Kara A. Snyder

Trauma is the 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, but the problem continues to go largely unrecognized.

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. Unintentional injury is no accident. Accident traditionally has implied an act of God or an unpredictable event. Domestic violence and alcohol-related issues are priority prevention areas with which health care providers must be actively involved.

Intimate partner violence (IPV) constitutes a major public health issue in the United States. IPV is the leading cause of injury to women, in the United States it is estimated that 4.8 million women and 2.9 million men every year are raped or physically assaulted each year.1 Up to one third of injuries from IPV result in medical attention being sought and 21% of those who present with acute injuries require emergency surgery.2

The Joint Commission has a standard of practice that all patients must be screened for IPV as part of the health history.3 Studies have shown that screening for IPV in healthcare settings is effective in identifying women who are victims and that patients are not offended when asked about current or past IPV.4 Key interventions for the victim of IPV are listed in Box 34-1.

In 2010, 10,228 people were killed in alcohol-impaired driving crashes, which account for 31% of the total motor vehicle traffic fatalities in the United States.5 Each year, alcohol-related crashes in the United States cost about $51 billion.6 Alcohol screening and intervention have been recommended as routine components of trauma care.7 The Alcohol Use Disorders Identification Test (AUDIT) (Table 34-1) is a screening questionnaire that can be used because it can be used to identify frequency of alcoholic drinking and problem drinking.8

TABLE 34-1


How often do you have a drink containing alcohol?
How many standard drinks containing alcohol do you have on a typical day when drinking?
How often do you have six or more drinks on one occasion?  
During the past year, how often have you found that you were not able to stop drinking once you had started? Never
During the past year, how often have you failed to do what was normally expected of you because of drinking?
During the past year, how often have you needed a drink in the morning to get yourself going after a heavy drinking session?
During the past year, how often have you had a feeling of guilt or remorse after drinking?  
During the past year, have you been unable to remember what happened the night before because you had been drinking?  
Have you or someone else been injured as a result of your drinking? No
Has a relative or friend, doctor or other health worker been concerned about your drinking or suggested you cut down? Yes, but not in the past year
Yes, during the past year


AUDIT, Alcohol Use Disorders Identification Test.

*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.

Over the past few decades, major advances have been made in the management of patients with traumatic injuries in the prehospital, emergency department, and critical care settings. Patients with complex, multisystem trauma are admitted to critical care units, and these patients require complex nursing care. This chapter reviews nursing management of patients with traumatic injuries in the critical care setting.

Mechanisms of Injury

Trauma occurs when an external force of energy impacts the body and causes structural or physiologic 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.

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.9

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. Pellets from a shotgun blast expand on impact and cause multiple injuries to internal structures. 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 more lives can be saved by decreasing the time from injury to definitive care. 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.

Statistics demonstrate that deaths as a result of trauma occur in a trimodal distribution (Fig. 34-1).9 The first peak includes victims who die before medical attention can be provided. The second peak occurs within a few hours after injury. This peak commonly is referred to as the golden hour for those critically injured. The golden hour is a 60-minute time frame that incorporates activation of the EMS system, stabilization in the prehospital setting, transportation to a medical facility, rapid resuscitation on arrival in the emergency department, and provision of definitive care. For the critically injured patient, the primary goal is to minimize the time from injury to definitive care. The third death peak occurs days to weeks after injury as a result of complications, including infection or multiple organ dysfunction syndrome (MODS). It is a nursing challenge to influence the quality of care the trauma patient receives in an attempt to “beat” the trimodal distribution of trauma deaths.

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.

Emergency Department Resuscitation

The American College of Surgeons developed guidelines (advanced trauma life support [ATLS]) for rapid assessment, resuscitation, and definitive care for trauma patients in the emergency department.9 These 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 34-2):


The patient’s airway is assessed for ineffective airway clearance and airway obstruction. The trauma patient is at risk for ineffective airway clearance, especially in the presence of altered consciousness, drugs and alcohol, and maxillofacial or thoracic injuries. Airway obstruction can be caused by foreign bodies, blood clots, or broken teeth. Airway patency should be assessed by inspecting the oropharynx for foreign body obstruction, listening for air movement at the nose and mouth, and auscultation of lung fields. Airway assessment must incorporate cervical spine immobilization. The patient’s head should not be rotated, hyperflexed, or hyperextended to establish and maintain an airway. The cervical spine must be immobilized in all trauma patients until a cervical spinal cord injury has been definitively ruled out. If the patient can verbally communicate, it is likely that the airway is patent. Patients who display nonpurposeful motor movements or who have a Glasgow Coma Scale (GCS) score of 8 or less usually require the placement of a definitive airway.9


The next step is to assess for decreased cardiac output, impaired tissue perfusion, and deficient fluid volume. External exsanguination is identified and controlled by direct manual pressure on the wound. Rapid assessment of the circulatory status includes assessment of level of consciousness, skin color, and pulse.9 Level of consciousness provides data on cerebral perfusion. Ashen, gray facial skin color or white, pale extremities may be ominous signs of hypovolemia.9 Central pulses (femoral or carotid artery) are assessed bilaterally for rate, regularity, and quality. If a pulse is not present, advanced cardiac life support (ACLS) protocols are instituted. ECG monitoring is initiated to assess for rhythm disturbances. Life-threatening dysrhythmias are treated according to ACLS protocols.

Resuscitation Phase

After the primary survey the resuscitation phase begins. Hypovolemic shock is the most common type of shock that occurs in trauma patients.9 Hemorrhage must be identified and treated rapidly. Two large-bore (14- to 16-gauge) peripheral intravenous catheters, intraosseous catheter, or central venous catheter is inserted. During the initiation of intravenous lines, blood samples are drawn (Box 34-2).

Resuscitation is aimed at ensuring adequate perfusion of tissues with oxygen and nutrients to support cellular function. Resuscitation end points (variables or parameters) must be viewed across the continuum of resuscitation from shock. During resuscitation from traumatic hemorrhagic shock, normalization of standard clinical parameters such as blood pressure, heart rate, and urine output are not adequate. The optimal resuscitation end point is a major focus of research in trauma care. During resuscitation, attempts should be made to improve cellular oxygenation. Base deficit and lactate and other assessment parameters have been well-studied to determine adequacy of cellular oxygenation during trauma resuscitation.10

Damage Control Resuscitation.

Resuscitation practices have been a focus for research in trauma care. Damage control resuscitation (DCR) is an emerging concept in trauma care. DCR is a strategy to provide only interventions to control hemorrhage and contamination. The strategy involves permissive hypotension, the use of blood products over isotonic fluid for volume replacement, and the rapid and early correction of coagulopathy with component therapy and begins in the field and continues through the emergency departments, operating rooms, and critical care units.11

Massive Transfusion Protocols.

Given the emphasis on use of blood products over crystalloids and correction of traumatic coagulopathy, many trauma centers have developed massive transfusion protocols for the 1% to 3% of all trauma patients who require DCR.12 Having a defined protocol serves as a system-based strategy to facilitate early, timely release of blood products in what can be an often-chaotic situation. The massive transfusion protocol outlines the ratio of packed red blood cells, fresh frozen plasma, platelets, and cryoprecipitate to be administered.12 The optimal ratio for these blood components has not yet been determined and is a focus for research.

Additional interventions during the resuscitation phase involve placement of urinary and gastric catheters. A gastric tube is inserted to reduce gastric distention and lower the risk of aspiration.9

Secondary Survey

The secondary survey begins when the primary survey is completed, resuscitation is well established, and the patient is demonstrating normalization of vital signs. 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. Often, head injury, shock, or the use of drugs or alcohol may preclude a good history, so the history must be pieced together from other sources. The prehospital providers (paramedics, emergency medical technicians) usually can provide most of the vital information pertaining to the unintentional injury. Specific information that must be elicited pertaining to the mechanism of injury is summarized in Box 34-3. This information can help predict internal injuries and facilitate rapid intervention. 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 ECG, radiographic studies (chest, cervical spine, thorax, and pelvis), ultrasonography, and, when required, diagnostic peritoneal lavage. Throughout this survey the nurse continuously monitors the patient’s vital signs and response to medical therapies. Emotional support to the patient and family also is imperative.

Critical Care Phase

Critically ill trauma patients are admitted into the critical care unit as direct transfers from the emergency department or operating room. Information the nurse must obtain from the emergency department or operating room nurse, or both, is summarized using the SBAR method: Situation, Background, Assessment, and Recommendations (Box 34-4). This information must be obtained before the patient’s admission to the critical care unit 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 34-3 summarizes the prehospital, emergency department, and operating room resuscitative measures that can affect the trauma patient’s care.

After the patient’s arrival in the critical care unit, the nurse uses the primary and secondary surveys and resuscitative measures in accordance with ATLS guidelines to assess the trauma patient’s status. Priority nursing care during the critical care phase includes ongoing physical assessments and monitoring the patient’s response to medical therapies. The nurse constantly is aware that the third peak of the trimodal distribution of trauma deaths occurs in the critical care setting as a result of complications, including acute respiratory distress syndrome (ARDS), sepsis, prolonged shock states, and MODS. Ongoing nursing assessments are imperative for early detection and treatment of complications.

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. The trauma patient is at high risk for impaired oxygenation as a result of a variety of factors (Table 34-4). 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.

Frequent and thorough nursing assessments of all body systems are the cornerstone of 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.

Specific Trauma Injuries

Traumatic Brain Injuries

More than 1.7 million traumatic brain injuries (TBIs) occur annually; approximately 52,000 Americans die each year of TBI with 275,000 hospitalized as a result of their injury.13 Children aged 0 to 4 years, older adolescents aged 15 to 19 years, and adults aged 65 years and older are most likely to sustain a TBI.13

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%), MVCs (17%), struck by or against objects (17%), and assaults (10%).14 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 injury causes the brain to crash against the skull after it has hit a hard surface such as the dashboard of a car. Acceleration injury occurs when the brain has been forcefully hit, such as with a baseball bat. In many instances, TBIs can be caused by acceleration and deceleration. Acceleration injuries occur when the skull is hit by a force that causes the brain to move forward to the point of impact, and then as the brain reverses direction and hits the other side of the skull, deceleration injuries occur.


Review of the pathophysiology of a TBI can be divided into two categories: primary injury and secondary injury. The critical care nurse must understand this pathophysiology, because goals of care focus on reducing morbidity and mortality from primary and secondary injuries.

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.15 A self-perpetuating cycle develops that may cause the expansion of a relatively focal primary injury as a result of uncontrolled refractory secondary injury.9,15

Brain Edema.

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. The extent of cerebral edema can be minimized by controlling the other aspects of secondary injury, such as oxygenation, ventilation, and perfusion.

Initial hypertension in the patient with severe TBI is common. As a result of the loss of autoregulation, increased blood pressure results in increased intracranial blood volume and elevates ICP. Every effort must be made to control hypertension to prevent the secondary injury caused by increased ICP (see “Intracranial Pressure Monitoring” in Chapter 24 and “Intracranial Hypertension” in Chapter 25). The effects of increased ICP are 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 of Brain Injuries

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 neurologic 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) is typically required. Assessment findings may include cerebrospinal fluid (CSF) loss—described as rhinorrhea (from nose) or otorrhea (from ear), Battle 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 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.


A concussion is a brain injury accompanied by a brief loss of neurologic function, especially loss of consciousness.14 When loss of consciousness occurs, it may last for seconds to an hour. The neurologic 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, or “bruising” of the brain, usually is related to acceleration–deceleration injuries, which result in hemorrhage into the superficial parenchyma. Frontal or temporal lobe contusions are most common and can be seen in a coupcontrecoup mechanism of injury (Fig. 34-2). 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 neurologic 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 are almost always associated with subdural hematoma (SDH).9

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 in level of consciousness and can lead to herniation. Because of the location, this deterioration can occur with little or no warning at a deceptively low ICP.

Diagnosis of contusion is made by CT. If the CT scan indicates contusion, especially in the temporal area, the nurse must pay specific attention to neurologic assessments and look for subtle changes in pupillary signs or vital signs, irrespective of a stable 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 neurologic assessments and possibly with ICP monitoring. Larger contusions that produce considerable mass effect require surgical intervention to prevent the increased edema and elevations in ICP as the contusion matures. Outcome of cerebral contusion varies, depending on the location and the size of the contused area.

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 (Fig. 34-3). The first two, epidural and SDH, 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 skull and the outermost layer of the dura (Fig. 34-3A). 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.9 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.9 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 requires 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 underlying arachnoid membrane, most often is related to a rupture in the bridging veins between the cerebral cortex and the dura (Fig. 34-3B). 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 timeframe from injury to clinical symptoms.

Chronic Subdural Hematoma.

Chronic SDH is diagnosed when symptoms appear days or months after injury. Most patients with chronic SDH usually are in late middle age or older adults. Individuals at risk for chronic SDH include those with coordination or balance disturbances, 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 neurologic status often depends on the degree of neurologic dysfunction before removal. Because this condition is most common in the older or debilitated patient, 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; however, late ICH into the necrotic center of a contused area also is possible (Fig. 34-3C). 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 management. It is thought that hemorrhages that do not cause significant ICP problems should be treated without surgery. Over time, the hemorrhage may be reabsorbed. If significant problems with ICP occur as a result of the ICH producing a mass effect, 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 are caused by objects that penetrate the skull to produce a significant focal damage but little acceleration–deceleration or rotational injury. The injury may be depressed, penetrating, or perforating (Fig. 34-4). Depressed injuries are caused by fractures of the skull, with penetration of bone into cerebral tissue. Penetrating injury is caused by a missile that enters the cranial cavity but does not exit. 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 neurologic 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 post-traumatic coma that is not caused by a mass lesion, although DAI with mass lesions has been reported. 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.

Neurologic Assessment of Traumatic Brain Injury

The neurologic 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.16 The cornerstone of the neurologic assessment is the GCS, although it is not a complete neurologic examination. Pupils and motor strength assessment must be incorporated into the early and ongoing assessments. After injuries are specifically identified, a more thorough, focused neurologic 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

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 critical care unit. Patients with moderate primary injury may deteriorate as a result of diffuse swelling or bleeding. A patient with severe TBI who is breathing spontaneously may require prophylactic endotracheal or nasotracheal intubation with mechanical ventilatory support to reduce the risk of hypoxia and hypercapnia. After stabilization of the ABCs is assured, a neurologic assessment is performed.

Level of consciousness, motor movements, pupillary response, respiratory function, and vital signs are all part of a complete neurologic assessment of the patient with a TBI. Level of consciousness can be elicited to assess wakefulness. Consciousness is assessed 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. Asymmetry must be reported immediately. Pupils are also assessed for constriction to a light source (parasympathetic innervation) or dilation (sympathetic innervation). Because parasympathetic fibers are present in the brainstem, pupils that are slow to react to light may indicate a brainstem injury. A “blown” pupil can be caused by compression of the third cranial nerve or transtentorial herniation. Bilateral fixed pupils can indicate midbrain involvement (see “Pupillary Function” in Chapter 23).

Neurologic assessments are ongoing throughout the patient’s critical care stay as part of the initial shift assessment and as part of ongoing assessments to detect subtle deterioration. Serial assessments include monitoring hemodynamic status and ICP. The use of muscle relaxants and sedation for ICP control may mask neurologic signs in the patient with a severe head injury. In these situations, observations for changes in pupils and vital signs become extremely important. Newer shorter-acting sedatives with a very short half-life, such as propofol, can be turned off, and within minutes, a neurologic 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 of ICP enables rapid intervention during these particularly vulnerable times.

Oct 29, 2016 | Posted by in NURSING | Comments Off on Trauma
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