In most situations, a brief history is obtained from prehospital personnel via radio communication or when the patient arrives at the hospital. In the case of motor vehicle crashes, for example, it is important to determine the circumstances of the injury, including the speed of impact, the condition of the vehicle, the position of the patient at the scene, type of restraint systems present, evidence of blood loss, and the condition of other passengers. The time that the injury occurred and the treatment rendered while en route is recorded. Knowing the mechanism of injury often gives a clue to concealed trauma. Information regarding serious underlying medical problems should be sought from Medic Alert bracelets or wallet cards. If the patient is conscious and stable, the examiner should obtain a complete history and use this information to direct the examination in order to avoid unnecessary tests.
Trauma victims require a precise, rapid, systematic approach to initial evaluation in order to ensure their survival. The ATLS system developed by the ACS Committee on Trauma represents the best current approach to the severely injured patient. The sequence of evaluation includes primary survey, resuscitation, secondary survey, and definitive management. The primary survey attempts to identify and treat immediate life-threatening conditions. Resuscitation is performed, and the response to therapy is evaluated. The secondary survey includes a comprehensive physical examination designed to detect all injuries and establish a treatment priority for potentially life-threatening and/or limb-threatening ones. During the primary and secondary surveys, appropriate laboratory and imaging studies are performed to aid in the identification of injuries and prepare the patient for definitive care.
The ATLS manual and provider course published by the ACS Committee on Trauma is the accepted guideline for the primary survey. The primary survey is a rapid assessment to detect life-threatening injuries following the ABCDE: airway, breathing, circulation, disability, and exposure/environment.
The establishment of an adequate airway has the highest priority in the primary survey. Oxygen by high-flow nasal cannula (10-12 L/min), 100% nonrebreather mask, or bag-mask ventilation with pulse oximetry should be started if not already in place. Maneuvers used in the trauma patient to establish an airway must consider a possible cervical spine injury. Any patient with multisystem trauma, especially those with an altered level of consciousness or blunt trauma above the clavicles, should be assumed to have a cervical spine injury. The rapid assessment for signs of airway obstruction should include inspection for foreign bodies and facial, jaw, or tracheal/laryngeal fractures that may result in acute loss of airway patency. Techniques that can be used to establish a patent airway while protecting the cervical spine include the chin lift or jaw thrust maneuvers (Figure 13–3).
Relief of airway obstruction.
Patients who can communicate verbally without difficulty are unlikely to have an impaired airway. Repeated assessment of airway patency is always prudent. Those patients with severe head injury, altered level of consciousness, or Glasgow Coma Scale (GCS) score 8 or less usually require placement of a definitive airway. Orotracheal or nasotracheal intubation can be attempted with cervical spine precautions if a second person maintains axial immobilization of the head to prevent destabilization of the spine (Figure 13–4). If ventilatory failure occurs and an adequate airway cannot be obtained readily by orotracheal or nasotracheal intubation, surgical cricothyroidotomy should be performed as rapidly as possible (Figure 13–5).
A. Nasotracheal intubation. B. Orotracheal intubation.
Once the airway has been established, it is necessary to ensure that oxygenation and ventilation is adequate. Examine the patient to determine the degree of chest expansion, breath sounds, tachypnea, crepitus from rib fractures, subcutaneous emphysema, and the presence of penetrating or open wounds. Immediately life-threatening pulmonary injuries that must be detected and treated promptly include tension pneumothorax, open pneumothorax, flail chest, and massive hemothorax. Chest injury has the second highest case fatality rate in the trauma patient. The following are examples of life-threatening pulmonary injuries and their treatment:
This condition occurs when air becomes trapped in the pleural space under pressure. The harmful effects result primarily from shift of the mediastinum, impairment of venous return, and potential occlusion of the airway. Tension pneumothorax is difficult to diagnose even when the patient reaches the hospital. The clinical findings consist of hypotension in the presence of distended neck veins, decreased or absent breath sounds on the affected side, hyperresonance to percussion, and tracheal shift away from the affected side. These signs may be difficult to detect in a hypovolemic patient with a cervical collar in place. Cyanosis may be a late manifestation. Emergency treatment consists of insertion of a large-bore needle or plastic intravenous cannula (angiocath) through the chest wall into the pleural space in the second intercostal space along the midclavicular line to relieve the pressure and convert the tension pneumothorax to a simple pneumothorax. The needle or cannula should be left in place until a thoracostomy tube is inserted for definitive management (Figure 13–6).
This condition results from an open wound of the chest wall with free communication between the pleural space and the atmosphere. The resulting impairment of the thoracic bellows, and its ability to expand the lung results in inadequate ventilation. With chest expansion during a breath, air moves in and out of the chest wall opening instead of through the trachea, producing hypoventilation that can be rapidly fatal. Emergency treatment consists of sealing the wound with an occlusive sterile dressing taped on three sides to act as a flutter-type valve or with any material if nothing sterile is available. Definitive treatment requires placement of a chest tube to reexpand the lung and surgical closure of the defect. Airway intubation with positive-pressure mechanical ventilation can be helpful in massive open pneumothorax.
Multiple rib fractures resulting in a free-floating segment of chest wall may produce paradoxical motion that impairs lung expansion (Figure 13–7). In patients with flail chest, injury-associated pulmonary contusion is common and is often the major cause of respiratory failure. The injury is identified by careful inspection and palpation during physical examination. Patients with large flail segments will almost always require endotracheal intubation and mechanical ventilation both to stabilize the flail segment and to optimize gas exchange. Smaller flail segments may be well tolerated if supplemental oxygen and adequate analgesia are provided. The work of breathing is increased considerably, and many patients who initially appear to be compensating well may suddenly deteriorate a few hours later. Therefore, most patients with flail chest require monitoring in an intensive care unit (ICU).
Relief of pneumothorax. Tension pneumothorax must be immediately decompressed by a needle introduced through the second anterior intercostal space. A chest tube is usually inserted in the midaxillary line at the level of the nipple and is directed posteriorly and superiorly toward the apex of the thorax. The tube is attached to a “three-bottle” suction device, and the rate of escape of air is indicated by the appearance of bubbles in the second of the three bottles. Cessation of bubbling suggests that the air leak has become sealed.
Free hemorrhage from accessible surface wounds is usually obvious and can be controlled in most cases by local pressure and elevation of the bleeding point. Firm and precise pressure on the major artery in the axilla, antecubital space, wrist, groin, popliteal space, or at the ankle may suffice for temporary control of arterial hemorrhage distal to these points. When all other measures have failed, a tourniquet may be necessary to control major hemorrhage from extensive wounds or major vessels in an extremity. Failure to manage a tourniquet properly may cause irreparable vascular or neurologic damage. For this reason, the tourniquet should be used only when necessary and must be kept exposed and loosened at least every 20 minutes for 1 or 2 minutes while the patient is in transit. Transport to definitive care where the tourniquet can be safely removed and treatment rendered should be a top priority. It is wise to write the time of tourniquet application in military time on the patient’s forehead with a skin-marking pen or on adhesive tape.
Vascular Access & Resuscitation
All patients with significant trauma should have large-caliber peripheral intravenous catheters inserted immediately for administration of crystalloid fluids as needed. If any degree of shock is present, at least two 14-16 gauge peripheral intravenous lines should be established usually in the antecubital fossa. If venous access cannot be obtained by percutaneous peripheral or central venous cannulation, an intraosseous line in the tibia or other uninjured site should be placed. A venous cutdown of the saphenous vein at the ankle using an angiocath or intravenous extension tubing with the tip cut off can be performed, but is a difficult procedure in the field. A blood sample for type and cross-match should be sent from the venous line, if not already drawn.
As soon as the first intravenous line is inserted, rapid crystalloid infusion should begin. Adult patients should be given 2 L of Ringer lactate or normal saline. For children, the initial administered crystalloid volume should be 20 mL/kg. Patients who experience a transient response should receive an additional infusion of 2 L of crystalloid. Patients in hemorrhagic shock for whom there is no improvement in blood pressure from initial crystalloid infusion or who transiently respond but fail a second crystalloid bolus should be switched to resuscitation with blood products. Beyond the administration of the first two units of packed red blood cells (PRBC), it is important to also administer fresh plasma or thawed fresh frozen plasma (FFP) to avoid coagulopathy in the massively transfused patient. Massive transfusion is defined as at least 10 units of PRBC. The exact ratio of FFP to PRBC is still under active investigation, but a target range of 1:1 or 2:3 is considered acceptable. Military data has shown that the early use of plasma can reduce mortality by up to 50% in the massively transfused trauma patient. Giving platelets as part of the massive transfusion protocol is also supported by military data demonstrating a 20% reduction in mortality for patients who received platelets as fresh whole blood or apheresis platelets in conjunction with PRBC. The exact platelet-to-PRBC ratio for optimal treatment of the hemorrhaging trauma patient is not known, but giving a unit of platelets for every five units of PRBC is a reasonable ratio. Type O, Rh-negative PRBC should be immediately available in the emergency department for any patient with impending cardiac arrest or massive hemorrhage. Some high-volume trauma centers now also stock fresh or “prethawed” AB plasma as well. Type-specific blood should be available within 15-20 minutes of patient arrival to the hospital.
Tranexamic acid is an antifibrinolytic agent which inhibits the breakdown of clotted blood. It does not promote new blood clot formation. Two large clinical trials, one in the military setting and another in civilian population, have demonstrated the efficacy of tranexamic acid when utilized as part of a blood product resuscitation strategy in patients with traumatic hemorrhage. The survival benefit is greatest in patients who received massive transfusion and those in whom early treatment was accomplished (≤ 1 hour after injury). Tranexamic acid started greater than 3 hours after injury increased the risk of death due to bleeding and is likely ineffective. Dosing is typically 1 g intravenously over 10 minutes, followed by a drip infusion of an additional 1 g over 8 hours.
Transfusion of blood products is not without risk. Despite rigorous screening programs, transmission of viral blood-borne diseases can occur. The current incidence of blood-borne pathogen transmission following red blood cell transfusion are hepatitis B, 1:350,000; hepatitis C 1:400,000; and HIV, 1:2 million. Transfusion of blood products is also associated with transfusion-related immunomodulation and transfusion-related acute lung injury. Both of these problems can increase morbidity and mortality. The storage age of blood transfused can also contribute to problems. Transfusion of a patient with older units of PRBC has been shown to cause generation of systemic proinflammatory mediators and increase the risk of wound infection.
As intravenous access is obtained, electrocardiogram leads for continuous cardiac monitoring should be placed. Noninvasive blood pressure measurements should be acquired with a time-cycled blood pressure cuff. Pulse oximetry is valuable in ensuring that adequate hemoglobin oxygen saturation is present in the injured patient. Temperature is a crucial vital sign, and it should be measured and recorded along with the first pulse and blood pressure in the emergency department.
A brief neurologic examination should be documented to assess patients’ degree of neurologic impairment. Many factors may contribute to altered levels of consciousness and should be considered in addition to central nervous system injury in all trauma patients. Other than the direct trauma, the most common contributing causes of altered mental status for trauma patients are alcohol intoxication, other central nervous system stimulants or depressants, diabetic ketoacidosis, cerebrovascular accident, and hypovolemic shock. Less common causes are epilepsy, eclampsia, electrolyte imbalances associated with metabolic and systemic diseases, anaphylaxis, heavy metal poisoning, electric shock, tumors, severe systemic infections, hypercalcemia, asphyxia, heat stroke, severe heart failure, and hysteria. These uncommon causes of coma or diminished mental status should be considered if routine testing such as blood alcohol and glucose level, urine toxicology, and head computerized tomography (CT) scanning are unrevealing as to the etiology of mental impairment. In such cases, further laboratory and diagnostic testing may be warranted.
The differential diagnosis depends upon a careful history and complete physical examination, with particular attention to the neurologic examination with documentation of the patient’s GCS score (Table 13–1), and an urgent head CT scan. The GCS score is useful in monitoring acute changes in neurologic function and is used for prognosticating outcomes after severe head injury. The motor component of the GCS score is the most accurate for predicting outcome and has a linear relationship with mortality. Lateralizing signs may also suggest evidence of an intracranial mass effect or carotid or vertebral artery injury, while loss of distal motor and/or sensory function may help localize potential spinal cord injuries.
Table 13–1.Glasgow Coma Scale score. ||Download (.pdf) Table 13–1. Glasgow Coma Scale score.
|Parameter ||Score |
|Best motor response |
|Normal ||6 |
|Localizes ||5 |
|Withdraws ||4 |
|Flexion ||3 |
|Extension ||2 |
|None ||1 |
|Best verbal response |
|Oriented ||5 |
|Confused ||4 |
|Verbalizes ||3 |
|Vocalizes ||2 |
|None ||1 |
|Eye opening |
|Spontaneous ||4 |
|To command ||3 |
|To pain ||2 |
|None ||1 |
All clothing should be removed (cut off with trauma shears, usually) from the seriously injured patient, with care taken to avoid unnecessary movement. The removal of helmets or other protective clothing may require additional personnel to stabilize the patient and prevent further injury. All skin surfaces should be examined to identify occult injuries that may not be readily apparent, such as posterior penetrating trauma or open fractures. After inspecting all surfaces, warm blankets or warming devices should be placed to avoid hypothermia in the seriously injured patient.
EMERGENCY ROOM THORACOTOMY
Certain injuries are so critical that operative treatment must be undertaken as soon as the diagnosis is made. In these cases, resuscitation is continued as the patient is being operated on. For cardiopulmonary arrest that occurs in the emergency room as a direct result of trauma, external cardiac compression is rarely successful in maintaining effective perfusion of vital organs. An emergency left anterolateral thoracotomy should be performed in the fourth or fifth intercostal space, and the pericardium should be opened anterior to the phrenic nerve (Figure 13–8). Open cardiac massage, cross-clamping of the descending thoracic aorta, repair of cardiac injuries, and internal defibrillation can be performed as appropriate. Wounds of the lung producing severe hemorrhage or systemic air embolus may require pulmonary hilar cross-clamping.
Emergency thoracotomy and open cardiac massage.
Emergency room thoracotomy is most useful for cardiac arrest due to penetrating thoracic trauma, particularly in patients with pericardial tamponade from stab wounds. This extreme procedure is ineffective for most patients with cardiac arrest due to blunt trauma and for all patients who have no detectable vital signs in the field (< 1% survival). If vital signs are present in the emergency room but arrest appears imminent, the patient should be transferred rapidly to the operating room if at all possible, since conditions in the operating room are optimal for surgical intervention.
Shock is defined as inadequate end-organ tissue perfusion. Some degree of shock accompanies most severe injuries and is manifested initially by pallor, cold sweat, weakness, lightheadedness, tachycardia, hypotension, thirst, air hunger, and, eventually, loss of consciousness. Patients with any of these signs should be presumed to be in shock and evaluated thoroughly. All patients determined to be in any degree of shock should be reexamined at regular intervals. The degree of shock has been categorized to guide resuscitation and help caregivers recognize the severity of symptoms (Table 13–2).
Table 13–2.Classification of hypovolemic shock. ||Download (.pdf) Table 13–2. Classification of hypovolemic shock.
| ||Class I ||Class II ||Class III ||Class IV |
|Blood loss (mL) ||Up to 750 ||750–1500 ||1500–2000 ||> 2000 |
|Blood loss (% BV) ||Up to 15% ||15–30% ||30–40% ||> 40% |
|Pulse rate (beats/min) ||< 100 ||> 100 ||> 120 ||> 140 |
|Blood pressure ||Normal ||Minimal decrease ||Decreased ||Significantly decreased |
|Pulse pressure ||Normal ||Narrowed ||Narrowed ||Unobtainable or very narrow |
|Hourly urine output ||≥ 0.5 mL/kg ||≥ 0.5 mL/kg ||< 0.5 cc/kg ||Minimal |
|CNS/mental status ||Slightly anxious ||Mildly anxious ||Anxious & confused ||Confused or lethargic |
Hypovolemic shock is due to loss of whole blood or plasma. Blood pressure may be maintained initially by vasoconstriction. Tissue hypoxia increases when hypotension ensues, and shock may become irreversible if irreparable damage occurs to the vital organs. Massive or prolonged hemorrhage, severe crush injuries, major fractures, and extensive burns are the most common causes. The presence of any of these conditions is an indication for prompt intravenous fluid infusion.
In mild or class 1 shock (< 15% blood volume loss), compensatory mechanisms may preserve adequate perfusion, and no skin or physiologic changes may be apparent. In moderate or class 2 shock (15%-30% blood loss), the skin on the extremities becomes pale, cool, and moist as a result of vasoconstriction and release of epinephrine. Systolic blood pressure is often maintained at near-normal levels, but urine output will usually decrease. With severe or class 3 shock (30%-40% blood volume loss), these changes—particularly diaphoresis—become more marked, and urine output declines significantly. Hypotension ensues. In addition, changes in cerebral function become evident consisting chiefly of agitation, disorientation, and memory loss. A common error is to attribute uncooperative behavior to intoxication, drug use, or brain injury when in fact it may be due to cerebral ischemia from blood loss. With class 4 shock (> 40% blood volume loss), profound hypotension is typically accompanied by loss of consciousness and anuria. In this situation, rapid resuscitation with crystalloid and blood products is necessary to prevent imminent death.
With any degree of shock, intravenous balanced salt solution (eg, lactated Ringer solution) should be given rapidly until the signs of shock abate and urine output returns to normal. If shock appears to be due to blood loss, blood transfusion should be given, starting with two units of uncross-matched O-negative blood if cross-matched blood is unavailable. Additional resuscitation with crystalloid and/or blood products is guided by the cause of volume loss and response to fluid administration. Successful resuscitation is indicated by warm, dry, well-perfused skin, a urine output of 30-60 mL/h, and an alert sensorium. Improvement in pH toward normal, correction of lactic acidosis, and minimization of base deficit as measured on an arterial blood gas sample are also indicators of successful resuscitation.
As a general principle, measurements of blood pressure and pulse are less reliable than changes in urine output in assessing the severity of shock. Young and athletic older patients may have compensatory mechanisms which maintain adequate blood pressure even with moderate volume loss. Older patients and those taking cardiac or blood pressure medications often do not exhibit tachycardia even with extreme volume loss. Therefore, a Foley catheter should be inserted into the bladder to monitor urine output in any patient with major injuries or shock. Oliguria is the most reliable sign of moderate shock, and successful resuscitation is indicated by a return of urine output to 0.5-1 mL/kg/h. Absence of oliguria is an unreliable index of the absence of shock if the patient has an osmotic diuresis due to alcohol, glucose, mannitol, or intravenous contrast material.
A patient who is receiving intravenous fluids at a high rate may not exhibit signs of shock even in the setting of ongoing hemorrhage. If a patient continues to require high volumes of fluid after initial resuscitation in order to maintain urine output, mental status, and blood pressure, further investigation must be performed to rule out occult hemorrhage. The patient must be kept recumbent and given reassurance and analgesics as necessary. If opioids are necessary for pain relief, they are best administered intravenously in small doses.
Neurogenic shock is due to the pooling of blood in autonomically denervated venules and small veins and is usually due to spinal cord injury. Neurogenic shock is not caused by an isolated head injury, and in those patients, other causes of shock should be sought. A patient exhibiting signs of neurogenic shock (warm and well-perfused distal extremities in the presence of hypotension) should be given a 2 L crystalloid fluid bolus—followed by an additional bolus if the response is suboptimal. If neurogenic shock persists with fluid resuscitation, phenylephrine or another vasopressor should be given as a drip with the dosage adjusted until the blood pressure is maintained at a satisfactory level. If the patient does not improve quickly, other kinds of shock must be considered. Patients with neurogenic shock may require central venous pressure monitoring to ensure an optimal volume status.
C. Cardiac Compressive Shock
Cardiac compressive shock is caused by compression of the thin-walled chambers of the heart—the atria and the right ventricle—or by compression or distortion of the great veins entering the heart. The usual causes of this type of shock in the trauma patient are pericardial tamponade, tension pneumothorax, massive hemothorax, diaphragmatic rupture with herniation of abdominal contents into the chest, and an elevated diaphragm from massive abdominal hemorrhage. Treatment consists of urgent decompression depending on the specific cause. In severe cases, emergency thoracotomy may be necessary to restore adequate cardiac function.
Cardiogenic shock is caused by decreased myocardial contractility and is most commonly caused by myocardial infarction or arrhythmia. Older trauma patients may develop a myocardial infarction as a complication of their injuries. On occasion an acute myocardial infarction may precede a traumatic event and be a cause of injury or loss of consciousness. Rarely, a severe myocardial contusion may lead to cardiogenic shock. Treatment is supportive, with volume replacement guided by hemodynamic monitoring and administration of inotropic agents to augment cardiac output as necessary to maintain adequate end-organ perfusion. Unfortunately, patients with traumatic injuries are not usually candidates for anticoagulant or lytic therapy, and treatment of their acute myocardial ischemia is sometimes hindered by concerns about bleeding. Echocardiography is helpful for assessment of wall motion abnormalities from severe cardiac contusion.
Immediately after intravenous catheters are placed, a blood sample should be drawn for blood typing and cross-matching. If the patient has a history of renal, hepatic, or cardiac disease or is taking diuretics or anticoagulants, serum electrolytes and coagulation parameters should be measured. In most patients with serious injuries, an arterial blood gas provides rapid data about acidosis and base deficit, both of which are markers of under-resuscitation in addition to oxygenation (Pao2) and ventilation (Paco2). Gross blood in the urine indicates the need for further diagnostic testing with abdominal CT scan or, in selected cases, a cystogram and urethrogram. Patients with obvious severe head injury, where intracranial pressure monitoring may be indicated, should have coagulation studies and a platelet count performed. Measurement of blood alcohol level and urine toxicology screen may be useful in patients with altered mental status.
Radiographic plain films of the chest and pelvis are required in all major injuries. Lateral C-spine films have been supplanted by formal CT scanning of the neck in patients with suspicion of or mechanism for cervical spine injury. Bedside focused assessment with sonography for trauma (FAST) is the preferred triage method for determining the presence of hemoperitoneum in blunt trauma patients or cardiac tamponade in blunt and penetrating trauma patients. The presence of hemoperitoneum in an unstable patient on FAST may be an indication for exploratory laparotomy. Presence of hemoperitoneum in a stable patient or a negative FAST in a patient with abdominal pain is indication for further evaluation with abdominal CT scan.
Patients who have an abnormal chest radiograph with a mechanism for blunt aortic injury should undergo further screening with either helical chest CT done at the time of abdominal imaging or with aortography, if necessary. Cervical spine CT scans should be obtained for patients who are unconscious, have pain in the cervical region, have neurologic deficits, or have painful or distracting injuries. CT scanning of the head should be performed in all patients with loss of consciousness or more serious neurologic impairment. Radiographs of the long bones and noncervical spine can usually be deferred until the more critical injuries of the thorax and abdomen have been delineated and stabilized.
2. SECONDARY SURVEY & PATTERNS OF INJURY
A rapid and complete history and physical examination are essential for patients with serious or multiple injuries. Progressive changes in clinical findings are often the key to correct diagnosis, and negative findings that change to positive may be of great importance in revising an initial clinical evaluation. This is particularly true in the case of abdominal, thoracic, and intracranial injuries, which frequently do not become manifest until hours after the trauma.
Recognition of injury patterns is also important in identifying all injuries. For example, fractures of the calcaneus resulting from a fall from a great height are often associated with central dislocation of the hip and fractures of the spine and of the skull base. A crushed pelvis is often combined with laceration of the posterior urethra or bladder, vagina, or rectum. Crush injuries of the chest are often associated with lacerations or rupture of the spleen, liver, or diaphragm. Penetrating wounds of the chest may involve not only the thoracic contents but also the abdominal viscera. These combinations occur frequently and should always be suspected.
In all cases of patients with multiple injuries, there must be a “captain of the team” who directs the resuscitation, decides which x-rays or special diagnostic tests should be obtained, and establishes priority for care by continuous consultation with other surgical specialists and anesthesiologists. A trauma surgeon or a general surgeon experienced in the care of injured patients usually has this role.
After controlling the airway if necessary, resuscitation and blood volume replacement have first priority. Deepening stupor in patients under observation should arouse suspicion of an expanding intracranial lesion requiring serial neurologic examinations and head CT. Too often, obvious signs of acute alcohol intoxication have been assumed to be the cause of unconsciousness, and intracranial hemorrhage has been overlooked.
Cerebral injuries take precedence in care when there is rapidly deepening coma. Extradural bleeding is a critical emergency, requiring operation for control of bleeding and cerebral decompression. Subdural bleeding may produce a similar emergency. If the patient’s condition permits, CT scanning should be performed for localization of the bleeding within the cranium prior to other operative interventions being initiated. In many cases of combined cerebral and abdominal injury with massive bleeding, laparotomy and craniotomy should be performed simultaneously.
Most urologic injuries are managed at the same time as associated intra-abdominal injuries. Pelvic fractures present special problems and are discussed in Chapter 40. Unless there is associated vascular injury with threatened ischemia of the limb, fractures of the long bones can be splinted and treated on an urgent basis. Open contaminated fractures should be cleansed and debrided as soon as possible. Injuries of the hand run the risk of infection that may result in a lifelong handicap without early effective treatment. Early treatment of the hand at the same time as treatment of any life-threatening injuries avoids infection and preserves the means of livelihood. Tetanus prophylaxis should be given in all instances of open contaminated wounds, puncture wounds, and burns.
Patients with a severe burden of trauma and shock may not be candidates for definitive treatment of all injuries in the immediate setting. Three physiological derangements comprise the “lethal triad” in the trauma literature: hypothermia, acidosis, and coagulopathy. These are boundaries of a patient’s physiologic envelope beyond which the patient will develop irreversible shock and eventual death. Bailing out of the abdomen with damage control maneuvers in a patient headed for the lethal triad is not a sign of defeat; instead it is usually the intelligent option. Early warning signs of physiologic compromise that could lead to the lethal triad are edema of the small bowel, midgut distension, dusky serosal surfaces, tissue that is cool to the touch, noncompliant swollen abdominal wall, diffuse oozing from surgical or raw surfaces, and lack of obvious clot formation. Successful packing relies on clot formation, so employing a strategy of early packing is recommended rather than turning to it as a last resort.
Details of definitive management of injuries are discussed in the sections on trauma that follow and in the various organ system chapters of this book.
American College of Surgeons Committee on Trauma: Advanced Trauma Life Support for Doctors Student Manual, 8th ed. Chicago, IL: American College of Surgeons, 2008.
Centers for Disease Control and Prevention: Injury Prevention and Control. Field triage. Available at http://www.cdc.gov/fieldtriage/
. Accessed August 18, 2012.
et al.: Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2): a randomized, placebo-controlled trial. Lancet. 2010;376:23.
et al.: The importance of early treatment with tranexamic acid in bleeding trauma patients: an exploratory analysis of the CRASH-2 randomised controlled trial. Lancet. 2011;377:1096.
et al.: The mortality benefit of direct trauma center transport in a regional trauma system: a population-based analysis. J Trauma Acute Care Surg. 2012;72:1510.
et al.: Military application of tranexamic acid in trauma emergency resuscitation (MATTERs) study. Arch Surg[Archives of Surgery Full Text]
All injuries to the neck are potentially life threatening because of the many vital structures in this area. Injuries to the neck are classified as blunt or penetrating, and the treatment is different for each. The patient must be examined closely for associated head and chest injuries. The initial level of consciousness is of paramount importance; progressive depression of the sensorium may signify intracranial bleeding or cerebral ischemia and requires neurosurgical evaluation. Trauma to the base of the neck may lacerate major blood vessels or have associated pneumothorax. Hemorrhage into the pleural cavity may occur suddenly as contained hematomas rupture.
Injuries to the larynx and trachea can be asymptomatic or may cause hoarseness, laryngeal stridor, or dyspnea secondary to airway compression or aspiration of blood. Subcutaneous emphysema in the neck can be present if the wall of the larynx or trachea has been disrupted.
Esophageal injuries are rarely isolated and by themselves may not cause immediate symptoms. Severe chest pain and dysphagia are characteristic of esophageal perforation. Hours later, as mediastinitis develops, progressive sepsis may occur. Mediastinitis results because the deep cervical space is in direct continuity with the mediastinum. Esophageal injuries can be recognized promptly if the surgeon is alert to the possibility and seeks out early diagnosis. Exploration of the neck, radiographic examination of the esophagus with contrast medium, and in selected cases flexible esophagoscopy confirms the diagnosis.
Cervical spine fractures and spinal cord injuries should always be suspected in deceleration injuries or following direct trauma to the neck. If the patient complains of cervical pain or tenderness or if the level of consciousness is depressed, the head and neck should be immobilized (eg, with a rigid cervical collar or sandbags) until cervical radiologic imaging can be performed to rule out a cervical fracture or ligamentous injury.
Injury to the great vessels (subclavian, common carotid, internal carotid, and external carotid arteries; subclavian, internal jugular, and external jugular veins) may follow blunt or penetrating trauma. Fractures of the clavicle or first rib may lacerate the subclavian artery and vein. With vascular injuries, the patient typically presents with visible external blood loss, neck hematoma formation, and in varying degrees of shock. Occasionally, bleeding may be contained and the injury may go undetected for a short time. Auscultation may reveal bruits that suggest arterial injury.
A. Penetrating Neck Injuries
Penetrating injuries of the neck are divided into three anatomic zones (Figure 13–9). Zone I injuries occur at the thoracic outlet, which extends from the level of the cricoid cartilage to the clavicles. Included in this area are the proximal carotid arteries, the subclavian vessels, and the major vessels of the chest. Proximal control of injuries to vascular structures in this zone often requires a thoracotomy or sternotomy. Zone II injuries occur in the area between the cricoid and the angle of the mandible. Injuries here are the easiest to expose and evaluate. Zone III injuries are between the angle of the mandible and the base of the skull. Exposure is much more difficult in this zone and in some cases may require disarticulation of the mandible. High injuries can be inaccessible, and control of hemorrhage may require ligation of major proximal vessels or angiographic embolization.
Penetrating trauma to the posterior neck may injure the vertebral column, the cervical spinal cord, the interosseous portion of the vertebral artery, and the neck musculature. Penetrating trauma to the anterior and lateral neck may injure the larynx, trachea, esophagus, thyroid, carotid arteries, subclavian arteries, jugular veins, subclavian veins, phrenic and vagus nerves, and thoracic duct.
With any penetrating cervical trauma, the likelihood of significant injury is high because there are so many vital structures in such a small space. Any patient with shock, expanding hematoma, or uncontrolled hemorrhage should be taken to the operating room for emergency exploration. The location of the injury suggests which structures may be involved. Vascular injuries at the base of the neck require thoracotomy or sternotomy to obtain proximal control of injured blood vessels before the site of probable injury is exposed. If the patient is stable after resuscitation, additional diagnostic testing may be considered.
Conventional angiography or computed tomography angiography is usually recommended for patients with stable injuries in zones I and III because precise identification of the location and extent of injury may alter the operative approach. If possible, angiography should be performed before exploration of any injury in which blood vessels may be damaged below the level of the cricoid cartilage or above a line connecting the mastoid process with the angle of the jaw. Arterial injuries above this line are practically inaccessible. If injury to the carotid artery at the base of the skull is confirmed by angiography, repair may not be possible and ligation may be required to control bleeding, or angiographic intervention may be required. Injured carotid arteries that have produced a neurologic deficit should be repaired if possible. The morbidity and mortality of patients undergoing carotid artery repair are significantly lower than those who have ligation of the carotid artery (15% vs 50%). Carotid artery ligation is indicated in the patient who presents with uncontrollable hemorrhage or coma with no prograde flow in the carotid artery.
Since exposure of injuries in zone II is relatively easy to obtain, a policy of mandatory exploration was the traditional recommendation for all injuries penetrating the platysma muscle. Although this approach is safe, reliable, and time-tested, studies have demonstrated that a selective approach is as safe provided that diagnostic testing does not detect a major injury and the patient is stable. High-resolution helical CT scanning of the neck can also be used to guide surgical decision making in zone II penetrating injuries. Invasive studies such as endoscopy and conventional angiography can often be eliminated if CT demonstrates a trajectory remote from vital structures such as blood vessels or the aerodigestive tract.
In the absence of an obvious vascular injury on clinical examination, ultrasound with color-flow Doppler has been demonstrated to be reliable in ruling out carotid artery injuries. Computed tomography angiography can also be used in this setting and may offer the advantage of identifying an unsuspected vertebral artery injury. Vertebral artery injuries should also be suspected when bleeding from a posterior or lateral neck wound cannot be controlled by pressure on the carotid artery or when there is bleeding from a posterolateral wound associated with fracture of a cervical transverse process. Flexible or rigid endoscopy can be used to evaluate the trachea and esophagus. A contrast study of the upper esophagus should be performed to identify esophageal injuries that might not be readily apparent on endoscopy. These injuries can be difficult to detect and are occasionally missed on surgical exploration. In either case, repeated, careful examinations should be performed.
The most important injuries resulting from blunt cervical trauma are: (1) cervical fracture, (2) cervical spinal cord injury, (3) vascular injury, and (4) laryngeal and tracheal injury. Radiographic examination of the cervical spine and soft tissues is essential. Careful neurologic examination can differentiate between injuries to the spinal cord, brachial plexus, and brain.
The diagnosis of a cervical spine fracture is reliant on the history, physical examination, and confirmatory studies. The use of plain radiographs has been supplanted by non-contrast computed tomography of the cervical spine. Awake, unimpaired patients with a negative physical examination are unlikely to have a clinically significant cervical spine injury. Obtunded patients with a negative CT scan and no clinical signs of cervical spine injury are also unlikely to have an injury. Following a negative CT scan, the cervical collar is typically removed once the patient is no longer obtunded and the examination can be repeated, or immediately if the patient is likely to remain obtunded/intubated in the ICU. The pediatric patient with an unreliable physical examination often requires additional imaging to clear the spine. Adult patients with a negative CT scan and pain often require flexion and extension views or a MRI to rule out ligamentous injury. Cervical fractures are often managed with external immobilization using rigid collars or a halo/vest apparatus. In some cases, unstable cervical spine fractures require reduction and internal fixation.
Vascular injuries may occur in cases of severe or localized blunt neck trauma. The common or internal carotid arteries can be torn or sustain intimal disruption and require intervention. Imaging of the cervical vessels is recommended in blunt trauma patients with lateralizing neurologic symptoms or GCS less than 8 with head CT findings that do not explain the neurologic symptoms. Screening should also be considered in patients with mandible or facial fractures, complex skull fractures, traumatic brain injury with thoracic injuries, scalp degloving, and thoracic vascular injuries. While four-vessel arteriography of bilateral carotid and vertebral arteries was the previous gold standard, newer imaging techniques such as a dedicated cervical CT-angiogram or MR-angiogram are the preferred screening tools. Formal arteriograms are reserved for patients who may have injuries amenable to angiographic intervention or if the diagnosis cannot be made by other means and would alter treatment. Most blunt carotid injuries are not amenable to operative intervention due to the location or extent of injury. The use of endovascular stent techniques to repair or control blunt carotid artery injuries is also an option. Patients with blunt carotid or vertebral artery injuries should be considered for anticoagulation or antiplatelet therapy. The value of anticoagulation continues to be debated due to associated bleeding complications, and antiplatelet therapy is a reasonable alternative to full systemic anticoagulation.
The complications of untreated neck trauma are related to the individual structures injured. Injuries to the larynx and trachea can result in acute airway obstruction, late tracheal stenosis, and sepsis. Cervicomediastinal sepsis can result from esophageal injuries. Carotid artery injuries can produce death from hemorrhage, stroke or cerebral ischemia, and arteriovenous fistula with cardiac decompensation. Major venous injury can result in exsanguination, air embolism, and arteriovenous fistula formation if there is concomitant arterial injury. Cervical fracture can result in paraplegia, quadriplegia, or death.
Prevention of these complications depends upon immediate resuscitation by intubation of the airway, prompt control of external hemorrhage and blood replacement, protection of the head and neck when cervical fracture is possible, accurate and rapid diagnosis, and prompt operative treatment when indicated.
Control of the airway with early intubation is the first key maneuver to successful management of severe neck injuries. Any wound of the neck that penetrates the platysma requires prompt surgical exploration or diagnostic workup to rule out major vascular injury. In patients with zone II injuries, color-flow Doppler imaging may provide a reliable way to assess for vascular injury and can be a safe alternative to contrast angiography. Arteries damaged by high-velocity missiles require debridement. End-to-end anastomosis of the mobilized vessels is preferred, but if a significant segment is lost, an autogenous vein graft can be used. Vertebral artery injury presents a formidable technical problem because of the interosseous course of the artery shortly after it arises from the subclavian artery. Although unilateral vertebral artery ligation has been followed by fatal midbrain or cerebellar necrosis, because of inadequate communication to the basilar artery, only 3% of patients with left vertebral ligation and 2% of patients with right vertebral ligation develop these complications. Therefore, in the face of massive hemorrhage from a partially severed vertebral artery, ligation with surgical clips applied to the vessel between the transverse processes above and below the laceration is accepted.
Subclavian artery injuries are best approached through a combined cervicothoracic incision. Proper exposure is the key to success in the management of these difficult and too-often fatal injuries. Ligation of the subclavian artery is relatively safe, but primary repair is preferable. Care should be taken to avoid phrenic nerve and thoracic duct injury when operating in this region of the neck. If the patient is stable and a subclavian injury is identified at arteriography, an endovascular stent is another therapeutic option.
Venous injuries are best managed by ligation. The possibility of air embolism must be kept constantly in mind. A simple means of preventing this complication is to lower the patient’s head using the Trendelenburg position until bleeding is controlled.
Esophageal injuries should be sutured closed primarily and drained. Use of muscle flaps using omohyoid or sternocleidomastoid muscles to cover the repair can be helpful. Drainage is the mainstay of treatment. Extensive injury to the esophagus is often immediately fatal because of associated injuries to the spinal cord. Systemic antibiotics should be administered routinely to patients with esophageal injuries.
Minor laryngeal and tracheal injuries do not require treatment, but immediate tracheostomy should be performed when airway obstruction exists. If there has been significant injury to the thyroid cartilage, a temporary laryngeal stent (Silastic) should be employed to provide support. Mucosal lacerations should be approximated before insertion of the stent. Conveniently located small perforations of the trachea can be utilized for tracheostomy. Otherwise, the wounds can be closed after they are debrided and a distal tracheostomy performed. Extensive circumferential tracheal injuries may require resection and anastomosis or reconstruction using synthetic materials.
Cervical spinal cord injury should be managed in such a way as to prevent further damage. When there is cervical cord compression from hematoma, vertebral fractures, or foreign bodies, decompression laminectomy is necessary.
Severe laceration of the cervical spinal cord often results in paralysis. Injuries to the soft tissues of the neck, trachea, and esophagus have a good to excellent prognosis if promptly treated. Major vascular injuries have a good prognosis if promptly treated before the onset of irreversible shock or neurologic deficit. The overall death rate for major cervical injuries is about 10%.
et al.: Blunt cerebrovascular injury practice management guidelines: Eastern Association for the Surgery of Trauma. J Trauma. 2010;68:471.
et al.: Blunt cerebrovascular injuries: redefining screening criteria in the era of noninvasive diagnosis. J Trauma Acute Care Surg. 2012;72:330.
et al.: Trauma association of Canada pediatric subcommittee national pediatric cervical spine evaluation pathway: consensus guidelines. J Trauma. 2011;70:873.
et al.: Computed tomography alone may clear the cervical spine in obtunded blunt trauma patients: a prospective evaluation of a revised protocol. J Trauma. 2011;70:345.
et al.: Optimal outcomes for patients with blunt cerebrovascular injury (BCVI): tailoring treatment to the lesion. J Am Coll Surg. 2011;212:549.
et al.: Improving the screening criteria for blunt cerebrovascular injury: the appropriate role for computed tomography angiography. J Trauma. 2011;70:1058.
et al.: Cervical spine clearance in obtunded blunt trauma patients: a prospective study. J Trauma. 2010;68:576.
et al.: Evaluation of multidetector computed tomography for penetrating neck injury: a prospective multicenter study. J Trauma Acute Care Surg. 2012;72:576.
et al.: Evaluating the use and utility of noninvasive angiography in diagnosing traumatic blunt cerebrovascular injury. J Trauma Acute Care Surg
Thoracic trauma accounts directly for or is a contributing factor in 50% of deaths from trauma. Early deaths are commonly due to: (1) airway obstruction, (2) flail chest, (3) open pneumothorax, (4) massive hemothorax, (5) tension pneumothorax, and (6) cardiac tamponade. Later deaths are due to respiratory failure, sepsis, and unrecognized injuries/complications. The majority of blunt thoracic injuries are the result of automobile accidents. Even what appears to be a minor blunt thoracic injury leading to rib fractures and pulmonary contusions can have a profound effect on patients. Near-side collisions are responsible for a higher incidence of blunt aortic injury among older adults and are associated with lower delta V forces compared to those in younger patients. Penetrating chest injuries from knives, bullets, etc, are deadly and can result in complex patterns of injury. The mortality rate in hospitalized patients with isolated chest injury is 4%-8%; it is 10%-15% when one other organ system is involved and rises to 35% if multiple additional organs are injured.
Combined injuries of multiple intrathoracic structures are typical. There are often other injuries to the abdomen, head, or skeletal system. When performing an operation on the chest for trauma, it is often necessary to operate on the abdomen as well. Therefore, when trauma patients are brought to the operating room for a laparotomy or thoracotomy, both body regions should be prepped into the operative field. Eighty-five percent of chest injuries do not require open thoracotomy, but immediate use of lifesaving measures is often necessary and should be within the competence of all surgeons.
A rapid estimate of cardiorespiratory status and possible associated injuries from the physical examination gives the physician a valuable overview of a patient who has sustained thoracic injuries. For example, patients with upper airway obstruction appear cyanotic, ashen, or gray; examination reveals stridor or gurgling sounds, ineffective respiratory excursion, constriction of cervical muscles, and retraction of the suprasternal, supraclavicular, intercostal, or epigastric regions. The character of chest wall excursions and the presence or absence of penetrating wounds should be observed. If respiratory excursions are not visible, ventilation is probably inadequate. Severe paradoxic chest wall movement in flail chest is usually located anteriorly and can be seen immediately. Sucking wounds of the chest wall should be obvious. A large hemothorax may be detected by percussion, and subcutaneous emphysema is easily detected on palpation as crepitus. Both massive hemothorax and tension pneumothorax may produce absent or diminished breath sounds and a shift of the trachea to the opposite side, but in massive hemothorax the neck veins are usually collapsed. If the patient has a thready or absent pulse and distended neck veins, the main differential diagnosis is between cardiac tamponade and tension pneumothorax.
In moribund patients, diagnosis must be immediate, and treatment may require chest tube placement, pericardiocentesis, or thoracotomy in the emergency room. The first priority of management should be to provide an airway and restore circulation. One can then reassess the patient and outline definitive measures. A cuffed endotracheal tube and assisted ventilation are required for apnea, ineffectual breathing, severe shock, deep coma, airway obstruction, flail chest, or open sucking chest wounds. Persistent shock or hypoxia due to thoracic trauma may be caused by any of the following: massive hemopneumothorax, cardiac tamponade, tension pneumothorax or massive air leak, or air embolism. If hemorrhagic shock is not explained readily by findings on chest x-ray or external losses, it is almost certainly due to intra-abdominal bleeding.
If time permits, the chest is prepared and draped in a sterile fashion. In awake patients, local anesthetic (1% lidocaine) is injected in the skin and surrounding tissues at the planned site of tube insertion. In an unconscious patient, this step is usually unnecessary. The location of the chest tube insertion site is the interspace between the fourth and fifth ribs in the midaxillary line. A 2- to 3-cm skin incision is created with a #10 scalpel and carried down into the subcutaneous tissue. Using a large hemostat, a soft tissue tunnel is created just superior to the cephalad edge of the fifth rib. A finger or blunt clamp is used to penetrate the parietal pleura and enter the pleural space. The wound is explored with an index finger to confirm entry into the pleural cavity and check for pulmonary adhesions. A 36F straight thoracostomy tube is inserted and directed posteriorly toward the apex of the lung. The tube is anchored to the skin with stitches and connected to a Pleur-Evac device set at 20 cm H2O suction with a water seal.
Rib fracture, the most common chest injury, varies across a spectrum from simple fracture to fracture with hemopneumothorax to severe multiple fractures with flail chest, pulmonary contusion, and internal injuries. With simple fractures, pain on inspiration is the principal symptom; treatment consists of providing adequate analgesia. In cases of multiple fractures, intercostal nerve blocks or epidural analgesia may be required to ensure adequate ventilation. Multiple fractures can be associated with decreased ventilation and subsequent pneumonia, particularly in the elderly patient.
Flail chest occurs when a portion of the chest wall becomes isolated by multiple fractures and paradoxically moves in and out with inspiration and expiration with a potentially severe reduction in ventilatory efficiency. The magnitude of the effect is determined by the size of the flail segment and the amount of pain with breathing. The rib fractures are usually anterior, and there are at least two fractures of the same rib. Bilateral costochondral separation and sternal fractures can also cause a flail segment. An associated lung contusion may produce a decrease in lung compliance not fully manifest until 12-48 hours after injury. Increased negative intrapleural pressure is then required for ventilation, and chest wall instability becomes apparent. If ventilation becomes inadequate, atelectasis, hypercapnia, hypoxia, accumulation of secretions, and ineffective cough occur. Arterial Pao2 is often low before clinical findings appear. Serial blood gas analysis is the best way to determine if a treatment regimen is adequate. For less severe cases, intercostal nerve block or continuous epidural analgesia may be adequate treatment. However, more severe cases require ventilatory assistance for variable periods of time with a cuffed endotracheal tube and a mechanical ventilator.
Most rib or sternal fractures will heal without treatment. In selected patients, internal fixation may be useful; however, determining the patient population who would most benefit is still under investigation. Commercially produced, implantable rib and sternal fracture plating systems are now available. A system with bioabsorbable plates has been described which allows fixation of fragments during the healing process and metabolism by the body within 24 months. Patients who would potentially benefit from an open reduction internal fixation procedure are those with nonunion, severely displaced rib fractures with overriding fragments, severe pain with respiratory compromise (eg, difficulty in being weaned off the mechanical ventilator), multiple unstable rib fractures, and those undergoing thoracotomy for other intrathoracic indication. Because of the peristomal bacterial burden associated with a tracheostomy, this procedure should be used with caution in patients with a prior tracheostomy and need for a surgical incision high on the chest wall.
Blunt tracheobronchial injuries are often due to compression of the airway between the sternum and the vertebral column in decelerating or high-velocity crush accidents. The distal trachea or main stem bronchi are usually involved, and 80% of all injuries are located within 2.5 cm from the carina. Penetrating tracheobronchial injuries may occur at any location. Most patients have pneumothorax, subcutaneous emphysema, pneumomediastinum, and hemoptysis. Cervicofacial emphysema may be dramatic. Tracheobronchial injury should be suspected when there is a massive air leak or when the lung does not readily reexpand after chest tube placement. In penetrating injuries of the trachea or main stem bronchi, there is usually massive hemorrhage and hemoptysis. Systemic air embolism resulting in cardiopulmonary arrest may occur if a bronchovenous fistula is present. If air embolism is suspected, emergency thoracotomy should be performed with cross-clamping of the pulmonary hilum on the affected side. The diagnosis is confirmed by aspiration of air from the heart. In blunt injuries, the tracheobronchial injury may not be obvious and may be suspected only after major atelectasis develops several days later. Diagnosis may require flexible or rigid bronchoscopy. Immediate primary repair with absorbable sutures is indicated for all tracheobronchial lacerations.
Hemothorax (blood within the pleural cavity) is classified according to the amount of blood: minimal, 350 mL; moderate, 350-1500 mL; or massive, 1500 mL or more. The rate of bleeding after evacuation of the hemothorax is clinically even more important. If air is also present, the condition is called hemopneumothorax.
Hemothorax should be suspected with penetrating or severe blunt thoracic injury. There may be decreased breath sounds and dullness to percussion, and a chest x-ray should be promptly obtained. In experienced hands, ultrasound can diagnose pneumothorax and hemothorax, but this technique is not widely employed at this time. Tube thoracostomy should be performed expeditiously for all hemothoraces. In 85% of cases, tube thoracostomy is the only treatment required. If bleeding is persistent, as noted by continued output from the chest tubes, it is more likely to be from the chest wall and an intercostal artery rather than a pulmonary artery. The use of positive end-expiratory pressure can help tamponade pulmonary parenchymal bleeding in trauma patients who are intubated. When the rate of bleeding shows a steady trend of greater than 200 mL/h or the total hemorrhagic output exceeds 1500 mL, thoracoscopy or thoracotomy should usually be performed. The trend and rate of thoracic bleeding is probably more important than the absolute numbers in deciding to perform surgical intervention. Thoracoscopy has been shown to be effective in controlling chest tube bleeding in 82% of cases. This technique has also been shown to be 90% effective in evacuating retained hemothoraces. In most of these cases, the chest wall is the source of hemorrhage. Thoracotomy is required for management of injuries to the lungs, heart, pericardium, and great vessels.
Pneumothorax occurs in lacerations of the lung or chest wall following penetrating or blunt chest trauma. Hyperinflation (eg, blast injuries and diving accidents) can also rupture the lungs. After penetrating injury, 80% of patients with pneumothorax also have blood in the pleural cavity. Most cases of pneumothorax are readily diagnosed on chest x-ray. In some cases, an occult pneumothorax will be identified on a chest or abdominal CT scan. Pneumothorax or hemothorax may be identified on the lateral scans performed as part of the FAST examination of the abdomen for trauma (see section on abdominal trauma). Most cases of traumatic pneumothorax should be treated with immediate tube thoracostomy; however, small occult pneumothoraces in stable patients can be observed.
Tension pneumothorax develops when a flap-valve leak allows air to enter the pleural space but prevents its escape; intrapleural pressure rises, causing total collapse of the lung and a shift of the mediastinal viscera to the opposite side, interfering with venous return to the heart. It must be relieved immediately to avoid impairment of cardiac function. Immediate treatment involves placement of a large-bore needle or plastic angiocath in the pleural space with care being taken to avoid injury to the intercostal vessels. After this emergency measure has been instituted, tension pneumothorax should be treated definitively by tube thoracostomy.
Sucking chest wounds, which allow air to pass in and out of the pleural cavity, should be promptly treated by a three-sided occlusive dressing and tube thoracostomy. The pathologic physiology resembles flail chest except that the extent of associated lung injury is usually less. Definitive management includes surgical closure of the defect in the chest wall.
Pulmonary contusion due to sudden parenchymal concussion occurs after blunt trauma or wounding with a high-velocity missile. Pulmonary contusion happens in 75% of patients with flail chest but can also occur following blunt trauma without rib fracture. Alveolar rupture with fluid transudation and extravasation of blood are early findings. Fluid and blood from ruptured alveoli enter alveolar spaces and bronchi, and produce localized airway obstruction and atelectasis. Increased mucous secretions and overzealous intravenous fluid therapy may combine to produce copious secretions and further atelectasis. The patient’s ability to cough and clear secretions effectively is weakened because of chest wall pain or mechanical inefficiency from fractures. Elasticity of the lungs is decreased, resistance to air flow increases, and as the work of breathing increases, blood oxygenation and pH drop and Paco2 rises. The cardiac compensatory response may be compromised, because as many as 35% of these patients have an associated myocardial contusion.
Treatment is often delayed because clinical and x-ray findings may not appear until 12-48 hours after injury. The clinical findings are copious, thin, blood-tinged secretions; chest pain; restlessness; apprehensiveness; and labored respirations. Eventually, dyspnea, cyanosis, tachypnea, and tachycardia develop. X-ray changes consist of patchy parenchymal opacification or diffuse linear peribronchial densities that may progress to diffuse opacification (“white-out”) characteristic for acute respiratory distress syndrome.
Mechanical ventilatory support permits adequate alveolar ventilation and reduces the work of breathing. Blood gases should be monitored and arterial saturation adequately maintained. There is some controversy over the best regimen for fluid management, but excessive hydration or blood transfusion should be avoided. Serial measurement of central venous pressure, mixed venous oxygen saturation, and cardiac output help avoid over- or underresuscitation. Despite optimal therapy, about 15% of patients with pulmonary contusion die. Use of protective mechanical ventilator strategies is essential in these patients to avoid progressive ventilator induced lung injury. Use of low-tidal volumes (6 mL/kg) and avoidance of plateau pressures greater than 35 cm H2O are recommended.
Most lung lacerations are caused by penetrating injuries, and hemopneumothorax is usually present. Tube thoracostomy is indicated to evacuate pleural air or blood and to monitor continuing leaks. Since expansion of the lung tamponades the laceration, most lung lacerations do not produce massive hemorrhage or persistent air leaks. Should a pulmonary laceration require operative intervention, lung-sparing techniques rather than formal anatomic lung resection should be employed when feasible to reduce morbidity and mortality.
Lung hematomas are the result of local parenchymal destruction and hemorrhage. The x-ray appearance is initially a poorly defined density that becomes more circumscribed a few days to 2 weeks after injury. Cystic cavities occasionally develop if damage is extensive. Most hematomas resolve adequately with expectant treatment.
Blunt injury to the heart occurs most often from compression against the steering wheel in automobile accidents. This injury is in decline with the increasing prevalence of airbag technology in motor vehicles. The injury varies from localized contusion to cardiac rupture. Autopsy studies of victims of immediately fatal accidents show that as many as 65% have rupture of one or more cardiac chambers, and 45% have pericardial lacerations. The incidence of blunt myocardial injury in patients who reach the hospital is unknown but is probably higher than generally suspected. The clinical relevance of this diagnosis is widely debated. Most trauma surgeons advocate the diagnosis and treatment of the actual clinical problem such as acute heart failure, valvular injury, cardiac rupture, or dysrhythmia.
Early clinical findings include friction rubs, chest pain, tachycardia, murmurs, dysrhythmias, or signs of low cardiac output. Patients with risk factors for blunt myocardial injury should undergo evaluation with a 12-lead electrocardiogram (EKG). If the EKG is normal and the patient is asymptomatic, the work up is complete. An abnormal EKG should prompt further evaluation with an echocardiogram. Patients with proven injury on echocardiogram and/or hemodynamic instability should be admitted to the ICU and managed appropriately for the diagnosed injury. An abnormal EKG with a normal echocardiogram merits at least 24 hours of monitoring in a telemetry unit and daily repeat EKGs until stable or the dysrhythmia resolves. Standard measurement of cardiac enzymes is not useful and has no role in the diagnosis of blunt myocardial injury. If the patient is suspected of having a myocardial infarction or acute myocardial ischemia, then cardiac enzymes should be obtained and a cardiology consultation arranged.
Management of symptomatic blunt myocardial injury should be the same as for acute myocardial infarction. Hemopericardium may occur without tamponade and can be treated by pericardiocentesis. Tamponade in blunt cardiac trauma is often due to myocardial rupture or coronary artery laceration. Tamponade produces distended neck veins, shock, and cyanosis. Immediate thoracotomy and control of the injury are indicated. If cardiopulmonary arrest occurs before the patient can be transported to the operating room, emergency room thoracotomy with relief of tamponade should be performed. Treatment of injuries to the valves, papillary muscles, and septum must be individualized; and when tolerated, delayed repair is usually recommended.
Pericardial lacerations from stab wounds tend to seal and cause tamponade, whereas gunshot wounds frequently leave a sufficient pericardial opening for drainage. Gunshot wounds produce more extensive myocardial damage, multiple perforations, and massive bleeding into the pleural space. Hemothorax, shock, and exsanguination occur in nearly all cases of cardiac gunshot wounds. The clinical findings are those of tamponade or acute blood loss. Use of ultrasound and the FAST examination technique can reveal the presence of clinically significant blood in the pericardial space.
Treatment of penetrating cardiac injuries requires prompt thoracotomy, pericardial decompression, and control of hemorrhage. Most patients do not require cardiopulmonary bypass. The standard approach has been to repair the laceration using mattress sutures with pledgets while controlling hemorrhage with a finger on the heart. Suture control of cardiac lacerations may be technically difficult when working with a beating heart or in patients with large or multiple lacerations. Several studies have demonstrated that in most cases, emergency temporary control of hemorrhage from cardiac lacerations can be achieved with the use of a skin stapler (Figure 13–10). Following stabilization of the patient, the staples can be removed after definitive suture repair is performed in the operating room. Hemostatic sealants such as FloSeal offer significant promise as additional tools in the surgical armamentarium when dealing with lacerations to the heart or great vessels. Regardless of the approach utilized, care must be taken to avoid injury to the coronary arteries.
Technique of cardiac stapling. Finger pressure (not shown) is used to maintain hemostasis during stapling. (Reproduced, with permission, from Macho JR, Markison RE, Schecter WP: Cardiac stapling in the management of penetrating injuries of the heart: rapid control of hemorrhage and decreased risk of personal contamination. J Trauma. 1993;34:711.)
Pericardiocentesis or creation of a pericardial window is reserved for selected cases when the diagnosis is uncertain or in preparation for thoracotomy. In approximately 75% of cases of stab wounds and 35% of cases of gunshot cardiac wounds, the patient survives the operation. However, it is estimated that 80%-90% of patients with gunshot wounds of the heart do not reach the hospital.
Anatomically, the esophagus is well protected, and perforation from external penetrating trauma is relatively infrequent. Blunt injuries are exceedingly rare. The most common symptom of esophageal perforation is pain; fever develops within hours in most patients. Hematemesis, hoarseness, dysphagia, or respiratory distress may also be present. Physical findings include shock, local tenderness, subcutaneous emphysema, or Hamman sign (pericardial or mediastinal “crunch” synchronous with cardiac sounds). Leukocytosis occurs soon after injury. X-ray findings on plain chest films include evidence of a foreign body or missile and mediastinal air or widening. Pleural effusion or hydropneumothorax is frequently seen, usually on the left side. Contrast x-rays of the esophagus should be performed but are positive in only about 70% of proven perforations.
A nasogastric tube should be passed to evacuate gastric contents. If recognized within 24-48 hours after injury, the esophageal perforation should be closed and pleural drainage instituted with large-bore catheters. Repair of these perforations requires special techniques that include buttressing of the esophageal closure with pleural or pericardial flaps; pedicles of intercostal, diaphragmatic, or cervical strap muscles; and serosal patches from stomach or jejunum. Illness and death are due to mediastinal and pleural infection.
Chylothorax and chylopericardium are rare complications of trauma but are difficult to manage when they occur. Penetrating injuries of the neck, thorax, or upper abdomen can injure the thoracic duct or its major tributaries.
Symptoms are due to mechanical effects of the accumulations (eg, shortness of breath from lung collapse or low cardiac output from tamponade). The diagnosis is established when the fluid is shown to have characteristics of chyle.
The patient should be maintained on a fat-free, high-carbohydrate, high-protein diet and the effusion aspirated. Chest tube drainage should be instituted if the effusion recurs. Lipid-free total parenteral nutrition with no oral intake may be effective in treating persistent leaks. Three or 4 weeks of conservative treatment usually are curative. If daily chyle loss exceeds 1500 mL for 5 successive days or persists after 2-3 weeks of conservative treatment, the thoracic duct should be ligated via a right thoracotomy. Intraoperative identification of the leak may be facilitated by preoperative administration of fat-containing a lipophilic dye.
Penetrating injuries of the diaphragm outnumber blunt diaphragmatic injuries by a ratio of at least 6:1. Diaphragmatic lacerations occur in 10%-15% of cases of penetrating wounds to the chest and in as many as 40% of cases of penetrating trauma to the left chest. Injuries to the right diaphragm are more common than previously thought. The injury is rarely obvious. Wounds of the diaphragm must not be overlooked because they rarely heal spontaneously and because herniation of abdominal viscera into the chest can occur with catastrophic complications either immediately or years after the injuries.
Associated injuries are usually present, and as many as 25% of patients are in shock when first seen. There may be abdominal tenderness, dyspnea, shoulder pain, or unilateral breath sounds. The diagnosis is often missed. Although chest radiography is a sensitive diagnostic tool, it may be entirely normal in 40% of cases. The most common finding is ipsilateral hemothorax, which is present in about 50% of patients. Occasionally, a distended, herniated stomach is confused with a pneumothorax. Passage of a nasogastric tube before x-rays will help to identify an intrathoracic stomach. CT scan or contrast x-rays may be necessary to establish the diagnosis in some cases. Newer generation helical CT scanners that allow sagittal reformatting can be helpful in definitively diagnosing diaphragmatic injury. Laparoscopy is a useful but invasive technique for detecting occult diaphragmatic injuries in patients who have no other indications for formal laparotomy.
Once the diagnosis is made, a transabdominal surgical approach should be used in cases of acute rupture. Laparoscopic suturing for repair of the injury may be possible in selected cases. The diaphragm should be reapproximated and closed with interrupted or running nonabsorbable sutures. Chronic herniation is associated with adhesions of the affected viscera to the thoracic structures and should be approached via thoracotomy, with the addition of a separate laparotomy when indicated. These cases can be quite challenging and appropriate preoperative planning is recommended.
et al.: Rib fracture fixation for flail chest: what is the benefit? J Am Coll Surg. 2012;215:201–205.
et al.: Great vessel and cardiac trauma. Surg Clin North Am. 2009;89:797.
et al.: Isolated severe traumatic brain injuries sustained during combat operations: demographics, mortality outcomes, and lessons to be learned from contrasts to civilian counterparts. J Trauma. 2011;70:11.
et al.: The clinical significance of occult thoracic injury in blunt trauma patients. Am Surg. 2010;76:1063.
et al.: Ultrasound detection of pneumothorax compared with chest x-ray and computed tomography scan. Am Surg. 2011;77:480.
et al.: Blunt aortic injury. N Engl J Med. 2008;359:1708.
et al.: Rib fracture fixation: controversies and technical challenges. Am Surg. 2010;76:793.
et al.: Penetrating cardiac injury. J R Army Med Corps. 2009;155:185.
The specific type of abdominal injury varies according to whether the trauma is penetrating or blunt. Blunt injuries predominate in rural areas, while penetrating injuries are more common in urban areas. The mechanism of injury in blunt trauma is rapid deceleration, and noncompliant organs such as the liver, spleen, pancreas, and kidneys are at greater risk of injury due to parenchymal fracture. Occasionally, hollow viscous organs may be injured, with the duodenum and urinary bladder being particularly susceptible. The small bowel occupies a large portion of the total abdominal volume and is more likely to be injured by penetrating trauma. Most blunt abdominal injuries are related to motor vehicle accidents. Although the use of restraints has been associated with a decrease in the incidence of head, chest, and solid organ injuries, their use may be associated with pancreatic, mesenteric, and intestinal injuries due to organ compression against the spinal column. These injuries should be considered in patients who have signs of seat belt-related contusions of the abdominal wall. Internal abdominal injury may be present in as many as 30% of these cases. In any abdominal trauma, hemoperitoneum may not manifest clinical signs of peritoneal irritation, particularly in patients with other distracting injuries or depressed mental status. Retroperitoneal injury may be more subtle and difficult to diagnose during the initial evaluation.
Deaths from abdominal trauma result largely from early severe hemorrhage and coagulopathy or from later sepsis. Most deaths from abdominal trauma are preventable. Patients at risk of abdominal injury should undergo prompt and thorough evaluation. In most trauma centers, after physical examination, the initial diagnostic evaluation includes bedside FAST and portable radiographs of the pelvis and chest to assess for other potential sites of bleeding. In unstable patients who cannot be adequately evaluated with FAST due to size, technical problems, or subcutaneous air, diagnostic peritoneal lavage is warranted. After the initial FAST examination, patients who are stable or who respond to initial fluid resuscitation should have a CT scan of the abdomen and pelvis to evaluate for intra-abdominal and retroperitoneal injuries. Patients with persistent hypotension requiring fluid and blood resuscitation in the face of a positive FAST or diagnostic peritoneal lavage should be transported to the operating room emergently for exploratory laparotomy.
In some cases, dramatic physical findings may be due to abdominal wall injury in the absence of intraperitoneal injury. If the results of diagnostic studies are equivocal, diagnostic laparoscopy or exploratory laparotomy should be considered, since they may be lifesaving if serious injuries are identified early. Evaluation always includes a comprehensive physical examination with pelvic and rectal examinations included and may require specific laboratory and radiologic tests (eg, retrograde urethrogram or cystogram, rigid sigmoidoscopy, abdominal CT). Serial physical examinations may be necessary to detect subtle findings.
Penetrating injuries to the abdomen that present with shock or ongoing resuscitation require prompt exploration. Lacerations of major blood vessels or the liver can cause severe and early shock. Penetrating injuries of the spleen, pancreas, or kidneys usually do not bleed massively unless a major vessel to the organ (eg, the renal artery) is damaged. Bleeding must be controlled promptly with packing and appropriate clamping for vascular control. A patient in shock with a penetrating injury of the abdomen who does not respond to 2 L of crystalloid fluid resuscitation should be operated on immediately following chest x-ray and switched blood product resuscitation.
Patients with hollow visceral injuries may have very few physical signs initially but will progress to sepsis if the injuries are not recognized. Increasing abdominal tenderness demands surgical exploration. White blood cell count elevations and fever appearing several hours following injury are keys to early diagnosis.
The treatment of hemodynamically stable patients with penetrating injuries to the lower chest or abdomen varies. All surgeons agree that patients with signs of peritonitis or hypovolemia should undergo surgical exploration, but operative treatment is less certain for patients with no signs of peritonitis or sepsis who are cardiovascularly stable.
Most stab wounds of the lower chest or abdomen should be explored, since a delay in treatment of a hollow viscous perforation can result in severe sepsis. Some surgeons recommend a selective policy in the management of these patients. When the depth of injury is in doubt, local wound exploration may rule out peritoneal penetration. Laparoscopy has a role in the evaluation of penetrating injuries in experienced hands, but requires considerable diligence to avoid missed injuries. All gunshot wounds of the lower chest and abdomen should be explored, unless there is a likely superficial scything wound, because the incidence of injury to major intra-abdominal structures exceeds 90% in such cases.
A major advance in management of blunt trauma has been the FAST examination. Ultrasound has proven to be an ideal modality in the immediate evaluation of the trauma patient because it is rapid and accurate for the detection of intra-abdominal fluid or blood and is readily repeatable. It provides valuable information that augments the surgeon’s diagnostic capabilities. Since its introduction in North America in 1989, ultrasonography has become commonplace, and a recent survey reports that 78% of United States trauma centers routinely use the FAST examination in the evaluation of patients.
The goal of the FAST examination is the identification of abnormal collections of blood or fluid. In this regard, it obviates the need for diagnostic peritoneal lavage. The primary focus is on the peritoneal cavity, but attention is also directed to the pericardium and to the pleural space. Unclotted blood or fluid allows transmission of ultrasound waves without echoes and thus appears black (Figure 13–11). In the standard FAST examination, four areas are scanned: the right upper quadrant, the subxiphoid area, the left upper quadrant, and the pelvis (Figure 13–12). Most surgeons recommend scanning initially in the right upper quadrant because more than half of the positive tests will reveal blood or fluid in this area. Unstable patients with a positive FAST examination should undergo urgent exploratory laparotomy.
A. Normal ultrasound of the right upper quadrant. B. Right upper quadrant ultrasound revealing blood between the liver and the kidney and between the liver and the diaphragm. (Courtesy of San Francisco General Hospital.)
Transducer positions for FAST. Pericardial area, right and left upper quadrants, and pelvis. (Reproduced, with permission, from Rozycki GS et al. Surgeon-performed ultrasound for the assessment of truncal injuries: lessons learned from 1540 patients. Ann Surg. 1998;228:557.)
The other diagnostic procedures most commonly used in patients without obvious indications for immediate laparotomy include diagnostic peritoneal lavage, CT scanning, and diagnostic laparoscopy.
Diagnostic Peritoneal Lavage
Diagnostic peritoneal lavage is designed to detect the presence of intraperitoneal blood. Although its use has decreased to virtually nil at many centers with the use of the FAST examination, it is still an important test in certain circumstances because of its high sensitivity for the presence of blood. Additional determinations of leukocytes, Gram stain, particulate matter, or amylase in the lavage fluid may indicate the presence of a bowel injury. Drainage of lavage fluid from a chest tube or urinary catheter may indicate a lacerated diaphragm or bladder. Lavage can be performed easily and rapidly, with minimal cost and morbidity. It is an invasive procedure that will affect the findings on physical examination and should be performed by a surgeon.
The procedure is neither qualitative nor quantitative. It cannot identify the source of hemorrhage, and relatively small amounts of intraperitoneal bleeding may result in a positive study. It may not detect small and large injuries to the diaphragm and cannot rule out injury to the bowel or retroperitoneal organs. The overall indications for diagnostic peritoneal lavage include abdominal pain or tenderness, low abdominal rib fractures, unexplained hypotension, spinal or pelvic fractures, paraplegia or quadriplegia, and assessment hampered by altered mental status due to neurologic injury or intoxication. Despite the many potential indications, FAST followed by abdominal pelvic CT scanning has replaced the need for most diagnostic peritoneal lavages. The only contraindication is a need for emergency laparotomy.
The procedure may be performed with careful technique on patients with prior abdominal surgery and in pregnant patients. It should usually be performed through a small infraumbilical incision with placement of the catheter under direct vision (Figure 13–13). In pregnant patients and those with pelvic fractures, a supraumbilical approach is indicated. Closed techniques of catheter placement utilizing trocars or guidewires have been shown to be almost as safe as the open technique, but the rate of failure with the closed technique is higher, thus eliminating most of the potential advantage. After placement of the catheter, 1 L of normal saline solution is instilled into the peritoneal cavity and then allowed to drain by gravity. At least 200 mL of lavage fluid should be recovered to allow for accurate interpretation. A portion of the recovered fluid is sent for laboratory analysis of cell counts, the presence of particulate matter, and amylase. Criteria for evaluation of results are summarized in Table 13–3.
Table 13–3.Criteria for evaluation of peritoneal lavage fluid. ||Download (.pdf) Table 13–3. Criteria for evaluation of peritoneal lavage fluid.
= 100,000 red cells/μL
= 500 white cells/μL
= 175 units amylase/dL
Bacteria on Gram-stained smear
Pink fluid on free aspiration
50,000–100,000 red cells/μL in blunt trauma
100–500 white cells/μL
75–175 units amylase/dL
< 100 white cells/μL
< 75 units amylase/dL
Diagnostic peritoneal lavage.
Computed tomography (CT) is noninvasive, qualitative, sensitive, and accurate for the diagnosis of intra-abdominal and retroperitoneal injuries. Modern multi-slice spiral scanners have greatly decreased the time required for obtaining high-quality images. However, CT scanning remains expensive, involves the use of intravenous contrast administration, exposes the patient to radiation, and requires an experienced radiologist for proper interpretation of the scans. CT scanning also involves transport from the acute care area and should not be attempted in the unstable patient.
Computed tomography scanning has a primary role in defining the location and magnitude of intra-abdominal injuries related to blunt trauma. It has the advantage of detecting most retroperitoneal injuries, but it may not identify all gastrointestinal injuries. The information provided on the magnitude of injury allows for potential nonoperative management of patients with solid organ injuries. Nonsurgical therapy is now used in more than 80% of blunt liver and spleen injuries. Detection of high-grade solid organ injuries or bleeding pelvic fractures by CT in relatively stable patients can also lead to other minimally invasive interventions, such as angiographic embolization, which increases the success of nonoperative management. Table 13–4 compares the time, costs, advantages, and disadvantages of nonoperative methods used for evaluation of the injured abdomen.
Table 13–4.Comparison of diagnostic methods for abdominal trauma. ||Download (.pdf) Table 13–4. Comparison of diagnostic methods for abdominal trauma.
|Methods ||Time/Cost ||Advantages/Disadvantages |
|Physical examination ||Quick/no cost ||Useful for serial examinations, very limited by other injuries, coma, drug intoxication, poor sensitivity and specificity. |
|Diagnostic peritoneal lavage (DPL) ||Quick/inexpensive ||Rapid results in unstable patient but invasive and may be overly sensitive for blood and not specific for site of injury; requires experience and may be limited if previous surgery. |
|Focused assessment with sonography for trauma (FAST) ||Quick/inexpensive ||Rapid detection of intra-abdominal fluid and pericardial tamponade; may be limited by operator experience, large body habitus, subcutaneous air; poor for detection of bowel injury. Fairly sensitive but not highly specific. |
|Helical computerized abdominal tomography (CT) ||Slower/expensive ||Most specific for site of injury and can evaluate retroperitoneum; very good sensitivity but may miss bowel injury; risk of reaction to contrast dye. |
Laparoscopy has an important diagnostic role in stable patients with penetrating abdominal trauma. It can quickly establish whether peritoneal penetration has occurred and thus reduce the number of negative and nontherapeutic trauma laparotomies performed. In selected patients, therapeutic laparoscopy has been used to repair injuries to the bowel and diaphragm. This approach offers all the advantages and disadvantages of minimally invasive surgery. Laparoscopy has also been applied safely and effectively as a screening tool in stable patients with blunt abdominal trauma. However, its use in this context requires further study. Concerns regarding the use of laparoscopy in trauma include the possibility of missed injuries, air embolism, hemodynamic instability related to the pneumoperitoneum, and complications related to trocar placement.
The three main indications for exploration of the abdomen following blunt trauma are peritonitis, ongoing intra-abdominal hemorrhage, and the presence of other injuries known to be frequently associated with intra-abdominal injuries. Peritonitis after blunt abdominal trauma is rare and can arise from rupture of a hollow organ, such as the duodenum, bladder, intestine, or gallbladder; from pancreatic injury; or occasionally from the presence of retroperitoneal blood.
Emergency abdominal exploration should be considered for patients with profound hypovolemic shock and a normal chest x-ray unless extra-abdominal blood loss is sufficient to account for the hypovolemia. In most cases, a rapidly performed FAST examination or peritoneal lavage will confirm the diagnosis of intraperitoneal hemorrhage. Patients with blunt trauma and hypovolemia should be examined first for intra-abdominal bleeding even if there is no overt evidence of abdominal trauma. For example, hypovolemia may be due to loss of blood from a large scalp laceration, but it may also be due to unsuspected rupture of the spleen. Hemoperitoneum may present with no signs except hypovolemia. The abdomen may be flat and nontender. Patients whose extra-abdominal bleeding has been controlled should respond to initial fluid resuscitation with an adequate urine output and stabilization of vital signs. If signs of hypovolemia (tachycardia, hypotension, low urine output, metabolic acidosis) recur, intra-abdominal bleeding must be considered to be the cause.
Other injuries frequently associated with abdominal trauma are rib fractures, pelvic fractures, abdominal wall injuries, and fractures of the thoracolumbar spine (eg, 20% of patients with fractures of the left lower ribs have a splenic laceration).
The spleen is the most commonly injured organ in cases of blunt abdominal trauma. Splenic injuries in children are typically managed without surgery. Currently, 50%-88% of adults with blunt splenic injuries are also treated nonoperatively. Patients must be monitored closely and immediate availability of an operating room is essential. Patients should be evaluated frequently for the possibility of other missed injuries or recurrent bleeding. Stable patients who have high-grade splenic injuries on CT scan or have evidence of ongoing bleeding on CT scan may be candidates for angiographic embolization. Unstable patients with splenic injuries should undergo splenectomy or attempts at splenic repair if appropriate.
Associated injuries are uncommon for patients in whom nonoperative management is attempted. In unstable patients, emergent celiotomy should be performed. Splenic salvage procedures such as splenorrhaphy, partial resection, wrapping with Vicryl mesh, or topical therapy with hemostatic agents should be attempted if the patient’s condition permits and there are a limited number of concomitant abdominal injuries. In the face of multiple injuries, ongoing cardiovascular compromise, or vascular avulsion of the spleen, total splenectomy is indicated. Following splenectomy, immunizations against Pneumococcus species, Meningococcus species, and Haemophilus influenzae are recommended postoperatively to reduce the risk of overwhelming postsplenectomy sepsis.
Approximately 85% of all patients with blunt hepatic trauma are stable following resuscitation. In this group, nonoperative management has been proven to be superior to open operation in avoiding complications and decreasing mortality. The primary requirement for nonoperative therapy is continued hemodynamic stability. Patients are monitored in the ICU with frequent assessment of vital signs and serial hematocrits. If transfusion with more than two units of PRBC is required, arteriography with possible embolization of bleeding vessels should be considered.
Nonoperative management of blunt hepatic trauma is successful in more than 90% of cases. With more severe injuries, repeat CT scanning may be necessary to evaluate for possible complications such as parenchymal infarction, hematoma, or biloma. Extrahepatic bile collections should generally be drained percutaneously. Intrahepatic collections of blood and bile usually resolve spontaneously over the course of several months. Patients with high-grade liver injuries have up to a 40% chance of developing bile leaks from the injured liver bed. Nuclear medicine scanning to delineate biliary flow with derivatives of iminodiacetic acid is useful in detection of bile leaks and should be done in the first few days after injury to reduce complications. Laparoscopic washout and placement of drains is an option for patients found to have evidence of extrahepatic bile leakage on HIDA scan. In addition, 1%-4% of patients with blunt liver injury will have injuries to other abdominal organs, which should prompt the clinician to consider the possibility of missed injury in patients who develop abdominal sepsis after injury.
Severe liver injury may result in exsanguinating hemorrhage with hypotension that does not respond to fluid resuscitation. For these patients, operative exploration is warranted. At laparotomy, immediate efforts should be directed to control of hemorrhage and stabilization of the patient by restoration of circulating blood volume. The initial techniques for the control of hepatic hemorrhage include manual compression, perihepatic packing, and the Pringle maneuver. Manual compression or perihepatic packing with laparotomy pads will control hemorrhage in most cases. The Pringle maneuver—clamping of the hepatic pedicle—should be performed when life-threatening hemorrhage is unresponsive to packing; it will control all hepatic bleeding except that from the hepatic veins or the intrahepatic vena cava. In most cases, the Pringle maneuver should not be maintained for more than 1 hour in order to prevent ischemic damage to the liver. Hepatic bleeding can be controlled by suture ligation or application of surgical clips directly to the bleeding vessels. Electrocautery or the argon beam coagulator can be used to control bleeding from raw surfaces of the liver. Microfibrillar collagen or hemostatic gelatin foam sponges soaked in thrombin can be applied to bleeding areas with pressure to control diffuse capillary bleeding. Fibrin glue has been used in treating both superficial and deep lacerations and appears to be the most effective topical agent but reports of fatal anaphylactic reactions have limited its use. When injury has already resulted in massive blood loss, packing of the abdomen with laparotomy pads and planned reexploration should be considered. Avoidance of the lethal triad of hypothermia, acidosis, and coagulopathy are paramount to successful surgical treatment of a major liver injury and may require further resuscitation in the ICU prior to return to the operating room. At the time of reexploration in 24-48 hours, hemorrhage is usually well controlled and can be managed with individual vessel ligation and debridement. Evidence of persistent hemorrhage should prompt earlier reexploration. Angiographic embolization may be a useful adjunct to surgical packing if arterial hemorrhage is still present or not well controlled. Rarely, selective hepatic artery ligation, resectional debridement, or hepatic lobectomy may be required to control hemorrhage. The raw surface of the liver may then be covered with omentum. Drains should always be used. Decompression of the biliary system is contraindicated, though sutures or clips should be used to control intraparenchymal bile ducts.
Hepatic vein injuries frequently bleed massively. Hepatic venous or intrahepatic vena caval injury should be suspected immediately when the Pringle maneuver fails to control bleeding. Several techniques have been described for isolation of the intrahepatic cava prior to attempted repair of these injuries. Unfortunately, even with the use of these techniques, mortality remains very high.
C. Biliary Tract Injuries
Biliary tract injuries are relatively uncommon, particularly for blunt trauma. Injury to the gallbladder should be treated in most cases by cholecystectomy. Minor injuries to the common bile duct can be treated by suture closure and insertion of a T-tube. Avulsion of the common bile duct or in combination with duodenal or ampullary trauma may require choledochojejunostomy in conjunction with total or partial pancreatectomy, duodenectomy, or other diversion procedures. Segmental loss of the common bile duct is best treated by choledochojejunostomy and drainage.
Pancreatic injuries may present with few clinical manifestations. Injury should be suspected whenever the upper abdomen has been traumatized, especially when serum amylase and lipase levels remain persistently elevated. The best diagnostic study for pancreatic injury (other than exploratory celiotomy) is CT scan of the abdomen. Peritoneal lavage is usually not helpful. Upper gastrointestinal studies with water-soluble contrast material may suggest pancreatic injury by demonstrating widening of the duodenal C-loop. Endoscopic retrograde cholangiopancreatography may be used in selected cases to evaluate for injuries to the major ducts.
The treatment of pancreatic injury depends on its grade and extent. Minor injuries not involving a major duct may be treated nonoperatively. Moderate injuries usually require operative exploration, debridement, and the placement of external drains. More severe injuries, including those with major duct injury or transection of the gland, may require distal resection or external drainage. Traumatic injuries to the head of the pancreas often include associated vascular injuries and carry a high mortality rate. Efforts should be directed at controlling hemorrhage, and drains can be placed in the area of the pancreatic injury. In most cases, pancreaticoduodenectomy should not be attempted in the setting of an unstable patient with multiple injuries.
The late complications of pancreatic injuries include pseudocyst, pancreatic fistula, and pancreatic abscess. Patients treated without resection may require reoperation for resection or Roux-en-Y internal gastrointestinal drainage.
E. Gastrointestinal Tract Injuries
Most injuries of the stomach can be repaired. Large injuries, such as those from shotgun blasts, may require subtotal or total resection. Failure to identify posterior stomach wall injuries by opening the lesser space is a pitfall to guard against.
Duodenal injuries may not be evident from the initial physical examination or x-ray studies. Abdominal films will reveal retroperitoneal gas within 6 hours after injury in most patients. CT performed with a contrast agent will frequently identify the site of perforation. Most duodenal injuries can be treated with lateral repair. Some may require resection with end-to-end anastomosis. Occasionally, pancreaticoduodenectomy or duodenal diversion with gastrojejunostomy and pyloric closure is required to manage a severe injury. A duodenostomy tube is useful in decompressing the duodenum and can be used to control a fistula caused by an injury. Jejunal or omental patches may also aid in preventing a suture line leak. A distal jejunostomy feeding tube is helpful in the long-term recovery from these injuries.
Duodenal hematomas causing high-grade obstruction usually resolve with nonoperative management. Patients may require total parenteral nutrition. In some cases, a small-bore enteral feeding tube can be passed beyond the area of obstruction utilizing interventional radiology techniques. Large hematomas may require operative evacuation, particularly when the obstruction lasts for more than 10-14 days and a persistent hematoma is seen on CT scan.
Most small bowel injuries can be treated with a two-layer sutured closure, though mesenteric injuries leading to devascularized segments of small bowel will require resection. The underlying principle is to preserve as much small bowel as possible.
For injuries to the colon, the past approach has been to divert the fecal stream or exteriorize the injury. However, more recent studies have shown a higher complication rate with colostomy formation than with primary repair. Wounds should be considered for primary repair if the blood supply is not compromised. Primary repair is more likely to be associated with complications in patients with ongoing shock, in those requiring multiple transfusions, if more than 6 hours elapse between injury and operation, or if there is gross contamination or peritonitis. Small, clean rectal injuries may be closed primarily if conditions are favorable. The treatment of larger rectal wounds involving pelvic fracture should include proximal diversion. Insertion of presacral drains is optional. In this latter case, direct repair of the rectal injury is not mandatory but should be performed if it can be readily exposed. Irrigation of the distal stump should be performed in most cases unless it would further contaminate the pelvic space.
F. Abdominal Wall Injuries
Abdominal wall injuries from blunt trauma are most often due to shear forces, such as being run over by the wheels of a tractor or bus. The shearing often devitalizes the subcutaneous tissue and skin, and if debridement is delayed, a serious necrotizing anaerobic infection may develop. The management of penetrating abdominal wall injuries is usually straightforward. Debridement and irrigation are appropriate surgical treatments. Every effort must be made to remove foreign material, shreds of clothing, necrotic muscle, and soft tissue. Abdominal wall defects may require insertion of absorbable mesh or coverage with a myocutaneous flap.
G. Genitourinary Tract Injuries
The most commonly injured genitourinary tract organs are the male genitalia, the uterus, the urethra, the bladder, the ureters, and the kidneys. The workup for these injuries consists primarily of radiologic examinations, which may include abdominal CT scan, cystogram, or retrograde urethrogram. In unstable patients with associated injuries, it may not be possible to obtain these studies prior to emergency laparotomy. In these patients, an intraoperative single-shot intravenous urogram is safe and of high quality in most cases. This study often provides important information that facilitates rapid and accurate decision making. It can confirm function in the noninjured kidney and help in identifying blunt renal injuries that may be safely observed.
Rupture of the bladder, like urethral disruption, is frequently associated with pelvic fractures. Seventy-five percent of ruptures are extraperitoneal and 25% intraperitoneal. Intraperitoneal bladder ruptures should be repaired through a mid-line abdominal incision. Rupture of the anterior wall of the bladder can be repaired by direct suture; rupture of the posterior wall can be repaired from inside the bladder after an opening has been made in the anterior wall. Care should be taken to avoid entering a pelvic hematoma. Retroperitoneal injuries can often be treated with urinary drainage, depending on the size of injury. Postoperatively, urine should be diverted for at least 7 days.
Membranous prostatic urethral disruption is often associated with pelvic fractures or deceleration injuries. Blood at the urethral meatus associated with scrotal hematoma and high-riding prostate on digital rectal examination are the classic signs of injury to the male urethra. The prostate may be elevated superiorly by the pelvic hematoma and will be free-riding and high on rectal examination. If these signs are present, a retrograde urethrogram should be performed before attempts at catheter placement, which may convert an incomplete injury to a complete disruption. If an injury is present, urethrography will demonstrate free extravasation of contrast from the urethra into the preperitoneal space.
Penetrating injuries are best treated with primary repair. Suprapubic bladder drainage and delayed reconstruction of blunt urethral disruption injuries are safe and effective in most cases. Immediate realignment with cystourethroscopy and placement of a urethral catheter is an attractive, minimally invasive alternative. In cases of partial disruption, it has been shown to result in stricture-free outcomes.
Major injuries to the bulbous or penile urethra should be managed by suprapubic urinary diversion. A voiding cystourethrogram may later reveal a stricture, but operative correction or dilation is usually not necessary.
Advances in the imaging and staging of renal trauma as well as in treatment strategies have decreased the need for operation and increased renal preservation. More than half of renal injuries can be treated nonoperatively. Management criteria are based on radiographic, laboratory, and clinical findings. Nonoperative treatment of penetrating renal lacerations is appropriate in hemodynamically stable patients without other injuries. Small to moderate injuries can be treated nonoperatively, but severe injuries are associated with a significant risk of delayed bleeding if treated expectantly. Stable patients may be candidates for angiographic procedures to control bleeding, revascularize a dissection or injuries leading to vessel thrombosis. Renal exploration should be considered if laparotomy is indicated for associated injuries. A mid-line transabdominal approach is preferred. The renal artery and vein are secured before the Gerota fascia is opened. The injury should be managed by suture repair, partial nephrectomy, or, rarely, total nephrectomy. Pedicle grafts of omentum or free peritoneal patch grafts can be used to cover defects. Renal vascular injuries require immediate operation to save the kidney. Meticulous attention to reconstructive techniques in renal exploration can ensure an excellent renal salvage rate. Adherence to the principles of early proximal vascular control, debridement of devitalized tissue, hemostasis, closure of the collecting system, and coverage of the defect will maximize the salvage of renal function while minimizing potential complications.
Perirenal hematomas found incidentally at celiotomy should be explored if they are expanding, pulsatile, or not contained by retroperitoneal tissues or if a preexploration urogram shows extensive urinary extravasation.
4. Injuries to the male genitalia
Injuries to the male genitalia usually result in skin loss only; the penis, penile urethra, and testes are usually spared. Skin loss from the penis should be treated with a primary skin graft. Scrotal skin loss should be treated by delayed reconstruction; an exposed testis can be temporarily protected by placing it in a subcutaneous tissue pocket in the thigh.
Injuries of the female reproductive organs are infrequent except in combination with genitourinary or rectal trauma. Injuries to the uterine fundus usually can be repaired with absorbable sutures; drainage is not necessary. In more extensive injuries, hysterectomy may be preferable. The vaginal cuff may be left open for drainage, particularly if there is an associated urinary tract or rectal injury. Injuries involving the uterus in a pregnant woman usually result in death of the fetus. Bleeding may be massive in such patients, particularly in women approaching parturition. Cesarean section plus hysterectomy may be the only alternative.
Ureteral injuries are easily missed because urinalysis and imaging studies can be unreliable. Most such injuries can be successfully reconstructed by primary repair over stents, ureteral reimplantations, or ureteroureterostomy depending on the level of injury.
et al.: Age does not affect outcomes of nonoperative management of blunt splenic trauma. J Am Coll Surg. 2012;214:958.
et al.: Selective angiographic embolization of blunt splenic traumatic injuries in adults decreases failure rate of nonoperative management. J Trauma Acute Care Surg. 2012;72:1127.
et al.: Comparison of nonoperative management with renorrhaphy and nephrectomy in penetrating renal injuries. J Trauma. 2011;71:554.
et al.: Sew it up! A Western Trauma Association multi-institutional study of enteric injury management in the postinjury open abdomen. J Trauma. 2011;70:273.
et al.: Treatment of major hepatic necrosis: lobectomy versus serial debridement. J Trauma. 2012;69:562.
et al.: FAST scan: is it worth doing in hemodynamically stable blunt trauma patients? Surgery. 2010;148:695.
et al.: Surgical treatment of injuries to the solid abdominal organs: a 50-year perspective from the Journal of Trauma. J Trauma. 2010;69:1011.
AB: Current management of hepatic trauma. Surg Clin North Am. 2010;90:775.
et al.: Adherence to a simplified management algorithm reduces morbidity and mortality after penetrating colon injuries: a 15-year experience. J Am Coll Surg. 2012;214:591.
et al.: Impact of a defined management algorithm on outcome after traumatic pancreatic injury. J Trauma Acute Care Surg. 2012;72;100.
et al.: Angioembolization reduces operative intervention for blunt splenic injury. J Trauma. 2008;64:1472.
Much of our knowledge of blood vessel injuries was developed during the course of military conflicts in the 20th century. Although techniques for the management of vascular injuries were in use prior to World War I, arterial ligation to save a life rather than arterial repair to salvage a limb was generally employed, and amputation frequently resulted after vascular injury.
The current mortality rate for lower extremity arterial injury is low in both civilian and recent military series: 2%-6%. Limb salvage rates in civilian series are 85%-90%, with best results obtained for interposition vein grafts. Ligation, need for reoperation, and failed revascularization are associated with worse outcomes and higher amputation rates. Low mortality and improved limb salvage is a result of more rapid transport of injured people, improved blood volume replacement, selective use of arteriography and shunts, and better operative techniques.
The Epidemiology of Vascular Trauma
The epidemiology of vascular trauma has been studied in three different settings: military conflicts, large urban locations, and, to a lesser extent, rural areas. The types of injuries seen in civilian vascular trauma, once much different from military settings, are now more similar to military wounds. The incidence is increasing as a result of the rise in urban violence, motor vehicle crashes, and iatrogenic injuries owing to more frequent use of minimally invasive diagnostic and therapeutic procedures.
Peripheral vascular trauma typically occurs in young men between the ages of 20 and 40 years. In both urban and rural environments, penetrating mechanisms dominate, accounting for 50%-90% of vascular injuries. Because many vascular injuries of the head, neck, and torso are immediately fatal, most patients with vascular injuries surviving transport have extremity trauma. This is especially true in the military experience where extremity vascular injuries account for approximately 90% of all arterial trauma. In the urban civilian experience, extremity vascular injuries comprise about 50% of arterial injuries. In rural vascular trauma, blunt injuries occur more frequently than in urban populations.
Mortality and utilization of medical resources is higher among patients with vascular injuries than among patients who do not have blood vessel injuries. Vascular injuries from automobile accidents or falls from heights and crush injuries account for up to half of all noniatrogenic vascular injuries in US hospitals. The likelihood of vascular injury after blunt trauma correlates with the overall severity of the injury and the presence of specific orthopedic injuries; for example, up to 45% of patients with posterior knee dislocations or severe instability from high-velocity blunt trauma sustain popliteal artery injury.
The number of iatrogenic vascular injuries has risen dramatically in recent decades. Most involve diagnostic and therapeutic procedures utilizing the femoral (less frequently the brachial or axillary) vessels, which serve as percutaneous access routes. In order of decreasing frequency, injuries include hemorrhage and hematoma, pseudoaneurysm, arteriovenous fistula formation, vessel thrombosis, and embolization. Rates of injury range from 0.5% for diagnostic procedures to as high as 10% for therapeutic procedures involving large catheters. Increasing age, female gender, use of anticoagulation, and the presence of atherosclerosis increase the risk of these complications. Complications remote from the puncture site include vessel rupture and dissection. Operative procedures (especially hepatic and pancreaticobiliary surgery) are associated with iatrogenic vascular trauma. In addition, anterior and retroperitoneal approaches to the lumbar spine and other orthopedic procedures such as total joint replacement and arthroscopy can produce vascular injuries.
The local and regional effects of penetrating wounds are determined by the mechanism of vessel injury. Stab wounds, low-velocity (< 2000 ft/s) bullet wounds, iatrogenic injuries from percutaneous catheterization, and inadvertent intra-arterial injection of drugs produce less soft tissue injury and disrupt collateral circulation less than injuries from sources with greater kinetic energy. The high-velocity missiles responsible for war wounds produce more extensive vascular injuries, which involve massive destruction and contamination of surrounding tissues. The temporary cavitational effect of high-velocity missiles causes additional trauma to the ends of severed arteries and may produce arterial thrombosis due to disrupted intima even when the artery has not been directly hit. This blast effect can also draw material such as clothing, dirt, or pieces of skin along the wound tract, which contributes to the risk of infection. Associated injuries are often major determinants of the eventual outcome.
Shotgun blasts present special problems. Although muzzle velocity is low (about 1200 ft/s), the multiple pellets produce widespread damage, and shotgun wadding entering the wound enhances the likelihood of infection. Similar to high-velocity injuries, the damage is often much greater than might be anticipated from inspection of the entry wound. Moreover, the multiplicity of potential sites of arterial damage often mandates diagnostic arteriography even in the presence of obvious arterial insufficiency.
Motor vehicle accidents are a major cause of blunt vascular trauma. Multiple injuries include fractures and dislocations; and while direct vascular injury may occur, in most instances the damage is indirect due to fractures. This is especially likely to occur with fractures near joints, where vessels are relatively fixed and vulnerable to shear forces. For example, the popliteal artery and vein are frequently injured in association with posterior dislocation of the knee. Fractures of large heavy bones such as the femur or tibia transmit forces that have cavitation effects similar to those caused by high-velocity bullets. There is extensive damage to soft tissues and neurovascular structures, and edema formation interferes with evaluation of pulses. Delay in diagnosis and the presence of associated injuries decrease the chances of limb salvage. Contusions or crush injuries may result in complete or partial disruption of arteries, producing intimal flaps or intramural hematomas that impede blood flow.
Blunt thoracic aortic injury (BTAI) is a serious traumatic injury that continues to have a high initial mortality and is associated with modern high-speed methods of transportation or significant falls. Autopsy data from cases of fatal BTAI demonstrated that 57% of patients were dead at the scene or on arrival to the hospital, 37% died during the first 4 hours at the hospital, and only 6% died after 4 hours in the hospital. The disruption generally occurs at the aortic isthmus (between the left subclavian artery and the ligamentum arteriosum) due to a deceleration injury in which the heart, the ascending aorta, and the transverse arch continue to move forward while movement of the isthmus and the descending aorta is limited by their posterior attachments. Clinical findings associated with traumatic rupture of the thoracic aorta are listed in Table 13–5 and radiographic findings in Table 13–6. Blunt traumatic injury to the abdominal aorta is uncommon, but it has been reported from lap seat belt trauma.
Table 13–5.Clinical features of traumatic aortic rupture. ||Download (.pdf) Table 13–5. Clinical features of traumatic aortic rupture.
History of high-speed deceleration injury
Superior vena cava syndrome
Multiple or first or second rib fractures
Upper extremity hypertension or pulse deficits
Hematoma in the carotid sheaths
Hoarseness with normal larynx
Table 13–6.Radiographic features of traumatic aortic rupture. ||Download (.pdf) Table 13–6. Radiographic features of traumatic aortic rupture.
Widening of mediastinum
Multiple or first rib or second rib fractures
Esophageal deviation to the right
Tracheal deviation to the right
Depression of left main stem bronchus
Obliteration of the aortic knob
Obliteration of the descending aorta
Obliteration of the aortopulmonary window
Obliteration of the medial left upper lobe
Widened paravertebral stripe
Almost any vessel can be injured by blunt trauma, including the extracranial cerebral and visceral arteries. Blunt carotid arterial injuries are associated with mortality rates of 20%-30%, with over 50% of survivors having permanent, severe neurologic deficits. Whereas in the past vertebral artery injuries were considered innocuous, recent studies have reported devastating complications related to these injuries, including a 70% incidence of coexistent cervical spine injuries. Traumatic injury to the superior mesenteric artery is associated with a 50% mortality rate. The brachial and popliteal arteries, which cross joints and are exposed to direct trauma, are particularly susceptible to injury as a result of fractures and dislocations.
When pulsatile external hemorrhage is present, the diagnosis of arterial injury is obvious, but when blood accumulates in deep tissues of the extremity, the thorax, abdomen, or retroperitoneum, the only manifestation may be shock. Peripheral vasoconstriction may make evaluation of peripheral pulses difficult until blood volume is restored. If the artery is completely severed, thrombus may form at the contracted vessel ends and a major vascular injury may not be suspected. The presence of arterial pulses distal to a penetrating wound does not preclude arterial injury; as many as 20% of patients with injuries of major arteries in an extremity have palpable pulses distal to the injury, either because the vessel has not thrombosed or because pulse waves are transmitted through soft clot. Conversely, the absence of a palpable pulse in an adequately resuscitated patient is a sensitive indicator of arterial injury.
Acute arterial insufficiency must be diagnosed promptly to prevent tissue loss. Ischemia should be suspected when the patient has one or more of the “five Ps”: pain, pallor, paralysis, paresthesia, or pulselessness. The susceptibility of different cells to hypoxia varies (eg, sudden occlusion of the carotid artery results in brain damage within minutes unless collateral circulation can maintain adequate perfusion, but a kidney can survive severe ischemia for up to an hour). Peripheral nerves are quite vulnerable to ischemia because they have a high basal energy requirement to maintain ion gradients over large membrane surfaces and because they have few glycogen stores. Hence, interruption of arterial flow for relatively short periods can result in nerve damage due to interrupted substrate delivery. In contrast, skeletal muscle is more tolerant of decreased arterial flow. Muscle can be ischemic for up to 4 hours without developing histologic changes. In general, complete interruption of all arterial inflow (including collateral blood supply) results in neuromuscular ischemic damage after 4-6 hours. Restoration of flow can actually worsen this damage as part of the reperfusion syndrome and can increase the severity of the original ischemic insult.
Prolonged ischemia can produce muscle necrosis and rhabdomyolysis, which releases potassium and myoglobin into the circulation. Myoglobin is an oxygen-transporting protein similar in structure to hemoglobin; it is innocuous unless it dissociates into hematin, which is nephrotoxic in an acidic milieu. Precipitation of hematin pigment also occurs when urine flow is reduced by hypotension or hypovolemia, obstructing renal tubules and worsening nephrotoxicity. Myoglobinemia can lead to acute tubular necrosis and renal failure, hyperkalemia, and a risk of life-threatening arrhythmias. Thus, in addition to limb loss, acute arterial ischemia can produce organ failure and death.
Disruption of an arterial wall as a result of trauma may lead to formation of a false aneurysm. The wall of a false aneurysm is composed primarily of fibrous tissue derived from nearby tissues, not arterial tissue. Because blood continues to flow past the fistulous opening, the extremity is seldom ischemic. False aneurysms may rupture at any time. They continue to expand because they lack vascular wall integrity. Spontaneous resolution of pseudoaneurysms larger than 3 cm is unlikely, and operative repair becomes increasingly difficult as the aneurysms increase in size and complexity with time. Symptoms gradually appear as a result of compression of adjacent nerves or collateral vessels or from rupture of the aneurysm—or as a result of thrombosis with ischemic symptoms. Iatrogenic false aneurysms after arterial puncture thrombose spontaneously within 4 weeks when they are less than 3 cm in diameter. Simple ultrasound follow-up rather than operative therapy is indicated. Color-flow duplex-guided compression of iatrogenic pseudoaneurysms is successful in 70%-90% of attempts, but the procedure is uncomfortable and may take hours of probe pressure. Ultrasound-guided thrombin injection has been effective for thrombosis of large false aneurysms in a matter of seconds, but distal arterial thrombosis has also been described using this technique.
With simultaneous injury of an adjacent artery and vein, a fistula may form that allows blood from the artery to enter the vein. Because venous pressure is lower than arterial pressure, flow through an arteriovenous fistula is continuous; accentuation of the bruit and thrill can be detected over the fistula during systole. Traumatic arteriovenous fistulas may occur as operative complications (eg, aortocaval fistula following removal of a herniated intervertebral disk). Iatrogenic femoral arteriovenous fistulas after arteriograms and cardiac catheterization are seen with increasing frequency. Long-standing large arteriovenous fistulas may result in high-output cardiac failure. Similar to iatrogenic pseudoaneurysms occurring after arteriography, spontaneous resolution of acute arteriovenous fistulas usually occurs.
Arterial injury must be considered in any injured patient. Patients who present in shock following penetrating injury or blunt trauma should be assumed to have vascular injury until proven otherwise. Any injury near a major artery should arouse suspicion. A plain film may be helpful in demonstrating a fracture whose fragments could jeopardize an adjacent vessel or a bullet fragment that could have passed near to a major vessel. Before the x-ray is taken, entrance and exit wounds should be marked with radiopaque objects such as a paper clip.
Diagnosis is usually established on the basis of physical examination looking for signs of injury (Table 13–7). In addition to checking for obvious hemorrhage and the five Ps, the physician should listen for a bruit, palpate for a thrill (eg, of an arteriovenous fistula), and look for an expanding hematoma (eg, of a false aneurysm). Secondary hemorrhage from a wound is an ominous sign that may herald massive hemorrhage. The finding of these “hard” signs reliably reflects the presence of a vascular injury; hard signs mandate immediate exploration in most instances. The presence of “soft” signs (history of bleeding, diminished but palpable pulse, injury in proximity to a major artery, neurapraxia) requires further tests or serial observation.
Table 13–7.Signs of extremity vascular injury. ||Download (.pdf) Table 13–7. Signs of extremity vascular injury.
Expanding or pulsatile hematoma
Bruit or thrill
Absence of distal pulse
History of hemorrhage at scene, now stopped
Deficit of nerve associated with vessel
Stable, nonexpanding hematoma
Proximity of wound to major extremity blood vessel
Ankle brachial index < 0.9
Doppler flow studies have gained importance in the diagnosis of arterial trauma. An ankle brachial index (ABI), determined by dividing the systolic pressure in the injured limb by the systolic pressure in an uninjured arm, is highly reliable for excluding arterial injury after both blunt and penetrating trauma. An ABI less than 0.9 has sensitivity of 95%, specificity of 97%, and negative predictive value of 99% for determining the presence of clinically significant arterial injury. Thus, only patients with soft signs and an ABI less than 0.9 require arteriography.
Color-flow duplex ultrasonography combines real-time B mode (brightness modulation) ultrasound imaging with a steerable pulsed Doppler flow detector. This technology can provide images of vessels and velocity spectral analysis. Color-flow duplex scanning of an area of injury is noninvasive, painless, portable, and easily repeated for follow-up examinations. When compared with arteriography and performed by experienced examiners, duplex ultrasound identifies nearly all major injuries that require treatment, potentially at considerable cost savings. In addition to screening for arterial trauma, duplex scanning has been used to detect pseudoaneurysms, arteriovenous fistulas, and intimal flaps. However, potential logistical and resource problems exist. The technology is sophisticated and requires skill in operation and interpretation, which is not always immediately available.
Arteriography is the most accurate diagnostic procedure for identifying vascular injuries (Figure 13–14). Arteriography to exclude vascular injury for soft signs results in a negative exploration rate of 20%-35% and an arteriography-related complication rate of 2%-4%. Proximity as the sole indication for arteriography has an extremely low yield, ranging from 0% to 10%. Patients with unequivocal signs of arterial injury on physical examination or plain films should have urgent operation. The false-negative rate of arteriography is low, and a normal arteriogram precludes the need for surgical exploration. Virtually all arteriographic errors are due to false-positives, which occur in 2%-8% of patients. Technical considerations in performing arteriography include the following: (1) entrance and exit wounds should be marked with a radiopaque marker; (2) the injection site should not be near the suspected injury; (3) an area 10-15 cm proximal and distal to the suspected injury should be included in the arteriographic field; (4) sequential films should be obtained to detect early venous filling; (5) any abnormality should be considered an indication of arterial injury unless it is obviously the result of preexisting disease; and (6) two different projections should be obtained.
Arteriogram showing traumatic pseudoaneurysm of subclavian/axillary artery from penetrating injury.
Emergency center arteriography using micropuncture Seldinger technique or cannulating the artery to be studied with an 18-gauge catheter (antegrade in the lower extremity and prograde in the upper extremity arteries) is quick and accurate. The use of fluoroscopy, especially if equipped with subtraction capability, simplifies the timing of contrast injection and x-ray exposure. Fluoroscopy is particularly helpful to visualize distal arteries and minimize the amount of contrast media needed. Arteriography may be particularly useful in differentiating arterial injury from spasm. In general, it is risky to attribute abnormal physical findings in an injured patient to arterial spasm; an arteriogram is indicated in such patients.
Arteriography is also valuable when arterial injuries may have occurred at multiple sites or to localize an injury when a long parallel penetration makes this determination difficult. Complications of arteriography include groin hematomas, iatrogenic pseudoaneurysms, arteriovenous fistulas, embolic occlusions, and delays in diagnosis that may lead to irreversible ischemia in marginally perfused limbs. The availability of CT angiograms with latest generation multidetector contrast-enhanced spiral scanners is a viable alternative to traditional angiography. CT angiograms can diagnose intimal dissections, pseudoaneurysms, arteriovenous fistulas, thrombosis or occlusion, and active bleeding. Metallic foreign bodies can create artifacts that interfere with generation of optimal CT angiogram studies.
For patients suspected of having BTAI based on mechanism of injury, the chest x-ray is a good screening tool to determine the need for further investigation. The most significant radiographic findings for possible BTAI include widened mediastinum, obscured aortic knob, deviation of the left mainstem bronchus or nasogastric tube, and opacification of the aortopulmonary window. Helical chest CT scanning is a useful diagnostic tool for screening and diagnosis of BTAI (Figure 13–15). A negative chest CT scan can obviate the need for further evaluation with a contrast aortogram. Patients with indeterminate CT scans or positive scans should have confirmation and delineation of the extent of BTAI with arteriography or a CT angiogram. In selected instances, cardiothoracic and/or trauma surgeons may consider helical CT scanning alone to be an adequate and complete work-up for BTAI. In addition, a helical CT angiogram with 3D reconstruction guides potential endovascular approach for treatment of BTAI. The use of either transesophageal echocardiography or intraluminal ultrasound in the diagnosis of BTAI continues to evolve, but they are not considered standard diagnostic modalities.
Computed tomography scan of the chest showing traumatic disruption of the aorta from blunt injury.
A rapid but thorough examination should be performed to determine the complete extent of injury. The physician must establish the priority of arterial injury in the overall management of the patient and should remember that delay in arterial repair decreases chances of a favorable outcome. When repair is performed within 12 hours after injury, amputation is rarely necessary; if repair is performed later, the incidence of amputation is about 50%. Depending on the degree of ischemia, delay in arterial repair will lead to lasting neuromuscular damage after as short a period as 4-6 hours.
Restoration of blood volume and control of hemorrhage are done simultaneously. If exsanguinating hemorrhage precludes resuscitation in the emergency room, the patient should be moved directly to the operating room. External bleeding is best controlled by firm direct pressure or packing. Probes or fingers should not be inserted into the wound because a clot may be dislodged, causing profuse bleeding. Tourniquets occlude venous return, disturb collateral flow, and further compromise circulation and should not be employed unless exsanguinating hemorrhage cannot be controlled by other means. Atraumatic vascular clamps may be applied to accessible vessels by trained surgeons, but blind clamping can increase damage and injure adjacent nerves and veins.
After hemorrhage has been controlled and general resuscitation accomplished, further assessment is possible. The extent of associated injuries is determined and a plan of management made. Large-bore intravenous catheters should be placed in extremities with no potential venous injuries. It is prudent to preserve the saphenous or cephalic vein in an uninjured extremity for use as a venous autograft for vascular repair.
B. Nonoperative Treatment
Some arterial injuries remain asymptomatic and heal. Data supporting the practice of observation of small or asymptomatic arterial injuries have emerged from experimental animal studies and clinical reports showing resolution, improvement, or stabilization of arterial injuries. In well-defined settings, this strategy has proved safe in follow-up reports covering periods of up to 10 years. Thus, a nonoperative approach may be appropriate for compliant patients willing to return for follow-up who have: (1) no active hemorrhage; (2) low-velocity injuries (particularly stab wounds or iatrogenic punctures); (3) minimal arterial wall disruptions (< 5 mm); (4) small (< 5 mm) intimal defects; and (5) intact distal circulation.
Follow-up must include frequent physical examinations and carefully performed noninvasive studies, and patients should be asymptomatic and the strategy must be reconsidered if symptoms develop. Adjuvant therapy with antiplatelet agents is usually recommended to improve patency in patients with intimal flaps.
Endovascular management has assumed a greater role in the treatment of arterial trauma in recent years. Transcatheter embolization with coils or balloons has been successful in managing selected arterial injuries such as pseudoaneurysms, arteriovenous fistulas, and active bleeding from nonessential arteries. Coils are made of stainless steel with wool or polyester tufts. They are extruded at the site of vessel injury through 5F or 7F catheters. After deployment, the coils expand and lodge at the extrusion site and the tufts promote thrombosis. Catheter-based intra-arterial infusion of vasodilators has also been used to treat vasospasm in small distal arteries.
The recent popularity of endovascular grafting in elective vascular surgery (Chapter 34) has been applied to the treatment of arterial trauma. A fixation device such as a stent is attached to a graft, and the Stent graft is inserted endoluminally from a remote site and deployed at the site of injury to repair false aneurysms or arteriovenous fistulas. The indications for endovascular grafting are likely to change as technology advances, but the most frequent application currently is in stable patients with delayed presentations who have complex false aneurysms or arteriovenous fistulas. Use of Stent grafts in the acute setting requires the availability of a wide variety of sizes and lengths of grafts and advanced catheter skills.
Endovascular repair of BTAI can be performed either electively or even emergently (Figure 13–16). In a recent American Association for the Surgery of Trauma (AAST) multicenter study, two-thirds of patients underwent endovascular Stent graph repair as compared to one-third who underwent traditional open repair. When adjusted for confounding variables, the endovascular approach was associated with reduced mortality (odds ratio 8.42, 95% confidence interval 2.76-25.69) and fewer blood transfusions. Further study is needed to determine the long-term outcome using endovascular techniques to repair BTAI. Commercial grafts have yielded better results than the noncommercial “homemade” grafts. Thoracic aorta lacerations of more than 1.5 cm resulting in graft apposition length less than 2 cm or those near or in the curvature of the aortic arch are associated with an increased risk of endoleak. Endoleak occurred in 14% of the AAST BTAI trial patients, with half being successfully managed with the deployment of additional stent grafts.
Aortogram and placement of aortic stent graft to repair a blunt aortic disruption.
In selected cases of BTAI repair, whether it is operative or endovascular, treatment is delayed because treatment and recovery from other more life-threatening injuries has priority (eg, severe pulmonary contusion, brain injury). This is acceptable, and the incidence of aortic rupture after 4 hours in the hospital is low. Systemic blood pressure and heart rate should be controlled with a beta-blocker and other pharmacologic agents as necessary to minimize the risk of rupture while waiting for definitive repair of the injured aorta.
General anesthesia is preferable to spinal or regional anesthesia. When vascular injuries involve the neck or thoracic outlet, endotracheal intubation must be performed carefully to avoid dislodging a clot and to protect the airway. Moreover, care is necessary to avoid neurologic damage in patients with associated cervical spine injuries. At least one uninjured extremity should also be prepared for surgery so that saphenous or cephalic vein conduit may be obtained if a vein graft is required. Provision should also be made for operative arteriography.
Incisions should be generous and parallel to the injured vessel. Meticulous care in handling incisions is essential to avoid secondary infections; all undamaged tissue should be conserved for use in covering repaired vessels. Preservation of all arterial branches is important in order to maintain collateral circulation. Atraumatic control of the vessel should be achieved proximal and distal to the injury so that the injured area may be dissected free of other tissues and inspected without risk of further bleeding. When large hematomas and multiple wounds make exposure and clamping of vessels difficult, it is wise to place a sterile orthopedic tourniquet proximal to the injury that can be inflated temporarily if needed.
The extent of arterial injury must be accurately determined. Arterial spasm generally responds to gentle hydraulic or mechanical dilation. Local application of warm saline or drugs such as papaverine, tolazoline, lidocaine, or nitroglycerin is occasionally effective in relieving spasm. Intra-arterial injection of nitroglycerin or papaverine is also very effective in alleviating spasm. If spasm persists, however, it is best to assume that it is caused by an intramural injury, and the vessel should be opened for direct inspection. An old adage is that spasm is spelled “c-l-o-t.”
All devitalized tissue, including damaged portions of the artery, must be debrided. One should resect only the grossly injured portion of the vessel. The method of reconstruction depends on the degree of arterial damage. In selected instances, the ends of injured vessels can be approximated and an end-to-end anastomosis created. If the vessels cannot be mobilized well enough to provide a tension-free anastomosis, an interposition graft should be used. Early experience with prosthetic interposition grafts was disappointing since postoperative infection, thrombosis, and anastomotic disruption were common. These problems have decreased considerably with the use of grafts made of expanded polytetrafluoroethylene (PTFE). Proponents of synthetic graphs focus on the fact that they fail well (eg, infected pseudoaneurysm), whereas a vein graft will disintegrate and result in a sudden blow-out type hemorrhage. Nevertheless, most surgeons still prefer to use an autogenous graft (ie, vein or artery) in severely contaminated wounds. Saphenous vein grafts should be obtained from the noninjured leg to avoid impairment of venous return on the side of the injury. Patch angioplasty using saphenous vein is performed when closure of a partially transected vessel would result in narrowing. Suturing should be done with fine 5-0 or 6-0 monofilament material.
In the unusual circumstance of isolated vascular injury, 5000-10,000 units of intravenous heparin can be given to prevent thrombosis. Otherwise, a small amount of dilute heparin solution (100 units/mL) may be gently injected into the proximal and distal lumen of the injured vessel before clamps are applied. Proximal and distal thrombi are removed with a Fogarty embolectomy catheter. Back-bleeding from the distal artery is not a sure indication that thrombus is absent. A completion operative arteriogram is indicated to determine distal patency and to check on the adequacy of the reconstruction—even when distal pulses are palpable.
It was formerly taught that fractures should be stabilized before vascular injuries were repaired so that manipulation of bones would not jeopardize vascular repair. The disadvantages of this dictum were delay in restoration of flow to ischemic tissue and interference with vascular reconstruction and subsequent arteriographic study of the completed repair by the fixation device. It is currently recommended that vascular repair be performed first, followed by careful application of external traction devices that allow easy access to the wound for observation and dressing changes. Another alternative is to place an intraluminal shunt temporarily across the vascular injury to decrease ischemia while fractures or other injuries are treated. Once the fracture is stabilized, the temporary shunt can be removed and definitive vascular repair completed. Improved outcomes similar to civilian lower extremity vascular trauma have been attributed to the use of temporary vascular shunts and damage control techniques in the current Iraq War.
Repaired vessels must be covered with healthy tissue. If left exposed, they invariably desiccate and rupture. Skin alone is inadequate, because subsequent necrosis of the skin would leave the vessels exposed, greatly endangering the reconstruction. Generally, an adjacent muscle (eg, sartorius muscle for coverage of the common femoral artery) can be mobilized and placed over the repair. Musculocutaneous flaps can be constructed by plastic surgeons to cover almost any site. In an extensive or severely contaminated wound, a remote bypass may be routed through clean tissue planes to circumvent difficult soft tissue coverage problems.
Venous injuries commonly accompany arterial injuries. In order of decreasing frequency, the most common extremity venous injuries are the superficial femoral vein, the popliteal vein, and the common femoral vein. The relative importance and timing of venous repair in an injured extremity is controversial. Advocates of routine venous repair contend that ligation is associated with significant postoperative morbidity, including more frequent failure of arterial repairs due to compromised outflow, venous insufficiency, compartment syndrome, and limb loss. Proponents of venous ligation argue that venous repairs are difficult (requiring interposition, compilation, and spiral grafting), time consuming (dangerous in the multiply-injured patient), and likely to cause occlusion (patency rates are only about 50%). The presence of postoperative edema after combined arterial and venous injuries is not reliably reduced by attempted venous repair. It seems reasonable to recommend repair of venous injuries when the repair is not too technically difficult (lateral venorrhaphy) and the patient is hemodynamically stable. Complex repair with autologous vein or ringed PTFE can yield good short-term patency in experienced hands (77% primary repair, 67% vein graft, 74% PTFE). Thus, the decision to repair the vein depends on the condition of the patient and the condition of the vein. When venous ligation is necessary, postoperative edema can be controlled by elevation of the extremity and use of compression stockings or wraps. In patients undergoing venous repair, patency should be monitored using duplex scanning. If thrombosis of the repair is detected and there are no contraindications, anticoagulation should be instituted and maintained for at least 3 months postoperatively.
Fasciotomy is an important adjunctive treatment in many cases of arterial trauma. Indications include the following: (1) combined arterial and venous injury; (2) massive soft tissue damage; (3) delay between injury and repair (4-6 hours); (4) prolonged hypotension; and (5) excessive swelling or high tissue pressure measured by one of several techniques. Whenever compartment pressures (measured with a needle and manometer) approach 25-30 mm Hg, fasciotomy should be considered. Fasciotomies must be performed through adequate skin incisions because when edema is massive, the skin envelope itself can compromise neurovascular function.
Fasciotomies are not benign procedures. They create large open wounds, and chronic venous insufficiency is a recognized late complication even in the absence of venous reflux or obstruction. The chronic swelling is thought to be related to loss of integrity of the ensheathing fascia of the calf muscles, reducing the efficiency of the calf muscle pump. Thus, some authorities recommend against routine use of fasciotomies at the initial operation. This approach is dependent on the ability to conduct frequent serial physical examinations and the ready availability of an operating room should problems arise. In the postoperative period, compartmental pressures can be measured using a handheld solid-state transducer as often as clinically indicated. Normal intracompartment pressure is less than 10 mm Hg. In general, a pressure of 25-30 mm Hg requires either fasciotomy or continuous monitoring. When the pressure exceeds 30 mm Hg, fasciotomy is mandatory. In patients who are obtunded or who cannot cooperate with serial physical examination, earlier fasciotomy should be considered.
High-energy or crush injuries of the extremities are associated with high morbidity and a poor prognosis for useful limb function—there is a high late amputation rate despite initial limb salvage. Vascular injuries are now repaired with a high rate of success, but associated orthopedic, soft tissue, and nerve injuries are the critical factors that determine long-term function. A number of scoring systems or indices have been proposed to help determine when to amputate immediately and thus reduce the number of protracted reconstructive procedures that ultimately fail. Management of the mangled extremity is particularly difficult, and none of the scoring systems are universally accepted. Evaluation and management of these patients should be multidisciplinary, and the decision to amputate emergently should be made by two independent surgeons whenever possible.
et al.: Evolving role of endovascular techniques for traumatic vascular injury: a changing landscape? J Trauma Acute Care Surg. 2012;72:41.
et al., the American Association for the Surgery of Trauma Thoracic Aortic Injury Study Group: Operative repair or endovascular stent graft in blunt traumatic thoracic aortic injuries: results of an American Association for the Surgery of Trauma Multicenter Study. J Trauma. 2008;64:561.
SR: Vascular injury: 50th anniversary year review article of the journal of trauma. J Trauma. 2010;68:1009.
et al.: Damage control resuscitation for vascular surgery in a combat support hospital. J Trauma. 2008;65:1.
et al.: Endovascular repair compared with operative repair of traumatic rupture of the thoracic aorta: a nonsystemic review and a plea for trauma-specific reporting guidelines. J Trauma. 2011;71:1059.
et al.: Minimal aortic injury after blunt trauma: selective nonoperative management is safe. J Trauma. 2011;71:1519.
et al.: Imaging vascular trauma. Br J Surg. 2012;99:494–505.
et al.: Tourniquets, vascular shunts, and endovascular technologies: esoteric or essential? A report from the 2011AAST military liaison panel. J Trauma Acute Care Surg. 2012;73:282.
et al.: Management of the left subclavian artery during endovascular stent grafting for traumatic aortic injury—a systematic review. Eur J Vasc Endovasc Surg. 2011;41:758.
et al.: A decade’s experience with temporary intravascular shunts at a civilian level I trauma center. J Trauma. 2008;65:316.
et al.: Penetrating femoropopliteal injury during modern warfare: experience of the Balad Vascular Registry. J Vasc Surg. 2008;47:1259.
Blast injuries in civilian populations occur as a result of fireworks, household explosions, or industrial accidents. Urban guerrilla warfare or terrorist tactics may take the form of letter bombs, suitcase bombs, vehicle bombs, and suicide bombers. Injuries occur from the effects of the blast itself, propelled foreign bodies, or, in large blasts, from falling objects. Military blast injuries may also involve personnel submerged in water. Water increases energy transmission and the possibility of injury to the viscera of the thorax or abdomen. The pathophysiology of blast injuries involves two mechanisms. Crush injury results from rapid displacement of the body wall and may result in laceration and contusion of underlying structures. Minor displacements may produce serious injury if the body wall velocity is high. In addition, the motion of the body wall generates waves that propagate within the body and transfer energy to internal sites.
The injury is dependent upon proximity to the blast, space confinement, and detonation size. Large explosions cause multiple foreign body impregnations, bruises, abrasions, and lacerations. Gross soilage of wounds from clothing, flying debris, or explosive powder is common. About 10% of all casualties have deep injuries to the chest or abdomen. Blast-induced circulatory shock may be caused by immediate myocardial depression without a compensatory vasoconstriction. Lung damage usually involves rupture of the alveolus with hemorrhage. Air embolism from bronchovenous fistula may cause sudden death. The mechanisms of lung injury are thought to be due to spalling effects (splintering forces produced when a pressure wave hits a fluid-air interface), implosion effects, and pressure differentials. Hypoxia may result from a ventilation-perfusion mismatch caused by the pulmonary hemorrhage. Patients with pulmonary blast injury may die despite intensive respiratory support.
Blast injury causing pneumatic disruption of the esophagus or bowel has been reported. Tension pneumoperitoneum is a known although rare complication of barotrauma. Letter bombs cause predominantly hand, face, eye, and ear injuries. Energy transmission within the fluid media of the eye can cause globe rupture, dialysis of the iris, hyphema of the anterior chamber, lens capsule tears, retinal rupture, or macular pucker. Ear injuries may consist of drum rupture or cochlear damage. There may be nerve or conduction hearing deficit or deafness. Tinnitus, vertigo, and anosmia are also seen in letter bomb casualties.
Chest x-ray may initially be normal or may show pneumothorax, pneumomediastinum, or parenchymal infiltrates. In mass casualty situations it may be necessary to reserve the use of CT scans for those patients with acute changing neurologic examinations during the immediate intake period. Patients with multiple penetrating injuries from shrapnel may benefit from full-body CT scanning following initial stabilization and evaluation. Correlation of radiologic imaging studies with clinical examination is useful in guiding which injuries may need operative intervention when the number of skin surface wounds is high and it is impractical to explore all of these wounds.
Severe injuries with shock from blood loss or hypoxia require resuscitative measures to restore perfusion and oxygenation. Penetrating injuries of the brain may require neurosurgical intervention along with intracranial pressure monitoring. The usual criteria for exploring penetrating wounds of the thorax or abdomen are employed. Perforation of hollow organs should be suspected in patients with appropriate histories, particularly those who were submerged at the time of injury. Respiratory insufficiency may result from pulmonary injury or may be secondary to shock, fat embolism, or other causes. Tracheal intubation and prolonged respiratory care with mechanical ventilation may be necessary. In cases of tension pneumoperitoneum, surgical decompression may dramatically improve respiratory and hemodynamic functions. Shrapnel is the main cause of abdominal injury following terrorist bombings. Surgical treatment of extremity injuries requires wide debridement of devitalized muscle, thorough cleansing of wounds, and removal of foreign materials. The possibility of gas gangrene in contaminated muscle injuries may warrant open treatment. Eye injuries may require immediate repair. Ear injuries are usually treated expectantly.
et al.: Abdominal trauma after terrorist bombing attacks exhibits a unique pattern of injury. Ann Surg. 2008;248:303.
et al.: The pattern of thoracic trauma after suicide terrorist bombing attacks. J Trauma. 2010;69:1022.
et al.: Improved characterization of combat injury. J Trauma. 2010;68:1139.
et al.: Management of post-traumatic retained hemothorax: a prospective, observational, multicenter AAST study. J Trauma Acute Care Surg. 2012;72:11.