Chapter 7: Trauma

1. Trauma remains the most common cause of death for all individuals between the ages of 1 and 44 years and is the third most common cause of death regardless of age.

2. The initial management of seriously injured patients consists of performing the primary survey (the “ABCs”—Airway with cervical spine protection, Breathing, and Circulation); the goals of the primary survey are to identify and treat conditions that constitute an immediate threat to life.

3. All patients with blunt injury should be assumed to have unstable cervical spine injuries until proven otherwise; one must maintain cervical spine precautions and in-line stabilization.

4. Patients with ongoing hemodynamic instability, whether “nonresponders” or “transient responders,” require prompt intervention; one must consider the four categories of shock that may represent the underlying pathophysiology: hemorrhagic, cardiogenic, neurogenic, and septic.

5. Indications for immediate operative intervention for penetrating cervical injury include hemodynamic instability and significant external arterial hemorrhage; the management algorithm for hemodynamically stable patients is based on the presenting symptoms and anatomic location of injury, with the neck being divided into three distinct zones.

6. The gold standard for determining if there is a blunt descending torn aorta injury is CT scanning; indications are primarily based on injury mechanisms.

7. The abdomen is a diagnostic black box. However, physical examination and ultrasound can rapidly identify patients requiring emergent laparotomy. Computed tomographic (CT) scanning is the mainstay of evaluation in the remaining patients to more precisely identify the site and magnitude of injury.

8. Manifestation of the “bloody vicious cycle” (the lethal combination of coagulopathy, hypothermia, and metabolic acidosis) is the most common indication for damage control surgery. The primary objectives of damage control laparotomy are to control bleeding and limit GI spillage.

9. Blunt injuries to the carotid and vertebral arteries are usually managed with systemic antithrombotic therapy.

10. The abdominal compartment syndrome may be primary (i.e., due to the injury of abdominal organs, bleeding, and packing) or secondary (i.e., due to reperfusion visceral edema, retroperitoneal edema, and ascites).

Trauma, or injury, is defined as cellular disruption caused by an exchange with environmental energy that is beyond the body’s resilience which is compounded by cell death due to ischemia/reperfusion. Trauma remains the most common cause of death for all individuals between the ages of 1 and 44 years and is the third most common cause of death regardless of age.¹ It is also the leading cause of years of productive life lost. Unintentional injuries account for over 110,000 deaths per year, with motor vehicle collisions accounting for over 40%. Homicides, suicides, and other causes are responsible for another 50,000 deaths each year. However, death rate underestimates the magnitude of the societal toll. For example, in 2004 there were approximately 167,000 injury-related deaths, but 29.6 million injured patients treated in emergency departments (EDs). Injury-related medical expenditures are estimated to be $117 billion each year in the United States.² The aggregate lifetime cost for all injured patients is estimated to be in excess of $260 trillion. For these reasons, trauma must be considered a major public health issue. The American College of Surgeons Committee on Trauma addresses this issue by assisting in the development of trauma centers and systems. The organization of trauma systems has had a significant favorable impact on patient outcomes.^3,4,5

Primary Survey

The Advanced Trauma Life Support (ATLS) course of the American College of Surgeons Committee on Trauma was developed in the late 1970s, based on the premise that appropriate and timely care can significantly improve the outcome for the injured patient.⁶ ATLS provides a structured approach to the trauma patient with standard algorithms of care; it emphasizes the “golden hour” concept that timely, prioritized interventions are necessary to prevent death and disability. The ATLS format and basic tenets are followed throughout this chapter, with some modifications. The initial management of seriously injured patients consists of phases that include the primary survey/ concurrent resuscitation, the secondary survey/diagnostic evaluation, definitive care, and the tertiary survey. The first step in patient management is performing the primary survey, the goal of which is to identify and treat conditions that constitute an immediate threat to life. The ATLS course refers to the primary survey as assessment of the “ABCs” (Airway with cervical spine protection, Breathing, and Circulation). Although the concepts within the primary survey are presented in a sequential fashion, in reality they are pursued simultaneously in coordinated team resuscitation. Life-threatening injuries must be identified (Table 7-1) and treated before being distracted by the secondary survey.

Airway Management with Cervical Spine Protection

Ensuring a patent airway is the first priority in the primary survey. This is essential, because efforts to restore cardiovascular integrity will be futile unless the oxygen content of the blood is adequate. Simultaneously, all patients with blunt trauma require cervical spine immobilization until injury is excluded. This is typically accomplished by applying a hard collar or placing sandbags on both sides of the head with the patient’s forehead taped across the bags to the backboard. Soft collars do not effectively immobilize the cervical spine. For penetrating neck wounds, however, cervical collars are not believed useful because they provide no benefit, but may interfere with assessment and treatment. ^7,8

In general, patients who are conscious, without tachypnea, and have a normal voice are unlikely to require early airway intervention. Exceptions are penetrating injuries to the neck with an expanding hematoma; evidence of chemical or thermal injury to the mouth, nares, or hypopharynx; extensive subcutaneous air in the neck; complex maxillofacial trauma; or airway bleeding. Although these patients may initially have an adequate airway, it may become obstructed if soft tissue swelling, hematoma formation, or edema progresses. In these cases, pre-emptive intubation should be performed before airway access becomes challenging.

Patients who have an abnormal voice, abnormal breathing sounds, tachypnea, or altered mental status require further airway evaluation. Blood, vomit, the tongue, foreign objects, and soft tissue swelling can cause airway obstruction; suctioning affords immediate relief in many patients. In the comatose patient, the tongue may fall backward and obstruct the hypopharynx; this can be relieved by either a chin lift or jaw thrust. An oral airway or a nasal trumpet is also helpful in maintaining airway patency, although the former is not usually tolerated by an awake patient. Establishing a definitive airway (i.e., endotracheal intubation) is indicated in patients with apnea; inability to protect the airway due to altered mental status; impending airway compromise due to inhalation injury, hematoma, facial bleeding, soft tissue swelling, or aspiration; and inability to maintain oxygenation. Altered mental status is the most common indication for intubation. Agitation or obtundation, often attributed to intoxication or drug use, may actually be due to hypoxia.

Options for endotracheal intubation include nasotracheal, orotracheal, or operative routes. Nasotracheal intubation can be accomplished only in patients who are breathing spontaneously. Although nasotracheal intubation is frequently used by prehospital providers, the application for this technique in the ED is limited to those patients requiring emergent airway support in whom chemical paralysis cannot be used. Orotracheal intubation is the preferred technique used to establish a definitive airway. Because all patients are presumed to have cervical spine injuries, manual in-line cervical immobilization is essential.⁶ Correct endotracheal placement is verified with direct laryngoscopy, capnography, audible bilateral breath sounds, and finally a chest film. The GlideScope^¯, a video laryngoscope that uses fiber optics to visualize the vocal cords, is being employed more frequently.⁹ Advantages of orotracheal intubation include the direct visualization of the vocal cords, ability to use larger-diameter endotracheal tubes, and applicability to apneic patients. The disadvantage of orotracheal intubation is that conscious patients usually require neuromuscular blockade, which may result in inability to intubate, aspiration, or medication complications. Those who attempt rapid-sequence induction must be thoroughly familiar with the procedure (see Chap. 13).

Patients in whom attempts at intubation have failed or who are precluded from intubation due to extensive facial injuries require operative establishment of an airway. Cricothyroidotomy (Fig. 7-1) is performed through a generous vertical incision, with sharp division of the subcutaneous tissues. Visualization may be improved by having an assistant retract laterally on the neck incision using army-navy retractors. The cricothyroid membrane is verified by digital palpation and opened in a horizontal direction. The airway may be stabilized before incision of the membrane using a tracheostomy hook; the hook should be placed under the thyroid cartilage to elevate the airway. A 6.0 endotracheal tube (maximum diameter in adults) is then advanced through the cricothyroid opening and sutured into place. In patients under the age of 11, cricothyroidotomy is relatively contraindicated due to the risk of subglottic stenosis, and tracheostomy should be performed.

Emergent tracheostomy is indicated in patients with laryngotracheal separation or laryngeal fractures, in whom cricothyroidotomy may cause further damage or result in complete loss of the airway. This procedure is best performed in the OR where there is optimal lighting and availability of more equipment (e.g., sternal saw). In these cases, often after a “clothesline” injury, direct visualization and instrumentation of the trachea usually is done through the traumatic anterior neck defect or after a generous collar skin incision (Fig. 7-2). If the trachea is completely transected, a nonpenetrating clamp should be placed on the distal aspect to prevent tracheal retraction into the mediastinum; this is particularly important before placement of the endotracheal tube.

Breathing and Ventilation

Once a secure airway is obtained, adequate oxygenation and ventilation must be ensured. All injured patients should receive supplemental oxygen and be monitored by pulse oximetry. The following conditions constitute an immediate threat to life due to inadequate ventilation and should be recognized during the primary survey: tension pneumothorax, open pneumothorax, flail chest with underlying pulmonary contusion, and massive air leak. All of these diagnoses should be made during the initial physical examination.

The diagnosis of tension pneumothorax is presumed in any patient manifesting respiratory distress and hypotension in combination with any of the following physical signs: tracheal deviation away from the affected side, lack of or decreased breath sounds on the affected side, and subcutaneous emphysema on the affected side. Patients may have distended neck veins due to impedance of venous return, but the neck veins may be flat due to concurrent systemic hypovolemia. Tension pneumothorax and simple pneumothorax have similar signs, symptoms, and examination findings, but hypotension qualifies the pneumothorax as a tension pneumothorax. Although immediate needle thoracostomy decompression with a 14-gauge angiocatheter in the second intercostal space in the midclavicular line may be indicated in the field, tube thoracostomy should be performed immediately in the ED before a chest radiograph is obtained (Fig. 7-3). Recent studies suggest the preferred location for needle decompression may be the 5^th intercostal space in the anterior axillary line due to body habitus.¹⁰ In cases of tension pneumothorax, the parenchymal tear in the lung acts as a one-way valve, with each inhalation allowing additional air to accumulate in the pleural space. The normally negative intrapleural pressure becomes positive, which depresses the ipsilateral hemidiaphragm and shifts the mediastinal structures into the contralateral chest. Subsequently, the contralateral lung is compressed and the heart rotates about the superior and inferior vena cava; this decreases venous return and ultimately cardiac output, which culminates in cardiovascular collapse.

An open pneumothorax or “sucking chest wound” occurs with full-thickness loss of the chest wall, permitting free communication between the pleural space and the atmosphere (Fig. 7-4). This compromises ventilation due to equilibration of atmospheric and pleural pressures, which prevents lung inflation and alveolar ventilation, and results in hypoxia and hypercarbia. Complete occlusion of the chest wall defect without a tube thoracostomy may convert an open pneumothorax to a tension pneumothorax. Temporary management of this injury includes covering the wound with an occlusive dressing that is taped on three sides. This acts as a flutter valve, permitting effective ventilation on inspiration while allowing accumulated air to escape from the pleural space on the untaped side, so that a tension pneumothorax is prevented. Definitive treatment requires closure of the chest wall defect and tube thoracostomy remote from the wound.

Flail chest occurs when three or more contiguous ribs are fractured in at least two locations. Paradoxical movement of this free-floating segment of chest wall is usually evident in patients with spontaneous ventilation, due to the negative intrapleural pressure of inspiration. However, the additional work of breathing and chest wall pain caused by the flail segment is rarely sufficient to compromise ventilation. Instead, it is the decreased compliance and increased shunt fraction caused by the associated pulmonary contusion that is the source of acute respiratory failure. Pulmonary contusion often progresses during the first 12 hours. Resultant hypoventilation and hypoxemia may require intubation and mechanical ventilation. The patient’s initial chest radiograph often underestimates the extent of the pulmonary parenchymal damage (Fig. 7-5); close monitoring and frequent clinical re-evaluation are warranted.

Massive air leak occurs from major tracheobronchial injuries. Type I injuries are those occurring within 2 cm of the carina.^11,12 These are often not associated with a pneumothorax due to the envelopment in the mediastinal pleura. Type II injuries are more distal injuries within the tracheobronchial tree and manifest with pneumothorax. Bronchoscopy confirms diagnosis and directs management.

Circulation with Hemorrhage Control

With a secure airway and adequate ventilation established, circulatory status is the next priority. An initial approximation of the patient’s cardiovascular status can be obtained by palpating peripheral pulses. In general, systolic blood pressure (SBP) must be 60 mm Hg for the carotid pulse to be palpable, 70 mm Hg for the femoral pulse, and 80 mm Hg for the radial pulse. Any episode of hypotension (defined as a SBP <90 mm Hg) is assumed to be caused by hemorrhage until proven otherwise. Patients with acute massive blood loss may have paradoxical bradycardia.¹³ Blood pressure and pulse should be measured at least every 5 minutes in patients with significant blood loss until normal vital sign values are restored. High energy auto-pedestrian victims should have their pelvis wrapped with a sheet until radiography can be done.

IV access for fluid resuscitation is obtained with two peripheral catheters, 16-gauge or larger in adults. For patients in whom peripheral angiocatheter access is difficult, intraosseous (IO) needles can be rapidly placed in the proximal tibia of the lower extremity (Fig. 7-6).^14,15 All medications administered IV may be administered in a similar dosage intraosseously. Although safe for emergent use, the needle should be removed once alternative access is established to prevent osteomyelitis. Blood should be drawn simultaneously for a bedside hemoglobin level and routine trauma laboratory tests. In the seriously injured patient arriving in shock, an arterial blood gas, cross-matching for possible red blood cell (RBC) transfusion, and a coagulation panel should be obtained. In these patients, secondary large bore cannulae should be obtained via the femoral or subclavian veins, or saphenous vein cutdown; Cordis introducer catheters are preferred over triple-lumen catheters. In general, initial access in trauma patients is best secured in the groin or ankle, so that the catheter will not interfere with the performance of other diagnostic and therapeutic thoracic procedures. Saphenous vein cutdowns at the ankle provide excellent access (Fig. 7-7). The saphenous vein is reliably found 1 cm anterior and 1 cm superior to the medial malleolus. Standard 14-gauge catheters can be quickly placed, even in an exsanguinating patient with collapsed veins. If IV access cannot be achieved readily, the IO route is very useful, particularly for drug administration.^14,15 Additional venous access often is obtained through the femoral or subclavian veins with Cordis introducer catheters. A rule of thumb to consider for secondary access is placement of femoral access for thoracic trauma and jugular or subclavian access for abdominal trauma. However, jugular or subclavian catheters provide a more reliable measurement of central venous pressure (CVP), which may be helpful in determining the volume status of the patient and in excluding cardiac tamponade. In severely injured children < 6 years of age, the preferred venous access is peripheral intravenous catheters followed by an IO needle. Central venous catheter placement or saphenous vein cutdown may be considered as the third choice of access based upon provider experience. Inadvertent femoral artery cannulation, however, may result in limb-threatening distal arterial spasm.

External control of any visible hemorrhage should be achieved promptly while circulating volume is restored. Manual compression of open wounds with ongoing bleeding should be done with a single 4 × 4 gauze and a gloved hand. Covering the wound with excessive dressings may permit ongoing unrecognized blood loss that is hidden underneath the dressing. Blind clamping of bleeding vessels should be avoided because of the risk to adjacent structures, including nerves. This is particularly true for penetrating injuries of the neck, thoracic outlet, and groin, where bleeding may be torrential and arising deep within the wound. In these situations, a gloved finger is placed through the wound directly onto the bleeding vessel and enough pressure is applied to control active bleeding. The surgeon performing this maneuver must then walk with the patient to the OR for definitive treatment. For bleeding of the extremities it is tempting to apply tourniquets for hemorrhage control, but digital occlusion will usually control the bleeding, and complete vascular occlusion risks permanent neuromuscular impairment. Patients in shock have a lower tolerance to warm ischemia, and an occluded extremity is prone to small vessel thrombosis. For patients with open fractures, fracture reduction with stabilization via splints will limit bleeding both externally and into the subcutaneous tissues. Scalp lacerations through the galea aponeurotica tend to bleed profusely; these can be temporarily controlled with skin staples, Raney clips, or a large full-thickness continuous running nylon stitch.

During the circulation section of the primary survey, four life-threatening injuries must be identified promptly: (a) massive hemothorax, (b) cardiac tamponade, (c) massive hemoperitoneum, and (d) mechanically unstable pelvic fractures with bleeding. Massive hemoperitoneum and mechanically unstable pelvic fractures are discussed in “Emergent Abdominal Exploration” and “Pelvic Fractures and Emergent Hemorrhage Control,” respectively. Three critical tools used to differentiate these in the multisystem trauma patient are chest radiograph, pelvis radiograph, and focused abdominal sonography for trauma (FAST) (see “Regional Assessment and Special Diagnostic Tests”). A massive hemothorax (life-threatening injury number one) is defined as >1500 mL of blood or, in the pediatric population, >25% of the patient’s blood volume in the pleural space (Fig. 7-8). Although it may be estimated on chest radiograph, tube thoracostomy is the only reliable means to quantify the amount of hemothorax. After blunt trauma, a major hemothorax usually is due to multiple rib fractures with severed intercostal arteries, but occasionally bleeding is from lacerated lung parenchyma which is usually associated with an air leak. After penetrating trauma, a great vessel or pulmonary hilar vessel injury should be presumed. In either scenario, a massive hemothorax is an indication for operative intervention, but tube thoracostomy is critical to facilitate lung re-expansion, which may improve oxygenation and cardiac performance as well as tamponade venous bleeding.

Cardiac tamponade (life-threatening injury number two) occurs most commonly after penetrating thoracic wounds, although occasionally blunt rupture of the heart, particularly the atrial appendage, is seen. Acutely, <100 mL of pericardial blood may cause pericardial tamponade.¹⁶ The classic Beck’s triad—dilated neck veins, muffled heart tones, and a decline in arterial pressure—is usually not appreciated in the trauma bay because of the noisy environment and associated hypovolemia. Because the pericardium is not acutely distensible, the pressure in the pericardial sac will rise to match that of the injured chamber. When this pressure exceeds that of the right atrium, right atrial filling is impaired and right ventricular preload is reduced. This ultimately leads to decreased right ventricular output. Additionally, increased intrapericardial pressure impedes myocardial blood flow, which leads to subendocardial ischemia and a further reduction in cardiac output.

Diagnosis of hemopericardium is best achieved by bedside ultrasound of the pericardium (Fig. 7-9). Early in the course of tamponade, blood pressure and cardiac output will transiently improve with fluid administration due to increased central venous pressure. In patients with any hemodynamic disturbance, a pericardial drain is placed using ultrasound guidance (Fig. 7-10). Removing as little as 15 to 20 mL of blood will often temporarily stabilize the patient’s hemodynamic status, and alleviate subendocardial ischemia with associated lethal arrhythmias, and allow safe transport to the OR for sternotomy. Pericardiocentesis is successful in decompressing tamponade in approximately 80% of cases; the majority of failures are due to the presence of clotted blood within the pericardium. Patients with a SBP <60 mm Hg warrant resuscitative thoracotomy (RT) with opening of the pericardium for rapid decompression and to address the injury.

The utility of RT has been debated for decades. Current indications are based on 30 years of prospective data, supported by a recent multicenter prospective study (Table 7-2).^17,18 RT is associated with the highest survival rate after isolated cardiac injury; 35% of patients presenting in shock and 20% without vital signs (i.e., no pulse or obtainable blood pressure) are salvaged after isolated penetrating injury to the heart. For all penetrating wounds, survival rate is 15%. Conversely, patient outcome is poor when RT is done for blunt trauma, with 2% survival among patients in shock and <1% survival among those with no vital signs. Thus, patients undergoing cardiopulmonary resuscitation upon arrival to the ED should undergo RT selectively based on injury and transport time (Fig. 7-11). RT is best accomplished using a generous left anterolateral thoracotomy, with the skin incision started to the right of the sternum (Fig. 7-12). A longitudinal pericardiotomy anterior to the phrenic nerve is used to release cardiac tamponade and permits access to the heart for cardiac repair and open cardiac massage. Cross-clamping of the aorta improves central circulation, augments cerebral and coronary blood flow, and limits further abdominal blood loss (Fig. 7-13). The patient must sustain a SBP of 70 mm Hg after RT and associated interventions to be considered resuscitatable, and hence transported to the OR.^17,18

Disability and Exposure

The Glasgow coma scale (GCS) score should be determined for all injured patients (Table 7-3). It is calculated by adding the scores of the best motor response, best verbal response, and the best eye response. Scores range from 3 (the lowest) to 15 (normal). Scores of 13 to 15 indicate mild head injury, 9 to 12 moderate injury, and ≤8 severe injury. The GCS is a quantifiable determination of neurologic function that is useful for triage, treatment, and prognosis.

Neurologic evaluation is critical before administration of neuromuscular blockade for intubation. Subtle changes in mental status can be caused by hypoxia, hypercarbia, or hypovolemia, or may be an early sign of increasing intracranial pressure. An abnormal mental status should prompt an immediate re-evaluation of the ABCs and consideration of central nervous system injury. Deterioration in mental status may be subtle and may not progress in a predictable fashion. For example, previously calm, cooperative patients may become anxious and combative as they become hypoxic. However, a patient who is agitated and combative from drugs or alcohol may become somnolent if hypovolemic shock develops. Patients with neurogenic shock are typified by hypotension with relative bradycardia, and are often first recognized due to paralysis, decreased rectal tone or priapism. Patients with high spinal cord disruption are at greatest risk for neurogenic shock due to physiologic disruption of sympathetic fibers; treatment consists of volume loading and a dopamine infusion which is both inotropic and chronotropic. Seriously injured patients must have all of their clothing removed to avoid overlooking limb- or life-threatening injuries.

Shock Classification and Initial Fluid Resuscitation

Classic signs and symptoms of shock are tachycardia, hypotension, tachypnea, altered mental status, diaphoresis, and pallor(Table 7-4). In general, the quantity of acute blood loss correlates with physiologic abnormalities. For example, patients in class II shock are tachycardic but they do not exhibit a reduction in blood pressure until over 1500 mL of blood loss, or class III shock. Physical findings should be used as an aid in the evaluation of the patient’s response to treatment. The goal of fluid resuscitation is to re-establish tissue perfusion. Fluid resuscitation begins with a 2 L (adult) or 20 mL/kg (child) IV bolus of isotonic crystalloid, typically Ringer’s lactate. For persistent hypotension (SBP <90 mm Hg in an adult), the current trend is to activate a massive transfusion protocol (MTP) in which red blood cells (RBC) and fresh-frozen plasma (FFP) are administered early. The details of a MTP are discussed later. Patients who have a good response to fluid infusion (i.e., normalization of vital signs, clearing of the sensorium) and evidence of good peripheral perfusion (warm fingers and toes with normal capillary refill) are presumed to have adequate overall perfusion. Urine output is a quantitative, reliable indicator of organ perfusion. Adequate urine output is 0.5 mL/kg per hour in an adult, 1 mL/kg per hour in a child, and 2 mL/kg per hour in an infant <1 year of age. Because measurement of this resuscitation-related variable is time dependent, it is generally more useful in the OR and intensive care unit (ICU) setting, than in initial evaluation in the trauma bay.

There are several caveats to be considered when evaluating the injured patient for shock. Tachycardia is often the earliest sign of ongoing blood loss, but the critical issue is change over time. Furthermore, individuals in good physical condition with a resting pulse rate in the fifties may manifest a relative tachycardia in the nineties; although clinically significant, this does not meet the standard definition of tachycardia. Conversely, patients receiving cardiac medications such as beta blockers may not be capable of increasing their heart rate to compensate for hypovolemia. Bradycardia can occur with rapid severe blood loss¹³; this is an ominous sign, often heralding impending cardiovascular collapse. Other physiologic stresses, aside from hypovolemia, may produce tachycardia, such as hypoxia, pain, anxiety, and stimulant drugs (cocaine, amphetamines). As noted previously, decreased SBP is not a reliable early sign of hypovolemia, because blood loss must exceed 30% before hypotension occurs. Additionally, younger patients may maintain their SBP due to sympathetic tone despite severe intravascular deficits until they are on the verge of cardiac arrest. Pregnant patients have a progressive increase in circulating blood volume over gestation; therefore, they must lose a relatively larger volume of blood before manifesting signs and symptoms of hypovolemia (see Special Trauma Populations).

Based on the initial response to fluid resuscitation, hypovolemic injured patients can be separated into three broad categories: responders, transient responders, and nonresponders. Individuals who are stable or have a good response to the initial fluid therapy as evidenced by normalization of vital signs, mental status, and urine output are unlikely to have significant ongoing hemorrhage, and further diagnostic evaluation for occult injuries can proceed in an orderly fashion (see “Secondary Survey”). At the other end of the spectrum are patients classified as “nonresponders” who have persistent hypotension despite aggressive resuscitation. These patients mandate immediate identification of the source of hypotension with appropriate intervention to prevent a fatal outcome. Transient responders are those who respond initially to volume loading with improvement in vital signs, but then deteriorate hemodynamically again. This group of patients can be challenging to triage for definitive management.

Persistent Hypotension

Patients with ongoing hemodynamic instability, whether “nonresponders” or “transient responders,” require systematic evaluation and prompt intervention.The spectrum of disease in patients with persistent hypotension ranges from overwhelming multisystem injury to easily reversible problems such as a tension pneumothorax. One must first consider the four categories of shock that may be the underlying cause: hemorrhagic, cardiogenic, neurogenic, and septic. In patients with persistent hypotension and tachycardia, cardiogenic or hemorrhagic shock are the likely causes. Ultrasound evaluation of the pericardium, pleural cavities, and abdomen in combination with plain radiographs of the chest and pelvis will usually identify the source of hemorrhagic and/or cardiogenic shock. Evaluation of the CVP may further assist in distinguishing between these two categories. A patient with distended neck veins and a CVP of >15 cm H₂O is likely to be in cardiogenic shock. The CVP may be falsely elevated, however, if the patient is agitated and straining, or fluid administration is overzealous; isolated readings must be interpreted with caution. A patient with flat neck veins and a CVP of <5 cm H₂O is likely hypovolemic due to ongoing hemorrhage. Serial base deficit measurements are helpful; a persistent base arterial deficit of >8 mmol/L implies ongoing cellular shock.^19,20 Serum lactate is also used to monitor the patient’s physiologic response to resuscitation.²¹ Evolving technology, such as near infrared spectroscopy, may provide noninvasive monitoring of oxygen delivery to tissue.²² Except for patients transferred from outside facilities >12 hours after injury, few patients present in septic shock in the trauma bay. Patients with neurogenic shock as a component of hemodynamic instability often are recognized during the disability section of the primary survey to have paralysis, but those patients chemically paralyzed before physical examination may be misdiagnosed.

The differential diagnosis of cardiogenic shock in trauma patients is: (a) tension pneumothorax, (b) pericardial tamponade, (c) blunt cardiac injury, (d) myocardial infarction, and (e) bronchovenous air embolism. Tension pneumothorax, the most frequent cause of cardiac failure, and pericardial tamponade have been discussed earlier. Although as many as one-third of patients sustaining significant blunt chest trauma experience some degree of blunt cardiac injury, few such injuries result in hemodynamic embarrassment. Patients with electrocardiographic (ECG) abnormalities or dysrhythmias require continuous ECG monitoring and antidysrrhythmic treatment as needed. Unless myocardial infarction is suspected, there is no role for routine serial measurement of cardiac enzyme levels—they lack specificity and do not predict significant dysrhythmias.²³ In patients who have no identified injuries who are being considered for discharge from the ED, the combination of a normal EKG and troponin level at admission and 8 hours later, rules out significant blunt cardiac injury.²⁴ The patient with hemodynamic instability requires appropriate resuscitation and may benefit from hemodynamic monitoring to optimize preload and guide inotropic support. Echocardiography (ECHO) is performed to exclude valvular or septal injuries, and the most common finding is right ventricular dyskinesia due to the anterior orientation of the right versus left ventricle. Transthoracic and transesophageal ECHO are now becoming routine in many surgical intensive care units (SICUs).^25,26 Patients with refractory cardiogenic shock may occasionally require placement of an intra-aortic balloon pump to decrease myocardial work and enhance coronary perfusion. Acute myocardial infarction may be the cause of a motor vehicle collision or other trauma in older patients. Although optimal initial management includes treatment for the evolving infarction, such as lytic therapy and emergent angioplasty, these decisions must be individualized in accordance with the patient’s other injuries.

Air embolism is a frequently overlooked lethal complication of pulmonary injury. Air emboli can occur after blunt or penetrating trauma, where air from an injured bronchus enters an adjacent injured pulmonary vein (bronchovenous fistula) and returns air to the left heart. Air accumulation in the left ventricle impedes diastolic filling, and during systole air is pumped into the coronary arteries, disrupting coronary perfusion. The typical case is a patient with a penetrating thoracic injury who is hemodynamically stable but experiences cardiac arrest after being intubated and placed on positive pressure ventilation. The patient should immediately be placed in Trendelenburg’s position to trap the air in the apex of the left ventricle. Emergency thoracotomy is followed by cross-clamping of the pulmonary hilum on the side of the injury to prevent further introduction of air (Fig. 7-14). Air is aspirated from the apex of the left ventricle and then the aortic root with an 18-gauge needle and 50-mL syringe. Vigorous massage is used to force the air bubbles through the coronary arteries; if this is unsuccessful, a tuberculin syringe is used to aspirate air bubbles from the right coronary artery. Once circulation is restored, the patient should be kept in Trendelenburg’s position with the pulmonary hilum clamped until the pulmonary venous injury is controlled operatively.

Persistent hypotension due to uncontrolled hemorrhage is associated with high mortality. A rapid search for the source or sources of hemorrhage includes visual inspection with knowledge of the injury mechanism, FAST, and chest and pelvic radiographs. During diagnostic evaluation, type O RBCs (O-negative for women of childbearing age) and thawed AB plasma should be administered at a ratio of 2:1. Type-specific RBCs should be administered as soon as available. The acute coagulopathy of trauma is now well recognized, and underscores the importance of pre-emptive blood component administration. The resurgent interest in viscoelastic hemostatic assays (thrombelastography [TEG] and thrombelastometry [ROTEM]) has facilitated the appropriate and timely use of clotting adjuncts, including the prompt recognition of fibrinolysis. In patients with clear indications for operation, essential films should be taken and the patient transported to the OR immediately. Such patients include those with blunt trauma and massive hemothorax, those with penetrating trauma and an initial chest tube output of >1 L, and those with abdominal trauma and ultrasound evidence of extensive hemoperitoneum. In patients with gunshot wounds to the chest or abdomen, a chest and abdominal film, with radiopaque markers at the wound sites, should be obtained to determine the trajectory of the bullet or location of a retained fragment. For example, a patient with a gunshot wound to the upper abdomen should have a chest radiograph to ensure that the bullet did not traverse the diaphragm causing intrathoracic injury. Similarly, a chest radiograph is important in a patient with a gunshot wound to the right chest to evaluate the left hemithorax. If a patient arrives with a penetrating weapon remaining in place, the weapon should not be removed in the ED, because it could be tamponading a lacerated blood vessel (Fig. 7-15). The surgeon should extract the offending instrument in the controlled environment of the OR, ideally once an incision has been made with adequate exposure. In situations where knives are embedded in the head or neck, preoperative imaging may be useful to anticipate arterial injuries.

In patients without clear operative indications and persistent hypotension, one should systematically evaluate the five potential sources of blood loss: scalp, chest, abdomen, pelvis, and extremities. Significant bleeding at the scene may be noted by paramedics, but its quantification is unreliable. Examination should seek active bleeding from a scalp laceration that may be readily controlled with clips or staples. Thoracoabdominal trauma should be evaluated with a combination of chest radiograph, FAST, and pelvic radiograph. If the FAST results are negative and no other source of hypotension is obvious, diagnostic peritoneal aspiration should be entertained.²⁷ Extremity examination and radiographs should be used to search for associated fractures. Fracture-related blood loss, when additive, may be a potential source of the patient’s hemodynamic instability. Each rib fracture can produce 100 to 200 mL of blood loss; for tibial fractures, 300 to 500 mL; for femur fractures, 800 to 1000 mL; and for pelvic fractures >2000 mL. Although no single injury can account for the patient’s hemodynamic instability, the sum of the injuries may result in life-threatening blood loss. The diagnostic measures advocated earlier are those that can be easily performed in the trauma bay. Transport of a hypotensive patient out of the ED for computed tomographic (CT) scanning is hazardous; monitoring is compromised, and the environment is suboptimal for dealing with acute problems. The surgeon must accompany the patient and be prepared to abort the CT scan with diversion to the OR. This dilemma is becoming less common in many trauma centers where CT scanning is done in the ED.

The concept of hypotensive resuscitation in the ED remains controversial, and it is primarily relevant for patients with penetrating vascular injuries. Experimental work suggests that an endogenous sealing clot of an injured artery may be disrupted at an SBP of >90 mm Hg²⁸; thus, many believe that this should be the preoperative blood pressure target for patients with potential torso arterial injuries. On the other hand, optimal management of traumatic brain injury (TBI) includes maintaining the SBP >100 mm Hg,²⁹ and thus, hypotensive resuscitation is not appropriate for most blunt trauma patients.

Secondary Survey

Once the immediate threats to life have been addressed, a thorough history is obtained and the patient is examined in a systematic fashion. The patient and surrogates should be queried to obtain an AMPLE history (Allergies, Medications, Past illnesses or Pregnancy, Last meal, and Events related to the injury). The physical examination should be literally head to toe, with special attention to the patient’s back, axillae, and perineum, because injuries here are easily overlooked. All potentially seriously injured patients should undergo digital rectal examination to evaluate for sphincter tone, presence of blood, rectal perforation, or a high-riding prostate; this is particularly critical in patients with suspected spinal cord injury, pelvic fracture, or transpelvic gunshot wounds. Vaginal examination with a speculum should be performed in women with pelvic fractures to exclude an open fracture. Specific injuries, their associated signs and symptoms, diagnostic options, and treatments are discussed in detail later in this chapter.

Adjuncts to the physical examination include vital sign and CVP monitoring, ECG monitoring, nasogastric tube placement, Foley catheter placement, radiographs, hemoglobin, urinalysis, and base deficit measurements, and repeat FAST exam. A nasogastric tube should be inserted in all intubated patients to decrease the risk of gastric aspiration but may not be necessary in the awake patient. Nasogastric tube placement in patients with complex mid-facial fractures is contraindicated; rather, a tube should be placed orally if required. Nasogastric tube evaluation of stomach contents for blood may suggest occult gastroduodenal injury or the errant path of the nasogastric tube on a chest film may indicate a left diaphragm injury. A Foley catheter should be inserted in patients unable to void to decompress the bladder, obtain a urine specimen, and monitor urine output. Gross hematuria demands evaluation of the genitourinary system for injury. Foley catheter placement should be deferred until urologic evaluation in patients with signs of urethral injury: blood at the meatus, perineal or scrotal hematomas, or a high-riding prostate. Although policies vary at individual institutions, most agree patients in extremis with need for Foley catheter placement should undergo one attempt at catheterization; if the catheter does not pass easily, a percutaneous suprapubic cystostomy should be considered.

Selective radiography and laboratory tests are done early in the evaluation after the primary survey. For patients with severe blunt trauma, chest and pelvic radiographs should be obtained. Historically, a lateral cervical spine radiograph was also obtained, hence the reference to the big three films, but currently patients preferentially undergo CT scanning of the spine rather than plain film radiography. For patients with truncal gunshot wounds, anteroposterior and at times lateral radiographs of the chest and abdomen are warranted. It is important to mark the entrance and exit sites of penetrating wounds with ECG pads, metallic clips, or staples so that the trajectory of the missile can be estimated. Limited one-shot extremity radiographs also may be taken. In critically injured patients, blood samples for a routine trauma panel (type and cross-match, complete blood count, blood chemistries, coagulation studies, and arterial blood gas analysis) should be sent to the laboratory. For less severely injured patients only a complete blood count and urinalysis may be required. Because older patients may present in subclinical shock, even with minor injuries, routine analysis of an arterial blood gas in patients over the age of 55 should be considered. Repeat FAST is performed if there are any signs of abdominal injury or unexplained blood loss.

Many trauma patients cannot provide specific information about the mechanism of their injury. Emergency medical service personnel and police are trained to evaluate an injury scene and should be questioned while they are present in the ED. For automobile collisions, the speed of the vehicles involved, angle of impact, use of restraints, airbag deployment, condition of the steering wheel and windshield, amount of intrusion, ejection of the patient from the vehicle, and fate of other passengers should be ascertained. For other injury mechanisms, critical information includes such things as height of a fall, surface impact, helmet use, and weight of an object by which the patient was crushed. In patients sustaining gunshot wounds, velocity, caliber, distance, and presumed path of the bullet are important, if known. For patients with stab wounds, the length and type of object is helpful. Finally, some patients experience a combination of blunt and penetrating trauma. Do not assume that someone who was stabbed was not also assaulted; the patient may have a multitude of injuries and cannot be presumed to have only injuries associated with the more obvious penetrating mechanism. In short, these details of information are critical to the clinician to determine overall mechanism of injury and anticipate its associated injury patterns.

Mechanisms and Patterns of Injury

In general, more energy is transferred over a wider area during blunt trauma than from a penetrating wound. As a result, blunt trauma is associated with multiple widely distributed injuries, whereas in penetrating wounds the damage is localized to the path of the bullet or knife. In blunt trauma, organs that cannot yield to impact by elastic deformation are most likely to be injured, namely, the solid organs (liver, spleen, and kidneys). For penetrating trauma, organs with the largest surface area when viewed from the front are most prone to injury (small bowel, liver, and colon). Additionally, because bullets and knives usually follow straight lines, adjacent structures are commonly injured (e.g., the pancreas and duodenum).

Trauma surgeons often separate patients who have sustained blunt trauma into categories according to their risk for multiple injuries: those sustaining high energy transfer injuries and those sustaining low energy transfer injuries. Injuries involving high energy transfer include auto-pedestrian accidents, motor vehicle collisions in which the car’s change of velocity (ΔV) exceeds 20 mph or in which the patient has been ejected, motorcycle collisions, and falls from heights >20 ft.³⁰ In fact, for motor vehicle accidents the variables strongly associated with life-threatening injuries, and hence reflective of the magnitude of the mechanism, are death of another occupant in the vehicle, extrication time of >20 minutes, ΔV >20 mph, lack of restraint use, and lateral impact.³⁰ Low-energy trauma, such as being struck with a club or falling from a bicycle, usually does not result in widely distributed injuries. However, potentially lethal lacerations of internal organs can occur, because the net energy transfer to any given location may be substantial.

In blunt trauma, particular constellations of injury or injury patterns are associated with specific injury mechanisms. For example, when an unrestrained driver sustains a frontal impact, the head strikes the windshield, the chest and upper abdomen hit the steering column, and the legs or knees contact the dashboard. The resultant injuries can include facial fractures, cervical spine fractures, laceration of the thoracic aorta, myocardial contusion, injury to the spleen and liver, and fractures of the pelvis and lower extremities. When such patients are evaluated, the discovery of one of these injuries should prompt a search for the others. Collisions with side impact also carry the risk of cervical spine and thoracic trauma, diaphragm rupture, and crush injuries of the pelvic ring, but solid organ injury usually is limited to either the liver or spleen based on the direction of impact. Not surprisingly, any time a patient is ejected from the vehicle or thrown a significant distance from a motorcycle, the risk of any injury exists.

Penetrating injuries are classified according to the wounding agent (i.e., stab wound, gunshot wound, or shotgun wound). Gunshot wounds are subdivided further into high- and low-velocity injuries, because the speed of the bullet is much more important than its weight in determining kinetic energy. High-velocity gunshot wounds (bullet speed >2000 ft/s) are infrequent in the civilian setting. Shotgun injuries are divided into close-range (<20 feet) and long-range wounds. Close-range shotgun wounds are tantamount to high-velocity wounds because the entire energy of the load is delivered to a small area, often with devastating results. In contrast, long-range shotgun blasts result in a diffuse pellet pattern in which many pellets miss the victim, and those that do strike are dispersed and of comparatively low energy.

Regional Assessment and Special Diagnostic Tests

Based on mechanism, location of injuries identified on physical examination, screening radiographs, and the patient’s overall condition, additional diagnostic studies often are indicated. However, the seriously injured patient is in constant jeopardy when undergoing special diagnostic testing; therefore, the surgeon must be in attendance and must be prepared to alter plans as circumstances demand. Hemodynamic, respiratory, and mental status will determine the most appropriate course of action. With these issues in mind, additional diagnostic tests are discussed on an anatomic basis.

Head

Evaluation of the head includes examination for injuries to the scalp, eyes, ears, nose, mouth, facial bones, and intracranial structures. Palpation of the head will identify scalp lacerations, which should be evaluated for depth, and depressed or open skull fractures. The eye examination includes not only pupillary size and reactivity, but also examination for visual acuity and for hemorrhage within the globe. Ocular entrapment, caused by orbital fractures with impingement on the ocular muscles, is evident when the patient cannot move his or her eyes through the entire range of motion. It is important to perform the eye examination early, because significant orbital swelling may prevent later evaluation. A lateral canthotomy may be needed to relieve periorbital pressure. The tympanic membrane is examined to identify hemotympanum, otorrhea, or rupture, which may signal an underlying head injury. Otorrhea, rhinorrhea, raccoon eyes, and Battle’s sign (ecchymosis behind the ear) suggest a basilar skull fracture. Although such fractures may not require treatment, there is an association with blunt cerebrovascular injuries, cranial nerve injuries, and risk of meningitis.

Anterior facial structures should be examined to rule out fractures. This entails palpating for bony step-off of the facial bones and instability of the midface (by grasping the upper palate and seeing if this moves separately from the patient’s head). A good question to ask awake patients is whether their bite feels normal to them; abnormal dental closure suggests malalignment of facial bones and a possibility for a mandible or maxillary fracture. Nasal fractures, which may be evident on direct inspection or palpation, typically bleed vigorously. This may result in the patient’s having airway compromise due to blood running down the posterior pharynx, or there may be vomiting provoked by swallowed blood. Nasal packing or balloon tamponade may be necessary to control bleeding. Examination of the oral cavity includes inspection for open fractures, loose or fractured teeth, and sublingual hematomas.

All patients with a significant closed head injury (GCS score <14) should undergo CT scanning of the head. Additionally, elderly patients or those patients on antiplatelet agents or anticoagulation should be imaged despite a GCS of 15.^31,32 For penetrating injuries, plain skull films may be helpful in the trauma bay to determine the trajectory of injury in hemodynamically unstable patients who cannot be transported for CT scan. The presence of lateralizing findings (e.g., a unilateral dilated pupil unreactive to light, asymmetric movement of the extremities either spontaneously or in response to noxious stimuli, or unilateral Babinski’s reflex) suggests an intracranial mass lesion or major structural damage.

Such lesions include hematomas, contusions, hemorrhage into ventricular and subarachnoid spaces, and diffuse axonal injury (DAI). Epidural hematomas occur when blood accumulates between the skull and dura, and are caused by disruption of the middle meningeal artery or other small arteries in that potential space, typically after a skull fracture (Fig. 7-16). Subdural hematomas occur between the dura and cortex and are caused by venous disruption or laceration of the parenchyma of the brain. Due to associated parenchymal injury, subdural hematomas have a much worse prognosis than epidural collections. Hemorrhage into the subarachnoid space may cause vasospasm and further reduce cerebral blood flow. Intraparenchymal hematomas and contusions can occur anywhere within the brain. DAI results from high-speed deceleration injury and represents direct axonal damage from shear effects. CT scan may demonstrate blurring of the gray and white matter interface and multiple small punctate hemorrhages, but magnetic resonance imaging is a more accurate test. Although prognosis for these injuries is extremely variable, early evidence of DAI is associated with a poor outcome. Stroke syndromes should prompt a search for carotid or vertebral artery injury using multislice CT angiography (CTA) (Fig. 7-17).

Significant intracranial penetrating injuries usually are produced by bullets from handguns, but an array of other weapons or instruments can injure the cerebrum via the orbit or through the thinner temporal region of the skull. Although the diagnosis usually is obvious, in some instances wounds in the auditory canal, mouth, and nose can be elusive. Prognosis is variable, but virtually all supratentorial wounds that injure both hemispheres are fatal.

Neck

All blunt trauma patients should be assumed to have cervical spine injuries until proven otherwise. During cervical examination one must maintain cervical spine precautions and in-line stabilization. Due to the devastating consequences of quadriplegia, a diligent evaluation for occult cervical spine injuries is mandatory. In the awake patient, the presence of posterior midline pain or tenderness should provoke a thorough radiologic evaluation. Additionally, intubated patients, patients with distracting injuries, or another identified spine fracture should undergo CT imaging. A ligamentous injury may not be visible with standard imaging techniques.³³ Flexion and extension views or MRI are obtained to further evaluate patients at risk or those with persistent symptoms, but generally are not done in the acute setting.

Spinal cord injuries can vary in severity. Complete injuries cause either quadriplegia or paraplegia, depending on the level of injury. These patients have a complete loss of motor function and sensation two or more levels below the bony injury. Patients with high spinal cord disruption are at risk for shock due to physiologic disruption of sympathetic fibers. Significant neurologic recovery is rare. However, there are several partial or incomplete spinal cord injury syndromes where the prognosis is better. Central cord syndrome typically occurs in older persons who experience hyperextension injuries. Motor function, pain, and temperature sensation are preserved in the lower extremities but diminished in the upper extremities. Some functional recovery usually occurs, but is often not a return to normal. Anterior cord syndrome is characterized by diminished motor function, pain, and temperature sensation below the level of the injury, but position sensing, vibratory sensation, and crude touch are maintained. Prognosis for recovery is poor. Brown-Séquard syndrome is usually the result of a penetrating injury in which one-half of the spinal cord is transected. This lesion is characterized by the ipsilateral loss of motor function, proprioception, and vibratory sensation, whereas pain and temperature sensation are lost on the contralateral side.

During the primary survey, identification of injuries to the neck with exsanguination, expanding hematomas, airway obstruction, or aerodigestive injuries is a priority. A more subtle injury that may not be identified is a fracture of the larynx due to blunt trauma. Signs and symptoms include hoarseness, subcutaneous emphysema (Fig. 7-18), and a palpable fracture. Penetrating injuries of the anterior neck that violate the platysma are potentially life-threatening because of the density of critical structures in this region. Although operative exploration is appropriate in some circumstances, selective nonoperative management has been proven safe (Fig. 7-19).³⁴ Indications for immediate operative intervention for penetrating cervical injury include hemodynamic instability, significant external hemorrhage, or evidence of aerodigestive injury. The management algorithm for hemodynamically stable patients is based on the presenting symptoms and anatomic location of injury, with the neck being divided into three distinct zones (Fig. 7-20). Zone I is inferior to the clavicles encompassing the thoracic outlet structures, zone II is between the thoracic outlet and the angle of the mandible, and zone III is above the angle of the mandible. Due to technical difficulties of injury exposure and varying operative approaches, a precise preoperative diagnosis is desirable for symptomatic zone I and III injuries. Therefore, these patients should ideally undergo diagnostic imaging before operation if they remain hemodynamically stable. Management of patients is further divided into those who are symptomatic and those who are not (Fig 7-19). Specific symptoms or signs that should be identified include dysphagia, hoarseness, hematoma, venous bleeding, minor hemoptysis, and subcutaneous emphysema. Symptomatic patients should undergo CTA with further evaluation or operation based upon the imaging findings; less than 15% of penetrating cervical trauma requires neck exploration.³⁵ Asymptomatic patients are typically observed for 6 to12 hours. The one caveat is asymptomatic patients with a transcervical gunshot wound; these patients should undergo CTA to determine the track of the bullet. CTA of the neck and chest determines trajectory of the injury tract; further studies are performed based on proximity to major structures.³⁵ Such additional imaging includes angiography, soluble contrast esophagram followed by barium esophagram, esophagoscopy, or bronchoscopy. Angiographic diagnosis, particularly of zone III injuries, can then be managed by selective angioembolization.

Chest

Blunt trauma to the chest may involve the chest wall, thoracic spine, heart, lungs, thoracic aorta and great vessels, and rarely the esophagus. Most of these injuries can be evaluated by physical examination and chest radiography, with supplemental CT scanning based on initial findings. Any patient who undergoes an intervention in the ED—endotracheal intubation, central line placement, tube thoracostomy—needs a repeat chest radiograph to document the adequacy of the procedure. This is particularly true in patients undergoing tube thoracostomy for a pneumothorax or hemothorax. Patients with persistent pneumothorax, large air leaks after tube thoracostomy, or difficulty ventilating should undergo fiber-optic bronchoscopy to exclude a tracheobronchial injury or presence of a foreign body. Patients with hemothorax must have a chest radiograph documenting complete evacuation of the chest; a persistent hemothorax that is not drained by two chest tubes is termed a caked hemothorax and mandates immediate thoracotomy (Fig. 7-21).

Occult thoracic vascular injury must be diligently sought due to the high mortality of a missed lesion. Widening of the mediastinum on initial anteroposterior chest radiograph, caused by a hematoma around an injured vessel that is contained by the mediastinal pleura, suggests an injury of the great vessels. The mediastinal abnormality may suggest the location of the arterial injury (i.e., left-sided hematomas are associated with descending torn aortas, whereas right-sided hematomas are commonly seen with innominate injuries) (Fig. 7-22). Posterior rib fractures, sternal fractures with laceration of small vessels, and mediastinal venous bleeding also can produce similar hematomas. Other chest radiographic findings suggestive of an aortic tear are summarized in Table 7-5 (Fig. 7-23). However, at least 7% of patients with a descending torn aorta have a normal chest radiograph.³⁶ Therefore, screening spiral CT scanning is performed based on the mechanism of injury: high-energy deceleration motor vehicle collision with frontal or lateral impact (> 30 mph frontal impact and >23 mph lateral impact), motor vehicle collision with ejection, falls of >25 ft, or direct impact (horse kick to chest, snowmobile or ski collision with tree). ^37,38 In >95% of patients who survive to reach the ED, the aortic injury occurs just distal to the left subclavian artery, where it is tethered by the ligamentum arteriosum (Fig. 7-24). In 2% to 5% of patients the injury occurs in the ascending aorta, in the transverse arch, or at the diaphragm. Reconstructions with multislice CTA obviate the need for invasive arteriography.³⁷

For penetrating thoracic trauma, physical examination, plain posteroanterior and lateral chest radiographs with metallic markings of wounds, pericardial ultrasound, and CVP measurement will identify the majority of injuries. Injuries of the esophagus and trachea are exceptions. Bronchoscopy should be performed to evaluate the trachea in patients with a persistent air leak from the chest tube or mediastinal air. Because esophagoscopy can miss injuries following an apparent normal endoscopy, patients at risk should undergo soluble contrast esophagraphy followed by barium examination to look for extravasation of contrast to identify an injury.³⁹ As with neck injuries, hemodynamically stable patients with transmediastinal gunshot wounds should undergo CT scanning to determine the path of the bullet; this identifies the vascular or visceral structures at risk for injury and directs angiography or endoscopy as appropriate. If there is a suspicion of a subclavian artery injury, brachial-brachial indices should be measured, but >60% of patients with an injury may not have a pulse deficit.⁴⁰ Therefore, CTA should be performed based on injury proximity to intrathoracic vasculature. Finally, with wounds identified on the chest, penetrating trauma should not be presumed to be isolated to the thorax. Injury to contiguous body cavities (i.e., the abdomen and neck) must be excluded; plain radiographs are a rapid, effective screening modality.

Abdomen

The abdomen is a diagnostic black box. Fortunately, with few exceptions, it is not necessary to determine in the emergency department which intra-abdominal organs are injured, only whether an exploratory laparotomy is necessary. However, physical examination of the abdomen can be unreliable in making this determination, and drugs, alcohol, and head and spinal cord injuries complicate clinical evaluation. The presence of abdominal rigidity and hemodynamic compromise is an undisputed indication for prompt surgical exploration. For the remainder of patients, a variety of diagnostic adjuncts are used to identify abdominal injury.

The diagnostic approach differs for penetrating trauma and blunt abdominal trauma. As a rule, minimal evaluation is required before laparotomy for gunshot or shotgun wounds that penetrate the peritoneal cavity, because over 90% of patients have significant internal injuries. Anterior truncal gunshot wounds between the fourth intercostal space and the pubic symphysis whose trajectory as determined by radiograph or wound location indicates peritoneal penetration should undergo laparotomy (Fig. 7-25). The exception is penetrating trauma isolated to the right upper quadrant; in hemodynamically stable patients with trajectory confined to the liver by CT scan, nonoperative observation may be reasonable.⁴¹ In obese patients, if the gunshot wound is thought to be tangential through the subcutaneous tissues, CT scan can delineate the track and exclude peritoneal violation. Laparoscopy is another option to assess peritoneal penetration for tangential wounds. If there is doubt, however, it is always safer to explore the abdomen. In the scenario of tangential high energy GSWs, however, it is possible to sustain a transmitted intraperitoneal hollow visceral injury due to a blast insult. Gunshot wounds to the back or flank are more difficult to evaluate because of the retroperitoneal location of the injured abdominal organs. Triple-contrast CT scan can delineate the trajectory of the bullet and identify peritoneal violation or retroperitoneal entry, but may not identify the specific injuries. In contrast to gunshot wounds, stab wounds that penetrate the peritoneal cavity are less likely to injure intra-abdominal organs. Anterior abdominal stab wounds (from costal margin to inguinal ligament and bilateral midaxillary lines) should be explored under local anesthesia in the ED to determine if the fascia has been violated. Injuries that do not penetrate the peritoneal cavity do not require further evaluation, and the patient may be discharged from the ED. Patients with fascial penetration must be further evaluated for intra-abdominal injury, because there is up to a 50% chance of requiring laparotomy. Debate remains over whether the optimal diagnostic approach is serial examination, diagnostic peritoneal lavage (DPL), or CT scanning; the most recent evidence supports serial examination and laboratory evaluation.^42,43 Patients with stab wounds to the right upper quadrant can undergo CT scanning to determine trajectory and confinement to the liver for potential nonoperative care.⁴¹ Those with stab wounds to the flank and back should undergo triple-contrast CT to assess for the potential risk of retroperitoneal injuries of the colon, duodenum, and urinary tract.

Penetrating thoracoabdominal wounds may cause occult injury to the diaphragm. Patients with gunshot or stab wounds to the left lower chest should be evaluated with diagnostic laparoscopy or DPL to exclude diaphragmatic injury. For patients undergoing DPL evaluation, laboratory value cutoffs to rule out diaphragm injury are different from traditional values formerly used for abdominal stab wounds (see Table 7-6). An RBC count of >10,000/μL is considered a positive finding and an indication for abdominal evaluation; patients with a DPL RBC count between 1000/μL and 10,000/μL should undergo laparoscopy or thoracoscopy. Diagnostic laparoscopy may be preferred in patients with a positive chest radiograph (hemothorax or pneumothorax) or in those who would not tolerate a DPL.

Blunt abdominal trauma is evaluated initially by FAST examination in most major trauma centers, and this has largely supplanted DPL (Fig. 7-26). FAST is not 100% sensitive, however, so diagnostic peritoneal aspiration is warranted in hemodynamically unstable patients without a defined source of blood loss to rule out abdominal hemorrhage.²⁷ FAST is used to identify free intraperitoneal fluid (Fig. 7-27) in Morrison’s pouch, the left upper quadrant, and the pelvis. Although this method is exquisitely sensitive for detecting intraperitoneal fluid of >250 mL, it does not reliably determine the source of hemorrhage nor grade solid organ injuries.⁴⁴ Patients with fluid on FAST examination, considered a “positive FAST,” who do not have immediate indications for laparotomy and are hemodynamically stable undergo CT scanning to quantify their injuries. Injury grading using the American Association for the Surgery of Trauma grading scale (Table 7-7) is an important component of nonoperative management of solid organ injuries. Additional findings that should be noted on CT scan in patients with solid organ injury include contrast extravasation (i.e., a “blush”), the amount of intra-abdominal hemorrhage, and presence of pseudoaneurysms (Fig. 7-28). CT also is indicated for hemodynamically stable patients for whom the physical examination is unreliable. Despite the increasing diagnostic accuracy of multidetector CT scanners, identification of intestinal injuries remains a limitation. Bowel injury is suggested by findings of thickened bowel wall, “streaking” in the mesentery, free fluid without associated solid organ injury, or free intraperitoneal air.^45,46 Patients with free intra-abdominal fluid without solid organ injury are closely monitored for evolving signs of peritonitis; if patients have a significant closed head injury or cannot be serially examined, DPL should be performed to exclude bowel injury. If DPL is pursued, an infraumbilical approach is used (Fig. 7-29). After placement of the catheter, a 10-mL syringe is connected and the abdominal contents aspirated (termed a diagnostic peritoneal aspiration). The aspirate is considered to show positive findings if >10 mL of blood is aspirated. If <10 mL is withdrawn, a liter of normal saline is instilled. The effluent is withdrawn via siphoning and sent to the laboratory for RBC count, white blood cell (WBC) count, and determination of amylase, bilirubin, and alkaline phosphatase levels. Values representing positive findings are summarized in Table 7-6.

Pelvis

Blunt injury to the pelvis may produce complex fractures with major hemorrhage (Fig. 7-30). Plain radiographs will reveal gross abnormalities, but CT scanning is necessary to determine the precise geometry. Sharp spicules of bone can lacerate the bladder, rectum, or vagina. Alternatively, bladder rupture may result from a direct blow to the torso if the bladder is full. CT cystography is performed if the urinalysis findings are positive for RBCs. Urethral injuries are suspected if examination reveals blood at the meatus, scrotal or perineal hematomas, or a high-riding prostate on rectal examination. Urethrograms should be obtained for stable patients before placing a Foley catheter to avoid false passage and subsequent stricture. Major vascular injuries causing exsanguination are uncommon in blunt pelvic trauma; however, thrombosis of either the arteries or veins in the iliofemoral system may occur, and CT angiography should be performed for evaluation. Life-threatening hemorrhage can be associated with pelvic fractures and may initially preclude definitive imaging. Treatment algorithms for patients with complex pelvic fractures and hemodynamic instability are presented later in the chapter.

Extremities

Physical examination often identifies arterial injuries, and findings are classified as either hard signs or soft signs of vascular injury (Table 7-8). In general, hard signs constitute indications for operative exploration, whereas soft signs are indications for further testing or observation. Bony fractures or knee dislocations should be realigned before definitive vascular examination. On-table angiography may be useful to localize the arterial injury and thus, limit tissue dissection in patients with hard signs of vascular injury. For example, a patient with an absent popliteal pulse and femoral shaft fracture due to a bullet that entered the lateral hip and exited below the medial knee could have injured either the femoral or popliteal artery anywhere along its course (Fig. 7-31). In management of vascular trauma, controversy exists regarding the treatment of patients with soft signs of injury, particularly those with injuries in proximity to major vessels. It is known that some of these patients will have arterial injuries that require repair. The most common approach has been to measure SBP using Doppler ultrasonography and compare the value for the injured side with that for the uninjured side, termed the A-A index.⁴⁷ If the pressures are within 10% of each other, a significant injury is unlikely and no further evaluation is performed. If the difference is >10%, CT angiography or arteriography is indicated. Others argue that there are occult injuries, such as pseudoaneurysms or injuries of the profunda femoris or peroneal arteries, which may not be detected with this technique. If hemorrhage occurs from these injuries, compartment syndrome and limb loss may occur. Although busy trauma centers continue to debate this issue, the surgeon who is obliged to treat the occasional injured patient may be better served by performing CT angiography in selected patients with soft signs. Blunt or penetrating trauma to the extremities requires an evaluation for fractures, ligamentous injury, and neurovascular injury. Plain radiographs are used to evaluate fractures, whereas ligamentous injuries, particularly those of the knee and shoulder, can be imaged with magnetic resonance imaging.

Over the past 25 years there has been a remarkable change in management practices and operative approach for the injured patient. With the advent of CT scanning, nonoperative management of solid organ injuries has replaced routine operative exploration. Those patients who do require operation may be treated with less radical resection techniques, such as splenorrhaphy or partial nephrectomy. Colonic injuries, previously mandating colostomy, are now repaired primarily in virtually all cases. Additionally, the type of anastomosis has shifted from a double-layer closure to a continuous running single-layer closure; this method is technically equivalent to and faster than the interrupted multilayer techniques.⁴⁸ Adoption of damage control surgical techniques in physiologically deranged patients has resulted in limited initial operative time, with definitive injury repair delayed until after resuscitation in the surgical intensive care unit (SICU) with physiologic restoration.⁴⁹ Abdominal drains, once considered mandatory for parenchymal injuries and some anastomoses, have disappeared; fluid collections are managed by percutaneous techniques. Newer endovascular techniques such as stenting of arterial injuries and angioembolization are routine adjuncts. Blunt cerebrovascular injuries have been recognized as a significant, preventable source of neurologic morbidity and mortality. The use of preperitoneal pelvic packing for unstable pelvic fractures as well as early fracture immobilization with external fixators are paradigm shifts in management. Finally, the institution of massive transfusion protocols balances the benefit of blood component therapy against immunologic risk. Viscoelastic hemostatic assays (TEG and ROTEM) have been shown to be superior to traditional laboratory tests, and have been central to the evolving concept of goal-directed hemostasis.⁵⁰ These conceptual changes have significantly improved survival of critically injured patients; they have been promoted and critically reviewed by academic trauma centers via forums such as the American College of Surgeons Committee on Trauma, the American Association for the Surgery of Trauma, the International Association of Trauma Surgery and Intensive Care, the Pan-American Trauma Congress, and other surgical organizations.

Transfusion Practices

Injured patients with life-threatening hemorrhage develop an acute coagulopathy of trauma (ACOT). Cohen et al⁵¹ have shown convincingly that activated protein C is a key element, although the complete mechanism remains to be elucidated. Fibrinolysis is another important component of the ACOT; present in only 5% of injured patients requiring hospitalization, but 20% in those requiring massive transfusion.⁵² Fresh whole blood, arguably the optimal replacement, is not available in the United States. Rather, its component parts, packed red blood cells (PRBCs), fresh-frozen plasma, platelets, and cryoprecipitate, are administered. Specific transfusion triggers for individual blood components exist. Although current critical care guidelines indicate that PRBC transfusion should occur once the patient’s hemoglobin level is <7 g/dL,⁵³ in the acute phase of resuscitation a hemoglobin of 10 g/dL is suggested to facilitate hemostasis.⁵⁴ The traditional thresholds for blood component replacement in the patient manifesting a coagulopathy have been INR >1.5, PTT >1.5 normal, platelet count > 50,000/μL, and fibrinogen >100 mg/dl. However, these guidelines have been replaced by TEG and ROTEM criteria in many trauma centers. Such guidelines are designed to limit the transfusion of immunologically active blood components and decrease the risk of transfusion-associated lung injury and secondary multiple organ failure.^55,56

In the critically injured patient requiring large amounts of blood component therapy, a massive transfusion protocol should be followed (Fig. 7-32). This approach calls for administration of various components in a specific ratio during transfusion to achieve restoration of blood volume and correction of coagulopathy. Although the optimal ratio is yet to be determined, current scientific evidence indicates a presumptive 1:2 red cell:plasma ratio in patients at risk for massive transfusion (10 units of PRBCs in 6 hours).^57,58,59,60 Because complete typing and cross-matching takes up to 45 minutes, patients requiring emergent transfusions are given type O, type-specific, or biologically compatible RBCs. Blood typing, and to a lesser extent cross-matching, is essential to avoid life-threatening intravascular hemolytic transfusion reactions. Trauma centers and their associated blood banks must have the capability of transfusing tremendous quantities of blood components, because it is not unusual to have 100 component units transfused during one procedure and have the patient survive. Massive transfusion protocols, established preemptively, permit coordination of the activities of surgeons, anesthesiologists, and blood bank directors to facilitate transfusion at these rates should a crisis occur.

Postinjury coagulopathy is associated with core hypothermia and metabolic acidosis, termed the bloody vicious cycle.⁴⁹ The pathophysiology is multifactorial and includes inhibition of temperature-dependent enzyme-activated coagulation cascades, platelet dysfunction, endothelial abnormalities, and fibrinolytic activity. Such coagulopathy may be insidious, so the surgeon must be cognizant of subtle signs such as excessive bleeding from the cut edges of skin. Although the coagulopathic “ooze” may seem minimal compared with the torrential hemorrhage from a hole in the aorta, blood loss from the entire area of dissection can lead to exsanguination. Point-of-care TEG results, which provide a comprehensive assessment of clot capacity and fibrinolysis, can be available within 10 minutes. This concept has been termed . In contrast, traditional laboratory tests of coagulation capability (i.e., INR, PTT, fibrinogen levels, and platelet count) requires at least 30 minutes. Such a delay is particularly troublesome for patients who have lost two blood volumes while waiting for the test results to return. Using damage control techniques to limit operative time and provide physiologic restoration in the SICU can be lifesaving (see section Damage Control Surgery).

Prophylactic Measures

All injured patients undergoing an operation should receive preoperative antibiotics. The type of antibiotic is determined by the anticipated source of contamination in the abdomen or other operative region; additional doses should be administered during the procedure based on blood loss and the half-life of the antibiotic. Extended postoperative antibiotic therapy is administered only for contaminated open fractures. Tetanus prophylaxis is administered to all patients according to published guidelines.

Trauma patients are at risk for venous thromboembolism and its associated morbidity and mortality. In fact, pulmonary embolus can occur much earlier in the patient’s hospital course than previously believed.⁶¹ Patients at higher risk for venous thromboembolism are those with multiple fractures of the pelvis and lower extremities, coma or spinal cord injury, and requiring ligation of large veins in the abdomen and lower extremities. Morbidly obese patients and those over 55 years of age are at additional risk. Administration of low molecular weight heparin (LMWH) is initiated as soon as bleeding has been controlled and there is stable intracranial pathology. Higher doses of LMWH are required in injured patients to attain adequate anti-Xa levels, and antiplatelet therapy should probably be added. In high-risk patients, removable inferior vena caval filters should be considered if there are prolonged contraindications to administration of LMWH. Additionally, pulsatile compression stockings (also termed sequential compression devices) are used routinely unless there is a fracture.

A final prophylactic measure that is usually not considered is thermal protection. Hemorrhagic shock impairs perfusion and metabolic activity throughout the body, with resultant decrease in heat production and body temperature. Removing the patient’s clothes causes a second thermal insult, and infusion of cold PRBCs or room temperature crystalloid exacerbates the problem. As a result, injured patients can become hypothermic, with temperatures below 34°C (93.2°F) upon arrival in the OR. Hypothermia aggravates coagulopathy and provokes myocardial irritability. Therefore, prevention must begin in the ED by maintaining a comfortable ambient temperature, covering patients with warm blankets, and administering warmed IV fluids and blood products. Additionally, in the OR a Bair Hugger^¯ warmer (the upper body or lower body blanket) and heated inhalation via the ventilatory circuit is instituted. For cases of severe hypothermia (temperature <30°C [86°F]), arteriovenous rewarming should be considered.

Operative Approaches and Exposure

Cervical Exposure

Operative exposure for midline structures of the neck (e.g.,trachea, thyroid, bilateral carotid sheaths) is obtained through a collar incision; this is typically performed two finger breadths above the sternal notch, but can be varied based on the level of anticipated injury. After subplatysmal flap elevation, the strap muscles are divided in the midline to gain access to the central neck compartment. More superior and lateral structures are accessed by extending the collar incision upward along the sternocleidomastoid muscle; this may be done bilaterally if necessary. Unilateral neck exploration is done through an incision extending from the mastoid down to the clavicle, along the anterior border of the sternocleidomastoid muscle (Fig. 7-33). The carotid sheath, containing the carotid artery, jugular vein, and vagus nerve, is opened widely to examine these structures. The facial vein, which marks the carotid bifurcation, is usually ligated for exposure of the internal carotid artery.

Exposure of the distal carotid artery in zone III is difficult (see Fig. 7-33). The first step is division of the ansa cervicalis to facilitate mobilization of the hypoglossal nerve. Next, the posterior portion of the digastric muscle, which overlies the internal carotid, is transected. The glossopharyngeal and vagus nerves are also mobilized and retracted as necessary. If accessible, the styloid process and attached muscles are removed. At this point anterior displacement of the mandible (subluxation) may be helpful. In desperate situations, the vertical ramus of the mandible may be divided. However, this maneuver often entails resection of the parotid gland and the facial nerve is at risk for exposure of the distal internal carotid.

Thoracic Incisions

An anterolateral thoracotomy, with the patient placed supine, is the most versatile incision for emergent thoracic exploration. The location of the incision is in the fifth interspace, in the inframammary line (Fig. 7-34). If access is needed to both pleural cavities, the original incision can be extended across the sternum with a Lebsche knife, into a “clamshell” thoracotomy (Fig. 7-35). If the sternum is divided, the internal mammary arteries should be ligated to prevent blood loss. The heart, lungs, descending aorta, pulmonary hilum, and esophagus are accessible with this approach. For control of the great vessels, the superior portion of the sternum may be divided with extension of the incision into the neck considered. A method advocated for access to the proximal left subclavian artery is through a fourth interspace anterolateral thoracotomy, superior sternal extension, and left supraclavicular incision (“trap door” thoracotomy). Although the trap door procedure is appropriate after resuscitative thoracotomy, the proximal left subclavian artery can be accessed more easily via a sternotomy with a supraclavicular extension. If the left subclavian artery is injured outside the thoracic outlet, vascular control can be obtained via the sternotomy and definitive repair done through the supraclavicular incision. Emergent median sternotomy is limited to anterior stab wounds to the heart. Typically, these patients have pericardial tamponade and undergo placement of a pericardial drain before a semiurgent median sternotomy is performed. Patients in extremis, however, should undergo anterolateral thoracotomy.

Median sternotomy with cervical extension is used for rapid exposure in patients with presumed proximal subclavian, innominate, or proximal carotid artery injuries. Care must be taken to avoid injury to the phrenic and vagus nerves that pass over the subclavian artery and to the recurrent laryngeal nerve passing posteriorly. Posterolateral thoracotomies are used for exposure of injuries to the trachea or main stem bronchi near the carina (right posterolateral thoracotomy), tears of the descending thoracic aorta (left posterolateral thoracotomy with left heart bypass), and intrathoracic esophageal injuries.

Emergent Abdominal Exploration

Abdominal exploration in adults is performed using a generous midline incision because of its versatility. For children under the age of 6, a transverse incision may be advantageous. Making the incision is faster with a scalpel than with an electrosurgical unit; incisional abdominal wall bleeding should be ignored until intra-abdominal sources of hemorrhage are controlled. Liquid and clotted blood are evacuated with multiple laparotomy pads to identify the major source(s) of active bleeding. After blunt trauma the spleen and liver should be palpated first and packed if fractured, and the infracolic mesentery inspected to exclude a zone I vascular injury. In contrast, after a penetrating wound the search for bleeding should pursue the trajectory of the penetrating device. If the patient has an SBP of <70 mmHg when the abdomen is opened, digital pressure or a clamp should be placed on the aorta at the diaphragmatic hiatus. After the source of hemorrhage is localized, direct digital occlusion (vascular injury) or laparotomy pad packing (solid organ injury) is used to control bleeding (Fig. 7-36). If the liver is the source in a hemodynamically unstable patient, additional control of bleeding is obtained by clamping the hepatic pedicle with a vascular clamp or Rummel tourniquet (Pringle maneuver) (Fig. 7-37). Similarly, clamping the splenic hilum may more effectively control bleeding than packing alone. When the spleen is mobilized, it should be gently rotated medially to expose the lateral peritoneum; this peritoneum and endoabdominal fascia are incised, which allows blunt dissection of the spleen and pancreas as a composite from the retroperitoneum anterior to Gerota’s fascia (Fig. 7-38).

Rapid exposure of the intra-abdominal vasculature can prove challenging in the face of exsanguinating hemorrhage. Proximal control of the aorta is obtained at the diaphragmatic hiatus; if an aortic injury is supraceliac, transecting the left crus of diaphragm or extending the laparotomy via a left thoracotomy may be necessary. The first decision is whether the patient has a supracolic or an infracolic vascular injury. Supracolic injuries (aorta, celiac axis, proximal superior mesenteric artery [SMA], and left renal arteries) are best approached a left medial visceral rotation (Fig. 7-39). This is done by incising the lateral peritoneal reflection (white line of Toldt) beginning at the distal descending colon and extending the incision along the colonic splenic flexure, around the posterior aspect of the spleen, and behind the gastric fundus, ending at the esophagus. The left colon, spleen, pancreas, and stomach are then rotated toward the midline. The authors prefer to leave the kidney in situ when mobilizing the viscera because this exaggerates the separation of the renal vessels from the SMA. The operative approach for SMA injuries is based on the level of injury. Fullen zone I SMA injuries, located posterior to the pancreas, are best exposed by a left medial visceral rotation. Fullen zone II SMA injuries, extending from the pancreatic edge to the middle colic branch, on the other hand, are approached via the lesser sac along the inferior edge of the pancreas at the base of the transverse mesocolon; the pancreatic body may be divided to gain proximal vascular access. More distal SMA injuries, Fullen zones III and IV, are approached directly within the mesentery. A venous injury behind the pancreas, from the junction of the superior mesenteric, splenic, and portal veins, is accessed by dividing the neck of the pancreas. Inferior vena cava injuries are approached by a right medial visceral rotation (Fig. 7-40). Proximal control is obtained just above the iliac bifurcation with direct pressure via a sponge stick; the injury is identified by cephalad dissection along the anterior surface of the inferior vena cava. A Satinsky clamp can be used to control anterior caval wounds.

Injuries of the iliac vessels pose a unique problem for emergent vascular control due to the number of vessels, their close proximity, and cross circulation. Proximal control at the infrarenal aorta arrests the arterial bleeding and avoids splanchnic and renal ischemia; however, venous injuries are not controlled with aortic clamping. Tamponade with a folded laparotomy pad held directly over the bleeding site usually will establish hemostasis sufficient to prevent exsanguination. If hemostasis is not adequate to expose the vessel proximal and distal to the injury, sponge sticks can be strategically placed on either side of the injury and carefully adjusted to improve hemostasis. Alternatively, complete pelvic vascular isolation (Fig. 7-41) may be required to control hemorrhage for adequate visualization of the injuries. The right common iliac artery obscures the bifurcation of the vena cava and the right iliac vein; the iliac artery may require division to expose venous injuries in this area (Fig. 7-42). The artery must be repaired after the venous injury is treated, however, because of limb-threatening ischemia.

Once overt hemorrhage is controlled, sources of enteric contamination are identified by serially running along the small and large bowel, looking at all surfaces. Associated hematomas should be unroofed to rule out adjacent bowel injury. The anterior and posterior aspects of the stomach should be inspected, which requires opening the lesser sac for complete visualization. Duodenal injuries should be evaluated with a wide Kocher maneuver. During exploration of the lesser sac, visualization and palpation of the pancreas is done to exclude injury. Palpating the anterior surface is not sufficient, because the investing fascia may mask a pancreatic injury; mobilization, including evaluation of the posterior aspect, is critical. After injuries are identified, whether to use damage control techniques or perform primary repair of injuries is based on the patient’s intraoperative physiologic status (see sections, Damage Control Surgery and Treatment of Specific Injuries). In a patient with multisystem trauma, enteral access via gastrostomy tube or needle-catheter jejunostomy should be considered. If abdominal closure is indicated after the patient’s injuries are addressed, the abdomen is irrigated with warm saline and the midline fascia is closed with a running heavy suture. The skin is closed selectively based on the amount of intra-abdominal contamination.

Vascular Repair Techniques

Initial control of vascular injuries is accomplished digitally by applying enough direct pressure to stop the hemorrhage. Sharp dissection with fine scissors is used to define the injury and mobilize sufficient length for proximal and distal control. Fogarty thromboembolectomy should be done proximally and distally to optimize collateral blood flow. Heparinized saline (50 units/mL) is then injected into the proximal and distal ends of the injured vessel to prevent small clot formation on the exposed intima and media. Ragged edges of the injury site should be débrided using sharp dissection. Intravascular shunts are used when there are multiple life-threatening injuries or the arterial injury is anticipated to require saphenous vein interposition reconstruction.

Options for the treatment of vascular injuries are listed in Table 7-9. Arterial repair should always be done for the aorta, carotid, innominate, brachial, superior mesenteric, proper hepatic, renal, iliac, femoral, and popliteal arteries. Named arteries that usually tolerate ligation include the right or left hepatic artery and the celiac artery. In the lower extremities, at least one artery with distal runoff should be salvaged. Arterial injuries that may be treated nonoperatively include small pseudoaneurysms, intimal dissections, small intimal flaps, and small arteriovenous fistulas in the extremities. Follow-up imaging is performed 1 to 2 weeks after injury to confirm healing. Venous repair should be performed for injuries of the superior vena cava, the inferior vena cava proximal to the renal veins, and the portal vein, although the portal vein may be ligated in extreme cases. The SMV should be repaired optimally, but >80% of patients will survive following ligation. Similarly the left renal vein can usually be ligated adjacent to the IVC due to collateral decompression.

The type of operative repair for a vascular injury is based on the extent and location of injury. Lateral suture repair is preferred for arterial injuries with minimal loss of tissue. End-to-end primary anastomosis is performed if the vessel can be repaired without tension. Arterial defects of 1 to 2 cm often can be bridged by mobilizing the severed ends of the vessel after ligating small branches. The surgeon should not be reluctant to divide small branches to obtain additional length, because most injured patients have normal vasculature, and the preservation of potential collateral flow is not as important as in revascularization for atherosclerosis. The aorta, subclavian artery, and brachial artery, however, are difficult to mobilize for additional length. To avoid postoperative stenosis, particularly in smaller arteries, beveling or spatulation should be used so that the completed anastomosis is slightly larger in diameter than the native artery (Fig. 7-43). The authors emphasize the parachute technique to ensure precision placement of the posterior suture line (Fig. 7-44). If this technique is used, traction must be maintained on both ends of the suture, or leakage from the posterior aspect of the suture line may occur. A single temporary suture 180 degrees from the posterior row may be used to maintain alignment for challenging anastomoses.

Interposition grafts are used when end-to-end anastomosis cannot be accomplished without tension despite mobilization. For vessels <6 mm in diameter (e.g., internal carotid, brachial, superficial femoral, and popliteal arteries), autogenous saphenous vein from the contralateral groin should be used, because polytetrafluoroethylene (PTFE) grafts of <6 mm have a prohibitive rate of thrombosis. Larger arteries (e.g., subclavian, innominate, aorta, common iliac) are bridged by PTFE grafts. PTFE is preferred over Dacron because of the reported decreased risk of infection.⁶² Aortic or iliac arterial injuries may be complicated by enteric contamination from colon or small bowel injuries. There is a natural reluctance to place artificial grafts in such circumstances, but graft infections are rare and the time required to perform an axillofemoral bypass is excessive.⁶³ Therefore, after the control of hemorrhage, bowel contamination is contained and the abdomen irrigated before placing PTFE grafts.⁶⁴ After placement of the graft, it is covered with peritoneum or omentum before definitive treatment of the enteric injuries.

Transposition procedures can be used when an artery has a bifurcation and one vessel can be ligated safely. Injuries of the proximal internal carotid can be treated by mobilizing the adjacent external carotid, dividing it distal to the internal injury, and performing an end-to-end anastomosis between it and the distal internal carotid (Fig. 7-45). The proximal stump of the internal carotid is oversewn, with care taken to avoid a blind pocket where a clot may form. Injuries of the common and external iliac arteries can be handled in a similar fashion (Fig. 7-46), while maintaining flow in at least one internal iliac artery.

Venous injuries are inherently more difficult to reconstruct due to their propensity to thrombose. Small injuries without loss of tissue can be treated with lateral suture repair. More complex repairs with interposition grafts may thrombose but this typically occurs gradually over 1 to 2 weeks. During this time adequate collateral circulation develops, which is sufficient to avoid acute venous hypertension. Therefore, it is reasonable to use ringed PTFE for venous interposition grafting and accept a gradual, but eventual, thrombosis while allowing time for collateral circulation to develop. Such an approach is reasonable for venous injuries of the superior vena cava, suprarenal vena cava, SMV, and popliteal vein because ligation of these is associated with significant morbidity. In the remainder of venous injuries the vein may be ligated. In such patients, chronic venous hypertensive complications in the lower extremities often can be avoided by (a) temporary use of elastic bandages (Ace wraps) applied from the toes to the hips at the end of the procedure, and (b) temporary continuous elevation of the lower extremities to 30 to 45 degrees. These measures should be maintained for 1 week; if the patient has no peripheral edema with ambulation, these maneuvers are no longer required.

Damage Control Surgery

The recognition of the bloody vicious cycle and the introduction of damage control surgery (DCS) have improved the survival of critically injured patients. Conceptually, the bloody vicious cycle, first described in 1981, is the lethal combination of coagulopathy, hypothermia, and metabolic acidosis (Fig. 7-47).⁴⁹ Hypothermia from evaporative and conductive heat loss and diminished heat production occurs despite the use of warming blankets and blood warmers. The metabolic acidosis of shock is exacerbated by aortic clamping, administration of vasopressors, massive RBC transfusions, and impaired myocardial performance. The acute coagulopathy of trauma, described previously, is compounded by hemodilution, hypothermia, and acidosis. Once the cycle starts, each component magnifies the other, which leads to a downward spiral and ultimately a fatal arrhythmia. The purpose of DCS is to limit operative time so that the patient can be returned to the SICU for physiologic restoration and the cycle thereby broken. Indications to limit the initial operation and institute DCS techniques include a combination of refractory hypothermia (temperature <35°C), profound acidosis, (arterial pH <7.2, base deficit <15 mmol/L), and refractory coagulopathy.^49,65 The decision to abbreviate a trauma laparotomy is made intraoperatively as the patient’s clinical course becomes clearer and laboratory values become available.⁶⁶

The goal of DCS is to control surgical bleeding and limit GI spillage. The operative techniques used are temporary measures, with definitive repair of injuries delayed until the patient is physiologically replete. Controlling surgical bleeding while preventing ischemia is of utmost importance during DCS. Aortic injuries must be repaired using an interposition PTFE graft. Although celiac artery injuries may be ligated, the SMA must maintain flow, and the early insertion of an intravascular shunt is advocated. Similarly, perfusion of the iliac system and infrainguinal vessels can be restored with a vascular shunt, with interposition graft placement delayed until hours later. Venous injuries are preferentially treated with ligation in damage control situations, except for the suprarenal inferior vena cava and popliteal vein. For extensive solid organ injuries to the spleen or one kidney, excision is indicated rather than an attempt at operative repair. For hepatic injuries, perihepatic packing of the liver will usually tamponade bleeding (see Fig. 7-36). Translobar gunshot wounds of the liver are best controlled with balloon catheter tamponade, whereas deep lacerations can be controlled with Foley catheter inflation deep within the injury track (Fig. 7-48). For thoracic injuries requiring DCS several options exist. For bleeding peripheral pulmonary injuries, wedge resection using a stapler is performed. In penetrating injuries, pulmonary tractotomy is used to divide the parenchyma (Fig. 7-49); individual vessels and bronchi are then ligated using a 3-0 polydioxanone suture (PDS) and the track left open. Patients who sustain more proximal injuries may require formal pulmonary resection but pneumonectomy is poorly tolerated. Cardiac injuries may be temporarily controlled using a running 3-0 nonabsorbable polypropylene suture or skin staples. Pledgeted repair should be performed for the relatively thin right ventricle.

The second key component of DCS is limiting enteric content spillage. Small GI injuries (stomach, duodenum, small intestine, and colon) may be controlled using a rapid whipstitch of 2-0 polypropylene. Complete transection of the bowel or segmental damage is controlled using a GIA stapler, often with resection of the injured segment. Alternatively, open ends of the bowel may be ligated using umbilical tapes to limit spillage. Pancreatic injuries, regardless of location, are packed and the evaluation of ductal integrity postponed. Urologic injuries may require catheter diversion. Before the patient is returned to the SICU, the abdomen must be temporarily closed. Originally, penetrating towel clips were used to approximate the skin; however, the ensuing bowel edema often produces a delayed abdominal compartment syndrome. Currently, temporary closure of the abdomen is accomplished using an antimicrobial surgical incise drape (Ioban, 3M Health Care, St Paul, MN) (Fig. 7-50). In this technique, the bowel is covered with a fenestrated subfascial sterile drape (45 × 60 cm Steri-Drape 3M Health Care), and two Jackson-Pratt drains are placed along the fascial edges; this is then covered using an Ioban drape, which allows closed suction to control reperfusion-related ascitic fluid egress while providing adequate space for bowel expansion to prevent abdominal compartment syndrome. During the initial DCS stage, the subfascial sterile drape is not covered by a blue towel so that the status of the bowel and hemorrhage control can be assessed. Return to the OR within 24 hours is planned once the patient clinically improves, as evidenced by normothermia, normalization of coagulation test results, and correction of acidosis.

Head Injuries

Intracranial Injuries

CT scanning, performed on all patients with a significant closed head injury (GCS score <14), identifies and quantitates intracranial lesions. Patients with intracranial hemorrhage, including epidural hematoma, subdural hematoma, subarachnoid hemorrhage, intracerebral hematoma or contusion, and diffuse axonal injury, are admitted to the SICU. In patients with abnormal findings on CT scans and GCS scores of ≤8, intracranial pressure (ICP) should be monitored using fiber-optic intraparenchymal devices or intraventricular catheters.²⁹ Although an ICP of 10 mm Hg is believed to be the upper limit of normal, therapy generally is not initiated until ICP is >20 mm Hg.²⁹ Indications for operative intervention to remove space-occupying hematomas are based on the clot volume, amount of midline shift, location of the clot, GCS score, and ICP.²⁹ A shift of >5 mm typically is considered an indication for evacuation, but this is not an absolute rule. Smaller hematomas that are in treacherous locations, such as the posterior fossa, may require drainage due to brain stem compression or impending herniation. Removal of small hematomas may also improve ICP and cerebral perfusion in patients with elevated ICP that is refractory to medical therapy. Patients with diffuse cerebral edema resulting in excessive ICP may require a decompressive craniectomy, although a recent AAST multicenter trial questions the benefits.^67,68 Patients with open or depressed skull fractures, with or without sinus involvement, may require operative intervention. Penetrating injuries to the head require operative intervention for hemorrhage control, evacuation of blood, skull fracture fixation, or débridement.

General surgeons in communities without emergency neurosurgical coverage should have a working knowledge of burr hole placement in the event that emergent evacuation is required for a life-threatening epidural hematoma (Fig. 7-51).⁶⁹ The typical clinical course of an epidural hematoma is an initial loss of consciousness, a lucid interval, and recurrent loss of consciousness with an ipsilateral fixed and dilated pupil. While decompression of subdural hematomas may be delayed, epidural hematomas require evacuation within 70 minutes.⁶⁸ The final stages of this sequence are caused by blood accumulation that forces the temporal lobe medially, with resultant compression of the third cranial nerve and eventually the brain stem. The burr hole is made on the side of the dilated pupil to decompress the intracranial space. After stabilization, the patient is transferred to a facility with neurosurgical capability for formal craniotomy.

In addition to operative intervention, postinjury care directed at limiting secondary injury to the brain is critical. The goal of resuscitation and management in patients with head injuries is to avoid hypotension (SBP of <100 mm Hg) and hypoxia (partial pressure of arterial oxygen of <60 or arterial oxygen saturation of <90).²⁹ Attention, therefore, is focused on maintaining cerebral perfusion rather than merely lowering ICP. Resuscitation efforts aim for a euvolemic state and an SBP of >100 mm Hg. Cerebral perfusion pressure (CPP) is equal to the mean arterial pressure minus the ICP, with a target range of >50 mm Hg.²⁹ CPP can be increased by either lowering ICP or raising mean arterial pressure. Sedation, osmotic diuresis, paralysis, ventricular drainage, and barbiturate coma are used in sequence, with coma induction being the last resort. The partial pressure of carbon dioxide (Pco₂) should be maintained in a normal range (35–40 mm Hg), but for temporary management of acute intracranial hypertension, inducing cerebral vasoconstriction by hyperventilation to a Pco₂ of <30 mm Hg is occasionally warranted. Moderate hypothermia (32°–33°C [89.6°–91.4°F]) has been proposed to improve neurologic outcomes when maintained for at least 48 hours, but studies to date have not validated this concept.^29,70,71 Patients with intracranial hemorrhage should be monitored for postinjury seizures, and prophylactic anticonvulsant therapy (e.g., phenytoin [dilantin]) is indicated for 7 days after injury. ^29,72

Maxillofacial Injuries

Maxillofacial injuries are common with multisystem trauma and require coordinated management by the trauma surgeon and the specialists in otolaryngology, plastic surgery, ophthalmology, and oral and maxillofacial surgery. Delay in addressing these systems that control vision, hearing, smelling, breathing, eating, and phonation may produce dysfunction and disfigurement with serious psychological impact. The maxillofacial complex is divided into three regions; the upper face containing the frontal sinus and brain, the midface containing the orbits, nose, and zygomaticomaxillary complex, and the lower face containing the mandible. High-impact kinetic energy is required to fracture the frontal sinus, orbital rims, and mandible, whereas low-impact forces will injure the nasal bones and zygoma.

The most common scenario, which at times may be life-threatening, is bleeding from facial fractures.⁷³ Temporizing measures include nasal packing, Foley catheter tamponade of posterior nasal bleeding, and oropharyngeal packing. Prompt angioembolization will halt exsanguinating hemorrhage. Fractures of tooth-bearing bone are considered open fractures and require antibiotic therapy and semiurgent repair to preserve the airway as well as the functional integrity of the occlusion (bite) and the aesthetics of the face. Orbital fractures may compromise vision, produce muscle injury causing diplopia, or change orbital volume to produce a sunken appearance to the orbit. Nose and nasoethmoidal fractures should be assessed carefully to identify damage to the lacrimal drainage system or to the cribriform plate producing cerebrospinal fluid rhinorrhea. After initial stabilization, a systematic physical examination of the head and neck should be performed that also includes cranial nerve examination and three-dimensional CT scanning of the maxillofacial complex (Fig. 7-52).

Cervical Injuries

Spine

Treatment of injuries to the cervical spine is based on the level of injury, the stability of the spine, the presence of subluxation, the extent of angulation, the level of neurologic deficit, and the overall condition of the patient. In general, physician-supervised axial traction, via cervical tongs or the more commonly used halo vest, is used to reduce subluxations and stabilize the injury. Immobilization of injuries also is achieved with spinal orthoses (braces), particularly in those with associated thoracolumbar injuries. Surgical fusion typically is performed in patients with neurologic deficit, those with angulation of >11 degrees or translation of >3.5 mm, and those who remain unstable after halo placement. Indications for immediate operative intervention are deterioration in neurologic function and fractures or dislocations with incomplete deficit. Historically, methylprednisolone was administered to patients with acute spinal cord injury after blunt injury, with clinical data suggesting a small benefit to initiating a 24-hour infusion if started within 3 hours and a 48-hour infusion if started 3 to 8 hours.⁷⁴ Current guidelines, however, no longer recommend steroids for acute injuries.⁷⁵ The role and timing of operative surgical decompression after acute spinal cord injury is debated. However, evidence supports urgent decompression of bilateral locked facets in patients with incomplete tetraplegia or with neurologic deterioration. Urgent decompression in acute cervical spinal cord injury is safe. Performing surgery within 24 hours may decrease length of stay and complications.⁷⁶ Complete injuries of the spinal cord remain essentially untreatable. Yet, approximately 3% of patients who present with flaccid quadriplegia have concussive injuries, and these patients represent the very few who seem to have miraculous recoveries.

Vascular

Cervical vascular injuries due to either blunt or penetrating trauma can result in devastating neurologic sequelae or exsanguination. Penetrating injuries to the carotid artery and internal jugular vein usually are obvious on operative neck exploration. The principles of vascular repair techniques (discussed previously) apply to carotid injuries, and options for repair include end-to-end primary repair (often possible with mobilization of the common carotid), graft interposition, and transposition procedures. All carotid injuries should be repaired except in patients who present in coma with a delay in transport. Prompt revascularization of the internal carotid artery, using a temporary Pruitt-Inahara shunt, should be considered in patients arriving in profound shock. Otherwise, carotid shunting should be done selectively as in elective carotid endarterectomy but the patient should be systemically anticoagulated. Currently, we administer heparin with an ACT target of 250 sec. Tangential wounds of the internal jugular vein should be repaired by lateral venorrhaphy, but extensive wounds are efficiently addressed by ligation. However, it is not advisable to ligate both jugular veins due to potential intracranial hypertension. Vertebral artery injuries due to penetrating trauma are difficult to control operatively because of the artery’s protected location within the foramen transversarium. Although exposure from an anterior approach can be accomplished by removing the anterior elements of the bony canal and the tough fascia covering the artery between the elements, typically the most efficacious control of such injuries is angioembolization. Fogarty catheter balloon occlusion, however, is useful for controlling acute bleeding if encountered during neck exploration.

Blunt injury to the carotid or vertebral arteries may cause dissection, thrombosis, or pseudoaneurysm, typically in the surgically inaccessible distal internal carotid (Fig. 7-53).⁷⁷ Early recognition and management of these injuries is paramount, because patients treated with antithrombotics have a stroke rate of <1% compared with stroke rates of 20% in untreated patients. Because treatment must be instituted during the latent period between injury and onset of neurologic sequelae, diagnostic imaging is performed based on identified risk factors (Fig. 7-54).⁷⁸ After identification of an injury, antithrombotics are administered if the patient does not have contraindications (intracranial hemorrhage, falling hemoglobin level with solid organ injury or pelvic fracture). Heparin, started without a loading dose at 15 units/kg per hour, is titrated to achieve a PTT between 40 and 50 seconds or antiplatelet agents are initiated (aspirin 325 mg/d or clopidogrel 75 mg/d). The types of antithrombotic treatment appear equivalent in published studies to date, and the duration of treatment is empirically recommended to be 6 months.^79,80 The role of carotid stenting for grade III internal carotid artery injuries remain controversial. Thrombosis of the internal jugular veins caused by blunt trauma can occur unilaterally or bilaterally and is often discovered incidentally, because most patients are asymptomatic. Bilateral thrombosis can aggravate cerebral edema in patients with serious head injuries; stent placement should be considered in such patients if ICP remains elevated.

Aerodigestive

Subclinical fractures of the larynx and trachea may manifest as cervical emphysema. Fractures documented by CT scan are usually repaired. Common injuries include thyroid cartilage fractures, rupture of the thyroepiglottic ligament, disruption of the arytenoids or vocal cord tears, and cricoid fractures. After débridement of devitalized tissue, tracheal injuries are repaired end-to-end using a single layer of interrupted absorbable sutures. Associated injuries of the esophagus are common in penetrating injuries due to its close proximity. After débridement and repair, vascularized tissue is interposed between the repaired esophagus and trachea, and a closed suction drain is placed. The sternocleidomastoid muscle or strap muscles are useful for interposition and help prevent postoperative fistulas.

Chest Injuries

The most common injuries from both blunt and penetrating thoracic trauma are hemothorax and pneumothorax. More than 85% of patients can be definitively treated with a chest tube. The indications for thoracotomy include significant initial or ongoing hemorrhage from the tube thoracostomy and specific imaging-identified diagnoses (Table 7-10). One caveat concerns the patient who presents after a delay. Even when the initial chest tube output is 1.5 L, if the output ceases and the lung is re-expanded, the patient may be managed nonoperatively if hemodynamically stable.

Great Vessels

Over 90% of thoracic great vessel injuries are due to penetrating trauma, although blunt injury to the innominate, subclavian, or descending aorta may cause a pseudoaneurysm or frank rupture.^40,81,82 Simple lacerations of the ascending or transverse aortic arch can be repaired with lateral aortorrhaphy. Repair of posterior injuries, or those requiring interposition grafting of the arch, require full cardiopulmonary bypass, and repair of complex injuries may require circulatory arrest. Innominate artery injuries are repaired using the bypass exclusion technique,⁸² which avoids the need for cardiopulmonary bypass. Bypass grafting from the proximal aorta to the distal innominate with a prosthetic tube graft is performed before the postinjury hematoma is entered. The PTFE graft is anastomosed end to side from the proximal undamaged aorta and anastomosed end-to-end to the innominate artery (Fig. 7-55). The origin of the innominate is then oversewn at its base to exclude the pseudoaneurysm or other injury. Subclavian artery injuries can be repaired using lateral arteriorrhaphy or PTFE graft interposition; due to its multiple branches and tethering of the artery, end-to-end anastomosis is not advocated if there is a significant segmental loss.

Descending thoracic aortic injuries may require urgent if not emergent intervention. However, operative intervention for intracranial or intra-abdominal hemorrhage or unstable pelvic fractures takes precedence. To prevent aortic rupture, pharmacologic therapy with a selective β1 antagonist, esmolol, should be instituted in the trauma bay, with a target SBP of <100 mm Hg and heart rate of <100/min.^36,83 Endovascular stenting is now the mainstay of treatment, but open operative reconstruction is warranted, or necessary, in select patients.^84,85 Endovascular techniques are particularly appropriate in patients who cannot tolerate single lung ventilation, patients >60- years-old who are at risk for cardiac decompensation with aortic clamping, or patients with uncontrolled intracranial hypertension. While endograft sizing has improved, the major question is long-term outcome in younger patients. Open repair of the descending aorta is accomplished using partial left heart bypass.⁸⁶ With the patient in a right lateral decubitus position, the patient’s hips and legs are rotated 45 degrees toward the supine position to gain access to the left groin for common femoral artery cannulation. Using a left posterolateral thoracotomy, the fourth rib is transected to expose the aortic arch and left pulmonary hilum. Partial left heart bypass is performed by cannulating the superior pulmonary vein with return through the left common femoral artery (Fig. 7-56). A centrifugal pump is used to provide flow rates of 2.5 to 4 L/min to maintain a distal perfusion pressure of >65 mm Hg. This prevents ischemic injury of the spinal cord as well as the splanchnic bed, and reduces left ventricular afterload.³⁶ Heparinization is not required, a significant benefit in patients with multiple injuries, particularly in those with intracranial hemorrhage. Unless contraindicated, however, low-dose heparin (100 units/kg) typically is administered to a target ACT of 250 sec to prevent thromboembolic events. Once bypass is initiated, vascular clamps are applied on the aorta between the left common carotid and left subclavian arteries, on the left subclavian, and on the aorta distal to the injury. In most patients a short PTFE graft (usually 18 mm in diameter) is placed using a running 3-0 polypropylene suture. However, primary arterial repair should be done when possible. Air and thrombus are flushed from the aortic graft before the final suture is tied, and the occluding vascular clamps are removed. The patient is then weaned from the centrifugal pump, the cannulas are removed, and primary repair of the cannulated vessels is performed. Removal of air or potential clot in the pulmonary vein is important during decannulation to avoid left heart emboli to the systemic circulation.

Heart

Blunt and penetrating cardiac injuries have widely differing presentations and therefore disparate treatments. Survivable penetrating cardiac injuries consist of wounds that can be repaired operatively; most are stab wounds. Before repair of the injury is attempted, hemorrhage should be controlled; injuries to the atria can be clamped with a Satinsky vascular clamp, whereas digital pressure is used to occlude the majority of ventricular wounds. Foley catheter occlusion of larger stellate lesions may be effective, but even minimal traction may enlarge the original injury. Temporary control of hemorrhage, and at times definitive repair, may be accomplished with skin staples for left ventricular lacerations; the myocardial edges of the laceration must coapt in diastole for stapling to be technically feasible. Definitive repair of cardiac injuries is performed with either running 3-0 polypropylene suture or interrupted, pledgeted 2-0 polypropylene suture (Fig. 7-57).⁸⁷ Use of pledgets may be particularly important in the right ventricle to prevent sutures from pulling through the thinner myocardium. Injuries adjacent to coronary arteries should be repaired using horizontal mattress sutures, because use of running sutures results in coronary occlusion and distal infarction. Gunshot wounds may result in stellate lesions or contused, extremely friable myocardium adjacent to the wound. When the edges of such complex wounds cannot be fully approximated and hence the repair is not hemostatic, the authors have used surgical adhesive (BioGlue) to achieve hemostasis.⁸⁸ Occasionally, interior structures of the heart may be damaged. Intraoperative auscultation or postoperative hemodynamic assessment usually identifies such injuries.⁸⁹ Echocardiography (ECHO) can diagnose the injury and quantitate its effect on cardiac output. Immediate repair of valvular damage or septal defects rarely is necessary and would require cardiopulmonary bypass, but structural intracardiac lesions may progress and, thus, patients must have a follow-up ECHO.

Patients with blunt cardiac injury typically present with persistent tachycardia or conduction disturbances, but occasionally present with tamponade due to atrial or right ventricular rupture. There are no pathognomonic ECG findings, and cardiac enzyme levels do not correlate with the risk of cardiac complications.²³ Therefore, patients for whom there is high clinical suspicion of cardiac contusion and who are hemodynamically stable should be monitored for dysrhythmias for 24 hours by telemetry. Patients with hemodynamic instability should undergo ECHO to evaluate for wall motion abnormalities, pericardial fluid, valvular dysfunction, chordae rupture, or diminished ejection fraction. If such findings are noted or if vasoactive agents are required, cardiac function can be continuously monitored using a pulmonary artery catheter and serial SICU transthoracic or transesophageal ECHO.

Trachea, Bronchi, and Lung Parenchyma

Less than 1% of all injured patients sustain intrathoracic tracheobronchial injuries, and only a small number require operative intervention. Although penetrating injuries may occur throughout the tracheobronchial system, blunt injuries most commonly occur within 2.5 cm of the carina. For patients with a massive air leak requiring emergent exploration, initial control of the injury to provide effective ventilation is obtained by passing an endotracheal tube either beyond the injury or into the contralateral mainstem bronchus. Principles of repair are similar to those for repair of cervical tracheal injuries. Devitalized tissue is débrided, and primary end-to-end anastomosis with 3-0 PDS suture is performed. Dissection should be limited to the area of injury to prevent disruption of surrounding bronchial vasculature and ensuing ischemia and stricture. Suture lines should be encircled with vascularized tissue, either pericardium, intercostal muscle, or pleura. Expectant management is employed for bronchial injuries that are less than one-third the circumference of the airway and have no evidence of a persistent major air leak.^11,12 In patients with peripheral bronchial injuries, indicated by persistent air leaks from the chest tube and documented by endoscopy, bronchoscopically directed fibrin glue sealing may be useful.

The majority of pulmonary parenchymal injuries are suspected based upon identification of a pneumothorax; the vast majority is managed by tube thoracostomy. Identified parenchymal injuries encountered during thoracic exploration for a massive hemothorax are managed without resection as much as possible. Peripheral lacerations with persistent bleeding can be managed with stapled wedge resection using a stapler. For central injuries, the current treatment is pulmonary tractotomy, which permits selective ligation of individual bronchioles and bleeders, prevents the development of an intraparenchymal hematoma or air embolism, and reduces the need for formal lobar resection (see Fig. 7-49).^90,91 A stapling device, preferably the longest stapler available, is inserted directly into the injury track and positioned along the thinnest section of overlying parenchyma. The injury track is thus filleted open, which allows direct access to the bleeding vessels and leaking bronchi. The majority of injuries are definitively managed with selective ligation, and the defect is left open. Occasionally, tractotomy reveals a more proximal vascular injury that must be treated with formal lobectomy. Injuries severe enough to mandate pneumonectomy usually are fatal because of right heart decompensation.⁹²

One parenchymal injury that may be discovered during thoracic imaging is a posttraumatic pulmonary pseudocyst, colloquially termed a pneumatocele.⁹³ Traumatic pneumatoceles typically follow a benign clinical course and are treated with aggressive pain management, pulmonary toilet, and serial chest radiography to monitor for resolution of the lesion. If the patient has persistent fever or leukocytosis, however, chest CT is done to evaluate for an evolving abscess, because pneumatoceles may become infected. CT-guided catheter drainage may be required in such cases, because 25% of patients do not respond to antibiotic therapy alone. Surgery, ranging from partial resection to anatomic lobectomy, is indicated for unresolving complex pneumatoceles or infected lesions refractory to antibiotic therapy and drainage.

The most common complication after thoracic injury is development of an empyema. Management is based on CT diagnostic criteria.⁹⁴ Percutaneous drainage is indicated for a single loculation without appreciable rind. While fibrinolytics are often used for empyema there is a paucity of data to support their use. Early decortication via video-assisted thoracic surgery should be done promptly in patients with multiple loculations or a pleural rind of >1 cm.⁹⁵ Antibiotic treatment is based on definitive culture results, but presumptive antibiotics should cover MRSA in the SICU.

Esophagus

Due to the proximity of the structures, esophageal injuries often occur with tracheobronchial injuries, particularly in cases of penetrating trauma. Operative options are based on the extent and location of esophageal injury. With sufficient mobilization, a primary single-layer end-to-end anastomosis may be performed after appropriate débridement. As with cervical repairs, if there are two suture lines in close approximation (trachea or bronchi and esophagus) interposition of a vascularized pedicle is warranted to prevent fistula formation. Perforations at the gastroesophageal junction may be treated with repair and Nissan fundoplication or, for destructive injuries, segmental resection and gastric pull-up. With large destructive injuries or delayed presentation of injuries, esophageal exclusion with wide drainage, diverting loop esophagostomy, and placement of a gastrostomy tube should be considered.

Chest Wall and Diaphragm

Virtually all chest wall injuries, consisting of rib fractures and laceration of intercostal vessels, are treated nonoperatively with pain control, pulmonary toilet or ventilatory management, and drainage of the pleural space as indicated. Early institution of effective pain control is essential. The authors advocate pre-emptive rib blocks with 0.25% bupivacaine hydrochloride (Marcaine) in the trauma bay, followed by thoracic wall pain catheters.⁹⁶ Epidural anesthesia is reserved for multiple segmental fractures. Persistent hemorrhage from a chest tube after blunt trauma most often is due to injured intercostal arteries; for unusual persistent bleeding (see Table 7-10), thoracotomy with direct ligation or angioembolization may be required to arrest hemorrhage. In cases of extensive flail chest segments or markedly displaced rib fractures, open reduction and internal fixation of the fracture with plates may be warranted. The current role of operative rib fixation remains controversial. Chest wall defects, particularly those seen with open pneumothorax, are repaired using local approximation of tissues or tissue transfer for coverage. Scapular and sternal fractures rarely require operative intervention but are markers for significant thoracoabdominal force during injury; significant displacement may benefit from sternal plating (Fig. 7-58). Careful examination and imaging should exclude associated injuries, including blunt cardiac injury and descending aortic tears. On the other hand, clavicle fractures often are isolated injuries and should be managed with pain control and immobilization. The exception is posterior dislocation of the clavicular head, which may injure the subclavian vessels.

Blunt diaphragmatic injuries usually result in a linear tear, and most injuries are large, whereas penetrating injuries are variable in size and location depending on the agent of injury. Regardless of the etiology, acute injuries are usually repaired through an abdominal approach to manage potential associated intraperitoneal visceral injury. After delineation of the injury, the chest should be evacuated of all blood and particulate matter, and thoracostomy tube placed if not previously done. Allis clamps are used to approximate the diaphragmatic edges, and the defect is closed with a running No. 1 polypropylene suture. Occasionally, large avulsions or shotgun wounds with extensive tissue loss will require polypropylene or biologic mesh to bridge the defect. Alternatively, transposition of the diaphragm cephalad one to two intercostal spaces may allow repair without undue tension.⁶¹

Abdominal Injuries

Liver and Extrahepatic Biliary Tract

The liver’s large size makes it the organ most susceptible to blunt trauma, and it is frequently involved in upper torso penetrating wounds. Nonoperative management of solid organ injuries is pursued in hemodynamically stable patients who do not have overt peritonitis or other indications for laparotomy. Patients with > grade II injuries should be admitted to the SICU with frequent hemodynamic monitoring, determination of hemoglobin, and abdominal examination. The only absolute contraindication to nonoperative management is hemodynamic instability. Factors such as high injury grade, large hemoperitoneum, contrast extravasation, or pseudoaneurysms may predict complications or failure of nonoperative management. Angioembolization and endoscopic retrograde cholangiopancreatography (ERCP) are useful adjuncts that can improve the success rate of nonoperative management.^97,98 The indication for angiography to control hepatic hemorrhage is transfusion of 4 units of RBCs in 6 hours or 6 units of RBCs in 24 hours without hemodynamic instability.

In the 15% of patients for whom emergent laparotomy is mandated, the primary goal is to arrest hemorrhage. Initial control of hemorrhage is best accomplished using perihepatic packing and manual compression. With extensive injuries and major hemorrhage a Pringle maneuver should be done immediately. Intermittent release of the Pringle is helpful to attenuate hepatic cellular loss. In either case, the edges of the liver laceration should be opposed for local pressure control of bleeding. Hemorrhage from most major hepatic injuries can be controlled with effective perihepatic packing. The right costal margin is elevated, and the pads are strategically placed over and around the bleeding site (see Fig. 7-36). Additional pads should be placed between the liver, diaphragm, and anterior chest wall until the bleeding has been controlled. Sometimes 10 to 15 pads may be required to control the hemorrhage from an extensive right lobar injury. Packing of injuries of the left lobe is not as effective, because there is insufficient abdominal and thoracic wall anterior to the left lobe to provide adequate compression with the abdomen open. Fortunately, hemorrhage from the left lobe usually can be controlled by mobilizing the lobe and compressing it between the surgeon’s hands. If the patient has persistent bleeding despite packing, injuries to the hepatic artery, portal vein, and retrohepatic vasculature should be considered. A Pringle maneuver can help delineate the source of hemorrhage. In fact, hemorrhage from hepatic artery and portal vein injuries will halt with the application of a vascular clamp across the portal triad; whereas, bleeding from the hepatic veins and retrohepatic vena cava will continue.

Injuries of the portal triad vasculature should be addressed immediately. In general, ligation from the celiac axis to the level of the common hepatic artery at the gastroduodenal arterial branch is tolerated due to the extensive collaterals, but the proper hepatic artery should be repaired. The right or left hepatic artery, or in urgent situations the portal vein, may be selectively ligated; occasionally, lobar necrosis will necessitate delayed anatomic resection. If the right hepatic artery is ligated, cholecystectomy also should be performed. If the vascular injury is a stab wound with clean transection of the vessels, primary end-to-end repair is done. If the injury is destructive, temporary shunting should be performed followed by interposition reversed saphenous vein graft (RSVG). Blunt avulsions of the portal structures are particularly problematic if located at the hepatic plate, flush with the liver; hemorrhage control at the liver can be attempted with directed packing or Fogarty catheters. If the avulsion is more proximal, at the superior border of the pancreatic body or even retropancreatic, the pancreas must be transected to gain access for hemorrhage control and repair.

If massive venous hemorrhage is seen from behind the liver despite use of the Pringle maneuver, the patient likely has a hepatic vein or retrohepatic vena cava injury. If bleeding can be controlled with perihepatic packing, the packing should be left undisturbed and the patient observed in the SICU. Placement of a hepatic vein stent by interventional radiology may be considered. If bleeding continues despite repeated attempts at packing, then direct repair, with or without hepatic vascular isolation, should be attempted. Three techniques have been used to accomplish hepatic vascular isolation: (a) direct repair with suprahepatic and infrahepatic clamping of the vena cava and stapled assisted parenchymal resection;⁹⁹ (b) temporary shunting of the retrohepatic vena cava; and (c) venovenous bypass (Fig. 7-59).¹⁰⁰

Numerous methods for the definitive control of hepatic parenchymal hemorrhage have been developed. Minor lacerations may be controlled with manual compression applied directly to the injury site. Topical hemostatic techniques include the use of an electrocautery (with the device set at 100 watts), argon beam coagulator, microcrystalline collagen, thrombin-soaked gelatin foam sponge, fibrin glue, and BioGlue. Suturing of the hepatic parenchyma with a blunt tipped 0 chromic suture (e.g., a “liver suture”) can be an effective hemostatic technique. A running suture is used to approximate the edges of shallow lacerations, whereas deeper lacerations are approximated using interrupted horizontal mattress sutures placed parallel to the edge of the laceration. When the suture is tied, tension is adequate when visible hemorrhage ceases or the liver blanches around the suture. Caution must be used to prevent hepatic necrosis. This technique of placing large liver sutures controls bleeding through reapproximation of the liver laceration rather than direct ligation of bleeding vessels. Aggressive finger fracture to identify bleeding vessels followed by individual clip or suture ligation was advocated previously but currently has a limited role in hemostasis. Hepatic lobar arterial ligation may be appropriate for patients with recalcitrant arterial hemorrhage from deep within the liver and is a reasonable alternative to a deep hepatotomy, particularly in unstable patients. Omentum can be used to fill large defects in the liver. The tongue of omentum not only obliterates potential dead space with viable tissue but also provides an excellent source of macrophages. Additionally, the omentum can provide buttressing support for parenchymal sutures.

Translumbar penetrating injuries are particularly challenging, because the extent of the injury cannot be fully visualized. As discussed later in “Damage Control Surgery,” options include intraparenchymal tamponade with a Foley catheter or balloon occlusion (see Fig. 7-48).¹⁰¹ If tamponade is successful with either modality, the balloon is left inflated for 24 to 48 hours followed by sequential deflation and removal at a second laparotomy. Hepatotomy with ligation of individual bleeders occasionally may be required; however, division of the overlying viable hepatic tissue may cause considerable blood loss in the coagulopathic patient. Finally, angioembolization is an effective adjunct in any of these scenarios and should be considered early in the course of treatment.

Several centers have reported patients with devastating hepatic injuries or necrosis of the entire liver who have undergone successful hepatic transplantation.¹⁰² Clearly this is dramatic therapy, and the patient must have all other injuries delineated, particularly those of the central nervous system, and have an excellent chance of survival excluding the hepatic injury. Because donor availability will limit such procedures, hepatic transplantation for trauma will continue to be performed only in extraordinary circumstances.

Cholecystectomy is performed for injuries of the gallbladder and after operative ligation of the right hepatic artery. Injuries of the extrahepatic bile ducts are a challenge due to their small size and thin walls. Because of the proximity of other portal structures and the vena cava, associated vascular injuries are common. These factors may preclude primary repair. Small lacerations with no accompanying loss or devitalization of adjacent tissue can be treated by the insertion of a T tube through the wound or by lateral suturing using 6-0 monofilament absorbable suture. Virtually all transections and any injury associated with significant tissue loss will require a Roux-en-Y choledochojejunostomy.¹⁰³ The anastomosis is performed using a single-layer interrupted technique with 5-0 monofilament absorbable suture. To reduce anastomotic tension, the jejunum should be sutured to the areolar tissue of the hepatic pedicle or porta hepatis. Injuries of the hepatic ducts are almost impossible to satisfactorily repair under emergent circumstances. One approach is to intubate the duct for external drainage and attempt a repair when the patient recovers or attempt stenting via ERC. Alternatively, the duct can be ligated if the opposite lobe is normal and uninjured.

Patients undergoing perihepatic packing for extensive liver injuries typically are returned to the OR for pack removal 24 hours after initial injury. Earlier exploration may be indicated in patients with evidence of ongoing hemorrhage. Signs of rebleeding are usually conspicuous, and include a falling hemoglobin, accumulation of blood clots under the temporary abdominal closure device, and bloody output from drains; the magnitude of hemorrhage is reflected in ongoing hemodynamic instability and metabolic monitoring. Postoperative hemorrhage should be re-evaluated in the OR once the patient’s coagulopathy is corrected. Alternatively, angioembolization is appropriate for complex injuries. Patients with hepatic ischemia due to prolonged intraoperative use of the Pringle maneuver have an expected elevation but subsequent resolution of transaminase levels, whereas patients requiring hepatic artery ligation may have frank hepatic necrosis. Although febrile patients should be evaluated for infectious complications, patients with complex hepatic injuries typically have intermittent “liver fever” for the first 5 days after injury.

Aside from hemorrhage and hepatic necrosis, additional complications after significant hepatic trauma include bilomas, arterial pseudoaneurysms, and biliary fistulas (Fig. 7-60). Bilomas are loculated collections of bile, which may or may not be infected. If infected, they should be treated like an abscess via percutaneous drainage. Although small, sterile bilomas eventually will be reabsorbed, larger fluid collections should be drained. Biliary ascites, due to the disruption of a major bile duct, often requires reoperation and wide drainage. Primary repair of the injured intrahepatic duct is unlikely to be successful. Resectional débridement is indicated for the removal of peripheral portions of nonviable hepatic parenchyma.

Pseudoaneurysms and biliary fistulas are rare complications in patients with hepatic injuries. Because hemorrhage from hepatic injuries often is treated without isolating individual bleeding vessels, arterial pseudoaneurysms may develop, with the potential for rupture. Rupture into a bile duct results in hemobilia, which is characterized by intermittent episodes of right upper quadrant pain, upper GI hemorrhage, and jaundice. If the aneurysm ruptures into a portal vein, portal venous hypertension with bleeding esophageal varices may occur. Either scenario is best managed with hepatic arteriography and embolization. Biliovenous fistulas, causing jaundice due to rapid increases in serum bilirubin levels, should be treated with ERCP and sphincterotomy. Rarely, a biliary fistulous communication will form with intrathoracic structures in patients with associated diaphragm injuries, resulting in a bronchobiliary or pleurobiliary fistula. Due to the pressure differential between the biliary tract (positive) and the pleural cavity (negative), the majority require operative closure. Occasionally, endoscopic sphincterotomy with stent placement will be required to address the pressure differential, and the pleurobiliary fistula will close spontaneously.

Spleen

Until the 1970s, splenectomy was considered mandatory for all splenic injuries. Recognition of the immune function of the spleen refocused efforts on operative splenic salvage in the 1980s.^104,105 After demonstrated success in pediatric patients, however, nonoperative management has become the preferred means of splenic salvage. The identification of contrast extravasation as a risk factor for failure of nonoperative management led to liberal use of angioembolization. The role of selective angioembolization (SAE) in splenic salvage remains controversial with some groups advocated pre-emptive SAE.¹⁰⁶ It is clear, however, that up to 20% of patients with splenic trauma warrant early splenectomy and that failure of nonoperative management often represents inappropriate patient selection.^107,108 Unlike hepatic injuries, which usually rebleed within 48 hours, delayed hemorrhage or rupture of the spleen can occur up to weeks after injury. Indications for early intervention include initiation of blood transfusion within the first 12 hours and hemodynamic instability.

Splenic injuries are managed operatively by splenectomy, partial splenectomy, or splenic repair (splenorrhaphy), based on the extent of the injury and the physiologic condition of the patient. Splenectomy is indicated for hilar injuries, pulverized splenic parenchyma, or any >grade II injury in a patient with coagulopathy or multiple injuries. The authors use autotransplantation of splenic implants (Fig. 7-61) to achieve partial immunocompetence in younger patients who do not have an associated enteric injury. Drains are not used. Partial splenectomy can be employed in patients in whom only the superior or inferior pole has been injured. Hemorrhage from the raw splenic edge is controlled with horizontal mattress sutures, with gentle compression of the parenchyma (Fig. 7-62). As with hepatic injuries, splenorrhaphy hemostasis is achieved by topical methods (electrocautery; argon beam coagulation; application of thrombin-soaked gelatin foam sponges, fibrin glue, or BioGlue), envelopment of the injured spleen in absorbable mesh, and pledgeted suture repair.

After splenectomy or splenorrhaphy, postoperative hemorrhage may be due to loosening of a tie around the splenic vessels, an improperly ligated or unrecognized short gastric artery, or recurrent bleeding from the spleen if splenic repair was used. An immediate postsplenectomy increase in platelets and WBCs is normal; however, beyond postoperative day 5, a WBC count above 15,000/mm³ and a platelet/WBC ratio of <20 are strongly associated with sepsis and should prompt a thorough search for underlying infection.¹⁰⁹ A common infectious complication after splenectomy is a subphrenic abscess, which should be managed with percutaneous drainage. Additional sources of morbidity include a concurrent but unrecognized iatrogenic injury to the pancreatic tail during rapid splenectomy resulting in pancreatic ascites or fistula, and a gastric perforation during short gastric ligation. Enthusiasm for splenic salvage was driven by the rare, but often fatal, complication of overwhelming postsplenectomy sepsis. Overwhelming postsplenectomy sepsis is caused by encapsulated bacteria, Streptococcus pneumoniae, Haemophilus influenzae, and Neisseria meningitidis, which are resistant to antimicrobial treatment. In patients undergoing splenectomy, prophylaxis against these bacteria is provided via vaccines administered optimally at 14 days.¹¹⁰

Stomach and Small Intestine

Little controversy exists regarding the repair of injuries to the stomach or small bowel because of a rich blood supply. Gastric wounds can be oversewn with a running single-layer suture line or closed with a stapler. If a single-layer closure is chosen, full-thickness bites should be taken to ensure hemostasis from the well-vascularized gastric wall. The most commonly missed gastric injury is the posterior wound of a totally penetrating injury. Injuries also can be overlooked if the wound is located within the mesentery of the lesser curvature or high in the posterior fundus. To delineate a questionable injury, the stomach can be digitally occluded at the pylorus while methylene blue-colored saline is instilled via a nasogastric tube. Alternatively, air can be introduced via the NG tube with the abdomen filled with saline. Partial gastrectomy may be required for destructive injuries, with resections of the distal antrum or pylorus reconstructed using a Billroth procedure. Patients with injuries that damage both Latarjet nerves or vagi should undergo a drainage procedure (see Chap. 26). Small intestine injuries can be repaired using a transverse running 3-0 PDS suture if the injury is less than one- third the circumference of the bowel. Destructive injuries or multiple penetrating injuries occurring close together are treated with segmental resection followed by end-to-end anastomosis using a continuous, single-layer 3-0 polypropylene suture.¹¹¹ Mesenteric injuries may result in an ischemic segment of intestine, which mandates resection.

Following repair of GI tract injuries, there is an obligatory postoperative ileus. Return of bowel function is indicated by a decrease in gastrostomy or nasogastric tube output. The topic of nutrition is well covered in other chapters, but a few issues warrant mention. Multiple studies have confirmed the importance of early total enteral nutrition (TEN) in the trauma population, particularly its impact in reducing septic complications.¹¹² The route of enteral feedings (stomach vs. small bowel) tends to be less important, because gut tolerance appears equivalent unless there is upper GI tract pathology. Although early enteral nutrition is the goal, evidence of bowel function should be apparent before advancing to goal tube feedings. Overzealous jejunal feeding can lead to small bowel necrosis in the patient recovering from profound shock. Patients undergoing monitoring for nonoperative management of grade II or higher solid organ injuries should receive nothing by mouth for at least 48 hours in case they require an operation. Although there is general reluctance to initiate TEN in patients with an open abdomen, a recent multicenter trial demonstrates TEN in the postinjury open abdomen is feasible.¹¹³ For those patients without a bowel injury, TEN was associated with higher fascial closure rates, decreased complications, and decreased mortality. TEN in patients with bowel injuries does not appear to alter fascial closure rates, complications, or mortality; hence EN appears to be neither advantageous nor detrimental in these patients. Prospective randomized controlled trials are warranted to further clarify the role of EN in this subgroup. Once resuscitation is complete, initiation of TEN, even at trophic levels (20 mL/h), should be considered in all injured patients with an open abdomen.

Duodenum and Pancreas

The spectrum of injuries to the duodenum includes hematomas, perforation (blunt blow-outs, lacerations from stab wounds, or blast injury from gunshot wounds), and combined pancreaticoduodenal injuries. The majority of duodenal hematomas are managed nonoperatively with nasogastric suction and parenteral nutrition. Patients with suspected associated perforation, suggested by clinical deterioration or imaging with retroperitoneal free air or contrast extravasation, should undergo operative exploration. A marked drop in nasogastric tube output heralds resolution of the hematoma, which typically occurs within 2 weeks; repeat imaging to confirm these clinical findings is optional. If the patient shows no clinical or radiographic improvement within 3 weeks, operative evaluation is warranted.

Small duodenal perforations or lacerations should be treated by primary repair using a running single-layer suture of 3-0 monofilament. The wound should be closed in a direction that results in the largest residual lumen. Challenges arise when there is a substantial loss of duodenal tissue. Extensive injuries of the first portion of the duodenum (proximal to the duct of Santorini) can be repaired by débridement and end-to-end anastomosis because of the mobility and rich blood supply of the distal gastric atrium and pylorus. In contrast, the second portion is tethered to the head of the pancreas by its blood supply and the ducts of Wirsung and Santorini; therefore, no more than 1 cm of duodenum can be mobilized away from the pancreas, and this does not effectively alleviate tension on the suture line. Moreover, suture repair using an end-to-end anastomosis in the second portion often results in an unacceptably narrow lumen. Therefore, defects in the second portion of the duodenum should be patched with a vascularized jejunal graft. Duodenal injuries with tissue loss distal to the papilla of Vater and proximal to the superior mesenteric vessels are best treated by Roux-en-Y duodenojejunostomy with the distal portion of the duodenum oversewn (Fig. 7-63). In particular, injuries in the distal third and fourth portions of the duodenum (behind the mesenteric vessels) should be resected, and a duodenojejunostomy performed on the left side of the superior mesenteric vessels.

Optimal management of pancreatic trauma is determined by where the parenchymal damage is located and whether the intrapancreatic common bile duct and main pancreatic duct remain intact. Patients with pancreatic contusions (defined as injuries that leave the ductal system intact) can be treated nonoperatively or with closed suction drainage if undergoing laparotomy for other indications. Patients with proximal pancreatic injuries, defined as those that lie to the right of the superior mesenteric vessels, are also managed with closed suction drainage,¹¹⁴ In contrast, distal pancreatic injuries are managed based upon ductal integrity. Pancreatic duct disruption can be identified through direct exploration of the parenchymal laceration, operative pancreatography, ERCP, or magnetic resonance cholangiopancreatography. Patients with distal ductal disruption undergo distal pancreatectomy, preferably with splenic preservation.

Injuries to the pancreatic head add an additional element of complexity because the intrapancreatic portion of the common bile duct traverses this area and often converges with the pancreatic duct. In contrast to diagnosis of pancreatic duct injuries, identification of intrapancreatic common bile duct disruption is relatively simple. The first method is to squeeze the gallbladder and look for bile leaking from the pancreatic wound. Otherwise, cholangiography, optimally via the cystic duct, is diagnostic. Definitive treatment of this injury entails division of the common bile duct superior to the first portion of the duodenum, with ligation of the distal duct and reconstruction with a Roux-en-Y choledochojejunostomy. For injuries to the head of the pancreas that involve the main pancreatic duct but not the intrapancreatic bile duct, there are few options. Distal pancreatectomy alone is rarely indicated due to the extended resection of normal gland and the resultant risk of pancreatic insufficiency. Central pancreatectomy preserves the common bile duct, and mobilization of the pancreatic body permits drainage into a Roux-en-Y pancreaticojejunostomy (Fig. 7-64). Although this approach avoids a pancreaticoduodenectomy (Whipple procedure), the complexity may make the pancreaticoduodenectomy more appropriate in patients with multiple injuries. Some injuries of the pancreatic head do not involve either the pancreatic or common bile duct; if no clear ductal injury is present, drains are placed. Rarely, patients sustain destructive injuries to the head of the pancreas or combined pancreaticoduodenal injuries that require pancreaticoduodenectomy. Examples of such injuries include transection of both the intrapancreatic bile duct and the main pancreatic duct in the head of the pancreas, avulsion of the papilla of Vater from the duodenum, and destruction of the entire second portion of the duodenum. In these cases of extensive injuries, damage control principles are often employed.

In contrast to proximal injuries, pancreatic resection continues to be advocated for major ductal disruption in the more distal pancreas. Several options exist for treating injuries of the pancreatic body and tail. In stable patients, spleen-preserving distal pancreatectomy should be performed. An alternative, which preserves both the spleen and distal transected end of the pancreas, is either a Roux-en-Y pancreaticojejunostomy or pancreaticogastrostomy. If the patient is physiologically compromised, distal pancreatectomy with splenectomy is the preferred approach. Regardless of the choice of definitive procedure, the pancreatic duct in the proximal edge of transected pancreas should be individually ligated or occluded with a TA stapler. Application of fibrin glue over the stump may be advantageous.

Pyloric exclusion often is used to divert the GI stream after high-risk, complex duodenal repairs (Fig. 7-65).¹¹⁵ If the duodenal repair breaks down, the resultant fistula is an end fistula, which is easier to manage and more likely to close than a lateral fistula. To perform a pyloric exclusion, first a gastrostomy is made on the greater curvature near the pylorus. The pylorus is then grasped with a Babcock clamp, via the gastrostomy, and oversewn with an O polypropylene suture. A gastrojejunostomy restores GI tract continuity. Vagotomy is not necessary because a risk of marginal ulceration has not been documented. Perhaps surprisingly, the sutures maintain diversion for only 3 to 4 weeks. Alternatively, the most durable pyloric closure is a double external staple line across the pylorus using a TA stapler.

Complications should be expected after major pancreaticoduodenal injuries. Delayed hemorrhage is rare but may occur with pancreatic necrosis or abdominal infection; this usually can be managed by angioembolization. If closed suction drains have been inserted for major pancreatic trauma, these should remain in place until the patient is tolerating an oral diet or enteral nutrition. Pancreatic fistula is diagnosed after postoperative day 5 in patients with drain output of >30 mL/d and a drain amylase level three times the serum value. Pancreatic fistula develops in over 20% of patients with combined injuries and should be managed similar to fistulas after elective surgery (see Chap. 33). Similarly, a duodenal fistula, presumptively an end fistula if a pyloric exclusion has been done, will typically heal in 6 to 8 weeks with adequate drainage and control of intra-abdominal sepsis. Pancreatic pseudocysts in patients managed nonoperatively suggest a missed injury, and ERCP should be done to evaluate the integrity of the pancreatic duct. Late pseudocysts may be a complication of operative management and are treated much like those in patients with pancreatitis (see Chap. 33). Intra-abdominal abscesses are common and routinely managed with percutaneous drainage.

Colon and Rectum

Currently, three methods for treating colonic injuries are used: primary repair, end colostomy, and primary repair with diverting ileostomy. Primary repairs include lateral suture repair or resection of the damaged segment with reconstruction by ileocolostomy or colocolostomy. All suturing and anastomoses are performed using a running single-layer technique (Fig. 7-66).¹¹¹ The advantage of definitive treatment must be balanced against the possibility of anastomotic leakage if suture lines are created under suboptimal conditions. Alternatively, although use of an end colostomy requires a second operation, an unprotected suture line with the potential for breakdown is avoided. Numerous large retrospective and several prospective studies have now clearly demonstrated that primary repair is safe and effective in virtually all patients with penetrating wounds.¹¹⁶ Colostomy is still appropriate in a few patients, but the current dilemma is how to select which patients should undergo the procedure. Currently, the overall physiologic status of the patient, rather than local factors, directs decision making. Patients with devastating left colon injuries requiring damage control are clearly candidates for temporary colostomy. Diverting ileostomy with colocolostomy, however, is used for most other high-risk patients.

Rectal injuries are similar to colonic injuries with respect to the ecology of the luminal contents, overall structure, and blood supply of the wall, but access to extraperitoneal injuries is limited due to the surrounding bony pelvis. Therefore, indirect treatment with intestinal diversion usually is required. The current options are loop ileostomy and sigmoid loop colostomy. These are preferred because they are quick and easy to perform, and provide essentially total fecal diversion. For sigmoid colostomy, technical elements include: (a) adequate mobilization of the sigmoid colon so that the loop will rest on the abdominal wall without tension, (b) maintenance of the spur of the colostomy (the common wall of the proximal and distal limbs after maturation) above the level of the skin with a one-half-inch nylon rod or similar device, (c) longitudinal incision in the tenia coli, and (d) immediate maturation in the OR (Fig. 7-67). If the injury is accessible (e.g., in the posterior intraperitoneal portion of the rectum), repair of the injury should also be attempted. However, it is not necessary to explore the extraperitoneal rectum to repair a distal perforation. If the rectal injury is extensive, another option is to divide the rectum at the level of the injury, oversew or staple the distal rectal pouch if possible, and create an end colostomy (Hartmann’s procedure). Extensive injuries may warrant presacral drainage with Penrose drains placed along Waldeyer’s fascia via a perianal incision (see Fig. 7-67). In rare instances in which destructive injuries are present, an abdominoperineal resection may be necessary to avert lethal pelvic sepsis.

Complications related to colorectal injuries include intra-abdominal abscess, fecal fistula, wound infection, and stomal complications. Intra-abdominal abscesses occur in approximately 10% of patients, and most are managed with percutaneous drainage. Fistulas occur in 1% to 3% of patients and usually present as an abscess or wound infection with subsequent continuous drainage of fecal output; the majority will heal spontaneously with routine care (see Chap. 29). Stomal complications (necrosis, stenosis, obstruction, and prolapse) occur in 5% of patients and may require either immediate or delayed reoperation. Stomal necrosis should be carefully monitored, because spread beyond the mucosa may result in septic complications, including necrotizing fasciitis of the abdominal wall. Penetrating injuries that involve both the rectum and adjacent bony structures are prone to development of osteomyelitis. Bone biopsy is performed for diagnosis and bacteriologic analysis, and treatment entails long-term IV antibiotic therapy and occasionally débridement.

Abdominal and Pelvic Vasculature

Injury to the major arteries and veins in the abdomen can be a technical challenge.^{117,118,119,120,121} Although penetrating trauma indiscriminately affects all blood vessels, blunt trauma most commonly involves renal vasculature and occasionally the abdominal aorta. Patients with a penetrating aortic wound who survive to reach the OR frequently have a contained hematoma within the retroperitoneum. Due to lack of mobility of the abdominal aorta, few injuries are amenable to primary repair. Small lateral perforations may be controlled with 4-0 polypropylene suture or a PTFE patch, but end-to-end interposition grafting with a PTFE tube graft is the most common repair. Blunt injuries are typically extensive intimal tears of the infrarenal aorta and are exposed via a direct approach; most require an interposition graft. To avoid future vascular-enteric fistulas, the vascular suture lines should be covered with omentum.

Penetrating wounds to the superior mesenteric artery (SMA) are typically encountered upon exploration for a gunshot wound, with “black bowel” and associated supramesocolic hematoma being pathognomonic. Blunt avulsions of the SMA are rare but should be considered in patients with a seat belt sign who have midepigastric pain or tenderness and associated hypotension. For injuries of the SMA, temporary damage control with a Pruitt-Inahara shunt can prevent extensive bowel necrosis; additionally, temporary shunting allows control of visceral contamination before placement of a PTFE graft. For definitive repair, end-to-end interposition RSVG from the proximal SMA to the SMA past the point of injury can be performed if there is no associated pancreatic injury. Alternatively, if the patient has an associated pancreatic injury, the graft should be tunneled from the distal aorta beneath the duodenum to the distal SMA. For proximal SMV injuries, digital compression for hemorrhage control is followed by attempted venorrhaphy; ligation is an option in a life-threatening situation, but the resultant bowel edema requires aggressive fluid resuscitation. Temporary abdominal closure and a second-look operation to evaluate bowel viability should be done.

Transpelvic gunshot wounds or blunt injuries with associated pelvic fractures are the most common scenarios in patients with iliac artery injuries. As with abdominal vascular injuries, a Pruitt-Inahara shunt can be used for temporary shunting of the vessel for damage control. Definitive interposition grafting with excision of the injured segment is appropriate (see “Vascular Repair Techniques”). Careful monitoring for distal embolic events and reperfusion injury necessitating fasciotomy is imperative.

In general, outcome after pelvic vascular injuries is related to (a) the technical success of the vascular reconstruction and (b) associated soft tissue and nerve injuries. Vascular repairs rarely fail after the first 12 hours, whereas, soft tissue infection is a limb threat for several weeks. Following aortic interposition grafting, the patient’s SBP should not exceed 120 mm Hg for at least the first 72 hours postoperatively. Patients requiring ligation of an inferior vena cava injury often develop marked bilateral lower extremity edema. To limit the associated morbidity the patient’s legs should be wrapped with elastic bandages from the toes to the hips and elevated at a 45- to 60-degree angle. For superior mesenteric vein injuries, either ligation or thrombosis after venorrhaphy results in marked bowel edema; fluid resuscitation should be aggressive and abdominal pressure monitoring routine in these patients. Prosthetic graft infections are rare complications, but prevention of bacteremia is imperative⁶⁷; administration of antibiotics perioperatively and treatment of secondary infections is indicated. Long-term arterial graft complications such as stenosis or pseudoaneurysms are uncommon, and routine graft surveillance rarely is performed. Consequently, long-term administration of antiplatelet agents or antithrombotics is not routine.

Genitourinary Tract

When undergoing laparotomy for trauma, the best policy is to explore all penetrating wounds to the kidneys.¹²² Parenchymal renal injuries are treated with hemostatic and reconstructive techniques similar to those used for injuries of the liver and spleen: topical methods (electrocautery; argon beam coagulation; application of thrombin-soaked gelatin foam sponge, fibrin glue, or BioGlue) and pledgeted suture repair. Two caveats are recognized, however: The collecting system should be closed separately, and the renal capsule should be preserved to close over the repair of the collecting system (Fig. 7-68). Renal vascular injuries are common after penetrating trauma and may be deceptively tamponaded, which results in delayed hemorrhage. Arterial reconstruction using graft interposition should be attempted for renal preservation. For destructive parenchymal or irreparable renovascular injuries, nephrectomy may be the only option; a normal contralateral kidney must be palpated, because unilateral renal agenesis occurs in 0.1% of patients.

Over 90% of blunt renal injuries are treated nonoperatively. Hematuria typically resolves within a few days with bed rest, although rarely bleeding is so persistent that bladder irrigation to dispel blood clots is warranted. Persistent gross hematuria may require embolization, whereas urinomas can be drained percutaneously. Operative intervention after blunt trauma is limited to renovascular injuries and destructive parenchymal injuries that result in hypotension. The renal arteries and veins are uniquely susceptible to traction injury caused by blunt trauma. As the artery is stretched, the inelastic intima and media may rupture, which causes thrombus formation and resultant stenosis or occlusion. The success rate for renal artery repair approaches 0%, but an attempt is reasonable if the injury is <5 hours old or if the patient has a solitary kidney or bilateral injuries.¹²³ Image-guided endostent placement is now employed for many of these injuries recognized by CT scanning. Reconstruction after blunt renal injuries may be difficult, however, because the injury is typically at the level of the aorta. If repair is not possible within this time frame, leaving the kidney in situ does not necessarily lead to hypertension or abscess formation. The renal vein may be torn or completely avulsed from the vena cava due to blunt trauma. Typically, the large hematoma causes hypotension, which leads to operative intervention. During laparotomy for blunt trauma, expanding or pulsatile perinephric hematomas should be explored. If necessary, emergent vascular control can be obtained by placing a curved vascular clamp across the hilum from an inferior approach. Techniques of repair and hemostasis are similar to those described earlier.

Injuries to the ureters are uncommon but may occur in patients with pelvic fractures and penetrating trauma. An injury may not be identified until a complication (i.e., a urinoma) becomes apparent. If an injury is suspected during operative exploration but is not clearly identified, methylene blue or indigo carmine is administered IV with observation for extravasation. Injuries are repaired using 5-0 absorbable monofilament, and mobilization of the kidney may reduce tension on the anastomosis. Distal ureteral injuries can be treated by reimplantation facilitated with a psoas hitch and/or Boari flap. In damage control circumstances, the ureter can be ligated on both sides of the injury and a nephrostomy tube placed.

Bladder injuries are subdivided into those with intraperitoneal extravasation and those with extraperitoneal extravasation. Ruptures or lacerations of the intraperitoneal bladder are operatively closed with a running, single-layer, 3-0 absorbable monofilament suture. Laparoscopic repair is becoming common in patients not requiring laparotomy for other injuries. Extraperitoneal ruptures are treated nonoperatively with bladder decompression for 2 weeks. Urethral injuries are managed by bridging the defect with a Foley catheter, with or without direct suture repair. Strictures are not uncommon but can be managed electively.

Female Reproductive Tract

Gynecologic injuries are rare. Occasionally the vaginal wall will be lacerated by a bone fragment from a pelvic fracture. Although repair is not mandated, it should be performed if physiologically feasible. More important, however, is recognition of the open fracture, need for possible drainage, and potential for pelvic sepsis. Penetrating injuries to the vagina, uterus, fallopian tubes, and ovaries are also uncommon, and routine hemostatic techniques are used. Repair of a transected fallopian tube can be attempted but probably is unjustified, because a suboptimal repair will increase the risk of tubal pregnancy. Transection at the injury site with proximal ligation and distal salpingectomy is a more prudent approach.

Pelvic Fracture Hemorrhage Control

Patients with pelvic fractures who are hemodynamically unstable are a diagnostic and therapeutic challenge for the trauma team. These injuries often occur in conjunction with other life-threatening injuries, and there is no universal agreement among clinicians on management. Current management algorithms in the United States incorporate variable time frames for bony stabilization and fixation, as well as hemorrhage control by preperitoneal pelvic packing and/or angioembolization. Early institution of a multidisciplinary approach with the involvement of trauma surgeons, orthopedic surgeons, interventional radiologists, the director of the blood bank, and anesthesiologists is imperative due to high associated mortality rates (Fig. 7-69).

Evaluation in the ED focuses on identification of injuries mandating operative intervention (e.g., massive hemothorax, ruptured spleen) and injuries related to pelvic fracture that alter management (e.g., injuries to the iliac artery). Immediate temporary stabilization with sheeting of the pelvis or application of commercially available compression devices should be performed. In high risk patients, (e.g. autopedestrian accident) with profound shock, this should be done before radiographic confirmation. If the patient’s primary source of bleeding is the fracture-related hematoma, several options exist for hemorrhage control. Because 85% of bleeding due to pelvic fractures is venous or bony in origin the authors advocate immediate external fixation and preperitoneal pelvic packing.^124,125 Anterior external fixation decreases pelvic volume, which promotes tamponade of venous bleeding and prevents secondary hemorrhage from the shifting of bony elements. Pelvic packing, in which six laparotomy pads (four in children) are placed directly into the paravesical space through a small suprapubic incision, provides tamponade for the bleeding (Fig. 7-70). Pelvic packing also eliminates the often difficult decision by the trauma surgeon: OR vs. interventional radiology? All patients can be rapidly transported to the OR and packing can be accomplished in under 30 minutes. In the authors’ experience, this results in hemodynamic stability and abrupt cessation of the need for ongoing blood transfusion in the majority of cases.¹²⁵ Patients also can undergo additional procedures such as laparotomy, thoracotomy, external fixation of extremity fractures, open fracture débridement, or craniotomy. Currently, angiography is reserved for patients with evidence of ongoing pelvic bleeding after admission to the SICU (>4 units of RBCs in the first 12 postoperative hours after the coagulopathy is corrected). Patients undergo standard posttrauma resuscitative SICU care, and the pelvic packs are removed within 48 hours, a time frame chosen empirically based on the authors’ experience with liver packing. The authors elect to repack the patient’s pelvis if there is persistent oozing and perform serial washouts of the preperitoneal space if it appears infected.

Another clinical challenge is the open pelvic fracture. In many instances the wounds are located in the perineum, and the risk of pelvic sepsis and osteomyelitis is high. To reduce the risk of infection, performance of a diverting sigmoid colostomy is recommended. The pelvic wound is manually débrided and then irrigated daily with a high-pressure pulsatile irrigation system until granulation tissue covers the wound. The wound is then left to heal by secondary intention with a wound vacuum-assisted wound closure (VAC) device.

Extremity Vascular Injuries, Fractures, and Compartment Syndromes

Patients with injured extremities often require a multidisciplinary approach with involvement of trauma, orthopedic, and plastic surgeons to address vascular injuries, fractures, soft tissue injuries, and compartment syndromes. Immediate stabilization of fractures or unstable joints is done in the ED using Hare traction, knee immobilizers, or plaster splints. In patients with open fractures the wound should be covered with povidoneiodine (Betadine)-soaked gauze and antibiotics administered. Options for fracture fixation include external fixation or open reduction and internal fixation with plates or intramedullary nails. Vascular injuries, either isolated or in combination with fractures, require emergent repair. Common combined injuries include clavicle/first rib fractures and subclavian artery injuries, dislocated shoulder/proximal humeral fractures and axillary artery injuries, supracondylar fractures/elbow dislocations and brachial artery injuries, femur fracture and superficial femoral artery injuries, and knee dislocation and popliteal vessel injuries. On-table angiography in the OR facilitates rapid intervention and is warranted in patients with evidence of limb threat at ED arrival. Arterial access for on-table lower extremity angiography can be obtained percutaneously at the femoral vessels with a standard arterial catheter, via femoral vessel exposure and direct cannulation, or with superficial femoral artery (SFA) exposure just above the medial knee. Controversy exists regarding which should be done first, fracture fixation or arterial repair. The authors prefer placement of temporary intravascular shunts first with arterial occlusions to minimize ischemia during fracture treatment, with definitive vascular repair following. Rarely, immediate amputation may be considered due to the severity of orthopedic and neurovascular injuries. This is particularly true if primary nerve transection is present in addition to fracture and arterial injury.¹²⁶ Collaborative decision making by the trauma, orthopedic, and plastic/reconstructive team is essential.

Operative intervention for vascular injuries should follow standard principles of repair (see “Vascular Repair Techniques”). For subclavian or axillary artery repairs, 6-mm PTFE graft and RSVG are used. Because associated injuries of the brachial plexus are common, a thorough neurologic examination of the extremity is mandated before operative intervention. Operative approach for a brachial artery injury is via a medial upper extremity longitudinal incision; proximal control may be obtained at the axillary artery, and an S-shaped extension through the antecubital fossa provides access to the distal brachial artery. The injured vessel segment is excised, and an end-to-end interposition RSVG graft is performed. Upper extremity fasciotomy is rarely required unless the patient manifests preoperative neurologic changes or diminished pulse upon revascularization, or the time to operative intervention is extended. For SFA injuries, external fixation of the femur typically is performed, followed by end-to-end RSVG of the injured SFA segment. Close monitoring for calf compartment syndrome is mandatory. Preferred access to the popliteal space for an acute injury is the medial one-incision approach with detachment of the semitendinosus, semimembranosus, and gracilis muscles (Fig. 7-71). Another option is a medial approach with two incisions using a longer RSVG, but this requires interval ligation of the popliteal artery and geniculate branches. Rarely, with open wounds a straight posterior approach with an S-shaped incision can be used. If the patient has an associated popliteal vein injury, this should be repaired first with a PTFE interposition graft while the artery is shunted. For an isolated popliteal artery injury, RSVG is performed with an end-to-end anastomosis. Compartment syndrome is common, and presumptive four-compartment fasciotomies are warranted in patients with combined arterial and venous injury. Once the vessel is repaired and restoration of arterial flow documented, completion angiography should be done in the OR if there is no palpable distal pulse. Vasoparalysis with verapamil, nitroglycerin, and papaverine may be used to treat vasoconstriction (Table 7-11).

Compartment syndromes, which can occur anywhere in the extremities, involve an acute increase in pressure inside a closed space, which impairs blood flow to the structures within. Causes of compartment syndrome include arterial hemorrhage into a compartment, venous ligation or thrombosis, crush injuries, and reperfusion injury. In conscious patients, pain is the prominent symptom, and active or passive motion of muscles in the involved compartment increases the pain. Paresthesias may also be described. In the lower extremity, numbness between the first and second toes is the hallmark of early compartment syndrome in the exquisitely sensitive anterior compartment and its enveloped deep peroneal nerve. Progression to paralysis can occur, and loss of pulses is a late sign. In comatose or obtunded patients, the diagnosis is more difficult to secure. In patients with a compatible history and a tense extremity, compartment pressures should be measured with a hand-held Stryker device. Fasciotomy is indicated in patients with a gradient of <35 mm Hg (gradient = diastolic pressure – compartment pressure), ischemic periods of >6 hours, or combined arterial and venous injuries. The lower extremity is most frequently involved, and compartment release is performed using a two-incision, four-compartment fasciotomy (Fig. 7-72). Of note, the soleus muscle must be detached from the tibia to decompress the deep flexor compartment.

Postinjury Resuscitation

ICU management of the trauma patient, either with direct admission from the ED or after emergent operative intervention, is considered in distinct phases, because there are differing goals and priorities. The period of acute resuscitation, typically lasting for the first 12 to 24 hours after injury, combines several key principles: optimizing tissue perfusion, ensuring normothermia, and restoring coagulation. There are a multitude of management algorithms aimed at accomplishing these goals, the majority of which involve goal-directed resuscitation with initial volume loading to attain adequate preload, followed by judicious use of inotropic agents or vasopressors.¹²⁷ Although the optimal hemoglobin level remains debated, during shock resuscitation a hemoglobin level of >10 g/dL is generally accepted to optimize hemostasis and ensure adequate oxygen delivery. After the first 24 hours of resuscitation, a more judicious transfusion trigger of a hemoglobin level of <7 g/dL in the euvolemic patient limits the adverse inflammatory effects of stored RBCs. The resuscitation of the severely injured trauma patient may require a considerable amount of crystalloid resuscitation, but recent trends have focused on limiting crystalloid loading. Although early colloid administration is appealing, evidence to date does not support this concept. In fact, optimizing crystalloid administration is a challenging aspect of early care (i.e., balancing cardiac performance against generation of an abdominal compartment syndrome and generalized tissue edema).

Invasive monitoring with pulmonary artery catheters is controversial but may be a necessary adjunct in occasional patients with multiple injuries who require advanced inotropic support. Not only do such devices allow minute-to-minute monitoring of the patient, but the added information on the patient’s volume status, cardiac function, peripheral vascular tone, and metabolic response to injury permits appropriate therapeutic intervention. With added information on the patient’s cardiac function, cardiac indices and oxygen delivery become important variables in the ongoing ICU management. Resuscitation to values of >500 mL/min per square meter for the oxygen delivery index and >3.8 L/min per square meter for the cardiac index are the goals.¹³³ Pulmonary artery catheters also enable the physician to monitor response to vasoactive agents. Although norepinephrine is the agent of choice for patients with low systemic vascular resistance who are unable to maintain a mean arterial pressure of >60 mm Hg, patients may have an element of myocardial dysfunction requiring inotropic support. The role of relative adrenal insufficiency is another controversial area.

Optimal early resuscitation is mandatory and determines when the patient can undergo definitive diagnosis as well as when the patient can be returned to the OR after initial damage control surgery. Specific goals of resuscitation before repeated “semielective” transport include a core temperature of >35°C (95°F), base deficit of <6 mmol/L, and normal coagulation indices. Although correction of metabolic acidosis is desirable, how quickly this should be accomplished requires careful consideration. Adverse sequelae of excessive crystalloid resuscitation include increased intracranial pressure, worsening pulmonary edema, and intra-abdominal visceral and retroperitoneal edema resulting in secondary abdominal compartment syndrome. Therefore, it should be the overall trend of the resuscitation rather than a rapid reduction of the base deficit that is the goal. The goal is to normalize lactate within 24 hours.

In general, wounds sustained from trauma should be examined daily for progression of healing and signs of infection. Complex soft tissue wounds of the abdomen, such as degloving injuries after blunt trauma (termed Morel-Lavallee lesions), shotgun wounds, and other destructive blast injuries, are particularly difficult to manage. Following initial débridement of devitalized tissue, wound care includes wet-to-dry dressing changes twice daily or application of a VAC device. Repeated operative débridement may be necessary, and early involvement of the reconstructive surgery service for possible flap coverage is advised. Midline laparotomy wounds are inspected 48 hours postoperatively by removing the sterile surgical dressing. If an ileostomy or colostomy is required, one should inspect it daily to ensure that it is viable. If the patient develops high-grade fever, the wound should be inspected sooner to exclude an early necrotizing infection. If a wound infection is identified—as evidenced by erythema, pain along the wound, or purulent drainage—the wound should be widely opened by removing skin staples. After ensuring that the midline fascia is intact with digital palpation, the wound is initially managed with wet-to-dry dressing changes. The most common intra-abdominal complications are anastomotic failure and abscess. The choice between percutaneous and operative therapy is based on the location, timing, and extent of the collection.

Abdominal Compartment Syndrome

The abdominal compartment syndrome is classified as pathologic intra-abdominal hypertension due to intra-abdominal injury (primary) or splanchnic reperfusion after massive resuscitation (secondary). Secondary abdominal compartment syndrome may result from any condition requiring extensive crystalloid resuscitation, including extremity trauma, chest trauma, or even postinjury sepsis. The sources of increased intra-abdominal pressure include gut edema, ascites, bleeding, and packs. A diagnosis of intra-abdominal hypertension cannot reliably be made by physical examination; therefore, it is obtained by measuring the intraperitoneal pressure. The most common technique is to measure the patient’s bladder pressure. Fifty milliliters of saline is instilled into the bladder via the aspiration port of the Foley catheter with the drainage tube clamped, and a three-way stopcock and water manometer is placed at the level of the pubic symphysis. Bladder pressure is then measured on the manometer in centimeters of water (Table 7-12) and correlated with the physiologic impact of abdominal compartment syndrome. Conditions in which the bladder pressure is unreliable include bladder rupture, external compression from pelvic packing, neurogenic bladder, and adhesive disease.

Increased abdominal pressure affects multiple organ systems (Fig. 7-73). Abdominal compartment syndrome, as noted earlier, is defined as intra-abdominal hypertension sufficient to produce physiologic deterioration and frequently manifests via such end-organ sequelae as decreased urine output, increased pulmonary inspiratory pressures, decreased cardiac preload, and increased cardiac afterload. Because any of these clinical symptoms of abdominal compartment syndrome may be attributed to the primary injury, a heightened awareness of this syndrome must be maintained. Organ failure can occur over a wide range of recorded bladder pressures. Generally, no specific bladder pressure prompts therapeutic intervention, except when the pressure is >35 mm Hg. Rather, emergent decompression is carried out when intra-abdominal hypertension reaches a level at which end-organ dysfunction occurs. Mortality is directly affected by the timing of decompression, with 60% mortality in patients undergoing presumptive decompression, 70% mortality in patients with a delay in decompression, and nearly uniform mortality in those not undergoing decompression. Usually decompression is performed operatively, either in the ICU if the patient is hemodynamically unstable or in the OR. ICU bedside laparotomy is easily accomplished, avoids transport of hemodynamically compromised patients, and requires minimal equipment (e.g., scalpel, suction device, cautery, and dressings for temporary abdominal closure). In patients with significant intra-abdominal fluid as the primary component of abdominal compartment syndrome, rather than bowel or retroperitoneal edema, decompression can be accomplished effectively via a percutaneous drain. This method is particularly applicable for nonoperative management of major liver injuries. These patients are identified by bedside ultrasound, and the morbidity of a laparotomy is avoided. When operative decompression is required with egress of the abdominal contents, temporary coverage is obtained using a subfascial 45 × 60 cm sterile drape and Ioban application (see Fig. 7-50).

The performance of damage control surgery and recognition of abdominal compartment syndrome have dramatically improved patient survival, but at the cost of an open abdomen. Several management points deserve attention. Despite having a widely open abdomen, patients can develop recurrent abdominal compartment syndrome, which increases their morbidity and mortality; therefore, bladder pressure should be monitored every 4 hours, with significant increases in pressures alerting the clinician to the possible need for repeat operative decompression. Patients with an open abdomen lose between 500 and 2500 mL per day of abdominal effluent. Appropriate volume compensation for this albumin-rich fluid remains controversial, with regard to both the amount administered (replacement based on clinical indices vs. routine ½ mL replacement for every milliliter lost) as well as the type of replacement (crystalloid vs. colloid).

Following resuscitation and management of specific injuries, the goal of the operative team is to close the abdomen as quickly as possible. Multiple techniques have been introduced to obtain fascial closure of the open abdomen to minimize morbidity and cost of care. Historically, for patients who could not be closed at repeat operation, approximation of the fascia with mesh (prosthetic or biologic) was used, with planned reoperation. Another option was split-thickness skin grafts applied directly to the exposed bowel for coverage; removal of the skin grafts was planned 9 to 12 months after the initial surgery, with definitive repair of the hernia by component separation. However, delayed abdominal wall reconstruction was resource invasive, with considerable patient morbidity. The advent of VAC technology has revolutionized fascial closure. The authors currently use a sequential closure technique with the wound VAC device that is based on constant fascial tension and return to the OR every 48 hours until closure is complete (Fig. 7-74). ¹²⁸ The authors’ success rate with this approach exceeds 95%. This is important because among patients not attaining fascial closure, 20% suffer GI tract complications that prolong their hospital course. These include intra-abdominal abscess, enteric fistula, and bowel perforations (Fig. 7-75). Management requires frequent operative or percutaneous drainage of abscesses, control of fistulas, and prolonged nutritional support.

Pregnant Patients

During pregnancy, 7% of women are injured. Motor vehicle collisions and falls are the leading causes of injury, accounting for 70% of cases. Fetal death after trauma most frequently occurs after motor vehicle collisions, but only 11% of fetal deaths are due to the death of the mother; therefore, early trauma resuscitation and management is directed not only at the mother but also at the fetus. Domestic violence is also common, affecting between 10% and 30% of pregnant women and resulting in fetal mortality of 5%.

Pregnancy results in physiologic changes that may impact postinjury evaluation (Table 7-13). Heart rate increases by 10 to 15 beats per minute during the first trimester and remains elevated until delivery. Blood pressure diminishes during the first two trimesters due to a decrease in systemic vascular resistance and rises again slightly during the third trimester (mean values: first = 105/60, second = 102/55, third = 108/67). Intravascular volume is increased by up to 8 L, which results in a relative anemia but also a relative hypervolemia. Consequently a pregnant woman may lose 35% of her blood volume before exhibiting signs of shock. Pregnant patients have an increase in tidal volume and minute ventilation but a decreased functional residual capacity; this results in a diminished Pco₂ and respiratory alkalosis. Also, pregnant patients may desaturate more rapidly, particularly in the supine position and during intubation. Supplemental oxygen is always warranted in the trauma patient but is particularly critical in the injured pregnant patient, because the oxygen dissociation curve is shifted to the left for the fetus compared to the mother (i.e., small changes in maternal oxygenation result in larger changes for the fetus because the fetus is operating in the steep portions of the dissociation curve). Anatomic changes contribute to these pulmonary functional alterations and are relevant in terms of procedures. With the gravid uterus enlarged, DPL should be performed in a supraumbilical site with the catheter directed cephalad. In addition, the upward pressure on the diaphragm calls for caution when placing a thoracostomy tube; standard positioning may result in an intra-abdominal location or perforation of the diaphragm.

Other physiologic changes during pregnancy affect the GI, renal, and hematologic systems. The lower esophageal sphincter has decreased competency, which increases the risk for aspiration. Liver function test values increase, with the alkaline phosphatase level nearly doubling. The high levels of progesterone impair gallbladder contractions, which results in bile stasis and an increased incidence of gallstone formation; this may not affect the trauma bay evaluation but becomes important in a prolonged ICU stay. Plasma albumin level decreases from a normal of around 4.3 g/dL to an average of 3.0 g/dL. Renal blood flow increases by 30% during pregnancy, which causes a decrease in serum level of blood urea nitrogen and creatinine. The uterus may also compress the ureters and bladder, causing hydronephrosis and hydroureter. Finally, as noted earlier there is a relative anemia during pregnancy, but a hemoglobin level of <11 g/dL is considered abnormal. Additional hematologic changes include a moderate leukocytosis (up to 20,000 mm³) and a relative hypercoagulable state due to increased levels of factors VII, VIII, IX, X, and XII and decreased fibrinolytic activity.

During evaluation in the ED, the primary and secondary surveys commence, with mindfulness that the mother always receives priority while conditions are still optimized for the fetus.¹²⁹ This management includes provision of supplemental oxygen (to prevent maternal and fetal hypoxia), aggressive fluid resuscitation (the hypervolemia of pregnancy may mask signs of shock), and placement of the patient in the left lateral decubitus position (or tilting of the backboard to the left) to avoid caval compression. Assessment of the fetal heart rate is the most valuable information regarding fetal viability. Fetal monitoring should be performed with a cardiotocographic device that measures both contractions and fetal heart tones (FHTs). Because change in heart rate is the primary response of the fetus to hypoxia or hypotension, anything above an FHT of 160 is a concern, whereas bradycardia (FHT of <120) is considered fetal distress. Ideally, if possible, a member of the obstetrics team should be present during initial evaluation to perform a pelvic examination using a sterile speculum. Vaginal bleeding can signal early cervical dilation and labor, abruptio placentae, or placenta previa. Amniotic sac rupture can result in prolapse of the umbilical cord with fetal compromise. Strong contractions are associated with true labor and should prompt consideration of delivery and resuscitation of the neonate. Focused prenatal history taking should elicit a history of pregnancy-induced hypertension, gestational diabetes, congenital heart disease, preterm labor, or placental abnormalities. Asking the patient when the baby first moved and if she is currently experiencing movement of the fetus is important. Determining fetal age is key for considerations of viability. Gestational age may be estimated by noting fundal height, with the fundus approximating the umbilicus at 20 weeks and the costal margin at 40 weeks. Discrepancy in dates and size may be due to uterine rupture or hemorrhage.

Initial evaluation for abdominopelvic trauma in pregnant patients should proceed in the standard manner. Ultrasound (FAST) of the abdomen should evaluate the four windows (pericardial, right and left upper quadrant, and bladder) and additionally assess FHTs, fetal movement, and sufficiency of amniotic fluid. DPL can be performed in pregnant women via a supraumbilical, open technique. Trauma radiography of pregnant patients presents a conundrum. Radiation damage has three distinct phases of damage and effect: preimplantation, during the period of organogenesis from 3 to 16 weeks, and after 16 weeks. Generally, it is accepted that “safe” doses of radiation from radiography are <5 rad.¹³⁰ A chest radiograph results in a dose of 0.07 mrad; CT scan of the chest, <1 rad; and CT scan of the abdomen, 3.5 rad. It is important, therefore, to limit radiographs to those that are essential and to shield the pelvis with a lead apron when possible. If clinically warranted, however, a radiograph should be obtained.

The vast majority of injuries are treated similarly whether the patient is pregnant or not. Following standard protocols for nonoperative management of blunt trauma avoids the risks associated with general anesthesia. A particular challenge in the pregnant trauma patient is a major pelvic fracture. Because uterine and retroperitoneal veins may dilate to 60 times their original size, hemorrhage from these vessels may be torrential. Fetal loss may be related to both maternal shock and direct injury to the uterus or fetal head. Penetrating injuries in this patient population also carry a high risk. The gravid uterus is a large target, and any penetrating injury to the abdomen may result in fetal injury depending on trajectory and uterine size. Gunshot wounds to the abdomen are associated with a 70% injury rate to the uterus and 35% mortality rate of the fetus. If the bullet traverses the uterus and the fetus is viable, cesarean section should be performed. On the other hand, stab wounds do not often penetrate the thick wall of the uterus. Indications for emergent cesarean section include: (a) severe maternal shock or impending death (if the fetus is delivered within 5 minutes, survival is estimated at 70%), (b) uterine injury or significant fetal distress (anticipated survival rates of >70% if FHTs are present and fetal gestational age is >28 weeks).¹³¹

Any patient with a viable pregnancy should be monitored after trauma, with the length of monitoring determined by the injury mechanism and patient physiology. Patients who are symptomatic, defined by the presence of uterine irritability or contractions, abdominal tenderness, vaginal bleeding, or blood pressure instability, should be monitored in the hospital for at least 24 hours. In addition, patients at high risk for fetal loss (those experiencing vehicle ejection or involved in motorcycle or pedestrian collisions and those with maternal tachycardia, Injury Severity Score of >9, gestational period of >35 weeks, or history of prior assault) also warrant careful monitoring.¹³² Patients without these risk factors who are asymptomatic can be monitored for 6 hours in the ED and sent home if no problems develop. They should be counseled regarding warning signs that mandate prompt return to the ED.

Geriatric Patients

Elderly trauma patients (>65 years of age) are hospitalized twice as often as those in any other age group, and this population accounts for one quarter of all trauma admissions. Although the physiology of aging separates older trauma patients from the younger generation (Table 7-14), treatment must remain individualized (some octogenarians look and physiologically act 50 years old, whereas others appear closer to 100 years). No chronologic age is associated with a higher morbidity or mortality, but a patient’s comorbidities do impact the individual’s postinjury course and outcome. For example, recognition that a patient is taking beta blockers affects the physician’s evaluation of vital signs in the ED and impacts treatment course in the ICU. Early monitoring of arterial blood gas values will identify occult shock. A base deficit of >6 mmol/L is associated with a twofold higher risk of mortality in patients over the age of 55 than in younger patients (67% vs. 30%).¹³³

Although the published literature on geriatric traumatic brain injury is relatively sparse and uncontrolled with regard to management, some interesting points are noted. First, outcomes are worse in this age group than in their younger counterparts. Based on data from the Traumatic Coma Databank, mortality in patients with severe head injury more than doubles after the age of 55. Moreover, 25% of patients with a normal GCS score of 15 had intracranial bleeding, with an associated mortality of 50%.¹²³ Just as there is no absolute age that predicts outcome, admission GCS score is a poor predictor of individual outcome. Therefore, the majority of trauma centers advocate an initial aggressive approach with re-evaluation at the 72-hour mark to determine subsequent care.

One of the most common sequelae of blunt thoracic trauma is rib fractures. In the aging population, perhaps due to osteoporosis, less force is required to cause a fracture. In fact, in one study, 50% of patients >65 years old sustained rib fractures from a fall of <6 ft, compared with only 1% of patients <65 years of age. Concurrent pulmonary contusion is noted in up to 35% of patients, and pneumonia complicates the injuries in 10% to 30% of patients with rib fractures, not surprisingly leading to longer ICU stays.^135,136 Additionally, mortality increases linearly with the number of rib fractures. Patients who sustain more than six rib fractures have pulmonary morbidity rates of >50% and overall mortality rates of >20%.

Chronologic age is not the best predictor of outcome, but the presence of pre-existing conditions, which affect a patient’s physiologic age, is associated with increased mortality rates. Injury Severity Score is probably the best overall predictor of patient outcome in the elderly; however, for any given individual its sensitivity may not be precise, and there is a time delay in obtaining sufficient information to calculate the final score. In addition to pre-existing conditions and severity of injury, the occurrence of complications compounds the risk for mortality.

Pediatric Patients

Twenty million children, or almost one in four children, are injured each year, with an associated cost of treating the injured child of $16 billion per year. Injury is the leading cause of death among children over the age of 1 year, with 15,000 to 25,000 pediatric deaths per year. Disability after traumatic injury is more devastating, with rates 3 to 10 times that of the death rate. Pediatric trauma involves different mechanisms, different constellations of injury, and the potential for long-term problems related to growth and development. As with adult trauma, over 85% of pediatric trauma has a blunt mechanism, with boys injured twice as often as girls.¹³⁷ Falls are the most common cause of injury in infants and toddlers. In children, bicycle mishaps are the most common cause of severe injury, whereas motor vehicle-related injury predominates in adolescence. Although unintentional injuries are by far the most common type of injuries in childhood, the number of intentional injuries, such as firearm-related injury and child abuse, is increasing.

ED preparation for the pediatric trauma patient includes assembling age-appropriate equipment (e.g., intubation equipment; IV catheters, including intraosseous needles and 4F single-lumen lines), laying out the Broselow Pediatric Emergency Tape (which allows effective approximation of the patient’s weight, medication doses, size of endotracheal tube, and chest tube size), and turning on heat lamps. Upon the pediatric patient’s arrival, the basic tenets of the ABCs apply, with some caveats. In children, the airway is smaller and more cephalad in position compared with that of adults, and in children younger than 10 years, the larynx is funnel shaped rather than cylindrical as in adults. Additionally, the child’s tongue is much larger in relation to the oropharynx. Therefore, a small amount of edema or obstruction can significantly reduce the diameter of the airway (thus increasing the work of breathing), and the tongue may posteriorly obstruct the airway, causing intubation to be difficult. During intubation, a Miller (straight) blade rather than a Macintosh (curved) blade may be more effective due to the acute angle of the cephalad, funnel-shaped larynx. Administration of atropine before rapid-sequence intubation will prevent bradycardia. Adequate ventilation is critical, because oxygen consumption in infants and young children is twice that in adults; onset of hypoxemia, followed by cardiac arrest, may be precipitous. Because gastric distension can inhibit adequate ventilation, placement of a nasogastric tube may facilitate effective gas exchange. Approximately one third of preventable deaths in children are related to airway management; therefore, if airway control cannot be obtained using a standard endotracheal method, surgical establishment of an airway should be considered. In children older than 11 years, standard cricothyroidotomy is performed. Due to the increased incidence of subglottic stenosis in younger patients, needle cricothyroidotomy with either a 14- or 16-gauge catheter is advocated, although it is rarely used. Alternatively, tracheostomy may be performed. In children, the standard physiologic response to hypovolemia is peripheral vasoconstriction and reflex tachycardia; this may mask significant hemorrhagic injury, because children can compensate for up to a 25% loss of circulating blood volume with minimal external signs. “Normal” values for vital signs should not necessarily make one feel more secure about the child’s volume status. Volume restoration is based on the child’s weight; two to three boluses of 20 mL/kg of crystalloid is appropriate.

After initial evaluation based on the trauma ABCs, identification and management of specific injuries proceeds. Acute traumatic brain injury is the most common cause of death and disability in any pediatric age group. Although falls are the most common mechanism overall, severe brain injury most often is due to child abuse (in children <2 years) or motor vehicle collisions (in those >2 years). Head CT should be performed to determine intracranial pathology, followed by skull radiography to diagnose skull fractures. As in adults, CPP is monitored, and appropriate resuscitation is critical to prevent the secondary insults of hypoxemia and hypovolemia. Although some data indicate that the pediatric brain recovers from traumatic injury better than the adult brain, this advantage may be eliminated if hypotension is allowed to occur.

As is true in adults, the vast majority of thoracic trauma is also blunt. However, because a child’s skeleton is not completely calcified, it is more pliable. Significant internal organ damage may occur without overlying bony fractures. For example, adult patients with significant chest trauma have a 70% incidence of rib fractures, whereas only 40% of children with significant chest trauma do. Pneumothorax is treated similarly in the pediatric population; patients who are asymptomatic with a pneumothorax of <15% are admitted for observation, whereas those who have a pneumothorax of >15% or who require positive pressure ventilation undergo tube decompression. Presence of a hemothorax in this age group may be particularly problematic, because the child’s chest may contain his or her entire blood volume. If the chest tube output is initially 20% of the patient’s blood volume (80 mL/kg) or is persistently >1 to 2 mL/kg per hour, thoracotomy should be considered. Aortic injuries are rare in children, and tracheobronchial injuries are more amenable to nonoperative management. Thoracic injuries are second only to brain injuries as the main cause of death according to the National Pediatric Trauma Registry; however, the overall mortality rate of 15% correlates with the levels in many adult studies.

The evaluation for abdominal trauma in the pediatric patient is similar to that in the adult. FAST is valid in the pediatric age group to detect intra-abdominal fluid.¹³⁸ The mechanism of injury often correlates with specific injury patterns. A child sustaining a blow to the epigastrium (e.g., hitting the handlebars during a bike accident) should be evaluated for a duodenal hematoma and/or a pancreatic transection. After a motor vehicle collision in which the patient was wearing a passenger restraint, injuries comprising the “lap belt complex” or “seat belt syndrome” (i.e., abdominal wall contusion, small bowel perforation, flexion-distraction injury of the lumbar spine, diaphragm rupture, and occasionally abdominal aortic dissection) may exist. Nonoperative management of solid organ injuries, first used in children, is the current standard of care in the hemodynamically stable patient. If the patient shows clinical deterioration or hemodynamic lability, has a hollow viscus injury, or requires >40 mL/kg of packed RBCs, continued nonoperative management is not an option. Success rates of nonoperative management approach 95%, with an associated 10% to 23% transfusion rate. Blood transfusion rates, however, are significantly lower in patients managed nonoperatively than in patients undergoing operation (13% vs. 44%).¹³⁹