Neurotrauma: Traumatic Brain Injury
Cynthia Blank-Reid, Ellen Barker

• TBI;
• primary versus secondary injury;
• mechanisms of injury;
• pathophysiology;
• diagnosis;
• types of brain injury;
• medical, surgical, and clinical management;
• nutrition, geriatric, and psychosocial considerations; and
• case management.

INCIDENCE

TBI occurs three times more often in males than in females. The average age of a TBI patient is between 15 and 30 years.¹³ TBI crosses all lines of race, religion and socioeconomic status, but the majority of patients tend to come from low-to median-income families and often do not have health insurance. The peak occurrence of TBI is during evenings, nights, and weekends.

ETIOLOGY

Injuries are usually classified by their mechanisms (e.g., blunt or penetrating) and by the type of injury (e.g., focal, diffuse, or fracture). The mechanism of injury is the event that caused the injury. Certain mechanisms of injury are associated with specific patterns and may be used to predict the severity of injury. Patients with TBI are injured from either a blunt mechanism, a penetrating mechanism, or a combination of both. Although the most common mechanism of injury associated with TBI is blunt force, neurotrauma cannot be discussed without mentioning penetrating injuries.^7,25

Blunt Injuries

Blunt trauma can result from many different causes. The majority of blunt TBI occurs from the following:

• Motor vehicle crashes (e.g., cars, trucks, motorcycles, pedestrians, or bicycle riders)
• Falls
• Acts of violence (e.g., assaults, baseball bats, or other objects)
• Sports-related injuries (e.g., rugby, football, lacrosse, field hockey)
• Other

The mechanism of injury affects outcome and can result from the following:

Deceleration forces: Injuries result when an individual’s head strikes an immovable object, such as the dashboard of a car.

Acceleration forces: Injuries occur when a moving object (e.g., baseball bat) strikes an individual’s head.

Acceleration-deceleration forces: Injuries often occur in combination because of the rapid changes in the velocity of the brain within the cranial vault.^28,29

Rotational forces: These forces refer to the movement of the brain in a side-to-side, twisting manner inside the cranial vault. Rotational injuries often occur in combination with acceleration / deceleration injuries and result in tension and shearing of the brain tissue.

Deformation forces: These injuries are usually the result of direct blows to the head that change the shape of the skull. Such injuries result in a compression of brain tissue. The velocity of the impact determines the extent of deformation and the subsequent injury.^28,29

Penetrating Injuries

A penetrating TBI can be caused by many things such as impalement injuries, nail guns, gunshot wounds (GSWs), and stab wounds (SWs). GSWs are the most lethal of all injuries to the brain, with a mortality rate of more than 90%.^6,7 The pathophysiology of cranial missile injuries is based on three primary events that occur at impact ^6,7:

1. Local parenchymal destruction occurs along the bullet track.
   
2. A temporary cavity (which may be much larger than the missile’s diameter) forms parallel to the primary track and then collapses within milliseconds.
   
3. A shock wave occurs immediately after the bullet enters the skull and is transmitted throughout the intracranial cavity.

Low-velocity injuries
Local parenchymal damage along the bullet path is the most important factor in determining the extent of injury. If the bullet has insufficient energy to exit the skull, it may ricochet off the inner table opposite the entry site or off a dural barrier such as the falx or tentorium, creating a second and occasionally a third track. The course of such a rebounding bullet is highly unpredictable.⁷

High-velocity injuries
As the impact energy of a missile increases, temporary cavitation and shock wave effects take on increasing significance in determining the ultimate extent of injury. If the missile transgresses vital brainstem structures, the patient usually dies instantaneously. Even without anatomic disruption of the brain’s vital centers, the shock waves themselves can be severe enough to produce transient or permanent medullary failure with cardiopulmonary arrest.⁷

(1) scalp lacerations and abrasions,

(2) skull fractures,

(3) cranial nerve injuries,

(4) mild injuries, and

(5) moderate to severe injuries.

• Scalp lacerations
• Skull fractures
• Contusions
• Concussions
• Penetrating injuries
• Hematomas

Skull Fractures

The skull has three layers:

1. inner table,
2. diploë, and
3. outer table.

The inner and outer table are hard layers of bone, and the diploë consists of cancellous or spongy bone. The skull is very hard and requires a significant amount of force to be fractured. Different types of skull fractures—including

• linear,
• basilar,
• anterior fossa,
• depressed, and
• comminuted fractures—

are described in Box 13-4 and in
Figs. 13-1 , 13-2 and 13-3.

The assessment of skull fractures is related to the type, extent, location, and signs and symptoms that accompany the fracture. A focused neurologic assessment is needed to determine the impact of the fracture on the underlying brain tissue, whether the fracture was from a blunt or a penetrating force, if the fracture required surgery or bone replacement with cranioplasty, and if there is evidence of any complications (e.g., cerebrospinal fluid [CSF] leak, infection, and brain swelling) associated with the fracture. Treatment is specific to the type of fracture and the need for surgery and patient follow-up.

Cranial Nerve Injuries

The 12 pairs of cranial nerves are often involved in TBI from direct injury, compression from edema, or stretching during periods of increased ICP (see RH1506). A careful and thorough assessment of the cranial nerves should be performed at frequent intervals following TBI. Treatment may focus on the primary injury, such as hemorrhage that can irritate or cause cranial nerve compression, edema that compresses the nerves, or trauma that directly injuries or destroys the nerves. Treatment focuses on relieving the compression or surgery to reattach or repair the nerves. Careful follow-up cranial nerve assessment is needed to evaluate the patient’s response to therapy. Box 13-5 provides a full review of cranial nerve injuries.

Mild Brain Injury

• Loss of consciousness that usually lasts less than 6 hours
• Posttraumatic amnesia as the result of the temporary disconnection of the RAS from the cortex^3,27
• No apparent structural sign of injury; may be undetectable by current means of diagnostic study
• Duration of unconsciousness as an indicator of the severity of the concussion (the longer the patient is unconscious, the worse the injury)
• Recovery that may appear complete
• Possible development of rapid, long-term sequelae (postconcussive syndrome [PCS])¹⁹

• Bruising to the cortex of the brain
  
• Tissue alteration and neurologic deficit without hematoma formation
  
• Significant alteration in consciousness without localizing signs
  
• A severe acceleration / deceleration force or blunt trauma to the head
  
• Dispersed hemorrhage into the tissue that varies in size from 1 to 3 ml to more than 50 ml²⁸
  
• Cortical and white matter petechial hemorrhages surrounded by hypodense brain edema
  
• Usual location in the frontal and temporal lobes at the poles, around the sylvian fissure, at the orbital areas and, less commonly, at the parietal and occipital areas (which are more prone to brain lacerations)

DAIs may be described as follows:

• Disconnection between the cerebral hemispheres and the RAS that produces widespread white matter injury and degeneration, neuronal dysfunction, and global cerebral edema
  
• Disconnection due to damage to nerve fibers produced by linear and rotational shear strains related to high-speed deceleration injuries¹¹
  
• Severity that correlates with the amount of shearing force applied

DAIs are commonly located on the corpus callosum and the brainstem.⁶ Patients present with an immediate loss of consciousness followed by a prolonged coma, abnormal posturing, increased ICP, hypertension, and elevated temperature.⁶ The mortality rate is 33%, with another 33% surviving with severe disabilities or remaining in a persistent vegetative state.⁶ DAIs create an increase in vasodilation and cerebral blood volume that precipitates increased ICP over time.²⁰

Microscopic lesions are not seen on the CT scan.⁶ They may appear on the CT scan as small areas of hemorrhage caused by the tearing of small blood vessels that occurs with shearing injuries.

DAIs are classified as mild, moderate, and severe:

Mild: Consists of loss of consciousness lasting 6 to 24 hours; occurs in only 8% of all severe head injuries⁶

Moderate: Consists of coma lasting less than 24 hours with incomplete recovery; represents 20% of all severe head injuries and 45% of all DAI injuries; often occurs with basal skull fractures

Severe: Occurs in 16% of all severe head injuries; usually involves primary brainstem injury

Brainstem Injury

Brainstem injuries may be caused by contusions or lacerations and are usually associated with other diffuse cerebral injuries. The prognosis associated with these injuries is poor due to the brainstem’s control of vital functions.²² Primary insult to the brainstem produces immediate dysfunction. The dysfunction may also appear in association with other TBIs as a result of secondary injury. Brainstem injuries produce an immediate loss of consciousness, pupillary changes, and posturing, along with cranial nerve deficits and changes in vital functions (e.g., respiratory rate and rhythm).^1,2 Brainstem injuries are also classified under diffuse axonal injuries.

Focal Brain Injury

Focal injuries account for about half of all head injuries. They are the direct result of trauma to the tissue. In contrast to a diffuse brain injury, a focal brain injury is a localized injury and is limited to a specific, well-defined area. It is the direct result of trauma to the tissue (e.g., contusion, laceration, or intracerebral bleed).

Subarachnoid hemorrhage
A subarachnoid hemorrhage (SAH) is the presence of blood in the subarachnoid space, which lies between the arachnoid and pia meningeal layers. When SAH occurs with trauma, it is often an incidental finding associated with other injuries. The patient’s CSF is bloody. If the patient is conscious, he or she may exhibit signs of meningeal irritation such as a headache.²⁵ Other types of cerebral hemorrhage are discussed in the following sections.

Hematoma
Three main types of hematomas result from trauma:

1. epidural,
2. subdural, and
3. intracerebral (Fig. 13-5).

One third to one half of all TBI patients develop some type of hematoma. One in four patients with skull fractures develop a surgically significant hematoma. The development of a hematoma should be explored if there is any change in LOC. Mortality rates vary according to the type of hematoma, with a subdural hematoma having the highest mortality rate.^3,4 Hematomas are often associated with a cerebral contusion.

Epidural hematoma
Epidural hematomas (EDHs) account for approximately 1% to 2% of all TBIs and for 20% to 30% of all hematomas.^1,2,28 The persons most affected are those in the 20- to 40-year age-group. The mortality rate is approximately 8%—the lowest of all hematomas.²⁸

1. Acute: An acute SDH presents within 48 hours after significant impact / injury to the brain. It is nearly always seen with cortical or brainstem injury⁶ and represents a mass lesion. An acute SDH results in significant mortality because there is injury to the brain tissue as well as the mass effect caused by the hematoma. The signs and symptoms mimic those of a rapidly expanding mass lesion or increased ICP, including herniation. Mortality decreases with surgical intervention within 4 hours of the injury.
   
2. Subacute: A subacute SDH occurs between 24 and 48 hours to 2 weeks postinjury and is associated with moderate TBI. Patients with a subacute SDH show a steady decline in level of response. Bleeding results from ruptured bridging veins, which allows it to occur at a slow rate.^1,2 The hematoma continues to act as a mass lesion; the slower it grows, the better the brain is able to compensate. Surgical removal is required before improvement in the patient’s condition is noted.^1,2
   
3. Chronic: A chronic SDH occurs from 2 weeks to several months postinjury. Older adults, chronic alcohol abusers, or those taking the anticoagulant warfarin have a higher incidence of this type of injury.^1,2 A chronic SDH acts as a space-occupying lesion that progressively enlarges. It is often surrounded by a characteristic membrane and may be referred to as a hygroma. The mortality rate is 15%.²² A chronic SDH is often bilateral and is usually the result of low-impact injuries such as falling or bumping the head. Patients may have no recall of injury but may be unable to relay the event. A chronic SDH is usually treated with burr holes and gradual drainage of the hematoma to prevent recurrence.

Intracerebral hematoma
Intracerebral hematomas can best be described as large, focal, intraparenchymal contusions. They are considered mass lesions when they are 25 ml or larger. Approximately 2% to 3% of these hematomas are associated with actual contusions.^1,2,18 They are caused by penetrating injuries (e.g., gunshot wounds, stab wounds, or lacerations of tissues), deep- depressed fractures, and DAI.^6,7 Intracerebral hematomas develop deep within the hemispheres from contused areas that become confluent and are surrounded by edema.

Summary of focal injuries
Lesion size and the patient’s overall status dictate treatment. The hematoma must be evacuated if it is large or if the patient’s neurologic status is deteriorating.⁶ Hematomas act as mass lesions and are often accompanied by progressive edema, producing a steady deterioration in the patient’s condition. This deterioration may occur immediately or be delayed from 72 hours to 7 to 10 days.⁶ Clot formation and deterioration within a few days after initial insult is called a delayed traumatic intracerebral hematoma (DTICH).³ DTICH occurs in the areas that were injured at the time of impact but appeared normal on the initial CT scan. DTICH is associated with a high incidence of increased ICP and a poor prognosis.²⁴ There is a higher risk of development of DTICH in patients with disseminated intravascular coagulation (DIC), hypotension, alcohol abuse, and hypoxia.

ASSESSMENT

Initial Assessment

Airway (A),

breathing (B), and

circulation (C) are the immediate priority as the trauma team members quickly complete the initial assessment.

Disability (D) of any neurologic function is noted, and total

exposure (E) of the patient by removing or cutting away all clothing allows the trauma team to assess the entire body for injuries.

• Provide unit-based quality improvement
  
• Serve as an educational tool for new staff
  
• Facilitate research
  
• Ensure continuity of care
  
• Bring a standard of care to the point of practice

FIG 13-7

Very early after admission to the emergency department, attention is focused on appropriate management for the prevention of secondary brain damage, such as hypoxia where the patient exhibits apnea or cyanosis and a partial pressure of oxygen in arterial blood (Pao₂) < 60 mm Hg, hypotension with a systolic blood pressure < 90 mm Hg, increased ICP with a surgical lesion or edema demonstrated on CT, or metabolic abnormalities.

Level of consciousness
The most important assessment of the patient with TBI is level of consciousness (LOC), followed by pupillary assessment and assessment of the extremities for lateralized weakness or loss of function. As the trauma team completes the initial assessment, the patient is preliminarily categorized as having mild, moderate, or severe TBI. A mini neurologic examination can be rapidly performed using the AVPU scale to determine if the patient is:

A Alert

V Responding to vocal stimuli

P Responding only to painful stimuli

U Unresponsive to all stimuli

The most widely used tool to assess a patient’s LOC is the Glasgow Coma Scale (GCS). Since its introduction in 1974, the GCS has become the tool most used to objectively score patient eye opening, motor response, and verbal performance to external stimuli. (See RH1501 for a discussion of GCS.) The highest GCS score is 15, which is normal. Any score less than 15 is considered abnormal. A score of 13 to 14 indicates a mild TBI, 9 to 12 a moderate injury, and 8 or less a severe head injury.^1,2,3

Pupillary changes
Pupillary changes range from a decrease in reactivity to bilateral fixation and dilation. (See RH1501 for pupil assessment.) Pupil changes indicate increased ICP resulting in CN III compression, as well as injury or ischemia to certain areas of the brain. The pupils are normally round, approximately 3 to 5 cm in diameter, equal in size, and briskly reactive to light. Several factors can influence the size, shape, and reactivity of pupils, such as a history of a previous ocular injury, alcohol ingestion, or the use of certain medications or illicit drugs.^1,2,3

A pupil that is oval in shape indicates increased ICP and CN III compression and develops into a fixed and dilated pupil if left untreated. This is seen most often in severe closed-head injuries.⁴ Bilaterally fixed and dilated pupils indicate massive elevations in ICP, which can result in brain death. A metabolically induced coma does not affect pupillary reaction (Fig. 13-8). Changes in pupil size, shape, and reactivity may indicate rising ICP and should be reported to the physician immediately.^1,2,3,20

Brainstem reflexes
Several reflexes that originate in the brainstem that should be assessed. These reflexes include the cough, gag, corneal, doll’s eyes, oculocephalic, cold calorics, and oculovestibular reflexes (see RH1500 and RH1501). These reflexes test CN V through CN X. The presence of these reflexes indicates that the integrity of the brainstem has not been disrupted.² An absence of these reflexes signifies a poor prognosis.

Vital signs
Vital sign changes are a late indication of increased ICP. Cushing’s reflex is seen in approximately 75% of patients with increased ICP and is a triad of late symptoms involving vital sign changes that indicate decompensation of the brainstem.² These changes include an increase in systolic blood pressure, a widening pulse pressure, and bradycardia. Patients with TBI and increased ICP show a reduced variability in heart rate regardless of activity. The vital signs must be routinely monitored; although the immediate response to TBI is an increase in blood pressure and ICP, these variables should return to normal within 1 to 2 minutes.²⁰ Blood pressure is often decreased with severe injuries and indicates a poor prognosis because of the negative effect on cerebral perfusion pressure (CPP).²⁰ A decreased blood pressure in the presence of increased ICP results in inadequate CPP, which precipitates further neuronal tissue damage from ischemia and a further increase in ICP. Systemic hypertension can also have deleterious effects on perfusion pressure. Hypertension increases cerebral blood flow, which in turn increases ICP and results in an inadequate CPP. Increased blood pressure may increase cerebral blood flow but, if autoregulation is intact, cerebral vasoconstriction will occur to control volume.²⁰

Cardiac changes
Intracranial injuries can produce changes in cardiac rate, rhythm, and conduction, and these changes may be neurogenic in origin.³⁴ Different intracranial lesions are associated with different cardiac changes. Atrial fibrillation and bundle branch blocks are associated with contusions. A subdural hematoma (SDH) may produce conduction defects as well as atrial and ventricular ectopy. Junctional escape rhythms, progressive bradycardia, and idioventricular rhythms are seen more often with hemorrhages and increased ICP. ST- and T-wave changes occur with severe TBIs.³¹ Neurogenic T waves (inverted T waves of increased amplitude and duration) are seen in a variety of neurologic diagnoses. There are little data to explain the cause of these changes, but they are thought to be related to the catecholamine response that occurs after injury.³¹ Because of the nature of these disease processes and their concurrent changes, continuous ECG monitoring is essential in patients with severe TBI.³¹

Respiratory changes
Respiratory rate and rhythm changes also occur in neurologically impaired patients. Cheyne-Stokes respiratory patterns are associated with damage to the bilateral hemispheres and the basal ganglia and often precede cerebral herniation. Central neurogenic hyperventilation (CNH) may occur as a compensatory mechanism to increased ICP. Hyperventilation reduces the PaO₂, resulting in vasoconstriction of cerebral vessels and reduced ICP. CNH is also associated with damage to the midbrain and pons.^6,20 Apneustic breathing is characterized by a prolonged inspiration followed by a pause and then a short expiratory phase. This also is associated with pontine injury. Ataxic or agonal respirations are associated with medullary damage and may progressively deteriorate to apnea. The clinician should be able to identify changes in a patient’s respiratory pattern, because these changes are often indicative of deterioration. Early detection of respiratory pattern changes and immediate, appropriate intervention prevents hypoxia, which contributes to secondary brain damage.⁶

Temperature changes
Temperature changes occur rapidly and are common in the TBI patient population. Ongoing monitoring is essential in preventing hyperthermia and hypothermia. Hypothermia has been defined as a core body temperature of less than 35° C (95° F). Hypothermia results when the body can no longer maintain an adequate temperature. It needs to be rapidly recognized and treated for life-threatening complications such as apnea, ventricular fibrillation, and acidosis.^17,33

Hypothermia is common with trauma patients as a result of environmental exposures, stress, and the administration of unwarmed IV fluids and blood products to correct massive hypovolemic shock. Age also plays a role in hypothermia, with older adults more at risk because of their high incidence of cardiovascular disease and decreased body fat. In addition, the patient’s ability to shiver can be affected by medications (e.g., phenothiazines, neuromuscular blocking agents), an elevated BAL, traumatic injuries, hypovolemic shock, and diseases such as diabetes. Active and passive rewarming are absolutely necessary in order to keep patients from becoming hypothermic.^17,22

Hypothalamic damage as well as infection often cause temperature increases. Hyperthermia increases the metabolic demands and oxygen consumption in an already overtaxed system. Oxygen consumption increases 10% for every degree of temperature elevation. Increased temperatures cause increased cerebral metabolic activity, increased CBF, and increased carbon dioxide production, all of which increase ICP.³³ Elevations above 38° C should be treated rapidly.³³ Elevated temperatures related to the neurologic injury and not to an infection may be refractory to acet-aminophen and aspirin. Other cooling methods such as cool sponge baths or hypothermia blankets may need to be instituted. Prevention, early detection, and intervention are essential in minimizing the metabolic demands on the brain. It is important to try to maintain a normothermia temperature with the use of antipyretics, antibiotics, and cooling blankets.^22,33

Neurologic deficits
Neurologic deficits are evaluated by completing and recording the neurologic assessment to include level of consciousness (LOC), motor and sensory evaluations, pupils, and cranial nerves.

Pain
Pain is the fifth vital sign and can be evaluated by asking the awake patient if he or she feels pain in any part of the body. The extent and severity of pain is determined by using a pain scale or, if patient is unable to report pain, by observing for facial expressions, body movements, crying, restlessness, and an increased heart rate or blood pressure (see RH1512). Sedating the neurotrauma patient should be avoided until the trauma team leader has cleared the patient to receive analgesics, because pain medications can cause hypotension. It is difficult to determine the extent of pain in patients who are unconscious or pharmacologically paralyzed. The clinician can use a variety of clues to deduce the pain status of an unresponsive patient. These clues can be determined by assessing the following:

• Vital signs (elevated blood pressure and heart rate)
• Elevated ICP
• Facial grimacing
• Agitation
• Restlessness
• Moaning

HIGH-RISK NURSING DIAGNOSIS

• Ineffective airway clearance related to decreased LOC and cranial nerve deficits
  
• Impaired gas exchange related to increased ICP, ventilation-perfusion (V / Q) mismatching
  
• Deficient fluid volume related to fluid restriction, diuresis, diabetes insipidus, inadequate volume resuscitation
  
• Excess fluid volume related to excessive fluid resuscitation and syndrome of inappropriate antidiuretic hormone (SIADH)
  
• Imbalanced nutrition: less than body requirements related to increased metabolic state and a delay in providing caloric replacement
  
• Impaired physical mobility related to injury, bedrest, unresponsive state
  
• Disturbed sensory perception related to impaired consciousness
  
• Acute pain related to any injuries from the trauma, invasive procedures, surgical procedures

NEURODIAGNOSTIC / LABORATORY STUDIES

Skull radiographs: Detects skull or facial fractures, tumors, or foreign bodies.⁷

CT: Best study for rapid diagnosis of type, location and extent of injury. A CT scan provides a quick comparison with serial scans and detects absent or compressed cisterns. A dual diagnosis of head and spinal injury can be ruled out with both a head and neck CT. CT images are usually repeated every 2 to 3 days after admission or as needed based on the patient’s clinical presentation.²⁹

MRI: Allows for a better definition of mass lesions, better visualization of the posterior fossa and brainstem, and an increased ability to detect subtle changes in tissue water content. An MRI scan requires more time than a CT scan and is not usually performed in acute or unstable patients, who are at high risk during scanning.

Cerebral angiography: Has limited use with trauma unless there are suspicions of cerebrovascular disease, vessel abnormality, or injury.

EEG: Detects abnormal electrical or seizure activity and the absence of electrical potentials as part of the diagnosis for brain death.

Cerebral blood flow studies (Xenon CT, Transcranial Doppler): Provide noninvasive measurements of cerebral blood flow (CBF) velocity, the diameter of cerebral blood vessels, or the presence of vasospasm. These studies can determine whether an increase in ICP is due to an increase in cerebral blood flow or to cerebral edema.

Evoked potentials (EPs): Measure the brain’s response to auditory, somatosensory, and visual stimuli.

Infrared spectroscopy: Noninvasive assessments of oxygen saturation.

SPECT: Measures abnormalities in regional blood flow.

PET (if available): Evaluates tissue blood flow and the use of oxygen glucose.

TREATMENT

Medical Management

Patient management is focused on preventing or treating the increased ICP that accompanies the primary injury. Box 13-7 describes the standard therapeutic regimen for the management of head injury.⁸

Fig. 13-6 illustrates the algorithm for initial management, and Table 13-1 provides a summary of head injury guidelines from the Brain Trauma Foundation and the American Association of Neurological Surgeons.

Other Variables That Affect Secondary Injury

1. Early: Occur within 7 days of the injury or when the patient is still suffering the direct effects of the primary injury. Early PTS may cause increased ICP, hypoxia, and increased metabolic demands that may compromise an already jeopardized brain.⁹
   
2. Late: Occur anytime after the first 7 days postinjury.

1. vasogenic and
2. cytotoxic.

Patients with an expanding epidural hematoma require emergency surgery for evacuation of the hematoma and cauterization of the bleeding vessel. Trauma patients with a subdural hematoma (SDH) may be managed medically when the clot is small unless the bleeding continues and a craniotomy is needed to locate and stop the bleeding (see RH1505). Patients with depressed skull fractures and other serious fractures may also be sent to the operating room (OR) for elevation of bone and repair of the dura and brain tissue. Most studies indicate that the prognosis for recovery from focal TBI is very good with early surgical intervention for mass lesions.

Once it is determined that the injury requires surgical intervention, the neurosurgeon will decide the type of procedure and the timing of surgery. Such decisions are made based on the injury. Surgery may range from burr holes to craniotomy, craniectomy, cranioplasty, or ventriculostomy.

Clinical Management

The use of mannitol can cause hypertension. It is important that the patient’s vital signs be closely monitored and that an MAP greater than 90 mm Hg is maintained. This can be done with the use of albumin, normal saline, packed red blood cells (RBCs) and vasopressors.^1,5

Lasix is a loop diuretic that is used as an adjunctive therapy in an effort to minimize the negative effects of mannitol. When Lasix and mannitol are used together, Lasix can do the following:

• Enhance the effect of mannitol
  
• Reduce the incidence of rebound ICP^1,5
  
• Decrease blood volume
  
• Reduce edema by pulling fluid out of the edematous tissue into the vasculature
  
• Decrease sodium uptake by the brain and reduce CSF production up to 70%⁵

Fluid replacement / restriction
Although it is not desirable for patients to be hypovolemic, fluid restriction may be necessary when ICP is elevated and becoming refractory to other therapies.⁵ The goal of fluid restriction is to improve mean arterial pressure (MAP), normalize CPP, and maintain euvolemia. Such therapy may be maintained for long periods to control ICP until compliance returns to normal.¹¹

The following measures are used to lower the patient’s cerebral metabolic requirement:

• Keep the patient seizure free.
  
• Maintain normothermia.
  
• Maintain a calm, quiet environment, and prevent loud noises and disturbing conversations. This restriction includes having one patient per room and having a door to the room so that the amount of noise and sensory stimulation can be controlled.
  
• Decrease ICP. Medical interventions that are used in an attempt to lower metabolic needs and decrease ICP include the administration of sedatives, paralytic agents, and anesthetic agents (propofol), as well as the induction of barbiturate coma when increased ICP is refractory to all other forms of therapy.^3,26,33

Sedation
Sedation reduces restlessness and agitation. It also decreases the metabolic rate and rate of oxygen consumption. Lorazepam (Ativan) or midazolam (Versed) may be required per the institution’s protocol. Opioids (narcotics) have the advantage of being reversed to allow for the completion of an accurate assessment. Morphine should be avoided due to its hypotensive effects. Propofol (Diprivan) may cause agitation and should be discontinued if this occurs.^2,22,26

Intubated patients may have an increase in ICP because the endotracheal tube can act as a noxious stimuli and require fentanyl (small boluses allow for pupil evaluation while decreasing the effect of noxious stimuli). Sedatives should be used very cautiously with nonventilated patients, because a decrease in respiratory rate and respiratory depression may precipitate an increase in ICP.²⁶

Paralytic agents
The objective and guidelines for pharmacologic paralysis includes reducing skeletal muscle activity, metabolic rate, and oxygen consumption. Paralytic agents offer no analgesic effect and do not adequately protect the patient from noxious stimuli. However, when used with sedatives, paralytics may help reduce the increase in cerebral metabolic rate related to agitation. The use of neuromuscular blocking agents (i.e., pancuronium [Pavulon], atracurium [Tracrium], vecuronium [Norcuron], and rocuronium [Zemuron]) without sedation should never be allowed.

Alert: Pancuronium can cause tachycardia, which may necessitate the use of a beta blocker.³

When paralytic agents are used with ICP monitoring and ventilation, the patient’s corneas are protected with artificial tears, and the eyes are taped shut or a moisture chamber is applied. The standard of care requires the use of “train of four” for monitoring the level of paralysis to ensure that the smallest amount of drug is used to achieve the desired level of paralysis. (The “train of four” refers to the application of a peripheral nerve stimulator to the ulnar nerve to determine neuromuscular function.)

Barbiturate coma
A barbiturate coma is used as therapy for hemodynamically stable patients with severe TBI and intracranial hypertension who are thought to be salvageable but who have been refractory to maximal medical and surgical therapies. The diagnosis of a delayed bleed / lesion should be ruled out before the induction of a barbiturate coma.

A barbiturate coma is a pharmacologically induced coma state that lowers cerebral metabolism and CBF. It acts as a neuroprotective therapy and decreases oxygen uptake in the brain, which decreases the cerebral metabolic rate of oxygen consumption (CMRo₂) and the CBF by as much as 50%. It may also assist in stabilizing cell membranes, producing a more uniform blood supply and decreasing the formation of vasogenic edema.^1,2,22

Pentobarbital is the drug of choice for barbiturate therapy because its half-life is 24 hours. It is administered as a loading dose of 36 mg / kg, with a maintenance dosage of 1 to 3 mg / kg / hr. Blood pressure and CPP may fall with the loading dose. Vasopressors, inotropes, and volume expanders may be used to help maintain systolic blood pressure and CPP.

Barbiturate infusion levels are regulated by burst suppression pattern appearance on EEG.³ The barbiturate coma is slowly decreased after the ICP is normal for 24 to 48 hours. This type of therapy requires complex monitoring, nursing care, and medical care. It is instituted only in specially equipped critical care areas.^3,22

Additional assessments
A complete neurologic assessment is performed for a baseline evaluation on admission to the NCCU. Subtle changes can be easily detected when subsequent assessments are charted on the neurologic flow sheet to document the patient’s changing status. The Rancho Los Amigos scale is a useful tool for identifying levels of dysfunction and for planning the appropriate nursing interventions (see Table 13-2).²⁷

In addition to the interventions described previously, acute care for the patient with TBI includes frequent and careful monitoring and documentation to manage the following parameters:

• Level of consciousness (LOC), Glasgow Coma Scale (GCS) score, neurologic status
  
• Cerebral hemodynamics (ICP: 0 to 15 mm Hg) and blood flow to the brain (CPP: 60 to 100 mm Hg)²⁰
  
• Airway clearance and respiratory rate and rhythm
  
• Pulmonary capillary wedge pressures, cardiac outputs

For patients with a GCS score of 8 or less, ICP monitoring is performed per protocol for drainage and placement of the drainage bag. For patients with a GCS score of 7 or less, hemodynamic monitoring is performed with a Swan-Ganz catheter and invasive lines. Airway clearance and respiratory rate and rhythm are monitored frequently. The cough, gag, and corneal reflexes are assessed, and the lungs are auscultated every 2 hours to detect adventitious lung sounds that may indicate respiratory failure. Intake and output (I&O) are monitored every shift.

Famotidine (Pepcid) 20 mg IV every 12 hours or and/or Maalox 30 ml PO or via nasogastric (NG) tube for a stomach pH less than 5 are administered to prevent stress ulcers.

Patients with TBI are turned every 1 to 2 hours to mobilize secretions. The use of specialty beds, when required, does not negate turning the patients.^1,2 Antiembolic stockings with sequential compression devices are also used.

Suctioning should never be done through the nose, because a basal skull fracture may be present. The patient is suctioned as often as needed but at least every 2 hours. The patient is premedicated with lidocaine 0.5 to 1.5 mg / kg IV or via endotracheal tube to suppress the cough reflex and to prevent ICP elevations^1,2; the patient is also preoxygenated with 100% oxygen. Suctioning is limited to two passes, and instilling saline down the endotracheal tube is avoided. Secretions are monitored for viscosity, color, and odor (a foul smell may indicate an infection). Humidified air may assist in decreasing secretion viscosity. Chest physiotherapy and postural drain-age are performed at least every 2 hours.

Prevention of complications
Several complications are described in detail in the following sections to emphasize their importance in preventing complications that could cause further neurologic impairment.

Impaired gas exchange
Impaired gas exchange is managed by the following:

• Clearing the airway (discussed earlier)
  
• Auscultating breath sounds every 2 hours to allow for early detection of compromised lung function
  
• Monitoring arterial blood gas (ABG) results to ensure that the appropriate interventions are provided to maintain adequate oxygenation and perfusion^5,6

Increased intracranial pressure
Nursing activities have been found to contribute to a rise in ICP.^8,20 The clinician should follow the guidelines in RH1506 to prevent elevated ICP^4,5,6:

• Calculate CPP before and after all activities to ensure adequate perfusion to the brain. If the CPP drops below 50 mm Hg, the activity should be interrupted and the patient allowed to rest.
  
• Provide a quiet, subdued environment to reduce stimuli and reduce ICP.
  
• If ICP remains greater than 20 mm Hg, use sedation to decrease agitation.
  
• For patients with an ICP monitor (Fig. 13-9), evaluate the ICP waveform for an elevated P₂ segment, which indicates decreased compliance.

For patients with a ventriculostomy, drain CSF by opening the stopcock to release a small amount of CSF, then reevaluate the patient’s ICP.

Deficient / excess fluid volume
Deficient or excess fluid volume is managed by the following:

• Judiciously monitoring I&O hourly during the acute phase
  
• Recording urine specific gravity a minimum of every 2 hours and every hour in the presence of diabetes insipidus (DI)
  
• Recording daily weights to identify a rapid loss of fluid or fluid retention
  
• Monitoring electrolytes frequently for DI (e.g., decrease in urine osmolarity, elevated serum sodium, serum osmolarity)^1,2
  
• Assessing the oral cavity for dry mucous membranes
  
• Monitoring for fluid loss (“neurogenic sweats” may cause a loss of 500 to 1000 ml of fluid daily)

Imbalanced nutrition
Nutrition must be adequate for the injured brain to heal. The following guidelines are recommended:

Nutrition consultation: To establish a feeding route within 24 hours of admission

Enteral feeding: Preferred over parenteral^12,32,34

• Problems of immobility lead to a reduction in gastrointestinal motility.
  
• Opioids (narcotics) affect the patient’s ability for elimination.
  
• Bowel sounds should be monitored and documented once every shift.
  
• All bowel movements should be recorded with regard to frequency, and type (soft, hard, small, large, bloody, diarrhea).
  
• Patients should not go more than 24 to 48 hours without a bowel movement.
  
• Patients should avoid Valsalva maneuvers, which raises ICP.
  
• A bowel program (e.g., bowel regimen, stool softeners, laxatives, fiber products) should be established to prevent constipation.
  
• Adequate hydration and calorie intake are also essential for proper elimination.

Impaired physical mobility
Patient immobility affects all body systems. The following guidelines will help prevent complications of immobility:

• Consult with the physiatrist from physical medicine and rehabilitation (PM&R) for a physical therapist and occupational therapist.
  
• Promote optimal level of mobility by following PM&R recommendations for ROM.
  
• Educate the patient and family on how to adapt to the patient’s mobility deficits.
  
• Provide interventions such as repositioning, provid- ing stimuli for all senses, and maintaining a safe environment.^1,2
  
• Ambulation: Assessment may indicate appropriate after 24 to 48 hours, bedside PT for passive ROM, out-of-bed to chair usually with assistants.

Disturbed sensory perception
Sensory alterations are important considerations, and treatment may include the following:

• Repositioning the patient every 2 hours
  
• Maintaining the bed in a low position with the side- rails up and the bed padded for agitated and combative patients
  
• Strictly following fall prevention assessment and guidelines at all times for patient safety
  
• Establishing a stimulation / rest routine based on independent patient needs
  
• Obtaining a physiatrist consultation and physical therapist / occupational therapist consultation to evaluate and intervene as soon as the patient is stabilized for range of motion (ROM) and other exercises as well as assist in preventing muscle atrophy and contractures.

• Pain has an adverse effect on ICP, vital signs, and CPP.
  
• Pain management is complicated due to the ability of certain agents to interfere with a neurologic assessment.^3,6,26
  
• Some agents do not affect pupillary response. Codeine and fentanyl allow for continued evaluation of pupils while decreasing noxious stimuli.
  
• Morphine sulfate (MS) should be avoided because of its effects on the blood pressure and cerebral vasculature.

Neuromuscular blocking agents should not be administered without analgesia because they have no effect on the perception of pain—only on the ability to respond to it.^1,3,11,26

Ineffective thermoregulation
Temperature control issues have been discussed previously. All other causes of fever should be evaluated for and eliminated before the cause is attributed to neurologic damage.^22,33 Tylenol 650 mg per rectum (PR) or PO every 4 hours is administered for a temperature over 101.5° F.

Postacute / nonacute care
After the patient is physiologically stable and his or her ICP has returned to normal, he or she is transferred to a nonacute unit. The patient is usually more awake and alert, and agitation may increase. There are potential problems for seizure activity, injury from falls, and aspiration as the patient starts oral feedings.

Assessment continues to play a key role. Neurobehavioral testing should be initiated^{2,15,19,27,28} to evaluate cognitive, adaptive, and emotional behaviors.²⁴ These behaviors or responses reflect cortical function. Neuropsychologic testing assists in planning ongoing care, determining rehabilitation potential, and identifying realistic individual goals.^15,27

The patient may need assistance to regain and build or maintain independent skills (activities of daily living), such as speaking, ambulating, eating, drinking, bathing, and performing personal hygiene to bridge the gap from dependence to independence and rehabilitation.

High-risk nursing diagnoses

• Disturbed thought processes related to cognitive deficits
  
• Self-care deficit related to physical and cognitive impairment
  
• Risk for injury related to impaired mobility and cognition
  
• Situational low self-esteem related to cognitive and physical limitations
  
• Compromised family coping related to the devastating long-term effects of head injury

Level of consciousness (LOC)
The higher Rancho Los Amigos Scale of Cognitive Functioning reflects the increased responsiveness that indicates recovery.^15,24 The patient’s responsiveness may vary between the following behaviors:

• Confusion
  
• Agitation
  
• Emotional lability
  
• Outbursts of anger, frustration, profanity, and inappropriate behavior

Interventions for this increased responsiveness include a structured environment to reduce overstimulation and distraction and acknowledging behavior calmly while correcting misperceptions and refocusing the patient. The family must be included and educated on how to intercede with the patient; this will help reduce their anxiety and prepare them for the future.^20,27

Physical or chemical restraints should be used judiciously and only when the patient poses a danger to himself or herself or others.²⁷ The least restrictive interventions should be used and should include a netted bed and family and/or sitters. Someone should be with the patient at all times during periods of confusion, restlessness, and agitation to prevent the patient from getting out of bed, falling, or self-harm.

Disturbed thought processes
The Rancho Los Amigos Scale of Cognitive Functioning assists in selecting the appropriate actions based on the patient’s cognitive status and abilities (Table 13-2).

The following guidelines are useful:

• Take care not to overwhelm or overstimulate a patient who has a low level of response or cognitive function.
  
• Modulate stimuli such as conversation, music, and environmental noise levels.
  
• Stimulate the senses by adding only one sensor stimulus at a time; this stimulation may be increased as the patient progresses.
  
• Provide a structured environment. Give directions in simple language with frequent repetition and reinforcement, and work closely with families and significant others on the type, duration and methods of stimulation.^2,19 Establish verbal cues and memory aids for the patient.

Self-care deficits
The goals of the TBI team are based on some of the following:

• Assist the patient with activities of daily living (ADLs), which may range from teaching patients to dress themselves to performing other self-care activities (e.g., eating, grooming, toileting).
  
• Teach / educate the patient. Separate activities into small steps, use repetition, and assist only when necessary.^2,19
  
• Encourage family involvement. Families can learn how to assist with ADLs and can provide support and encouragement for the patient.

The physical therapist, occupational therapist, speech therapist, and neuropsychologist should evaluate and develop a rehabilitation plan that includes weekly evaluations.

Risk for injury
The patient with a TBI can be injured as a result of the following:

• Falls: To prevent falls, assess for fall precautions, place the patient’s bed in the low position, place the patient’s call bell within reach (the patient may be ignoring it or may have forgotten how it is used), and remind the patient to call for assistance (he or she will often forget). Use commercial bed alarm systems, net or “mesh beds,” or video surveillance, and have a hospital “sitter”/ “patient extender” or family member stay with the patient at all times.
  
• Unattended or unsupervised activities.
  
• Inappropriate behavior: This includes a reluctance or inability to summon assistance and continuously climbing over the siderails to get out of bed (OOB), most often to use the bathroom.
  
• Failure to orient the patient to his or her surroundings or not providing adequate lighting or visual aids.
  
• Failure to provide regularly scheduled toileting that results in patient getting OOB without assistance.

Restraints are used as a last resort to keep the patient from self-harm.²⁷ Their use should be discussed with family members, and hospital policy should be followed.

Posttraumatic epilepsy
Posttraumatic epilepsy occurs after TBI, with both focal and grand mal (tonic-clonic) seizures occurring. Their incidence appears to be greater in those who experience penetrating as opposed to blunt head injuries.^7,9 The onset of posttraumatic epilepsy varies greatly—from 1 month up to 2 years after the original injury. This condition is best controlled with anticonvulsant therapy.⁹ It has a propensity to decrease over the years, with some patients becoming seizure free.^9,22

• Give the patient as much control as possible and as early as possible.
  
• Spend time with the patient to enable caregivers to assess the patient’s self-concept and direct activities toward his or her abilities as well as strengthen weaknesses. This will provide a reality base.^2,19
  
• Use talk and touch as simple ways of supporting and encouraging the patient.
  
• Set realistic and patient-directed goals.
  
• Encourage the family to allow the patient to do as much as possible.
  
• Help the patient and family locate the nearest TBI support group.

Compromised family coping
Like the patient, family members experience a loss of control and feelings of fear and helplessness. Assist the family by using some of the following interventions:

• To reduce their anxiety, identify tasks they can do, and include them in the plan of care.
  
• Encourage family members to communicate their feelings.
  
• Answer questions honestly, and provide verbal and written information.
  
• Mobilize support personnel, such as social services, pastoral care, family liaisons, and case managers.

COMPREHENSIVE PATIENT MANAGEMENT: TRAUMATIC BRAIN INJURY

The psychosocial dysfunction experienced by patients with TBI is perhaps the major obstacle faced after survival. Their lives and the lives of their families are altered forever. Patients and their families must cope with many stressors as they face the fear of unknown and unpredictable outcomes. Psychosocial support is needed to deal with these concerns, to help reduce stress and anxiety, and to promote adequate coping skills. Patient outcomes range from mild with no residual deficits to a persistent vegetative state, with every condition in between possible. Neurologic deficits may include impairments in language, cognition, personality, mentation, and movement. The patient is evaluated for the need for professional psychologic counseling.

Rehabilitation and education of both the patient and family must start on admission. Families require education and crisis intervention during the initial stages and support throughout hospitalization and often for an extended time after discharge. The Brain Injury Association (BIA) has chapters in every state that can help inform and support families. In the last decade, support groups for patients with TBI and their families have grown in size and number throughout the country. Unfortunately, TBI and its long-term effects (including behavior issues) are not well understood by society, which results in misconceptions about patient behavior and needs and often creates fear and mistreatment for many TBI survivors.

Living with a Brain Injury

Because of the advances in emergency medical systems during the past 20 years and because of the current state-of-the-art trauma centers with specialists and new technology, patients who would have died at the scene from a head injury are surviving and living a normal life expectancy. These individuals, however, are not normal. They live each day in communities across the country and struggle with their lifelong disability and cognitive impairments that often lead to early dementia, a shortened work life, the need for early retirement or disability pay, and premature aging with an early onset of medical problems. This population may be at higher risk for Alzheimer’s disease and other types of dementia. They are also at a higher risk for sustaining a fall and other injury if their home has not been evaluated and equipped with equipment and safety devices that enable them to live with their special needs. A patient who has lived at home may require early admission to a long-term care facility. The patient’s physical limitations and lack of endurance may qualify / classify him or her for disability and the need for expensive equipment (e.g., power wheelchairs, hospital wheelchairs) and for the services of physical or occupational therapists. Research on aging and brain injury is needed for patients and their families to successfully prepare them for the final years following a TBI.

Older Adult Considerations

Trauma is the fifth leading cause of death in older adults. The geriatric population (aged 65 years and older) has the second highest TBI incidence of all age-groups. The most common causes of TBI in the older are falls and motor vehicle crashes (MVCs). Older patients are more likely to develop chronic subdural hematomas (SDHs) and experience secondary injury than are their younger counterparts. Indeed, intracranial bleeding in older adults may occur even with minor head trauma due to the cerebral changes associated with aging.

Although TBI is not uncommon in older adults, the diagnosis is often complicated by an atypical presentation. For example, headache is the classic sign of SDH, yet in older adults it is often not a complaint. The presentation of an SDH is delayed weeks or even months, and unfortunately the insidious onset may be attributed to the normal aging process. Chronic SDHs are tolerated better by older adults because of the brain atrophy associated with aging. As the brain decreases in size, the space within the cranial vault increases.^1,2,18 Therefore a hematoma can collect over time without obvious changes in neurologic status until its size is sufficient to produce a mass effect.

The assessment and management of older patients should follow the same algorithm as the care of younger TBI patients. The goals of treatment should focus on returning to the patient’s preinjury functional status and future quality of life. It is important to realize that the metabolic, anatomic, and psychosocial changes associated with aging may influence the assessment and care of the older patient with TBI.¹⁴ Injuries that are relatively survivable in younger adults can lead to complications and life-threatening events, including death, in older adults. Thus, in addition to hospital care, nursing interventions should also focus on injury prevention.

Environmental assessments, fall-risk profiles, and appropriate prostheses, assistive devices, and therapies can reduce the older patient’s risk for TBI related to falls. A rehabilitation focus that includes an acute-phase prevention of complications should be initiated as soon as the injury is discovered and should be continued throughout the course of recovery.

CONTINUUM OF CARE

Home Care / Rehabilitation

• Maximizing the patient’s ability to return to his or her highest level of functioning and to his or her home and the community
  
• Addressing all concerns before discharge for a smooth transmission to home or rehabilitation
  
• Promoting independence with adaptation to deficits (this becomes a crucial part of care)

• Impaired physical mobility related to weakness and / or hypertonicity
  
• Disturbed thought processes related to a disturbance in cognitive functioning
  
• Risk for injury related to behavioral changes
  
• Imbalanced nutrition: less than body requirements related to difficulty swallowing (dysphagia)

Impaired physical mobility
Interventions for the patient with impaired physical mobility include the following:

• Performing ROM exercises on all extremities several times per day
  
• Splinting weakened extremities and using serial lower extremity casting and upper extremity splinting to treat spasticity and maintain functional position of the extremity, especially during the acute phase of care
  
• Performing strengthening exercises to prevent atrophy and improve the mobility of the involved extremities (Hypertonicity varies from a mild increase in motor tone to rigid states, as seen in flexor and extensor posturing.)
  
• Administering antispasmodic agents such as baclofen, dantrolene (Dantrium), and diazepam
  
• Performing surgical procedures such as myotomy or muscle / tendon release, peripheral nerve simulator implants, and nerve blocks

Complications of impaired mobility include prolonged spasticity, contractures, and heterotrophic ossification (HO). HO involves the deposition of bone around the major joints and has the potential to cause a frozen joint and a functional loss of the use of the extremity.

Disturbed thought processes
Using the behaviors outlined on the Ranchos Los Amigos Scale of Cognitive Functioning, a care plan can be designed to decrease sensory overload. The plan may include the following:

• A strict and consistent schedule to decrease confusion and increase compliance, because the ability to process information is severely impaired. Short-term memory is also affected in these patients, which means they are unable to understand new information about people, places, and events.
  
• Sensory stimulation programs: These programs are usually started in the NCCU and should be continued in rehabilitation.
  
• Cognitive retraining: Such retraining improves the patient’s executive functioning, judgment, and reasoning.
  
• Controlled stimulation, order, repetition, and consistency: These are important in assisting the patient to regain optimal cognitive functioning.
  
• Cognitive remediation based on an assessment of the deficits and strengths, remedial cuing interventions, and the patient’s ability to respond.

This program focuses on five core deficit areas:

1. arousal and attention,
2. skill structures,
3. memory, language and
4. thought processes, and
5. emotional activity.

Risk for injury
Unpredictable and eccentric behavior is often seen in a patient with TBI when arousal occurs. Behaviors include the following:

• Agitation
  
• Screaming, angry outbursts
  
• Delusions, disinhibitions

Interventions include controlling the environment by placing the patients in a quiet room, providing consistent caregivers, maintaining a strict schedule, and avoiding loud noises (radio, television), confusion, and too many visitors. Medications include haloperidol (Haldol) and lorazepam (Ativan). Sensory stimuli should be meaningful to the patient and presented in a structured format, because he or she has poor insight and judgment and requires careful monitoring. The use of restraints is discouraged unless no other avenues of preventing harm are successful.

Case Management Considerations

Case managers usually become involved with a TBI case when it becomes clear that the discharge plan will be complex and complicated. The exception is the case manager who becomes involved in the coordination of services and medical care for a patient who has problems from a concussion beyond 6 to 12 months. Almost half of all individuals recovering from a concussion experience symptoms afterwards, but fewer than 10% experience disabling symptoms that actually intensify instead of resolving. To help the individual return to work or school, a case manager can facilitate evaluation by a specialist for diagnostic studies, neuropsychologic testing, and treatment. Testing may include the following:

• Evoked potentials
  
• SPECT or MRI imaging
  
• EEG with a 24-hour Holter monitor or a sleep EEG
  
• Audiologic evaluation
  
• Brainstem auditory evoked responses (BAERs)
  
• Transcranial Doppler (TCD)
  
• Nocturnal penile tumescence (NPT) monitoring

The goals of cognitive and behavioral rehabilitation after TBI are to enhance the patient’s capacity to process and interpret information and to improve his or her ability to function in all aspects of family and community life.²⁷ Restorative training focuses on improving a specific cognitive function, whereas compensatory training focuses on adapting to the presence of a cognitive deficit. The case manager should be aware that these recommendations include the following:

• Comprehensive, interdisciplinary rehabilitation treatment provided by a diverse team of experienced professionals that contains individualized tailored interventions that are both restorative and compensatory
  
• Computer-assisted strategies for attention, memory, and executive skills
  
• Compensatory devices (e.g., memory books and electronic paging systems) to improve cognitive function
  
• Teaching that uses sequenced and repetitive practice
  
• Psychotherapy to treat depression and the loss of self-esteem and cognitive dysfunction
  
• Individual and family / significant other psychotherapy for emotional support, self-assessment, reduction of denial, and improvement in interpersonal skills related to family members and the community
  
• Pharmacologic agents for affective and behavioral disturbances associated with TBI, with additional monitoring provided for detrimental side effects
  
• Behavior modification for personality and the behavioral effects of TBI
  
• Short- and long-term vocational rehabilitation and job coaching for individuals who will return to work (a “return to work” is considered prognostic of successful rehabilitation)
  
• Special education services for students who will return to the classroom
  
• Structured adult education for nutritional support
  
• Music and art therapy, therapeutic recreation, acupuncture and other alternative approaches

The case manager assessment includes a thorough patient assessment and chart review, interviews with family members and members of the health care team and, in many instances, an evaluation of the patient’s home. Placement of the patient following hospitalization and inpatient rehabilitation is the first consideration. If the patient is in a persistent vegetative state or coma, a decision must be made for institutional care versus home care with 24-hour caregivers.

Case managers should be aware and review the 2000 Medical Rehabilitation Standards for Brain Injury Programs of the Commission on Accreditation of Rehabilitation Facilities. These standards cover rehabilitation programs, outpatient medical rehabilitation, home and community-based programs, long-term residential services, and vocational services. Through a case management approach, the CARF program addresses the following²⁴:

• Ongoing access to information about the services available within a coordinated continuum of care
  
• Movement through the brain injury continuum of care
  
• Conservation of funding to meet lifelong needs
  
• Linkages with the community
  
• Family / support systems and the community
  
• Education of the person served, his or her family / support systems, and the community
  
• Facilitation of opportunities for interaction with individuals with similar activity limitations

The most prevalent impairment subsequent to a brain injury are severe cognitive deficits. With this awareness, a plan of care is developed with the health care team, patient and family members, and approval of the payer. Realistic short- and long-term measurable goals are included. Once approval has been received, the case manager implements the plan in a cost-effective manner to ensure continuity of care, monitors patient compliance, and includes patient and family satisfaction with the plan. The goal is functional restoration, compensatory training, prevention of complications, and avoidance of rehospitalization. The responsibility of the case manager may also include provisions for patient transportation, physician visits, and therapy sessions. Follow-up case management includes arranging for caregivers with appropriate home visits to provide wound care and dressing changes, medications, and nutritional evaluation, with frequent written reports from all members of the home health team.

Issues for the case manager to address include inappropriate client behavior that may interfere with social relationships and interpersonal relationships that could cause rejection by the spouse, relatives, friends, and associates. Sexuality and inappropriate sexual behavior can be another disturbing consequence of TBI. The use and abuse of drugs and alcohol may have contributed to the cause of the head injury and may also be a significant problem after discharge from the hospital or rehabilitation center. The need for a very consistent and structured lifestyle may create problems within a family unit. After TBI some individuals experience altered sleep patterns (e.g., napping versus sleeping at night, wandering during the night) that require 24-hour supervision. Quality of life issues are some of the more difficult challenges in case management.

The patient and family should be provided with a 24-hour telephone number to call for emergencies following TBI (with the understanding of what constitutes a medical emergency). The consequences of TBI may be lifelong, and the patient may require lifelong services. Preventing a second TBI requires care and injury prevention by all members of the team (and teaching for the family).

CONCLUSION

TBI affects 2 million people per year. The cost is staggering, and the outcome can be devastating. In a time when allocation of limited resources is a growing reality, the care of this population needs to be continually reevaluated, organized, cost-effective, and individualized. Nursing care of the patient with TBI is both challenging and complex. Clinicians must carefully consider how interventions affect patients. Care of the TBI patient is an area in which patient condition and response to care truly dictate the methods of nursing practice. Advanced technologic interventions, new pharmacologic agents, and research have improved the diagnosis and treatment of TBI. This has resulted in an increase in the number of survivors and has helped to reduce disability significantly. As scientists develop modalities for neuronal regeneration and repair, neuroscience nurses will play a key role in the patient’s return to functional independence.

E-mail: info@aacn.org

http://www.aacn.org

E-mail: info@AANS.org

http://www.neurosurgery.org/aans

E-mail: info@aann.org

http://www.aann.org

http://www.aast.org

http://www.facs.org

American Trauma Society
(800) 556-7890

http://www.amtrauma.org

Brain Injury Association
105 N. Alfred Street
Alexandria, Virginia
(800) 321-7037

http://www.biausa.org

Brain Trauma Foundation
523 East 72nd Street
New York, NY 10021
(212) 772-0608

http://www.braintrauma.org

Copies of their publications are available:

Epilepsy Foundation of America
(800) EFA-1000

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