Running head: TBI
Traumatic Brain Injury
Makenzie Welch
Colby-Sawyer College Traumatic Brain Injury
The brain is the most vital organ in the human body for survival. It is the main control center, which is responsible for everything from breathing and sleeping to walking and running. The brain also controls the body’s heart rate, immune response, and learning abilities (Perkins, 2015). At a more in-depth level, the brain works with the nervous system to send and receive messages. Neurons are responsible for communicating with other nerve cells, muscle cells, and gland cells (Perkins, 2015). Each cell receives information that drives the body to complete its specific function (Perkins, 2015). It is evident that the brain is a very powerful organ. However, it is also very fragile. When a person experiences an injury to the head, they are at increased risk of experiencing a traumatic brain injury (TBI), which can be life-threatening and irreversible. The Department of Defense and the Department of Veterans Affairs define a TBI as any traumatically-induced structural injury or physiological disruption of brain function (Lump, 2014). This is due to an external force that causes a change in level of consciousness, a neurologic deficit, or an alteration in mental status (Lump, 2014).
The intent of this paper is to discuss the different classifications of TBI and to examine the pathophysiology. This paper will address specific signs and symptoms, assessment strategies, complication prevention, and discharge teaching.
Background
On average, there are close to 5.3 million Americans who are currently living with disabilities as a result of a TBI (Zink & McQuilian, 2005). The incidence of TBIs is highest among young adults aged 15 to 24 and adults over the age of 75 (Zink & McQuilian, 2005). Males are two times more likely than females to sustain a TBI, especially during the 15 to 24 age range, due to risk-taking behavior and sport injuries (Zink & McQuilian, 2005). Sport injuries cause an estimated 1.6 million to 3.8 million TBIs a year (Clark & Guskiewicz, 2016). Adults over the age of 75 experience TBI due to falls, which usually occur in their homes. In any given year, there are 108 to 332 new cases of TBI admitted to hospitals per 100,000 people (Rosenfeld et al., 2012). Of these admissions, 39% of the patients die from their injuries and 60% have unfavorable outcomes on the Glasgow Outcome Scale (Rosenfeld et al., 2012). Those who survive a TBI have a lower life expectancy and will die three times faster than the general population (Rosenfeld et al., 2012). During this short amount of time, most survivors face prolonged care and rehabilitation. They experience long-term physical, cognitive, and psychological disorders, which can affect their independence, relationships, and employment (Rosenfeld et al., 2012).
Classifications of TBIs
TBIs are measured based on their severity, which is determined by the Glasgow Coma Scale (GCS) and their duration of loss of consciousness. The GCS evaluates the best eye-opening response, the best verbal response, and the best motor response (Zink & McQuilian, 2005). The lowest score an individual can receive is three, while the highest score a person can receive is 15 (Zink & McQuilian, 2005). A score of 15 indicates that the individual is fully alert and oriented, whereas a score of three indicates severe impairment (Zink & McQuilian, 2005).
A mild TBI is represented with a GCS score of 13 to 15. The patient may experience a mental status change or loss of consciousness for less than 30 minutes (Lump, 2014). This compares to a moderate TBI which has a GCS score of nine to 12 and symptoms lasting for 30 minutes to six hours (Lump, 2014). Finally, a GCS score of three to eight indicates that the patient sustains a severe TBI and may have symptoms that last for more than six hours (Lump, 2014).
Pathophysiology
Etiology
TBI can be caused by many different types of injuries, all of which result in damage to brain cells. A penetrating injury occurs when an object breaks through the skull and enters the cranial vault, causing damage to the protective meningeal layers, cerebral blood vessels, and brain tissue (Zink & McQuilian, 2005). Gunshot wounds are the most common type of penetrating injuries (Zink & McQuilian, 2005). They are the deadliest cause of TBI in patients under the age of 35 (Zink & McQuilian, 2005). A contact phenomena, or non-penetrating injury, occurs when an object strikes the head, such as a baseball bat or the dashboard of a vehicle in a motor vehicle crash. This can lead to a skull fracture, concussion, cerebral contusion, or intracranial hemorrhage (Zink & McQuilian, 2005). During an acceleration-deceleration injury, the head’s velocity quickly increases, causing the brain to strike the skull. The brain’s velocity then decreases during deceleration, which causes the brain to strike the skull on the opposite side (Zink & McQuilian, 2005). The rapid coup-countercoup injury causes tearing of neuronal tissue and cerebral blood vessels. Finally, a rotational acceleration-deceleration injury is caused by nonlinear acceleration-deceleration forces, which results in a twisting motion inside the skull (Zink & McQuilian, 2005). Maximal stress is induced on the brain, which can lead to torsion and shearing of neuronal tissue and vascular disruption (Zink & McQuilian, 2005).
Risk Factors
TBIs are caused by several different types of traumas. The likelihood of sustaining a TBI increases with age. As a person ages, they become more unstable on their feet and they are more likely to experience a fall (Ignatavicius & Workman, 2016). Inadequate lighting and throw rugs are environmental hazards that can increase the risk of a fall in older adults (Ignatavicius & Workman, 2016). Other risk factors include not partaking in safe practices, including wearing a seatbelt while in a car or wearing a helmet while riding a bike (Ignatavicius & Workman, 2016).
Cellular and Tissue Disruption
A TBI is a type of injury that evolves through different phases, which causes the pathophysiology to change over time.
Primary injury. The first phase of a TBI is primary injury, which occurs at the time of injury. A primary injury can be either penetrating or non-penetrating. During a penetrating injury, like a gunshot to the head, an object breaks through the skin and the skull, causing direct impact (Lump, 2014). A non-penetrating injury is different because it results from the direct impact of neuronal tissue against the skull or bone. For example, during a motor vehicle crash, a person’s head may hit the dashboard, which causes rapid deceleration to the body and causes the brain to strike the inside of the skull. When the brain initially strikes the inside of the skull, the person experiences coup, which means there is an injury at the site of impact (Lump, 2014). Countercoup happens exactly 180 degrees from the site of the impact as the brain hits the skull and bounces back in return, causing another injury. This complete motion may also be referred to as whiplash (Lump, 2014). In this pathophysiology paper, the focus will be on non-penetrating injuries and how the rapid acceleration and deceleration leads to many other pathophysiological problems (Lump, 2014).
Axonal damage. The mechanical effects of rapid acceleration and deceleration are the primary cause of injury producing strains and distortion within the brain (McCance & Huether, 2015). Notably, the brain is attached to the spinal cord. This produces an issue when the head is forced in a direction that the rest of the body is not, resulting in stretching and tearing of nerve fibers. The stretching and tearing causes axonal damage (McCance & Huether, 2015). The closer the axonal damage is to the brainstem, the more severe the effects are. For example, injuries located more peripheral to the brainstem cause extensive cognitive and affective impairments. The axonal damage reduces the speed of information processing and can disrupt a person’s attention span (McCance & Huether, 2015). Due to each axon being so small, an electron microscope must be used to see axonal damage, and there must be numerous axons or actual tissue tears (McCance & Huether, 2015). When this happens, small blood vessels are torn apart, causing a hemorrhage or bleeding in the brain. Over the next several hours to days after the initial injury, the axonal damage becomes more apparent (McCance & Huether, 2015).
There are three different levels of axonal damage, mild, moderate, and severe (McCance & Huether, 2015). In mild axonal injury, death is uncommon, but a posttraumatic coma may last from six to 24 hours following the injury. The person may experience a prolonged period of stupor or restlessness and display decerebrate or decorticate posturing (McCance & Huether, 2015). In moderate axonal injury, actual tearing of some axons in both hemispheres occurs. The patient usually suffers from a basal skull fracture. Patients tend to experience a prolonged coma, lasting over 24 hours due to their GCS score, which averages between four and eight (McCance & Huether, 2015). Unfortunately, recovery is often incomplete and the patient may remain unconscious for days or weeks (McCance & Huether, 2015). The patient tends to experience a long period of posttraumatic anterograde and retrograde amnesia, along with affect and mood changes and deficits in memory, selective attention, and language difficulties. Finally, severe axonal injury involves mechanical disruption of many axons in both the cerebral hemispheres and axons extending to the diencephalon and brainstem (McCance & Huether, 2015). Usually, an individual with severe axonal injury has an initial GCS score of three (McCance & Huether, 2015). After the immediate injury, increased intracranial pressure (ICP) may appear in the following four to six days, which may lead to pulmonary complications and cognitive system deficits. At this state, the patient may have compromised coordinated movements and may struggle with verbal and written communication (McCance & Huether, 2015).
Secondary injury. Secondary brain injury can begin immediately following the primary injury and can continue for hours or days. Hypoxia, which means decreased oxygen, and hypoperfusion, which means decreased blood flow, are two of the leading contributors to secondary brain injury (Lump, 2014). Both hypoxia and hypoperfusion result in decreased cerebral perfusion pressure, which indicates that the gradient required to push blood towards the brain is not being maintained. If blood flow to the brain is not being maintained then the brain will eventually become ischemic, resulting in dysfunctional tissue (McCance & Huether, 2015). Once a brain injury occurs, cerebrovascular autoregulation, which controls cerebral perfusion pressure is impaired, leading to alterations in carbon dioxide reactivity (McCance & Huether, 2015).
During the secondary injury, a variety of excitatory neurotransmitters are released, including glutamate and aspartate (McCance & Huether, 2015). The release of these neurotransmitters causes a calcium and sodium influx, which is neurotoxic or excitotoxic. Excitotoxicity is defined as the process by which neurons are damaged and killed by the over-activation of receptors for glutamate (McCance & Huether, 2015). Normally, glutamate is absorbed by astrocytes, which convert it into glutamine (McCance & Huether, 2015). The glutamine is then delivered back to neurons as an alternative source of energy (McCance & Huether, 2015). When glutamate is being produced excessively due to the secondary injury, the astrocytes cannot remove all the glutamate from the extracellular space (McCance & Huether, 2015). The extra glutamate needs some place to go. Therefore, it binds to neuronal receptors, which cause the influx of calcium and sodium and the efflux of potassium (McCance & Huether, 2015).
The influx of calcium leads to mitochondrial failure, anaerobic metabolism, lactic acid production, and increased levels of reactive oxygen species and phospholipase, along with an increased level of other enzymes (McCance & Huether, 2015). Reactive oxygen species and phospholipase damage proteins, phospholipid component, and organelle membranes. This causes cell swelling, vacuolization, and inevitability cell death (McCance & Huether, 2015). Specifically, the influx of the sodium attracts water, which leads to cytotoxic edema in neurons, astrocytes, and microglia regardless of the integrity of the vascular wall (McCance & Huether, 2015). The new edema increases ICP which, once again, contributes to tissue hypoxia and cerebral ischemia (McCance & Huether, 2015).
Signs and Symptoms
TBIs have a variety of physical, psychological, and cognitive symptoms, which vary depending on the severity of the injury. Mild TBIs result in headaches, confusion, lightheadedness, dizziness, fatigue, blurred vision, and ringing in the ears (Kirwan, 2013). A patient with a moderate to severe TBI will experience prolonged or worsening headaches, repeated nausea and vomiting, weakness or numbness in the extremities, loss of coordination, increasing confusion, agitation, restlessness, and convulsions or seizures (Kirwan, 2013). All severities experience mood, behavioral, and sleep changes, along with depression, memory and concentration difficulties, slowed thinking, and difficulty finding words (Kirwan, 2013). The major difference between mild, moderate, and severe TBIs are how long the symptoms last and how intense the patient experiences them (Kirwan, 2013). For example, a patient with a severe TBI may experience a constant headache, while a person with a mild TBI may experience intermittent headaches (Kirwan, 2013).
Inflammation
Inflammation in the brain is caused by both the primary and secondary injury. Inflammation may start immediately and last for several weeks. While inflammation is necessary for the healing of wounds, an over-reactive response leads to blockage of microvasculatures, which are the smallest blood vessels in the brain (McCance & Huether, 2015). For inflammation to take place, there is a release of inflammatory cytokines, proteases, free radicals, and prostaglandins, which in excess alter the blood-brain barrier and cause vasoconstriction. Vasoconstriction then leads to brain edema, increased ICP, reduced cerebral perfusion and ischemia (McCance & Huether, 2015). Ischemia is irreversible, therefore, as more brain cells suffer from it the more brain function is lost (McCane & Huether, 2015).
Increased Intracranial Pressure (ICP)
Inflammation and edema lead to increased ICP, which reflects the pressure of the cerebral fluid, brain tissue, and blood (Zerfoss, 2016). If edema is severe, it must be controlled or it may lead to death. The increased ICP causes the structures inside the brain to become displaced and squeezed together, which results in them no longer being able to function properly (Zerfoss, 2016). Cognitive, emotional, and behavioral symptoms may appear and patients may experience aphasia and amnesia. Mental clouding and difficulty making decisions are also common with a TBI (Zerfoss, 2016). Besides cognitive problems, emotional changes, including mood swings, irritability, depression, and anxiety, may also occur (Auday & Abrahamsen, 2014).
Post-Concussion Syndrome
When individuals experience more than one TBI they are at risk for post-concussion syndrome. This leads to headaches, irritability, dizziness, lack of concentration, fatigue, anxiety, light and noise sensitivity, and impaired memory (Auday & Abrahamsen, 2014). Post-concussion syndrome typically occurs seven to ten days after the initial injury and it may last from a few weeks to a year (Davis, 2014). An individual may notice a decrease in functional status including difficulty with activities of daily living, school or work-related activities, leisure and recreational activities, and social interactions (Davis, 2014).
Assessment
History
Obtaining a history from a patient who experiences a TBI may be difficult due to confusion or amnesia that they may be experiencing. Patients may even be unconscious. Therefore, if the TBI was unwitnessed, no history can be given. The most important information to obtain is where, how, and when the injury happened, and whether the patient lost consciousness or not. It should also be determined if the patient has a history of alcohol or drug use because these substances may interfere with the baseline assessment (Ignatavicius & Workman, 2016).
The most comprehensive type of assessment for a TBI is a neuropsychological assessment, which is performed by a clinical neuropsychologist. The neuropsychologist will review the patient’s chart and determine the cause of injury, history of previous TBIs, and if there are any complicating factors (Franzen, 2000). The presence of post-traumatic amnesia should be determined because there is a parallel relationship between length of post-traumatic amnesia and a worsening outcome (Franzen, 2000). Essential areas of neurobehavioral functions, including attention and memory, are evaluated. Attention and memory are the focus of the assessment because they provide important information needed to continue care and to plan for discharge (Franzen, 2000).
Another important aspect of the neuropsychological assessment is the change in emotional reactions after the injury. Significant depression, anxiety, and apathy will affect the patient’s plan of care and may lead to specific controls in the environment to promote healing (Franzen, 2000).
Physical Examination
Every brain injury is different and can lead to different complications. The patient should immediately be assessed for signs of increased ICP, hypotension, hypoxia, and hypercarbia. The earlier these manifestations are addressed, the more likely the providers can prevent or treat life-threatening complications (Ignatavicius & Workman, 2016).
Airway and breathing pattern. While the patient should be assessed for complications, the highest priority assessment should be the patient’s airway, breathing, and circulation. When the brainstem is injured, patients may experience changes in their breathing pattern, including central neurogenic hyperventilation, apnea, or Cheyne-Stokes respirations. If patients can no longer support their own respirations, mechanical ventilation may be needed (Ignatavicius & Workman, 2016).
Spinal cord injuries. Patients who experience a TBI should be assessed for spinal cord injuries, especially the older adult population. Patients are usually transported to the hospital with a cervical collar on to prevent new and secondary spine injuries. Spinal precautions should be maintained until radiography provides evidence that there are no injuries to the cervical, thoracic, and lumbar spine. If there is an injury to the cervical spine, the patient should remain on spinal precautions until future notice (Ignatavicius & Workman, 2016).
Vital signs assessment. When a person experiences a TBI, the body goes into autoregulation. This decreases the ability of the body to modify the systemic pressure to ensure adequate blood flow to the brain. The patient’s blood pressure and pulse should be monitored for signs of increased ICP. Cushing’s triad, which includes severe hypertension, irregular respirations, and bradycardia, are the last manifestations of increased ICP. In opposition, if severe hypotension and tachycardia occur, the patient is experiencing hypovolemic shock. Hypovolemic shock is caused by severe blood loss. This inhibits the heart’s ability to pump blood throughout the body. Therefore, the patient should also be assessed for bleeding (Ignatavicius & Workman, 2016).
Neurologic assessment. A decrease or change in the level of consciousness is one of the first signs of deteriorating neurologic status. Early assessment of level of consciousness should include noticing behavior changes and disorientation. Pupils should be assessed with a bright light to determine reactivity. Pinpoint or nonresponsive pupils indicate a brainstem dysfunction at the level of the pons, which is life-threatening. In contrast, patients with nonreactive and dilated pupils are also experiencing a poor prognosis, but this is indicative of an injury further up the brainstem. If a patient is awake and alert, the provider should ask the patient to participate in cranial nerve tests to determine if any nerves are not intact (Ignatavicius & Workman, 2016).
The patient should also be monitored for late signs of increased ICP. These include a severe headache, nausea, vomiting, and seizures. Papilledema, which is increased blood flow to the optic disc, is a definite sign of increased ICP (Ignatavicius & Workman, 2016).
Motor loss appears on the opposite side of the body to which the injury occurred. Injuries to the brain may cause loss of balance, decreased or increased muscle tone, weakness, or complete absence of muscle tone. Ears and nose should be observed for any signs of cerebrospinal fluid leakage. Bruises behind the ears usually indicate a fracture of the middle cranial fossa of the skull (Ignatavicius & Workman, 2016).
Bedside examinations. Depending on the severity of the TBI, different tests should be performed to evaluate the patient’s brain function and extent of the injury. For all patients, a brain computerized tomography scan should be performed to diagnose the intracranial injury and determine if there is a need for surgery (Zink & McQuilian, 2005). If there is not a need for surgery, and the patient is stable, bedside tests should be administered to evaluate the patient’s memory and attention span. For example, verbal memory can be evaluated through the Hopkins Verbal Learning Test, or the California Verbal Learning Test (Franzen, 2000). In both tests, the patient is required to learn a string of words in any order over multiple trials. The provider waits 20 minutes before determining if the recall is available (Franzen, 2000).
Attention span can be evaluated through the Digit Span subtest from the Wechsler Adult Intelligence Scale. This test requires the patient to repeat a string of numbers in order or in reverse order. The numbers are only presented once; therefore, the test is determining vigilance and maximum span of apprehension (Franzen, 2000). The tests are scored in a standardized manner and results are interpreted in terms of what consequences there might be for changes in behavior (Franzen, 2000). Care and discharge planning are also based on the scores (Franzen, 2000).
Psychosocial assessment. Disabilities from a mild TBI may last for up to a year after the injury, while disabilities from a severe TBI may last a lifetime. The most common changes in a person include personality changes, depression, and memory loss. The ability to concentrate, communicate, and understand language may also be altered. These changes lead to difficulties in social interactions and relationships with family and friends (Ignatavicius & Workman, 2016).
Nursing Diagnoses
Ineffective Breathing Pattern Related to Increased ICP or Brain Stem Injury
The provider of a patient with a TBI should be consistently monitoring respiratory rate, depth, and pattern. Any abnormalities including Cheyne-Stokes or periods of apnea should be reported. If the patient’s respiratory status diminishes, ventilation and intubation should occur. The provider should obtain frequent arterial blood gases to ensure that oxygen is above 100 mm Hg and carbon dioxide is between 35 and 45 mm Hg (Nettina, 2006).
Outcomes should include respirations of 18 breaths per minute with regular rate and rhythm. The patient should also maintain an oxygen level above 100 mm Hg and a carbon dioxide level between 35 and 45 mm Hg (Nettina, 2006).
Ineffective Tissue Perfusion Related to Increased ICP
The patient should maintain a systolic blood pressure above 90 mm Hg to ensure cerebral perfusion. If tachycardia and hypotension are present, the patient should be evaluated for a source of bleeding. The patient may experience sympathetic storming, which is an abnormal stress response to trauma. This includes alterations in level of consciousness, along with hypertension, hyperthermia, tachycardia, and tachypnea. Providers should monitor for these signs and identify triggers and effective treatment (Nettina, 2006).
Outcomes should include the patient having no signs of increased ICP or change in level of consciousness. Ideally, the patient will avoid sympathetic storming, but effective management should take place immediately if storming occurs (Nettina, 2006).
Imbalanced Nutrition Related to Compromised Neurologic Function and Stress of Injury
Nutritional support should begin as soon as possible after injury to provide the body with adequate energy for healing. Enteric feedings can start once bowel sounds are present. To prevent aspiration, the head of the bed should be elevated to at least 30 degrees during and after feedings. If a person cannot tolerate nasogastric feedings, nutrition can be obtained through intravenous hyperalimentation. Oral feeding may begin when adequate swallowing mechanisms are present. To determine if the patient is receiving adequate nutrition, blood glucose levels should be monitored frequently (Nettina, 2006).
Outcomes should include well-tolerated tube or enteric feeding. The patient should maintain a blood glucose level of less than 100 mg/dl before meals, and less than 140 mg/dl after meals (Nettina, 2006).
Goals of Therapy and Reduction of Complications
The main goal of taking care of a patient with a TBI is to prevent complications and to reduce the risk of increased ICP.
Seizure Prevention
Standard seizure precautions, including seizure pads and suction equipment, should be implemented with all patients who experience a TBI. Post-traumatic seizures may exacerbate secondary brain injury by increasing ICP, altering blood pressure, and triggering excessive neurotransmitter release (Zink & McQuilian, 2005). Seizure activity should be assessed daily, and blood levels should be monitored for the therapeutic range of anti-seizure medications (Zink & McQuilian, 2005).
Adequate Nutrition
When a patient experiences a TBI, his or her body goes into a hypermetabolic state, which requires more calories to prevent malnutrition (Zink & McQuilian, 2005). After a TBI, nitrogen excretion rises, and at least 15% of the caloric intake should be provided as proteins (Zink & McQuilian, 2005). Feedings should be initiated within 72 hours of the injury so the patient can have the full caloric replacement by day seven. Blood glucose levels should be kept stable because hyperglycemia and hypoglycemia can exacerbate secondary brain injury (Zink & McQuilian, 2005).
Pulmonary Care
Patients are at risk for many pulmonary complications, including acute respiratory distress syndrome, pneumonia, atelectasis, and pulmonary embolus. To decrease the risk of these complications, pulmonary hygiene and aspiration precautions should be implemented. Excessive suctioning may lead to neurologic compromise; therefore, providers should take the necessary steps to prevent this. These steps include hyperoxygenating the patient before and after suctioning, not suctioning for longer than ten seconds, and using the fewest catheter passes necessary (Zink & McQuilian, 2005).
Monitor Fluid and Electrolytes
When a TBI occurs, the pituitary gland may be injured or compressed due to edema. This compression or injury can lead to diabetes insipidus and syndrome of inappropriate antidiuretic hormone. Due to cerebral edema, there is a shift in fluids and electrolytes. The patient may experience fluid overload. Fluid administration should be titrated to optimize volume resuscitation and minimize brain swelling and elevation in ICP (Ignatavicius & Workman, 2016).
Disease Management
Managing a TBI must start with an initial trauma assessment, which begins with the rapid assessment of airway, breathing, circulation, and disability (Zink & McQuilian, 2005). The provider should establish a patent airway to allow adequate ventilation and supporting circulation (Zink & McQuilian, 2005). A patient with a GCS score below nine, which indicates a severe TBI, should be intubated immediately to allow mechanical ventilation. Once a patient’s hemodynamics and respiratory status are stabilized, an ICP monitoring device should be inserted (Zink & McQuilian, 2005). A ICP monitoring device can be placed in the epidural, subdural, subarachnoid, parenchymal, or ventricular of the brain. Potential risks include catheter misplacement, infection, or hemorrhage (Bratton et al., 2007). After inserting the ICP monitoring device, the providers can calculate cerebral perfusion pressure. One goal of treatment should be to keep the cerebral perfusion pressure greater than 60 mm Hg to ensure adequate brain oxygenation and blood flow (Zink & McQuilian, 2005). Typically, patients begin to show signs of neurological deterioration when their ICP is greater than 20 to 25 mm Hg, therefore ICP should be kept under 20 mm Hg (Bratton et al., 2007).
Treatment Options and Interventions
A TBI cannot be cured or treated immediately. Many interventions can be initiated once the trauma happens to decrease the chance of complications. TBI patients benefit from oxygenation to compensate for hypoxemia. Along with hypoxemia, patients experience hypotensive episodes therefore a systolic blood pressure above 90 mm Hg should be maintained with fluids or blood products. It is important to determine a specific threshold tailored to the individual to determine acceptable values for oxygenation and blood pressure support (Bratton, et al., 2007).
To prevent continuous brain edema and refractory ICP management, the use of hypothermia has been widely studied. Therapeutic hypothermia is the intentional lowering of the body temperature to reduce tissue damage in the central nervous system (Anderson, Gazmuri, Marin, Regueria, & Rovegno, 2015). There are two ways to induce and maintain hypothermia, external and internal. External cooling methods include using cooling blankets, ice packs, cold-water immersion, cold-saline gastric lavage, and cooling helmet devices. Limitations for this method include intense skin vasoconstriction and slow onset of desired temperature with unpredictable temperature maintenance (Anderson, et al., 2015).
Internal cooling methods include using central venous catheters to infuse cool saline or directly reducing blood temperature by convection. This is the easiest and most effective method to induce hypothermia. Hypothermia induction should be started immediately to decrease neurologic damage (Anderson, et al., 2015). During hypothermia, the patient’s core temperature should be monitored closely (Anderson, et al., 2015).
Hypothermia-related complication include cardiac arrhythmias, coagulopathy, hypokalemia, and infections (Anderson, et al., 2015). Specifically, internal cooling methods may cause catheter-related infections, deep venous thrombosis, and vascular dissection. Shivering may cause increase in systemic and cerebral energy consumptions which may increase ICP. Sedation and neuromuscular blockades should be used in conjunction to prevent shivering (Anderson, et al., 2015).
Medications. While there is no medication that can cure a TBI, medications can help with symptom treatment. Mannitol, an osmotic diuretic, should be given to treat cerebral edema. Mannitol works by pulling water out of the extracellular space of the edematous brain tissue, and it has the greatest effect when pushed intravenously (Ignatavicius & Workman, 2016). Mannitol’s presence in the blood vessels of the brain creates a force that draws the edematous fluid from the brain to the blood (Burcham & Rosenthal, 2016). With this force, there is no risk of increasing cerebral edema because mannitol cannot exit the capillary beds of the brain (Burcham & Rosenthal, 2016). Common side effects that may occur with mannitol include, headache, nausea, and vomiting (Burcham & Rosenthal, 2016). The patient should also be monitored for fluid and electrolyte imbalance (Burcham & Rosenthal, 2016).
Furosemide, a loop diuretic, should be used in conjunction with mannitol to enhance the therapeutic action of mannitol by decreasing blood volume, edema, sodium uptake, and production of CSF. Furosemide acts in the ascending limb of the loop of Henle, to block reabsorption of sodium and chloride (Burcham & Rosenthal, 2016). Furosemide is a powerful drug. It is generally reserved for situations that require rapid mobilization of fluids (Burcham & Rosenthal, 2016). Common sides effects include excessive sodium, chloride, and water loss. Patients should be monitored closely for signs of dehydration (Burcham & Rosenthal, 2016). Furosemide can also cause hypotension, hypokalemia, and ototoxicity (Burcham & Rosenthal, 2016). When the patient is on a diuretic, intake and output should be monitored closely (Ignatavicius & Workman, 2016).
Agitation and ventilator asynchrony may be managed with sedative agents like dexmedetomidine and propofol. Due to their short duration of action, these medications can be stopped daily to reassess neurologic status. If a patient has increased ICP, it is not recommended to stop sedative agents until ICP is lowered (Ignatavicius & Workman, 2016).
Opioids, including morphine sulfate or fentanyl can be used to control pain, and agitation due to ventilator use. Morphine has strong effects on blood pressure and heart rate; therefore, fentanyl is the preferred medication (Ignatavicius & Workman, 2016).
Medications for increased ICP. The most important factor with increased ICP and a TBI is to have adequate blood flow and perfusion to the brain. The patient may require vasopressors to maintain a systolic blood pressure above 90mm Hg (Zerfoss, 2016). When a vasopressor is given, blood vessels constrict to push more blood to the needed area.
Hypertonic saline, like three percent normal saline can be given to dehydrate the endothelial cells and erythrocytes in the blood vessels. This increases the diameter of the vessels, allowing plasma volume expansion and improved blood flow. One risk factor of hypertonic saline is that it may lead to central pontine myelinolysis when given to patients with preexisting chronic hyponatremia. Central pontine myelinolysis is caused by severe damage to the myelin sheath of the nerve cells in the brainstem (Bratton et al., 2007). Hyponatremia must be ruled out before hypertonic saline can be given (Bratton et al., 2007)
In contrast, as a stress response to a TBI, a patient may experience hypertension, which would require the nurse to administer an antihypertensive agent. Some hypertensive agents, including nitroglycerin, nitroprusside, and nicardipine, may cause side effects that lead to ICP. Therefore, monitoring ICP is a balancing act (Zerfoss, 2016).
Discharge and Patient Teaching
Rehabilitation
Patients who suffer from a mild TBI may be sent home from the Emergency Department with instructions to rest and monitor for a change in neurological status. Those who experience a severe brain injury will require ongoing rehabilitation in a specialized brain injury rehabilitation center. The goal of rehabilitation is to have the patient reach their highest level of functioning (Ignatavicius & Workman, 2016). Some patients may require speech rehabilitation, while other patients may require fine motor skills rehabilitation. Due to each TBI being different, every plan of care will be specific towards the patient.
Emotional Support
Most patients who experience a moderate or severe TBI are discharged with many physical and emotional changes. These changes may be hard on the family, which can lead to struggles with coping to a new lifestyle. The primary caregiver may experience depression and feelings of loneliness. He or she may also experience anger towards the patient. Family members should attend local brain injury support groups and have regular respite care (Ignatavicius & Workman, 2016).
Self-Management Education
The teaching plan for the patient and family should include instructions about seizure safety at home and ways to adapt to sensory dysfunction. The family should be taught to encourage the patient to participate in activities he or she enjoys, as tolerated. Appointments for regular follow-up visits with therapists and other healthcare providers should be attended. Patients with personality and behavior problems respond better in a structured environment. The family should develop a home routine that provides structure and consistency (Ignatavicius & Workman, 2016).
Conclusion
TBIs can vary in both severity and the effect on the patient’s life. Through immediate treatment and careful monitoring, most patients can adapt to a new lifestyle or continue with their lives. Close to 5.3 million Americans are currently living with disabilities due to TBI (Zink & McQuilian, 2005). This has a drastic influence on both the patients and their families. The patient should be monitored for complications, and effective treatment must be utilized when complications arise.
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