Brendan L. Howes
Mark L. Shapiro
1. Frequent causes of immediate death must be ruled out during the primary survey. These include (1) critical airway obstruction, (2) tension pneumothorax, (3) open pneumothorax, (4) massive hemothorax, and (5) cardiac tamponade.
2. Adequate management of rib fracture pain using multimodal analgesia is critical in preventing further morbidity and mortality.
3. Delayed repair of aortic transection can be associated with improved mortality, and endovascular stent grafting may become the technique of choice for definitive treatment of BTAI.
This 22-year-old male was the unrestrained passenger of a pickup truck who suffered a head-on collision at high speed. The patient was ejected and suffered severe facial and chest trauma. He was found conscious upon arrival of the emergency medial team but soon deteriorated, requiring tracheal intubation at the scene.
He has multiple facial and chest contusions, is wearing a Philadelphia collar and is positioned on a trauma board. A CXR in the ED showed opacification of the entire left hemithorax. A chest tube was placed which was followed by brisk 2 liter blood loss. He is moved to the OR for emergency thoracotomy.
Trauma is the most common cause of death in the United States for persons between the age of 1 and 44 years, and thoracic trauma accounts for 25% to 50% of all trauma-related mortality.1,2 Patients with thoracic trauma may be managed conservatively in many cases, but the 10% that require urgent or emergent thoracotomy can present tremendous challenges to the anesthesiologists and intensivists involved in their care.2 In particular, members of the trauma care team must simultaneously manage profound hemodynamic instability from massive hemorrhagic or obstructive shock, significant metabolic and acid/base abnormalities, and complex intra- and extrathoracic airway and pulmonary pathology. The complexity and severity of these injuries mandate that the trauma anesthesiologist possess expertise in massive resuscitation, invasive monitoring and line placement, and advanced airway management techniques and equipment. Airway management is further complicated by concerns for associated cervical spine injury and by the fact that the trauma patient is considered to have a full stomach, necessitating a rapid sequence induction and intubation if not already intubated. Thoracic injuries can require prolonged stays in the intensive care unit (ICU) with significant morbidity, including the need for prolonged mechanical ventilation and invasive monitoring. The anesthesiologist may also play a significant role as a pain management consultant and as such must be familiar with a variety of analgesic strategies.
BLUNT VERSUS PENETRATING TRAUMA
The mechanism of chest injury has important implications for the likelihood of specific organ injury, type of injury present, and its management. Blunt injury can be associated with significant injury to the heart, lungs, great vessels, and esophagus and involves three major mechanisms: compression between osseous structures, direct energy transfer from the impact, and deceleration.3 Compression injury can occur whenever the heart, aorta, or innominate artery is trapped and crushed between the sternum and the thoracic spine as seen when the steering wheel or seatbelt impacts the chest of the driver in a motor vehicle crash (MVC). This mechanism, along with high-speed side impact crashes, is also a significant cause of direct energy transfer injury to intrathoracic organs. Compression and direct energy transfer may result in pulmonary and/or myocardial injury in addition to chest wall injuries. Finally, sudden deceleration may result in injury to the heart or aorta, usually occurring at one of several points of fibrous attachment of the heart and major vessels. The most frequent of these is aortic disruption originating at the attachment of the ligamentum arteriosum; however, sites of other clinically significant attachments include the junctions of the vena cava and the pulmonary veins with the atria, the aortic valve annulus, the origins of the great vessels from the aortic arch, and the aortic hiatus (Figure 20–1).4 Penetrating trauma can be subdivided into high-and low-velocity mechanisms, also referred to as high- and low-energy transfer wounds. Most knife and small-caliber handgun injuries are considered low-energy transfer wounds, while shotgun and rifle injuries are considered medium- to high-energy and high-energy transfer wounds, respectively. In addition to the direct tissue injury caused by the specific pathway of penetrating objects, high-velocity injuries can be associated with significant damage to surrounding tissues caused by a large energy dissipation into surrounding tissues.5 The severity of this process of “cavitation” is directly proportional to (1) the surface area of the point of impact, (2) the density of the tissue impacted, and (3) the velocity of the missile at the moment of impact.6 Cavitation injury is most likely to be significant in waterbearing tissues such as the central nervous system (CNS), liver, and spleen, while tissues such as lung and muscle are less susceptible.
Figure 20–1. Common sites of blunt injury to the heart and aorta. (Reproduced with permission from Pretre R, Chilcott M. Blunt trauma to the heart and great vessels. N Engl J Med. 1997 Feb 27;336(9):628, with permission. Copyright © Massachusetts Medical Society. All rights reserved.)
A growing concern related to the increasing incidence of terrorist attacks is the use of explosives and bombs and the resulting blast injuries. While there is concern that terrorists will gain access to biological and nonconventional weapons of mass destruction, the majority of terrorist attacks both overseas and in the United States to date have involved the detonation of explosive devices.7 In addition to the threat from terrorist attacks, trauma physicians may also care for patients injured by explosions resulting from industrial accidents. The detonation of a conventional bomb results in the creation of a blast wave consisting of two parts: (1) a shockwave of high pressure resulting from the chemical reaction of the explosion, the peak amplitude of which is termed the blast overpressure, which is closely followed by (2) a blast wind, consisting of air in rapid motion outward from the source of explosion.5,7 Blast overpressure of 35 psi can result in significant pulmonary injury, while pressures above 65 psi are usually fatal.5 The peak amplitude decreases exponentially with increasing distance from the explosion, whereas the blast waves in confined spaces such as buildings or buses can be amplified due to the complex effects of reflected and standing waves.8 So-called enhanced-blast explosive devices are associated with a different and potentially more dangerous overpressure pattern—the primary blast from these devices distributes the explosives into a larger area and then triggers a secondary explosion. This dual-stage explosion results in a prolonged duration of the overpressurization phase and greatly increases the total energy released.7 As the outwardly directed energy dissipates, the blast wind returns to the source of the explosion, resulting in underpressurization, which can also result in significant injury.
Blast injuries are caused by one of four mechanisms related to the explosion: primary, secondary, tertiary, and quaternary effects. Primary effects are direct results of the overpressurization and underpressurization, which occur as a result of the blast wave. Tympanic membrane rupture, pulmonary injury (including contusion, hemorrhage, pneumothorax, and hemothorax), and rupture of the abdominal viscera, usually the colon, are the most common injuries caused by primary blast effects. Secondary effects include penetrating injury related to the release of fragments that are part of the device itself or released from the environment as a result of the blast. Tertiary effects include blunt and/or penetrating injuries that result from persons or objects being thrown by the blast wind or from collapse of structures. Finally, quaternary effects include burns, asphyxiation, and exposure to toxic substances.7
TRIAGE AND INITIAL MANAGEMENT
Patients with thoracic trauma should initially be evaluated according to the guidelines of the American College of Surgeons Advanced Trauma Life Support protocol.9 Briefly, as for most trauma patients, this initial treatment consists of the primary survey, followed by resuscitation, secondary survey, diagnostic evaluation, and definitive treatment. While these are often presented as discrete or “stepwise” elements, they frequently occur simultaneously.10 It is during the primary survey that the “ABCDEs” are evaluated: Airway (with special considerations and precautions for cervical spine injury), Breathing,Circulation, Disability (or neurologic status), and Exposure (removal of clothes) and Environment (temperature control). A major goal of the primary survey in the patient with thoracic trauma is the early diagnosis of hypoxia and any of 5 major injuries which may cause immediate death, including (1) critical airway obstruction, (2) tension pneumothorax, (3) open pneumothorax, (4) massive hemothorax, and (5) cardiac tamponade (Table 20–1). To accomplish the primary survey, the entire thorax including the back must be exposed and examined in a systematic fashion.
Table 20–1. Life-Threatening Injuries Which Must Be Diagnosed in the Primary Survey
Of particular concern to all members of the trauma team is the potential need for emergent thoracotomy, either in the emergency department (ED) or operating suite. The goals and indications for this “resuscitative thoracotomy” include (1) immediate treatment of pericardial tamponade, (2) control of massive intrathoracic hemorrhage, (3) control of bronchopleural fistula or bronchovenous air embolism (which accounts for up to 25% deaths), (4) performance of open cardiac massage, and (5) occlusion of the descending thoracic aorta to redistribute limited cardiac output to the brain and myocardium.10 On the other hand, many patients with thoracic trauma may be managed with a tube thoracostomy or with a more controlled thoracotomy in the operating suite after initial stabilization. We will review these varied management strategies, together with the anesthetic and perioperative concerns for these patients by examining specific thoracic injuries that may be diagnosed in the primary and/or secondary surveys.
Pleural Space Injuries—Pneumothorax
Pneumothorax is a common result of thoracic trauma and patients may have no signs or symptoms (occult, simple pneumothorax) or may be in overt respiratory failure and circulatory shock (tensionpneumothorax). Pneumothorax can develop whenever there is disruption of the visceral pleura causing a communication between the airways and the pleural space. This can result in the passage of air into the pleural space, typically through a “one-way valve” mechanism in which air enters the pleural space with inspiration but is not expelled from the chest with exhalation. A one-way valve created through a chest wall injury that communicates with the pleural space will also result in the accumulation of air in the pleural space. Both injuries can result in sequestration of air and positive pressure in the ipsilateral hemithorax leading to varying degrees of lung consolidation, tracheal deviation, jugular venous distension (JVD), hypotension, and mediastinal shift toward the contralateral hemithorax. In addition to the ipsilateral lung volume loss, gas exchange may also be significantly impaired by mediastinal compression of the contralateral lung, with the combined mechanisms leading to critical respiratory failure. Impedance to venous return by the increased thoracic pressure and vena caval compression may result in hemodynamic embarrassment.
Clinical signs and symptoms of pneumothorax include chest pain, dyspnea, tachycardia and hypotension, subcutaneous emphysema, JVD, tracheal deviation away from the affected side, hyperresonanceto percussion and absence of breath sounds or chest rise on the affected side. Chest x-ray (CXR) findings may include tracheal and mediastinal deviation to the contralateral side along with downward displacement of the diaphragm and widening of the intercostal spaces on the ipsilateral side. Treatment of clinically significant pneumothorax should not be delayed for a confirmatory radiographic study. A tension pneumothorax may be temporized with decompression by needle thoracostomy. This has classically been performed by placing a needle or 14-gauge angiocatheter through the second intercostal space in the midclavicular line; however, some argue that a safer technique involves placement through the fifth intercostal space in the midaxillary line, as this may be associated with a lower likelihood of injury to the great vessels.10
Definitive management of a pneumothorax usually requires tube thoracostomy. The procedure, while not technically difficult, does require considerable training and experience as significant complications are possible including transdiaphragmatic, extrapleural, or interlobar fissure placement, lung parenchymal injury, and rarely cardiac injury.10 In most cases, tension pneumothorax will be adequately resolved with chest tube placement. If there is persistent severe air leak or failure of the affected lung to re-expand, the airways should be examined with bronchos-copy to evaluate for bronchopleural fistula, which would likely be associated with decreased tidal volumes and decreased oxygen saturation (SpO2) despite increasing levels of suction in the pleural drainage system used to drain the ipsilateral hemithorax.
Anesthetic considerations should include a high degree of suspicion for occult pneumothorax in any trauma patient. While many argue that occult pneumothorax can be managed conservatively, there is the possibility of a simple pneumothorax being converted to a tension type upon intubation and initiation of positive pressure ventilation.2 Strong consideration should be given to placement of a chest tube prior to the initiation of positive pressure ventilation whenever circumstances permit. The diagnosis of de novo tension pneumothorax may be difficult during general anesthesia, but it should always be suspected if there is unexplained hypotension, hypoxia, absent or diminished breath sounds on one side, or a sudden increase in airway pressure. Intraoperative management should include immediate placement of a chest tube or needle thoracostomy if tube thoracostomy is not feasible. Patients with a persistent air leak in the setting of pneumothorax already treated with tube thoracostomy may require surgical repair of a bronchopleural fistula. If performed with video-assisted thoracic surgery (VATS) airway management will require one-lung ventilation. In addition to the usual considerations for lung isolation, the technique may be complicated by facial and cervical spine injures in the trauma patient. These considerations may dictate which device can be used successfully (ie, placement of a double-lumen endotracheal tube vs use of a bronchial blocker through a single-lumen endotracheal tube already in place). In all cases of pneumothorax, nitrous oxide and positive end-expiratory pressure (PEEP) should be avoided until the injury has been definitively controlled (ie, with tube thoracostomy). Care must be taken to maintain adequate intravascular volume status to avoid a critical decrease in central venous return and attendant hemodynamic compromise.
Pleural Space Injuries—Open Pneumothorax
The open pneumothorax or “sucking chest wound” is caused by a full-thickness injury to the chest wall without a “one-way valve” effect. Theoretically, if the diameter of the defect exceeds two-thirds of the tracheal diameter, the negative pleural pressure associated with inspiration will cause air to preferentially enter the chest via the wound instead of through the trachea. Tension pneumothorax is unlikely in this case because the large size of the injury allows two-way gas exchange between the atmosphere and the pleural space; however, adequate ventilation and oxygenation will quickly become impossible, as air is no longer exchanged between the alveoli and the atmosphere through the trachea.
The open pneumothorax is managed by placement of an occlusive dressing (usually with petrolatum gauze) secured on 3 of the 4 sides. The remaining unsecured side of the dressing allows air in the pleural space to exit the chest, but air will no longer preferentially enter the chest via low resistance pathway and will instead pass normally through the upper airway and trachea. Patients with an open pneumothorax can be safely intubated and placed on positive pressure ventilation prior to placement of a chest tube or surgical repair of the wound.
Pleural Space Injuries—Hemothorax
Similar to a pneumothorax, the signs and symptoms caused by the collection of blood within the thorax can vary greatly. A small hemothorax may be asymptomatic and must be at least 200 mL to create blunting of the costophrenic angle on an upright chest film. A larger hemothorax on the other hand, will likely have similar signs and symptoms to a tension pneumothorax including varying degrees of respiratory failure and cardiovascular collapse. Physical findings of hemothorax include decreased or muffled breath sounds and dullness to percussion on the affected side.
Massive hemothorax is defined as the accumulation of more than 1500 mL of fluid within the pleural space. These are usually caused by large lacerations to the pulmonary parenchyma or injury to intercostal or great vessels. Up to 60% patient’s blood volume can accumulate in one hemithorax, so it must be appreciated that profound hemodynamic instability and intravascular volume loss can be accounted for by this injury alone. Indications for thoracotomy include an initial output of 1500 mL or more of blood at the time of chest tube placement or the continued output of 200 mL or more from the chest tubes for 2 to 3 consecutive hours. In stable patients who have less severe hemorrhage, management with VATS can be successful in up to 80% patients.11 Common indications include retained hemothorax and entrapped lung; many trauma surgeons advocate for the VATS to be performed on post-trauma day 3.
Lung laceration, intercostal vessel bleeding, and great vessel injuries are etio-logic in the majority of injuries associated with hemothorax requiring surgery. The source of the hemorrhage will dictate the definitive treatment and therefore the anesthetic considerations. If VATS or thoracotomy is required, the management may include considerations for lung isolation, whereas for embolization procedures, as in the case of intercostal arterial bleeding for example, conventional ventilation with a single-lumen endotracheal tube will likely be sufficient. As with any trauma associated with major hemorrhage, large bore intravenous access and direct arterial blood pressure monitoring should be obtained immediately. Central venous access and invasive hemodynamic monitoring may also be useful for the management of resuscitation in some cases, especially in the presence of severe coexisting cardiopulmonary disease. If available, consideration should be given to the use of autotransfusion techniques. Hemorrhagic shock should not be treated primarily with vasopressors, sodium bicarbonate, or continued crystalloid infusion, but with cross-matched packed red blood cells (PRBCs) or O-negative blood to maintain adequate oxygen-carrying capacity.
Chest Wall—Rib, Clavicle, and Sternum Injuries
Rib fractures are present in at least 10% patients who present with trauma, and in up to 94% who are associated with serious injuries including pneumothorax, hemothorax, and lung contusion.12 Injuries of multiple ribs, first and second rib fractures, and injuries of the clavicle and scapula are usually associated with high-energy mechanisms of injury and should raise awareness of the possibility of serious associated intra-abdominal and thoracic injuries including aortic transection and great vessel disruption.
In the absence of flail-chest physiology (see next section), the most significant consequences of rib and sternal fractures are usually related to severe pain and the associated effects on pulmonary function (Table 20–2). Particularly in the elderly, inadequate pain management can lead to significant morbidity and mortality, usually from pneumonia because of impaired coughing and clearance of secretions. In one series, mortality in patients 65 years or older increased by 19% for each rib fracture while the risk of pneumonia increased by 27%.13
Table 20–2. Adverse Effects of Rib Fracture Pain
Management of rib fracture pain can be achieved with a number of analgesic modalities including systemic administration of opioids, intercostal nerve blocks, single-injection or continuous paravertebral blocks, intrapleural administration of local anesthetics, and continuous epidural catheters (Figure 20–2). The use of parenteral opioids in the management of rib fracture pain is well described, and its main advantage is absence of any need for a regional analgesic intervention and the associated risks of bleeding, infection, or pneumothorax. However, the usual problems of respiratory and CNS depression related to their administration and the relative inferiority to regional techniques limit the utility of systemic opioids for the treatment of multiple rib fractures. If a regional technique is not feasible (coagulopathy, localized or systemic infection, limitation of patient positioning, etc), patients can be managed adequately with an intravenous (IV) narcotic either as a continuous infusion, intermittent IV dosing, or in the form of a patient-controlled analgesia (PCA) technique.14
Figure 20–2. Locations for delivery of anesthetic/analgesic solutions for rib fractures.
Intercostal nerve blocks (ICNB) are a simple and universally practiced technique for the management of rib fractures. The main disadvantage of intercostal nerve blocks is the brief duration of pain control, but there are also limitations due to the chest wall sensory anatomy and the technique itself. Because of sensory contributions from segments adjacent to the injury, multiple levels must be injected to achieve adequate sensory block. Further, firm palpation of the chest wall necessary during the technique may cause intolerable pain. However, the 6 to 12 hour duration of this block may be used as a “bridging” technique until a more definitive continuous technique can be initiated. The blocks may also be placed internally by the surgeon at the completion of the operation if the patient requires thoracotomy.
Continuous thoracic paravertebral blockade (TPB) is effective for unilateral analgesia and may be technically easier to place than a continuous epidural catheter, depending upon the preference and skill of the practitioner. In a prospective, controlled pilot study, patients with unilateral multiple level rib fractures treated with continuous TPB achieved equivalent pain relief as patients treated with thoracic epidurals.15 While there was a slight increase in the incidence of pneumonia in the TPB group, there was no difference in outcome. Continuous TPB may be associated with fewer hemodynamic changes, but increased serum levels of local anesthetic and systemic toxicity are possible.14
The infusion of a local anesthetic solution into the pleural space with a percutaneously placed catheter was first described by Kvalheim and Reiestad in 1984.16 The use of intrapleural analgesia (IPA) was then described for patients with multiple rib fractures by Rocco et al in 1987.17 Although the mechanism of analgesia is incompletely understood, the technique probably results in a unilateral, multi-level ICNB.14 While the technique may result in analgesia equivalent to that achieved with systemic opioids or epidural techniques, there are multiple limitations and drawbacks to the technique. In particular, because the anesthetic solution tends to settle in dependent portions of the chest, upper chest wall injuries will likely have poor coverage in the ICU patient with the head of the bead ideally elevated to 30 degrees. There is also the concern that accumulation of the solution on the diaphragm could result in impaired diaphragmatic function and respiratory compromise. Further, there is the possibility of inadvertent removal of the solution by an ipsilateral chest tube that may be in place. IPA can result in high plasma concentrations of local anesthetics that could lead to systemic toxicity. Given these and numerous other problems with the technique, IPA cannot be considered a first-line measure, especially given the efficacy and safety of the other regional techniques described.14
Perhaps the most effective and universally accepted analgesic modality for multiple rib fractures is continuous thoracic epidural analgesia (TEA) with local anesthetics, with or without the addition of opioids. In addition to analgesia which is superior to that achieved with systemic opioids and IPA,18,19 TEA results in superior pulmonary function including improvement in functional residual capacity, dynamic lung compliance, arterial PO2, and airway resistance.20 There is also the possibility of immune modulation as suggested by a TEA-induced decrease in plasma levels of interleukin (IL)-8, which may contribute to the development of acute lung injury (although this has not been directly correlated with clinical benefit).18 There is evidence that patients treated with TEA may require a shorter duration of mechanical ventilation, shorter ICU stays, and shorter hospitalizations.14 TEA is not appropriate for all trauma patients and contraindications include coagulopathy, infection or significant tissue injury at the intended insertion site, coexisting cardiac disease such as mitral or aortic stenosis, increased intracranial pressure, and ongoing hemodynamic instability. It is incumbent upon the practitioner to rule out associated intra-abdominal trauma as TEA may mask symptoms from these injuries. The addition of opioids to the epidural solution can result in pruritus, nausea, vomiting, urinary retention, and rarely respiratory suppression. In general, all of these side effects are less severe when compared with IV opioid administration.
The specific analgesic modality used in a given patient depends on many variables including the anesthesiologist’s preference and skill set, the preference of the thoracic or trauma surgeon, and the limitations of the institution’s infrastructure and nursing capabilities. It is important to recognize that the optimal method of analgesia for patients with multiple rib fractures remains a matter of significant controversy, and no single modality can be recommended in all situations. For any patient with acute pain resulting from chest wall injury, multimodal analgesia including the above methods with the addition of nonsteroidal anti-inflammatory drugs (NSAIDs), low-dose ketamine infusion, transcutaneous electrical nerve stimulation (TENS), anticonvulsant drugs, and pain specialist consultation should be considered early during the course of treatment.
Chest Wall—Flail chest
When two or more adjacent ribs are fractured in two or more places, anteriorly and posteriorly, a so-called flail segment can develop. Flail chest may develop in as many as 20% patients hospitalized for blunt chest trauma.21 The injured portion of the chest wall will demonstrate paradoxical movement with inspiration—that is, the segment will move inward with inspiration, and outward with exhalation. This pattern of movement occurs because the flail segment becomes mechanically separated from the chest wall and its movement becomes dependent upon the changes in pleural pressure present during spontaneous respiration. If the segment is large enough, pulmonary function may be impaired as a result of this counterproductive motion. However, the pulmonary decline is probably more frequently related to the injury to the lung or chest wall itself (pulmonary contusion, hemothorax, or pneumothorax) and its associated pain. Management of the flail chest thus no longer focuses primarily on surgical stabilization of the segment (see discussion on rib stabilization below), but instead is concerned with the management of the associated pain and lung injury which can result in decreased FRC and vital capacity (VC) and significant V/Q mismatch. Indeed, the management should be similar to that of any patient with multiple rib fractures (see previous discussion), assuming that the segment is not so large that its negative impact on spontaneous ventilation necessitates endotracheal intubation and mechanical ventilation. The management of the patient with flail chest may ultimately be determined by the extent and severity of coexisting injuries. In the setting of multiple severe intrathoracic or intracranial injuries, the patient will likely remain intubated and mechanically ventilated until these injuries are addressed or stabilized. Conversely, in the absence of other significant injuries, the patient may be successfully managed with parenteral narcotics or TEA,5 and the use of noninvasive positive pressure ventilation (NIPV), which avoids the complications of endotracheal intubation and is showing promise for those patients who still require supportive ventilation.21
Historically, reduction and fixation for rib fractures have met with resistance and failure. Traditional management since the early trials of rib traction and wiring has yielded more complications and morbidity than success and relief. Fortunately for some patients, industry has revisited the patient with flail chest and revised the stabilization approach to the fractured rib segments. Formerly, Kirschner wires were subject to fracture and therefore would add to morbidity rather than prevent complications. Newer devices attempt to be specific to ribs and even specific to rib size and side of the chest.22-25
Indications for rib stabilization include intractable pain leading to failure to liberate from mechanical ventilation, repeated trauma (as in hemothoraces), and chest wall instability leading to intubation, pneumonia, and failure to thrive.26-28 Newer techniques and devices have shown promise and several trauma centers have ongoing trials looking at length of stay (LOS), duration of mechanical ventilation, ICU stay, and amount of narcotic use.29 Many investigations are underpowered and retrospective in their analysis, but a few prospective studies exist that demonstrate significant improvement in LOS, and decreased duration of mechanical ventilation.
In summary, the approach to surgical rib stabilization has been revitalized and appears to improve patient comfort and decrease morbidity, even expedite patient throughput. Time will tell however, if this procedure holds up to the scrutiny of critical review.
Pulmonary contusion is a common consequence of thoracic trauma, and it may result in significant morbidity and mortality, usually due to the severe hypoxemia. The contusion may arise from any of the common injury mechanisms including deceleration forces, direct energy transfer, or from a shockwave associated with blast injury. The severity of contusions correlates closely with the overall severity of the chest trauma.5 The pathologic changes include hemorrhage and edema, which can result in complete consolidation of the lung parenchyma. This leads to varying degrees of hypercarbia and hypoxia due to decreased pulmonary compliance and increased pulmonary shunt fraction. The severity of the alveolar hemorrhage and parenchymal injury generally peaks during the first 24 hours after the injury, and the injury usually resolves within 7 days.30
Pulmonary contusion should be considered in any trauma patient with dyspnea, hypoxia, cyanosis and tachycardia. Unfortunately, the contusion(s) may not be radiologically apparent upon initial presentation, but they will usually be evident on CXR within the first 6 hours after the injury. Computed tomography (CT) may be more sensitive than CXR in the diagnosis of early contusion.10
The management of pulmonary contusion is frequently supportive, including the administration of supplemental oxygen and successful pain management with the goals of maintaining pulmonary toilet and minimizing atelectasis. This may be accomplished by any of the analgesic modalities described above (see Chest Wall—Rib, Clavicle, and Sternum Injuries). In severe injury, pulmonary function may decline to an extent necessitating intubation and mechanical ventilation. Antibiotics and steroids should not be used routinely.30 In the absence of pneumonia and/or the development of the acute respiratory distress syndrome (ARDS), patients are likely to make a complete recovery, although long-term morbidity manifesting as dyspnea related to persistently decreased FRC is possible.31 This decrease in FRC may make adequate pre-oxygenation prior to anesthetic induction difficult. Approximately 3% patients with pulmonary contusions develop pulmonary pseudocysts, cavitary lesions which are frequently asymptomatic but rarely are complicated by infection, bleeding, or rupture requiring surgical intervention.32 Anesthetic management of these patients will likely include the need for lung isolation and arterial line placement for arterial blood gas (ABG) analysis. Optimal fluid management for patients with acute pulmonary contusion is controversial, but a balanced approach with judicious crystalloid administration to optimize intravascular volume status makes physiologic sense, as the injury is associated with increased lung water accumulation and excessive administration of crystalloid may exacerbate the pulmonary injury and further impair gas exchange.
Pulmonary laceration can result from penetrating trauma, blunt shearing forces, missile injury associated with a gunshot wound, blast, or explosion, or from the exposed portions of fractured ribs or clavicles. The most common finding from the primary survey and CXR is a hemopneumothorax. Hemorrhage associated with pulmonary laceration is usually self-limited and can be managed definitively with tube thoracostomy.10 Approximately 10% patients will require thoracotomy, and up to 20% will require anatomic lung resection (lobectomy or pneumonectomy), a procedure which has been associated with a high mortality. Nonanatomic resection, including tractotomy or wedge resection may be associated with a significantly improved mortality and should be considered the operation of choice in non-hilar injuries.33
Traumatic diaphragmatic rupture (TDR) is a fairly uncommonly diagnosed injury associated with severe thoracoabdominal trauma. It occurs in 0.5% to 8% patients hospitalized for motor vehicle crashes and is found in approximately 5% blunt trauma victims who undergo laparotomy.34 It is also present in 10% to 15% victims of penetrating lower thoracic trauma.35 The injury is more likely to be diagnosed on the left side for 2 major reasons: (1) the liver probably provides some degree of protection to the right hemidiaphragm, especially in blunt injury, and (2) victims of stab wounds are usually attacked by right-handed assailants who are more likely to penetrate the victim’s chest or abdomen on the left side.36 Diaphragmatic rupture can occur as a result of three major mechanisms in blunt trauma: (1) the abdominal to thoracic pressure gradient may exceed the normal maximum value of 100 cmH2O, especially if the patient gasps against a closed glottis at the time of impact, (2) thoracic compression and distortion during the trauma can result in large shearing forces causing tears in the diaphragm’s musculoaponeurotic structure, and (3) the patient may have congenital abnormalities leading to areas of relative weakness in the diaphragm.37 A defect in the diaphragm may allow the herniation of abdominal structures into the pleural space, usually the stomach, omentum, transverse colon, or portions of the small bowel. Respiratory and hemodynamic compromise can follow if a significant volume of viscera becomes sequestered in the thorax, leading to a clinical picture similar to that seen with hemothorax or tension pneumothorax.
Diagnosis of diaphragmatic injury is frequently delayed and the initial CXR may be misinterpreted as representing an elevated diaphragm related to phrenic nerve injury, a “pseudodiaphragm” formed by the wall of a herniated viscus, a loculated hemopneumothorax, gastric dilatation, or subpulmonary hematoma. The delay of diagnosis may be associated with an increase in mortality.35 As such, the diagnosis of TDR requires a high degree of clinical suspicion in any patient with penetrating injuries below the fifth intercostal space, osseous injuries associated with high energy mechanisms (clavicle, sternum, scapulae, first or second ribs, pelvic, or thoracolumbar spine fractures), or with associated high speed blunt abdominal injuries.37 If there is no contraindication, a nasogastric tube should be placed as this may appear coiled in the stomach above the diaphragm on the CXR. If CXR findings are inconclusive and TDR is still suspected, further diagnostic studies including inspiratory and expiratory films (which can better detect the visceral herniation), contrast studies, or even diagnostic laparoscopy may be required. CT with reconstructed images may be the study of choice for the diagnosis of TDR.36
Anesthetic management for patients with known TDR should be similar to those patients with hemothorax and/or tension pneumothorax as similar pulmonary and cardiovascular considerations apply. In addition, it seems prudent to minimize or avoid entirely the use of positive pressure mask ventilation whenever possible, as this may result in entrainment of air into the stomach and proximal small intestine, possibly worsening the compression of intrathoracic organs by the herniated abdominal contents. Rapid sequence induction and intubation may be necessary for this reason and to decrease the risk of pulmonary aspiration of gastric contents. Placement of a gastric tube prior to induction should be considered to decompress the herniated visceral organs, perhaps reducing the risk of aspiration and potentially mitigating the adverse effects of the herniated contents on cardio-pulmonary function. Re-expansion pulmonary edema is possible in the setting of rapid decompression of the affected lung and should be suspected if there is sudden hypoxia at the time of thoracic decompression. If thoracotomy or VATS (for chronic diaphragmatic hernias) is required for surgical correction of the TDR, one-lung ventilation may be necessary.
LARYNGEAL AND TRACHEOBRONCHIAL TRAUMA
Injuries to the larynx and tracheobronchial tree are relatively uncommon but can result in immediate death from airway obstruction, and complex injuries can present tremendous challenges for airway and ventilatory management. The incidence of this rare injury is difficult to estimate, but may occur in 3% to 6% patients with penetrating neck injuries, less than 1% patients with penetrating thoracic trauma, and from 0.5% to 2% patients with blunt trauma to the neck or chest.38 Eighty percent of tracheobronchial injuries occur within 2.5 cm of the carina, but complex injuries may involve multiple areas of the larynx and/or tracheobronchial tree. Clinical symptoms and signs of significant airway injury may include dyspnea and respiratory distress, dysphonia or hoarseness, hemoptysis, pneumothorax, and subcutaneous and/or mediastinal emphysema. Persistent air leak after otherwise successful chest tube placement (as indicated by continuous bubbling in the water seal chamber of the drainage system, or worsening SpO2 when suction intensity is increased), or failure of the lung to re-expand with suction are possible in the setting of significant airway injury. The CXR and cervical spine films obtained during the primary survey are important in the diagnosis of tracheobronchial injury as cervical mediastinal emphysema and pneumothorax will be seen in 60% and 70% patients, respectively. CT images of the cervical spine (perhaps obtained to evaluate cervical spinal cord injury) are sensitive for diagnosing laryngeal injuries. CT of the chest may be helpful in the diagnosis of tracheobronchial injury, but a negative study does not obviate the need for flexible fiberoptic bronchoscopy (FOB) if there is still a high suspicion of airway injury. While FOB is considered the definitive study for the diagnosis of tracheobronchial disruption, both in the acute and late stages of evaluation, the modality may still fail to diagnose the injury in up to 6% injuries.38
Laryngeal trauma can result from a “clothesline” injury mechanism, with a narrow and focused band of energy causing compression of the cervical portion of the trachea against the vertebral bodies. Shear and deceleration forces can injure the trachea at points of relative airway fixation, such as at the cricoid cartilage and the carina, leading to tears and even complete transection of the airway. The sudden widening of the thorax that occurs during antero-posterior compression of the thoracic cage may produce enough bilateral traction on the trachea to cause an injury at the level of the carina. Finally, the airways may rupture as a consequence of sudden thoracic compression in association with a closed glottis at the time of blunt impact. This usually results in linear tears either at the junction of the membranous and cartilaginous portions of the trachea or between cartilaginous rings.38
Successful airway management is both the most critical and potentially challenging aspect of the management of patients with laryngeal or tracheobronchial trauma. FOB is perhaps the most useful modality for initial airway examination and intubation. Assuming a significant degree of patient cooperation, the broncho-scope can be introduced into the airway of the trauma patient and used both for evaluation of the location and extent of injury and for directly visualized intubation across injured or transected portions of the airway. This can be accomplished with topical anesthesia if necessary and without any requirement for extension of the neck in patients with actual or suspected cervical spine injury. Adequate control of the airway may necessitate lung isolation, depending upon the location of the injury. This may be accomplished with either a double-lumen endotracheal tube or a single-lumen tube combined with a bronchial blocker. Some argue that double-lumen endotracheal tubes should be avoided as they are stiffer and larger than conventional tubes and may worsen or extend the airway injury. With either technique, bronchoscopic skill and precision are required to ensure that the airway is controlled and the area of injury is successfully traversed and isolated by the tracheal or bronchial tube prior to the initiation of positive pressure ventilation.
Surgical management of the airway may be necessary, and this situation demands close cooperation and communication between the surgeon and anesthesiologist. This may involve a tracheostomy in the setting of laryngeal injury, or for more distal tracheal injury, a sterile endotracheal tube may need to be inserted directly by the surgeon through the operative field. Jet ventilation through small caliber tubes may also be effective as their smaller diameter creates less interference in the operative field during the repair.38 Cardiopulmonary bypass (CPB) may be necessary in the setting of extremely complex airway injuries or if coexisting cardiac or great vessel injury necessitate its use. The main limitation of CPB is the requirement of profound systemic anticoagulation, which will likely be contraindicated in the patient with multiple injuries or intracranial trauma. Thus, careful and skillful management of the airway by the anesthesiologist and surgeon is usually required if early repair of airway injury is necessary. Indeed, immediate and definitive repair of airway injuries is almost always required as delayed intervention may increase the risk of pulmonary or mediastinal infection and bronchial stenosis.5
The heart can be injured by blunt or penetrating injuries, or by a combination of these mechanisms as may occur with a blast injury. Penetrating cardiac injuries can be caused by relatively low-energy mechanisms such as knife stab wounds, or by high-energy mechanisms in the case of gunshot wounds (GSWs). Complete penetration of the heart and pericardial sac usually results in immediate death from hemorrhage at the scene, whereas patients may survive the initial injury if the pericardium is intact thereby limiting the rate of exsanguination. Blunt cardiac injury (BCI), formerly referred to as myocardial or cardiac contusion, is most commonly caused by a MVC, but any trauma to the chest wall including that resulting from falls, assaults with blunt implements, blast injury, or even cardiopulmonary resuscitation (CPR) can cause injury to the heart. It is estimated that 20% MVC-related fatalities are caused by injury to the heart, and 50% patients will die before arrival to the hospital.39 Injuries can include cardiac rupture, valvular or septal rupture, damage to coronary arteries, or nonspecific myocardial injury manifesting only as electrophysiologic (rhythm or conduction) disturbances noted on electrocardiography (ECG). Patients may present with no signs or symptoms during the primary survey or may be in overt cardiogenic shock. Patients with blunt cardiac injury will usually have other signs of significant thoracic trauma, but the absence of other findings on the physical exam does not rule out the possibility of significant BCI. Conversely, the presence of an isolated sternal fracture does not warrant further work-up for BCI in the absence of other clinical signs or symptoms.40
Cardiac rupture is the most severe form of penetrating injury and is usually fatal at the scene within seconds or minutes of the injury. The chambers most commonly ruptured (in descending order of frequency) are the right atrium, right ventricle, left atrium, and left ventricle.4 If there is concomitant rupture of the pericardium, the patient will usually exsanguinate rapidly in the field. The patient may survive to hospital admission if the pericardium remains intact, although if there is significant accumulation of pericardial blood the victim will likely develop pericardial tamponade. It should be noted that volumes as small as 15 to 30 mL can be associated with clinically evident tamponade. Stab wounds are likely to be associated with tamponade, which is protective and associated with improved survival, whereas GSWs usually pierce the pericardial sac and result in uncontrolled bleeding into the chest. Pericardial tamponade should be suspected in any victim of blunt or penetrating thoracic trauma with hypotension unresponsive to rapid volume resuscitation, and should be rapidly diagnosed in the primary survey. The diagnosis is frequently made as part of the focused assessment with sonography for trauma (FAST) exam (using subxiphoid or parasternal views) which can approach 100% sensitivity and specificity by experienced practitioners.41 The diagnosis may also be suggested by persistently elevated central venous pressures (CVP) in the setting of persistent hypotension. The findings of Beck’s triad (hypotension, muffled heart sounds, and distended neck veins) are present in only 10% victims, while Kussmaul’s sign (swelling of neck veins with inspiration) and pulsus paradoxus (decrease in systolic blood pressure upon inspiration) are similarly unreliable.10 Unstable patients with pericardial tamponade should undergo immediate subxiphoid pericardial window with local anesthesia either in the ED or OR. Median sternotomy may be necessary if hemorrhage is difficult to control through the pericardial window. The utility of pericardiocentesis is highly controversial, as the procedure may be both unhelpful diagnostically and of little therapeutic value, especially if the fluid collection is not continuous with the entire pericardial space.
Valvular injuries occur in approximately 2% patients with documented BCI.42 The aortic valve is the most frequently injured, and injury usually results from a sudden increase in aortic pressure associated with thoracic compression. The sudden increase in pressure can cause laceration or avulsion of any of the three aortic valve cusps. Aortic valvular trauma may cause severe acute pump failure or may present in the days or weeks following the initial trauma with only angina or syncope. The mitral valve apparatus may also be injured when thoracic compression coincides with early systole and may result in tearing of the mitral valve leaflets or rupture of a papillary muscle or chordae tendinae. If the resulting mitral regurgitation is severe, cardiac failure and flash pulmonary edema may ensue, and a holosystolic murmur at the apex will likely be present. Injuries to the tricuspid valve may occur, but are much less frequent and less likely to be of immediate hemodynamic consequence. Definitive diagnosis of valve injury resulting from BCI will likely require either transesophageal echocardiography (TEE) or cardiac catheterization, neither of which may be feasible during the initial stabilization and evaluation of the trauma patient. The majority of injuries can be managed conservatively until other associated injuries have been addressed and stabilized.
Septal injuries are present in approximately 5% to 7% patients who die from blunt trauma. Ventricular septal injuries are more common than traumatic atrial septal ruptures, and they usually occur in the muscular portion of the septum near the cardiac apex.39 Significant injuries can result in left-to-right shunting or hemodynamic compromise that may require urgent repair, whereas smaller injuries frequently can be allowed to heal primarily. Physical findings may include a systolic thrill and/or a harsh holosystolic murmur heard best at the left sternal edge; echocardiography or cardiac catheterization will confirm the diagnosis. If penetrating cardiac injury (of any type) represents a significant concern, TEE should be performed prior to leaving the OR.
Injuries to the coronary arteries are rare, occurring in less than 2% patients with BCI, but can be life-threatening and associated with significant myocardial ischemia.42 The most commonly involved vessels (in descending order of frequency) are the left anterior descending (LAD), right coronary (RCA), and circumflex coronary arteries. Vessel obstruction may be caused by traumatic rupture of an existing plaque, de novo thrombosis, spasm or contusion of the vessel, or even laceration or dissection. Patients may demonstrate any of the usual signs and symptoms of myocardial ischemia including angina, ST segment elevation, and varying degrees of cardiac failure depending on the extent of the coronary distribution involved. Most patients can be managed medically while associated traumatic injuries are addressed, but severe ischemia may mandate urgent percutaneous coronary intervention (PCI) with stenting or angioplasty or even surgical coronary bypass grafting or vessel repair.
Perhaps the most common yet diagnostically challenging clinical entity associated with BCI is otherwise unexplained sinus tachycardia. The incidence of BCI depends upon the diagnostic criteria used, but may be present in up to one-third of patients with blunt chest trauma.39 Injury to the myocardium can be associated with hemorrhage, edema, inflammation, and even myocyte necrosis, all of which may result in ECG changes, elevation of cardiac enzymes such as troponin I and CK-MB (which are probably unhelpful in making the diagnosis or guiding therapy), or regions of impaired contractility. Blunt cardiac injury must be differentiated from the distinct clinical phenomenon of commotio cordis which is caused by blunt impact to the precordium occurring either 15 to 30 milliseconds prior to the peak of the T wave, or during the QRS complex, leading to ventricular fibrillation or complete heart block, respectively. The impact is not associated with demonstrable contusion of the myocardium and the effects are related to the precise timing of the impact and its associated disruption of normal electrical activity of the heart.3
ECG is a simple and inexpensive test that should be performed in all patients suspected of having BCI. The most frequent findings are sinus tachycardia, followed by premature atrial and ventricular contractions. Other abnormalities in descending order of frequency include nonspecific T-wave changes, atrial fibrillation or flutter, ST segment elevation or depression, conduction delays, ventricular arrhythmias, and new Q waves.42 Of note, ventricular fibrillation and pulseless ventricular tachycardia are extremely rare, but obviously require immediate treatment with defibrillation. A normal ECG in a hemodynamically stable patient with minor thoracic trauma and no preexisting cardiac disease effectively rules out significant BCI, and these patients do not require further cardiac telemetry unless other injuries necessitate continuous monitoring.42 Asymptomatic patients with a history of cardiac disease may develop delayed ECG changes and should therefore be monitored with telemetry for 24 hours with serial 12-lead ECGs. Echocardiography (transthoracic or transesophageal) is indicated for patients with ongoing hemodynamic instability. New symptoms (angina or shock) in the setting of ECG changes necessitate ICU admission and monitoring for at least 24 hours and evaluation with echocardiography which may show segmental wall motion abnormalities (SWMAs).39
The measurement of cardiac enzymes such as creatinine kinase (CK), creatinine kinase myocardial type B fraction (CK-MB), and Troponin I and T as a screening tool for BCI is based on the rationale that myocyte injury caused by blunt trauma should be associated with their release into the serum. Historically, CK and CK-MB were the most frequently measured enzymes, but they have been shown to be nonspecific and of little to no value in the screening of patients for BCI.39,42,43 Troponins T and I, on the other hand, are highly specific for myocyte injury, and while some consider them to be useful in screening for myocardial contusion, practice guidelines do not recommend that cardiac enzymes be obtained routinely.40 However, the combination of a normal admission ECG and normal troponin levels after 4 to 6 hours makes the likelihood of BCI in asymptomatic patients highly unlikely.43
Given the variation and severity of injuries resulting from BCI, anesthetic management can be understandably complex. Large bore intravenous access should be obtained immediately and blood products and rapid infusion devices must be prepared as soon as possible in anticipation of a massive resuscitation, especially in the patient with myocardial rupture. The use of pulmonary artery catheterization (PAC) may be useful to monitor the progress of the resuscitation and in the diagnosis of pericardial tamponade. TEE may be necessary for accurate assessment of volume status, however, as BCI may be associated with reduced ventricular compliance, thereby complicating the interpretation of cardiac filling pressures as measured by PAC. TEE may also have the added benefit of diagnosing valvular injury that may not have been detected in the primary survey. Diagnosis of significant aortic or mitral regurgitation with TEE may improve the anesthesiologist’s ability to maintain hemodynamic stability by guiding the optimization of heart rate, intravascular volume, and afterload. Blunt trauma victims with coexisting right ventricular myocardial injury and pulmonary trauma (pulmonary contusion, hemothorax, or pneumothorax) resulting in pulmonary hypertension are at increased risk for right heart failure; inhaled nitric oxide (NO) or a combination of epinephrine and nitroglycerine infusions may be required to maintain adequate right ventricular function. Patients with myocardial injury are also at increased risk for the development of arrhythmias. No single anesthetic technique is less likely to exacerbate this problem, but the immediate ability to defibrillate or pace, either with externally placed pads or internal paddles, must be available at all times. The use of catecholamines, which may exacerbate or induce arrhythmias in patients with injured myocardium, may not be avoidable in patients with hypotension and shock.
GREAT VESSEL TRAUMA
Significant trauma to the aorta and aortic arch vessels can result from all traumatic mechanisms including those associated with blunt, penetrating, and blast injuries. Victims of penetrating injuries to the thoracic vessels often die in the field immediately due to their injury; however, patients may occasionally survive if the hematoma is sufficiently contained. Thus, early evaluation with CXR is extremely important for the early recognition of radiographic signs of blunt traumatic aortic injury (BTAI) that may be present. Rapid control of hemorrhage is critical in unstable patients with penetrating injuries to the thoracic vessels. As such, victims of penetrating thoracic trauma with massive hemorrhage who arrive in the emergency department with signs of life (pupillary activity, respiratory effort, or narrow complex QRS activity) are likely candidates for resuscitative thoracotomy (RT) in the ED.10 Conversely, victims of blunt thoracic trauma are unlikely to be considered candidates for RT, as those who do undergo RT rarely survive.
Bleeding from arch vessels, most commonly originating at the base of the innominate artery, is usually contained by local tissues but can rarely result in massive hemorrhage into the pericardial or pleural spaces. Great vessel injury leading to common carotid artery occlusion may result in cerebral ischemia and varying degrees of neurological deficit, which may or may not be detectable at presentation. Injury to most minor thoracic veins is usually not clinically devastating, but the hemorrhage may create a widened mediastinum on CXR necessitating further work-up for aortic transection (see below). Notable exceptions include injuries to the azygos or pulmonary veins, which may cause massive intrapleural hemorrhage.4 Injuries to the proximal pulmonary arteries, terminal pulmonary veins, or the vena cava have a mortality rate approaching 75%.5
The majority (70%) of injuries to the thoracic aorta occur as a result of blunt trauma sustained in MVCs; however, falls from higher than 30 ft (9 meters), motorcycle crashes, and automobile-pedestrian collisions may also be associated with BTAI (Table 20–3). While the injury occurs in less than 1% MVCs, it represents the cause of death in up to 15% MVC victims.44 Approximately 80% patients will die at the scene, and a majority of those who survive to hospital admission will die without a definitive procedure.45 It was formerly thought that head-on crashes were the most likely to result in aortic transection, but it is now recognized that any MVC with significant energy transfer, regardless of directionality or side of impact may be associated with aortic transection.10 The mechanism of the injury is probably related to shearing forces resulting from rapid deceleration. These forces usually cause a tear just distal to the takeoff of the left subclavian artery which represents the junction of the relatively mobile aortic arch with the comparably fixed descending aorta (Figure 20–3).4 While the tear occurs at this aortic isthmus in around 90% cases, between 3% and 10% transections may originate in the ascending aorta, aortic arch, or distal descending aorta.44 In addition to the shearing forces resulting from sudden deceleration, it is also possible that a “water-hammer” effect from simultaneous occlusion of the aorta coinciding with a sudden increase in blood pressure, along with pinching of the vessel between osseous structures during the thoracic compression may contribute to the injury.45 The injury is characterized by complete disruption of all three layers of the aorta; this should be distinguished from aneurysmal disease, which involves variable amounts of weakening and expansion of the layers of the aorta. When all three layers are completely disrupted, the patient will usually die within minutes at the scene. However, the hemorrhage may be contained in the form of a pseudoaneurysm, permitting survival for transport and definitive treatment.
Table 20–3. Factors Associated with Thoracic Aortic Injury
Figure 20–3. Aortic disruption in the proximal descending aorta. (Image courtesy of Mark L. Shapiro, MD.)
Plain CXR is the most important initial study in the evaluation of suspected aortic transection. Suggestive findings include mediastinal widening, an obscured aortic knob, downward deviation of the left mainstem bronchus, rightward deviation of the normal path of the nasogastric tube, and opacification of the aortopulmonary window.10,45 However, up to 44% patients may have a normal mediastinal appearance on CXR, leading to the recommendation that the diagnosis should be further investigated whenever there is a high suspicion based on the mechanism or circumstances of the injury (Table 20–3).45 While angiography was considered the gold standard diagnostic modality as recently as 10 years ago, helical CT is currently considered the test of choice.45,46 Helical CT has a sensitivity approaching 100% and is considered to have an excellent negative predictive value.47
Perhaps the most important recent development in the management of blunt aortic injury is a shift in management strategy from emergent surgical repair to one of hemodynamic stabilization followed by delayed repair, either with an open technique or endovascular stent grafting. This strategy is particularly applicable to patients with other life-threatening injuries, such as intracranial trauma, exsanguinating abdominal or pelvic injuries, or severe lung injury, all of which may significantly complicate open repair.48 The primary goal of this hemodynamic management strategy centers upon lowering cardiac contractility (dP/dt), thereby decreasing the intra-aortic shear forces present at the site of injury. The increasing preference for delayed repair has also been driven by the high morbidity and mortality historically associated with emergent open repair. In a 20-year metaanalysis of over 1700 patients, overall mortality was 32%, and 19% patients for whom a “clamp-and-sew” technique was employed developed paraplegia.49 Despite this high mortality, there has classically been a sense that patients with contained aortic ruptures represent “ticking time-bombs.” However, in a prospective study involving 71 patients with proven BAI, there were no cases of in-hospital aortic rupture when a strategy to keep the heart rate less than 100 bpm and the systolic blood pressure near 100 mm Hg was used. Infusions of either labetalol or esmolol with or without the addition of nitroprusside were used to achieve the hemodynamic goals.50 It should be noted that sodium nitroprusside is contraindicated in patients with significant intracranial injury due to its potent cerebrovasodilatory effects.
Patients who do require urgent or delayed open surgical repair will present significant perioperative anesthetic and hemodynamic challenges. Whenever possible, the heart rate and systolic blood pressure should be kept below 100 bpm and 110 mm Hg, respectively, to reduce shear stress at the site of the transection. This is probably best achieved with short-acting, titratable agents such as esmolol, which will effectively lower contractility (dP/dt). If patients are more stable and rapid titratability is not as important, the decrease in blood pressure and contractility may also be achieved with labetalol, either intermittently or as an infusion. Monitoring with PAC may be useful both for optimization of filling pressures and to ensure adequate oxygen delivery by measurement of mixed venous oxygen saturation (SvO2). Lung isolation with selective ventilation of the right lung will be required for surgical access through a left posterolateral thoracotomy at the fourth intercostal space. This may not be well-tolerated by patients with significant pulmonary contusion, and maintenance of adequate oxygenation may be very difficult. For descending aortic injuries, the arterial line should be placed in the right radial artery, whereas placement in the left radial artery may be necessary if repair of an ascending aortic injury will require clamping of the inominate artery. Repair of arch injuries will necessitate full cardiopulmonary bypass (CPB) and hypothermic circulatory arrest. In the traditional “clamp-and-sew” technique utilized in the repair of descending aortic injuries, proximal and distal control of the injury is achieved with two clamps, and an interposition graft is placed as quickly as possible to bridge the defect. This technique is associated with rates of paraplegia as high as 19%,49 so most centers employ some degree of active bypass to provide perfusion to the distal aorta during clamping of the injured segment. This can be achieved by one of two techniques: (1) bypassing oxygenated blood from the left atrium to the femoral artery with a simple centrifugal pump, or (2) venoarterial bypass with a pump oxygenator, either through direct cannulation of the pulmonary artery or by placing a right atrial catheter via the femoral vein. Both techniques require only minimal systemic heparinization or the use of heparin-coated tubing.45
While still not widely accepted as the standard of care, endovascular repair of aortic injuries with placement of stent grafts is becoming more popular, and the technique can greatly simplify the intraoperative management of patients with aortic trauma. There is no requirement for lung isolation and if necessary the procedure can even be performed under local anesthesia. Thoracotomy is not necessary, greatly minimizing concerns for post-operative pain. Of importance to the patient with head injury and concern for increased ICP, the procedure can also be performed with the head of the bed elevated. In addition to simplifying management, outcomes are also improved with this technique. In a recent meta-analysis comparing open with endovascular repair, mortality was reduced from 15.2% in the open-repair group to 7.6% in the group treated with endovascular repair, while paraplegia was similarly reduced from 5.6% to 0%.51 Patients undergoing endovascular stent grafting still require meticulous management of heart rate and blood pressure as described for patients requiring open repair. Invasive hemodynamic monitoring with a PAC may still be useful despite the greatly simplified operative requirements to ensure adequate oxygen during controlled hypotension.
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