- Introduction
- Assessment of a patient with chest trauma
- Injuries to the chest wall and underlying lung
- Management guidelines for injuries to the chest wall and underlying lung
- Technique of insertion of intercostal catheters
- Tracheobronchial and oesophageal injury
- Diaphragmatic injury
- Penetrating cardiac injury
- Blunt injury to the heart and sternal fractures
- Great vessel injury
- Summary
Introduction
Motor vehicle accidents and other deceleration injuries are the common causes of chest trauma. Early fatalities following severe trauma can be accounted for by injury to the chest and its contents. In patients surviving beyond 30 minutes, chest trauma may be unrecognized or its severity underestimated. Patients with isolated chest trauma and not in extremis at presentation are likely to survive although their management may require aggressive investigation and treatment.
Major disruptions of the aorta, heart and pulmonary vessels are associated with immediate death due to exsanguination. Injuries initially compensated for by peripheral vasoconstriction and tachypnoea - such as cardiac tamponade and haemo/pneumo-thoraces - may subsequently cause a precipitous decline. Several hours after the initial injury, seemingly minor injuries may be associated with clinical deterioration as is the case with lung contusion following blunt injury.
Key points
Motor vehicle accidents and other deceleration injuries are the common causes of chest trauma Major disruptions of the aorta, heart and pulmonary vessels are associated with immediate death due to exsanguination
Assessment of a patient with chest trauma
Assessment and initial management of injured patients should follow a described trauma protocol (ATLS / EMST)(RACS 1997). It is essential to obtain as much pre-hospital information as possible.
B 'MIST' - pre-hospital information to seek
1. Mechanism of injury
2. Injury sustained
3. Signs evident at the scene
4. Treatment to the point of arrival
Severe chest injuries will be evident during the primary and secondary surveys and may necessitate early intubation, ventilation and volume replacement. Eliciting tracheal deviation, observing chest wall movement, identifying obvious blunt or penetrating injury, as well as auscultation and percussion of the lung fields are important parts of the initial survey.
Findings from physical examination, and possible explanations and associations are outlined in Table 8.1
Isolated pneumothoraces occupying less than 40% of the pleural space are unlikely to compromise normal individuals. Tension pneumothorax should be suspected in any injured patient with respiratory distress. A high index of suspicion is required, as some of the 'classical' signs may be difficult to elicit in an acute situation. Intervention (needle thoracocentesis if in extremis - 14g hollow needle in 2nd intercostal space, mid clavicular line - or immediate ICC insertion) should be instigated if there is any clinical suspicion and not delayed until a chest x-ray is available. If a tension pneumothorax is diagnosed during the initial assessment, it should be treated before an x-ray is obtained, because the patient is likely to arrest due to cardiovascular compromise, before the x-ray is taken, reviewed and acted upon.
Key points
- Isolated pneumothoraces occupying less than 40% of the pleural space are unlikely to compromise normal individuals
- Drainage of a suspected tension pneumothorax should be immediately performed, and not delayed by obtaining a confirmatory xray.
Tension pneumothorax:
- Respiratory distress
- Decreased breath sounds
- Tracheal deviation
- Increased resonance to percussion
- Distended neck veins
Investigations required early in the assessment include a plain chest x-ray, assessment of oxygenation (pulse oximetry ABG as indicated) and an ECG.
A history of smoking and significant co-morbidity (airways disease, asthma, and ischaemic heart disease) is important to elicit.
The initial chest x-ray is performed supine and over 1L of blood may be present before this is evident, seen as a diffuse haziness over the entire lung field. This contrasts with an erect film where 200-300ml of blood will be visible as blunting of the costophrenic angle.
B What to look for on the initial chest x-ray:
- Trachea - deviation
- Lungs - pneumothorax, contusion, lobar collapse
- Pleural spaces - haemothoraces, pleural cap
- Mediastinum - widening, aortic contour, shape of cardiac silhouette (see section on blunt aortic injury)
- Bones - rib fractures, scapular fractures
- Soft tissues - subcutaneous emphysema, swellings in the neck
- Diaphragm - shape, position and free abdominal gas
Injuries to the chest wall and underlying lung
Fractured ribs, haemopneumothorax, flail chest and pulmonary contusion result from injury to the chest wall and the underlying lung. Blood loss and hypoxia are the main concerns. Hypoxia may result from hypoventilation due to pain, increased work of breathing due to air or blood in the pleural spaces, large flail segments, lung collapse and ventilation / perfusion mismatching.
Key points
- Blood loss and hypoxia are the main concerns
Rib fractures
Fractured ribs are a common cause of pneumothorax, due to laceration of the underlying lung. First and second rib fractures are caused by extreme force and are commonly associated with major vascular injury (see blunt injury to aorta). Sub-diaphragmatic injury, especially to the liver and spleen may occur with fracture of lower ribs (especially ribs 7 to 9). When three or more adjacent ribs are broken in two or more places, instability results and the affected segment of chest wall moves paradoxically with respiration. This 'flail' segment increases the work of breathing, however the predominant problem is the underlying lung contusion.
Key points
- Fractured ribs are a common cause of pneumothorax
Lung contusion
Lung contusion due to blunt injury is associated with significant force. Injury to the alveolo-capillary membrane causes micro-haemorrhages and fluid transudation, promoting the development of interstitial and alveolar fluid accumulation. This causes decreased compliance with the development of hypoxaemia. Contusion is commonly associated with haemopneumothoraces. The patient's clinical condition may worsen after initial stabilization, as the effects of contusion worsen. Its onset may be insidious with only mild chest wall bruising, tachycardia and tachypnoea evident. Contusion appears as a patchy irregular alveolar infiltrate on chest x-ray but may not be apparent on the initial film.
Lung contusion may be difficult to differentiate from ARDS. Contusion however usually occurs earlier, is usually localized to the injured area affected (eg unilateral and lower or upper zones) and improves over 48-72 hours. ARDS tends to be more generalized, is later in onset and slower to resolve.
Key points
- The patient's clinical condition may worsen after initial stabilization
- Lung contusion may be difficult to differentiate from ARDS.
Bleeding
Blunt and penetrating injury may cause disruption of chest wall vessels (intercostal and internal thoracic vessels) and damage to arteries and veins within the lung parenchyma. The resulting haemothorax and intra-pulmonary haemorrhage is usually self-limiting. Lung tissue surrounding parenchymal vessels commonly tamponades the bleeding. Great vessel disruption should be considered with ongoing blood loss (see section on chest tubes).
Open pneumothoraces
Open chest wounds with underlying lung injury cause 'sucking' wounds (also known as an 'open pneumothorax'). When the communication between the lung and the atmosphere is more than 2/3 the diameter of the trachea, air will preferentially enter the wound rather than the trachea and neither lung will be effectively ventilated causing severe respiratory distress. Emergency treatment involves creating a flap valve using petroleum jelly gauze taped on three sides to allow air out but not in, together with formal ICC drainage of the pleural space.
Subcutaneous emphysema
Subcutaneous emphysema is caused by leakage of air into the tissues usually from lung injury at the site of a rib fracture. Pneumomediastinum such as that caused by a ruptured oesophagus may progress to subcutaneous emphysema over the neck and shoulders. Subcutaneous emphysema is a benign condition and does not cause airway obstruction in itself. Evacuation of the pneumothorax and treatment of the underlying injury is usually followed by rapid improvement.
Management guidelines for injuries to the chest wall and underlying lung
Patients with chest trauma require regular review of their cardio-respiratory status. Optimal management involves assessment of analgesic requirements and timely treatment of any clinical deterioration.
Analgesia options
Good analgesia allows the patient to cough to clear secretions and move in the bed without severe pain. It allows effective physiotherapy and promotes early recovery and reduces the likelihood of pneumonia. Table 8.2 is a guide to analgesic options.
Patient controlled analgesia (PCA) has advantages in the minimization of narcotic dosing and ensuring timely administration ie before moving, for coughing etc. Standard ward admission is usually appropriate for this modality. Narcotic infusions require high dependency or intensive care level monitoring in most institutions. Thoracic epidurals are particularly useful in the management of flail chest and may reduce the requirement for intubation and positive pressure ventilation. Patients with thoracic epidurals require admission to a 'high dependency' or intensive care unit, for monitoring of epidural effectiveness and safety.
Management of hypoxia
Continuous cardio-respiratory monitoring is required for at least 4 hours, for all patients requiring ICC insertion. During that time, it will become clear what intensity of nursing and medical care is required for ongoing management. In most institutions it will be a choice between ward-, high dependency- or intensive care bed.
Supplemental oxygen, humidified if possible, should be titrated to oxygen saturation. This should be maintained at or above 92% and arterial blood gas measurements should be performed at least once in the first 2 hours to ascertain the PaCO2.
When the saturations fall below 90% or the PaO2 below 65mmHg, oxygen delivery must be increased. This may involve use of a higher FiO2, CPAP (continuous positive airway pressure) or consideration of intubation and positive pressure ventilation. Transfer to a higher intensity nursing and medical environment may be required. Repeated clinical assessment to exclude evolving problems (such as a new pneumothorax or worsening of lung contusion) should be undertaken. Remember both CPAP and IPPV may cause or enlarge pneumothoraces and other barotrauma.
Key points
- Continuous cardiorespiratory monitoring is required for at least 4 hours
Management of pneumothoraces
Traumatic pneumothoraces are treated by intercostal catheter insertion. Intramuscular narcotic analgesia is generally sufficient for patients with isolated pneumothoraces. Provided the lung fully re-expands after ICC insertion, the tube may be removed 24 hours after cessation of any air leak (bubbling on coughing) and another x-ray is performed after removal. Provided the lung is fully expanded on this film the patient may be discharged with oral analgesia on the same day.
Patients with severe lung injury undergoing general anaesthesia or transport, involving positive pressure ventilation, may require 'prophylactic' ICC insertion. This is a reasonable approach if the risk of pneumothorax is considered high.
Management of haemothoraces
Traumatic haemothoraces should undergo drainage by ICC. Drain output should be monitored constantly and measured hourly. A total output of 1500ml or drainage greater than 200ml/hour should prompt consideration of thoracotomy for haemostasis and evacuation of clot. This should also be considered when the haemothorax is incompletely cleared by ICC insertion, or the patient is haemodynamically unstable despite adequate fluid replacement in the absence of other injuries.
Key points
- Traumatic haemothoraces should undergo drainage by ICC
Consider thoracotomy when
- Total loss 1500ml (blunt trauma)
- Drainage > 200ml/hr (blunt trauma)
- Initial output > 1000ml (penetrating trauma)
- Drainage > 100ml/hr (penetrating trauma)
- Haemodynamic instability (blunt and penetrating trauma)
The ICC should be removed 24 hours after drainage has ceased. Serous pleural fluid, up to 100ml/day, will continue to drain after the blood has been completely cleared, but should not delay tube removal.
A word of caution on the management of small haemothorax and pneumothorax without ICC insertion
Rarely, small traumatic pneumothoraces may be observed without drainage. These patients need to be admitted to a monitored environment because of the risk of rapid pneumothorax expansion causing respiratory embarrassment and/or tension and should have a repeat chest x-ray 4-6 hours after admission.
Large amounts of blood left in the pleural space form a clotted haemothorax. Thoracotomy may be required to clear the pleural space and allow re-expansion of the lung. If this is not performed, a clotted haemothorax may progress to form a fibrothorax with the possibility of late chest wall deformities and trapped lung. Small haemothoraces (<15%) may be observed without drainage, however this requires repeat chest x-ray 4 hours after the initial film to detect any further accumulation of blood. A further chest x-ray is required one week after the injury to detect the development of a sympathetic effusion. This may occur as part of the inflammatory response to blood in the pleural space.
All haemo-pneumothoraces, and bilateral pneumothoraces should be drained regardless of size.
Penetrating injury to the lung may be initially managed without open exploration when there is a small initial drainage (less than 400ml after ICC insertion) but with a low threshold for thoracotomy if there is ongoing bleeding. Thoracoscopy is an alternative to thoracotomy in stable patients requiring exploration.
Key points
Rarely, small traumatic pneumothoraces may be observed without drainage All haemopneumothoraces, and bilateral pneumothoraces should be drained regardless of size.
Antibiotics
It is recommended that 24 hours of antibiotics using a first generation cephalosporin be used following insertion of an ICC (Barie et al. 1998).
Prophylactic antibiotics with extended gram negative cover should be considered in smokers because of the increase in mucus production and stasis of secretions that occurs with cessation on admission.
Technique of insertion of intercostal catheters
Insertion of an ICC can be a life saving procedure but guidelines should be followed for safe insertion. The sharp trocar is not used as part of standard ICC insertion because of the risk of causing further injury.
Site: The anterior axillary line in the 5th or 6th intercostal spaces is easily accessible and free of overlying muscle. Since the diaphragm is often elevated in trauma, either due to collapsed lung or increased intra-abdominal pressure, it is unwise to go below the level of the nipple.
Tube: Size32 French tubes are the minimum acceptable size. Smaller tubes will not effectively drain large volumes of blood because clot obstructs the tube. Smaller tubes may be used for draining isolated pneumothoraces in stable patients. There is no place for fine 'pleurocath' or 'pleuovac' style catheters in major trauma, since they are too small to effectively drain blood, require a blind insertion technique and easily kink.
Insertion: An aseptic technique is used. In conscious patients, local anaesthetic is infiltrated beneath the skin, into the subcutaneous tissues and over the rib. A 3cm incision is made over the site of insertion directly through the dermis into the subcutaneous fat. Artery forceps are used to separate the intercostal muscles and localize the rib. The artery forceps are then pushed over the top of the rib (since the intercostal vessels run beneath the rib), through the intercostal muscles then the pleura, which 'gives way' with moderate pressure. Spreading the artery forceps then dilates this tract.
The operator confirms that the hole made in the chest enters the pleural space, by digital examination, sweeping the index finger in all directions. This confirms that there is a space for insertion of the chest tube, and that adhesions between lung and chest wall are not present at that site. It guards against the blind insertion of a tube directly into the lung, and into a high rising diaphragm or even the heart.
The chest tube is then inserted in the direction required - apically for air or basally for blood. The basal drain is directed by running the tube postero-medially around the chest wall. Drains pushed horizontally may lodge within a lung fissure, and incompletely drain blood and air. The tube is then connected to the underwater seal drain and secured to the skin with a suture and adhesive tape.
Low wall suction (-5kPa, 10-20cm H2O) should be applied to all chest tubes except where major bronchopleural fistulae exist. In these circumstances, suction may increase the air leak without improving ventilation.
A chest x-ray should be performed following ICC insertion to confirm the position of the tube, and evacuation of air blood as required. If a collection is incompletely drained, a further ICC may be required, usually at a different site. Where large blood loss is expected, two drains may be placed initially, one directed apically and one basally.
Removal of the chest drain is performed 24 hours after drainage of air (bubbling) has ceased or when daily drainage of serous pleural fluid is less than 150 ml. Suction should be disconnected before removal. Removal is performed in full inspiration and the wound is covered with petroleum jelly gauze followed by an occlusive dressing before expiration. Purse-string sutures may be used but are not necessary since the defect closes spontaneously within 24 hours, under an occlusive dressing. Furthermore, purse strings may give a poor cosmetic result because of hurried insertion, skin necrosis where they are pulled up and propensity to infection.
Tracheobronchial and oesophageal injury
Major airways (such as trachea and bronchi) are injured in blunt trauma by rapid deceleration and shearing of more mobile bronchi from fixed proximal structures. Injury due to deceleration is usually within 2cm of the carina or at the origin of lobar bronchi. Tracheal injuries in the neck are usually associated with direct trauma eg neck struck by car dashboard.
Complete atelectasis of a lung, or pneumomediastinum (possibly with Hamman's sign or pericardial 'crunch' on auscultation) may be evident. Pneumomediastinum is also associated with injury to the pharynx, larynx and oesophagus. Intra-pleural bronchial injuries are associated with tension pneumothoraces, with massive air leak after tube insertion due to the bronchopleural fistula. More subtle injuries may require bronchoscopic evaluation if there is a high index of suspicion. A further clue may be the failure of supplemental oxygen to improve systemic saturations
Tracheobronchial injuries are associated with oesophageal injuries in 25% of patients, and complicated in the early period by infection (pulmonary, mediastinal). Isolated oesophageal trauma is uncommon in blunt injury, although blows to the abdomen may cause linear tears in the lower oesophagus due to forced regurgitation of gastric contents. Management of the ruptured oesophagus involves delineation of the injury with a contrast study, drainage of any collection in the mediastinum and pleural space, and antibiotic treatment. Mediastinitis and empyema are potential complications.
In major airway trauma, the endotracheal tube cuff may be positioned beyond a tracheal injury. Double lumen endotracheal intubation may be required for more distal injuries. For a major tracheal disruption, a stoma may need to be fashioned from the distal end of the trachea to accommodate a tracheostomy tube.
Systemic air embolism is possible when there is a communication between a bronchus and pulmonary vein. This uncommon injury usually manifests with high pressure PPV, and is a cause of rapid deterioration often immediately following intubation. Another presentation is with neurological signs in the absence of head trauma. Froth in the blood gas syringe or haemoptysis may also be noted. The patient should be positioned head down and fluid resuscitated. Cardiac compression may be required however emergent thoracotomy and securing of the vascular and bronchial injury is the only real means of treatment.
Key points
- Major airways (such as trachea and bronchi) are injured in blunt trauma by rapid deceleration and shearing
A Diaphragmatic injury
Diaphragmatic injuries due to penetrating and blunt trauma are common. Blunt trauma causes large defects, and ten percent of pelvic fractures are associated with diaphragmatic rupture.
In blunt trauma, the sudden increase in intra-abdominal pressure causes a 'blow out' at the weakest point, the left posterolateral diaphragm (over 80%). The stronger right side is also 'protected' by the liver. Intra-abdominal contents, commonly colon, stomach and spleen may herniate into the chest, often not detected in multiply injured and ventilated patients. Difficulty passing a nasogastric tube or the intra-thoracic position of a successfully placed one may assist in the diagnosis. Diaphragmatic ruptures without herniation are difficult to demonstrate on CT scan, and diagnosis is often serendipitous, such as the appearance of abdominal lavage fluid in an ICC drainage bottle, or the appearance of a pneumoperitoneum on plain x-ray with coexisting thoracic trauma.
Diaphragmatic defects do not spontaneously close, regardless of the size, because of the pleuroperitoneal pressure gradient caused by respiration. If undetected in the early period, non-specific abdominal complaints due to intermittent herniation of abdominal contents may be the presenting symptom. Bowel obstruction and incarceration may also occur.
Operative closure and relocation of abdominal contents is required. The diaphragm may be approached from either the chest or the abdomen, and in a stable patient this may be performed laparoscopically.
Key points
• In blunt trauma, the sudden increase in intraabdominal pressure causes a 'blow out' at the weakest point, the left posterolateral diaphragm (over 80%).
• Diaphragmatic defects do not spontaneously close, regardless of the size
A Penetrating cardiac injury
Penetrating injuries to the heart are usually fatal, with less than 25% surviving to hospital. Those alive at presentation survive because the bleeding has slowed due to pericardial tamponade, which the patient is able to tolerate for a short time. It is wise to assume that any penetrating injury between the right mid-clavicular line and the left anterior axillary line involves the heart.
The anterior lie of the right ventricle makes it the most susceptible to injury, and is involved in over 40% of cases. The left ventricle is injured in over 30% of cases, the right atrium in 15%. The intra-pericardial vessels and coronary arteries are infrequently involved (<5%).
Beck's triad of distended neck veins, hypotension and muffled heart sounds is present in only 10-40% of patients. The venous pressure may not be elevated because of volume depletion, and muffled heart sounds are unreliable. Furthermore, other injuries such as blunt cardiac trauma and tension pneumothorax may also manifest these signs. In practical terms, haemodynamic compromise and an entry wound over the cardiac silhouette are all that are required to make a diagnosis of significant penetrating cardiac injury.
Knife and gunshot wounds are common causes of penetrating trauma, and in these conditions, there is always an element of pericardial tamponade. Aggressive fluid resuscitation is required even when the filling pressures appear elevated, since this is initially the only way of increasing cardiac output. In shocked patients, emergency room thoracotomy is required.
It is rare for patients with penetrating cardiac injuries to be haemodynamically stable. In this event, pericardiocentesis may be performed and the drainage of even a small amount of blood may improve the patient's blood pressure, although this does nothing to address the injury itself. Echocardiographic confirmation of tamponade is desirable if available and time permits.
Key points
• Penetrating injuries to the heart are usually fatal
• Beck's triad of distended neck veins, hypotension and muffled heart sounds is present in only 10-40% of patients
B Technique of needle pericardiocentesis
Continuous ECG monitoring is required during needle pericardiocentesis. An aseptic technique is used. Purpose-built kits are available, containing a 16 or 18-gauge needle within a plastic cannula, at least 10 cm in length. Most central line insertion kits also have such a needle, alternatively an 18 gauge spinal needle may be used. The needle is inserted on the left-hand side, at the junction between the costal margin and the xiphisternum, at 45 degrees to the skin, heading toward the left scapula.
Aspirate the needle as it enters the pericardial space, and withdraw the needle as fluid returns freely, leaving the cannula in place. If the needle touches the heart, ectopics or ST-T changes may appear on the ECG trace, and the needle should be withdrawn. An ECG monitoring lead may be attached to a metal pericardiocentesis needle, and when displayed as a 'v' lead, may further assist in insertion.
If no blood is aspirated, then it is possible that the collection is clotted, that tamponade does not exist, or that the needle is incorrectly positioned. False positives may occur by aspiration of right ventricular blood if the needle is inserted too far. If time permits, echocardiography is useful to confirm the diagnosis and guide needle insertion. Pericardiocentesis is a difficult procedure often with an unsatisfactory outcome because of the blind nature of the procedure and operator inexperience. For this reason, either emergent thoracotomy or operative exploration is preferred for penetrating trauma.
Rarely, needle pericardiocentesis may be required in blunt trauma, when the patient does not respond to resuscitation and a suspicion of tamponade exists.
B Technique of emergency room thoracotomy
Penetrating wounds of the chest with significant compromise, or rapid deterioration after arrival in the emergency department with a penetrating wound are indications for emergency room thoracotomy. It is not useful for patients who have no signs of life after prolonged resuscitation (more than 15 minutes of CPR), or are multiply injured by blunt trauma.
The patient is intubated and fluid resuscitated whilst preparations are made for an antero-lateral thoracotomy. After the chest is entered, ventilation is briefly ceased, the pericardium opened and the injury identified. At that point, haemorrhage may be controlled by digital pressure, and fluid resuscitation should be continued. Relief of tamponade is usually associated with an improvement in haemodynamics after which the cardiac injury can be repaired by direct suture.
A left anterolateral thoracotomy permits open cardiac massage, treatment of cardiac lacerations and clamping of the descending thoracic aorta. Torrential lung bleeding may also be controlled through a thoracotomy. The best outcomes are for patients with isolated right ventricular lacerations and tamponade and a systolic blood pressure of 50mmHg or more on arrival. Where the left ventricle or two cardiac chambers are involved or tamponade is not present on opening, the prognosis is poor.
A Blunt injury to the heart and sternal fractures
Severe cases of blunt cardiac trauma causing rupture of cardiac chambers result in immediate death due to tamponade and pump failure. Deceleration injuries, causing the heart to impact against the sternum and vertebrae may cause injury to the myocardium, valvular structures and pericardial attachments.
Acute valvular incompetence, usually affecting the aortic valve and less commonly the mitral valve, present with shock out of proportion to the degree of external injury. Acute regurgitation is poorly tolerated although these injuries are uncommon as in most circumstances the myocardium absorbs most of the impact. This injury to the myocardium was previously known as 'cardiac contusion'. More recently it has been labelled blunt cardiac injury ('BCI'). The diagnosis and management of BCI, has been simplified as result of an evidence-based review of this condition (Pasquale et al. 1998).
The suspicion of BCI must be raised when there is evidence of direct trauma to the precordium (often caused by the steering wheel in motor vehicle accidents). BCI may manifest as ischaemic like chest pain which is unrelieved by nitrate therapy, or failure to respond in a normal way to fluid resuscitation for other injuries.
All patients in whom blunt cardiac injury is suspected should have an ECG on admission. The ECG revealing potential BCI may show arrhythmia (especially ventricular ectopics and atrial fibrillation), ischaemia, heart block, and bundle branch block or non-specific ST changes. Patients with an abnormal ECG should be admitted for cardiac monitoring for 24 hours. If the admission ECG is normal, it is unlikely that blunt cardiac injury exists, and no further investigations are required after a four-hour period of cardio-respiratory monitoring. Patients under 55 years of age and without significant co-morbidity or other injury can be discharged from the emergency department after 4 hours. Older patients should be admitted and observed for 24 hours.
If the patient is haemodynamically unstable and BCI is suspected, then an echocardiogram should be obtained. This allows quantification of wall motion abnormalities, detects pericardial fluid collections and confirms valvular competence.
It is unnecessary to perform cardiac enzyme analysis on patients in whom BCI is suspected. It is uncommon for CK-MB to be elevated in patients with a normal ECG. Whilst troponin assays are more specific and sensitive, their use does not significantly contribute to patient management since all unstable patients should undergo echocardiography and the ECG is a better screening test for stable patients.
Blunt cardiac injury is generally self-limiting, and specific complications are treated on their merits, such as anti-arrhythmic medication, or inotropes and intra-aortic balloon pumping for low output states.
Key points
- Use ECG as a screening test
- Observe all for 4 hours
- Admit and perform echocardiography on all with abnormal ECG or signs of BCI
- Exclude other injury (fractured sternum, ruptured aorta)
Sternal fractures
Sternal fractures are a common cause of blunt cardiac injury, but clearly not all sternal fractures have BCI. If the admission ECG is normal, then it is not necessary to monitor these patients, nor is measurement of cardiac enzymes. These patients may require admission for analgesia, particularly in displaced bi-cortical fractures, however most patients with unicortical sternal fractures and normal admission ECGs may be safely discharged after four hours of cardiorespiratory observation. The majority of sternal fractures involve the upper or mid portion, and are associated with other injuries, especially rib fractures in 50% of cases.
Sternal fracture management
- Lateral chest x-ray
- Identify displacement as a guide to magnitude of force
- Screen for BCI with ECG
- Echo those with abnormal ECGs
- Admit those requiring opiate pain relief
- Observe all for 4 hours
- Discharge those with minor discomfort only
Great vessel injury
The great vessels are the major intra-thoracic arteries and veins, principally the aorta and its branches, the pulmonary arteries, the vena cavae, and the subclavian vessels. Injury to these vessels accounts for 10 to 15% of motor vehicle accident deaths, most of whom die at the scene or during transport. There is a high rate of death and serious complications in those surviving to hospital (Pasquale and Fabian 1998).
The most common injury is to the aorta, which is subject to shearing forces caused by the relative mobility of the arch and the fixed descending aorta. The tethering point is the ligamentum arteriosum, just distal to the origin of the left subclavian. In blunt aortic injury (BAI), over 80% of ruptures are at this point.
In patients who survive the initial injury, the aortic rupture is contained by a thin layer of aortic adventitia and surrounding haematoma, explaining the precarious nature of this condition and its propensity to complete rupture. In a recent series the overall mortality of patients with injuries including BAI, was 31%. Aortic rupture was the cause of death in 63% of these(Fabian et al. 1997).
Despite significant force being required to cause this injury, 50% of patients have no other injuries and are quite stable, reinforcing that a high index of suspicion of blunt aortic injury (BAI) must be exercised (Table 8.3).
Key points
- There is a high rate of death and serious complications in those surviving to hospital
Investigations for BAI
The initial chest x-ray is often abnormal in blunt aortic injury, and is a guide to the need for other investigations.
The most important findings are:
1 A widened mediastinum
2 Loss of definition of the aortic knob
3 Downward deviation of the left main bronchus (normally 30º below horizontal) or rightward deviation of a nasogastric tube. Both are due to displacement by peri-aortic haematoma.
4 Loss of (opacification of) the aortopulmonary window.
Less important signs include:
5 A pleural cap, due to mediastinal haematoma tracking superiorly.
6 Associated fractures of the first and second ribs.
7 Rightward deviation of the trachea, usually at T4.
Interpreting mediastinal widening
If the mediastinum looks wider than normal following a high-risk accident, then this warrants further investigation. A subjective assessment of widening is more important than direct measurement. As a guide to typical values, if the mediastinum is more than 6cm in width on an erect PA film, or 8cm on a supine AP film, then mediastinal widening is probably present.
The chest x-ray is a screening tool for BAI. If there are any positive signs as listed above, then definitive test/s must be performed (Table 8.4).
Key points regarding BAI
- Sensitivity = correctly identified true positives (ruptured aortas)
- Specificity = correctly identified true negatives (non - ruptured aortas)
- If mediastinal haematoma is present on CT, BAI cannot be ruled out except by aortography. If helical CT shows a normal mediastinum, and there are no suggestive clinical signs, BAI is very unlikely, and an aortogram is not necessary (Pate et al. 1999).
- Chest X-ray is a good screening tool, however BAI may exist even with a normal chest x-ray and some centres advocate chest CT in all high risk patients. In one such trial, over 40% of patients with angiogram-proven rupture had a normal mediastinum on chest x-ray (Demetriades et al. 1998).
- Conventional (non - helical) CT systems are not recommended as investigations for BAI. They are significantly slower, and do not have the sensitivity or specificity of the newer generation machines.
A recommended approach is as follows (see Figure 8.1):
a) Patients with suspected aortic rupture on chest x-ray and no other injury undergo aortography as the first line of investigation.
b) Patients with a chest x-ray suggestive of BAI and requiring other CT imaging (eg abdominal or head scan) we perform a helical contrast CT of the chest as a screening tool.
c) A CT finding of mediastinal haematoma prompts definitive evaluation by aortography. Although fractures of the vertebral column may cause mediastinal haematoma, it should be assumed that mediastinal haematoma is due to a ruptured aorta until cleared by aortography.
d) Patients with normal CT scans of the chest, clearly demonstrating a normal sized mediastinum and intact contrast filled aorta, do not require aortography.
e) Trans-oesophageal echo is not used routinely in our institution. Despite obvious advantages, it is not regarded as a definitive test.
This algorithm is summarized in Figure 8.1
Management of BAI
It is common for patients with BAI to be hypertensive, unless hypovolaemic because of other injuries. In stable patients, minimal volume replacement and maintenance of the systolic blood pressure below 110mmHg is preferred. A beta-blocker such as esmolol or metoprolol administered intravenously, and intravenous sodium nitroprusside as required are used for this purpose(Fabian et al. 1998). Beta blockade is preferred because of the reduction in aortic wall dP/dt, which is actually increased by dilators. Coughing and straining should be avoided by adequate sedation or paralysis particularly during insertion of nasogastric tubes or during intubation and TOE probe insertion.
Frequently, transport to an institution with cardiothoracic surgical facilities will be required. Surgical repair of a ruptured aorta usually involves control of the aorta above and below the rupture and insertion of a vascular graft. There is a significant risk of paraplegia due to spinal cord ischaemia during surgical repair, particularly when the ischaemic time exceeds 30 minutes. To reduce this risk, some institutions perform the repair with cardiopulmonary bypass or use a bypass circuit from proximal to distal aorta, to maintain peripheral and possibly spinal perfusion. Systemic anticoagulation is usually required for these approaches and this may be contraindicated with concomitant injuries. Paraplegia occurs in around 9% of operative repairs (Fabian et al. 1997).
Summary
The treatment of chest trauma requires an assessment of problems that may potentially cause death. A high index of suspicion should be maintained in all high-velocity accidents for internal chest injuries.
Algorithms based on available evidence should be developed in individual institutions to improve outcomes for patients with chest trauma.
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