Anesthetic Considerations in the Acutely Injured Patient
Few situations are more challenging than the management of the acutely traumatized patient. It is the leading cause of death in individuals younger than 45 years.1,2 Up to 75% of these deaths occur within hours of injury. Effective management requires cooperation and communication between a team of physicians.
The initial survey of the patient should occur immediately on arrival to the health care facility and must assess if the patient is in an imminent life-threatening condition. A systematic approach should be followed. The Advanced Trauma Life Support (ATLS) protocol describes a process of assessment and resuscitation that involves the evaluation of airway patency, breathing, circulation, and neurologic function. For the critically injured patient, the primary anesthetic responsibilities focus on assessing, maintaining, or obtaining an airway and providing respiratory support. If the injury warrants, surgical intervention will occur in the operating room. Anesthetic management in this phase of the patient’s care will focus on drug selection to facilitate the surgical procedure. The anesthetic objective will be to achieve anxiolysis, analgesia, amnesia, and hemodynamic stability. The selection of drugs may be modified secondary to the injury and by the fact that resuscitation of the patient may be ongoing.
This chapter will focus on anesthetic and airway considerations in the management of the patient with oral and maxillofacial injuries. Many of the topics relevant to anesthetic trauma management are presented in the chapters pertaining to the assessment and evaluation of neurologic, thoracic, and abdominal injuries. This chapter will emphasize aspects that have significant anesthetic implications while minimizing repetition of the material presented elsewhere in this text.
The patient presenting with maxillofacial trauma presents a potentially complex and emergent scenario. Of significant concern is the susceptibility of the airway to injury in association with trauma to the head and neck. Airway narrowing or obstruction can result from edema, vascular congestion, or hemorrhage into the soft tissues or fascial spaces. These processes are dynamic and minimal; even an absence of early findings in the patient with significant trauma does not ensure that such problems will not occur or not worsen. Fracture of the skeletal complex may also result in airway narrowing and/or distortion. This may be a direct result associated with the displacement of bony fragments or may be secondary to the instability of bony segments with an unfavorable effect on normal muscle function. Airway irritability may also occur secondary to hemorrhage within upper airway. This could contribute to airway obstruction, laryngospasm, or aspiration.
Maxillofacial trauma may also impede the ability to secure the airway. Trismus may occur secondary to edema, skeletal mechanical obstruction, or inflammation of the muscles of mastication. The cervical spine is susceptible to injury and, until an injury is ruled out, modifications in airway management will be dictated.
The initial airway survey occurs immediately and consists of making a gross observation. Is the patient breathing spontaneously? Does the patient have adequate exchange? A negative response to either of these questions will necessitate emergent intervention. The initial assessment should also determine the patient’s adequacy of oxygenation. Observation for cyanosis may not be evident secondary to significant blood loss. Use of a pulse oximeter to determine oxygen saturation may be difficult for numerous reasons, including cold extremities, decreased perfusion, burns, and smoke inhalation. Centrally positioned probes should decrease the incidence of artifact associated with cold extremities and decreased peripheral perfusion. An oxygen saturation above 92% on room air confers some degree of safety, but this has to be interpreted based on the specific situation. For example, the patient with a decreased hematocrit may reflect a satisfactory oxygen saturation but in reality have a compromised oxygen content because of the diminished blood volume. Rapidly obtained initial laboratory studies, such as arterial blood gas (ABG) or venous blood gas (VBG), can provide data useful for evaluating the adequacy of ventilation and oxygenation. The astute clinician will also look for subtle changes, such as irritability and agitation, that may be early signs of hypoxia. Apprehension and restlessness may be suggestive of hypoxia as opposed to fear or anxiety caused by the ongoing events. As the hypoxia worsens, this may progress to deteriorating levels of altered consciousness, ultimately progressing to unconsciousness. Maxillofacial trauma patients who demonstrate an altered mental status, whether it be apprehension or confusion, must also be considered in the differential diagnosis to have a cerebral injury. The emergent need to manage the airway will preclude the ability to evaluate the patient fully and assess the extent of the head and neck injuries. Management of the airway will thus necessitate the assumption of concomitant injuries and dictate appropriate care.
If emergent intervention is not required, the examination must then identify injuries that may complicate or impede airway management. The examination must identify injuries that although not initially of an emergent matter, may potentially worsen and result in adverse respiratory consequences at some future point. The practitioner must also ensure that the examination focuses beyond the maxillofacial injury, determining whether the patient has other injuries that increase the risk of respiratory complications or would benefit from ventilatory assistance.
The complexity of managing the airway in the traumatized patient is that the decision to intubate may not be clearly defined. There are patients who, on admission, will appear to be ventilating and oxygenating adequately, but who will have less morbidity if the airway is controlled. Conversely, there are also patients in whom aggressive airway intervention on retrospect was contributory to an adverse event.
To provide optimal care, all patients should have a complete medical history and physical examination. If the patient is in acute distress, there frequently is inadequate time to perform such a complete history and physical examination. Emergent resuscitation and surgery may need to proceed with little or no background information. Whatever information is available should be obtained expeditiously. Information about the past medical history or the events surrounding the injury may be ascertained from the patient, family members, friends, or bystanders.
The emergency response personnel may also provide information about the events surrounding the traumatic event. Information about the mechanism of the injury may facilitate the diagnosis of associated clinical conditions. Information such as the death of another occupant of the vehicle may alert the practitioner to the potential for severe injuries that might otherwise go undetected. The report of the use of shoulder belts may alert the practitioner to blunt cervical injuries, such as a hematoma, that may displace the airway and produce pharyngeal and laryngeal congestion. A history of fire or smoke in a closed space will raise concern about the potential for airway injury.
Many trauma patients have major systemic diseases in addition to the injuries that currently brought them to the hospital. These systemic diseases may directly affect the patient’s care. Cardiovascular, pulmonary, hepatic, or renal disease may decrease the patient’s reserve and increase the patient’s risk. Trauma patients frequently have histories of alcohol and illicit drug use. These drugs can cause various physiologic changes and interactions with anesthetic drugs. Their actions could affect preoperative, intraoperative, and postoperative care.
The trauma patient may also be pregnant. Pregnancy in the traumatized patient presents special problems. Changes in cardiovascular and respiratory parameters can alter the patient’s response to anesthetic drugs. Additionally, many anesthetic drugs cross the placenta, having adverse effects on the fetus, and thus may be contraindicated.
An additional factor that needs to be considered during the intake visit is patient maturity. The child or mentally impaired patient poses a unique challenge. These individuals may lack the ability to cooperate. Techniques that may be selected for the typical adult patient may need to be foregone for safety purposes because they require a degree of patient cooperation.
The anesthesiologist first inspects for injuries that decrease airway patency and impair the ability to ventilate and intubate the patient. Stridor, dyspnea, dysphonia, dysphagia, odynophagia, or gurgling may be suggestive of obstruction or swelling of the airway. Coughing or hemoptysis may be associated with significant hemorrhage and an inability to maintain a patent airway. A muffled voice, hoarseness, or inability to speak may be suggestive of a laryngeal fracture. Subcutaneous emphysema may be suggestive of a disruption of the airway. The physical examination of the maxillofacial region must identify congenital abnormalities in addition to the following: (1) displacement of teeth or oral appliances; (2) hemorrhage; (3) soft tissue edema; (4) maxillofacial fractures; (5) limited interincisal opening; (6) cervical spine injury, instability, or hypomobility; and (7) burns and smoke inhalation. An extended examination must assess for neurologic, ophthalmologic, thoracic, abdominal, and orthopedic injuries, all of which may affect the anesthetic decisions that are made.
The initial examination may be limited. Injuries may be missed during the primary assessment, both in the emergency department and operating room. Undiagnosed cervical spine injuries, pneumothorax, or thoracoabdominal vascular injuries may cause significant intraoperative or postoperative morbidity or mortality. A secondary assessment or reexamination of the patient, including a review of the radiographs and laboratory results before surgery if the patient is not immediately operated on, or postoperatively, has been shown to diagnose 90% of significant injuries missed during the initial examination.3
Although unusual, teeth and/or associated structures may be aspirated. These foreign objects may become lodged in the supraglottic, glottic, or laryngeal area, or below the carina in the bronchi. A foreign object in the supraglottic, glottic, or laryngeal area may cause partial or complete obstruction. Immediate removal is indicated. General anesthesia should be considered for the patient with a partial obstruction, because anything that causes agitation of the patient could result in movement, resulting in a total obstruction. Alternatively, a foreign object that is aspirated into a bronchus is an urgent situation as opposed to an emergent situation. Maneuvers such as coughing should be avoided because they could dislodge the object so that it becomes wedged above the carina, causing a complete as opposed to a partial obstruction. The surgeon must also be cognizant that aspirated foreign objects are not always symptomatic. They frequently are not considered and may be only incidentally detected during laryngoscopy or evaluation of a chest radiograph, which should always be inspected for foreign material.
Maxillofacial injuries usually do not result in significant hemorrhage. However, in the traumatized patient, hemorrhage into the airway may increase airway irritability or cause laryngospasm, both of which impair ventilation. Impaired reflexes in the obtunded patient or significant hemorrhage may also lead to aspiration of blood. Patients are actually at more risk for aspirating blood than gastric contents. Vascular injury does not have to produce evident hemorrhage. A hematoma may cause a narrowing of the pharynx or superior-posterior displacement of the tongue, which will lead to partial or complete obstruction of the airway. The hematoma or edema may also cause vascular congestion that compounds the narrowing of the airway, contributing to respiratory distress. The edema or hematoma formation may not necessarily be noted extraorally. The swelling may also take several hours to become clinically significant and occlude the airway. An injury to the tongue represents an example of this, in which the extent of swelling may be unimpressive on initial examination, with delayed edema causing airway obstruction. Hemorrhage within soft tissue is more common with penetrating head and neck injuries as opposed to blunt injuries. Another consideration with soft tissue injuries is the potential distortion of the anatomy so that a mask fit cannot be satisfactorily achieved.
Certain fractures of the maxillofacial complex have the potential to compromise the airway. Mandibular fractures (e.g., bilateral parasymphyseal or condylar fractures) can result in posterior displacement of the tongue and paraglottic soft tissue, resulting in partial or complete respiratory obstruction. Establishment of a patent airway can usually be achieved by traction on the anterior mandibular segment and/or tongue, pulling either or both forward, away from the posterior pharyngeal wall. One method used to maintain anterior traction on the tongue is to place a heavy suture or towel clamp through the anterior midline of the tongue. The placement of the suture through the midline avoids injuring a vessel. Reducing the fracture using maxillomandibular fixation or interdental wires may also reduce the posterior displacement of the tongue and paraglottic soft tissue, alleviating the airway obstruction. The placement of a nasopharyngeal or oropharyngeal airway may also assist in establishing a patent airway when the tongue is displaced posteriorly.
Le Fort fractures produce a disruption of the pterygoid plates that may result in the posterior displacement of the maxilla. At the Le Fort I level, this may result in an anterior open bite but generally does not produce airway obstruction secondary to the skeletal displacement. The severity of the open bite, however, may cause difficulty in achieving a satisfactory mask fit. Posterior and downward displacement of a Le Fort III fracture may result in obstruction of the nasopharynx. The disruption of the skeletal stability, with its associated effect on the soft tissue of the pharynx, may contribute to obstruction during negative pressure inspiration.4 Nasal fractures may also cause nasopharyngeal obstruction. The hemorrhage associated with a nasal fracture may be sufficient to result in airway irritability and aspiration of blood.
Aspects of the examination seek to identify injuries that may necessitate modifications in airway management. A restricted interincisal opening may be seen with mandibular and midface trauma. The restricted movement may be secondary to soft tissue edema, muscle splinting, or mechanical bony obstruction. Frequently, it is secondary to pain and muscle splinting and should be alleviated on induction of anesthesia. An actual mechanical limitation may exist. A condylar or high subcondylar fracture of the mandible, the displacement of the zygomatic buttress or zygomatic arch so that either impinges on the path of the coronoid process of the mandible, or significant edema may limit mandibular opening and is not relieved with the induction of anesthesia.
Le Fort II and III fractures, along with naso-orbital-ethmoidal (NOE) fractures, may involve a fracture of the cribriform plate of the ethmoid bone or the medial wall of the orbit. The fracture of these bones creates the risk for the endotracheal tube to enter the cranium or orbit with nasal intubation. This is a relative contraindication to nasotracheal intubation until a cranial base fracture has been ruled out. There is also a potential risk for bacteria or air to be forced into the cranial cavity with positive-pressure ventilation.5
Cervical spine injury must be suspected in any patient with a maxillofacial injury. The incidence of cervical injury in the presence of facial fractures has been reported to be 1% to 6%.6–8 The higher percentage is among patients who were involved in a motor vehicle accident (MVA). The increased incidence probably is secondary to the forces sustained in the MVA and the associated hyperextension, hyperflexion, compression, and rotation of the cervical spine.9 However, no definitive relationship has been found between the mechanism of injury and a specific maxillofacial or cervical spine injury.
In the conscious patient, cervical spine injury is unlikely if the patient subjectively is without pain or paresthesia and objectively is without deformity or tenderness to palpation in a neutral position and during flexion and extension.10 If there is any positive finding, or if the patient is obtunded or not fully alert and able to concentrate, further investigation is warranted. The pediatric patient may be unable to provide reliable information and a lower threshold for further investigation is warranted. In the unconscious patient, flaccid areflexia, loss of rectal sphincter tone, diaphragmatic breathing, and bradycardia are suggestive of a cervical spine injury.
If further investigation is required, the diagnosis of a cervical injury is made radiographically. The examination must be able to detect fractures and ligamentous injuries. The examination must visualize all seven cervical vertebrae and the first thoracic vertebrae to be able to rule out a cervical injury. Fractures of the cervical spine are more reliably detected with a computed tomography (CT) scan compared with plain films (90% versus 58%), but ligamentous injuries are more reliably detected with plain films compared with CT scans (93% versus 54%).11 Immobilization of the neck in a neutral position is required until a definitive diagnosis is established, with the understanding that the urgency of the resuscitation may preclude the ability to obtain a definitive diagnosis for several hours to days. The best method of immobilization is achieved with a combination of a rigid cervical collar, a cervical-head immobilizer, and a backboard.12 Rigid cervical collars by themselves limit rotation and lateral movement to only 50% of normal and flexion and extension to only 30% of normal and do not provide adequate stabilization. An anesthetized or paralyzed patient should not remain on a backboard for a period exceeding 1 hour because of the risk for decubitus ulcers.
Respiratory complications are common with cervical spine injuries. The extent of the respiratory derangement is associated with the level of the injury to the cervical spine. Diaphragmatic paralysis occurs with injuries at C4 or above. This will necessitate ventilatory support. Although injuries at C5 or below spare the phrenic nerve and therefore diaphragmatic breathing, expiratory reserve may be adversely affected secondary to accessory muscle paresis. This may be further compounded by the respiratory depressant effects of alcohol and/or illicit drugs and any concomitant injuries to the brain, chest, or abdomen. Respiratory function may also be impaired because of pulmonary edema. This is secondary to pulmonary capillary damage and left ventricular dysfunction associated with the acute transient hypertension that frequently follows a spinal cord injury.
Injuries to the cervical airway may result from blunt or penetrating trauma. The incidence of these injuries is low. Blunt trauma to the airway from a direct blow to the cervical airway or from severe flexion-extension injuries may result in a thyroid, cricoid, or laryngeal cartilage fracture, or laryngotracheal separation.13 A fracture of the thyroid cartilage is frequently associated with edema. Stridor, dyspnea, dysphagia, odynophagia, or gurgling may be suggestive of swelling of the airway. A muffled voice, hoarseness, or inability to speak may also be suggestive of a laryngeal fracture. A fracture of the cricoid cartilage is less common. It is frequently associated with an injury to the recurrent laryngeal nerve. Injury to this nerve results in vocal cord paralysis. Vocal cord paralysis impairs the ability to protect the airway, which can lead to pulmonary aspiration. Although the incidence of a cricoid cartilage fracture is rarer, there is a mortality of 43% associated with this injury compared with 11% seen with a thyroid fracture.14,15 Up to 70% of patients sustaining blunt airway trauma have a concurrent cervical spine injury.16
Thermal and/or inhalation injury to the airway must be suspected in any patient presenting with a history of exposure to fire or smoke. Injury to the respiratory system may extend from the mouth to the alveoli. The heat and noxious chemicals from exposure to fire or smoke can produce upper airway edema, resulting in airway obstruction, periglottic edema, which potentially impairs laryngeal function, resulting in compromised protection of the lower airway, chemical injury, resulting in impaired pulmonary gas exchange, and carbon monoxide and cyanide toxicity. Patients with facial burns or a history of being in an enclosed space with a fire or smoke have a high risk of developing airway damage.
When the patient presents with a risk of thermal or inhalation injury, the examination must include looking for signs such as facial burns, singed facial hair, and/or carbonaceous debris in the nasal or oral secretions. These may be the only indications of potential respiratory problems because some patients may not demonstrate respiratory dysfunction on initial presentation. However, approximately 15% to 30% of burn patients develop some degree of respiratory dysfunction.17,18 Other early physical findings include wheezing, cough, dysphonia, and hoarseness. Upper airway edema, which may appear unremarkable initially, is an early contributing factor to respiratory distress. Within 2 hours, it may become notable, progressively worsening and necessitating intubation within 4 to 8 hours.19 The pediatric patient’s airway, with its relatively smaller diameter, is more susceptible to airway obstruction because any edema will have a more profound effect on airway patency. Late complications, such as parenchymal lung damage, may take several days to develop.
Periodic examination over the first 12 to 24 hours should be done to assess the severity of the injury. Fiber optic laryngoscopy and bronchoscopy will provide direct visualization of the periglottic region and lower airways, respectively. Serial ABGs and pulmonary function tests may also aid in assessing and differentiating upper from lower airway obstruction and pulmonary injury.
Carbon monoxide and cyanide are products of combustion; both cause tissue hypoxia. Hypoxia secondary to carbon monoxide toxicity occurs because carbon monoxide has a 250 times greater affinity for hemoglobin compared with oxygen. This displaces oxygen from its hemoglobin binding site and results in a lower oxygen-carrying capacity and lower blood oxygen content. The oxyhemoglobin dissociation curve is also shifted to the left. The leftward shift of the oxyhemoglobin dissociation curve results in less oxygen being released to the peripheral tissue.20
Monitoring oxygen saturation by pulse oximetry is inaccurate because these devices do not differentiate between oxyhemoglobin and carboxyhemoglobin.21,22 Serum carboxyhemoglobin levels should be obtained to establish the actual level of carbon monoxide present. Carboxyhemoglobin levels less than 20% cause headache and possible confusion. Carboxyhemoglobin levels between 20% and 40% present symptoms that include nausea, vomiting, disorientation, and visual impairment. Levels between 40% and 60% result in agitation, hallucinations, and coma, whereas levels greater than 60% are fatal.23 The half-life of carboxyhemoglobin is 4 hours. Oxygen therapy is indicated. The administration of 100% oxygen can shorten the half-life of carboxyhemoglobin to less than 1 hour. Hyperbaric oxygen (HBO) therapy has been recommended for carboxyhemoglobin levels of 30% or higher.24 Patients with neurologic symptoms should be considered for HBO regardless of their carboxyhemoglobin level.
Cyanide interferes with mitochondrial cytochrome function, resulting in tissue hypoxia. Nonspecific neurologic findings, including agitation and coma, are seen with cyanide toxicity. Lactic acidosis is also found with cyanide toxicity because it occurs with carbon monoxide toxicity. However, elevated levels in the patient without a significant burn injury and with ventilatory correction are more suggestive of cyanide toxicity.25 The mixed venous partial pressure of oxygen is also elevated in these patients. Cardiac rhythm disturbances are also not uncommon in these patients. Cyanide levels above 0.2 mg/liter are toxic and above 1 mg/liter are fatal.26