trauma maksilo facial

8/13/2019 Trauma Maksilo Facial

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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...22Definitive 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


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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.40Maxilla .42

Orbital walls.44

Complications

Lid damage...47

Vision loss.49

Implant visibility..49

Malocclusion 50

Temporomandibular joint injury...50Recent technical adjuvant

Bioresorbable implants...51

Endoscopic surgery.51

Surgical model and computer-aided surgery51

Intraoperative CT scanning ...52

Highlights...52

References .53


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Principles of TraumaJames ChanPeter J. Koltai

Trauma is the leading cause of death and disability of Americans younger than 40 years1. Inthe United States, more than 150,000 violent deaths occur each year, and more than 500,000trauma victims are left with permanent disabilities. Annually, approximately 30 to 40 millionvisits are made to emergency departments for injury treatment (2). The cost to our society issignificant. In 2000, $117 billion was spent by Americans, which accounts for 10% of allmedical expenditures (3). This is comparable to the percentages attributable to other publichealth issues such as obesity (9.1%) and smoking (14.4%)4.

Deaths from trauma fall into three categories immediate, early, and late. Immediate deathoccurs within minutes of injury and is caused by acute airway obstruction or major vesseldisruptions of the brain, heart, or other internal organs. Early death occurs in the first fewhours after injury and is associated with excessive hemorrhage, blood accumulation aroundthe 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 wayto decrease this number. Many public health injury-prevention strategies have beensuccessfully implemented, including use of seat belts (5)and bicycle helmets (6),implementation of blood alcohol limits (7), and fire-safety education, including widespreadsmoke 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 anddefinitive response. This requires a parallel system of prehospital care and hospital care atdedicated trauma centers.

Death at an accident scene is usually related to head injury with associated hypoventilationdue to loss of consciousness. Intubation in the field can thus be lifesaving. Another commoncause of prehospital death is massive hemorrhage. When intravenous catheters are inserted atthe scene, circulatory volume can be maintained until the hemorrhage can be surgicallycontrolled. 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, includinghemorrhage, 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 fluidinto the circulatory system, redistribution of blood flow to the heart and brain, and alterationsin 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-intensiveresponse to trauma. Local responses include immunologic activation with leukocytesmobilization, 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


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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 ResponseHemostatic adjustments to trauma are mediated by the neuroendocrine system. Stimuli such

as hemorrhage, hypoxia, and tissue damage stimulate a graded response that increases to apeak level, after which additional response is no longer possible. Pain is the first signal fromthe central nervous system (CNS) to reestablish homeostasis. The hypothalamic response to

pain stimulates the pituitary gland to release corticotropin, which stimulates adrenal secretionof cortisol. Pain causes elaboration of antidiuretic hormone for fluid conservation. Painactivates the sympathetic nervous system and stimulates direct adrenal secretion ofepinephrine.

Blood loss stimulates vascular pressure and volume receptors and precipitates a CNS-mediated decrease in cardiac output, an increase in peripheral vascular resistance, andredistribution of blood flow to the vital organs. Hypoxia and hypercapnia cause

chemoreceptor stimulation, vasomotor activation, and increased respiratory drive. At laterstages, stimulation of the hypothalamus by interleukin 1 initiates the hypermetabolic responseto 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. Incontrast, plasma concentrations of the primaryanabolic hormone, insulin, are decreased

because of CNS-mediated sympathetic inhibition of the pancreas. Posttraumatichyperglycemia provides non-insulin-mediated tissues such as the brain with a preferentialsupply of glucose.

Glucagon, cortisol, and catecholamines maintain blood glucose levels and preventhypoglycemia. The primary function of glucagon, which is produced in the pancreas, is to

promote gluconeogenesis in the liver. After trauma, direct sympathetic stimulation of thepancreas enhances glucagon secretion. Corticotropin release by the anterior pituitary glandcauses adrenal elaboration of cortisol, which promotes the breakdown of skeletal muscle intoamino acids and facilitates gluconeogenesis in the liver. The hypoglycemic effect of cortisolcounteracts 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 increasedmyocardial contractility and conductivity. Epinephrine also promotes glucose production byenhancing hepatic gluconeogenesis and inhibiting insulin release. Norepinephrine, the

primary sympathetic nervous system neurotransmitter, exerts a direct effect on the circulatorysystem and vital organs. With massive and prolonged sympathetic discharge, norepinephrinecan enter the bloodstream and exert a direct vasoconstrictive effect on the vascular systemsimilar to that of epinephrine(9,10).

Metabolic ResponseThe 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 sustainedrelease of circulating catecholamines and increased activity of the sympathetic nervous


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system. The primary energy source during this period comes from oxidation of lipidspromoted by the elaboration of the catabolic hormones (9,10).Although fat is the primary energy source after injury, protein also is broken down to produceenergy. 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 toform precursors for new glucose synthesis in a trauma patient in the catabolic state. The resultis rapid loss of muscle mass. The depth and the length of the catabolic state are related to theseverity of the trauma. Although it represents an adaptive mechanism, a persistently

prolonged and severe catabolic state leads to severe malnutrition, multiple organ failure, anddeath (9,10,13,14,15).

Treatment of a Patient who has Sustained TraumaThe key to improving survival and managing disablity in the trauma patient are the initialevaluation and resuscitation performed at a dedicated trauma center. The American Collegeof 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 primaryand 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 life-sustaining maneuvers. Resuscitation is performed simultaneously with the primary survey.The secondary survey consists of a rapid but systematic head-to-toe physical examinationwith the patient completely disrobed. This global assessment is done to identify all potentiallylife-threatening and occult injuries. An important part of the primary and secondary surveyare radiographic studies including the use of ultrasonography. Samples are drawn for baseline

blood studies, typing, and cross-matching. Once these priorities have been addressed, vitalsigns are rechecked. When the patient's condition is stable, a detailed management plan isestablished.

Primary Survey

Airway

The foremost emergency measure is establishing the airway, which may be lost to a variety ofcauses. The oropharynx, larynx, and trachea can be obstructed by secretions, blood, andforeign 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 belowthe oropharynx. Maneuvers to secure an adequate airway range from the simple to thecomplex and begin with manual cleaning of the oropharynx followed by suctioning ofsecretions.


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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 cervicalspinal fracture is present. The airway must be controlled with the assumption that such afracture exists. The neck must be completely immobilized in a neutral position. One memberof the trauma team must be assigned to kneel at the head of the stretcher to maintain inlinemanual head stabilization and avoid hyperextension by holding the cervical spine with thehands while immobilizing the head with the forearms (Fig. 66.1). Traction on the head isavoided, because distraction with further injury to the spinal cord can occur if the patient hasan 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 isconscious, a nasopharyngeal airway is used. Once the airway has been established and the

patient is spontaneously breathing, supplemental oxygen can be provided through nasalprongs or a face mask.

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


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tongue and mandible is performed.

When these simple measures are unsuccessful, more aggressive airway management isneeded. Nasotracheal intubation is the preferred technique for establishing an airway in aconscious 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 intubationand does not necessitate sedation or muscle relaxation. Nasotracheal intubation is precludedif the patient has extensive maxillofacial injuries.

If the nasotracheal route cannot be used, orotracheal intubation is the next step. In idealcircumstances, a cross-table lateral cervical spine radiograph is obtained before orotrachealintubation to evaluate for a possible cervical spinal fracture. It is nevertheless important toremember that even a normal cross-table lateral radiograph of the cervical spine does notdefinitively exclude the presence of cervical spinal fracture or instability(16). When

emergency airway control with orotracheal intubation is indicated, intubation proceeds withinline 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 patientis unconscious and cervical spinal injury has been ruled out, orotracheal intubation can bereadily accomplished. A patient who is awake must be paralyzed with succinylcholine forsuccessful orotracheal intubation.

After intubation, the chest is auscultated to ensure that the tube is in the trachea and not in theesophagus or in one of the main-stem bronchi. Correct endotracheal tube positioning can beconfirmed reliably by the presence of end-tidal carbon dioxide. Carbon dioxide from thelungs can be detected rapidly by observing a color change on a disk that can be connectedrapidly to the endotracheal tube. If no carbon dioxide is detected, the endotracheal tube is inthe esophagus, and a new airway is attempted. If the patient is in cardiac arrest, end-tidalcarbon dioxide is unreliable in confirming the positioning of an endotracheal tube. A follow-up 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 hassustained laryngotracheal trauma, surgical airway intervention may be needed. Four surgicalmethods 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 sheaththrough the cricothyroid membrane into the tracheal lumen. Once it is in the airway, theneedle is withdrawn and the plastic sheath is advanced. When properly positioned, the sheathis 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-secondintermittent injections of oxygen followed by 4-second exhalations. Patients can bemaintained 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 airwayintervention (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 membraneitself. The blunt end of the scalpel is inserted between the cricoid and the thyroid cartilages


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

Figure 66.3 Cricothyrotomy.


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Tension pneumothorax develops when a pleural, bronchial, or tracheal tear allows air to beforced into the pleural space without a means of egress. The result is collapse of theipsilateral lung. As pleural pressure increases, the mediastinum and trachea shift to theopposite side, compress the contralateral lung, and compromise oxygenation. The mediastinalshift 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 ofbreath, tracheal deviation away from the injury, increased resonance to percussion, distentionof the neck veins, and decreased breath sounds over the injured hemithorax. Tension

pneumothorax is a clinical diagnosis made on these clinical grounds. Diagnostic chestradiographs 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 needlethoracocentesis with a large-bore,12-gauge intravenous cannula inserted into the secondintercostal space in the midclavicular line (Fig. 66.5), followed by definitive treatment withchest-tube insertion. Pneumothorax also can cause hypotension, owing to its effect onmyocardial 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 insertedinto the second intercostal space in the clavicular line.

Cir culation and Shock

Once the airway and breathing have been reestablished, the next step is to assess theadequacy of the circulatory system. Shock is the clinical manifestation of the inability of theheart to maintain adequate circulation to vital organs. This low-flow state can be caused bycardiac dysfunction, loss of blood volume, loss of vascular resistance, and an increase invenous capacity(13). The cellular response to shock is a shift from aerobic to anaerobicmetabolism in nonvital organ systems. The result is lactic acidosis. If hypoperfusion persists,oxygen delivery to vital organs becomes inadequate, and acidosis deepens. Unlessoxygenation 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 beanxious and restless; if shock is severe, the patient appears listless or exhausted. The skin is


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cool and sallow with decreased capillary filling in the nail beds. Thirst, nausea, and vomitingarecommon. Blood pressure is low, and the pulse is fast and weak. Poor filling of peripheralveins makes it difficult to place intravenous catheters. The four categories of shock arehypovolemic shock, neurogenic shock, cardiogenic shock, and septic shock. The first threeare associated with the acute phase of trauma.

Hypovolemic ShockHypovolemia is the most common cause of shock after trauma. Hemorrhage is assumed to bethe cause unless proved otherwise. Attempts have been made to classify the severity ofhemorrhagic shock as follows to give better guidelines for resuscitation:

Class I hemorrhage is the loss of about 15% of blood volume. The primarymanifestation is mild anxiety.

Class II hemorrhage is the loss of 15% to 30% of blood volume. The result istachycardia and tachypnea, anxiety, decreased capillary refill, and decreased urineoutput. Supine blood pressure remainsnormal.

Class III hemorrhage is the loss of 30% to 40% of blood volume. Patients often areextremely anxious or combative and have marked tachycardia and tachypnea,

prolonged capillary refill time, and a marked decrease in urine output. Only at thisstage of severe hypovolemia does supine hypotension occur.

Class IV hemorrhage is the loss of more than 40% of blood volume. The result ismarked hypotension and tachycardia. Urine output is almost completely shut off, andmental status can range from anxiety to coma. Losses of this magnitude often arelethal.

Hypovolemia should be managed with rapid volume replacement. Patients needing acutefluid 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 littledifficulty. If the systolic blood pressure is so low that percutaneous access in the antecubitalspaces is precluded, greater saphenous vein cutdown can be performed. Percutaneous femoralvein or subclavian catheterization is another alternative, but the surgeon must be familiar withthe 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 preferredfluids for resuscitation. In adults, blood volume is about 7% of total body weight (about 5 Lfor a normal-sized man). In children, blood volume is 8% or 9% of total body weight; ininfants, 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 approximateblood volume of the patient. Circulating volume can be restored by infusing 3 mL crystalloidsolution for each milliliter of estimated blood loss. This ratio can be much greater in massivehemorrhage. The crystalloid solution is infused as rapidly as possible until blood pressure andheart rate return to acceptable levels. Further fluid replacement can be monitored according tothe adequacy of the urine output(1,2,3,4,5,6,7,10,12).

When crystalloid replacement is inadequate, blood replacement becomes necessary. As arule, trauma patients who arrive in the emergency department with supine hypotension likelyneed 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 mosthospitals and rarely causes serious complications. If type-specific blood is unavailable, type


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O-negative (universal donor) blood can be given safely to a trauma patient in need ofemergency blood transfusion. The risk of transfusion reactions with O-negative blood in thissituation is minimal.

Substantial clotting problems can occur with massive crystalloid and blood-replacement

therapy for hemorrhagic shock. Although blood components are not used in earlyresuscitation, dilutional coagulopathy can develop after substantial transfusion. Thisdilutional coagulopathy is managed with fresh-frozen plasma and platelet transfusion,depending on the degree of ongoing bleeding. Platelets and fresh-frozen plasma areadministered 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 tenthunit of banked blood and then after every fourth unit. Use of platelets can be considered afterthe 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. Incases of external hemorrhage, the bleeding often can be controlled with minimal pressure.

Tourniquets usually are not helpful, because direct compression can control blood loss. Blindclamping must be avoided to prevent injury to adjacent nerves. The scalp may be the sourceof profuse bleeding, and rapid temporary suturing may be needed.

Military antishock trousers (MASTs), which are inflatable pants, can be placed around thepatient's legs and pelvis to decrease circulation to the extremities and thereby improve centralcirculation. 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 MASTsbecause abdominal compartment inflation can impair respiration, and leg compartmentoverinflation for long periods can cause compartment syndrome.

Neurogenic ShockThe purpose of fluid restoration is to reestablish adequate perfusion to vital organs.Measurements such as blood pressure, heart rate, urinary output, and level of consciousnesshelp measure the success of fluid resuscitation. When these signs do not change in responseto adequate resuscitation, other causes must be suspected. One such cause can be neurogenicshock, which is caused by brainstem dysfunction or spinal cord injury that denervates thesympathetic nervous system. The result is vasodilatation, decreased peripheral vascularresistance, and consequent loss of blood pressure. Neurogenic shock is characterized by theabsence 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 repleteintravascular volume, vasopressors to restore lost vascular tone, and appropriateneurosurgical intervention(13).

Cardiogenic ShockCardiogenic shock is loss of circulatory perfusion because the myocardium cannot producesufficient flow to maintain tissue oxygenation. Among trauma patients, cardiogenic shock isgenerally associated with three injuries: tension pneumothorax, cardiac tamponade, andmyocardial contusion. Cardiogenic shock is suspected when hypotension persists despiteappropriate resuscitation. The most common features of cardiogenic shock are distended

jugular veins and elevated central venous pressure in the presence of hypotension. These


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signs may not occur until the patient has undergone adequate fluid replacement. Cardiogenicshock may coexist with hypovolemic shock.

A common feature of tension pneumothorax is impaired myocardial function due todecreased venous return. Increasing intrathoracic pressure distends the jugular veins and

causes hypotension. In an emergency, tension pneumothorax can be confused with cardiactamponade because both conditions are associated with hypotension and neck-vein distention.In some instances, it is impossible to differentiate these two conditions, and empiricalthoracocentesis is necessary on the side most likely to be affected. If a rush of air is seen withrestoration of hemodynamic status, the diagnosis of tension pneumothorax is confirmed. Ifnot, the procedure is repeated on the opposite side of the chest. If the patient's condition doesnot improve, cardiac tamponade is considered, and the patient is empirically treated.

Cardiac tamponade in a trauma patient is caused by blood accumulation between themyocardium and its pericardial covering. Because the pericardium is nondistensible, smallvolumes of blood can accumulate in the acute setting, resulting in marked myocardial

impairment. The pathophysiologic changes leading to cardiogenic shockare caused by adecrease in ventricular filling during diastole and myocardial contractility impairment due toischemia from coronary circulation impairment. The classic cardiac tamponade signs arehypotension, 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 ofsuspicion based on an injury such as a penetrating chest wound.

Figure 66.6 Pericardiocentesis for acute cardiac tamponade performed through the leftsubxyphoid 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 leftsubxyphoid 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 inmyocardial function; however, frequent false-negative and false-positive results under


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extreme circumstances may prompt a left anterior thoracotomy with direct pericardialdecompression.

Emergency thoracotomy is an option when a trauma patient does not respond to resuscitationand is in cardiac arrest. Other considerations for emergency thoracotomy include initiating

direct cardiac massage and controlling massive hemothorax due to cardiac puncture or tearsin the thoracic aorta.

Myocardial contusion, another cause of cardiogenic shock after trauma, is caused by bluntinjury, typically when the chest hits a steering wheel. Physical signs include ecchymoticdiscoloration of the anterior chest wall and flail chest. Severe myocardial contusion isunusual, whereas blunt chest trauma is common. Marked myocardial contusion can beconfirmed with transthoracic or transesophageal electrocardiography. Wall motion, valvulardysfunction, and the presence of pericardial fluid or tamponade can be seen withechocardiography. Management is aimed at preventing fluid overload while maintainingcardiac 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 stronglyconsidered(13).

Secondary SurveyThe secondary survey consists of a detailed physical examination with the patient fullyexposed. It is undertaken once the lifesaving priorities of the primary survey have beenaddressed. The breadth and speed of this examination depend in large measure on the

patient's injuries and the need for definitive surgical intervention. Valuable informationregarding the patient's history must be collected, including the mechanism of injury,

preexisting medical problems, current medications, known drug allergies, and when thepatient last ate. Routine objective studies also can be performed at this time, including acomplete blood cell count, chest radiography, and urinalysis. If drug overdose or alcoholconsumption is suspected, appropriate toxicologic studies can be performed. Hypotensionwarrants blood typing and cross-matching.

Head and Spine I njur ies

Altered mentation is the most frequent sign of injury to the CNS and is presumed to becaused by injury until proved otherwise. Cervical spinal and spinal cord injuries are commonamong patients with multiple injuries, and the greatest concern is to avoid further injury tovital neurologic structures. Rigid immobilization of the cervical spine is imperative until a

complete set of spinal radiographs, including cervical, thoracic, and lumbar spineradiographs, has been obtained. The entire spine is palpated for tenderness and alteredcontour. For patients with definitive cervical spinal injuries, use of a rigid collar reinforcedwith 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 increasedintracranial pressure (ICP), or by decreased cerebral perfusion. Whereas the first twoconditions necessitate formal neurosurgical intervention, the changes in pressure and

perfusion can be managed in the emergency department. The tool used to assess mental statusis an abbreviated neurologic examination to define the Glasgow Coma Scale score (Table66.1). This graded evaluation is performed to assess the functions of eye opening, verbalresponse, 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. Furtherneurologic assessment includes evaluation of pupillary reflexes, deep tendon reflexes, and


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rectal sphincter tone. A serious head injury can have nonneurologic signs such ashypoventilation and hypertension.

Emergency department treatment of a patient with a head injury is aimed at minimizingcerebral 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 levelof about35 mm Hg. Patients with suspected cerebral trauma and a Glasgow Coma Scale scoreless 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, toreduce the amount of intracellular water in the brain. Ventriculostomy can be used to monitorICP 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 gainingincreasing acceptance. Any patient who has changes in mental status after injury needscranial computed tomography (CT) as part of the secondary survey(17).

Figure 66.7 For patients with definitive cervical spinal injuries, use of a rigid collarreinforced with sandbags on either side and wide tape across the forehead is mandatory.

TABLE 66.1 GLASGOW COMA SCALE

Function Score

Eye openingSpontaneous 4Verbal stimulus 3

Painful stimulus 2None 1

Verbal responseOriented 5Confused 4Inappropriate 3Incomprehensible sounds 2

No response 1Intubated 1T

Best motor responseObeys commands 6

Localizes painful stimulus 5Withdraws from painful stimulus4


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Flexion response 3Extensor response 2

No response 1

Score rangeExtubated 3-15

Intubated 3T-11T

The management of spinal cord injury with distal deficits has changed over the last severalyears. Emphasis remains on maintaining spinal immobilization to prevent additional spinalcord injury. Recent research(18)has found that administering steroids may play a role inminimizing neurologic deficits for patients with spinal cord injuries. Administeringmethylprednisolone 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 withassessment 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 thefacial bones, hemotympanum, cerebral spinal fluid otorrhea and rhinorrhea, and periorbitaland mastoid ecchymosis.

Neck I nju ri es

All injuries to the neck are potentially life threatening because numerous vital structurestraverse this area. Neck injuries are classified as blunt or penetrating. Blunt trauma to theneck can cause cervical spinal injury, pharyngeal and tracheal injuries, and carotid arteryinjury. 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 thejaw, and zone III injuries are above the angle of the jaw (Fig. 66.8). Posterior injuries candamage the cervical spine. Anterior and lateral wounds can injure the great vessels of theneck, the larynx, the trachea, and the esophagus as well as important nerves such as thevagus, 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; penetratinginjuries 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, includingevaluation for hoarseness, stridor, dyspnea, and hemoptysis. Subcutaneous emphysema,crepitus, and distorted laryngeal landmarks indicate laryngotracheal injury. Dysphagia andchest 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 useand provides an excellent way to evaluate the patency of the airway and the function of thelarynx. Fiberoptic laryngoscopy also can aid in diagnosing laryngeal fractures and vagalinjuries. CT of the neck also can help to delineate laryngeal fractures.


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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 theaw. 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 ofthe 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 personnelare available, especially when the patient has sustained blunt laryngotracheal disruption. Thisinjury usually is caused by severe compression of the laryngotracheal complexbetween thesteering wheel and the vertebral column or from clothesline injury, such as catching the neckon a barbed-wire fence while riding a snowmobile or a motorcycle. Under thesecircumstances, active airway management can be fraught with danger. Intubation may not befeasible, and tracheotomy can cause retraction of the distal trachea into the mediastinum.

Patients with penetrating neck injuries are at risk of airway obstruction, hemorrhage, andinjury to the cervical spine. Important clinical signs include stridor, hoarseness, subcutaneousemphysema, expanding hematoma, external hemorrhage, hemoptysis, dysphagia, cranial

nerve dysfunction, and branchial plexus injury. Active airway intervention is important withevidence of airway distress. It is best accomplished with nasotracheal or orotrachealintubation. Bleeding in the oropharyngeal area may preclude intubation and necessitateemergency 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 neckinjuries, not only as definitive treatment but also as a diagnostic technique. Some authorsadvocate routine exploration of all injuries penetrating the platysma. Others advocateselective exploration and observation based on preoperative arteriographic findings and onthe presence or absence of symptoms that suggest vascular, airway, and neurologic injury.


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Most patients in stable condition with penetrating injuries to the base of the neck (zone I) arebest examined by means of arteriography, laryngoscopy, and esophagoscopy or a barium-swallow radiographic study. Patients in stable condition with penetrating injuries above theangle of the mandible (zone III) are best examined with arteriography to exclude carotid orvertebral 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 ofarteriography, 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 CTof the head are normal, the possibility of blunt carotid injury with carotid occlusion ordissection is considered and excluded with arteriography. Management of these injuriesinvolves anticoagulation with heparin or reconstruction, depending on the nature of theinjury.

Thoracic In ju ri es

Thoracic injuries are classified as blunt or penetrating. Most blunt injuries are caused bymotor vehicle accidents. Penetrating injuries typically are from violence with knives or guns.The principal forms of life-threatening blunt chest trauma are flail chest, pulmonarycontusion, tracheobronchial disruption, and torn thoracic aorta.

Flail chest occurs when part of the chest wall becomes isolated owing to multiple fractures ofthe 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 thatinvariably accompanies a severe flail chest. If ventilation becomes inadequate, hypoxia andhypercapnia occur, and the patient needs intubation and ventilatory assistance.

Pulmonary contusion is a common finding in blunt chest trauma. It often is associated withflail chest and hemopneumothorax and is common in multisystem trauma. Pulmonarycontusion causes alveolar edema and impairs gas exchange. The primary sign of pulmonarycontusion is hypoxia. Initial management is adequate oxygenation and avoidance of fluidoverload, which can promote pulmonary edema. If a patient has hypovolemia and pulmonarycontusion, 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. Theareas most commonly involved are the proximal main-stem bronchi and the distal trachea.Common features of this injury include pneumothorax, subcutaneous emphysema, andhemoptysis. Initial therapy often entails venting the pneumothorax. Bronchoscopy isindicated for diagnosis.


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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'shemodynamic status.

Abdominal I nju ri es

Abdominal injuries are life threatening because the peritoneal cavity can harbor occult bloodloss and fecal contamination. Unrecognized abdominal injury is a common cause of deathafter trauma, and prompt recognition is of primary importance in its prevention. Diagnosiscan be delayed by the silent nature of the injury, other life-threatening problems, or an alteredstate of consciousness.

Examination of the abdomen begins at the level of the nipples and extends to the pubicsymphysis. 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 notcorrelate 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 areassociated with injury to solid organs, such as the liver, spleen, pancreas, and kidneys. Themost common finding among patients with blunt abdominal trauma and solid-organ injuriesis hemoperitoneum with shock. Trauma patients with persistent hypotension and possible

blunt abdominal trauma require a search for occult bleeding. This can be done expeditiouslywith focused assessment for the sonographic evaluation of the trauma patient (FAST) ordiagnostic peritoneal lavage (DPL). These studies can be done rapidly in the trauma bay.FAST is an ultrasonographic examination performed by the trauma surgeon or emergencydepartment 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 performFAST, a DPL can be performed. Initial peritoneal aspiration of more than 10 mL of blood isan indication for laparotomy.

Lavage is performed by means of instilling 15 mg/kg normal saline solution into theperitoneal cavity and letting the fluid drain out by means of gravity. When the totalerythrocyte count in the lavage effluent exceeds 100,000 per milliliter, most patients haveabnormal 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 abdominalCT has increased, it has become clear that many patients with minor liver and spleen injurieswith hemoperitoneum stop bleeding spontaneously and never need abdominal exploration.

Patients with penetrating abdominal trauma and overt signs of peritonitis or hypovolemianeed surgical exploration; however, therapy is less clear-cut when the patient's condition ishemodynamically stable or when signs of peritonitis have yet to evolve. The commonmechanisms of penetrating trauma are gunshot wounds and stab wounds. With gunshotwounds, laparotomy is indicated when the missile penetrates the peritoneum. Plain abdominalradiographs are obtained to outline the missile trajectory. Broad-spectrum antibiotics areadministered in anticipation of definitive surgical therapy.


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Stab wounds of the abdomen can be managed selectively because the likelihood of visceralinjury, even with peritoneal violation, is inconsistent. The first diagnostic steps are toascertain 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 patientunder 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 lavageresult differ in blunt injuries from stab wounds. Although 100,000 erythrocytes per milliliteris the accepted positive result for blunt injuries, an erythrocyte count of 5,000 to 10,000 permilliliter is accepted as a positive result in a stab wound and indicates that laparotomy isneeded. Patients with positive peritoneal lavage results need exploratory laparotomy. Thosewith negative peritoneal lavage results can be admitted for observation.

Extremity In jur ies

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 femoralfractures. Pelvic fractures associated with hypovolemia are stabilized with application ofMASTs. An expanding hematoma or pulsatile, bright-red bleeding indicates acute arterialinjury and is controlled with manual pressure.

Before it is assumed that bleeding is coming from a pelvic fracture when the patient'scondition is unstable, it is necessary to exclude ongoing intrathoracic or intraabdominalhemorrhage. Supraumbilical DPL may be indicated to exclude an intraabdominal source ofhemorrhage in these patients. In the care of patients with persistent pelvic hemorrhage,angiography is indicated for diagnosis and definitive management by means of embolizationof 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, andurethra. A high-riding prostate or a positive result of a heme test of stool can alert theclinician to this possibility. Bladder rupture also is considered if a patient has a pelvic fractureand hematuria. An abnormal result of a prostate examination or blood at the urethralmeatusindicates 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 isconfirmed with arteriography. Knee dislocation is often associated with popliteal artery injuryand distal ischemia. Popliteal artery angiography is usually recommended to exclude injury ifa patient has a knee dislocation.

Crush injuries to the lower leg and forearm can cause compartment syndrome due tohemorrhage 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 ofperipheral pulses is a relatively late finding and often implies irreversible damage to the limb.


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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. Bleedingfrom 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 beprovided(11,12).

I nhalation I njur ies

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 arecaused 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 ofinhalation include a decreased level of consciousness, singed nasal hairs, carbon deposits inthe oral cavity, carbonaceous sputum, and the finding of inflammatory changes in thesupraglottic 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 ofsupraglottic inhalation injuries need early endotracheal intubation with mechanicalventilation. The subglottic airway often is protected from burns unless the patient is exposedto superheated gas or steam. The vocal cords form an anatomic barrier. In addition, reflexclosure of the glottis serves to protect the subglottis and trachea. Carbon monoxide levels inthe blood should be measured, and oxygen therapy should be given immediately. Hyperbaricoxygen therapy is considered when a patient has marked carbon monoxide poisoning(12).

Definitive ManagementOnce the primary and secondary surveys have been completed, the patient has beenadequately resuscitated, and the patient's condition is judged to be stable, a plan for definitivecare is formulated. This plan begins with a ranking of the injuries in the order in which theyare to be managed. If at any point the vital signs become unstable, the primary and secondarysurveys are repeated. If the instability is from an injury that warrants definitive surgicalintervention, 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 furtherobservation. Transfer errors include inadequate management of the airway, poorly securedintravenous lines and drainage tubes, and inadequate patient monitoring. It is a tragedy toresuscitate a patient in the emergency department successfully only to lose the patient ontransfer to the operating room.

Role of the OtolaryngologistSince the early 1970s, the responsibility of otolaryngologists as members of the trauma teamhas continued to expand. In most institutions, otolaryngologists are viewed as experts inmanaging the airway and are expected to perform difficult intubations and provideemergency surgical airways. They also are recognized for expertise in the management of

maxillofacial trauma and penetrating injuries to the neck. Otolaryngologists often are calledon to assist in the immediate care of trauma victims in the emergency department.


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As valued members of the trauma team, otolaryngologists must continue to refinemanagement skills for injuries associated with the specialty but also need to beknowledgeable about the general care of trauma patients. Otolaryngologists shouldunderstand 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 alsoshould be able to perform the complete examinations needed in the secondary survey andknow 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 ofcatecholamines, which cause vasoconstriction, increase cardiac rate, increasemyocardial 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 initialevaluation and resuscitation performed partly in the field and partly in the emergencydepartment. Primary and secondary surveys allow physicians to manage complexmultisystem 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 primaryrisk during early airway management is movement of the neck when an occultcervical spinal fracture is present. When the airway is being controlled, it must beassumed that such a fracture exists.

Correct positioning of the endotracheal tube can be confirmed reliably by the presenceof end-tidal carbon dioxide. If no carbon dioxide is detected, the endotracheal tube isin the esophagus, and a new attempt at intubation is made immediately.

In the trauma patient, continuous monitoring with pulse oximetry is extremely helpfulin determining the adequacy of oxygenation and is used in the care of all criticallyinjured patients.

Techniques of surgical airway management include needle cricothyrotomy, standardcricothyrotomy, tracheotomy, and percutaneous tracheal ventilation. Needlecricothyrotomy is the best procedure for children; surgical cricothyrotomy is preferredfor adults.

Loss of respiratory drive among trauma patients most commonly is caused by severehead 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 arerestored. The most common cause of shock after trauma and hemorrhage ishypovolemia. Treatment is rapid volume replacement with crystalloids, such aslactated Ringer solution or normal saline solution through two 14-gauge catheters inthe antecubital fossa.

Cardiogenic shock is the loss of circulatory perfusion that occurs when themyocardium does not generate sufficient blood flow for tissue oxygenation. Amongtrauma 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


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that acute myocardial infarction or arrhythmia has precipitated an accident must beconsidered.

In the care of patients with head trauma, ventilation is adjusted to maintain a carbondioxide level of about35 mm Hg. Patients with cerebral edema or coma needcontinuous 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 asmeasured by cerebral perfusion pressure is best accomplished with the use of fluidsand vasopressors.

In the care of patients with spinal cord injury, administration of methylprednisoloneas 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 ifadministered within 8 hours of injury.

The decision to perform thoracic arteriography to exclude aortic disruption must bemade early in resuscitation. The decision is based on findings of mediastinal wideningon 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 ofassessment and management. Peritoneal lavage is an acceptable alternative. A totalerythrocyte count of 100,000 per milliliter correlates with positive findings atlaparotomy after blunt abdominal trauma. For patients with penetrating abdominaltrauma, 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 byangiography.

The earliest sign of compartment syndrome is the patient's report of paresthesia orsensory deficit in the limb. Loss of peripheral pulse is a relatively late finding andoften implies irreversible damage to the limb. Compartment syndrome occurs mostoften with closed fractures of the tibia and fibula. Amputated body parts must be keptin a moist and sterile towel and placed in crushed ice until definitive reimplantationcan 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 thesupraglottic structures. Signs of this type of injury are indications for earlyendotracheal intubation and mechanical ventilation.

Definitive management follows the primary and secondary surveys and begins withranking of the injuries in the order in which they are to be managed. If at any point thevital signs become unstable once again, the primary and secondary surveys arerepeated. Transfer out of the emergency department for definitive management can bea period of risk. Transfer errors include inadequate management of the airway, poorlysecured intravenous lines and drainage tubes, and inadequate patient monitoring.


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References1. National Center for Injury Prevention and Control. Web-Based Injury Prevention andControl. Web-Based Injury Statistics Query and Reporting System (WISQARS). 2001.Available athttp://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 andPrevention. Am J Public Health 2004;94(4): 522-534.5. Dinh-Sarr TB, Sleet DA, Shults RA, et al. Reviews of evidence regarding intervention toincrease 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 bicylesafety helmets. N Engl J Med 1989;320: 1361-1367.7. Shults RA, Elder RW, Sleet DA, et al. Reviews of evidence regarding interventions toreduce 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-fireinjuries. 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. Essentialsof 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 adifference? Intens Care Med 1998;24:28-36.16. Hastings RH, Marks JD. Airway management in patientswith potential cervical spineinjuries. Anesth Analg 1991;73:471-482.17. Bullock R, et al. Guidelines for the management of severe head injury Brain TraumaFoundation, 1995.

18. Hadley MN, Walters BC, Grabb PA, et al. Guidelines for the management of acutecervical spine and spinal cord injuries. Clin Neurosurg 2002;49:407-498.19. McCarter FD, Luchette FA, Molloy M, et al. Institutional and individual learning curvesfor focused abdominal ultrasound for trauma: cum sum analysis. Ann Surg 2000;231(5):689-700.
http://www.cdc.gov/ncipc/wisquarshttp://www.cdc.gov/ncipc/wisquars


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Maxillary and Periorbital FracturesBrendan 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 thefacial skeleton were traditionally evaluated and managed in a segmental manner, even ifcomplex injuries were obvious during the initial evaluation. This approach usually producedacceptable results if the fractures were from low-velocity impact and displacement wasminimal. However, similar successes in managing injuries due to high-velocity impact oftenwere not achieved. Experienced maxillofacial trauma surgeons have recognized that thesuboptimal results were caused by the segmental approach. Therefore, all fractures of themiddle third of the face must be evaluated as possible orbitozygomaticomaxillary injuries andnot as blowout, malar, or Le Fort fractures, each in isolation. The goal of treatment must bethe exact anatomic restoration of the midfacial skeletal unit rather than approximaterepositioning of its component parts.

AnatomyThe structure of the midfacial skeleton is related to its mechanical adaptation to forcesgenerated by mastication. Forces of up to 200 pounds per square inch are developed duringchewing. The concept of buttresses describes the relatively stronger areas of the midfacialskeleton that bear the bulk of these vertically oriented forces. Horizontally oriented buttressesalso exist for supporting vertical buttresses.

Buttresses

The vertical buttress system has seven components, including three paired pillars and oneunpaired structure: (a) the paired medial, or nasomaxillary (a.k.a., nasofrontal), buttressesextend 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, orzygomaticomaxillary, buttresses extend from the lateral maxillary alveolus along the lateralmaxilla to the malar eminence of the zygoma, then superiorly along the lateral orbital rim tothe 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 andperpendicular plate of the ethmoid bone, connects the palatine process of the maxilla to thefrontal 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, thezygomatic 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 containsa 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 thezygoma. 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).


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The bone of the maxilla is for the most part quite thin. The lateral wall of the maxillaryantrum, however, includes a wedge of thicker, compact bone. It is in this area that thezygomaticomaxillary 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 integralcomponent of the buttress system, and also forms the aesthetically vital malar prominence. Itis a keystone as it integrates the vertical zygomaticomaxillary and zygomaticofrontal (zf)

buttresses to the horizontal infraorbital and zygomatic arch buttresses. It is related to thesurrounding 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, runningfrom the zygomatic process of the frontal bone, over the zygoma itself to the lateral antralwall 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 intersectionof 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 wallwith the orbital plate of the sphenoid bone and the orbital floor projection that articulates withthe orbital surface of the maxilla in the extreme lateral aspect of the orbital floor. Thesphenoid 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 therim.


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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 calledorbital 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 zygomaand the maxilla(3). No true medial rim exists in the area of confluence of the orbit, lacrimalfossa, glabella, and nasal dorsum. The orbital rims form a frame of relatively sturdy bone atthe 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 theinferior orbital rim, where the orbital roof has a concavity that places it approximately 5 mmabove the superior orbital rim. The orbital floor is also concave with a depth of approximately3 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). Laterallyand posteriorly, the floor is separated from the greater wing of the sphenoid bone by theinferior orbital fissure. The optic foramen lies posteriorly in the plane of the medial orbitalwall; 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 portionof the orbital floor, and the retrobulbar soft tissues are supported by the convex posteriorfloor. The millimeter scale identifies the position of the two areas of opposite floor contourrelative to the inferior orbital rim and orbital apex.


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

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


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description of the injuries.

Pathophysiology/Mechanism of TraumaWith the midfacial skeleton adapted to the vertical forces of mastication, it is force deliveredat other vectors that cause the bulk of midface fractures. Common etiologies of midfacial

fractures include motor vehicle accidents, assaults, and sporting events.

Le Fort F ractures

Rene Le Fort introduced a classification of midfacial fractures on the basis of cadaverexperiments he performed in the early part of the 20th century. He noted that fractures tend tooccur at characteristic locations, which correspond with relatively weak areas of the facialskeleton.

Le Fort Level I fractures are transverse fractures separating the maxillary alveolus from therest of the midfacial skeleton (Fig. 70.5). These injuries generally result from anterior forcedirected at the lower midface. The nasomaxillary and zygomaticomaxillary buttresses are

disrupted at their inferior extent (6). The fracture line then extends transversely through themaxillary 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 uppercraniofacial skeleton. They result from either direct anterior force against the midface or frominferior impact at the mandibular symphysis transmitted to the midface via the dentoalveolarsegments of the mandible. Once again the nasomaxillary and zygomaticomaxillary buttressesare disrupted, this time more superiorly. The fracture line extends from the nasal root via thelacrimal bone and medial orbital wall, then anteriorly along the orbital floor to the infraorbitalcanal. From this point, the fracture line follows the zygomaticomaxillary suture to theanterolateral maxillary wall. Posteriorly, the fracture line passes across the infratemporalsurface 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 ofthe vertical buttresses. The vertical buttresses are disrupted at their superior most extent. Thefracture line extends through the root of the nose, across the lacrimal bone and medial orbitalwall, across the orbital floor to the inferior orbital fissure. From this point, one fracture linetraverses 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 theprevious discussion suggests. A reading of Le Fort's original work demonstrates that he wascertainly not unaware of this. The Level I to III classification scheme is a distillation of someof his most significant experimental observations but is not comprehensive. In hisexperiments, and most definitely in real-life trauma, force is delivered unevenly to each sideof the face, at varying angles, and with variable locations of impact. The resulting fracturesmay be asymmetric from one side of the face to the other (i.e., Le Fort II on the left, Le FortIII on the right), may combine with other fractures to create a more complex pattern [i.e., aLe 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 notdescribed by the classification at all.


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Figure 70.5 External arcs of contour of the zygoma disrupted (dotted lines) with comminutionof 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 Maxill ary F ractures

Anterior forces localized between the nose and malar prominence may produce anteriormaxillary wall fractures. Significant force delivered to the lower anterior midface, in additionto generating the classic fracture patterns described by Le Fort, may less commonly causefractures of the palate. Although they may occur in isolation, palatal fractures tend toaccompany 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 widenedmaxillary alveolar arch.

Palatal fractures, and in particular those oriented sagittally, alter the width of the maxilla andpermit the rotation of the maxillary dentoalveolar segments. One of the fundamentals inmanagement of severe facial fractures is the intraoperative restoration of normalmaxillomandibular occlusion, with anatomic reduction of fractures following from this basis.Palatal fractures, by complicating the restoration of occlusion, can confound this strategy ifnot addressed appropriately first(8).

Zygomaticomaxil lary Complex Fractures

A number of terms are used in the literature to describe fractures involving the zygoma andthe bones with which it articulates. These include malar fractures, zygoma or zygomatic


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fractures, ZMC fractures(9), tripod fractures, tetrapod fractures, trimalar fractures,zygomatico-orbital fractures, and orbitozygomatic fractures(10). All of these terms emphasizecertain salient features of this type of injury. For example, the term tripod underscores theobservation 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 andother articulating bones in these injuries.

ZMC fractures generally result from blunt trauma to the malar eminence, the most prominentfeature of the lateral midface. They are the second most common midface fracture, after nasalfractures. Routinely, they involve disruption of the projections of the zygoma; in more severeinjuries, the sturdy body of the zygoma itself may be fractured. Additional fracturesfrequently occur concomitantly, including the anterior maxillary wall and the orbit. Anothercommon clinical feature of ZMC fractures is facial numbness/paresthesias. This is caused bydamage 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 fracturesseems most related to the force and velocity of impact(9)(Fig. 70.5).

Orbital Fl oor F racture

The complex anatomy of the bony orbit presages a wide array of possible fracture types andterminology. One simple method of categorizing orbital fractures is 1, fractures in which theexternal 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 thefirst, bone conduction theory, force contacting the inferior orbital rim is transmitted to theweaker bone of the floor behind it, resulting in a floor fracture and an intact rim. In thesecond, hydrostatic theory, a force impacting the globe itself causes a transient compressionof the orbital soft tissue contents. The resultant increased pressure within the bony orbit, ifsufficient, causes fracturing of the internal orbit in its weakest areas, primarily the floor andmedial wall. The originators of this theory coined the term blowout fracture to describe this

phenomenon. A third mechanism, recently reintroduced, describes translational movement ofthe globe (after a force is delivered to it), with fractures resulting directly from impact of theglobe 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 areactually much more common in combination with orbital rim injuries. Excellent examples ofthis type of injury are the orbital fractures that accompany all displaced ZMC fractures. Thezygoma comprises the entirety of the lateral orbital rim, as well as significant portions of thelateral orbital wall, inferior rim, and floor. A ZMC fracture with any significant displacementof the zygoma is thus, by definition, a lateral rim fracture and orbital floor fracture as well(13).


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Figure 70.6 Fisticuffs resulting in a classic orbital blowout fracture.

Other Orbital F ractures

Fractures of the strong supraorbital rim are relatively uncommon. They result from anteriorforces high on the face and are frequently associated with frontal sinus fractures andintracranial injuries. Nasoorbitalethmoid (NOE) fractures are caused by anterior forcedirected 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 inthese 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 bythe use of high-resolution computed tomography (CT). This modality is the work horse forevaluation of maxillary and periorbital trauma. Axial and coronal scans will documentfracture lines through the entire facial skeleton. The expense of CT evaluation of patientswith facial fractures other than simple nasal and mandibular fractures appears justified andcan be done in many emergency rooms (14).

The buttress system, particularly the vertical struts, must be systematically inspectedpreoperatively to document the degree of malalignment because of fracture fragment

displacement. Fracture lines themselves through the buttresses do not mandate openreduction, but comminution and gross malalignment strongly suggest the need for reductionof the fractures under direct visualization to restore facial length and projection. Ultrasoundhas also been reported in evaluation of orbital trauma. Its advantages include no use ofirradiation and the ability to perform a bedside examination (15). Its incorporation into astandardized 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 anorbitozygomatic fracture is a goal that is not always realized. However, reconstructivesurgeons must be sensitive to the possibility of direct ocular trauma and obtain selected

consultation as indicated. A minimal preoperative examination includes testing of visualacuity (subjective and objective in both eyes), papillary function, and ocular motility;


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inspection of the anterior chamber for hyphema; and visualization of the fundus for grossdisruption. A decrease in visual acuity or any abnormality observed on the other portions ofthis screening examination warrants detailed examination by an ophthalmologist beforereconstruction of the bony injuries is undertaken. The value of forced duction testing formuscle 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 ofthe bony architecture of the injured facial skeleton (Table 70.2). Immediate reconstructionusually is less difficult and more successful than delayed reconstruction, mainly because thelatter 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 arepliable enough to allow restoration of the underlying bony configurations with local bonefragments or autogenous bone grafts. If the soft tissues are allowed to contract into a bonedefect, restoration of the soft tissue to a normal position by delayed restoration of thesupporting bone invariably produces a less desirable result. If revision surgery for minorresidual bone defects or lacerations is required, it is greatly facilitated if the overall soft tissueenvelope has been maintained in a normal position by a previous anatomic reduction of thefacial skeleton.

TABLE 70.2 TREATMENT

Early repair of midface fractures prevents soft tissue contracture that can be difficultto normalize in a delayed approach.

Meticulous attention to soft tissue closure and facial soft tissue re-draping is essentialto achieving a pretraumatic facial appearance.

Anatomic reduction prior to plate fixation is key. Rigidly fixated, malreducedstructures will result in a persistent facial deformity requiring revision surgery.

Maxillomandibular Fi xation

Closed manipulation of the maxilla to obtain maximal intercuspation of the teeth beforeapplication of maxillomandibular fixation restores the position of the maxilla in thehorizontal 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 byfracture dislocations. Closed reduction and maxillomandibular fixation are adequate


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management of less complex, minimally displaced maxillary fractures. Maxillomandibularfixation puts the jaws at rest for the 4 to 6 weeks needed for fracture healing. Maxillaryfractures found to be displaced on CT scans are best managed by means of extended accessapproaches 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 archbar wiring and can reduce operative time. Other innovations in maxillomandibular fixationthat reduce surgeon risk and decrease operative time include four point screw fixation whentooth bearing structures are intact and/or rapid plastic zip tie fixation with laced dental chainelastics (16,17,18,19).

Extended Access Approaches

Paralleling advances in radiographic evaluation of facial fractures has been the developmentof extended access approaches. These approaches (coronal, transconjunctival, buccogingival,and midfacial degloving) allow more accurate reduction of fracture displacements whilecamouflaging 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 ofcoronal, sublabial,

trauma maksilo facial

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