte Unfallheilkd 1990;212:104–5. Clark GC, Schechter WP, Trunkey DD. Variables affecting outcome in blunt chest trauma: flail chest versus pulmonary contusion. J Trauma 1988;28:298–304. Johnson JA, Cogbill TH, Winga ER. Determinants of outcome after pulmonary contusion. J Trauma 1986;26:695–7. Pape HC, Auf’m Kolk M, Paffrath T, Regel G, Sturm JA, Tscherne H. Primary intramedullary femur fixation in multiple injured patients with associated lung contusion – a cause of posttraumatic ARDS. J Trauma 1993;34:540–8. Gaillard M, Herve C, Mandin L, Raynaud P. Mortality prognostic factors in chest injury. J Trauma 1990;30:93–6. Inthorn F, Huf R. Das Thoraxtrauma beim Mehrfachverletzten. Anästh Intensivther Notfallmed 1992;27:498–501. Lewis RF. Thoracic trauma. Surg Clin North Am 1982;62:97–102. Trupka A, Nast-Kolb D, Schweiberer L. Das Thoraxtrauma. Unfallchirurg 1998;101:244–58. Gams E, Kalweit G. Thoraxverletzungen. In: Mutschler W, Haas N, Hrsg. Praxis der Unfallchirurgie. Stuttgart–New York: Thieme, 1998. LoCicero J, Mattox KL. Epidemiology of chest trauma. Surg Clin North Am 1989;69:15–9. Miller HAB, Taylor GA. Flail chest and pulmonary contusion. In: McMutry RY, McLellan BA, eds. Management of blunt trauma. Baltimore: Williams & Wilkins, 1990:186–98. Waydhas C. Thoraxtrauma. Unfallchirurg 2000;103:871–90.


18. Richardson J, Miller F, Carillo E, Spain D. Complex thoracic injuries. Surg Clin North Am 1996;76:725–46. 19. Boyd AD. Pneumothorax and hemothorax. In: Hood RM, Culliford AT, eds. Thoracic trauma. Philadelphia: Saunders, 1989: 133–49. 20. Bertichant J, Polge A, Mohty D, Nguyen-Ngoc-Lam R, Estorc J. Evaluation of incidence, clinical significance, and prognostic value of circulating troponin I and T elevation in hemodynamically stable patients with suspected myocardial contusion after blunt chest trauma. J Trauma 2000;48:924–31. 21. Bayer M, Burdick D. Diagnosis of myocardial contusion in blunt chest trauma. J Am Coll Emerg Phys 1977;6:238–43. 22. Obertacke U, Neudeck F, Hellinger A, Schmit-Neuburg KP. Pathophysiologie, Diagnostik und Therapie der Lungenkontusion. Akt Chir 1997;32:32–48. 23. Shorr RM, Crittenden M, Indeck M, Hartunian SL, Rodriguez A. Blunt thoracic trauma. Ann Surg 1987;206:200–5. 24. Ertel W, Trentz O. Causes of shock in the severely traumatized patient: emergency treatment. In: Goris RJA, Trentz O, eds. The integrated approach to trauma care: the first 24 hours. Berlin–Heidelberg–New York: Springer, 1995:78–87. 25. Allen GS, Coatee NE. Pulmonary contusion: a collective review. Am Surg 1996;62:895–900. 26. Schlag G, Redl H, Buchinger W, Dinges HP. Pathophysiologie der Lungenkontusion. Hefte Unfallheilkd 1992;223:13–9. 27. Fulton RL, Peter ET. The progressive nature of pulmonary contusion. Surgery 1970;67:499–506. 28. Regel G, Sturm JA, Friedl HP, Nerlich M, Bosch U, Tscherne H. Die Bedeutung der Lungenkontusion für die Letalität nach Polytrauma – Möglichkeiten der therapeutischen Beeinflussung. Chirurg 1998;59:771–6. 29. Richardson JD, Woods D, Johannson WG. Lung bacterial clearance following pulmonary contusion. Surgery 1979;86:730–5. 30. Obertacke U, Redl H, Schlag G, Schmit-Neuerburg KP. Lokale und systemische Reaktionen nach Lungenkontusion. Berlin–Heidelberg–New York: Springer, 1994. 31. Rose S, Marzi I. Pathophysiologie des Polytraumas. Zentralbl Chir 1996;121:896–913. 32. Ware L, Mattay M. The acute respiratory distress syndrome. N Engl J Med 2000;342:1334–49. 33. Jacobs RR, McClain OM. Effects of fracture stabilization by internal fixation. Injury 1977;12:194–201.

165


34. Lhowe DW, Hansen ST. Immediate nailing of fractures of the femoral shaft. J Bone Joint Surg [Am] 1988;70: 812–20. 35. Johnson KD, Cadambi A, Seibert GB. Incidence of adult respiratory distress syndrome in patients with multiskeletal injuries: effect of early operative stabilization of fractures. J Trauma 1985;25:375–84. 36. Bone LB, Johnson KD, Weigelt J, Scheinberg R. Early versus delayed stabilization of fractures. A prospective randomised study. J Bone Joint Surg [Am] 1989;71:336–40. 37. Riseborough EJ, Herndon JH. Alterations in pulmonary function, coagulation and fat metabolism in patients with fractures of the lower limbs. Clin Orthop 1976;311:281–6. 38. Tscherne H, Regel G, Pape HC, Pohlemann T, Krettek C. Internal fixation of multiple fractures in patients with polytrauma. Clin Orthop 1998;347:62–78. 39. Stürmer KM, Suchardt W. Neue Aspekte der gedeckten Marknagelung und des Aufbohrens im Tierexperiment. Unfallheilkunde 1980;83:341–52, 433–45. 40. Wenda K, Ritter G, Ahlers J, Issendorf W von. Nachweis und Effekt von Knochenmarkeinschwemmungen bei Operationen im Bereich der Femurmarkhöhle. Unfallchirurg 1990;93: 56–61. 41. Barie PS, Minnear FL, Malik AB. Increased pulmonary vascular permeability after bone marrow injection in sheep. Am Rev Respir Dis 1981;123:648–53. 42. Nerlich ML, Wisner DH, Albes JM, Sturm JA, Tscherne H. Pulmonary effects of iv-injection of bone marrow fat and endotoxemia in sheep. Langenbecks Arch Chir 1985;13:55–8. 43. Waydhas C, Nast-Kolb D, Kick M, Richter-Turnur M, Trupka A, Machleidt W, Jochum M, Schweiberer L. Operationstrauma Wirbelsäule in der Behandlung polytraumatisierter Patienten. Unfallchirurg 1993;96:62–5. 44. Waydhas C, Nast-Kolb D, Kick M, Richter-Turnur M, Schweiberer L. Operationsplanung von sekundären Eingriffen nach Polytrauma. Unfallchirurg 1994;97:244–9. 45. Giannoudis PV, Smith RM, Bellamy MC. Stimulation of the inflammatory system by reamed and unreamed nailing of femoral fractures. J Bone Joint Surg [Br] 1999;81:356–61. 46. Pape HC, Dwenger A, Regel G, Schweitzer G, Jonas M, Remmers D, Neumann K, Sturm JA, Tscherne H. Pulmonary damage after intermedullary femoral nailing in traumatized sheep – is there an effect from different nailing methods? J Trauma 1992;33: 574–81. 47. Pape HC, Regel G, Dwenger A, Krumm K, Schweitzer G, Krettek K, Sturm JA, Tscherne H. Influences of different methods of intramedullary femoral nailing on lung function in patients with multiple trauma. J Trauma 1993;35:709–15. 48. Stalp M, van Griensven M, Pape HC, Regel G, Tscherne H. Substitution of b-endorphin in severe trauma – modulation of the respiratory burst of PMNL. Suppl Shock 1998;9:98–9. 49. van Griensven M, Stalp M, Seekamp A. Ischemia-reperfusion directly increases ovine pulmonal endothelial permeability in vitro. Shock 1999;11:259–63. 50. Pape HC, Hoffmann M, Zwipp H, Tscherne H. Chronic diaphyseal osteomyelitis of long bones refractory to conventional therapy – benefits and risks of reaming of the femoral medullary cavity. Eur J Orthop Surg Trauma 1995;5:53–8. 51. Pape HC, Regel G, Dwenger A, Grotz M, Remmers D, Tscherne H. The risk of early intramedullary nailing of long bone fractures in multiply traumatized patients. Compl Orthop 1995;10:15–23. 52. Pape HC, Krettek C, Maschek HJ, Regel G, Tscherne H. Fatal pulmonary embolization after reaming of the femoral medullary cavity in sclerosing osteomyelitis. J Orthop Trauma 1996;10:429–32.

166

53. Pape HC, Stalp M, Dahlweid M, Regel G, Tscherne H. Der Polytraumapatient im „Borderline-Zustand“: Welche primäre OPDauer ist vertretbar? Unfallchirurg 1999;102:105–12. 54. Nast-Kolb D, Waydhas C, Jochum M, Spannagel M, Duswald KH, Schweiberer L. Günstigster Operationszeitpunkt für die Versorgung von Femurschaftfrakturen beim Polytrauma. Chirurg 1990;61:259–65. 55. Uffmann M, Fuchs M, Herold CJ. Radiologie des Thoraxtraumas. Radiologie 1998;38:683–92. 56. Dörr F. Differenzierte Beurteilung und Therapiekontrolle beim Thoraxverletzten durch die Computertomographie. Anästhesiol Intensivmed Notfallmed Schmerzther 1999;34:41–4. 57. Regel G, Sturm JA, Neumann C, Bosch U, Tscherne H. Bronchoskopie der Lungenkontusion bei schwerem Thoraxtrauma. Unfallchirurg 1987;90:20–6. 58. Perry JF, Galway CF. Chest injury due to blunt trauma. J Thorac Cardivasc Surg 1965;49:684–90. 59. Marths B, Durham R, Shapiro M, Mazuski JE, Zuckermann D, Sundaram M, Luchtefeld WB. Computed tomography in the diagnosis of blunt thoracic injury. Am J Surg 1994;168:688–92. 60. Greene R. Lung alterations in thoracic trauma. J Thorac Imaging 1987;2:1–8. 61. Tocino IM, Miller MH, Frederick PR. CT detection of occult pneumothorax in head trauma. AJR Am J Roentgenol 1984;143: 987–90. 62. Rhea JT, Novelline RA, Lawrason J. The frequency and significance of thoracic injuries detected on abdominal CT scans of multiple trauma patients. J Trauma 1989;29:502–5. 63. McGonigal MD, Schwab W, Kauder DR. Supplemental emergent chest computed tomography in the management of blunt torso trauma. J Trauma 1990;30:1431–5. 64. Rizzo AG, Steinberg SM, Flint LM. Prospective assessment of the value of computed tomography for trauma. J Trauma 1995;38:338–43. 65. Nelson JB, Bresticker MA, Nahrwold DL. Computed tomography in the initial evaluation of patients with blunt trauma. J Trauma 1993;33:722–7. 66. Pillgram-Larsen J, Lovstakken K, Hafsahl G. Initial axial computerized tomography examination in chest injuries. Injury 1993;24:182–4. 67. Blostein PA, Hodgam CG. Computed tomography of the chest in blunt thoracic trauma: results of a prospective study. J Trauma 1997;43:13–8. 68. Guerrero-Lopez F, Vazquez-Mata G, Alcazar PP, Fernandez-Mondejar E, Aguayo-Hoyos E, Linde-Valverde CM. Evaluation of the utility of computed tomography in the initial assessment of the critical care patient with chest trauma. Crit Care Med 2000;28:1370–5. 69. Karaaslan T, Meuli T, Androux RE, Duvoisin B, Hessler C, Schnyder P. Traumatic chest lesion in patients with severe head trauma: a comparative study with computed tomography and conventional chest roentgenograms. J Trauma 1995;39:1081–6. 70. Ivatury RR, Sugerman HJ. Chest radiograph or computed tomography in the intensive care unit? Crit Care Med 2000;28:1234–5. 71. Exadaktylos AK, Sclabas G, Schmid SW, Schaller B, Zimmermann H. Do we really need routine computed tomographic scanning in the primary evaluation of blunt chest trauma in patients with “normal” chest radiograph? J Trauma 2001;51:1173–6. 72. Trupka A, Kierse R, Waydhas C, Nast-Kolb D, Schweiberer L, Pfeifer KJ. Schockraumdiagnostik beim Polytrauma – Wertigkeit der Thorax-CT. Unfallchirurg 1997;100:469–76. 73. Tello R, Munden RF, Hooton S, Kandarpa K, Pugatch R. Value of spiral CT in hemodynamically stable patients following blunt chest trauma. Comput Med Imaging Graph 1998;22:447–52.



74. Scaglione M, Pinto A, Pinto E, Romano L, Ragazzino A, Grassi R. Role of contrast-enhanced helical CT in the evaluation of acute thoracic aortic injuries after blunt chest trauma. Eur Radiol 2001;11:2444–8. 75. Röthlin MA, Näf R, Amgwerd M, Candinas D, Frick T, Trentz O. Ultrasound in blunt abdominal and thoracic trauma. J Trauma 1993;34:488–95. 76. Walz M, Muhr G. Sonographische Diagnostik beim stumpfen Thoraxtrauma. Unfallchirurg 1990;93:359–65. 77. Börner N, Kelbel C, Lorenz J. Sonographische Volumenbestimmung und Drainage von Pleuraergüssen. Ultraschall Klin Prax 1987;2:148–53. 78. Hara KS, Prakash UBS. Fiberoptic bronchoscopy in the evaluation of acute chest and upper airway trauma. Chest 1989;96:627–30. 79. Regel G, Seekamp A, Aebert H, Wegener G, Sturm JA. Bronchoscopy in severe blunt chest trauma. Surg Endosc 1990;4:31–5. 80. Hoffmann P, Gahr R. Frühdiagnostik der Lungenkontusion durch Bronchoskopie. Unfallchirurg 1989;92:92–4. 81. Merkle P, Ahrendt J. Funktionelle Untersuchungen beim stumpfen Thoraxtrauma unter besonderer Berücksichtigung der Perfusions- und Ventilationsszintigraphie. Chirurg 1985;56:147–50. 82. Van Eeden SF, Klopper JF, Alheit B, Bardin PG. Ventilation-perfusion imaging in evaluating regional lung function in nonpenetrating injury to the chest. Chest 1989;95:632–8. 83. Helm M, Hauke J, Esser M, Lampl L, Bock KH. Diagnosis of blunt thoracic trauma in emergency care. Use of continuous pulse oximetry monitoring. Chirurg 1997;68:606–12. 84. Bone RC, Maunder R, Slotman G. An early test of survival in patients with the adult respiratory distress syndrome. Chest 1985;85:849–51. 85. Erickson DR, Shinozaki T, Beekman E, Davis J. Relationship of arterial blood gases and pulmonary radiographs to the degree of pulmonary damage in experimental pulmonary contusion. J Trauma 1971;11:689–94. 86. Voggenreiter G, Majetschak M, Auf’m Kolk M, Assenmacher S, Schmit-Neuerburg KP. Estimation of condensed pulmonary parenchyma from gas exchange parameters in patients with multiple trauma and blunt chest trauma. J Trauma 1997;43:8–12. 87. Sturm JA, Lewis FR, Trentz O. Cardiopulmonary parameters and prognosis after severe multiple trauma. J Trauma 1979;19:305–17. 88. Wagner RB, Slivko B, Jamieson PM, Dills MS, Edwards FH. Effect of lung contusion on pulmonary hemodynamics. Ann Thorac Surg 1991;52:51–8.


89. Sturm JA, Wisner HD, Oestern HJ. Increased lung capillary permeability after trauma: a prospective clinical study. J Trauma 1986;26:409–15. 90. Lewis FR, Ellings VB, Sturm JA. Bedside measurement of lung water. J Surg Res 1979;27:250–3. 91. Shepard GH, Ferguson JL, Foster JH. Pulmonary contusion. Ann Thorac Surg 1969;7:110–5. 92. Wagner RB, Jamieson PM. Pulmonary contusion. Evaluation and classification of computed tomography. Surg Clin North Am 1989;69:31–40. 93. Svenning JL, Bugge-Asperheim B, Geiran O, Vaage J, PillgramLarsen J, Fjeld NB, Birkeland S. High-dose corticosteroids in thoracic trauma. Acta Chir Scand 1985;526:110–9. 94. Tybursky JG, Collinge JD, Wilson RF, Eachempati SR. Pulmonary contusion: quantifying the lesions on chest x-ray films and the factors affecting prognosis. J Trauma 1999;46:833–8. 95. Shulman HS, Samuels TH. The radiology of blunt chest trauma. J Can Assoc Radiol 1983;34:204–17. 96. Thompson BM, Finger W, Tonsfeldt D, Aprahamian C, Troiano P, Hendley G, Mateer J, Stueven H. Rib radiographs for trauma: useful or wasteful? Ann Emerg Med 1986;15:261–5. 97. Civil ID, Schwab CW. The Abbreviated Injury Scale, 1985 revision: a condensed chart for clinical use. J Trauma 1988;28:87–90. 98. Oestern KJ, Kabus K. Klassifikation Schwer- und Mehrverletzter – Was hat sich bewährt? Chirurg 1997;68:1059–65. 99. Pape HC, Remmers D, Rice J, Ebisch M, Krettek C, Tscherne H. 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.

Correspondence Address Frank Hildebrand, MD Department of Trauma Surgery Hannover Medical School Carl-Neuberg-Straße 1 30625 Hannover Germany Phone (+49/511) 532-2050, Fax -5877 e-mail: [email protected]

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