Trauma

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Trauma

Kara Snyder

Objectives

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Be sure to check out the bonus material, including free self-assessment exercises, on the Evolve web site at

evolve.elsevier.com/Urden/priorities/.

Trauma is a leading cause of death for all age groups younger than 44 years. Injury costs the United States hundreds of billions of dollars annually. It is one of the most pressing health problems in the United States today.

Injury as a result of trauma is no longer considered to be an accident. The term motor vehicle accident (MVA) has been replaced with motor vehicle crash (MVC), and the term accident has been replaced with unintentional injury. A program for prevention, recognition, and treatment of intimate partner violence is described in Box 25-1.

Clinicians working with trauma patients, however, are uniquely poised to impact the person who presents to the trauma center following a traumatic event that may be related to drugs or alcohol. The American College of Surgeons Committee on Trauma recommends that all patients presenting to a trauma center be screened for alcohol use and history that could have contributed to the traumatic event that brought them to the trauma center.1 The program of alcohol screening, brief interventions, and recommendations for rehabilitation (SBIRT) reduces recidivism and cost for trauma care.2 There are several alcohol use screening tools available, including the Alcohol Use Disorders Identification Test (AUDIT), and the CAGE tool, which is an acronym for Cut down, Annoyed, Guilty, Eye opener morning alcoholic drink. The AUDIT is outlined in Table 25-1.

TABLE 25-1

AUDIT ALCOHOL SCREENING QUESTIONNAIRE

QUESTION SCORE*
1. How often do you have a drink containing alcohol? Never

2. How many standard drinks containing alcohol do you have on a typical day when drinking?

3. How often do you have six or more drinks on one occasion?

4. During the past year, how often have you found that you were not able to stop drinking once you had started?

5. During the past year, how often have you failed to do what was normally expected of you because of drinking?

6. During the past year, how often have you needed a drink in the morning to get yourself going after a heavy drinking session?

7. During the past year, how often have you had a feeling of guilt or remorse after drinking?

8. During the past year, have you been unable to remember what happened the night before because you had been drinking?

9. Have you or someone else been injured as a result of your drinking?

10. Has a relative or friend, doctor or other health worker been concerned about your drinking or suggested you cut down?

Total Points  

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*Scores for each question range from 0 to 4, with the first response for each question (never) scoring 0, the second (less than monthly) scoring 1, the third (monthly) scoring 2, the fourth (weekly) scoring 3, and the fifth response (daily or almost daily) scoring 4. For the last two questions, which only have three responses, the scoring is 0, 2, and 4. A score of 8 or more is associated with harmful or hazardous drinking, and a score of 13 or more by women or 15 or more by men is likely to indicate alcohol dependence.

A patient who screens positive is recommended to undergo “brief interventions” for alcohol use. Brief interventions are by their very name short and are based upon motivational interviewing. Once a rapport is built with the patient, the following motivational-style interview questions may be used:3 1) What is a typical day like for you on a day when you drink? 2) How important is it to you to make a change in your drinking? 3) How confident are you that you can make a change? 4) What do you like and dislike about your drinking habits? 5) How would your life be different if you were to change your drinking? 6) What are some of the most important things to you? These questions serve to help the patient dichotomize the impact of drinking, both positively and negatively.

Major advances have been made in the management of patients with traumatic injuries. This chapter reviews selected critical care nursing management of patients with traumatic injuries.

Mechanisms of Injury

Trauma occurs when an external force of energy impacts the body and causes structural or physiological alterations, or injuries. External forces can be radiation, electrical, thermal, chemical, or mechanical forms of energy. This chapter focuses on trauma from mechanical energy. Mechanical energy can produce blunt or penetrating traumatic injuries. Understanding the mechanism of injury helps health care providers anticipate and predict potential internal injuries.

Blunt Trauma

Blunt trauma is seen most often with MVCs, contact sports, blunt force injuries (e.g., trauma caused by a baseball bat), or falls. Injuries occur because of the forces sustained during a rapid change in velocity (deceleration). To estimate the amount of force sustained in an MVC, multiply the person’s weight by the miles per hour (speed) the vehicle was traveling. A 130-pound woman in a vehicle traveling at 60 miles per hour that hits a brick wall, for example, would sustain 7800 pounds of force within milliseconds. As the body stops suddenly, tissues and organs continue to move forward. This sudden change in velocity causes injuries that result in lacerations or crush injuries of internal body structures.

Penetrating Trauma

Penetrating injuries occur with stabbings, firearms, or impalement—injuries that penetrate the skin and result in damage to internal structures. Damage is created along the path of penetration. Penetrating injuries can be misleading inasmuch as the condition of the outside of the wound does not determine the extent of internal injury. Bullets can create internal cavities 5 to 30 times larger than the diameter of the bullet.

Several factors determine the extent of damage sustained as a result of penetrating trauma. Different weapons cause different types of injuries. The severity of a gunshot wound depends on the type of gun, type of ammunition used, and the distance and angle from which the gun was fired. At close range, shotgun pellets expand on impact and cause multiple injuries to internal structures. From a distance, shotgun pellets cause only minor injuries. Handgun bullets usually damage what is directly in the bullet’s path. Inside the body, the bullet can ricochet off bone and create further damage along its pathway. With penetrating stab wounds, factors that determine the extent of injury include the type and length of object used and the angle of insertion.

Phases of Trauma Care

Care of trauma victims during wartime enhanced principles of triage and rapid transport of the injured to medical facilities. The military experience has demonstrated that decreasing the time from injury to definitive care saves more lives. It also has enhanced incentives and models for improvements in civilian trauma care, such as emergency medical service (EMS) systems and trauma care centers. The goal with critically injured patients is to minimize the time from initial insult to definitive care and to optimize prehospital care so that the patient arrives at the hospital alive.

Nursing management of the patient with traumatic injuries begins the moment a call for help is received and continues until the patient’s death or return to the community. Care of the trauma patient is seen as a continuum that includes six phases: prehospital resuscitation, hospital resuscitation, definitive care and operative phase, critical care, intermediate care, and rehabilitation.

Prehospital Resuscitation

The goal of prehospital care is immediate stabilization and transportation. This is achieved through airway maintenance, control of external bleeding and shock, immobilization of the patient, and immediate transport (ground or air) to the closest appropriate medical facility.4 Prehospital personnel should communicate information needed for triage at the hospital. Advanced planning for the injured patient is essential.

Emergency Department Resuscitation

The American College of Surgeons developed Advanced Trauma Life Support (ATLS) guidelines for rapid assessment, resuscitation, and definitive care for trauma patients in the emergency department.4 The ATLS guidelines delineate a systematic approach to care of the trauma patient: rapid primary survey, resuscitation of vital functions, more detailed secondary survey, and initiation of definitive care. This process constitutes the ABCDEs of trauma care and assists in identifying injuries.

Primary Survey

On arrival of the trauma patient in the emergency department, the primary survey is initiated. During this assessment, life-threatening injuries are discovered and treated. The five steps in the trauma primary survey are performed in ABCDE sequence (Table 25-2):

TABLE 25-2

PRIMARY SURVEY OF THE TRAUMA PATIENT

SURVEY COMPONENT NURSING DIAGNOSIS NURSING ASSESSMENT, CARE
Airway Ineffective Airway Clearance related to obstruction or actual injury Immobilize cervical spine.

Secure airway.

Breathing Ineffective Breathing
Pattern related to actual injury
Impaired Gas Exchange related to actual injury or disrupted tissue perfusion
Assess for:

For absent breathing:

If breathing, but ineffective:

Circulation Decreased Cardiac Output related to actual injury
Alteration in Tissue Perfusion related to actual injury or shock
Deficient Fluid Volume related to actual loss of circulating volume
Assess pulse quality and rate.
Use ECG monitoring.
If no pulse:

If pulse, but ineffective

Initiate two large-bore IVs or central catheter; obtain serum samples for laboratory tests.
Provide fluid replacement.

Disability Ineffective Cerebral Tissue Perfusion
Risk for Injury related to actual injury of brain or spinal cord
Determine Glasgow Coma Scale score.
Assess pupil size and reactivity.
Exposure or environmental control Risk for Imbalanced Body Temperature Remove all clothing to inspect all body regions.
Prevent hypothermia.

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ACLS, advanced cardiac life support; ECG, electrocardiogram; IV, intravenous line.

Resuscitation Phase

Concurrent with the primary survey is the resuscitation phase. Hypovolemic shock is the most common type of shock that occurs in trauma patients.4 Hemorrhage must be identified and treated rapidly. Two large-bore (14- to 16-gauge) peripheral intravenous catheters, a central venous catheter or intraosseous access is inserted. Management of hemorrhagic shock starts with IV fluids followed quickly by O-negative blood or type-specific blood.4 Many trauma centers have developed massive transfusion protocols to make sure adequate blood products are available as needed. Fluid warmers are used to prevent hypothermia. Blood samples are also drawn (Box 25-2).

Placement of urinary and gastric catheters is part of the resuscitation phase. An indwelling urinary catheter can help evaluate urine output as an indicator of volume status and kidney perfusion. A gastric tube is inserted to reduce gastric distention and lower the risk of aspiration.

The resuscitation phase begins in the emergency department and may continue well into the critical care phase. During resuscitation from traumatic hemorrhagic shock, normalization of standard clinical parameters such as blood pressure, heart rate, and urine output are important but do not represent the end-point.5 Optimal resuscitation goals are to improve oxygen tissue delivery and normalize base deficit, lactate, or gastric pH during the first 24 hours after injury.6

Secondary Survey

The secondary survey begins when the primary survey is completed, resuscitation is well established, and the patient is hemodynamically stable. During the secondary survey, a head-to-toe approach is used to thoroughly examine each body region. The history is one of the most important aspects of the secondary survey. Prehospital providers can usually provide vital information pertaining to the unintentional injury. Specific information that must be elicited about mechanism of injury is summarized in Box 25-3. The patient’s pertinent past history can be assessed by use of the mnemonic AMPLE:

During the secondary survey, the nurse ensures the completion of special procedures, such as an electrocardiogram (ECG), radiographic studies, and the FAST exam (Focused Assessment Sonography for Trauma). Throughout the secondary survey, the nurse continuously monitors the patient’s vital signs and response to medical therapies. Emotional support to the patient and family is imperative.

Definitive Care and Operative Phase

After the secondary survey has been completed, specific injuries are diagnosed. Trauma is often referred to as a “surgical disease” because the nature and extent of injuries may require operative management. After surgery, depending on the patient’s status, transfer to a critical care unit may be indicated.

Critical Care Phase

Critically ill trauma patients are admitted into the intensive care unit (ICU) as direct transfers from the emergency department or operating room. Information the ICU nurse must obtain from the emergency department, operating room nurse, or both, is summarized using the SBAR method: Situation, Background, Assessment, and Recommendation (Box 25-4). This information must be obtained before the patient’s admission to the ICU to ensure availability of needed personnel, equipment, and supplies. This information also helps the nurse to assess the impact of trauma resuscitation on the patient’s presentation and course. Table 25-3 summarizes the prehospital, emergency department, and operating room resuscitative measures that can affect the trauma patient’s care in the ICU.

TABLE 25-3

EFFECTS OF TRAUMA RESUSCITATION

ASPECT OF INJURY OR RESUSCITATION EFFECT ON ICU COURSE
Prolonged extrication time Gives an indication of length of time patient may have been hypotensive and/or hypothermic before medical care
Period of respiratory or cardiac arrest Effects of loss of perfusion to brain (anoxic injury), kidneys, and other vital organs
Time on backboard Potentiates risk of sacral or occipital breakdown
Number of units of blood; whether any were not fully cross-matched; packed cells versus whole blood used Potentiates risk of ARDS, MODS

ARDS, acute respiratory distress syndrome; ICU, intensive care unit; MODS, multiple organ dysfunction syndrome.

One of the most important nursing roles is assessment of the balance between oxygen delivery and oxygen demand. Oxygen delivery must be optimized to prevent further system damage. Assessment of circulatory status includes the use of noninvasive and invasive techniques. The trauma patient is at high risk for impaired oxygenation as a result of a variety of factors (Table 25-4). These risk factors must be promptly identified and treated to prevent life-threatening sequelae. Prevention and treatment of hypoxemia depend on accurate assessment of the adequacy of pulmonary gas exchange, oxygen delivery, and oxygen consumption.

TABLE 25-4

FACTORS PREDISPOSING THE TRAUMA PATIENT TO IMPAIRED OXYGENATION

FACTOR IMPAIRMENT
Impaired ventilation Injury to airway structures, loss of central nervous system regulation of breathing, impaired level of consciousness
Impaired pulmonary gas diffusion Pneumothorax, hemothorax, aspiration of gastric contents
Shifts to the left of the oxyhemoglobin dissociation curve (can result from infusion of large volumes of banked blood, hypocarbia or alkalosis, or hypothermia)
Decreased oxygen supply Reduced hemoglobin (from hemorrhage)
Reduced cardiac output (cardiovascular injury, decreased preload)
Increased oxygen supply Increased metabolic demands (associated with the stress response to injury)

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Frequent and thorough nursing assessments of all body systems are important because these assessments are the cornerstone of the medical and nursing management of the critically ill trauma patient. The nurse can detect subtle changes and facilitate the implementation of timely therapeutic interventions to prevent complications often associated with trauma. The nurse must be knowledgeable about specific organ injuries and their associated sequelae.

Trauma Injuries

Traumatic Brain Injuries

More than 1.7 million traumatic brain injuries (TBIs) occur annually, with approximately 275,000 patients hospitalized as a result of their injuries. Approximately 52,000 Americans die each year of TBI.7 At least 5.3 million Americans are living with disabilities resulting from TBI.8

Mechanism of Injury

TBIs occur when mechanical forces are transmitted to brain tissue. Mechanisms of injury include penetrating or blunt trauma to the head. The leading causes of TBI include falls (35.2%), MVCs (17.3%), struck by or against events (16.5%), and assaults (10%).7 Penetrating trauma can result from the penetration of a foreign object such as a bullet, which causes direct damage to cerebral tissue. Blunt trauma can be the result of deceleration, acceleration, or rotational forces. Deceleration causes the brain to crash against the skull after it has hit something such as the dashboard of a car. Acceleration injuries occur when the brain has been forcefully hit, such as with a baseball bat. Brian injury occurs when the brain moves toward the point of impact (acceleration) and then as the brain reverses direction (deceleration) it hits the other side of the skull. These injuries are described as coup and contrecoup; this injury is shown in Figure 25-1.

Pathophysiology

Review of the pathophysiology of a TBI can be divided into two categories: primary injury and secondary injury. The critical care nurse uses knowledge of this pathophysiology to provide interventions that reduce morbidity and mortality from secondary injury.

Primary Injury.

The primary injury occurs at the moment of impact as a result of mechanical forces to the head. The extent of and recovery from injury are related to whether the primary injury was localized to an area or whether it was diffuse or widespread throughout the brain. Primary injuries may include direct damage to the parenchyma or injury to the vessels that causes hemorrhage, compressing nearby structures. Examples of primary injuries include contusion, laceration, shearing injuries, and hemorrhage. Primary injury may be mild, with little or no neurological damage, or severe, with major tissue damage. Immediately after the injury, a cascade of neural and vascular processes is activated.

Secondary Injury.

Secondary injury is the biochemical and cellular response to the initial trauma that can exacerbate the primary injury and cause loss of brain tissue not originally damaged. Secondary injury can be caused by ischemia, hypercapnia, hypotension, cerebral edema, sustained hypertension, calcium toxicity, or metabolic derangements. Hypoxia or hypotension, the best known culprits for secondary injury, typically are the result of extracranial trauma.9 A detrimental cycle may develop causing a focal primary injury to expand as a result of uncontrolled, refractory secondary injury.

Tissue ischemia occurs in areas of poor cerebral perfusion as a result of hypotension or hypoxia. The cells in ischemic areas become edematous. Extreme vasodilation of the cerebral vasculature occurs in an attempt to supply oxygen to the cerebral tissue. This increase in blood volume increases intracranial volume and raises intracranial pressure (ICP).

Significant hypotension causes inadequate perfusion to neural tissue. Hypotension rarely is associated with TBI. Hypotension typically is not caused by brain injury unless terminal medullary failure occurs.10 If a trauma patient is unconscious and hypotensive, a detailed assessment of the chest, abdomen, and pelvis is performed to rule out internal injuries.

Hypercapnia (elevated CO2) is a powerful vasodilator. Most often caused by hypoventilation in an unconscious patient, hypercapnia results in cerebral vasodilation and increased cerebral blood volume and ICP.

Cerebral edema occurs as a result of the changes in the cellular environment caused by contusion, loss of autoregulation, and increased permeability of the blood-brain barrier. Cerebral edema can be focal as it localizes around the area of contusion, or diffuse as a result of hypotension or hypoxia. Optimizing other aspects of secondary injury, such as oxygenation, ventilation, and perfusion can limit the extent of cerebral edema.

Initial hypertension in the patient with severe TBI is common. Because of the loss of autoregulation, increased blood pressure results in increased intracranial blood volume and ICP. The effects of increased ICP may be varied. As pressure increases inside the closed skull vault, cerebral perfusion decreases, which further compromises the brain. The combined effects of increasing pressure and decreasing perfusion precipitate a downward spiral of events.

Classification

Injuries of the brain are described by the functional changes or losses that occur. Some of the major functional abnormalities seen in head injury are described here.

Skull Fracture.

Skull fractures are common, but they do not by themselves cause neurological deficits. Skull fractures can be classified as open (dura is torn) or closed (dura is not torn), or they can be classified as those of the vault or those of the base. Common vault fractures occur in the parietal and temporal regions. Basilar skull fractures usually are not visible on conventional skull films and a computed tomography (CT) scan is typically required. Assessment findings may include cerebral spinal fluid rhinorrhea (from nose) or otorrhea (from ear), Battle’s sign (ecchymosis overlying the mastoid process behind the ear), “raccoon eyes” (subconjunctival and periorbital ecchymosis), or palsy of the seventh cranial nerve.

The significance of a skull fracture is that it identifies the patient with a higher probability of having or developing an intracranial hematoma. Open skull fractures require surgical intervention to remove bony fragments and to close the dura. The major complications of basilar skull fractures are cranial nerve injury and leakage of cerebrospinal fluid (CSF). CSF leakage may result in a fistula, which increases the possibility of bacterial contamination and resultant meningitis. Because fistula formation may be delayed, patients with a basilar skull fracture are admitted to the hospital for observation and possible surgical intervention.

Concussion.

A concussion is a brain injury accompanied by a brief loss of neurological function, especially loss of consciousness. When loss of consciousness occurs, it may last for seconds to an hour. The neurological dysfunctions include confusion, disorientation, and sometimes a period of antegrade or retrograde amnesia. Other clinical manifestations that occur after concussion are headache, dizziness, nausea, irritability, inability to concentrate, impaired memory, and fatigue. The diagnosis of concussion is based on the loss of consciousness inasmuch as the brain remains structurally intact despite functional impairment.

Contusion.

Contusion, or bruising of the brain, usually is related to acceleration-deceleration injuries, which result in hemorrhage into the superficial parenchyma, often the frontal and temporal lobes. Frontal or temporal contusions are most common and can be seen in a coup-contrecoup mechanism of injury (see Figure 25-1). Coup injury affects the cerebral tissue directly under the point of impact. Contrecoup injury occurs in a line directly opposite the point of impact.

The clinical manifestations of contusion are related to the location of the contusion, the degree of contusion, and the presence of associated lesions. Contusions can be small, in which localized areas of dysfunction result in a focal neurological deficit. Larger contusions can evolve over 2 to 3 days after injury as a result of edema and further hemorrhaging. A large contusion can produce a mass effect that can cause a significant increase in ICP.

Contusions of the tips of the temporal lobe are a common occurrence and are of particular concern. Because the inner aspects of the temporal lobe surround the opening in the tentorium where the midbrain enters the cerebrum, edema in this area can cause rapid deterioration of the patient’s condition and can lead to herniation. Because of the location, this deterioration can occur with little or no warning at a deceptively low ICP.

Medical management of cerebral contusions may consist of medical or surgical therapies. Because a contusion can progress over 3 to 5 days after injury, secondary injury may occur. If contusions are small, focal, or multiple, they are treated medically with serial neurological assessments and possibly with ICP monitoring. Larger contusions that produce considerable mass effect require surgical intervention to prevent the increased edema and ICP as the contusion matures. Outcome of cerebral contusion varies, depending on the location and the degree of contusion.

Cerebral Hematomas.

Extravasation of blood creates a space-occupying lesion within the cranial vault that can lead to increased ICP. Three types of hematomas are discussed here (Figure 25-2). The first two, epidural and subdural hematomas, are extraparenchymal (outside of brain tissue) and produce injury by pressure effect and displacement of intracranial contents. The third type, intracerebral hematoma, directly damages neural tissue and can produce further injury as a result of pressure and displacement of intracranial contents.

Epidural Hematoma.

Epidural hematoma (EDH) is a collection of blood between the inner table of the skull and the outermost layer of the dura. EDHs are most often associated with patients with skull fractures and middle meningeal artery lacerations (two thirds of patients) or skull fractures with venous bleeding.4 A blow to the head that causes a linear skull fracture on the lateral surface of the head may tear the middle meningeal artery. As the artery bleeds, it pulls the dura away from the skull, creating a pouch that expands into the intracranial space.

The incidence of EDH is relatively low. EDH can occur as a result of low-impact injuries (e.g., falls) or high-impact injuries (e.g., MVCs). EDH occurs from trauma to the skull and meninges rather than from the acceleration-deceleration forces seen in other types of head trauma.

The classic clinical manifestations of EDH include brief loss of consciousness followed by a period of lucidity. Rapid deterioration in the level of consciousness should be anticipated because arterial bleeding into the epidural space can occur quickly. A dilated and fixed pupil on the same side as the impact area is a hallmark of EDH.4 The patient may complain of a severe, localized headache and may be sleepy. Diagnosis of EDH is based on clinical symptoms and evidence of a collection of epidural blood identified on the CT scan. Treatment of EDH involves surgical intervention to remove the blood and to cauterize the bleeding vessels.

Subdural Hematoma.

Subdural hematoma (SDH), which is the accumulation of blood between the dura and the underlying arachnoid membrane, most often is related to a rupture in the bridging veins between the cerebral cortex and the dura. Acceleration-deceleration and rotational forces are the major causes of SDH, which often is associated with cerebral contusions and intracerebral hemorrhage. SDH is common, representing about 30% of severe head injuries. The three types of SDH—acute, subacute, and chronic—are based on the time frame from injury to clinical symptoms.

Acute Subdural Hematoma.

Acute SDHs are hematomas that occur after a severe blow to the head. The clinical presentation of acute SDH is determined by the severity of injury to the underlying brain at the time of impact and the rate of blood accumulation in the subdural space. In other situations, the patient has a lucid period before deterioration. Careful observation for deterioration of the level of consciousness or lateralizing signs, such as inequality of pupils or motor movements, is essential. Rapid surgical intervention—including craniectomy, craniotomy, or burr hole evacuation—and aggressive intervention can reduce mortality.

Subacute Subdural Hematoma.

Subacute SDHs are hematomas that develop symptomatically 2 days to 2 weeks after trauma. In subacute SDHs, the expansion of the hematoma occurs at a rate slower than that in acute SDH, and it takes longer for symptoms to become obvious. Clinical deterioration of the patient with a subacute SDH is slower than with an acute SDH, but treatment by surgical intervention, when appropriate, is identical.

Chronic Subdural Hematoma.

Chronic SDH is diagnosed when symptoms appear days or months after injury. Most patients with chronic SDH are older or in late middle age. Patients at risk for chronic SDH include those with coordination or balance disturbances, older adults, and those receiving anticoagulation therapy. Clinical manifestations of chronic SDH are insidious. The patient may report a variety of symptoms, such as lethargy, absent-mindedness, headache, vomiting, stiff neck, and photophobia and may show signs of transient ischemic attack, seizures, pupillary changes, or hemiparesis. Because a history of trauma often is not significant enough to be recalled, chronic SDH seldom is seen as an initial diagnosis. CT evaluation can confirm the diagnosis of chronic SDH.

If surgical intervention is required, evacuation of the chronic SDH may occur by craniotomy, burr holes, or catheter drainage. Evacuation by burr hole involves drilling a hole in the skull over the site of the chronic SDH and draining the fluid. Drains or catheters are left in place for at least 24 hours to facilitate total drainage. Outcome after chronic SDH evacuation varies. Return of neurological status often depends on the degree of neurological dysfunction before removal. Because this condition is most common in older or debilitated patients, recovery is a slow process. Recurrence of chronic SDH is not infrequent.

Intracerebral Hematoma.

Intracerebral hematoma (ICH) results when bleeding occurs within cerebral tissue. Traumatic causes of ICH include depressed skull fractures, penetrating injuries (bullet, knife), or sudden acceleration-deceleration motion. The ICH can act as a rapidly expanding lesion; late ICH into the necrotic center of a contused area also is possible. Sudden clinical deterioration of a patient 6 to 10 days after trauma may be the result of ICH.

Medical management of ICH may include surgical or nonsurgical treatment. Hemorrhages that do not cause significant ICP elevation are treated without surgery. Over time, the hemorrhage may be reabsorbed. If significant problems with ICH mass effect occur, surgical removal is necessary. The outcome of a patient with an ICH depends greatly on the location of the hemorrhage. Size, mass effect, and displacement of other intracranial structures also affect the outcome.

Missile Injuries.

Missile injuries penetrate the skull and produce significant focal damage, but little acceleration-deceleration or rotational injury. The injury may be depressed, penetrating, or perforating (Figure 25-3). Depressed injuries are caused by fractures of the skull, with penetration of bone into cerebral tissue. A low-velocity penetrating injury (knife) may involve only focal damage and no loss of consciousness. A high-velocity missile (bullet) can produce shock waves that are transmitted throughout the brain in addition to the injury caused by the bullet. Perforating injuries are missile injuries that enter and then exit the brain. Perforating injuries have much less ricochet effect but are still responsible for significant injury.

Risk of infection and cerebral abscess is a concern in cases of missile injuries. If fragments of the missile are embedded within the brain, careful consideration of the location and risk of increasing neurological deficit is weighed against the risk of abscess or infection. The outcome after missile injury is based on the degree of penetration, the location of the injury, and the velocity of the missile.

Diffuse Axonal Injury.

Diffuse axonal injury (DAI) is a term used to describe prolonged posttraumatic coma that is typically not caused by a mass lesion. DAI covers a wide range of brain dysfunction typically caused by acceleration-deceleration and rotational forces. DAI occurs as a result of damage to the axons or disruption of axonal transmission of the neural impulses.

The pathophysiology of DAI is related to the stretching and tearing of axons as a result of movement of the brain inside the cranium at the time of impact. The stretching and tearing of axons result in microscopic lesions throughout the brain, but especially deep within cerebral tissue and the base of the cerebrum. Disruption of axonal transmission of impulses results in loss of consciousness. Unless surrounding tissue areas are significantly injured, causing small hemorrhages, DAI may not be visible on CT or magnetic resonance imaging (MRI). DAI can be classified as one of three grades based on the extent of lesions: mild, moderate, or severe. The patient with mild DAI may be in a coma for 24 hours and may exhibit periods of decorticate and decerebrate posturing. Patients with moderate DAI may be in a coma for longer than 24 hours and exhibit periods of decorticate and decerebrate posturing. Severe DAI usually manifests as a prolonged, deep coma with periods of hypertension, hyperthermia, and excessive sweating. Treatment of DAI includes support of vital functions and maintenance of ICP within normal limits. The outcome after severe DAI is poor because of the extensive dysfunction of cerebral pathways.

Neurological Assessment of Traumatic Brain Injury

The neurological assessment is the most important tool for evaluating the patient with a severe TBI, because it can indicate the severity of injury, provide prognostic information, and dictate the speed with which further evaluation and treatment must proceed. The cornerstone of the neurological assessment is the Glasgow Coma Scale (GCS),4 although it is not a complete neurological examination. Pupils and motor strength assessment must be incorporated into the early and ongoing assessments. After injuries are specifically identified, a more thorough, focused neurological assessment, such as examination of the cranial nerves, is warranted. To assist with the initial assessment, TBIs are divided into three descriptive categories—mild, moderate, or severe—on the basis of the patient’s GCS score and duration of the unconscious state.

Degree of Injury

Mild Injury.

Mild TBI is described as a GCS score of 13 to 15, with a loss of consciousness that lasts up to 15 minutes. Patients with mild injury often are seen in the emergency department and discharged home with a family member who is instructed to evaluate the patient routinely and to bring the patient back to the hospital if any further neurological symptoms appear.

Moderate Injury.

Moderate TBI is described as a GCS score of 9 to 12, with a loss of consciousness for up to 6 hours. Patients with this type of TBI usually are hospitalized. They are at high risk for deterioration from increasing cerebral edema and ICP, and serial clinical assessments are an important function of the nurse. Hemodynamic and ICP monitoring and ventilatory support may not be required for these patients unless other systemic injuries make them necessary. A CT scan usually is obtained on admission. Repeat CT scans are indicated if the patient’s neurological status deteriorates.

Severe Injury.

Patients with a GCS score of 8 or less after resuscitation or those who deteriorate to that level within 48 hours of admission have a severe TBI. Patients with severe TBI often receive ventilatory support along with ICP and hemodynamic monitoring. A CT scan is performed to rule out mass lesions that can be surgically removed. Patients are placed in a critical care setting for continual assessment, monitoring, and management.

Nursing Assessment of the Patient with Traumatic Brain Injury

As in all traumatic injuries, evaluation of the airway, breathing, and circulation (ABCs) is the first step in the assessment of the patient with TBI in the ICU. After stabilization of the ABCs is ensured, a neurological assessment is performed.

Level of consciousness, motor movements, pupillary response, respiratory function, and vital signs are all part of a complete neurological assessment in the patient with a TBI. Level of consciousness to assess wakefulness is elicited by obtaining the patient’s response to verbal and painful stimuli. Determination of orientation to person, place, and time assesses mental alertness. Pupils are assessed for size, shape, equality, and reactivity. Pupil asymmetry must be reported immediately. Pupils are also assessed for constriction to a light source (parasympathetic innervation) or dilation (sympathetic innervation). A dilated or “blown” pupil can be caused by compression of the third ocular nerve or by transtentorial herniation.

Neurological assessments are ongoing as part of the initial shift assessment and as part of ongoing assessments to detect subtle deterioration. Serial assessments include hemodynamic status and ICP monitoring. The use of muscle relaxants and sedation for ICP control can mask neurological signs in the patient with a severe head injury. In these situations, observations for changes in pupils and vital signs become extremely important. Sedatives with a very short half-life, such as propofol, can be turned off, and within minutes, a neurological examination can be performed.

Diagnostic Procedures

The cornerstone of diagnostic procedures for evaluation of TBI is the CT scan. CT is a rapid, noninvasive procedure that can provide invaluable information about the presence of mass lesions and cerebral edema. Serial CT scans may be used over a period of several days to assess areas of contusion and ischemia and to detect delayed hematomas. A nurse must always remain with a TBI patient during a CT scan to provide continued observation and monitoring and during transport to and from the scanner. Transporting the patient, moving the patient from the bed to the CT table, and positioning the head flat during the CT scan are all stressful events and can cause severe increases in ICP. Continuous monitoring enables rapid intervention.

Medical Management

Surgical Management.

If a lesion identified on CT is causing a shift of intracranial contents or increasing ICP, surgical intervention is necessary. Space-occupying hematomas such as EDH or SDH are removed via craniotomy. To alleviate excessive intracranial pressure and prevent herniation, a part of the skull may be removed (decompressive craniectomy). Patients who have had penetrating head trauma have an increased incidence of posttraumatic seizures, and may receive anticonvulsants.

Nonsurgical Management.

Most of the TBI management occurs in the ICU. Nonsurgical management includes management of ICP, maintenance of adequate cerebral perfusion pressure and oxygenation, and treatment of any complications (e.g., pneumonia, infection). ICP monitoring may be required for patients with a GCS score less than 8 and abnormal findings on a head CT scan.9

Nursing Management

Nursing priorities in management of traumatic brain injury focus on (1) stabilizing vital signs, (2) preventing further injury, and (3) reducing increased ICP and maintaining adequate CPP.

Nursing diagnoses for the patient with TBI are listed in the Nursing Diagnosis Priorities Box on Traumatic Brain Injury. Ongoing nursing assessments are the cornerstone of the care of patients with TBI. These assessments are the primary mechanism for determining secondary brain injury from cerebral edema and increased ICP.

Hemodynamic and fluid management are vital. Arterial blood pressure should be monitored because hypotension in a patient with TBI is rare and may indicate additional injuries. Cerebral perfusion pressure (CPP) should be maintained at a minimum of 60 mm Hg.9

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