This course is directed at practicing nurses to assist them when caring for the patient with a traumatic brain injury (TBI). The course will provide a general overview of TBI. The incidence, risk factors, causes, treatment options and prevention will be discussed. The course will also discuss sports related concussion including its assessment, management and long-term complications.
After completing this course, the learner will be able to:
Traumatic brain injury (TBI) is a major cause of death and disability. In the United States, TBIs affects 1.7 million people every year and is responsible for about 40% of all deaths from acute injuries (CDC, 2013). Annually, 200,000 victims of TBIs need hospitalization, and 1.74 million people need at least one day off after TBI (Dawodu, 2013). In 2005, it was estimated that 1.1 percent of those in the United States are living with long-term disability from TBI (Zaloshnja, Miller, Langlois, & Selassie, 2008).
TBI is sudden trauma that damages the brain. Damage is either focal, in one area, or diffuse. When the head hits an object, and the skull does not break, the injury is considered a closed head injury. When the skull breaks and the object penetrates brain tissue than the injury is considered a penetrating injury.
About 75% of TBIs are mild. Repeated TBIs over a period of time can lead to multiple problems such as a cumulative cognitive or neurological deterioration. TBIs have many complications including an increased risk of dementing illnesses such as Alzheimer's disease, Parkinson's disease and seizures (CDC 2012).
Falls are the leading cause of TBI, accounting for 35.2 percent of TBIs in the United States (CDC, 2013). Falls lead to 61 percent of all TBIs in those over the age of 65. They also account for about 50 percent of TBIs in children under 15 years-old.
Motor vehicle accidents are the second leading cause of TBI, accounting for 17.3 percent of all TBIs. Due to the violent nature of many motor vehicle accidents, they result in the highest percentage of deaths from TBI (CDC, 2013).
Running into a stationary object or getting struck in the head is another common cause of TBI, which accounts for 16.5% of TBIs (CDC, 2013). Other causes of TBI include: violence, assaults, firearms and blasts (particularly among military personal).
Sports related injuries account for a large number of TBIs every year. TBIs commonly occur in sports such as football, boxing, ice hockey, soccer and rugby. Every year in the United States there are 1.6 to 3.8 million sports related concussions. (McKee, Cantu, Nowinski, Hedley-Whyte, Gavett, Budson, Santini, Lee, Kubilus, & Stern, 2009).
Rates of concussion are about six times higher in competition than during practice. American football (47.1% of all concussions) accounted for the most concussions. Female soccer (8.2%) accounted for the second most concussions followed by male wrestling (5.8%) and female basketball (5.5%). The most common way concussions were obtained were from player-to-player contact accounting for 7 out of 10 concussions followed by player-to-surface contact accounting for 17.2 percent of concussions. Most athletes (55.3%) returned to play in 1 to 3 weeks with 22.8 percent returning in under 7 days (Marar, McIlvain, Fields, & Comstock, 2012).
Approximately 20% of professional boxers have chronic traumatic brain injury. This will present with cognitive, motor and/or behavioral disturbances. When it becomes severe it is classified as dementia pugilistica. Pathologically, chronic traumatic brain injury is similar to Alzheimer's disease (Jordon, 2000). Factors that increase the risk of dementia pugilistica include the number of professional bouts, number of total head blows and number of knockouts. Other sports that have repeated head blows may lead to dementia pugilistica.
A fifty-three year old male who is retired boxer presents to his primary care provider after his wife is concerned of his increasing aggressive and irritable behavior. Over the next three years he was diagnosed with advanced dementia. He also suffered from features of parkinsonism (shuffling gait, tremor and slow movements). After his death an autopsy was done which showed chronic traumatic encephalopathy.
Men account for 59 percent of the diagnosed TBIs (CDC, 2012). This may be due to the fact that men are more commonly involved in higher risk activities such as sports that involve collisions (e.g., football, hockey), faster driving, and fighting.
Age is a risk for TBI. Those over 75 years-old are at greatest risk of being hospitalized or dying from a TBI. Younger age is a risk factor for TBI as 18% of all TBI-related emergency room visits are for children under five years-old (CDC, 2012).
Other risk factors for TBI include (CDC, 2012 and Dawadu, 2013):
Female athletes are at higher risk for concussion than males. Males have a higher percentage of player-to-player contact concussions and females have a higher percentage of surface or ball-to-head contact concussions. Outcome studies showed females had worse outcomes in TBI than males. It is unclear if this higher risk in females is a true incidence or a reporting bias (Dick, 2009).
Cerebral perfusion pressure is the blood pressure minus the intracranial pressure (ICP) and should be above 70 mm Hg in adults and 60 mm Hg in children. Pressure to the brain is critical. If pressure gets too low, below 12 ml/mg/min, than irreversible brain damage may occur (Tolias, 2011). Autoregulation helps maintain adequate perfusion to the brain. When there is a traumatic event, autoregulation does not work and cerebral blood flow is decreased. Thus, maintaining adequate blood pressure during a TBI is critical.
Inside the skull is a closed space and the pressure in the cavity is constant. On average, the adult has an intracranial volume of about 1500 mL. The brain makes up about 85-90%, the intravascular cerebral blood volume consumes about 10% of that volume, and the cerebrospinal fluid (CSF) accounts for less than three percent of the volume (Crippen, 2012). Any alteration in one of the components will result in an alteration in the other. When ICP increases the brain may herniate. This is when part of the brain is pushed through a natural opening.
The CSF acts as a shock absorber for compressive forces. Certain areas of the brain are more prone to trauma due to rough spots in the skull including the floor of the frontal lobe and a tops and floor of the temporal lobes.
A stationary head is most likely to be damaged in the area of the blow. When the head is in motion the injury most commonly occurs on the opposite side of the trauma because the brain lags slightly behind the body falling and the brain bounces off the other side of the skull (Cantu, 2013).
TBI can be primary or secondary. Primary injuries occur at the moment of the injury due to mechanical forces. They can occur when the object strikes the head, the brain hits the inside of the skull or from acceleration-deceleration (Crippen, 2012).
Secondary injury happens sometime after trauma and often leads to long-term problems. Secondary injury often compounds the primary injury. Swelling, bleeding, or increased ICP may result in decreased blood flow to the brain. Reduced blood flow leads to cell death. Secondary injury may be noted clinically by low blood pressure, hyperthermia, hypoxia, intracranial hemorrhage or malignant brain edema (Dawodu, 2013).
A contusion is bruising of the brain and is formed in 2 ways: 1) direct trauma and 2) acceleration/deceleration injury. Direct trauma causes injury at the site of impact, which is termed a coup contusion. Acceleration/deceleration causes injury at a site opposite to the site of impact, which is termed a contrecoup contusion. Contrecoup typical results in a bruised brain when the brain bounces off the skull. This often occurs in shaken baby syndrome or a car accident. It can cause damage to individual nerve cells.
Skull fractures occur when there is break in the integrity of the skull bone. When the skull pushes into the brain it is called a depressed skull fracture. When an object penetrates into the skull a penetrating skull fracture occurs.
Hematoma is bleeding into or around the brain and is a common injury seen in TBI. Hematoma is the most common cause of death in TBI (Crippen, 2012). A hematoma should be considered when there is neurological deterioration such as a worsening headache, confusion, lethargy, focal neurological signs or loss of consciousness.
Multiple types of hematomas can occur including: a subdural hematoma, epidural hematoma and an intracerebral hematoma. A subdural hematoma (SDH) is bleeding into the subdural space. SDH can act like a mass lesion and lead to death or disability.
An epidural hematoma is bleeding between the skull and the dura. This is often caused by a break in the temporal bone and rupture of the middle meningeal artery. This type of hematoma can grow rapidly because the bleeding is coming from a high pressure artery and can quickly elevate pressure in the brain. An intracerebral hematoma is bleeding into the brain.
Diffuse axonal injury is an important feature of TBIs. It results from damage on a microscopic level and therefore not seen on imaging studies. It is believed that the rapid stretching of the axon damages the neuron and reduces its function.
Symptom severity is related to the severity of the injury. Some signs and symptoms occur immediately while others occur days or even weeks after the injury.
Mild traumatic brain injury (Glasgow Coma Scale [GCS] between 13 and 15, which is measured 30 minutes after the injury) is typically a benign problem, but it must be considered carefully, because there is potential for significant long-term and short-term complications. Mild TBIs often have subtle symptoms such as the patient acting a little strange, a little dazed or not acting like themselves. Patients may complain of headache, blurred vision, tinnitus, confusion, dizziness, fatigue, mood change, sleep disturbance, or inability to concentrate.
When a patient presents with a worsening or persistent headache, convulsions, persistent vomiting, decreased level of consciousness, slurred speech, incoordination, agitation, restlessness, abnormal pupil response, or weakness/numbness in the extremities a moderate to severe TBI should be suspected.
Children with head injuries may present with persistent crying, irritability, refusal to eat, abnormal sleeping patterns, tiredness, listlessness, inconsolability, changed behavior or playing patterns, reduced performance in school, regression of development, emesis, or incoordination.
Some symptoms persist long into the recovery period. Six months after mild TBI, some patients still report weakness, fatigue, memory problems, dizziness, and headache. Eighty-three percent of patients with mild TBI report at least one symptom after six months (Crippen, 2012).
When evaluating a head injury it is important to evaluate for other injuries such as neck injury, spinal cord injury, facial bone fracture, eye injury or skull fracture.
Seizures, generalized or partial, are a common complication of head trauma, especially moderate to severe TBIs. They are more common in those who have brain contusions, hematomas, or penetrating head injuries. Seizures can occur shortly after the injury or can occur for an extended period of time after the injury in a condition called post-injury epilepsy. Those who have early seizures are at higher risk to develop post-traumatic epilepsy.
Phenytoin is often used the first week after TBI. If seizures do not develop, the medication can be discontinued as there is little evidence that it prevents late onset seizures (Crippen, 2012) (Buck, 2005). If seizures do occur, epilepsy can last for years after a TBI, even for a mild TBI. The relative risk of epilepsy ten years after a TBI is 1.51 for a mild TBI and 4.29 for a severe TBI (Christensen, Pedersen, Pedersen, Sidenius, Olsen, & Vestergaard, 2009).
Brain injuries have the potential to lead to a coagulopathy (disorder of blood coagulation) as they lead to a systemic release of tissue factors and brain phospholipids into the circulation leading to abnormal intravascular coagulation and a consumptive coagulopathy (Zehtabchi, Soghoian, Liu, Carmody, Shah, Whittaker, & Sinert, 2008). Those with a coagulopathy after a TBI have a worse prognosis.
The ventricles can dilate when CSF builds up in the brain leading to hydrocephalus and an increased ICP. It often occurs soon after an injury but can occur after an extended period of time. Increased ICP may lead to cerebral edema, cerebral ischemia, cerebral hypoxia and brain herniation.
Skull fractures are another complication. When the matter between the dura and the arachnoid membrane tears, CSF can leak out in a condition called a subdural hygroma. Fluid can leak out the nose, ears and the mouth. Any tear in the brain's protective matter increases the risk that bacteria can enter these spaces leading to meningitis.
Hemorrhagic stroke can results from an arterial bleed in the brain. Ischemic stroke can occur when a clot forms in the brain's blood vessels. Blood clots can occur in the sinuses next to the brain. These clots usually occur within a few days of the injury. They present with seizures, headache, emesis, hemiparesis and a decreased level of consciousness.
The cranial nerves can also be injured when there is a TBI. It is estimated that only 0.3 percent of mild TBIs result in cranial nerve injuries (Coello, Canals, Gonzalez, & Martin, 2010). It is more common when there is a fracture and it is near the base of the skull. The most commonly injured cranial nerve is the facial nerve (CN VII), which can result in paralysis of the face. Cranial nerve injury may lead to an impaired sense of smell or taste. If patients lose their sense of smell it will likely be permanent if it lasts one year after injury (Yousem, Geckle, & Bilker, 1996). Double vision may occur and if it is to occur it is likely that cranial nerve IV has been affected. Damage to the trigeminal nerve (CN V) leads to facial pain.
Post concussion syndrome can occur days or even months after a TBI. This can occur with any degree of head injury from the mild to severe. It is characterized by dizziness, vertigo, headache, reduced concentration, apathy, depression, sleep disturbance, confusion, irritability, and anxiety.
Amnesia can also occur after a head injury. Anterograde amnesia is impaired memory of events after the injury where retrograde amnesia is memory deficits of events prior to the injury.
Brain dysfunction can take many forms after a TBI. The following are problems that may be noted after a TBI.
Most of the recovery from a TBI occurs in the first six months, and can be more gradual after the first six months.
Some problems may occur years after the head injury (CDC, 2013). Alzheimer's disease is the most common type of dementia and is linked to prior history of head injury. Parkinson's disease can occur when there is a remote history of damage to the basal ganglia. As mentioned above, dementia pugilistica occurs in patients who have a history of head trauma. Posttraumatic dementia is dementia that occurs after a single TBI that results in coma.
Agitation is commonly seen after a head injury. Other causes of agitation seen after a head injury may include: pain, depression, infection, side effects of medications, sleep deprivation, or electrolyte imbalance.
A myriad of other problems may occur after TBI including:
Different diagnostic tests are available to help determine the severity of the injury. Imaging helps with determining if there is a fracture and assists in the determination of prognosis.
Computed tomography (CT) scans are the best test for moderate to severe head trauma. CT scans can identify bone fractures, hemorrhages, contusions, cerebral edema, hematoma, and tumors. Neuronal damage can be underestimated. Most mild TBIs have no evident changes on neuroimaging, but a mild TBI may be associated with cortical contusion or an intracrainial hemorrhage.
Magnetic resonance imaging (MRI) is another commonly used test in the diagnostic work up of TBI. It is not the best initial test as it is more time consuming and not as readily available. The MRI is a more accurate test for detecting contusions and diffuse axonal injury (Morales, & Diaz-Daza, 2007).
For those with a mild TBI, a head CT should be considered if: there is a Glasgow Coma Scale (GCS) score less than 15, two hours after injury; vomiting; any loss of consciousness; the individuals is 60-65 years-old or older; scalp laceration to the bone of greater than 5 cm; significant maxillofacial injuries; persistent headache; amnesia before impact of 30 minutes or more; dangerous mechanism of injury (e.g., pedestrian struck by motor vehicle, occupant ejected from a motor vehicle, fall from =3 feet or =5 stairs); or suspected skull fracture (e.g., CSF leak [clear fluid from nose or out of ears], raccoon eyes [bruising around eyes], Battle's sign [bruising behind ears], or hemotympanum [blood behind ear drum]). Those with seizure, neurological deficit, those who take oral anticoagulants or those with a bleeding diathesis typically require a CT scan (Levine, 2010).
Mild TBIs often present to their primary care doctor's office, urgent care clinic, or as a walk in patient at an emergency department. More severe cases may present to the emergency department after transport by emergency medical personal.
Those with severe injury need to be medically stabilized as a primary priority. Pre-hospital care needs to assure that the patient is triaged appropriately, stabilized, and has any life threatening complications such as increased intracranial pressure or cerebral herniation recognized (Stiver, & Manley, 2008).
The ABCs are of primary importance in any severe injury. Assuring there is an airway present to maintain adequate oxygen flow to the brain and the rest of the body. Intubation is often done to those with moderate or severe head injuries. Blood pressure control is necessary as is controlling any other injuries that may accompany head injury. Often times head injury cases are multi-trauma cases, including spinal cord injury, and patients need to be managed systemically as other injuries may be more immediately life threatening.
Regular assessment of the GCS is necessary. This test is rated from one to fifteen and looks at eye opening, verbal response, and motor response. GCS describes the severity of a TBI.
The ability to open the eyes is rated from 1 to 4.
|4||Spontaneously opens the eyes|
|3||Opens eyes with verbal command|
|2||Opens eyes only in response to painful stimulus|
|1||Unable to open eyes|
|5||Patient is oriented and speaks coherently|
|4||Disoriented but can speak coherently|
|2||Makes incomprehensible sounds|
|1||No verbal response|
The best motor response:
|6||Moves arms and legs in response to verbal commands|
|5||Able to localize pain|
|4||Withdrawals to pain|
|3||Abnormal flexion (decoriticate)|
|2||Abnormal extension (decerebrate)|
|1||No movement to any stimulus|
The scores given to each section are added up and based on the total score a severity is given.
|3-8||Severe head injury|
|9-12||Moderate head injury|
|13-15||Mild head injury|
A minor head injury is indicated by a GCS sore of greater than 12. Minor head injuries usually do not progress; but, about 3% of mild head injuries advance to more severe injuries (Crippen, 2012).
Patients who are discharged with a mild head injury should be awakened every 2 hours and assessed neurologically. Patients and their caregivers should return to the hospital if there is any seizure, confusion, severe/worsening headache, watery discharge from the ear or nose, or persistent nausea and vomiting (Crippen, 2012).
Certain indications necessitate consideration for admission (Tolias, 2011). These include:
CT scan helps determine the degree of intracranial injury and helps predict outcome. In those with normal CT scans hospitalizations may be avoided. CT scans can detect skull fracture, hemorrhage, midline shift, mass effect, and herniation. A repeat exam should occur in 4-8 hours for those with coagulopathies or an intracranial hemorrhage. Abnormal findings on the CT scan, prolonged unconsciousness, persistent mental status changes or an abnormal neurological exam necessitate referral to a neurosurgeon. Patients with normal CT scans after head injury will clinically improve within hours. Those who fail to improve should have a repeat CT scan (Rangel-Castillia, 2012).
Neurological checks should be done frequently. The patient should consume nothing orally until they are alert. Intravenous fluids will help prevent dehydration and help maintain pressure. Comfort measures should ensue with the use of mild analgesics and an antiemetic. Do not use phenothiazines (e.g., Compazine, Thorazine) as this increases the risk of seizure (Tolias, 2012).
A Glasgow Coma Score under 8 indicates severe injury. Severe injury requires CT scan, admission to the hospital and neurosurgical referral. ICP should be lowered using a variety of measures including:
Among those with a moderate to severe head injury fewer than 10% have an initial surgical lesion (Crippen, 2012). Indications for surgery include: an open skull fracture, a depressed skull fracture of more than 1 cm, extra-axial hematoma with a midline shift of greater an 0.5 cm, intra-axial hematoma with a volume greater than 30 ml, or a temporal or cerebellar hematoma more than 3 cm (Crippen, 2012).
Corticosteroids have been used in the past in the management of TBI. Research suggests that corticosteroids increase the risk of death and should not be routinely used (Alderson & Roberts, 2005).
Multiple steps should be implemented in the prevention of TBI. These include:
In the United States, concussion occurs in 128 people per 100,000 people every year. The highest rates of concussions are seen in children between the ages of 5 and 14 from bicycle accidents or sports. In adults, falls and motor vehicle accidents are the most common cause (Bey and Ostick, 2012). A concussion is considered a mild traumatic brain injury and involves an induced alteration in mental status that may or may not involve loss of consciousness. As many as 50 percent of concussions are unreported (Harmon, 2013).
A concussion is caused by a blow, often to the head, but can occur on another part of the body that leads to impulsive force transmitted to the head. It leads to a rapid onset of short-lived impairment in the neurological function and resolves on its own. It typically leads to a functional disturbance, but not necessarily a structural one and neuroimaging tests are typically normal.
A simple concussion resolves within 10 days. A complex concussion has symptoms that persist beyond 10 days or has additional symptoms such as confusion, seizures, or an exertion headache (Bey and Ostick 2012).
The post concussive syndrome is a combination of symptoms (headache, irritability, concentration impairment, dizziness, fatigue, insomnia, alcohol intolerance, memory impairments, or intellectual difficulties) that occur after a head injury. During this time it is critical to maintain rest both cognitively and physically. If rest is not maintained recovery can be prolonged. Symptoms typically resolve in one week to 10 days, but may persist for months.
The Cantu guidelines classify concussions into three grades. Grade I concussions do not present with a loss of consciousness. Post-traumatic amnesia is not present or present for less than 30 minutes. A grade II concussion is associated with a loss of consciousness for less than five minutes or has posttraumatic amnesia between 30 minutes and 24 hours. In grade III concussions the athlete is unconscious for more than five minutes or has post-traumatic amnesia greater than 24 hours.
Acute symptoms of concussion include amnesia, confusion and loss of consciousness. The amnesia usually involves an inability to recall the traumatic event, but may also include the inability to remember events before or after the injury. The athlete may also complain of headache, dizziness, nausea/vomiting, tinnitus, balance impairment, or photophobia. The athlete may not be able to report details of the game, appear dazed, feel foggy/hazy/sluggish or stunned. The athlete may ask the same question over and over even though it has been answered.
Many people will experience headaches after mild TBI. The headaches typically occur within seven days after the TBI but sometimes they may start up to three months after the head injury (Haas, 1996).
After a concussion the physical exam may show memory problems, slurred speech, a vacant stare, confusion, incoordination, emotional fluctuation, slow to answer questions, and easy distraction.
Athletes who experience any of the signs and symptoms after a bump, blow, or jolt to the head or body should not participate in sports until a health care professional who is experienced in concussion management clears the patient.
On the field there are multiple tests that can be used to assess the athlete for concussion. The Standardized Assessment of Concussion (SAC) assesses orientation, immediate memory, concentration, delayed recall, neurologic screening, and exertion maneuvers. This test works best when there is a baseline measure and should not be used in isolation as a test to determine if the athlete should go back to play.
The Sport Concussion Assessment Tool-2 (SCAT2), a more involved test than the SAC, is used to evaluate an injured athlete on the sideline. This test works best when there is a baseline evaluation to determine the degree of impairment after an injury. The test is associated with significant variability among high school students. Because of the variable on testing (especially balance scores and concentration), this test should be used cautiously without a baseline measure.
Observation is recommended for at least 24 hours after a concussion because there is risk for an intracranial complication. Admitting to the hospital may be considered for those with a GCS less than 15; any seizures activity; CT scan evidence of cerebral edema or intracranial bleeding; those on an anticoagulation medication; or those who have a bleeding diathesis. Those with no one to monitor them at home should be admitted to the hospital for observation. For those who do not have someone to watch them at home and a GCS score of 15, an immediate CT scan can be considered and if normal the patient is unlikely to have a neurological complication (Norlund, Mark, af Geijerstam, Oredsson, & Britton, 2006).
If an athlete is monitored at home it is important to teach the observer that the athlete should be awakened from sleep every two hours the first night and if the athlete is unable to be awoken immediate help should be attained. The athlete should not perform any strenuous activity for 24 hours. Other signs that should prompt the athlete to attain immediate medical help include: confusion, somnolence, vision difficulties, urinary or bowel incontinence, severe or worsening headaches, vomiting, stiff neck, fever, seizure, restlessness, unsteadiness, or weakness/numbness of any body part. These findings suggest that there is a potential intracrainial bleed/cerebral edema secondary to a contusion. These signs warrant evaluation including a head CT.
Second impact syndrome is a rare complication of mild head injury. This is diffuse cerebral swelling after a second concussion during the time the athlete is still symptomatic from the first. If the athlete returns to play too soon and develops another injury, when not fully recovered from the first, swelling of the brain, herniation or death may occur. It is not a common condition, but athletes may die within a few minutes if it does occur.
When evaluating a patient with a TBI, the first priority is always airway, breathing and circulation. It is also important to rule out any spinal cord/cervical spine injury and if suspected immobilization and radiography should occur. Paresthesia, reduced consciousness, posterior midline tenderness/pain and/or extremity weakness may suggest spinal cord/cervical spine injury.
Athletes who have experienced head injuries over the years may experience chronic traumatic encephalopathy (CTE) which is a neurodegenerative disease likely caused by repetitive brain trauma. It may result in memory problems, executive dysfunction, poor impulse control, depression, apathy, suicide, aggression, violence, substance abuse, and an increase in high risk behaviors (e. g., increased food intake, risky sexual behavior and gambling). Motor disturbances may present in CTE such as rigidity with a slow shuffling gait. It may eventually lead to dementia.
CTE is thought to be secondary to hyperphosphorylated tau and TDP-43 in the brain. Once thought to be only a problem in boxers, now has been shown to be prevalent in football players (Baugh, 2012).
CTE is likely caused by repetitive trauma to the brain (both concussions and subconcussive trauma). CTE is difficult to diagnose because it overlaps with multiple other syndromes. CTE may start during the post-concussive syndrome. As the disease progresses it presents similarly to other dementing illnesses such as frontotemporal dementia and Alzheimer's disease.
Multiple guidelines are available to determine when it is safe to return to play. The Cantu guidelines (Cantu, 1998) recommend that for grade I or grade II concussions athletes may return to play if asymptomatic for one week. For athletes with grade III concussions the athlete may return to play in one month if asymptomatic for seven days.
It is important to assure that concussion symptoms are fully resolved before the athlete can return to exercise. Some student athletes may require reduced school work while recovering from a concussion. Student athletes who are experiencing symptoms from their concussion need to rest the brain from cognitive activity to not worsen or lead to a reemergence in the symptoms of the concussion.
A newer protocol utilizes a graduated return to play protocol that is made up of six stages. The first stage is no activity; the athlete is to have complete rest (physical and cognitive). The second stage is light aerobic exercise with the goal of increased heart rate. The third stage is participating in sports specific drills such as running with no head impact. The fourth stage is non-contact training such as passing drills or resistance training. The fifth stage is full practice with contact and the sixth stage is return to play. The athlete is allowed to progress to the next stage each successive day if they are without symptoms (McCroy, 2008). When return to activity is too soon there is a reduction in reaction time and an increased risk for re-injury or another concussion.
The Cantu guidelines recommend that for the second concussion, if it is grade I, the athlete may return to play in two weeks if no symptoms are present for one week. For the second grade II concussion, the athlete should be out at least one month, but may return if after that month they are without symptoms for one week. For the second grade III concussion the athlete should be out for the season. The Cantu guidelines recommended stopping play for the season after the third concussion. If an athlete returns to play to quickly there is a risk for recurrent concussion and cumulative brain injury. With each concussion there is an increased risk for future concussion.
A 14 year-old boy is playing soccer and after heading the ball in for a goal, he comes off the field and asks the coach, "Who won the game?" Since it is only the first half, the coach realizes that the player is confused. The player is taken out of the game and one of the parents, who is a nurse, comes over to evaluate the athlete. The nurse determines that the athlete has a GCS score of 15, but is unclear of the game's score (this suggests retrograde amnesia). The nurse tells the coach that the boy should not reenter the game.
After calling his primary doctor, the boy takes the next day off of school and has an appointment with his primary care doctor. At the doctor's office he complains of a slight headache and feels a little dizzy. The following day he reports no symptoms, therefore, he goes to school and participates in light running at practice. He feels well after running. He goes back to practice the next day and does some light drills with the team. Since he continues to have no symptoms he advances his practice and includes some more intense drills the following day. The next practice he fully participates, but wakes up the next day with a headache. At the request of his primary care doctor, the next day, he sits out the game and then resumes practice the next week. He plays without incident the following week.
Head injuries are common, costly and at times devastating. Nurses should know how to assess, educate and monitor patients with TBI. With recent information learned about mild traumatic brain injury in sports, it is becoming more important for all health care providers to have a full understanding of TBI, its recognition, management and prevention.
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This course is applicable for the following professions:
Advanced Registered Nurse Practitioner (ARNP), Clinical Nurse Specialist (CNS), Licensed Practical Nurse (LPN), Licensed Vocational Nurses (LVN), Registered Nurse (RN)
CPD: Practice Effectively, Neurology, Psychiatric, Rehabilitation