Thoracic Trauma Management

Brendan L. Howes
Mark L. Shapiro

Clinical Vignette

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.)

Blast Injury

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 (tension pneumothorax). 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, hyperresonance to 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

Related posts:

Practice Improvement and Patient Safety in Thoracic Anesthesia: A Human Factors Perspective Lung Separation Techniques Bronchoscopy, Mediastinoscopy, and Chamberlain Procedure Bronchopleural Fistula: Anesthetic Management Pericardial Window Procedures Therapeutic Bronchoscopy, Airway Stents, and Other Closed Thorax Procedures

Stay updated, free articles. Join our Telegram channel

Join