CONTENT PART 1: PRINCIPLE OF TRAUMA..3 Neuroendocrine response..4 Metabolic Response...4 Treatment of patient who has sustained trauma.

5 Primary survey Airway5 Breathing9 Circulation & shock.10 Hypovolemic shock...11 Neurogenic shock..12 Cardiogenic shock.12 Secondary survey Head & spine injuries......14 Neck injuries.16 Thoracic injuries..18 Abdominal injuries..20 Extremity injuries21 Inhalation injuries...22 Definitive management.22 Role of otolaryngologist22 Highlights...23 Reference...25 PART 2: MAXILLARY AND PREORBOTAL FRACTURE Anatomy Buttresses..26 Maxilla..26 Zygoma.27 Orbit..28 Patophysiology/ mechanism of trauma Le Fort Fractures.30 Others maxillaries fractures...31 Zygomaticomaxillary complex fractures...31

Orbital floor fracture..32 Other orbital fracture.33 Patient evaluation Computed tomography...33 Ophthalmologic evaluation.33 Fracture management: Principles Immediate reconstruction...34 Maxillomandibular fixation34 Extended access approaches...35 Stable external fixation36 Fracture management: surgical techniques Zygoma.36 Palate.40 Maxilla .42 Orbital walls.44 Complications Lid damage...47 Vision loss.49 Implant visibility..49 Malocclusion 50 Temporomandibular joint injury...50 Recent technical adjuvant Bioresorbable implants...51 Endoscopic surgery.51 Surgical model and computer-aided surgery51 Intraoperative CT scanning ...52 Highlights...52 References .53

Principles of Trauma
James Chan Peter J. Koltai Trauma is the leading cause of death and disability of Americans younger than 40 years1. In the United States, more than 150,000 violent deaths occur each year, and more than 500,000 trauma victims are left with permanent disabilities. Annually, approximately 30 to 40 million visits are made to emergency departments for injury treatment (2). The cost to our society is significant. In 2000, $117 billion was spent by Americans, which accounts for 10% of all medical expenditures (3). This is comparable to the percentages attributable to other public health issues such as obesity (9.1%) and smoking (14.4%)4. Deaths from trauma fall into three categories immediate, early, and late. Immediate death occurs within minutes of injury and is caused by acute airway obstruction or major vessel disruptions of the brain, heart, or other internal organs. Early death occurs in the first few hours after injury and is associated with excessive hemorrhage, blood accumulation around the brain, or respiratory failure. Late death occurs days to weeks after trauma and is caused by sepsis and multiple organ failure. More than half the deaths due to trauma occur within several minutes of the accident. Because immediate treatment is rarely available, accident prevention is the most logical way to decrease this number. Many public health injury-prevention strategies have been successfully implemented, including use of seat belts (5) and bicycle helmets (6), implementation of blood alcohol limits (7), and fire-safety education, including widespread smoke alarm use (8). Early deaths account for about one third of all trauma deaths. Although not all of these patients can be saved, many can be treated effectively with a rapid and definitive response. This requires a parallel system of prehospital care and hospital care at dedicated trauma centers. Death at an accident scene is usually related to head injury with associated hypoventilation due to loss of consciousness. Intubation in the field can thus be lifesaving. Another common cause of prehospital death is massive hemorrhage. When intravenous catheters are inserted at the scene, circulatory volume can be maintained until the hemorrhage can be surgically controlled. Rapid transport to a hospital with an organized team of surgeons, anesthesiologists, and trauma professionals is vital for the effective treatment of trauma patients. In urban areas, ambulances usually provide efficient transportation to the hospital. In rural areas, distance becomes a critical factor, and helicopters or airplanes can be lifesaving. Trauma patients undergo rapid and severe changes in normal body function, including hemorrhage, tissue hypoxia, cellular damage, and disrupted function of vital organs. The physiologic response to massive injury is dramatic and occurs both systemically and locally. Systemic responses include activation of the clotting sequence, shifts of extravascular fluid into the circulatory system, redistribution of blood flow to the heart and brain, and alterations in renal and pulmonary function to maintain acidbase balance. Metabolic changes include skeletal muscle and fat breakdown to provide a substrate for the body's fuel-intensive response to trauma. Local responses include immunologic activation with leukocytes mobilization, acute-phase protein synthesis, inflammatory cell migration into the injured area, and onset of fibroblast proliferation and blood vessel ingrowth to begin the wound-repair process. Understanding of the restorative mechanisms that occur in an acutely injured patient

is necessary for the complex task of treating these patients with regard to fluid maintenance, nutritional requirements, wound healing, and susceptibility to infection (9,10). Neuroendocrine Response Hemostatic adjustments to trauma are mediated by the neuroendocrine system. Stimuli such as hemorrhage, hypoxia, and tissue damage stimulate a graded response that increases to a peak level, after which additional response is no longer possible. Pain is the first signal from the central nervous system (CNS) to reestablish homeostasis. The hypothalamic response to pain stimulates the pituitary gland to release corticotropin, which stimulates adrenal secretion of cortisol. Pain causes elaboration of antidiuretic hormone for fluid conservation. Pain activates the sympathetic nervous system and stimulates direct adrenal secretion of epinephrine. Blood loss stimulates vascular pressure and volume receptors and precipitates a CNSmediated decrease in cardiac output, an increase in peripheral vascular resistance, and redistribution of blood flow to the vital organs. Hypoxia and hypercapnia cause chemoreceptor stimulation, vasomotor activation, and increased respiratory drive. At later stages, stimulation of the hypothalamus by interleukin 1 initiates the hypermetabolic response to injury manifested by the elevated temperatures experienced by injured patients (11,12). The hormonal response to trauma is marked by an increase in the catabolic hormones, corticotropin, cortisol, growth hormone, glucagon, epinephrine, and norepinephrine. In contrast, plasma concentrations of the primaryanabolic hormone, insulin, are decreased because of CNS-mediated sympathetic inhibition of the pancreas. Posttraumatic hyperglycemia provides non-insulin-mediated tissues such as the brain with a preferential supply of glucose. Glucagon, cortisol, and catecholamines maintain blood glucose levels and prevent hypoglycemia. The primary function of glucagon, which is produced in the pancreas, is to promote gluconeogenesis in the liver. After trauma, direct sympathetic stimulation of the pancreas enhances glucagon secretion. Corticotropin release by the anterior pituitary gland causes adrenal elaboration of cortisol, which promotes the breakdown of skeletal muscle into amino acids and facilitates gluconeogenesis in the liver. The hypoglycemic effect of cortisol counteracts insulin. The hormonal reaction most fundamental to trauma is the release of catecholamines. Epinephrine, released by the adrenal medulla in response to direct neurostimulation, is a potent regulator of the circulatory system and systemic metabolism. The hemodynamic effects of epinephrine include vasoconstriction, increased cardiac rate, and increased myocardial contractility and conductivity. Epinephrine also promotes glucose production by enhancing hepatic gluconeogenesis and inhibiting insulin release. Norepinephrine, the primary sympathetic nervous system neurotransmitter, exerts a direct effect on the circulatory system and vital organs. With massive and prolonged sympathetic discharge, norepinephrine can enter the bloodstream and exert a direct vasoconstrictive effect on the vascular system similar to that of epinephrine(9,10). Metabolic Response The postinjury period is characterized by catabolism. Negative nitrogen balance, hyperglycemia, and heat production reflect the increased energy requirements for ongoing reparative and inflammatory processes. Increased energy expenditure is due to sustained release of circulating catecholamines and increased activity of the sympathetic nervous

system. The primary energy source during this period comes from oxidation of lipids promoted by the elaboration of the catabolic hormones (9,10). Although fat is the primary energy source after injury, protein also is broken down to produce energy. In a fasting catabolic patient, glucose can be generated only from the breakdown of protein. Lipid breakdown to triglycerides and glycerol contributes minimally to form precursors for the synthesis for new glucose. As a result, protein is rapidly broken down to form precursors for new glucose synthesis in a trauma patient in the catabolic state. The result is rapid loss of muscle mass. The depth and the length of the catabolic state are related to the severity of the trauma. Although it represents an adaptive mechanism, a persistently prolonged and severe catabolic state leads to severe malnutrition, multiple organ failure, and death (9,10,13,14,15). Treatment of a Patient who has Sustained Trauma The key to improving survival and managing disablity in the trauma patient are the initial evaluation and resuscitation performed at a dedicated trauma center. The American College of Surgeons has developed a protocol taught in advanced trauma life support courses to improve the care of injured patients during the early hospital phase. It is based on a primary and secondary survey approach that allows physicians to handle the complex, multisystem problems of trauma patients. This treatment algorithm can be divided into four categories; primary survey, resuscitation, secondary survey, and definitive care. The primary survey involves hierarchical assessment of airway, breathing, and circulation. The purpose is to identify extreme, life-threatening injuries and institute immediate lifesustaining maneuvers. Resuscitation is performed simultaneously with the primary survey. The secondary survey consists of a rapid but systematic head-to-toe physical examination with the patient completely disrobed. This global assessment is done to identify all potentially life-threatening and occult injuries. An important part of the primary and secondary survey are radiographic studies including the use of ultrasonography. Samples are drawn for baseline blood studies, typing, and cross-matching. Once these priorities have been addressed, vital signs are rechecked. When the patient's condition is stable, a detailed management plan is established. Primary Survey Airway The foremost emergency measure is establishing the airway, which may be lost to a variety of causes. The oropharynx, larynx, and trachea can be obstructed by secretions, blood, and foreign bodies. Oropharyngeal airway collapse can occur with loss of consciousness and from facial fractures. Direct trauma to the larynx and trachea may cause airway obstruction below the oropharynx. Maneuvers to secure an adequate airway range from the simple to the complex and begin with manual cleaning of the oropharynx followed by suctioning of secretions.

Figure 66.1 Stabilization of the cervical spine during primary survey of an injured patient. The primary risk during early airway management is neck movement when an occult cervical spinal fracture is present. The airway must be controlled with the assumption that such a fracture exists. The neck must be completely immobilized in a neutral position. One member of the trauma team must be assigned to kneel at the head of the stretcher to maintain inline manual head stabilization and avoid hyperextension by holding the cervical spine with the hands while immobilizing the head with the forearms (Fig. 66.1). Traction on the head is avoided, because distraction with further injury to the spinal cord can occur if the patient has an unstable cervical spinal injury. Once the neck of an unconscious patient has been secured, forward traction of the mandible is performed to overcome pharyngeal collapse (Fig. 66.2). The next step is oropharyngeal airway placement in the unconscious patient. If the patient is conscious, a nasopharyngeal airway is used. Once the airway has been established and the patient is spontaneously breathing, supplemental oxygen can be provided through nasal prongs or a face mask.

Figure 66.2 Once the neck of an unconscious patient has been secured, forward traction of the

tongue and mandible is performed. When these simple measures are unsuccessful, more aggressive airway management is needed. Nasotracheal intubation is the preferred technique for establishing an airway in a conscious patient who may have a cervical spinal injury because it can be done without excessive neck mobility. Nasotracheal intubation is better tolerated by an awake patient than is orotracheal intubation and does not necessitate sedation or muscle relaxation. Nasotracheal intubation is precluded if the patient has extensive maxillofacial injuries. If the nasotracheal route cannot be used, orotracheal intubation is the next step. In ideal circumstances, a cross-table lateral cervical spine radiograph is obtained before orotracheal intubation to evaluate for a possible cervical spinal fracture. It is nevertheless important to remember that even a normal cross-table lateral radiograph of the cervical spine does not definitively exclude the presence of cervical spinal fracture or instability(16). When emergency airway control with orotracheal intubation is indicated, intubation proceeds with inline stabilization, whether or not radiographs have been obtained. Bag-mask intubation can be an effective method of maintaining the airway until radiographs are obtained. If the patient is unconscious and cervical spinal injury has been ruled out, orotracheal intubation can be readily accomplished. A patient who is awake must be paralyzed with succinylcholine for successful orotracheal intubation. After intubation, the chest is auscultated to ensure that the tube is in the trachea and not in the esophagus or in one of the main-stem bronchi. Correct endotracheal tube positioning can be confirmed reliably by the presence of end-tidal carbon dioxide. Carbon dioxide from the lungs can be detected rapidly by observing a color change on a disk that can be connected rapidly to the endotracheal tube. If no carbon dioxide is detected, the endotracheal tube is in the esophagus, and a new airway is attempted. If the patient is in cardiac arrest, end-tidal carbon dioxide is unreliable in confirming the positioning of an endotracheal tube. A followup chest radiograph to confirm the position of the tube must be obtained expeditiously. If an endotracheal tube cannot be inserted, as when a patient has major facial fractures or has sustained laryngotracheal trauma, surgical airway intervention may be needed. Four surgical methods exist for obtaining anairway needle cricothyrotomy, conventional cricothyrotomy, tracheotomy, and percutaneous transtracheal ventilation. For children, needle cricothyrotomy is the best procedure. The procedure is performed by means of placing a number 12 or number 14 intravenous cannula with a plastic sheath through the cricothyroid membrane into the tracheal lumen. Once it is in the airway, the needle is withdrawn and the plastic sheath is advanced. When properly positioned, the sheath is connected with intravenous tubing to wall or bottled oxygen at 50 pounds per inch of pressure (about 15 L oxygen per minute). Ventilation is accomplished by means of 1-second intermittent injections of oxygen followed by 4-second exhalations. Patients can be maintained for up to 30 minutes with this technique, after which, hypercapnia becomes a problem. Surgical cricothyrotomy is the preferred approach for adult patients who need surgical airway intervention (Fig. 66.3). It consists of a small vertical skin incision over the area of the cricothyroid membrane followed by a horizontal incision through the cricothyroid membrane itself. The blunt end of the scalpel is inserted between the cricoid and the thyroid cartilages

and rotated 90 degrees to make an opening through which an endotracheal tube or tracheostomy tube can be inserted.

Figure 66.3 Cricothyrotomy.

For patients with laryngeal trauma, tracheal trauma, or tracheal disruption, cricothyrotomy is inadvisable, and emergency tracheotomy is performed. Percutaneous transtracheal ventilation, a technique similar to needle cricothyrotomy, is an acceptable alternative in the treatment of these patients. In the trauma patient, continuous pulse oximetry monitoring is extremely helpful in determining the adequacy of oxygenation and is used in the care of all critically injured patients to allow early detection of arterial oxygen desaturation. Breathing Loss of respiratory drive among trauma patients is most commonly caused by severe head trauma. Ventilation is provided with a bag mask until cervical spinal injury is ruled out. An endotracheal tube is then inserted, and mechanical ventilation begun. As part of the primary survey, injuries to the chest wall and structures within the thoracic cavity that can cause hypoventilation must be recognized and rapidly managed. These injuries include sucking pneumothorax, massive pneumothorax, and tension pneumothorax. Sucking pneumothorax occurs when a defect in the chest wall is larger than the tracheal diameter. Because of reduced resistance through this opening, inspiratory and expiratory efforts result in movement of air through the opening in the chest wall into the pleural space rather than through the trachea. Occluding the chest-wall defect and chest-tube placement followed by intubation with positive pressure ventilation is the best management of this injury.

Figure 66.4 Tube thoracostomy. An incision is made in the fourth or fifth intercostal space in the midaxillary line. A: A short subcutaneous intrapleural track is developed by means of finger dissection. B: The tube is passed posteriorly and superiorly toward the pleural apex. Massive hemothorax is vented promptly. Although blood loss of 1,000 to 1,500 mL into the thoracic cavity almost always necessitates emergency thoracotomy, initial management is aimed at decompressing the chest cavity so that adequate ventilation can proceed. Tube thoracotomy is performed by means of making an incision at the fourth or fifth intercostal space in the midaxillary line (Fig. 66.4). A short subcutaneous tunnel is developed by means of finger dissection, and the tube is passed posterosuperiorly along an intrapleural tract toward the pleural apex. Continued hemorrhage at a rate of greater than 200 mL per hour is an indication for thoracotomy.

Tension pneumothorax develops when a pleural, bronchial, or tracheal tear allows air to be forced into the pleural space without a means of egress. The result is collapse of the ipsilateral lung. As pleural pressure increases, the mediastinum and trachea shift to the opposite side, compress the contralateral lung, and compromise oxygenation. The mediastinal shift kinks the inferior and the superior vena cava, the kink impairs venous return, and hypotension develops. Signs and symptoms of tension pneumothorax are acute shortness of breath, tracheal deviation away from the injury, increased resonance to percussion, distention of the neck veins, and decreased breath sounds over the injured hemithorax. Tension pneumothorax is a clinical diagnosis made on these clinical grounds. Diagnostic chest radiographs should not delay chest decompression, as this may lead to the patient's death. Tension pneumothorax is managed by means of allowing air to escape through needle thoracocentesis with a large-bore,12-gauge intravenous cannula inserted into the second intercostal space in the midclavicular line (Fig. 66.5), followed by definitive treatment with chest-tube insertion. Pneumothorax also can cause hypotension, owing to its effect on myocardial performance. Any patient who remains in shock after chest trauma needs empirical chest ventilation.

Figure 66.5 Needle thoracentesis for management of pneumothorax. The needle is inserted into the second intercostal space in the clavicular line. Circulation and Shock Once the airway and breathing have been reestablished, the next step is to assess the adequacy of the circulatory system. Shock is the clinical manifestation of the inability of the heart to maintain adequate circulation to vital organs. This low-flow state can be caused by cardiac dysfunction, loss of blood volume, loss of vascular resistance, and an increase in venous capacity(13). The cellular response to shock is a shift from aerobic to anaerobic metabolism in nonvital organ systems. The result is lactic acidosis. If hypoperfusion persists, oxygen delivery to vital organs becomes inadequate, and acidosis deepens. Unless oxygenation and perfusion are restored, organ failure progresses, and the patient dies. The clinical presentation of shock depends on the severity. A patient with mild shock may be anxious and restless; if shock is severe, the patient appears listless or exhausted. The skin is

cool and sallow with decreased capillary filling in the nail beds. Thirst, nausea, and vomiting arecommon. Blood pressure is low, and the pulse is fast and weak. Poor filling of peripheral veins makes it difficult to place intravenous catheters. The four categories of shock are hypovolemic shock, neurogenic shock, cardiogenic shock, and septic shock. The first three are associated with the acute phase of trauma. Hypovolemic Shock Hypovolemia is the most common cause of shock after trauma. Hemorrhage is assumed to be the cause unless proved otherwise. Attempts have been made to classify the severity of hemorrhagic shock as follows to give better guidelines for resuscitation:

Class I hemorrhage is the loss of about 15% of blood volume. The primary manifestation is mild anxiety. Class II hemorrhage is the loss of 15% to 30% of blood volume. The result is tachycardia and tachypnea, anxiety, decreased capillary refill, and decreased urine output. Supine blood pressure remainsnormal. Class III hemorrhage is the loss of 30% to 40% of blood volume. Patients often are extremely anxious or combative and have marked tachycardia and tachypnea, prolonged capillary refill time, and a marked decrease in urine output. Only at this stage of severe hypovolemia does supine hypotension occur. Class IV hemorrhage is the loss of more than 40% of blood volume. The result is marked hypotension and tachycardia. Urine output is almost completely shut off, and mental status can range from anxiety to coma. Losses of this magnitude often are lethal.

Hypovolemia should be managed with rapid volume replacement. Patients needing acute fluid resuscitation are usually those in whom venous access is most difficult. For most patients, 14-gauge intravenous catheters can be inserted into the antecubital veins with little difficulty. If the systolic blood pressure is so low that percutaneous access in the antecubital spaces is precluded, greater saphenous vein cutdown can be performed. Percutaneous femoral vein or subclavian catheterization is another alternative, but the surgeon must be familiar with the anatomic features of the area(1,2,3,4,5,6,7,10,12). Crystalloids, such as lactated Ringer solution or normal saline solution, are the preferred fluids for resuscitation. In adults, blood volume is about 7% of total body weight (about 5 L for a normal-sized man). In children, blood volume is 8% or 9% of total body weight; in infants, 10%. The requirements for crystalloid resuscitation can be based on the results of clinical assessment of the percentage of blood loss and the knowledge of the approximate blood volume of the patient. Circulating volume can be restored by infusing 3 mL crystalloid solution for each milliliter of estimated blood loss. This ratio can be much greater in massive hemorrhage. The crystalloid solution is infused as rapidly as possible until blood pressure and heart rate return to acceptable levels. Further fluid replacement can be monitored according to the adequacy of the urine output(1,2,3,4,5,6,7,10,12). When crystalloid replacement is inadequate, blood replacement becomes necessary. As a rule, trauma patients who arrive in the emergency department with supine hypotension likely need transfusion. Blood is added to resuscitation when the crystalloid infusion exceeds 50 mL per kilogram. Cross-matched, type-specific blood rarely is available to acutely injured patients, but uncross-matched, type-specific whole blood can be obtained rapidly in most hospitals and rarely causes serious complications. If type-specific blood is unavailable, type

O-negative (universal donor) blood can be given safely to a trauma patient in need of emergency blood transfusion. The risk of transfusion reactions with O-negative blood in this situation is minimal. Substantial clotting problems can occur with massive crystalloid and blood-replacement therapy for hemorrhagic shock. Although blood components are not used in early resuscitation, dilutional coagulopathy can develop after substantial transfusion. This dilutional coagulopathy is managed with fresh-frozen plasma and platelet transfusion, depending on the degree of ongoing bleeding. Platelets and fresh-frozen plasma are administered according to the degree of coagulopathy, not the specific number of units of blood administered. As a rule, using fresh-frozen plasma can be considered after the tenth unit of banked blood and then after every fourth unit. Use of platelets can be considered after the 15th unit of blood, and then after every fifth unit. Coagulation profiles can be monitored. Adjunctive steps can be helpful in the care of patients sustaining hemorrhagic trauma. In cases of external hemorrhage, the bleeding often can be controlled with minimal pressure. Tourniquets usually are not helpful, because direct compression can control blood loss. Blind clamping must be avoided to prevent injury to adjacent nerves. The scalp may be the source of profuse bleeding, and rapid temporary suturing may be needed. Military antishock trousers (MASTs), which are inflatable pants, can be placed around the patient's legs and pelvis to decrease circulation to the extremities and thereby improve central circulation. They are not meant to replace adequate fluid therapy but can be useful in the prehospital phase of the trauma delivery system. Caution must be exercised in using MASTs because abdominal compartment inflation can impair respiration, and leg compartment overinflation for long periods can cause compartment syndrome. Neurogenic Shock The purpose of fluid restoration is to reestablish adequate perfusion to vital organs. Measurements such as blood pressure, heart rate, urinary output, and level of consciousness help measure the success of fluid resuscitation. When these signs do not change in response to adequate resuscitation, other causes must be suspected. One such cause can be neurogenic shock, which is caused by brainstem dysfunction or spinal cord injury that denervates the sympathetic nervous system. The result is vasodilatation, decreased peripheral vascular resistance, and consequent loss of blood pressure. Neurogenic shock is characterized by the absence of tachycardia, warm extremities, and lack of anxiety in the presence of hypotension. No patient should be presumed to have neurogenic shock, despite evidence of neurologic injury, until all other causes of shock have been systematically evaluated and eliminated. Once this has been done, neurogenic shock management is fluid resuscitation to replete intravascular volume, vasopressors to restore lost vascular tone, and appropriate neurosurgical intervention(13). Cardiogenic Shock Cardiogenic shock is loss of circulatory perfusion because the myocardium cannot produce sufficient flow to maintain tissue oxygenation. Among trauma patients, cardiogenic shock is generally associated with three injuries: tension pneumothorax, cardiac tamponade, and myocardial contusion. Cardiogenic shock is suspected when hypotension persists despite appropriate resuscitation. The most common features of cardiogenic shock are distended jugular veins and elevated central venous pressure in the presence of hypotension. These

signs may not occur until the patient has undergone adequate fluid replacement. Cardiogenic shock may coexist with hypovolemic shock. A common feature of tension pneumothorax is impaired myocardial function due to decreased venous return. Increasing intrathoracic pressure distends the jugular veins and causes hypotension. In an emergency, tension pneumothorax can be confused with cardiac tamponade because both conditions are associated with hypotension and neck-vein distention. In some instances, it is impossible to differentiate these two conditions, and empirical thoracocentesis is necessary on the side most likely to be affected. If a rush of air is seen with restoration of hemodynamic status, the diagnosis of tension pneumothorax is confirmed. If not, the procedure is repeated on the opposite side of the chest. If the patient's condition does not improve, cardiac tamponade is considered, and the patient is empirically treated. Cardiac tamponade in a trauma patient is caused by blood accumulation between the myocardium and its pericardial covering. Because the pericardium is nondistensible, small volumes of blood can accumulate in the acute setting, resulting in marked myocardial impairment. The pathophysiologic changes leading to cardiogenic shockare caused by a decrease in ventricular filling during diastole and myocardial contractility impairment due to ischemia from coronary circulation impairment. The classic cardiac tamponade signs are hypotension, jugular venous distention, and distant heart sounds. The jugular veins may not become distended if the patient has hypovolemia; thus diagnosis often is made as the result of suspicion based on an injury such as a penetrating chest wound.

Figure 66.6 Pericardiocentesis for acute cardiac tamponade performed through the left subxyphoid approach. Emergency department treatment of a patient with cardiac tamponade is pericardiocentesis (Fig. 66.6). The procedure is performed by inserting a 14- or a 16-gauge catheter in the left subxyphoid position with the needle aimed toward the posterior portion of the left shoulder. Aspirating as little as 10 to 20 mL of blood can bring about dramatic improvement in myocardial function; however, frequent false-negative and false-positive results under

extreme circumstances may prompt a left anterior thoracotomy with direct pericardial decompression. Emergency thoracotomy is an option when a trauma patient does not respond to resuscitation and is in cardiac arrest. Other considerations for emergency thoracotomy include initiating direct cardiac massage and controlling massive hemothorax due to cardiac puncture or tears in the thoracic aorta. Myocardial contusion, another cause of cardiogenic shock after trauma, is caused by blunt injury, typically when the chest hits a steering wheel. Physical signs include ecchymotic discoloration of the anterior chest wall and flail chest. Severe myocardial contusion is unusual, whereas blunt chest trauma is common. Marked myocardial contusion can be confirmed with transthoracic or transesophageal electrocardiography. Wall motion, valvular dysfunction, and the presence of pericardial fluid or tamponade can be seen with echocardiography. Management is aimed at preventing fluid overload while maintaining cardiac output and medically suppressing ventricular arrhythmia. With the increasing frequency of trauma among elderly patients, the possibility of an acute myocardial infarction, arrhythmia, or congestive heart failure precipitating an accident must be strongly considered(13). Secondary Survey The secondary survey consists of a detailed physical examination with the patient fully exposed. It is undertaken once the lifesaving priorities of the primary survey have been addressed. The breadth and speed of this examination depend in large measure on the patient's injuries and the need for definitive surgical intervention. Valuable information regarding the patient's history must be collected, including the mechanism of injury, preexisting medical problems, current medications, known drug allergies, and when the patient last ate. Routine objective studies also can be performed at this time, including a complete blood cell count, chest radiography, and urinalysis. If drug overdose or alcohol consumption is suspected, appropriate toxicologic studies can be performed. Hypotension warrants blood typing and cross-matching. Head and Spine Injuries Altered mentation is the most frequent sign of injury to the CNS and is presumed to be caused by injury until proved otherwise. Cervical spinal and spinal cord injuries are common among patients with multiple injuries, and the greatest concern is to avoid further injury to vital neurologic structures. Rigid immobilization of the cervical spine is imperative until a complete set of spinal radiographs, including cervical, thoracic, and lumbar spine radiographs, has been obtained. The entire spine is palpated for tenderness and altered contour. For patients with definitive cervical spinal injuries, use of a rigid collar reinforced with sandbags on either side and wide tape across the forehead is mandatory (Fig. 66.7). Altered mental status can be caused by direct injury to the cortex and brainstem, by increased intracranial pressure (ICP), or by decreased cerebral perfusion. Whereas the first two conditions necessitate formal neurosurgical intervention, the changes in pressure and perfusion can be managed in the emergency department. The tool used to assess mental status is an abbreviated neurologic examination to define the Glasgow Coma Scale score (Table 66.1). This graded evaluation is performed to assess the functions of eye opening, verbal response, and motor response. A Glasgow score less than 8 indicates serious head injury, although the score can be artificially low if an endotracheal tube is in place. Further neurologic assessment includes evaluation of pupillary reflexes, deep tendon reflexes, and

rectal sphincter tone. A serious head injury can have nonneurologic signs such as hypoventilation and hypertension. Emergency department treatment of a patient with a head injury is aimed at minimizing cerebral edema and reducing ICP. These goals are met by means of controlling the airway to maintain acceptable oxygenation. Ventilation is adjusted to maintain a carbon dioxide level of about35 mm Hg. Patients with suspected cerebral trauma and a Glasgow Coma Scale score less than 8 need continuous monitoring of ICP. The ICP is maintained at less than20 mm Hg. Elevations in ICP are managed by means of administering mannitol, an osmotic diuretic, to reduce the amount of intracellular water in the brain. Ventriculostomy can be used to monitor ICP and can be therapeutic in that it allows cerebrospinal fluid removal to control ICP. Maintenance of cerebral blood flow, measured as a cerebral perfusion pressure (mean arterial pressure minus ICP) of 70 mm Hg with the use of fluids and vasopressors, is gaining increasing acceptance. Any patient who has changes in mental status after injury needs cranial computed tomography (CT) as part of the secondary survey(17).

Figure 66.7 For patients with definitive cervical spinal injuries, use of a rigid collar reinforced with sandbags on either side and wide tape across the forehead is mandatory. TABLE 66.1 GLASGOW COMA SCALE Function Score Eye opening Spontaneous 4 Verbal stimulus 3 Painful stimulus 2 None 1 Verbal response Oriented 5 Confused 4 Inappropriate 3 Incomprehensible sounds 2 No response 1 Intubated 1T Best motor response Obeys commands 6 Localizes painful stimulus 5 Withdraws from painful stimulus4

Flexion response Extensor response No response Score range Extubated Intubated

3 2 1 3-15 3T-11T

The management of spinal cord injury with distal deficits has changed over the last several years. Emphasis remains on maintaining spinal immobilization to prevent additional spinal cord injury. Recent research(18) has found that administering steroids may play a role in minimizing neurologic deficits for patients with spinal cord injuries. Administering methylprednisolone for either 24 or 48 hours is recommended as an option in the treatment of patients with acute spinal cord injuries. Once the neurologic system has been evaluated, the secondary survey continues with assessment of the rest of the head. The scalp can be a source of considerable blood loss, and immediate suturing may be needed. Basilar skull fractures can manifest as mobility of the facial bones, hemotympanum, cerebral spinal fluid otorrhea and rhinorrhea, and periorbital and mastoid ecchymosis. Neck Injuries All injuries to the neck are potentially life threatening because numerous vital structures traverse this area. Neck injuries are classified as blunt or penetrating. Blunt trauma to the neck can cause cervical spinal injury, pharyngeal and tracheal injuries, and carotid artery injury. Penetrating neck wounds are classified according to location. Zone I injuries are below the level of the clavicles, zone II injuries are between the clavicles and the angle of the jaw, and zone III injuries are above the angle of the jaw (Fig. 66.8). Posterior injuries can damage the cervical spine. Anterior and lateral wounds can injure the great vessels of the neck, the larynx, the trachea, and the esophagus as well as important nerves such as the vagus, phrenic, hypoglossal, spinal accessory, and branchial plexus. High penetrating injuries (zone III) threaten the great vessels and cranial nerves at the base of the skull; penetrating injuries at the base of the neck (zone I) threaten the great vessels exiting the thorax. Clinical examination of an injured neck involves careful airway assessment, including evaluation for hoarseness, stridor, dyspnea, and hemoptysis. Subcutaneous emphysema, crepitus, and distorted laryngeal landmarks indicate laryngotracheal injury. Dysphagia and chest pain are characteristic of esophageal injuries. Fiberoptic laryngoscopy is an excellent tool for examining the hypopharynx and larynx after neck injuries. It is rapid and easy to use and provides an excellent way to evaluate the patency of the airway and the function of the larynx. Fiberoptic laryngoscopy also can aid in diagnosing laryngeal fractures and vagal injuries. CT of the neck also can help to delineate laryngeal fractures.

Figure 66.8 Penetrating neck wounds are classified according to location. Zone I injuries are below the level of the clavicles. Zone II injuries are between the clavicles and the angle of the jaw. Zone III injuries are above the angle of the jaw. When laryngeal or tracheal injury is apparent and airway compromise is imminent, tracheotomy is performed. Cricothyrotomy is not used under such circumstances because of the risk of further injury to the larynx and upper trachea. Although it may be necessary to perform a tracheotomy in the emergency department, this procedure is best done in the operating room, where proper instrumentation, optimal lighting, and appropriate personnel are available, especially when the patient has sustained blunt laryngotracheal disruption. This injury usually is caused by severe compression of the laryngotracheal complexbetween the steering wheel and the vertebral column or from clothesline injury, such as catching the neck on a barbed-wire fence while riding a snowmobile or a motorcycle. Under these circumstances, active airway management can be fraught with danger. Intubation may not be feasible, and tracheotomy can cause retraction of the distal trachea into the mediastinum. Patients with penetrating neck injuries are at risk of airway obstruction, hemorrhage, and injury to the cervical spine. Important clinical signs include stridor, hoarseness, subcutaneous emphysema, expanding hematoma, external hemorrhage, hemoptysis, dysphagia, cranial nerve dysfunction, and branchial plexus injury. Active airway intervention is important with evidence of airway distress. It is best accomplished with nasotracheal or orotracheal intubation. Bleeding in the oropharyngeal area may preclude intubation and necessitate emergency surgical airway intervention, which can cause great difficulty if bleeding is present in the deeper layers of the neck. External hemorrhage is controlled with compression, and no effort is made to gain hemostasis by means of blind clamping. Much controversy has occurred with regard to routine exploration of penetrating neck injuries, not only as definitive treatment but also as a diagnostic technique. Some authors advocate routine exploration of all injuries penetrating the platysma. Others advocate selective exploration and observation based on preoperative arteriographic findings and on the presence or absence of symptoms that suggest vascular, airway, and neurologic injury.

Most patients in stable condition with penetrating injuries to the base of the neck (zone I) are best examined by means of arteriography, laryngoscopy, and esophagoscopy or a bariumswallow radiographic study. Patients in stable condition with penetrating injuries above the angle of the mandible (zone III) are best examined with arteriography to exclude carotid or vertebral artery injury. Patients with injuries between the angle of the mandible and the base of the neck (zone II) can be examined by means of routine exploration or combinations of arteriography, laryngoscopy, and esophageal evaluation if the injury has penetrated the platysma. Patients in unstable condition with active hemorrhage need surgical exploration. When a patient has marked neurologic deficits after blunt neck trauma and the findings of CT of the head are normal, the possibility of blunt carotid injury with carotid occlusion or dissection is considered and excluded with arteriography. Management of these injuries involves anticoagulation with heparin or reconstruction, depending on the nature of the injury. Thoracic Injuries Thoracic injuries are classified as blunt or penetrating. Most blunt injuries are caused by motor vehicle accidents. Penetrating injuries typically are from violence with knives or guns. The principal forms of life-threatening blunt chest trauma are flail chest, pulmonary contusion, tracheobronchial disruption, and torn thoracic aorta. Flail chest occurs when part of the chest wall becomes isolated owing to multiple fractures of the ribs or sternum (Fig. 66.9). The severity is determined by the size of the flail segment, which moves paradoxically with inspiration and thus reduces ventilatory efficiency. Ventilation is further compromised by the size of the underlying pulmonary contusion that invariably accompanies a severe flail chest. If ventilation becomes inadequate, hypoxia and hypercapnia occur, and the patient needs intubation and ventilatory assistance. Pulmonary contusion is a common finding in blunt chest trauma. It often is associated with flail chest and hemopneumothorax and is common in multisystem trauma. Pulmonary contusion causes alveolar edema and impairs gas exchange. The primary sign of pulmonary contusion is hypoxia. Initial management is adequate oxygenation and avoidance of fluid overload, which can promote pulmonary edema. If a patient has hypovolemia and pulmonary contusion, aggressive fluid resuscitation is indicated, regardless of whether lung injury is present. Intubation and mechanical ventilation often are needed to support respiration. Most intrathoracic blunt tracheobronchial injuries are caused by compression of the trachea and bronchi between the sternum and the vertebral column in motor vehicle accidents. The areas most commonly involved are the proximal main-stem bronchi and the distal trachea. Common features of this injury include pneumothorax, subcutaneous emphysema, and hemoptysis. Initial therapy often entails venting the pneumothorax. Bronchoscopy is indicated for diagnosis.

Figure 66.9 Flail chest. Traumatic rupture of the thoracic aorta is the most common cause of immediate death after motor vehicle accidents. In 90% of cases, the aortic injury occurs beyond the origin of the left subclavian artery at the level of the ligamentum arteriosum, where the descending aorta is relatively fixed. Motion between the more mobile aortic arch and fixed descending aorta can cause aortic injury when rapid deceleration is the mechanism. In about 10% to 20% of cases, thoracic aortic rupture does not cause immediate death because intrathoracic hemorrhage is contained by the aortic adventitia, and the patients can be saved if the injury is rapidly recognized. Although arteriography is the only definitive study for diagnosing this injury, the first indication of an aortic tear usually is evidence of superior mediastinal widening on routine chest radiographs. Clinical features, such as retrosternal or interscapular pain from mediastinal blood dissection and hypertension from sympathetic stimulation of the nerves around the aorta, can provide clues to the presence of aortic rupture. Early recognition and definitive surgical repair are crucial because the rupture becomes complete in a high percentage of patients within the first 24 to 48 hours after injury. The decision to perform thoracic arteriography to exclude aortic disruption is made early in the resuscitation and is based on findings of mediastinal widening on the initial supine chest radiograph obtained in the emergency department. The injuries associated with penetrating thoracic trauma; hemopneumothorax, tension pneumothorax, and cardiac tamponade, were discussed earlier. After immediate management, a decision must be made regarding surgical thoracotomy when persistent bleeding from a

chest wound is found. Considerations include the volume of the initial chest-tube drainage, the rate of ongoing hemorrhage once the lung has been reexpanded, and the patient's hemodynamic status. Abdominal Injuries Abdominal injuries are life threatening because the peritoneal cavity can harbor occult blood loss and fecal contamination. Unrecognized abdominal injury is a common cause of death after trauma, and prompt recognition is of primary importance in its prevention. Diagnosis can be delayed by the silent nature of the injury, other life-threatening problems, or an altered state of consciousness. Examination of the abdomen begins at the level of the nipples and extends to the pubic symphysis. The examination includes inspection, auscultation, percussion, and palpation. Rectal examination is mandatory for assessment of sphincter tone, pelvic crepitus, prostate position, and hemorrhage. Although the absence or presence of bowel sounds may not correlate well with the presence of injury, other signs, such as abdominal tenderness, are highly suggestive of peritoneal inflammation and can indicate the need for laparotomy. Abdominal injuries are classified as blunt or penetrating. Blunt abdominal injuries usually are associated with injury to solid organs, such as the liver, spleen, pancreas, and kidneys. The most common finding among patients with blunt abdominal trauma and solid-organ injuries is hemoperitoneum with shock. Trauma patients with persistent hypotension and possible blunt abdominal trauma require a search for occult bleeding. This can be done expeditiously with focused assessment for the sonographic evaluation of the trauma patient (FAST) or diagnostic peritoneal lavage (DPL). These studies can be done rapidly in the trauma bay. FAST is an ultrasonographic examination performed by the trauma surgeon or emergency department physician and can detect fluid in the peritoneal cavity(19). In addition, the pericardial sac can be evaluated. In hospitals without the expertise or equipment to perform FAST, a DPL can be performed. Initial peritoneal aspiration of more than 10 mL of blood is an indication for laparotomy. Lavage is performed by means of instilling 15 mg/kg normal saline solution into the peritoneal cavity and letting the fluid drain out by means of gravity. When the total erythrocyte count in the lavage effluent exceeds 100,000 per milliliter, most patients have abnormal findings at laparotomy. Abdominal CT is an excellent diagnostic study to exclude intraperitoneal or retroperitoneal injury if the patient is in hemodynamically stable condition. As experience with abdominal CT has increased, it has become clear that many patients with minor liver and spleen injuries with hemoperitoneum stop bleeding spontaneously and never need abdominal exploration. Patients with penetrating abdominal trauma and overt signs of peritonitis or hypovolemia need surgical exploration; however, therapy is less clear-cut when the patient's condition is hemodynamically stable or when signs of peritonitis have yet to evolve. The common mechanisms of penetrating trauma are gunshot wounds and stab wounds. With gunshot wounds, laparotomy is indicated when the missile penetrates the peritoneum. Plain abdominal radiographs are obtained to outline the missile trajectory. Broad-spectrum antibiotics are administered in anticipation of definitive surgical therapy.

Stab wounds of the abdomen can be managed selectively because the likelihood of visceral injury, even with peritoneal violation, is inconsistent. The first diagnostic steps are to ascertain the depth of the injury and to assess the integrity of the peritoneum. These steps are best done by means of exploring the wound in the emergency department with the patient under local anesthesia. Peritoneal lavage follows local exploration if an indication is present that the anterior muscular fascia has been penetrated. Criteria for a positive peritoneal lavage result differ in blunt injuries from stab wounds. Although 100,000 erythrocytes per milliliter is the accepted positive result for blunt injuries, an erythrocyte count of 5,000 to 10,000 per milliliter is accepted as a positive result in a stab wound and indicates that laparotomy is needed. Patients with positive peritoneal lavage results need exploratory laparotomy. Those with negative peritoneal lavage results can be admitted for observation. Extremity Injuries During the secondary survey, the arms and legs are examined carefully to assess perfusion, neurologic function, deformity, and range of motion. Serious injuries include fractures, dislocations, amputations, and compartment syndromes. Life-threatening injuries involve massive blood loss due to pelvic fractures, traumatic amputations, and open femoral fractures. Pelvic fractures associated with hypovolemia are stabilized with application of MASTs. An expanding hematoma or pulsatile, bright-red bleeding indicates acute arterial injury and is controlled with manual pressure. Before it is assumed that bleeding is coming from a pelvic fracture when the patient's condition is unstable, it is necessary to exclude ongoing intrathoracic or intraabdominal hemorrhage. Supraumbilical DPL may be indicated to exclude an intraabdominal source of hemorrhage in these patients. In the care of patients with persistent pelvic hemorrhage, angiography is indicated for diagnosis and definitive management by means of embolization of the bleeding vessels by interventional radiologists. A direct surgical approach to the bleeding pelvis rarely is indicated. Rectal and vaginal examinations are an important part of the management of pelvic fractures. Patients with severe pelvic fractures may have associated injuries to the vagina, rectum, and urethra. A high-riding prostate or a positive result of a heme test of stool can alert the clinician to this possibility. Bladder rupture also is considered if a patient has a pelvic fracture and hematuria. An abnormal result of a prostate examination or blood at the urethral meatusindicates urethral injury and is a contraindication to insertion of a Foley catheter. Under this circumstance, retrograde urethrography is performed before a Foley catheter is placed. Vascular injuries can be associated with penetrating wounds, fractures, and joint dislocation. Signs are typically those of ischemia, and the patient has pain, pallor, paralysis, paresthesia, and pulselessness. Recognition is important to preserve the extremity, and the diagnosis is confirmed with arteriography. Knee dislocation is often associated with popliteal artery injury and distal ischemia. Popliteal artery angiography is usually recommended to exclude injury if a patient has a knee dislocation. Crush injuries to the lower leg and forearm can cause compartment syndrome due to hemorrhage and edema within recognized fascial planes. The patient typically has a painful, pale extremity with decreased sensation and pulse. The earliest sign of compartment syndrome is the patient's report of paresthesia or sensory deficit in the limb. Loss of peripheral pulses is a relatively late finding and often implies irreversible damage to the limb.

Compartment syndrome occurs most often with closed fractures of the tibia and fibula. Emergency fasciotomy is the appropriate therapy. Traumatic amputation necessitates microsurgical reimplantation when possible. Bleeding from the proximal limb is controlled with manual pressure. The amputated parts must be kept in a moistened sterile towel and placed in crushed ice until definitive therapy can be provided(11,12). Inhalation Injuries Thermal injuries must be managed in an orderly way, as with all serious traumatic injuries. Inhalation injuries occur in 3% to 20% of all burn patients. Most inhalation injuries are caused by fires in closed spaces, but the possibility of blunt injuries to the throat or abdomen, as in blast injuries or car accidents with fires, must be considered. An otolaryngologist may be asked to facilitate airway management for patients with inhalation injuries. Although all types of trauma are suspect, specific types, such as explosive burns and burns sustained in a confined building, are associated with inhalation injury. Physical signs of inhalation include a decreased level of consciousness, singed nasal hairs, carbon deposits in the oral cavity, carbonaceous sputum, and the finding of inflammatory changes in the supraglottic larynx at fiberoptic laryngoscopy. The glottic and supraglottic airway can sustain marked edema from routine thermal trauma. The result is immediate or delayed airway obstruction. Patients with clear signs of supraglottic inhalation injuries need early endotracheal intubation with mechanical ventilation. The subglottic airway often is protected from burns unless the patient is exposed to superheated gas or steam. The vocal cords form an anatomic barrier. In addition, reflex closure of the glottis serves to protect the subglottis and trachea. Carbon monoxide levels in the blood should be measured, and oxygen therapy should be given immediately. Hyperbaric oxygen therapy is considered when a patient has marked carbon monoxide poisoning(12). Definitive Management Once the primary and secondary surveys have been completed, the patient has been adequately resuscitated, and the patient's condition is judged to be stable, a plan for definitive care is formulated. This plan begins with a ranking of the injuries in the order in which they are to be managed. If at any point the vital signs become unstable, the primary and secondary surveys are repeated. If the instability is from an injury that warrants definitive surgical intervention, the patient is transferred to the operating room. Patients who do not need further surgical intervention are transferred to the intensive care unit or to a surgical floor for further observation. Transfer errors include inadequate management of the airway, poorly secured intravenous lines and drainage tubes, and inadequate patient monitoring. It is a tragedy to resuscitate a patient in the emergency department successfully only to lose the patient on transfer to the operating room. Role of the Otolaryngologist Since the early 1970s, the responsibility of otolaryngologists as members of the trauma team has continued to expand. In most institutions, otolaryngologists are viewed as experts in managing the airway and are expected to perform difficult intubations and provide emergency surgical airways. They also are recognized for expertise in the management of maxillofacial trauma and penetrating injuries to the neck. Otolaryngologists often are called on to assist in the immediate care of trauma victims in the emergency department.

As valued members of the trauma team, otolaryngologists must continue to refine management skills for injuries associated with the specialty but also need to be knowledgeable about the general care of trauma patients. Otolaryngologists should understand the concepts of the primary and secondary survey and be capable of stabilizing the neck, securing the airway, placing chest tubes, and starting intravenous lines. They also should be able to perform the complete examinations needed in the secondary survey and know how to interpret the diagnostic procedures that must be performed as part of the survey. Highlights

The most fundamental neuroendocrine reaction to trauma is the release of catecholamines, which cause vasoconstriction, increase cardiac rate, increase myocardial contractility and conductivity, and stimulate gluconeogenesis. The postinjury period is characterized by catabolism with negative nitrogen balance, hyperglycemia, and heat production, all of which reflect the reparative processes. The most important factor in the successful care of trauma patients is the initial evaluation and resuscitation performed partly in the field and partly in the emergency department. Primary and secondary surveys allow physicians to manage complex multisystem problems. This treatment algorithm has four steps: primary survey, resuscitation, secondary survey, and definitive care. The foremost emergency measure after trauma is airway establishment. The primary risk during early airway management is movement of the neck when an occult cervical spinal fracture is present. When the airway is being controlled, it must be assumed that such a fracture exists. Correct positioning of the endotracheal tube can be confirmed reliably by the presence of end-tidal carbon dioxide. If no carbon dioxide is detected, the endotracheal tube is in the esophagus, and a new attempt at intubation is made immediately. In the trauma patient, continuous monitoring with pulse oximetry is extremely helpful in determining the adequacy of oxygenation and is used in the care of all critically injured patients. Techniques of surgical airway management include needle cricothyrotomy, standard cricothyrotomy, tracheotomy, and percutaneous tracheal ventilation. Needle cricothyrotomy is the best procedure for children; surgical cricothyrotomy is preferred for adults. Loss of respiratory drive among trauma patients most commonly is caused by severe head trauma; however, injuries to the chest wall and thoracic structures can cause hypoventilation, which must be recognized and rapidly treated. Shock is the clinical manifestation of the inability of the heart to maintain adequate circulation to vital organs. The patient dies unless oxygenation and perfusion are restored. The most common cause of shock after trauma and hemorrhage is hypovolemia. Treatment is rapid volume replacement with crystalloids, such as lactated Ringer solution or normal saline solution through two 14-gauge catheters in the antecubital fossa. Cardiogenic shock is the loss of circulatory perfusion that occurs when the myocardium does not generate sufficient blood flow for tissue oxygenation. Among trauma patients, cardiogenic shock usually is precipitated by tension pneumothorax, cardiac tamponade, or myocardial contusion. The presence of myocardial contusion is best confirmed with echocardiography. Among elderly trauma patients, the possibility

that acute myocardial infarction or arrhythmia has precipitated an accident must be considered. In the care of patients with head trauma, ventilation is adjusted to maintain a carbon dioxide level of about35 mm Hg. Patients with cerebral edema or coma need continuous monitoring of ICP. The ICP must be maintained at less than 20 mm Hg. Elevation in ICP is managed with mannitol. Maintenance of cerebral blood flow as measured by cerebral perfusion pressure is best accomplished with the use of fluids and vasopressors. In the care of patients with spinal cord injury, administration of methylprednisolone as a bolus of30 mg/kg followed by a drip at 5.4 mg/kg each hour for 23 hours has been shown to lead to small but important improvements in neurologic function if administered within 8 hours of injury. The decision to perform thoracic arteriography to exclude aortic disruption must be made early in resuscitation. The decision is based on findings of mediastinal widening on the initial supine chest radiograph obtained in the emergency department. Unrecognized abdominal injury is a common cause of death after trauma. Ultrasonography, when available, is the preferred step in the initial phase of assessment and management. Peritoneal lavage is an acceptable alternative. A total erythrocyte count of 100,000 per milliliter correlates with positive findings at laparotomy after blunt abdominal trauma. For patients with penetrating abdominal trauma, a total erythrocyte count of 5,000 to 10,000 per milliliter correlates with positive findings at laparotomy. Abdominal CT is an excellent diagnostic study to exclude intraperitoneal and retroperitoneal injury if the patient is in hemodynamically stable condition. The extremity injury that poses the greatest risk to life is a pelvic fracture, resulting in massive blood loss. The best initial management is application of MASTs followed by angiography. The earliest sign of compartment syndrome is the patient's report of paresthesia or sensory deficit in the limb. Loss of peripheral pulse is a relatively late finding and often implies irreversible damage to the limb. Compartment syndrome occurs most often with closed fractures of the tibia and fibula. Amputated body parts must be kept in a moist and sterile towel and placed in crushed ice until definitive reimplantation can be provided. The physical signs of inhalation injury include a decreased level of consciousness, burned nasal hairs, carbon deposits in the oral cavity, and inflammation of the supraglottic structures. Signs of this type of injury are indications for early endotracheal intubation and mechanical ventilation. Definitive management follows the primary and secondary surveys and begins with ranking of the injuries in the order in which they are to be managed. If at any point the vital signs become unstable once again, the primary and secondary surveys are repeated. Transfer out of the emergency department for definitive management can be a period of risk. Transfer errors include inadequate management of the airway, poorly secured intravenous lines and drainage tubes, and inadequate patient monitoring.

References 1. National Center for Injury Prevention and Control. Web-Based Injury Prevention and Control. Web-Based Injury Statistics Query and Reporting System (WISQARS). 2001. Available at http://www.cdc.gov/ncipc/wisquars. Accessed November 13,2004. 2. Bonnie RJ, Fulco CE, Liverman CT, eds. Reducing the burden of injury: advancing prevention and treatment Washington, DC: National Academies Press, 1999. 3. Finkelstein E, Fiebelkorn I, Corso P, et al. Medical expenditures attributable to injuries: United States, 2000. MMWR Morb Mortal Wkly Rep 2004;52:1-9. 4. Doll L, Binder S. Injury prevention research at the Centers for Disease Control and Prevention. Am J Public Health 2004;94(4): 522-534. 5. Dinh-Sarr TB, Sleet DA, Shults RA, et al. Reviews of evidence regarding intervention to increase use of safety belts. Am J Prev Med 2001;21(suppl 4):48-65. 6. Thompson RS, Rivara FP, Thomson DC. A case-control study of effectiveness of bicyle safety helmets. N Engl J Med 1989;320: 1361-1367. 7. Shults RA, Elder RW, Sleet DA, et al. Reviews of evidence regarding interventions to reduce alcohol-impaired driving. Am J Prev Med 2001;21(4 suppl):66-88. 8. Mallonee S, Istre GR, Rosenberg M, et al. Surveillance and prevention of residential-fire injuries. N Engl J Med 1996;335:27-31. 9. Gann DS, Foster AH. Endocrine and metabolic response to injury. In: Schwartz SI, ed. Principles of surgery, 6th ed. New York: McGraw-Hill, 1994:3-60. 10. Wildmore DW. Homeostasis: bodily changes in trauma and surgery. In: Sabiston DC Jr, ed. Textbook of surgery: the biologic basis of modern surgical practice, 15th ed. Philadelphia: WB Saunders, 1997:55-67. 11. Macho JR, Lewis FR, Krupski WC. Management of the injured patient. In: Way LW, ed. Current surgical diagnosis and treatment, 10th ed. Norwalk, CT: Appleton & Lange, 1994:214-240. 12. Eddy AC, Heimbach DM, Frame SB. Trauma and burns. In: Lawrence PF, ed. Essentials of general surgery, 2nd ed. Baltimore: Williams & Wilkins, 1992:145-165. 13. Shires GT III, Shires GT, Carrico CJ. Shock. In: Schwartz SI, ed. Principles of surgery, 6th ed. New York: McGraw-Hill, 1994:119-144. 14. Hill AG, Hill GL. Metabolic response to severe injury. Br J Surg 1998;85:884-890. 15. Boldt J, Muller M, Mentges D, et al. Volume therapy in the critically ill: is there a difference? Intens Care Med 1998;24:28-36. 16. Hastings RH, Marks JD. Airway management in patientswith potential cervical spine injuries. Anesth Analg 1991;73:471-482. 17. Bullock R, et al. Guidelines for the management of severe head injury Brain Trauma Foundation, 1995. 18. Hadley MN, Walters BC, Grabb PA, et al. Guidelines for the management of acute cervical spine and spinal cord injuries. Clin Neurosurg 2002;49:407-498. 19. McCarter FD, Luchette FA, Molloy M, et al. Institutional and individual learning curves for focused abdominal ultrasound for trauma: cum sum analysis. Ann Surg 2000;231(5):689700.

Maxillary and Periorbital Fractures

Brendan C. Stack Jr. Francis P. Ruggiero Maxillofacial trauma is a serious medical and socioeconomic problem that continued to increase over recent decades but has appeared to level off or even decrease in some settings, perhaps due to improved vehicular restraints and air bag deployment (1). Fractures of the facial skeleton were traditionally evaluated and managed in a segmental manner, even if complex injuries were obvious during the initial evaluation. This approach usually produced acceptable results if the fractures were from low-velocity impact and displacement was minimal. However, similar successes in managing injuries due to high-velocity impact often were not achieved. Experienced maxillofacial trauma surgeons have recognized that the suboptimal results were caused by the segmental approach. Therefore, all fractures of the middle third of the face must be evaluated as possible orbitozygomaticomaxillary injuries and not as blowout, malar, or Le Fort fractures, each in isolation. The goal of treatment must be the exact anatomic restoration of the midfacial skeletal unit rather than approximate repositioning of its component parts. Anatomy The structure of the midfacial skeleton is related to its mechanical adaptation to forces generated by mastication. Forces of up to 200 pounds per square inch are developed during chewing. The concept of buttresses describes the relatively stronger areas of the midfacial skeleton that bear the bulk of these vertically oriented forces. Horizontally oriented buttresses also exist for supporting vertical buttresses. Buttresses The vertical buttress system has seven components, including three paired pillars and one unpaired structure: (a) the paired medial, or nasomaxillary (a.k.a., nasofrontal), buttresses extend from the anterior maxillary alveolus along the pyriform aperture and medial orbit, through the nasal and lacrimal bones to the frontal bone; (b) the paired lateral, or zygomaticomaxillary, buttresses extend from the lateral maxillary alveolus along the lateral maxilla to the malar eminence of the zygoma, then superiorly along the lateral orbital rim to the frontal bone. They also extend laterally to the temporal bone via the zygomatic arch; (c) the paired pterygomaxillary buttresses extend posteriorly from the maxilla to the pterygoid plates of the sphenoid bone; (d) the midline bony nasal septum, consisting of the vomer and perpendicular plate of the ethmoid bone, connects the palatine process of the maxilla to the frontal bone (2). The mostly curved, vertical buttresses are reinforced by a number of horizontal buttresses. These include the superior and inferior orbital rims, the maxillary alveolus and palate, the zygomatic process of the temporal bone, the edge of the greater wing of the sphenoid bone, and the pterygoid plates of the sphenoid bone. Maxilla The maxilla, or upper jaw, consists of paired bones also called maxilla. Each maxilla contains a hollow body, encompassing the maxillary sinus, or antrum. Projections from the maxillary body extend superiorly and medially to the frontal and nasal bones and laterally to the zygoma. The inferior and medial palatine process of the maxilla forms the bulk of the hard palate. The alveolar process of the maxilla extends inferiorly and holds the upper teeth (3).

The bone of the maxilla is for the most part quite thin. The lateral wall of the maxillary antrum, however, includes a wedge of thicker, compact bone. It is in this area that the zygomaticomaxillary buttress arises. It appears that the greatest occlusal load is borne by this buttress(4).

Figure 70.1 Vertical and horizontal external arcs of contour (zygomatic complex). Intersection at X (dashed lines) marks the position of the malar prominence. Zygoma The zygoma is a relatively sturdy bone that is important structurally, as an integral component of the buttress system, and also forms the aesthetically vital malar prominence. It is a keystone as it integrates the vertical zygomaticomaxillary and zygomaticofrontal (zf) buttresses to the horizontal infraorbital and zygomatic arch buttresses. It is related to the surrounding facial bones via four superficial and two deep projections. The superficial projections of the zygoma define two critical external arcs of facial contour (Fig. 70.1). The vertical arc follows the course of the zygomaticomaxillary buttress, running from the zygomatic process of the frontal bone, over the zygoma itself to the lateral antral wall of the maxilla. The horizontal arc runs from the maxilla in the area of the lacrimal fossa, across the zygoma, to the zygomatic process of the temporal bone. The point of intersection of the vertical and horizontal arcs defines the location of the malar prominence. The deep projections are the sphenoid projection that articulates along the lateral orbital wall with the orbital plate of the sphenoid bone and the orbital floor projection that articulates with the orbital surface of the maxilla in the extreme lateral aspect of the orbital floor. The sphenoid and orbital floor projections lie beneath and perpendicular to the external arcs of contour in the area of the inferolateral orbital rim, greatly strengthening this portion of the rim.

Orbit Contributions from of seven bones make up each orbit: frontal, sphenoid, lacrimal, ethmoid, maxilla, zygoma, and palatine(5). The palpable anterior projections of the bony orbit are called orbital rims. The superior orbital rim is formed by the frontal bone; the lateral orbital rim is comprised entirely of zygoma; the inferior rim features contributions from both the zygoma and the maxilla(3). No true medial rim exists in the area of confluence of the orbit, lacrimal fossa, glabella, and nasal dorsum. The orbital rims form a frame of relatively sturdy bone at the anterior limits of the orbit. The internal orbit is roughly pyramidal in shape and composed of the thinner orbital roof, walls, and floor. The greatest diameter of the orbit is approximately 1.5 cm posterior to the inferior orbital rim, where the orbital roof has a concavity that places it approximately 5 mm above the superior orbital rim. The orbital floor is also concave with a depth of approximately 3 mm in relation to the inferior orbital rim. The globe rests within this concavity (Fig. 70.2). In the posterior aspect, the floor is convex. The posteromedial aspect of the orbital floor slopes upward into the medial orbital wall without a sharp demarcation (Fig. 70.3). Laterally and posteriorly, the floor is separated from the greater wing of the sphenoid bone by the inferior orbital fissure. The optic foramen lies posteriorly in the plane of the medial orbital wall; thus, it is medial and superior to the true orbital apex (Fig. 70.4) (4).

Figure 70.2 Longitudinal section of the orbit. The globe lies in the area of the concave portion of the orbital floor, and the retrobulbar soft tissues are supported by the convex posterior floor. The millimeter scale identifies the position of the two areas of opposite floor contour relative to the inferior orbital rim and orbital apex.

Figure 70.3 The convex posterior orbital floor (large arrow) slopes gradually into the medial wall. A dissection 40 mm into the orbit from the inferior rim may be needed for repair of this area. The optic foramen (small arrow) is immediately medial and superior to this posterior limit of dissection.

Figure 70.4 Le Fort fracture levels. Although these levels usually do not describe the extent or exact nature of midfacial fractures, they are still appropriately used for a general

description of the injuries. Pathophysiology/Mechanism of Trauma With the midfacial skeleton adapted to the vertical forces of mastication, it is force delivered at other vectors that cause the bulk of midface fractures. Common etiologies of midfacial fractures include motor vehicle accidents, assaults, and sporting events. Le Fort Fractures Rene Le Fort introduced a classification of midfacial fractures on the basis of cadaver experiments he performed in the early part of the 20th century. He noted that fractures tend to occur at characteristic locations, which correspond with relatively weak areas of the facial skeleton. Le Fort Level I fractures are transverse fractures separating the maxillary alveolus from the rest of the midfacial skeleton (Fig. 70.5). These injuries generally result from anterior force directed at the lower midface. The nasomaxillary and zygomaticomaxillary buttresses are disrupted at their inferior extent (6). The fracture line then extends transversely through the maxillary sinus and nasal septum and posteriorly across the pyramidal process of the palatine bone and pterygoid processes of the sphenoid bone (2). Level II fractures create a pyramidal nasomaxillary fragment separate from the upper craniofacial skeleton. They result from either direct anterior force against the midface or from inferior impact at the mandibular symphysis transmitted to the midface via the dentoalveolar segments of the mandible. Once again the nasomaxillary and zygomaticomaxillary buttresses are disrupted, this time more superiorly. The fracture line extends from the nasal root via the lacrimal bone and medial orbital wall, then anteriorly along the orbital floor to the infraorbital canal. From this point, the fracture line follows the zygomaticomaxillary suture to the anterolateral maxillary wall. Posteriorly, the fracture line passes across the infratemporal surface of the maxilla through the lower pterygoid plates (6,7). Level III fractures, which result in complete separation of facial skeleton from the skull base, are less common. They usually result from anterior force directed obliquely to the plane of the vertical buttresses. The vertical buttresses are disrupted at their superior most extent. The fracture line extends through the root of the nose, across the lacrimal bone and medial orbital wall, across the orbital floor to the inferior orbital fissure. From this point, one fracture line traverses the lateral orbital wall as it approaches the frontozygomatic suture; a second line passes over the back of the maxilla to the lower pterygoid plates. An additional fracture line through the zygomatic arch completes the craniofacial dysjunction (6,7). In clinical practice, the patterns of maxillary fractures encountered are rarely as orderly as the previous discussion suggests. A reading of Le Fort's original work demonstrates that he was certainly not unaware of this. The Level I to III classification scheme is a distillation of some of his most significant experimental observations but is not comprehensive. In his experiments, and most definitely in real-life trauma, force is delivered unevenly to each side of the face, at varying angles, and with variable locations of impact. The resulting fractures may be asymmetric from one side of the face to the other (i.e., Le Fort II on the left, Le Fort III on the right), may combine with other fractures to create a more complex pattern [i.e., a Le Fort II fracture and a zygomaticomaxillary complex (ZMC) fracture on the same side of the face constituting a complex Le Fort III fracture], or may be maxillary fractures not described by the classification at all.

Figure 70.5 External arcs of contour of the zygoma disrupted (dotted lines) with comminution of the inferior orbital rim and lateral antral wall. Totally accurate three-point reduction of the lower end of the vertical arc and the anterior end of the horizontal arc may not be possible. Open reduction of the zygomatic arch may be needed. Other Maxillary Fractures Anterior forces localized between the nose and malar prominence may produce anterior maxillary wall fractures. Significant force delivered to the lower anterior midface, in addition to generating the classic fracture patterns described by Le Fort, may less commonly cause fractures of the palate. Although they may occur in isolation, palatal fractures tend to accompany extensive facial injuries. Most often, the palate is fractured in a sagittal fashion, in a paramedian plane. Fractures in a number of other orientations and locations are also possible. Clinical indicators of palatal fractures include palatal lacerations, lip lacerations that extend into the gingivolabial sulcus, maxillary tooth loss, and malocclusion from a widened maxillary alveolar arch. Palatal fractures, and in particular those oriented sagittally, alter the width of the maxilla and permit the rotation of the maxillary dentoalveolar segments. One of the fundamentals in management of severe facial fractures is the intraoperative restoration of normal maxillomandibular occlusion, with anatomic reduction of fractures following from this basis. Palatal fractures, by complicating the restoration of occlusion, can confound this strategy if not addressed appropriately first(8). Zygomaticomaxillary Complex Fractures A number of terms are used in the literature to describe fractures involving the zygoma and the bones with which it articulates. These include malar fractures, zygoma or zygomatic

fractures, ZMC fractures(9), tripod fractures, tetrapod fractures, trimalar fractures, zygomatico-orbital fractures, and orbitozygomatic fractures(10). All of these terms emphasize certain salient features of this type of injury. For example, the term tripod underscores the observation that blunt force to the zygoma tends to disrupt its three superficial articulations: frontal, maxillary, and temporal concomitantly; the term tetrapod accentuates the frequent involvement of a fourth, deep articulationthat to the sphenoid. Henceforth in this chapter, the term ZMC fracture is used to connote nearly universal involvement of the maxilla and other articulating bones in these injuries. ZMC fractures generally result from blunt trauma to the malar eminence, the most prominent feature of the lateral midface. They are the second most common midface fracture, after nasal fractures. Routinely, they involve disruption of the projections of the zygoma; in more severe injuries, the sturdy body of the zygoma itself may be fractured. Additional fractures frequently occur concomitantly, including the anterior maxillary wall and the orbit. Another common clinical feature of ZMC fractures is facial numbness/paresthesias. This is caused by damage to the infraorbital nerve (V2) as it exits from the midportion of the inferior orbital rim, which lies directly within one of the typical fracture lines. The severity of ZMC fractures seems most related to the force and velocity of impact(9) (Fig. 70.5). Orbital Floor Fracture The complex anatomy of the bony orbit presages a wide array of possible fracture types and terminology. One simple method of categorizing orbital fractures is 1, fractures in which the external bony orbital rim is intact, and 2, those in which it is disrupted. The classic orbital floor blowout fracture occurs in the absence of an orbital rim fracture (Fig. 70.6). At least three distinct mechanisms for this type of injury have been proposed. In the first, bone conduction theory, force contacting the inferior orbital rim is transmitted to the weaker bone of the floor behind it, resulting in a floor fracture and an intact rim. In the second, hydrostatic theory, a force impacting the globe itself causes a transient compression of the orbital soft tissue contents. The resultant increased pressure within the bony orbit, if sufficient, causes fracturing of the internal orbit in its weakest areas, primarily the floor and medial wall. The originators of this theory coined the term blowout fracture to describe this phenomenon. A third mechanism, recently reintroduced, describes translational movement of the globe (after a force is delivered to it), with fractures resulting directly from impact of the globe on the thin bone of the floor and medial wall (11,12). In the clinical realm, these mechanisms are not mutually exclusive; it is likely that each, alone or in combination, accounts for a significant number of orbital floor and medial wall fractures (11). In any event, the most common etiology of orbital blowout fractures is assault, often with a fist. Other causes include falls, auto accidents, and projectiles. Despite the familiarity of the term orbital blowout fracture, internal orbital fractures are actually much more common in combination with orbital rim injuries. Excellent examples of this type of injury are the orbital fractures that accompany all displaced ZMC fractures. The zygoma comprises the entirety of the lateral orbital rim, as well as significant portions of the lateral orbital wall, inferior rim, and floor. A ZMC fracture with any significant displacement of the zygoma is thus, by definition, a lateral rim fracture and orbital floor fracture as well(13).

Figure 70.6 Fisticuffs resulting in a classic orbital blowout fracture. Other Orbital Fractures Fractures of the strong supraorbital rim are relatively uncommon. They result from anterior forces high on the face and are frequently associated with frontal sinus fractures and intracranial injuries. Nasoorbitalethmoid (NOE) fractures are caused by anterior force directed at the mid-portion of the midface. The medial orbital wall; ethmoid sinuses; nasal, lacrimal and frontal bones; the maxilla; and the medial canthal apparatus are involved in these challenging injuries. NOE fractures are discussed in greater detail in Chapter 71A, 71B. Patient Evaluation Computed Tomography Evaluation of a patient with maxillary and periorbital trauma has been greatly improved by the use of high-resolution computed tomography (CT). This modality is the work horse for evaluation of maxillary and periorbital trauma. Axial and coronal scans will document fracture lines through the entire facial skeleton. The expense of CT evaluation of patients with facial fractures other than simple nasal and mandibular fractures appears justified and can be done in many emergency rooms (14). The buttress system, particularly the vertical struts, must be systematically inspected preoperatively to document the degree of malalignment because of fracture fragment displacement. Fracture lines themselves through the buttresses do not mandate open reduction, but comminution and gross malalignment strongly suggest the need for reduction of the fractures under direct visualization to restore facial length and projection. Ultrasound has also been reported in evaluation of orbital trauma. Its advantages include no use of irradiation and the ability to perform a bedside examination (15). Its incorporation into a standardized evaluation of the facial trauma patient has yet to occur (Table 70.1). Ophthalmologic Evaluation Complete preoperative ophthalmologic evaluation of every patient who has sustained an orbitozygomatic fracture is a goal that is not always realized. However, reconstructive surgeons must be sensitive to the possibility of direct ocular trauma and obtain selected consultation as indicated. A minimal preoperative examination includes testing of visual acuity (subjective and objective in both eyes), papillary function, and ocular motility;

inspection of the anterior chamber for hyphema; and visualization of the fundus for gross disruption. A decrease in visual acuity or any abnormality observed on the other portions of this screening examination warrants detailed examination by an ophthalmologist before reconstruction of the bony injuries is undertaken. The value of forced duction testing for muscle entrapment has diminished with the increased use of CT to document the status of the orbital walls and floor. TABLE 70.1 DIAGNOSIS/EVALUATION

CT scan is the workhorse imaging study for the evaluation of mid facial trauma. Review of facial CT scan should include the status of the buttress system, zygomatic arches, orbital volume, and herniation of orbital contents. Direct coronal imaging for orbital floor and skull base imaging. Newer reformatting software of thin axial slice images offers high quality image and avoids cervical extension. Sagittal imaging can facilitate orbital trauma evaluation. Postoperative CT imaging can document anatomic reduction. Basic evaluation of visual function (and documentation thereof) should precede operative management.

Fracture Management: Principles Immediate Reconstruction The goal of modern fracture management is acute near-total or total initial reconstruction of the bony architecture of the injured facial skeleton (Table 70.2). Immediate reconstruction usually is less difficult and more successful than delayed reconstruction, mainly because the latter can be complicated by cicatricial contraction of the facial soft tissues if the underlying skeletal support collapses or is lost. During the acute phase of injury, the soft tissues are pliable enough to allow restoration of the underlying bony configurations with local bone fragments or autogenous bone grafts. If the soft tissues are allowed to contract into a bone defect, restoration of the soft tissue to a normal position by delayed restoration of the supporting bone invariably produces a less desirable result. If revision surgery for minor residual bone defects or lacerations is required, it is greatly facilitated if the overall soft tissue envelope has been maintained in a normal position by a previous anatomic reduction of the facial skeleton. TABLE 70.2 TREATMENT

Early repair of midface fractures prevents soft tissue contracture that can be difficult to normalize in a delayed approach. Meticulous attention to soft tissue closure and facial soft tissue re-draping is essential to achieving a pretraumatic facial appearance. Anatomic reduction prior to plate fixation is key. Rigidly fixated, malreduced structures will result in a persistent facial deformity requiring revision surgery.

Maxillomandibular Fixation Closed manipulation of the maxilla to obtain maximal intercuspation of the teeth before application of maxillomandibular fixation restores the position of the maxilla in the horizontal plane if the mandible is correctly related to the skull base. However, it does not automatically reestablish midfacial height if the vertical buttresses have been disrupted by fracture dislocations. Closed reduction and maxillomandibular fixation are adequate

management of less complex, minimally displaced maxillary fractures. Maxillomandibular fixation puts the jaws at rest for the 4 to 6 weeks needed for fracture healing. Maxillary fractures found to be displaced on CT scans are best managed by means of extended access approaches that allow direct visualization and anatomic reconstruction of the buttress system. Maxillomandibular fixation can be accomplished with directly bonded orthodontic brackets applied before open reduction and fracture-line plating. This method reduces the risk of arch bar wiring and can reduce operative time. Other innovations in maxillomandibular fixation that reduce surgeon risk and decrease operative time include four point screw fixation when tooth bearing structures are intact and/or rapid plastic zip tie fixation with laced dental chain elastics (16,17,18,19). Extended Access Approaches Paralleling advances in radiographic evaluation of facial fractures has been the development of extended access approaches. These approaches (coronal, transconjunctival, buccogingival, and midfacial degloving) allow more accurate reduction of fracture displacements while camouflaging incisions. The zygoma and all of its projections, including the zygomatic arch, and all walls of the orbit can be safely and almost totally exposed through a combination of coronal, sublabial, and transconjunctival incisions. Dissection of the orbital floor often cannot be limited to the concave area immediately behind the orbital rim but must be extended deeply into the orbit to repair the convex posteromedial floor. Deep dissection to within 5 to 10 mm of the orbital apex may be needed to return the orbital soft tissues as completely as possible to their normal location and for placing grafts for restoration of the normal shape and volume of the orbit (Figs. 70.2 and 70.7). The lower ends of the vertical buttresses can be exposed through extended sublabial incisions that essentially deglove the maxilla. Although this frequently removes all residual external periosteal attachments to displaced maxillary fracture fragments, bony union should proceed in a timely manner if the fragments are adequately stabilized and the periosteum is redraped over them.

Figure 70.7 Transconjunctival approach to the orbital floor. A: Lateral canthotomy/cantholysis and conjunctival incision. B: The pretarsal plane of dissection. C: Upward retraction of orbital contents exposing the orbital floor defect.

A surgeon may be hesitant to perform these extended access approaches in favor of more limited approaches in the hope that any facial asymmetry resulting from incomplete fracture reduction will be imperceptible. However, the range of imperceptible asymmetry is small, and the surgeon cannot rely on it to hide suboptimal results from nonanatomic reductions that might have been improved with more extensive exposure and reconstruction. The classic clinical example is an incompletely reduced zygoma, which results in unilateral facial widening. Extended approaches can be precisely placed and well camouflaged so as not to compromise patient cosmesis and to facilitate achieving precise anatomic reduction. When extended access approaches are used, care should be taken to close them meticulously with attention to periosteal closure, soft tissue resuspension, hemostasis, and wound drainage. Stable Internal Fixation Although the term rigid is used to describe the fixation achieved with these implants, it is somewhat overstated when applied to maxillary fractures. Rigidity sufficient to allow removal of maxillomandibular fixation can be obtained, but it is not sufficient to allow the patient to return immediately to a normal diet. Fixation devices do maintain the position of the maxillary dentoalveolar complex under the stresses of forces generated by mastication of very soft foods, speech, and deglutition. They will preserve the anatomic reduction achieved and allow for bone healing. Fracture Management: Surgical Techniques Zygoma Precise relocation of the displaced zygoma can be greatly simplified if the surgeon concentrates on reconstruction of the two main external arcs of contour. Restoration of the horizontal arc reestablishes anterior and lateral projections of the cheek, and restoration of the vertical arc reestablishes height of malar prominence in relation to the middle third of the face (Fig. 70.2). The repositioned zygoma can be used as a framework for repair of associated fractures of the orbital wall. Any form of orbitozygomatic repair relies heavily on palpation and external visualization of the position of the zygoma and direct visualization of deep structures through a small incision. Therefore, these procedures are delayed for 5 to 7 days to allow resolution of facial soft tissue edema. Preoperative and intraoperative administration of steroids can reduce the progression of swelling during surgery and facilitate evaluation of reduction and application of fixation. The repair is not delayed more than 10 days because the masseter muscle begins to shorten after this time, making elevation of the zygoma and its anatomic reduction more difficult.

Figure 70.8 Algorithm for restoration and stabilization of the position of the malar prominence. OR, open reduction; RIF, rigid internal fixation. Treatment to attain the multidimensional restoration of the position of the zygoma becomes increasingly complex as the injury to each arc of contour worsens (Fig. 70.8). Only patients with absolutely no comminution of any of the projections of the arcs of contour are treated with limited-exposure reduction techniques, such as the Gillies operation with or without transzygomatic Steinmann pin fixation. The lateral wall of the maxillary antrum often is comminuted, even if the other projections of the arcs of contour sustain simple fractures or separation (diastasis) of a suture line. In these cases, exposure through a sublabial incision is needed to allow assessment of reduction. Subperiosteal dissection around the infraorbital nerve to the inferior orbital rim allows evaluation of alignment of the inferior rim and the anterior wall of the antrum. Displaced fragments of the lateral antral wall can be repositioned to confirm alignment and bridged with a miniadaptation plate to stabilize the reconstruction of the zygomaticomaxillary buttress against the downward pull of the masseter muscle (Fig.

70.9). Because the fixation device does not resist heavy occlusal forces, as in a Le Fort fracture, only two screws into the body of the zygoma above and two screws into the maxilla below are needed for stability. An alternative site for placement of a single rigid fixation device for less severe zygomatic injuries is the reduced zf suture line. The thickness of the bone above and below the suture lines makes screw placement easy and gives even greater stability to the reduction. However, this greater stability is unnecessary in most cases, and direct visualization of the suture line reduction gives little more information about the overall position of the zygoma than does direct visualization of the lateral antral wall. The lateral brow or superior blepharoplasty incision needed to expose the suture line can leave a noticeable scar.

Figure 70.9 Single-point fixation of an orbitozygomatic fracture with a miniadaptation plate on the comminuted lateral antral wall. The progression to more complex fractures usually involves comminution of the lateral antral wall and the medial aspect of the inferior orbital rim as well as displacement at the zf suture line. In these cases, accurate realignment necessitates exposure of the inferior rim through a transconjunctival incision and exposure of the zf suture line through either the same incision after detachment of the lateral canthal ligament, through a separate lateral brow incision, or through a coronal incision if indicated for other fractures. Initial reduction of the zygoma is performed at the zf suture line. This reduction is temporarily held in place with a single wire passed through holes made well away from the thick portion of the rim that later is used for a rigid fixation implant. Because this temporary wire allows rotational movement of the zygoma, the position of the malar prominence can be appropriately adjusted in the lateral and anterior dimensions. This adjustment is accomplished by means of realigning the orbital rim and lateral antral wall fragments. Resistance to the pull of the masseter muscle is accomplished with a miniadaptation plate positioned over the lower end of the zygomaticomaxillary buttress. Additional stability can be obtained with microadaptation

(very low profile) plates placed on the inferior rim and across the zf suture line. Thicker plates at these sites can become visible with time through the overlying thin skin.

Figure 70.10 Completed unilateral frontotemporal flap needed for the approach to the lateral orbital rim and entire length of the zygomatic arch. Elevation of the flap in the correct plane protects all branches of the facial nerve. In some cases, a full coronal flap offers greater tissue relaxation and improved exposure of the body of the zygoma and the zygomatic arch. If the inferior rim and lateral wall fragments are too small to manipulate or are missing, traditional three-point reduction usually is inadequate for accurate restoration of the position of the malar prominence. The prominence typically is displaced posteriorly and laterally to its normal location. Failure to recognize the amount and direction of displacement at the time of reduction can leave a flattened cheek and widened face. In these situations, the fourth point of alignment, the zygomatic arch, must be used to reposition the point of intersection of the arcs of contour. If CT scans show that the arch has a single displaced fracture or two greenstick fractures with bending of the arch, dissection can be carried out over the malar eminence through the transconjunctival incision to expose the fractures. The fractures are elevated and realigned. In this step the surgeon must remember that the bone of the middle portion of the arch is straight and must be reconstructed as such to reestablish both anterior and lateral projections of the malar prominence. Although the bone of the arch is thin, accurate end-to-end realignment usually can be obtained to reconstruct the true length and contour of the arch. Fixation is applied at the other three points of reduction of the zygoma. If the arch has a displaced central segment, access to the full length of the horizontal arc is needed, and a coronal or extended pretragal incision is necessary in addition to the

transconjunctival incision. Dissection toward the lateral orbital rim and the zygomatic arch is in a plane deep to the superficial layer of the deep temporal fascia, allowing the frontal and zygomatic branches of the facial nerve to be elevated within the flap (Fig. 70.10). The periosteum is incised along the orbital rim and along the arch fragments deep to the attachment of the superficial layer of this fascia. A subperiosteal dissection is carried over the body of the zygoma to connect with the subciliary dissection, and all of the components of the zygomatic arch are exposed and realigned. Fixation with microadaptation plates must be applied to the arch in these cases in addition to fixation, as previously described at the other three points of reduction. If extreme difficulty is encountered in mobilizing the zygoma to its correct position, even with the extended access approaches, the masseter muscle can be detached from the zygoma and the arch. This step often is necessary in operations on patients not treated within the recommended 7 to 10 days following fractures. This maneuver does not have long-term effects on jaw mobility or masticatory function, but the additional soft tissue trauma and subsequent scarring can accentuate the prominence of the reconstructed arch, especially if a plate spans the length of the arch. Accurate draping of the soft tissues over the reconstructed arch helps to prevent this. Simultaneous upward traction on the skin flap and incised temporal fascia allows a tight closure that holds the periosteum in correct position over the arch and zygoma.

Figure 70.11 Exposure of the maxilla through a midfacial degloving approach. Plate 1 provides fixation for the anterior aspect of a parasagittal palatal fracture. Plates marked 2 provide fixation across the fractured zygomaticomaxillary buttresses and complete triangular fixation of the palatal fracture. Plates marked 3 were placed across the fractured nasomaxillary buttresses for inferior repair of a nasoorbitoethmoidal fracture. (From Stanley RB. Rigid fixation of fractures of the maxillary complex. Facial Plast Surg 1990;7:176, with permission.) Palate The integrity of a fractured palate must be reestablished. Palatal fractures, most commonly parasagittal splits, must be reduced anteriorly at the inferior rim of the piriform aperture and posteriorly to allow a solid, structurally accurate dentoalveolar complex to be related to the

mandibular teeth. Open reduction and internal fixation of the anterior extent of a palatal fracture can be accomplished through the same extended gingivobuccal incision used to expose and repair the vertical buttresses (Fig. 70.11). The bone above the anterior teeth is more than adequate for placement of a miniadaptation plate with multiple monocortical screws. In some instances, a small amount of bone can be removed immediately below the anterior nasal spine to facilitate placement of a plate with a flat contour under the upper lip and base of the columella. Care to prevent tooth root injuries should be exercised. The posterior extent of a palatal fracture usually can be reduced in a closed manner if the overlying palatal mucoperiosteum is intact. Difficulty manifests as inability to align the lower end of the zygomaticomaxillary buttress with an accurately reconstructed zygoma above. Also the need to overtighten the maxillomandibular fixation wires to pull the lingual cusp tips of the maxillary molars and premolars into the central fossae of the mandibular teeth can be problematic. In these cases, an incision can be made over the posterior extent of the palatal fracture, and a transosseous wire can be placed across the fracture. This wire does not serve as a point of rigid fixation of the palatal fracture, but it reduces the fracture gap posteriorly after it is tightened. Stable fixation is obtained with superficial triangulation of the palate with plates and screws placed across the anterior extent of the palatal fracture and across both zygomaticomaxillary buttress areas (Fig. 70.12). Posterior distraction of a parasagittal palatal fracture can be overlooked easily if a presymphyseal mandibular fracture is present that has been incompletely reduced at the lingual cortex. Both dental arches are widened posteriorly, and the maxillary and mandibular teeth can appear to interdigitate correctly. However, when facial edema resolves, the patient may notice widening of the intergonial distance and have a cheeky appearance.

Figure 70.12 Reduction of the posterior gap of a displaced parasagittal fracture of the palate with a transosseous wire. Arrows indicate points of triangular fixation that hold the palatal fracture in reduction (Fig. 70.15). Palatal fractures exposed by means of laceration of the mucoperiosteum usually are widely separated and impossible to reduce without a transosseous wire to pull the palatal shelves together posteriorly. If this method of reduction is not used, and tightening of the maxillomandibular fixation wires only is used to pull the teeth into occlusion, the maxillary teeth probably will be lingually tipped or left in some degree of unilateral or bilateral posterior crossbite deformity. The exposure through the laceration may be adequate to allow placement of a plate across the split palate; however, this procedure can be technically difficult, and these plates frequently become exposed in the mouth and must be removed. Acrylic palatal splints are essential adjuncts for stabilization of teeth in a segment of maxillary bone separated from the palate by an alveolar fracture. Even if a rigid fixation device cannot be used to attach the isolated alveolar segment to the surrounding maxillary bone, the combination of a sturdy buccal arch bar, a palatal splint, and circumdental wires to cinch the involved teeth between the bar and the splint usually provides enough stability to allow removal of the maxillomandibular fixation.

Figure 70.13 Algorithm for management of fractures of the vertical buttresses. Maxilla

Restoration of the pretrauma relations of the tooth-bearing segments of the maxilla to the mandible and skull base necessitates reestablishment of the proper occlusal relation of the maxillary and mandibular teeth and stabilization of the midfacial buttress system (Fig. 70.13). If the mandible also is fractured, the lower dental arch must first be stabilized and accurately related to the skull base; proper alignment of the mandibular condyles in the glenoid fossae is an absolute requirement. The anteroposterior position of the maxilla can be set by means of occluding the teeth in stable maxillomandibular fixation. The midfacial vertical dimension is stabilized by means of reduction and fixation of all fracture lines between the palatoalveolar complex and the base of the skull. When subcondylar fractures or fractures of the condylar head cannot or should not be managed with open reduction, the midfacial buttress system can be reconstructed first to establish vertical and horizontal positioning of the occlusal plane. This alternative approach may not restore the relation of the maxilla to the base of the skull with the same accuracy that can be achieved if it is first related to an intact or totally reconstructed lower arch. This sequence, however, is the preferred sequence if mandibular vertical ramus height cannot be accurately restored because of the presence of a posterior mandible injury. Although not a part of the maxilla, each zygoma must be accurately repositioned and stabilized before reattachment of the maxilla to the upper ends of vertical buttresses. Zygomatic fractures associated with Le Fort fractures of the middle third of the facial skeleton often necessitate open reduction and internal fixation of the zygomatic arch to position the zygoma correctly before reattachment of the maxilla. This is particularly critical if mandibular condylar fractures necessitate reconstruction of the upper jaw first. Failure to recognize and correct the amount and direction of displacement at the time of reduction leaves a flattened cheek and widened face and can produce a rotation and possibly tilting of the maxilla when it is reattached to the malpositioned zygoma. Only after the zygomatic and palatal fractures have been repaired can the maxillary complex be reattached superiorly. Reattachment begins with the zygomaticomaxillary buttress that has the less severe injury. Unlike the anterior wall of the maxilla, which often is severely comminuted, the zygomaticomaxillary buttress often is traversed by a single fracture line that can be easily reduced, or it has a single free-floating fragment that can be accurately related to the zygoma above and the lower maxilla below. At least one zygomaticomaxillary buttress usually can be reduced in this way to set the correct vertical dimension of the middle third of the face. After stabilization of this buttress, reduction and fixation of the other zygomaticomaxillary buttress and the nasomaxillary buttresses can proceed. If both zygomaticomaxillary buttresses are severely comminuted, reconstruction of the nasomaxillary buttresses can facilitate reestablishment of the vertical dimension. In most cases of comminution of the zygomaticomaxillary struts, however, the nasomaxillary buttresses are even more fragmented and difficult to realign. Stability of the reattachment of the maxillary complex is gained mainly through reconstruction of the zygomaticomaxillary buttresses. Reconstruction of the nasomaxillary buttresses can provide some supplementary vertical stability to the overall reconstruction, but only if the upper confluence of these struts (nasoorbitoethmoidal complex) is intact. If plates and screws are used for fixation and the patient is allowed to function early, a delicate nasoorbitoethmoidal repair cannot be relied on to transmit occlusal forces to the base of the skull. Instead, zygomaticomaxillary buttress reconstruction must be used to hold the repositioned maxilla in place during healing. Plates must be positioned to overlie the zygomaticomaxillary buttresses as closely as possible, and three screws are used to anchor

the plate to the zygoma above and the maxilla below. Placement of screws into the lower end of a plate or a bone graft can be difficult if the fracture line closely parallels the apices of the molar and premolar teeth. This problem usually can be overcome with L-shaped plates that allow placement of more screws close to (often in between) but not through the root tips (Fig. 70.11). Comminution of the lower ends of the vertical buttresses severe enough to mandate bone grafting for adequate stabilization is uncommon, although occasional cases occur in which gaps of 1 to 2 cm of severely comminuted or absent bone exist in one or both lateral antral walls. Onlay split cranial bone grafts are attached across these gaps. The grafts can be contoured and positioned to allow placement of lag screws that do not damage the root tips. Reconstruction of the vertical dimension cannot be done with the same precision for these patients as for those who undergo successful edge-to-edge approximation of in situ fracture fragments. Orbital Walls Reconstruction of the orbital walls can begin only after total reconstruction of the zygoma and any other injuries of the horizontal and vertical buttress system (13). This includes an accurate anatomic reconstruction of the frontal bar, to the lateral ends of which the orbitozygomatic complexes are reattached. During repair of fractures of the roof of the orbit, the surgeon must be aware of an essential difference in positioning of bone fragments or bone grafts during the repair. Although the goal of reconstruction of the lateral, inferior, and medial walls of the orbit is an exact reconstruction of contour and position, the goal of reconstruction of the roof is to position it higher than its pretrauma level. The normal upward convexity of the roof is difficult to duplicate. A reconstructed roof that appears to be at the correct level often is too flat and pushes the globe inferiorly. This problem is avoided if the rebuilt roof is attached to the frontal bar at a level approximating the normal height of convexity of the roof and not the level of its normal junction with the frontal bar (Fig. 70.14). The zygomatic contribution to the lateral orbital wall most often remains attached to the body of the zygoma and is correctly rearticulated to the greater wing of the sphenoid bone with reconstruction of the zygoma. In some cases, reduction of this suture line can be used as an indicator of adequacy of the overall realignment of a displaced zygoma. However, the serrated edge of this projection of the zygoma is frequently comminuted, and realignment of the suture line cannot be relied on as a main indicator. In the unlikely event of a displaced sphenoid wing fracture, the lateral wall component of the zygoma can be used as a landmark for repositioning the orbital plate of the sphenoid bone. Only rarely is an alloplastic or autogenous graft needed to reconstruct a lateral wall defect to correct herniation of orbital soft tissues into the infratemporal fossae. However, if a high-impact injury does produce comminution and displacement of the lateral orbital wall, a split calvarial graft is the ideal choice of graft material. Because a lateral approach must be used to expose these retrobulbar bone injuries safely, the calvarial donor site is already in the surgical field. A fairly flat area of skull usually can produce a graft that closely matches the contour of the lateral orbital wall. The inserted graft can be stabilized to the frontal bone or the zygoma with a microplate and screws.

Figure 70.14 A: Upwardly convex configuration of the orbital roof above a normally positioned globe. B: Flat bone graft attached to the lower edge of the superior orbital rim has displaced the globe inferiorly. C: Similar graft attached at a higher point on the frontal bar has not displaced the globe. The orbital floor projection of the zygoma usually remains intact and is restored to a normal position after the zygoma is repositioned. The medial floor (orbital plate of the maxilla) can be reconstructed with the intact lateral floor as a stable landmark. Reconstruction of a defect involving only the concave anterior aspect of the floor usually can be accomplished with an alloplastic implant. Dissection of the floor must expose the entire circumference of the defect so that an almost 360-degree ledge is formed to support the implant. Of the various alloplasts available, polypropylene mesh has many properties that make it an ideal choice. It is readily available, is easily trimmed, and can be layered to strengthen the reconstruction. Clotted blood and fibrous tissue eventually fill the mesh to prevent implant migration, obviating fixation of the implant to the orbital rim or residual floor. Reconstruction of defects of the concave anterior and convex posterior floor requires an implant with rigidity greater than that of polypropylene because there often is no ledge of residual floor to stabilize the implant posteriorly or medially, even when the orbital floor dissection is carried well into the posterior third of the orbit (20). A stiffer alloplastic material that is well suited for larger defects that have medial and lateral ledges for support is porous high-density polyethylene. This material, which has the same favorable properties as polypropylene mesh, does not require full 360-degree support to remain in place. For defects that extend to the junction of the floor and lamina papyracea, a graft with even more rigidity is needed to overcome the lack of posterior and medial support of the implant. Outer-table calvarial bone is ideally suited for reconstruction of these larger defects. This bone is easily

harvested and contoured to match most large defects in the floor, and its rigidity eliminates the need for medial and posterior support (Fig. 70.15). The graft can be stabilized by means of attaching it to the orbital floor projection of the zygoma with one or two lag screws or to the reconstructed orbital rim with miniplates and screws in a cantilevered manner (Fig. 70.16A). The calvarial bone graft cannot restore an accurate position of the globe if the surgeon is hesitant in floor dissection and does not venture the sometimes necessary 35 to 40 mm into the posterior third of the orbit to allow maximal reconstruction of the convex posterior floor (Fig. 70.2).

Figure 70.15 Harvesting the outer table of calvarial bone from the parietal skull. A: Outline area of graft on bone stripped of periosteum, 2 cm behind the coronal suture and 2 cm lateral to the sagittal suture. B: A cutting bur is used to make a monocortical trough through the outer table of calvarium. C: A straight osteotome is used to gently elevate the outer table off of the diploic space without injury to the inner table of the skull. Reconstruction of defects that involve the concave anterior floor, convex posterior floor, and medial orbital wall (lamina papyracea) offers the greatest challenge. Although these severe orbital injuries usually are part of a panfacial fracture, they can occur with isolated orbitozygomatic injuries. Complete exposure of the medial wall of the orbit is mandatory and is best accomplished through a coronal incision. Reconstruction is made difficult by the need to restore the integrity of walls themselves and the exact relation of the medial wall to the floor. Cranial bone grafts cannot be bent without fracturing, but they can be joined together with microplates to reproduce a correct medial wall-to-floor relation (Fig. 70.16B). An alternative is to use prefabricated titanium orbital floor plates with medial and lateral wings that act as a cradle for bone implants and greatly facilitate placement and stabilization. However, insertion of these plates puts a large amount of metal in contact with the maxillary and ethmoidal sinuses, and problems with chronic infection become a consideration. Complications

The complications of malocclusion and facial asymmetry that can be caused by lack of recognition and management of midfacial skeletal injuries have been discussed. Other serious occurrences include various iatrogenic complications introduced by the surgical intervention itself (Tables 70.3 and 70.4). Lid Damage Even the most experienced surgeon occasionally notices increased scleral show or even gross ectropion after any incision that violates the lower eyelid to approach the orbit. A transconjunctival incision greatly reduces this risk, and with the addition of lateral cantholysis approximately 2 mm medial to the lateral canthus, even the medialmost aspect of the inferior rim and medial wall of the orbit can be exposed. The cornea can be adequately protected during dissection of the deep orbit and placement of large alloplastic or autogenous grafts with traction sutures that pull the bulbar conjunctiva over the globe (Fig. 70.17). TABLE 70.3 COMPLICATIONS

Midfacial fractures are frequently accompanied by significant nonfacial injuries; patients should be managed in accordance with ATLS principles. Facial asymmetry and malocclusion result from poor recognition of extent of injuries, inadequate exposure of fractures, incomplete fracture reduction, and/or inadequate fracture stabilization. Other complications of midfacial fracture management include ectropion, epiphora, visible implants (plates), enophthalmos, ptosis of soft tissue, and trismus.

Figure 70.16 A: Reconstruction of a large defect of the entire orbital floor medial to the infraorbital nerve. An outer-table cranial bone graft is cantilevered from the inferior rim with

a miniadaptation plate. B: A second graft is attached to the floor graft with microplates to reconstruct a defect that involves the floor and medial wall of the orbit. The preassembled bone grafts are inserted through the transconjunctival incision and manipulated into position through a medial orbital or coronal incision. Iatrogenic lid damage can be lessened with careful dissection that adds no injury to the orbicularis muscle or the orbital septum. The periosteum overlying the inferior orbital rim is not incised immediately over the crest of the rim but on the downward slope of the rim 2 to 3 mm anterior to the crest. If the rim is comminuted and the fragments are depressed, correct placement of the periosteal incision is difficult and the risk of damage to the orbital septum increases. Reduction of the fragments to a more anatomic position through a sublabial incision before incision of the rim periosteum reduces the risk. The rim incision is not sutured during closure of the lid to reduce the risk of tethering the orbital septum to the reconstructed rim. The conjunctival incision is closed with continuous 6-0 fast-absorbing catgut suture, and the tarsal plate is reattached to the inferior limb of the lateral canthal ligament with buried 4-0 polyglactin 910 suture. A Frost suture between the upper and lower eyelids offers no additional protection against lower lid retraction if the transconjunctival opening and closure are correctly performed. If the soft tissues over the inferior orbital rim, malar prominence, and anterior maxillary wall have been completely elevated during reconstruction, absorbable suspension sutures can be placed from the periosteum of the cheek tissues to the reconstructed rim. This maneuver helps to maintain the length of the lower lid as the infraorbital soft tissues redrape over the reconstructed inferior orbital rim. TABLE 70.4 EMERGENCIES

Visual loss due to globe damage or optic nerve injury is a possible complication of any surgery performed within the orbit. Occasionally, placement of a large orbital floor implant can cause an acute increase in intraocular pressure, necessitating early removal and modification of the implant. Early recognition is key to preventing blindness. Acute intervention to release increased intraocular pressure includes a bedside canthotomy and cantholysis. Life-threatening hemorrhage is sometimes associated with extensive midfacial trauma. This can be managed by attention to large wound closure (especially scalp) and management of epistaxis (which may involve nasal packing). Emergent airway management may be necessary. Fracture reduction will reduce blood loss when it is practical in the acute setting. An alternative means in the patient who is not fit for surgery may include interventional radiology and vessel embolization.

Figure 70.17 Transconjunctival incision with cantholysis of lower tarsal plate attachment to lateral canthal ligament. Traction sutures are used to pull the conjunctiva superiorly to protect the cornea. The orbital rim is exposed through an incision 2 to 3 mm below the junction of the orbital septum and rim periosteum (see also Fig. 70.11).

Vision Loss Damage to the globe or the optic nerve with resultant loss of vision is a risk of any surgical procedure within the orbit. In some instances, ocular injury from the trauma itself can prevent management of the fractures if manipulation of the globe is likely to worsen the ocular injury and precipitate total loss of vision in the eye. If the fractured orbit houses the patient's only seeing eye, reconstruction is limited to returning the globe to functional position if the orbit is severely disrupted and marked displacement of the globe has occurred. Bone grafting is directed at providing basic support for the globe and not at total reconstruction of the orbital volume and shape. Intraoperative tonometry and funduscopic examination are considered in these and all other cases in which large implants are placed into the posterior orbit. Forward positioning of the globe by an oversized implant occasionally causes an acute increase in intraocular pressure, and the implant must be removed and reduced in size. Implant Visibility Miniplates and screws along the lateral orbital rim and zygomatic arch usually are visually undetectable if low-profile titanium or cobalt-chromium alloy plates with screws 1.3 mm or less in diameter are used. These fixation devices can be left in place permanently. Because a plate positioned on the inferior rim can produce an irregular contour visible through the thin

skin of the lower eyelid, it is preferable not to use rigid fixation devices on the inferior orbital rim unless absolutely necessary for stability of the reconstruction. If such a plate is placed and is visible after healing is complete, a second surgical violation of this lower lid to remove the plate does expose the patient to a higher risk for lid complication. Use of high-profile plates on the zf suture are at risk for developing postoperative visibility. Malocclusion Rigid fixation is an unforgiving technique that produces serious occlusal disturbances if used inappropriately to manage fractures of tooth-bearing segments. If the plates are not correctly adapted to the bone, tightening of the screws can produce torque in the system, and the fragments can be distracted so that malocclusion is produced when the maxillomandibular fixation is removed. This is less likely to occur now that thinner, more malleable titanium or cobalt-chromium alloy plates are being used rather than the stiffer, harder to bend stainless steel plates. The surgeon must consider the risk of inaccurate condylar seating in the glenoid fossae in all cases involving tooth-bearing segments of bone. Patients with complex maxillary injuries can have a deranged occlusal relation that is difficult to correct and prevents the teeth from interdigitating in a passive manner before application of maxillomandibular fixation. One or both mandibular condylar heads invariably are displaced from their normal centric occlusion position in the glenoid fossae if the maxillomandibular fixation is used to pull the patient into occlusion. Even if the plates are subsequently and accurately adapted to the repositioned maxillary fragments, malocclusion develops after maxillomandibular fixation is removed and the patient's normal muscle balances return the mandible to its correct position. If gross malocclusion does not result and the patient learns to function in this altered position, chronic temporomandibular joint (TMJ) discomfort is likely to develop. If rigid fixation is used and an error in postoperative occlusion is discovered, the patient must be returned to the operating room for revision surgery. Reapplication of maxillomandibular fixation exclusively to allow the patient's muscles or orthodontic traction bands to pull on misaligned fragments is uniformly unsuccessful because of the rigidity of the fixation devices. Internal fixation must be revised. Temporomandibular Joint Injury An altered relation within the TMJ can be a problem for patients who have associated mandibular injuries. Edema, effusion, or hematoma can exist within the joint structures and displace the condylar head to an abnormal position. This produces a risky situation for rigid fixation on the maxillary fractures. If there is doubt about the position of the condylar heads within the glenoid fossae, plates and screws can be used for rigid fixation of any associated Le Fort III or zygomatic fractures, and wire osteosynthesis can be used for the Le Fort I and II components. Although the patient must endure maxillomandibular fixation for 4 to6 weeks, the semirigid wire fixation at the maxillary level of the buttresses allows the patient to adjust the relation of the maxillomandibular complex to the base of the skull during the early postsurgical period as the soft tissue TMJ injury resolves. Recent Technical Adjuvants Bioresorbable Implants Fixation implants ultimately are fabricated from bioresorbable materials that can be contoured, remain rigid during fracture healing, resorb over time, and leave no permanent evidence of their presence. Polyglycolic acid implants have been used to treat humans, but the rate of resorption has been erratic. In some cases, implant breakdown products have

initiated an intense inflammatory response with subsequent fibrosis. For the immediate future, metallic implants remain the best rigid fixation devices for the management of orbitozygomaticomaxillary fractures. Endoscopic Surgery Isolated orbital floor fractures often required operative evaluation. New innovations in endoscopic surgery have allowed for minimal access to this class of fractures, fracture reduction, and even placement of alloplast to reconstruct larger defects that would otherwise result in enophthalmos if left untreated (20). Endoscopic approaches can be combined with computer aided surgical navigation for precise localization of fractured structures (Fig. 70.18).

Figure 70.18 A transantral approach to the endoscopic repair of the orbital floor requires a mini Caldwell-Luc approach on the anterior maxillary face between buttresses. The inset shows the repositioned bone segment after antrostomy. Surgical Models and Computer-Aided Surgery Although most information necessary to evaluate orbitozygomaticomaxillary fractures can be seen on standard axial and coronal CT scans, three-dimensional reconstructions can help surgeons better conceptualize the overall injury. Precise calculation of changes in orbital volume and the amount of displacement of superficial bony landmarks is possible with threedimensional images (21,22). This is particularly valuable for patients who cannot be positioned for true coronal CT for optimal evaluation of the orbital walls. However, coronal reformations generated from fine-cut axial CT scans are less expensive and more readily obtained than three-dimensional reconstructions. Although they do not supply the same detail

in equal clarity, the coronal reformations usually supply adequate information for orbital wall evaluation. Perhaps more important, technical limitations placed on surgery on the craniofacial skeleton by surrounding soft tissue structures probably always prevent the surgeon from full use of the additional information gained from multidimensional imaging. Stereoscopic three-dimensional CT images are useful in evaluating facial fractures. These are made when an image in a pair is different from its mate by a 6-degree shift of the z-axis. Additional technologic enhancements to aid the surgeon in repair of complex facial trauma include sagittal CT reconstruction for orbital floor fractures (23), computer-aided surgery (CAS) navigation for facial fragment reduction (24), and preoperative computer generated models for surgical planning (particularly helpful for reconstruction in the delayed setting and revision cases). Intraoperative CT Scanning Portable CT scanners allow immediate radiographic evaluation of fracture reduction in the operating room (25). The quality of these scans appears sufficient to allow evaluation of relocation of the malar prominence on axial scans and realignment of the orbital walls on coronal reformations. The expense of the scanner and technologist time can be offset by elimination of the need for extended access approaches to evaluate reduction of each fracture line, thus decreasing operating room time and expense. Intraoperative CT to confirm alignment of unexposed fractures can increase the feasibility of endoscopic management of selected orbitozygomaticomaxillary fractures. Acknowledgment The authors wish to acknowledge the work of Robert B. Stanley, Jr., M.D., the original author of this chapter whose material was revised, updated, and augmented for this edition. Highlights

Return to normal masticatory function and facial appearance after orbitozygomaticomaxillary fractures necessitates total anatomic restoration of the skeletal unit that maintains the position of the tooth-bearing segments of alveolar bone and the critical soft tissue structures occupying the middle third of the face. Posttraumatic evaluation of midfacial injuries should include CT evaluation of the horizontal and vertical buttress system, the external arcs of contour of the zygoma, the orbital walls, and the mandibular condyles. Visual acuity should be documented in both eyes before reconstructive orbital surgery. Ocular injuries can delay or contraindicate reconstruction of the involved orbit. If the patient has only one seeing eye, reconstruction of the orbit housing this eye is directed at returning the eye to a functional position. Total reconstruction of the orbit is contraindicated if extensive posterior orbital dissection or forceful retraction of the globe is necessary for placement of large alloplastic or autogenous grafts. The zygomatic arch can be used as a fourth point of reduction during repair of orbitozygomatic fractures due to high-velocity impacts that have caused severe comminution of the inferior orbital rim and lateral antral wall. Total reconstruction of the arch, in particular its straight central portion, gives the most accurate anterior repositioning of the malar prominence. Orbital reconstruction should return the floor, medial wall, and lateral wall to their normal positions. Because its normal upward convexity is difficult to recreate, a reconstructed orbital roof is reattached to the frontal bar of the cranium at a level approximating the highest convexity of the orbital roof, not at the level of the

insertion to the orbital rim. If this is not done, the globe usually is depressed by the flat bony reconstruction. The most common error in orbital reconstruction is failure to repair the convex posterior orbital floor and its gradual slope into the medial orbital wall. This area is behind the globe, and the dissection needed for reconstruction can extend 35 to 40 mm posterior to the orbital rim. This can be added by pre/postoperative sagittal reconstruction of thin-cut CT scans. The most accurate reconstruction of the vertical dimension of the middle third of the face is achieved with open reduction of the vertical buttresses if fracture dislocations are seen on CT scans. Loss of vertical dimension is more likely to be caused by use of internal suspension (circumzygomatic or craniofacial) than by reduction of the Le Fort fractures themselves. The occlusal relation of the maxillary and mandibular teeth must be reestablished in treating patients with fractures of the tooth-bearing segments of the maxilla. Maxillomandibular fixation, however, does not automatically restore the correct relation of the palatoalveolar complex to the base of the skull if one or both mandibular condyles are incorrectly seated in the glenoid fossae. Displacement of a condyle from the centric occlusion position that it normally occupies during maximal interdigitation of the teeth can be caused by trauma to the joint structures themselves or by overzealous use of the fixation wires to pull the patient into occlusion. Rigid (plate and screw) fixation is an acceptable alternative therapy for fractures that separate the maxillary complex from the midfacial skeleton. Rigid fixation allows immediate removal of maxillomandibular fixation and early, limited function. However, the procedure is much more technique sensitive than is closed or open reduction with interosseous wire fixation. Reduction errors produce an unacceptably high rate of iatrogenic complications (malocclusion) that necessitate revision surgery.

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