The cause of traumatic injury to the chest varies greatly in different parts of the world. Currently, in large American cities and parts of South Africa, black males have a 1 in 20 chance of being fatally shot or stabbed before the age of 30. Although terrorism and civilian violence are on the increase throughout Europe, the absolute numbers of victims remains small in comparison. In England and Wales, the annual death rate from stabbing and gunshot wounds is less than 200. Britain and Europe, nevertheless, have increasing figures for road casualties. Road traffic accidents in England and Wales account for 60000 hospital admissions per year, and London and south-east England have 57 fatal or serious road traffic accidents per 100 km of road. Blunt thoracic injury is almost exclusively caused by rapid deceleration in motor vehicle collisions. A small number of injuries follow crushing industrial accidents.

Although less than 15 per cent of patients with chest trauma require surgical intervention, many needless deaths occur through inadequate or delayed treatment of an easily remediable injury. The majority of chest injuries are confined to the thoracic cage. These consist of rib fractures with underlying pulmonary contusion, haemothorax, or pneumothorax, which can usually be dealt with simply and effectively by chest drain insertion and fluid restriction. When ignored, underestimated, or inadequately treated, chest injuries may cause the death of a patient during surgical intervention for seemingly more pressing intracranial or abdominal haemorrhage. The basis for successful management of thoracic trauma is effective cardiopulmonary resuscitation followed by early detection and treatment of life-threatening injuries. The former is based on the ABC principle.

A. Establish a reliable airway

B. Restore the mechanics of breathing

C. Stabilize the cardiovascular system.

The most serious intrathoracic injuries often occur in the absence of significant chest wall damage. Recognition must depend upon exclusion rather than direct manifestation of injury. The latter depends upon prediction of likely lesions according to the mechanism of injury. Important injuries to rule out are aortic transection or dissection, major airways disruption, ruptured diaphragm, and severe cardiac contusion or valvular regurgitation. Although all are relatively rare, they may coexist after major trauma. A high index of suspicion is the key to early diagnosis.

The existence of serious visceral injury can usually be predicted with knowledge of the type of accident or assault and should be confirmed or excluded by appropriate investigation such as chest radiographs and CT scan. There are three broad categories for the mechanism of injury associated with blunt thoracic trauma (Table 1) 547. The patterns of injuries sustained are different in each case.

Sudden profound deceleration (Fig. 1) 2011 produces the so called intrathoracic ‘bell clanger’ effect. The chest wall suffers direct impact. The aorta, a heavy column of blood with inertia, swings like the clanger of a bell within the thorax, producing severe shear forces. These forces may tear the vessel at its fixed points above the aortic valve or, more frequently, at the posterior chest wall, causing transection. The main bronchi situated beneath the aortic arch are subject to similar forces and may rupture. Impact of the neck may transect the trachea, and compression of the abdominal viscera may rupture the diaphragm, the spleen, or the liver. There may be little or no injury to the bony chest wall, though bilateral clavicular fractures or a fractured sternum must arouse suspicion. Anterior chest wall contusion is an indicator of underlying myocardial injury.

Low velocity impact causes direct damage to the bony thorax, with or without contusion of the underlying lungs or myocardium (Fig. 2) 2012. This type of injury does not usually create stress or compression forces sufficient to damage the aorta, bronchi, or diaphragm, although the liver or spleen may be ruptured by a direct blow over the lower part of the thoracic cage.

Following compression, multiple bilateral rib fractures are likely. However, in the young the sternum may be forced backwards to touch the spine without fracture (Fig. 3) 2013. Such low velocity forces seldom damage the aorta or myocardium, but may rupture the diaphragm or lacerate the bronchi by a different mechanism from that above (Fig. 4) 2014. When sudden forceful compression of the thoracic cage decreases the anteroposterior diameter and produces a widening of the transverse diameter, the negative intrapleural pressure ensures that the lungs remain in contact with the chest wall. Lateral motion pulls the two lungs apart thus producing traction on the trachea at the carina. Rupture occurs when the elasticity of the tracheobronchial tree is exceeded. If the glottis is closed at the moment of impact, intrabronchial pressure may rise suddenly. The greatest tension develops in the larger bronchi and increases the tendency to rupture.

Knife and gunshot wounds are now more commonplace in British accident departments and in some North American cities they are responsible for up to 40 per cent of trauma admissions. The extent of damage inflicted by a penetrating agent depends on the size, shape, stability, and above all, the velocity of the missile (Fig. 5) 2015. The vast majority of civilian gunshot wounds and accidental industrial or road traffic penetrating injuries occur with low velocity. Such missiles core out a hole through the body and damage only those tissues with which they are in direct contact. They cause death by damage to vital structures or exsanguinating haemorrhage. Because of their low kinetic energy, the path taken by a hand gun bullet through the body is unpredictable, deflection being caused by bone or even parenchymal organs such as the liver or spleen. Chest wounds may be accompanied by abdominal injury, and vice versa. The greater the mass of the penetrating object the greater the damage inflicted.

In contrast, high velocity rifle bullets and fragments from explosive devices over a short range have a large amount of energy which causes damage remote from the path of the missile itself. High velocity bullets cause extensive tissue damage by cavitation and shock waves (Fig. 6) 2016. Energy from the bullet is dissipated into the surrounding tissues, which are violently accelerated forwards and outwards. This creates a large temporary cavity 30 to 40 times the diameter of the missile. The greatest extent of cavitation occurs only after the missile has passed through the tissues. This has subatmospheric pressures and is open at both entrance and exit holes. The cavity then collapses in a pulsatile fashion sucking air, debris, and bacteria into the wound and producing a large amount of dead or devitalized contaminated tissue.

Damage is directly proportional to the density of the tissue: homogeneous structures such as brain, liver, spleen, or muscle are very sensitive, whereas light tissues like lung, which mainly consists of air, are resistant. The destruction is also inversely proportional to the proportion of elastic fibres present: skin and lung are resistant whereas bone is shattered. The external appearance of a bullet wound in the chest is therefore deceptive. The elasticity of the skin produces tiny entry and exit holes that disguise extensive internal destruction.

Chest injuries adversely affect pulmonary function by three separate mechanisms: altered mechanics of breathing, ventilation/perfusion imbalance, and impairment of gas transfer.

The great majority of blunt injuries to the thoracic cage and those penetrating injuries that cause haemothorax or pneumothorax impair ventilation (Fig. 7) 2017. Even relatively minor trauma with fractured ribs but no underlying pathology may cause pain sufficiently to lead to hypoventilation, atelectasis, failure to clear secretions, pneumonia, septicaemia, respiratory failure, and even death in an elderly or bronchitic patient. More serious problems which cause severe impairment of the mechanics of breathing include pneumothorax (particularly tension pneumothorax), haemothorax, ruptured diaphragm, multiple rib fractures with unstable segments, and injuries to the major airways (Fig. 8) 2018. The most extensive disruption of the chest wall tends to occur with crush injuries where multiple bilateral rib fractures, ruptured diaphragm, or fractures of the spine or sternum coexist. A single rib fracture is associated with a blood loss of 150 ml. Multiple fractures may cause substantial blood loss into the chest wall and pleural cavity; this may be increased by laceration of the underlying lung by sharp edges.

There are two main types of chest wall derangement, a functionally important traumatic defect (sucking chest wound) or a flail segment (Fig. 9) 2019. The latter may be unilateral with double fractures of three or more ribs, or anterior with fractures of three or more ribs on both sides of the sternum (Fig. 10) 2020. Some fractures may occur through the costochondral junctions, and are therefore invisible on plain chest radiographs. The unstable segment moves inwards on inspiration (paradoxical movement) and consequently compromises ventilation by reducing tidal volume. Following diaphragmatic rupture, the abdominal contents are similarly sucked into the chest on inspiration (Fig. 11) 2021,2022. If the pleural cavity is filled with air or blood, ventilation of partially collapsed lung is similarly compromised. Injuries to the major airways or inhalation of foreign material including teeth, windscreen glass, or stomach contents may physically occlude the large or small airways, thereby obstructing air entry.

Effective oxygenation of the blood and elimination of CO&sub2; depends on a balance between ventilation of the lung and its blood supply. Thoracic injuries compromise ventilation perfusion balance by a number of different mechanisms. Mechanical obstruction of the airway is an obvious cause of impaired ventilation, but in practice other mechanisms predominate. Distribution of ventilation in the lung is influenced by regional variations in airways resistance and compliance. The latter is governed by gravity-dependent intrapleural pressure gradients, and gas distribution in the lung is therefore uneven during normal resting tidal ventilation. In the lower or more dependent pleural space the pressure is closest to atmospheric (least negative). It becomes increasingly negative towards the apex or non-dependent region of the lung. When a normal inspiration is taken from end-expiration (functional residual capacity) expansion of the initially smaller dependent alveoli is governed by the steep portion of the compliance curve. Consequently, they expand more for each unit of pressure change than do those at the apices which are influenced by the upper, flatter portion of the curve. These differences result in preferential distribution of inspired gases to the areas of greater expansion in the dependent portions of the lungs. However, if terminal air spaces have collapsed due to haemopneumothorax or adult respiratory distress syndrome, inspiration results in preferential distribution to already expanded areas because of the influence of the compliance curve. The maldistribution of ventilation is worsened by airflow obstruction in terminal airways due to external compression, elevated intrapleural pressure, or interstitial oedema fluid. When a whole lobe or lung eventually collapses, there is perfusion of non-ventilated lung and a serious veno-arterial shunt effect. Ineffective oxygenation of the venous blood is reflected by widening of the alveolar–arterial oxygen tension difference and systemic hypoxia.

Movement of blood through the lungs is also influenced by gravity and the pressure gradient between the pulmonary arteries and left atrium. Blood flow is normally directed preferentially to the dependent parts of normal lung where ventilation is also most efficient. However, perfusion is often impaired by thrombosis of vessels in contused lung or widespread pulmonary microembolism by fat from bone marrow or platelet/neutrophil microemboli in patients with disseminated intravascular coagulation or adult respiratory distress syndrome.

In many patients after even minor thoracic trauma, the effects of ventilation/perfusion mismatch may lead to unsuspectedly severe hypoxia which is seldom recognized without blood gas analysis. Pulmonary contusion, intrapulmonary haemorrhage, and haemothorax or pneumothorax are invariably associated with serious deterioration in pulmonary function.

Passive diffusion of gas across the alveolar capillary barrier is dependent on the surface area available, the width of the membrane, certain plasma and erythrocyte enzymic factors, and the partial pressure gradient between the alveolar and vascular spaces. Following thoracic trauma a number of factors, including injury to the pulmonary parenchyma by contusion, damage to the alveolar capillary barrier by inhalation of gastric contents or smoke, impaired cardiac output, and interstitial pulmonary oedema due to overtransfusion of crystalloid, colloid, or blood (elevated left atrial pressure) may adversely affect gas exchange. However, the most sinister process involved is that which begins with the pathophysiological effects of shock and, if uninterrupted by prompt resuscitation, may progress to adult respiratory distress syndrome (Fig. 12) 2023. It is not appropriate to discuss the detailed humoral and cytological changes that culminate in this syndrome (see Section 4.3 11). Nevertheless, they are important, are probably triggered by activation and interaction of the complement, coagulation, kallikrein, and plasminogen cascades, and result in trapping of ‘activated’, neutrophils in the pulmonary microvasculature. Here they release protease enzymes and generate oxygen free radicals with the potential to damage the alveolar capillary membrane. The clinical and radiological stages of adult respiratory distress syndrome are summarized in Table 2 548. When full-blown adult respiratory distress syndrome occurs in a patient with thoracic trauma, particularly following multiple injuries, the chances of survival decrease markedly. Gas exchange is impaired by extension of the diffusion pathway by the presence of hyaline membrane and oedema fluid in the alveoli; accumulation of interstitial fluid within the septum and of proliterated type II cells along its alveolar border; reduction in the surface for diffusion because of terminal air space collapse and closure of capillary channels; and the detrimental influence of consequent hypoxaemia, hypercapnia, and acid–base shifts in erythrocyte enzyme kinetics. Some of the consequences of this process precipitate further deterioration in pulmonary dysfunction. Pulmonary arterial hypertension develops because of hypoxic arteriolar vasoconstriction. Higher flow resistance in small vessels can be made worse by increased interstitial fluid pressure. Intravascular coagulation may exacerbate these problems and contribute to ventilation/perfusion mismatch.

Hypoxaemia is the first objective sign of the onset of adult respiratory distress syndrome, and is the cardinal index of its progressive severity. At a later stage CO&sub2; retention develops, with its consequent disturbances of acid–base balance. Unless blood gases are monitored continuously in patients with thoracic trauma the primary effects in the lung may be misinterpreted. The manifestations of respiratory insufficiency are reflected principally in deterioration of cardiovascular and central nervous system dysfunction.

Advances in pre-hospital transportation have provided an opportunity to sustain life in patients who would previously have died (Fig. 13) 2024. In the United States, Europe, and Japan helicopter retrieval with resuscitation en route by positive pressure ventilation, external cardiac massage, and blood volume replacement are employed routinely for patients with major trauma. Relief of cardiac tamponade, control of exsanguinating haemorrhage, stabilization of respiratory dynamics, and the use of mechanical circulatory assistance should therefore be integral steps in accident department resuscitation rather than sequels to resuscitation. The decision to employ such procedures must be undertaken on clinical judgement and without recourse to radiology or special investigations.

More than 80 per cent of all patients with ruptured aorta, trachea or bronchus die rapidly at the site of injury. Those who reach hospital alive are a self-selected group who should survive with appropriate treatment. Once in hospital, resuscitative manoeuvres are best carried out with caution and in an unhurried way, since most survivors have reached an impaired but balanced respiratory and haemodynamic status compatible with life. More drastic measures, such as thoracotomy in the accident department, are reserved strictly for those with penetrating injuries or severe chest wall disruption who arrive moribund and in circulatory arrest. The admitting department should have an area set aside for patients with severe injuries. This should contain a trolley that can be tipped, and that has adequate space around it on all sides for manoeuvre. An anaesthetic trolley should be readily at hand with chest drains, peritoneal lavage cannulas, and a variety of intravenous and central venous cannulas for use in the large veins. An overhead radiograph machine and CT scanner should be available and an autotransfusion system is desirable (Fig. 14) 2025. Once in the accident department, the airways, breathing, and cardiovascular status are reviewed and take priority over other procedures as appropriate (Table 3) 549. A brief but thorough history is obtained from the patient, witnesses, or police officers. The time and mechanism of injury, type of weapon, and condition of the victim during transport are noted. Nursing and medical staff remove all the patient's clothes but, in the case of penetrating wounds, must preserve them carefully for future forensic or medicolegal investigation. Orientation of the garment on the patient, traces of gunpowder, or missile fragments may constitute important evidence, and even tissue debrided from wound edges should be retained. The vital signs, pulse and respiratory rate, blood pressure, and central venous pressure are measured, and the haemodynamic state and volume of overt or concealed haemorrhage assessed. A central venous catheter and one or more large bore peripheral cannulae are inserted.

In the collapsed patient a Ryle's nasogastric tube, quickly inserted by cutting down into an antecubital vein and passing into the superior vena cava, is excellent for rapid blood transfusion, venous pressure measurement, and repeated venous sampling (Fig. 15) 2026. An arterial line facilitates blood pressure recording and blood gas analysis. Blood volume replacement is initially carried out using crystalloid or colloid substitutes, but after massive blood loss or continued rapid bleeding, oxygen carrying capacity and coagulation must be preserved with group O Rhesus negative blood or the bleeding stopped by immediate surgical intervention. No attempt should be made to attain normal blood pressure at this stage: this may precipitate fatal haemorrhage from lacerated major vessels, intracranial bleeding, or cardiac tamponade. Controlled hypotension is desirable until the extent of injury is determined or surgical access to damaged structures is obtained. Whenever feasible, initial evaluation (including radiology) and resuscitation should be completed within 5 to 10 min. A patient whose vital signs cease or continue to deteriorate should undergo rapid endotracheal intubation and should be removed immediately to an area where operative resuscitation and repair can begin. For some moribund patients operation is a co-ordinated part of resuscitation.

External cardiac massage is seldom successful in restoring cardiac activity in patients who have suffered penetrating trauma. Immediate thoracotomy for control of haemorrhage, cardiac compression, preservation of available blood volume, and direct repair of critical injuries can be life saving in patients who present in extremis with injuries that preclude transportation to the operating theatre, and in those whose condition deteriorates during the first few minutes following arrival, suggesting impending death despite resuscitation. ‘Do not meddle with an obviously dead patient’ is an important dictum: patients with detectable vital signs can usually be sustained as far as the operating theatre. However, within these constraints there have been encouraging results from the use of immediate anterolateral thoracotomy for release of cardiac tamponade, suture repair of great vessels and cardiac wounds, internal cardiac massage, and cross-clamping of the descending thoracic aorta (Fig. 17) 2028. This last manoeuvre improves perfusion of the coronary and cerebral circulation in patients with profound hypovolaemia and stems exsanguinating haemorrhage in the abdomen.

In one group of patients with no immediately discernible vital signs or with systolic blood pressure less than 60 mmHg, and with preterminal respiratory pattern and cerebral activity, who did not respond to volume replacement and ventilatory support, there was a 66 per cent survival rate following immediate thoracotomy when the injuries were limited to intrathoracic organs. This contrasted strongly with only 20 per cent survival when thoracotomy was performed for cardiac resuscitation in patients whose injuries were totally extrathoracic.

The blood pressure level at 60 mmHg is important: young and fit individuals compensate for blood loss by vasoconstriction and pressure is maintained until critical hypovolaemia and acidosis occur. The extent of blood loss is disclosed by insertion of a central venous pressure line, though false elevation of venous pressure occurs with cardiac tamponade, shivering, straining, or poor position of the catheter. Measurement of base deficit is a sensitive index of the efficacy of resuscitation. Typing and cross-matching for at least six units of blood is performed at the same time.

In victims of assault or attempted homicide, the entire body should be examined for signs of penetration, each site being marked with a radio-opaque marker so that the track of the missile can be established. Decreased or absent breath sounds, subcutaneous emphysema, tracheal displacement, and neck vein distension are sought. The girth of the abdomen is measured and the presence of abdominal distension, localized and rebound tenderness, guarding, rigidity, frank dullness on percussion, and hyperaesthesia over the shoulder (Kehr's sign indicative of subdiaphragmatic irritation by blood) are sought. When the patient is unconscious it is easy to miss serious injuries such as paraplegia. A catheter is inserted into the bladder to monitor urine flow. A nasogastric tube is used to empty the stomach.

After basic steps, including clearance of blood and mucus from the pharynx, conventional endotracheal intubation can usually be used to secure an airway. This may prove impossible or undesirable in patients with direct injury to the major airways or severe facio-maxillary trauma (Fig. 19) 2030. Clues to disruption of the larynx, trachea, or major bronchi include aphonia, stridor, haemoptysis, and free air in the subcutaneous tissues or thorax (radiologically, pneumothorax, pneumomediastinum, or pneumopericardium). The severity of such injuries may be deceptive (Fig. 20) 2031.

Direct negotiation of the airway by rigid bronchoscopy or flexible intubating fibrescope is safer than blind intubation, which may completely obliterate a critical narrowing. If a patient with stridor is breathing spontaneously a helium–oxygen mixture may alleviate asphyxia until the bronchoscope is passed. Severe laryngeal injuries usually require tracheostomy.

In patients with tracheal trauma tracheostomy adds a second tracheal injury and may fail to secure an airway when the lesion is intrathoracic. In those with tracheal transection an endotracheal tube can be passed distal to the injury over a guide bougie inserted at bronchoscopy. Alternatively, high frequency jet ventilation can be used via a narrow catheter inserted into the distal segment pending direct surgical exposure. In desperate circumstances, immediate exploration of the neck is required. The distal trachea is located by a finger passed into the superior mediastinum, grasped in forceps, delivered, and intubated directly.

Arterial blood gases should be analysed in all patients with chest injury since apparently minor chest wall injuries may cause major degrees of hypoxaemia. In those with uncomplicated chest wall injuries pain and anxiety are usually the biggest barrier to adequate respiratory excursion; once these are relieved ventilation improves substantially. It is imperative to restore both gas exchange and acid–base balance as soon as possible, by whatever means, since these abnormalities seriously compromise cardiovascular function.

The mechanics of breathing may be compromised by disruption of the bony chest wall or diaphragm, accumulation of blood or air in the pleural cavities, or haemorrhage and oedema in the lung itself, which reduces compliance (Fig. 21) 2032. A neurological injury may alter the respiratory drive and pattern of breathing. Early resuscitative measures include stabilization of a flail segment or covering a chest wall defect (sucking chest wound), intercostal drainage of a haemopneumothorax, and, sometimes, positive pressure ventilation from the outset. A large plastic adhesive membrane such as ‘Opsite’ is useful for covering or stabilizing the chest wall; this can be supported by dressings and strapping until surgical debridement. A tension pneumothorax is always readily apparent on clinical examination and should never wait for radiological confirmation. A needle inserted through the chest wall will confirm the diagnosis but is useless therapeutically. A scalpel incision will relieve tension and restore both ventilation and venous return; an intercostal drain can then be inserted with aseptic technique. At this point remember that by lowering intrathoracic pressure venous return will increase, as will bleeding from damaged structures. Ventilatory support is initiated promptly when respiratory efforts are inadequate or obstructed. If a bronchial or pulmonary air leak coexists, it is important to allow air to escape continuously, otherwise tension pneumothorax results. A large volume suction pump (Tubbs-Barrett) should be applied to chest drains inserted for haemopneumothorax (Fig. 22) 2033. Negative pressures of −15 to 20 cmH&sub2;O are applied unless a large bronchial air leak results in extraction of a significant proportion of the tidal volume. Low volume (Roberts) pumps should never be used in trauma patients because they may obstruct air flow.

Assessment of external or concealed blood loss is particularly difficult in patients with chest trauma accompanied by multiple long bone fractures or abdominal injury. Physical signs and measurement of systemic and central venous pressure may be deceptive for the following reasons. First, cardiac contusion (predominantly of the right ventricle) or cardiac tamponade produces spuriously elevated right atrial pressure. After substantial haemorrhage this may fall within normal limits even in the presence of severe tamponade. Second, major vascular injuries such as aortic transection separate the baroreceptors from the vessel lumen and reflexly produce systemic hypertension. After serious blood loss the systolic blood pressure can still be normal. Lastly, fit young adults compensate for blood loss remarkably well. For these reasons it is imperative to measure and continue to monitor central venous pressure in every patient who is thought to require volume replacement. Peripheral pulses are checked and the presence of bruits sought in the neck. The possibility of injury to the heart or great vessels must be considered, however unlikely, since it is the unexpected rather than the obvious which most often leads to disaster. When there is no exit wound in the chest an abdominal injury may coexist. In patients surviving with either cardiac tamponade or a ruptured aorta, a balance is established between systemic hypotension and occlusion of the traumatic defect by blood clot or haematoma, which can create pressure beneath the surrounding tissues (Fig. 23) 2034. Over-aggressive blood volume replacement raises intravascular pressures, upsets this equilibrium, and may cause fatal bleeding or tamponade. In these circumstances, controlled hypotension is maintained until surgical repair. A systolic pressure of 80 to 100 mmHg should not be exceeded, especially in the presence of satisfactory acid–base balance and urine flow.

Needle pericardiocentesis is usually a waste of valuable time in trauma patients: cardiac tamponade is diagnosed clinically and should be relieved surgically. Except in the moribund patient, this procedure should be performed in the operating theatre to enable control of the source of haemorrhage.

In patients with severe myocardial contusion or unexplained haemodynamic deterioration, a Swan-Ganz catheter is used both to measure the right ventricular, pulmonary arterial, and left atrial (wedge) pressures, and to monitor the need for, and efficacy of, inotropic support. Contused lungs are very sensitive to volume overload and often contain fat emboli. The goal of fluid and blood replacement in such cases is to restore the intravascular volume, tissue perfusion, and oxygen carrying capacity as rapidly as possible, without causing pulmonary dysfunction or reactionary haemorrhage. The debate regarding composition of such an infusion is self-perpetuating. There is general agreement that acute massive blood loss requires resuscitation, at least in part, with whole blood and/or blood components. When packed cell volume falls below a critical value, oxygen delivery to the tissues is severely impaired as a result of insufficient circulating red cells. In healthy adults, compensatory cardiac and pulmonary mechanisms are effective when packed cell volume falls below 0.20 but generally if this falls below 0.30 red cells should be infused. Thus, in acute loss of 1 to 1.5litres, whole blood is not essential and blood volume can safely be restored with a plasma substitute. If the volume of haemorrhage is larger than this, whole blood should be available early in order that fluid volume and oxygen carrying capacity can be simultaneously replaced.

When the patient is haemodynamically stable an upright chest and abdominal radiograph (preferably posteroanterior) is obtained in full inspiration. The patient may require physical support and care must be taken not to disconnect catheters, since air embolism may occur on inspiration in the presence of low venous pressure. Supine radiographs are of limited value for assessment of intrapleural haemorrhage or intra-abdominal injury but may be the only alternative in the patient with multiple injuries. Sometimes there is surprisingly little abnormality, especially when direct injury to the mediastinum leaves the pleural cavities unscathed. Heart size may prove deceptively normal despite cardiac laceration and tamponade, and this should not cast doubt on a clinical diagnosis based on circulatory collapse with raised venous pressure ( Fig. 24 2035,2036 (a), (b)). Widening of the mediastinum occurs after damage to the major vessels, and if ruptured aorta is suspected an aortogram (not CT scan) must follow. Mediastinal air, subcutaneous emphysema, pneumothorax, and pneumopericardium are good evidence for injury to the bronchial tree or lung parenchyma (Fig. 25) 2037. Haemopneumothorax is the most common finding after penetration of the pleural cavity. The CT scan provides little information that cannot be derived from plain chest radiographs but is excellent for identifying associated head and abdominal injuries.

In practice, insertion of an intercostal drain (size 28–36 F) is the only intervention required in up to 85 per cent of patients with penetrating thoracic wounds (Fig. 26) 2038. This allows evaluation of blood loss and re-expansion of the lung. The usual approach is via the sixth or seventh interspace in the mid-axillary line. The tube is directed towards the apex of the chest posteriorly, and is immediately placed on suction. The initial blood loss and presence of an air leak are noted so that ongoing drainage can be assessed. Subsequent management is based upon the results of chest drainage.

When the wound is several hours old the blood is dark in colour. Initial drainage may be large in volume, due to reactive pleural effusion stimulated by blood in the pleural cavity. Continued bleeding and the increasing or decreasing hourly trend is more important than the initial value and determines what further intervention must be undertaken. A persistent air leak associated with bleeding and haemopneumothorax indicates major pulmonary laceration, though in a stable patient this may not require surgical treatment. Damage to a large bronchus usually produces a massive air leak with surgical emphysema (Fig. 27) 2039; this does require early intervention. With blood transfusion and intercostal drainage, most pulmonary lacerations resolve. When the chest tube drainage yields less than 250 ml/h without a large or continuous air leak, and if diagnostic studies show no major structural damage to the trachea, bronchial tree, oesophagus or cardiovascular system, chest drainage and supportive measures are sufficient. If the patient's haemodynamics are stable and an arterial bruit, absent pulse, widened mediastinum, or a wound track passing across the mediastinum is observed an aortogram should be performed to assess major vessel injury, bleeding from which may be deceptively controlled by a haematoma under tension. Signs of cardiac tamponade or failure to stabilize the haemodynamics mitigate against this course and prompt early surgical exploration (Table 4) 550. When a missile path is known to traverse the mediastinum and the patient remains stable bronchoscopy and oesophagoscopy are useful before exploration, particularly if mediastinal emphysema is seen on the chest radiograph or subcutaneous emphysema is felt in the neck.

Well-defined protocols exist for thoracotomy either on an urgent or delayed basis (Table 4) 550. The most frequent indications for emergency surgery are exsanguinating haemorrhage via the intercostal drain from pulmonary hilar wounds, or tamponade from cardiac laceration. Unless the patient is moribund and thoracotomy is required for resuscitation, it is preferable to maintain a state of controlled hypotension, insert the appropriate lines for transfusion, correct acid–base deficit and move quickly towards the appropriate facilities in the operating theatre.

Approximately 80 per cent of patients with penetrating cardiac wounds are dead on arrival in the accident department or are taken directly to the coroner. Major intracardiac injuries such as valve disruption, coronary artery transection, or septal defects are therefore rare in patients but more frequent in autopsy series. Autopsy series have a preponderance of gunshot wounds whilst, with few exceptions, clinical papers discuss predominantly stab wounds. This reflects the relative severity of these modes of injury. The triad of a mediastinal entrance wound, clinical evidence of cardiac tamponade, and a pulseless patient with profound systemic hypotension are pathognomonic of important cardiac injury. Though a posterior, subxiphoid, or subcostal penetrating wound may also produce cardiac injury, a mediastinal site of penetration is responsible for 57 to 85 per cent of cases. The diagnosis must be made rapidly from the clinical condition and will seldom await elective diagnostic studies other than the plain chest radiograph or two-dimensional echocardiography in a few stable and equivocal cases with tamponade. Many patients appear lifeless but have not sustained irreversible brain damage. The first question, therefore, is whether the patient is dead or alive. Those patients who reach hospital alive are a self-selected group who survive through arrest of haemorrhage by cardiac tamponade, or who are conveyed rapidly with bleeding from potentially fatal injuries. Cardiac wounds consequently present with one or two distinct syndromes—pericardial tamponade or haemorrhagic shock. The key to successful management of penetrating cardiac injuries is prompt diagnosis and immediate resuscitation and repair.

Haemorrhagic shock follows cardiac wounding when the pericardial laceration is large enough to allow free exit of blood so that tamponade cannot occur. Those patients who arrive moribund with haemorrhagic shock should undergo immediate thoracotomy on the side of injury, with the objective of controlling haemorrhage from the cardiac laceration and restoring blood volume and acid–base status. Thoracotomy is performed in the accident department only when the patient arrives warm with reactive pupils but with circulatory arrest, or when acute deterioration, uncontrolled haemorrhage, or cardiac arrest occurs in a patient whose injuries suggest cardiac involvement. In this situation, transfer to an operating theatre is not feasible, since a 5- to 10-min delay is not compatible with survival. The patient is rapidly intubated before thoracotomy and infused with a crystalloid solution such as Ringer's lactate. Unmatched type-specific or non-specific universal donor blood is given as soon as possible. Arterial pH and blood gas measurements are taken early and bicarbonate administered to correct profound acidosis. Anaesthesia is not required for the incision in a moribund patient: survivors will not recall the events.

An anterolateral thoracotomy through the 5th intercostal space is used most frequently. The incision can be taken across the sternum for access to the right atrium and venae cavae or through the costal cartilages on the left side superiorly for involvement of the great vessels. This approach is also useful for patients with blunt trauma or flail or crushed chest who have suffered cardiopulmonary arrest and cannot undergo external cardiac compression safely. Moribund or profoundly hypotensive patients who have suffered blunt or penetrating abdominal trauma can be stabilized by resuscitative thoracotomy and cross-clamping of the descending thoracic aorta. This arrests intra-abdominal haemorrhage, facilitates internal cardiac massage, and allows perfusion of the brain and myocardium in preference to other organs. Patients with ruptured abdominal aortic aneurysms can be revived in the same way. Median sternotomy gives a better access to all cardiac chambers but sternal saws are not readily available in most United Kingdom accident departments.

Surgical management of cardiac laceration depends on the location. Control of haemorrhage can usually be obtained by digital or manual compression, and the wound can be sutured directly or over felt pledgets. A small number of patients who survive laceration of a major coronary artery or valvular or septal disruption may require cardiopulmonary bypass after urgent thoracotomy. Left or right atrial lacerations may be controlled by inserting a Foley catheter and inflating the balloon. This facilitates direct suture repair of the defect. Autotransfusion is a valuable adjunct in patients with a major cardiac laceration, though few of these patients survive to reach hospital. Frequently, the lacerated heart has already arrested or is fibrillating. Control of the penetrating wound must then be carried out in association with cardiac massage and defibrillation.

All patients who respond to treatment are transferred to an operating theatre for formal exploration, and more secure cardiorrhaphy if necessary. Cleansing and closure of the chest are then undertaken in sterile surroundings. Intravenous antibiotics, such as gentamicin, flucloxacillin, and penicillin, are administered postoperatively for 5 days or more. Treatment with steroids, mannitol, calcium channel blockers, or hypothermia may be considered for patients with signs of cerebral hypoxia. Complications of the procedure often relate to the uncontrolled operative circumstances and the need for rapid intervention. Iatrogenic lacerations of the heart, coronary arteries, and lung may contribute to failure. Considerable experience is essential in deciding which patient should be explored in the accident department. The heart is relatively easy to resuscitate. The outcome depends more on the cerebral status.

Reviews of large series of patients undergoing immediate thoracotomy in the United States demonstrate two groups with clear prognostic differences. Patients who suffer circulatory arrest more than 4 min prior to admission to the accident department and who are virtually dead on arrival rarely survive. Those patients who are admitted with some minimal signs of life have a better prognosis. Survival correlates well with neurological status immediately after resuscitation. Those patients who show prompt improvement in neurological status with resuscitation usually have a satisfactory outcome. Young age, a brief period of cerebral hypoxia, and lack of major intracardiac structural injury are good prognostic features. Factors associated with high mortality in penetrating cardiac injuries include shotgun wounds (100 per cent mortality), left ventricular injury (47 per cent mortality), unconsciousness at the time of arrival (86 per cent mortality), and the absence of measurable blood pressure on arrival (66 per cent mortality). The mortality associated with knife wounds is usually lower than that associated with gunshot wounds.

Tamponade occurs when the pericardial laceration is small so that blood accumulates within the sac and clots, thus arresting haemorrhage. Patients presenting with cardiac tamponade are easily recognized by the combination of an appropriate entrance wound, systemic hypotension and tachycardia, and distended neck veins despite haemorrhage (Fig. 24) 2035,2036. The majority of these patients remain conscious but are extremely anxious, cold, clammy, and cerebrally obtunded. The cardiac wound is usually small, and bleeding stops when intracardiac pressures fall and intrapericardial pressure and blood clot in the wounds arrests haemorrhage. The distended pericardium usually contains blood clot equivalent to between 500 to 1500 ml of blood. Bleeding of this degree may not lower the systemic pressure and the patient's overall condition may not suggest a cardiac wound.

On arrival in the accident department, large bore central and the peripheral venous cannulae are inserted, though it is important at this stage to avoid transfusion, which may elevate the intracardiac and systemic pressures beyond 100 mmHg. This upsets the homeostatic mechanisms of cardiac tamponade and may cause fatal reactive haemorrhage. Full volume replacement and administration of a muscle relaxant must wait until the tamponaded patient is prepared and draped on the operating table with sternotomy or thoracotomy underway.

For patients whose circulatory status remains good and where there is doubt as to whether the heart has been damaged, plain chest radiographs or two-dimensional echocardiography can be carried out once venous lines have been inserted. In tamponade patients the cardiac shadow is typically globular shaped. Two-dimensional echocardiography shows a pericardial effusion with compression of the cardiac chambers and abnormal ventricular filling.

Patients with tamponade who survive a prolonged journey to hospital can usually survive the further short transfer to an operating theatre. Most centres who treat large numbers of penetrating cardiac wounds have abandoned pericardiocentesis in favour of early thoracotomy since the pericardial blood has usually clotted. Some advocate surgical transdiaphragmatic pericardotomy through a small subxiphoid incision for diagnosis and relief of suspected tamponade. This may produce temporary clinical improvement until median sternotomy or thoracotomy can be carried out. However, it may also disturb the blood clot in the cardiac wound and precipitate fatal haemorrhage before adequate surgical access is possible. If the knife or wounding implement is still in place it is important not to withdraw this until exposure of the damaged structures has been obtained.

Median sternotomy is the incision of choice for cardiac wounds. This provides access to all aspects of the heart and both pleural cavities, and the pulmonary hila, mediastinal trachea, and upper oesophagus area are also accessible. Penetrating wounds involving the heart can be approached via lateral thoracotomy, the position of which depends upon the site of penetration and predicted track of the weapon. Wounds above the nipple line require an incision through the fifth interspace. Those below, with possible diaphragmatic and abdominal damage, should be approached through the seventh interspace.

Opening of the sternum and evacuation of blood clot is usually followed by fresh bleeding from the site of penetration. Most bleeding areas in the ventricles or great vessels can be controlled with finger pressure followed by suture. It is important to inspect the rest of the heart carefully for an exit wound. Only rarely is cardiopulmonary bypass required at this stage.

Excessive bleeding from the lung can be arrested by a clamp across the hilum. In the profoundly hypotensive patient, bleeding is minimal; once haemorrhage is stopped, blood or crystalloid infusion can be used to restore the intravascular volume and blood pressure. If ventricular fibrillation occurs during thoracotomy, cross-clamping of the descending aorta allows perfusion of the cerebral and coronary vessels while blood volume is restored. Severe pulmonary laceration or contusion may require debridement or resection, whereas cardiac, bronchial, or oesophageal lacerations can usually be repaired by direct suture. Suture of cardiac lacerations should avoid the coronary arteries. If a major coronary artery is divided proximally, a saphenous vein or internal mammary arterial graft may be required.

Damage to intracardiac structures such as the interventricular septum or valves may require open repair at a later stage but cardiopulmonary bypass is rarely required in the acute phase. In difficult situations such as inaccessible hole in the left atrium, balloon tamponade with a Foley catheter can allow time to organize appropriate equipment and personnel.

Gunshot or stab wounds below the nipple line may produce combined thoracoabdominal injuries. The abdominal component may be recognized by preoperative peritoneal lavage or examination of the diaphragm during thoracotomy. Diaphragmatic injury must be repaired carefully since the morbidity associated with strangulated diaphragmatic herniation is considerable.

Any patient who has sustained high-speed deceleration trauma with head, thoracic, or abdominal injuries may also have cardiac contusion. Clinical and autopsy studies report a 15 to 75 per cent incidence of myocardial contusion in patients with blunt chest trauma, and life-threatening cardiac injury can occur with minimal or absent external signs. If cardiac contusion is not excluded by deliberate investigation and treated appropriately if present, the first clinical event may be cardiogenic shock, ventricular fibrillation, or complete heart block. Cardiogenic shock may cause death during surgery or rehabilitation for other injuries.

High speed deceleration impact of the anterior chest wall, for example, against a steering wheel, and severe crush injuries cause acute depression of the sternum and costal cartilages which compress the heart against the vertebral column posteriorly. In children and young adults the chest wall may spring back into position, leaving no external evidence of the severity of injury. Older adults may sustain a transverse fracture of the sternum, anterior costochondral dislocation, or multiple rib fractures, producing an anterior flail segment. These findings guarantee some degree of blunt cardiac injury. Pulmonary contusion, ruptured diaphragm, liver, or spleen, head injury, faciomaxillary trauma, aortic transection, and long bone fractures may coexist.

The range of potential cardiac lesions is shown in Table 5 551. Pericardial effusion and partial or full thickness myocardial contusion with conduction disturbances or dysrhythmia are common. Valve disruption, cardiac rupture, and ventricular septal defect are rare in patients who reach hospital alive. In order of frequency, traumatic cardiac rupture affects the right ventricle, left ventricle, right atrium, and left atrium. Rupture of the ventricular septum occurs as a delayed event, recognized after acute recovery; the patient develops cardiac failure with a loud systolic murmur. Injuries to the tricuspid, mitral, and aortic valves are usually apparent at an early stage, although papillary muscle ischaemia may lead to late development of tricuspid and mitral regurgitation. Rupture of the cordae tendineae and mitral or tricuspid leaflets is extremely rare. Aortic valve tears usually occur at the base where the cusps attach to the annulus. Acute occlusion of a non-atherosclerotic left anterior descending coronary artery may cause acute myocardial infarction, cardiogenic shock, or late left ventricular aneurysm formation. Right ventricular aneurysm formation has been described following severe right ventricular contusion.

Although cardiac contusion is usually considered as equivalent to acute myocardial infarction, there are important morphological and clinical differences between the two. Coronary artery injury is rare in patients with cardiac contusion, and coronary flow may be normal or increased in the contused myocardium. Nevertheless, in severe cases, transmural injury causes the same sequelae as infarction. Most patients show limited areas of necrosis restricted to portions of muscle bundles rather than complete coagulation necrosis. Myocardial haemorrhage and oedema produce a decrease in compliance, though the transition from normal to abnormal myocardium is more abrupt than in an acute myocardial infarction. Healing is by patchy scarring rather than fibrosis.

The possibility of cardiac trauma should be considered in every patient who sustains a high-velocity deceleration injury. Precordial bruising, and tyre or seatbelt marks reinforce suspicion of cardiac injury. Petechial haemorrhages over the chest and neck, together with subconjunctival haemorrhage, suggest traumatic asphyxia due to severe anteroposterior crush injury (Fig. 30) 2043. Cardiac contusion should be assumed to coexist in patients with aortic transection, blunt tracheobronchial injuries, lacerated diaphragm, and ruptured liver or spleen, all of which indicate the severity of trauma. A pericardial friction rub, cardiac murmur, or irregular pulse suggest acute cardiac injury in a patient with no previous history of cardiac disease.

Elevated jugular venous pressure prior to volume replacement is worrisome, especially when combined with blood loss from other injuries. Central venous pressure should therefore be measured from the outset. An inappropriately raised venous pressure suggests either cardiac tamponade or severe right ventricular dysfunction due to myocardial contusion or tricuspid regurgitation. It is extremely difficult to assess the severity of myocardial contusion, the spectrum of which ranges from barely perceptible to that sufficient to cause complete myocardial disruption.

The appearance of the heart shadow on chest radiographs may be entirely normal, but radiological evidence of pulmonary contusion or oedema implies an element of cardiac contusion. More severe cardiac trauma causes the radiograph to show cardiac enlargement or pulmonary venous congestion. Apparent cardiac dilatation may result from a haemopericardium; true dilatation results from an acute valve injury with left ventricular failure. Pneumopericardium may occur after severe pulmonary contusion, when air tracks from the lungs through the sheath around the pulmonary veins or when a lacerated pericardium allows free communication from a pneumothorax to the pericardial cavity. A large amount of air in the pericardium is often associated with rupture of a main bronchus, and tension pneumopericardium has been reported. Pneumopericardium can be distinguished from pneumomediastinum by tipping the patient into the left lateral decubitus position.

Electrocardiographic findings are variable. The ECG may show non-specific ST and T wave changes, sinus tachycardia, supraventricular tachycardia, and conduction abnormalities such as right bundle branch block. Bundle branch block, left anterior hemiblock, or first or second degree heart block may progress to complete heart block and sudden death, with worsening of the oedema around the conduction tissue. The most frequent clinical manifestation of cardiac contusion is ventricular tachycardia, the likelihood of which seems unrelated to the size of contusion or the extent of morphological damage. Electrical instability at sites of unevenly perfused tissue may initiate re-entry responses conducive to tachyarrhythmia. These electrical events often occur in the convalescent period, when no chest or cardiac injury has been suspected.

It is difficult to assess the degree of myocardial injury following trauma in the same way as acute myocardial infarction. In patients who do not have clinically obvious cardiac dilatation, raised filling pressures, pulmonary oedema, or electrocardiographic changes myocardial contusion can be reliably confirmed by two-dimensional echocardiographic imaging of ventricular wall motion abnormalities, and by the measurement of the myocardial isoenzyme of creatine phosphatase. Echocardiographic demonstration of pericardial effusion and either right or left ventricular dyskinesia indicates serious myocardial damage. Septal akinesia is often associated with electrocardiographic conduction abnormalities and ST segment and T wave changes. A rise in creatine phosphatase isoenzyme levels to more than 6 per cent of total creatine kinase is a sensitive and accurate index of important myocardial injury. Such patients have a high incidence of conduction defects and dysrhythmia on ECG, and of associated pulmonary contusion, which constitutes the best radiological correlate of important myocardial contusion. In the future troponin-T levels may provide a better quantitative assessment of direct myocardial injury.

Early intervention depends on the extent of associated injuries. Hypoxia and acidosis due to blood loss, haemopneumothorax, or airways obstruction seriously compound a head or cardiac injury and must be corrected at the earliest opportunity. There should be a low threshold for intubation and ventilation, and care must be taken not to overtransfuse the patient. There is an early and consistent depression of cardiac output following myocardial contusion. The damaged heart has less reserve with which to compensate for abnormal haemodynamic states. Meticulous fluid management is therefore necessary to avoid the sequelae of hyper- or hypovolaemia.

With careful treatment most patients with myocardial contusion make a complete functional recovery within a relatively short period (4–6 weeks), with no residual disability. Patients with severe damage, characterized by wall motion abnormalities, raised creatine kinase and ECG changes are subject to the same consequences as those suffering acute myocardial infarction, including ventricular septal rupture, left or right ventricular scar formation with dysrhythmia, and ventricular aneurysms. Cardiogenic shock is rarely seen following myocardial contusion alone but occurs in patients with cardiac tamponade, valve disruption, or ventricular septal defect. The thin-walled right ventricle which lies directly behind the sternum may fail acutely. This may contribute to death from chest trauma of apparently moderate severity (particularly when subject to volume overload).

Patients who sustain cardiac injury should be managed similarly to those suffering acute myocardial infarction. Such a history should cause concern during prolonged surgery for associated abdominal trauma or long bone injuries. Although operations for associated injuries are mandatory, they must be undertaken by experienced surgeons and anaesthetists who can minimize the duration of surgery. In particular, dysrhythmia prophylaxis should be discussed beforehand, if necessary with a cardiologist. Bed rest with continuous ECG monitoring, serial creatine kinase measurement, and repeat two-dimensional echocardiography should be employed until the risks of complete heart block, ventricular fibrillation, or delayed cardiac rupture are considered extinct.

In patients with cardiogenic shock, it is important to use two-dimensional echocardiography to diagnose or rule out cardiac tamponade, pericardial laceration with cardiac herniation, or acute laceration of the tricuspid, mitral, or aortic valves. We have undertaken successful immediate thoracotomy in the accident department for pericardial laceration and herniation of the ventricles, and for blunt left ventricular rupture (Fig. 32) 2045. Injury to the cardiac valves can usually be managed conservatively until the patient's condition is stabilized. These then require cardiopulmonary bypass for valve replacement or repair.

Patients with established cardiogenic shock may require early treatment with inotropic drugs. However, inotropic support in isolation increases cardiac work and oxygen consumption and provides an ideal setting for fatal dysrhythmias. Maintenance of adequate perfusion pressure to uninjured areas of cardiac muscle is vital, and the intra-aortic balloon pump provides an effective means of increasing coronary perfusion and reducing afterload.

If multiple injuries have been sustained cardiac filling pressure must be optimized by invasive monitoring. Following severe right ventricular contusion, the right atrial pressure may substantially exceed the left atrial or pulmonary arterial wedge pressure. Tricuspid regurgitation due to papillary muscle dysfunction, ruptured cordae, or laceration of the anterior leaflet will result in a characteristic right atrial pressure trace. In cardiac tamponade, both left and right atrial pressures are elevated and equal. Pericardial effusion may compound the effects of myocardial contusion and lead to late deterioration. Post-traumatic pericardial effusions may be reactive and serous or traumatic (frank blood). Serous effusions can be successfully tapped with a needle and, if necessary, an indwelling catheter. Whole blood in the pericardium may clot and require surgical decompression. Blood clot that is not evacuated will eventually liquefy, causing an increase in volume due to osmosis and the risk of progressive cardiac compression. Two-dimensional echocardiography should be repeated daily, and more frequently if haemodynamic deterioration occurs. Delayed haemodynamic deterioration may also follow worsening oedema in the myocardium of the right or left ventricles, thrombosis of the left anterior descending coronary artery with myocardial infarction, increasing papillary muscle dysfunction, or ventricular septal or free wall rupture following haemorrhage into ischaemic myocardium. Cardiac catheterization may then be necessary to check the status of the coronary arteries or the significance of a new murmur.

A lacerated aortic valve requires early repair or replacement. The tricuspid valve can be repaired satisfactorily, even following leaflet laceration (Fig. 33) 2046. Care should be taken when assessing a severely regurgitant mitral valve: if the leaflets and cordae are intact the valve will appear normal and the problem lies in an infarcted papillary muscle. Under these circumstances the mitral valve should be replaced. Traumatic ventricular septal defects have been repaired successfully in a manner similar to post-myocardial infarction ventricular septal defect.

Experience has shown that patients with normal ECG, creatine kinase, and echocardiographic findings will not deteriorate subsequently. However, all patients with evidence of myocardial injury should be monitored carefully in hospital and subsequently as an outpatient for 2 years.

Sixteen per cent of patients who die in automobile accidents have some form of aortic injury. The most common location of this injury is just distal to the origin of the left subclavian artery and ligamentum arteriosum (Fig. 34) 2047. The aortic tear may be partial (usually on the posteromedial aspect of the aorta), complete, or spiral. The exact physical mechanism of the injury is not completely understood but is probably a combination of a shearing effect at the ligamentum attachment caused by displacement of the aorta during deceleration due to mass–inertia effect and its high density, and profound intraluminal hypertension during impact.

Immediate survival depends upon the formation of an acute false aneurysm. The intima and media rupture but the adventitia and adjacent mediastinal structures contain the bleeding. Only 10 to 20 per cent of patients with this type of injury survive to reach hospital.

The classical physical findings in patients with aortic transection are normal or elevated blood pressure in the right arm with absent or low pressure pulses in the legs. Urine flow is absent or decreased. In rare cases where dissection has occurred, there may be asymmetry of the pulses, a pericardial rub, and the diastolic murmur of aortic regurgitation.

In practice the chest radiograph provides the first evidence of aortic injury (Fig. 35) 2048. The widened mediastinum has been widely discussed in this context, though several other signs are also of importance. Marsh and Sturm highlight six radiographic findings strongly predictive of aortic rupture.

1.Widening of the superior mediastinum to 8 cm on the 100-cm anteroposterior supine radiograph.

2.Tracheal shift to the right.

3.Blurring of the aortic outline.

4.Obliteration of the medial aspect of the left upper lobe.

5.Opacification of the clear space between the aorta and left pulmonary artery.

6.Depression of the left main bronchus below a 40° angle with the trachea.

Although fracture of the first and second ribs is a hallmark of severe trauma, patients with this injury are no more likely to have a damaged aorta than patients with other rib fractures or no bony injury at all.

The natural history of aortic rupture is immediate death in 82 per cent of patients; death within 24 h in a further 6 per cent, within 2 to 7 days in 6 per cent, and during the second week in 4 per cent. Chronic traumatic aneurysm persists in 2 per cent of patients although stability is doubtful; delayed deaths occur without surgical intervention. Primary repair is indicated in all patients unless the extent of associated injuries clearly mitigates against survival.

The patient should be taken directly from the aortogram to the operating room, though in some cases laparotomy for exsanguinating intra-abdominal haemorrhage or craniotomy for a blown pupil may be needed first.

During preparation and transfer to the operating theatre, care is taken to keep the blood pressure below 100 mmHg. Use of nitroprusside is avoided due to its adverse effects on the spinal cord. When transection of the descending thoracic aorta is confirmed, the patient is positioned for left thoracotomy with the left groin exposed to allow access to the femoral vessels. Surgical access is obtained through the left fourth intercostal space and dissection is performed to gain exposure for cross-clamping of the aortic arch between the carotid and left subclavian arteries: the left subclavian artery proximal to the vertebral origin, and the descending thoracic aorta distal to the transection. Only after clamps have been placed is the pleura over the transection opened and the injury examined. The tear may be amenable to repair by direct suture. More often a woven Dacron tube graft is inserted by continuous Prolene suture anastomosis (Fig. 36) 2049.

Heparin-bonded shunts, partial left heart bypass, and femoral vein to femoral artery bypass are used by some surgeons for treatment of both acute transection and traumatic aneurysms. These are used to convey blood from the aortic arch or apex of the left ventricle to the descending aorta, thereby bypassing the injured area. However, the need for bypass procedures is questionable. Cardiopulmonary bypass requires systemic heparinization, which is clearly dangerous in patients with head injuries and multiple fractures.

With the exception of tears in the aortic arch or ascending aorta, surgery of this lesion can be accomplished safely and expeditiously without the use of shunts or extracorporeal bypass. Bypass techniques have not been shown to decrease the incidence of paraplegia (5 to 7 per cent) or renal failure compared with simple cross-clamping of the thoracic aorta. Interruption of proximal intercostal branches associated with the aortic transection itself may produce sufficient spinal cord ischaemia to cause paraplegia before surgery is undertaken. Paraplegia results from unfavourable spinal vascular anatomy and has been reported with as little as 15 min cross-clamping. Some 20 to 40 min cross-clamping is usually required for graft anastomoses and up to 110 min has been reported without paraplegia.

Postoperatively, these patients should be treated as if it were certain that progressive post-traumatic respiratory insufficiency will develop. Blood gases should be monitored frequently and appropriate changes in respiratory and metabolic therapy should be made rapidly and aggressively. Microfiltration of transfused blood should be routine. Since cardiac contusion frequently accompanies this injury, serial electrocardiograms should be evaluated. Unexplained cardiovascular instability may be the hallmark of severe cardiac contusion.

All levels of the trachea or main bronchi may be involved. More than 80 per cent of injuries occur within 2.5 cm of the carina, equally distributed between right and left sides. Mainstem bronchi are injured in 80 per cent of patients and the distal bronchi in only 9 per cent. The type of lesion varies from simple linear mucosal lacerations to extensive full thickness tears involving the trachea, main bronchi, and branch bronchi. Following complete transverse rupture and separation of the trachea, some continuity is usually maintained by the intact elastic mucosa or loose peribronchial tissue. In some patients the bronchial cartilage and muscle fractures, leaving an unsupported mucosal tube with a ‘flap valve’ effect.

Pathogenic features of airways injury are free air in the soft tissues, signs of airways obstruction, and haemoptysis (Table 6) 552. When the chest is crushed, petechial haemorrhage of the upper chest and face may develop. This traumatic asphyxia syndrome is caused by retrograde venous flow from the right side of the heart.

Patients with intrathoracic tracheal or bronchial disruption show distinct clinical patterns, depending on whether or not there is free communication between the site of disruption and the pleural cavity (Fig. 37) 2050. In the first group (70 per cent) the damaged bronchus opens into the pleural cavity causing a large (often tension) pneumothorax which continues to leak air after insertion of an intercostal drain. As a rule the lung fails to re-expand. The usual signs of injury are dyspnoea, haemoptysis, subcutaneous and mediastinal emphysema, and, in severe cases, cyanosis. Pericardial laceration in proximity to a bronchial rupture causes pneumopericardium.

In the second group rupture occurs proximal to the pleural sheath and there is little or no communication between the site of injury and the pleural cavity, even when disruption is complete. There is usually no pneumothorax; if one is present it is small and does not recur after chest drainage. Small pleural lacerations become sealed by fibrin or blood clot, allowing the lung to re-expand providing bronchial continuity is not immediately lost. Air generally escapes into the mediastinum and tracks under the deep cervical fascia. Mediastinal emphysema may be insufficient to be clinically detectable, or may be massive. Positive pressure ventilation worsens the subcutaneous emphysema or pneumothorax, and complete respiratory obstruction may occur.

Chest and neck radiographs are essential since they may disclose free air not detectable on physical examination. Pneumomediastinum is an early diagnostic sign but may easily be overlooked because of the technical quality of the film. The deep cervical fascia is in direct continuity with the mediastinum and air almost invariably tracks into the cervical region. Since this area is easily penetrated by X-rays and is not obscured by overlying soft tissue structures, deep cervical emphysema is easily recognized on lateral radiographs of the neck. Other important radiological signs include hyoid bone elevation (indicating tracheal transection), pneumothorax, subcutaneous air, pneumopericardium, fractures limited to the upper rib cage or sternum, air surrounding the bronchus, and obstruction in the course of an air-filled bronchus. Air trapping distal to a ‘flap valve’ causes over-distension of the ipsilateral lung with mediastinal shift to the opposite side or herniation of the hyperinflated lung across the anterior mediastinum. When a main bronchus is transected within its pleural sheath, the characteristic radiographic appearance is of the affected lung dropped down onto the diaphragm (Fig. 38) 2051. This picture contrasts with the findings in patients with pneumothorax without transection, in whom the lung collapses towards the mediastinum. Definitive diagnosis depends on bronchoscopy. This is best performed in a thoracic surgical unit with experienced anaesthetic support and facilities for complex intubation, thoracotomy, and respiratory support. However, it is often better for a thoracic surgeon to take his equipment to a referring hospital rather than risk interhospital transfer for bronchoscopy in circumstances where complete respiratory obstruction may occur en route.

Bronchoscopy is performed only when initial resuscitative measures such as restoration of circulatory blood volume correction of acid–base balance, and stabilization of the mechanics of breathing (e.g. insertion of an intercostal drain) have been carried out. An exception to this rule occurs when bronchoscopy is required to establish an airway after intrathoracic tracheal transection. A rigid Negus or Stortz instrument is preferable since bronchoscopy must also be used to remove blood clot, broken teeth, and secretions.

The site, nature, and extent of injury must be carefully defined. The airways may be full of blood clot and mucus. Torn bronchial mucosa and oedema may obscure the true extent of the injury. Care must be taken not to displace the ends of a transected trachea or bronchus if a satisfactory airway exists. Details of surgical techniques are beyond the scope of this chapter. A successful outcome depends on prompt diagnosis, procurement of a reliable airway, stabilization of the cardiovascular status and the mechanics of breathing, correction of acid–base balance, and early primary repair.

Conservative treatment is permissible only in certain well-defined circumstances. The first is when a longitudinal tear involves only a short length of posterior tracheal membrane, following thoracic compression against a closed glottis. This ‘bursting’ injury self-seals when the intratracheal pressure is normal. ‘Minitracheostomy’ can be used to maintain a low intratracheal pressure and discourage air leakage into the mediastinum whilst the mucosal laceration heals spontaneously (Fig. 39) 2052. The second is when bronchoscopy shows the tear to be less than one-third the circumference of the bronchus and chest tube drainage re-expands the lung completely with early cessation of air leak. Repair is then usually unnecessary.

When the acute injury is undiagnosed, and the patient survives, symptoms of respiratory distress usually follow in 7 to 10 days. These are caused by an ingrowth of granulation tissue, displacement of the injured segment, oedema, and surrounding haematoma. Untreated partial rupture of a mainstem bronchus leads to bronchopulmonary suppuration, atelectasis, and fibrosis. Reconstructive surgery with excision of the granulation tissue is indicated at this stage, otherwise stenosis will develop at the site. In complete bronchial rupture the separated lung is atelectatic and uninfected, and is often capable of circulatory and ventilatory function after being re-expanded. Normal pulmonary function has been observed following re-anastomosis 2 months after the initial injury. However, the chances of performing successful delayed primary repair for the missed bronchial injury complicated by infection, are poor and pneumonectomy is often required. Bronchial stenosis has a similarly poor outlook unless the segment is short and resection with reconstruction can be performed.

Considerable compression forces are required to rupture the diaphragm. Such forces are usually encountered during deceleration road traffic accidents, when associated visceral and musculoskeletal injuries are the rule. In the absence of respiratory distress, delay in diagnosis is almost invariable.

In one large series, the injury remained undiagnosed in 94 per cent of patients, the average interval until recognition being 4 to 5 years. Positive pressure ventilation, often undertaken on an urgent basis before the chest radiograph, masks respiratory distress and signs such as bowel sounds in the left chest. This may also replace some of the herniated contents back into the abdomen and prevent gastric distension.

Rupture is said to be more common on the left side than on the right, which is protected by the liver. This has not been our experience, but right-sided rupture is diagnosed less often. Bilateral rupture is very rare, but is seen, even in the absence of visceral injury (Fig. 40) 2053. Diagnosis of left-sided rupture usually follows radiological detection of bowel in the left chest. On the right side, appearances are those of a raised right hemidiaphragm (Fig. 41) 2054; other non-invasive means of diagnosis such as CT or ultrasound scanning are notoriously unreliable. It is easy to overlook diaphragmatic rupture during laparotomy for hepatic or splenic rupture.

The surgical approach depends on the stage of recognition and the presence of associated injuries. If the tear is recognized early in a patient with intra-abdominal injuries, the transabdominal approach is acceptable, although access to the right hemidiaphragm is difficult. Epstein and Lempke reported 36 cases of right-sided rupture in which the diagnosis was made only six times preoperatively. They concluded that an approach through the right chest wall was necessary for accurate and safe repair. This also applies for left-sided rupture diagnosed late or when the diagnosis is made early and no intra-abdominal injury is suspected. Repair is undertaken with a two-layer closure since dehiscence of the suture line occurs frequently. If this cannot be performed without tension, particularly after delayed diagnosis, Marlex mesh or a pericardial flap are employed.

In most patients with thoracic trauma injuries are limited to the thoracic cage, with or without underlying pulmonary contusion, pneumothorax, or haemothorax. The extent of chest wall derangement varies considerably. The most extensive disruption occurs in patients with severe crush injuries, in whom multiple bilateral rib fractures and fractures of the spine and sternum coexist.

A flail segment moves inwards on inspiration (paradoxical movement) and consequently compromises ventilation by reducing tidal flow. Physical examination is more valuable than radiology in defining the nature and extent of such an injury. Both pleural cavities act as single bellows. If the bellows are damaged and cannot produce sufficient negative pressure in the presence of a large flail segment, then to and fro movement of the segment may equal the attempted tidal volume of that side of the chest and ventilation is seriously compromised.

It is important to restore full expansion of the lungs as soon as possible by drainage of a haemopneumothorax. The two almost always coexist to some extent after trauma, and the size and position of the intercostal drain is important. This must be sufficiently large to drain blood and some fresh blood clot. A size 32 to 36 F Argyle tube is appropriate and is usually inserted laterally between the anterior and mid-axillary lines. The intercostal space and precise site chosen depends upon the site of injury and the location of blood or air. It is important not to enter the bony thorax too low or penetration of the diaphragm and abdominal viscera may occur: the fifth to seventh interspaces laterally at the anterior axillary line are usually safe. It is unnecessary for the drain to be in the ‘basal’ position to drain blood, or in the apical position for air. A safe insertion is the first consideration, especially when radiological landmarks are obscured by a haemothorax and the chest wall itself is bruised or deformed. Liquid, blood, and air will ‘find’ the drain as the lung expands. Established blood clots will not drain and an extensive clotted haemothorax requires surgical evacuation. It is important to incise the chest wall through to the pleura with a scalpel and to complete the entry with scissors or an artery forcep. Blood or air will then drain through the entry wound and the large drain can be inserted and directed to its required position without difficulty. Blood loss is measured carefully, since the need for thoracotomy is determined on the basis of the initial volume lost and the continued rate of bleeding. A guide for this is given in Table 4 550. There is no contradiction against insertion of the drain through the area of injury. Three commonly performed manoeuvres are inadvisable. These are, first, insertion of a chest drain ‘prophylactically’ after injury on the pretext of preventing pneumothorax during positive pressure ventilation. If there is no pneumo- or haemothorax the underlying lung may be damaged by the procedure, thus creating an air leak or bleeding. This applies particularly to the 15 per cent of patients whose pleural cavity has been obliterated by fibrous adhesions from previous ‘pleurisy’. In the presence of a pneumothorax, a drain should always be inserted prior to positive pressure ventilation.

Second, insertion of a chest drain anteriorly in the second intercostal space. This causes pain and transfixes the principal accessory respiratory muscle, the pectoralis major. If an apical drain is specifically required then the posterior suprascapular route to the second interspace can be used.

Third, clamping of a chest drain at any time in the presence of an airleak. This produces serious risk of tension pneumothorax. The alternative, without clamping, is disconnection of the drain from its underwater seal. This merely produces a simple pneumothorax which is rapidly resolved by reconnection.

When the chest drain has served its purpose, it should be removed directly. It will otherwise act as a conduit for bacterial infection and hamper chest wall movement and mobility during physiotherapy. Further management is aimed not at the chest wall itself but at preservation of respiratory function.

Two or three simple fractures may lead to the death of a patient with chronic bronchitis: pain causes decreased respiratory excursion and failure to ventilate the basal segments. Atelectasis supervenes. Pain may also inhibit cough, so that secretions are not cleared from the bronchial tree. Pneumonia follows and profuse retained secretions cause respiratory obstruction. The patient then rapidly deteriorates into acute respiratory failure.

Pain relief is of paramount importance from the outset. This allows the most affective therapeutic option, physiotherapy, to be carried out frequently and with the full co-operation of the patient. A few stable rib fractures are usually manageable with potent antipyretic oral or intravenous opiate analgesia. Patients with multiple fractures, or those with instability, require specialized attention.

Intercostal or paravertebral nerve blocks provide temporary relief for some patients with unilateral rib fractures. Nevertheless, the need for multiple injections is a distinct disadvantage. Thoracic epidural anaesthesia is an effective alternative that has radically improved the overall management of patients with chest wall trauma. Recent studies show a decreased mortality in patients with extensive rib fractures following epidural anaesthesia without ventilatory support, compared to those treated without routine mechanical ventilation. This applies equally to those who have undergone surgery for concomitant abdominal or orthopaedic injuries, those with flail segments, and those with pulmonary or cardiac contusion as long as arterial po&sub2; exceeds 50 mmHg (with 50 per cent inspired oxygen) and vital capacity exceeds 10 ml/kg.

Analgesia is planned to provide a sensory block of the dermatome area of up to, but no higher than, the level of T4. Only if the arterial po&sub2; falls below 50 mmHg on supplemental oxygen or if there is an increase in the respiratory rate to more than 40/min with an inability to cough, is intubation and ventilation considered for further management. In borderline patients, clearance of secretions by minitracheostomy (Portex) may tip the balance in favour of continued conservative management. There are potential complications attached to the thoracic epidural anaesthesia, however. The procedure should be carried out by experts and managed in the intensive care unit. Patients are excluded if they have spinal damage, pre-existing chronic neurological disease, skin infection overlying the area for insertion of the epidural catheter, or are unconscious, unco-operative, or unwilling to undergo a spinal anaesthetic procedure. Autonomic nerve block may produce hypotension, and motor blockade may decrease maximum ventilatory capacity in a few patients. However, in one excellent study, the requirement for mechanical ventilation in patients with ‘severe’ chest wall injury was reduced from 100 per cent to 9 per cent. Pain relief with epidural anaesthesia was dramatic and sedation was not required, thereby providing an alert, co-operative patient who was able to comply with physiotherapy demands.

While a conservative approach should be used in the first instance, mechanical ventilation has an important role to play in managing patients who are unconscious and unco-operative, those in severe respiratory failure, or with worsening respiratory failure despite adequate analgesia and clearance of secretions by physiotherapy and minitracheostomy.

The disadvantages of prolonged intermittent positive pressure ventilation include the need for prolonged intubation or formal tracheostomy (with the risks of accidents), prolonged sedation, inadequate nutrition, and immobility with the risk of respiratory infections and pressure sores. Effective physiotherapy is more difficult and repeated passage of suction catheters causes trauma to the major airways. Patients with chronic obstructive airways disease and those with severe pulmonary contusion are more likely to require mechanical ventilation. A flail segment in itself is not an indication for mechanical ventilation: it is the functional rather than the anatomical consequence of injury which determine the necessity for ventilatory support.

This is only rarely undertaken for fracture fixation and stabilization of the bony chest wall, or correction of serious deformity with functional sequelae. Chest wall fixation may also be performed during evacuation of an extensive clotted haemothorax or for haemostasis in a severely lacerated lung.

The vogue for nail or clip fixation of fractured ribs in flail chest waned with widespread use of positive pressure ventilation for these patients. However, it has recently been resurrected, particularly in the United States, with the trend towards ‘conservative’, non-ventilatory management. Provided that rib fractures are not too comminuted, internal fixation may eliminate the need for artificial ventilation in a few patients and lessen the risks of pulmonary infection.

When a clotted haemothorax is left in situ the long-term complications are debilitating. The haematoma deposits fibrin on the chest wall and lung and fibrotic contraction eventually causes crowding of the ribs, with severe restriction of lung compliance and expansion. There is also a significant risk of infection and emphysema. Thoracotomy should therefore be performed early when intercostal drainage fails to evacuate a substantial haemothorax. Respiratory function and recovery rate are improved by this procedure. Surgical morbidity and mortality are negligible when the patient is haemodynamically stable beforehand.

Substantial force is required to fracture the sternum. These fractures are usually transverse and may overlap, causing agonizing pain. Internal fixation is required to correct deformity and relieve the discomfort of instability. This is performed by making an incision in the xiphisternum and passing a Steinmann pin up through the medulla of both sternum fragments from underneath. A separate incision over the fracture itself aids alignment of the bone ends.

Similarly, stabilization of an anterior flail segment can be performed by passing a flat metal plate behind the sternum with its ends resting on the ribs lateral to the fracture. Both of the above procedures can be performed to great effect through small skin incisions. This is in contraindication to the extensive dissection required for multiple rib fixation.

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