Traumatic Brain Injury – Causes, Symptoms, Treatment

Traumatic Brain Injury – Causes, Symptoms, Treatment

Brain trauma or traumatic brain injury (TBI) results from a blow, bump, jolt, or penetrating injury to the head that disrupts the normal function of the brain. Symptoms vary greatly and may range from mild to severe depending on the degree of damage; imaging may or may not reveal changes. Patients with mild TBI may have transient changes in consciousness or mentation, while those with severe TBI may experience prolonged periods of unconsciousness, coma, or death.

Traumatic brain injury (TBI) is a common presentation in emergency departments, which accounts for more than one million visits annually. It is a common cause of death and disability among children and adults.

Based on the Glasgow Coma Scale (GCS) score, it is classified as:

  • Mild = GCS 13 to 15, also called concussion
  • Moderate = GCS 9 to 12
  • Severe = GCS 3 to 8

Pathophysiology

The following concepts are involved in the regulation of blood flow and should be considered.

1) Monroe-Kellie Doctrine

  • Related to the understanding of intracranial pressure (ICP) dynamics.
  • Any individual component of the intracranial vault may undergo alterations, but the total volume of intracranial contents remains constant since the space within the skull is fixed. In other words, the brain has a compensatory mechanism to maintain an equilibrium thereby maintaining normal intracranial pressure.
  • According to this, the displacement of cerebrospinal fluid (CSF) or blood occurs to maintain normal ICP. A rise in ICP will occur when the compensatory mechanisms are exhausted.

2) Regulation of Cerebral Blood Flow (CBF) (Autoregulation)

  • Under normal circumstances, the brain maintains CBF via auto-regulation which maintains equilibrium between oxygen delivery and metabolism.
  • Autoregulation adjusts Cerebral perfusion pressure (CPP) from 50 to 150 mm Hg. Beyond this range, autoregulation is lost, and blood flow is only dependent on blood pressure.
  • Severe brain injury may disrupt the autoregulation of CBF.

3) Cerebral Perfusion Pressure (CPP)

  • The difference between the mean arterial pressure (MAP) and the ICP (CPP = MAP – ICP)
  • Target CPP is 55 mm Hg  to 60 mm Hg
  • An increase in ICP can decrease the CPP
  • A decrease in ICP may improve CPP
  • Remember, lowering MAP in a hypotensive patient may lower CPP.
  • A minimum CPP should be maintained to avoid cerebral insult. It is age-dependent and is as follows: Infants – 50 mm Hg, Children – 60 mm Hg, and Adults – 70 mm Hg.
  • CBF is quite sensitive to oxygen and carbon dioxide.
  • Hypoxia causes vasodilation and therefore increases CBF and may worsen ICP.
  • Hypercarbia also results in vasodilation and can alter ICP via effects on cerebrospinal fluid (CSF) pH and increases CBF.

4) Mean arterial pressure (MAP)

  • Maintain = 80 mm Hg
  • 60 mm Hg = cerebral vessels maximally dilated
  • < 60 mm Hg = cerebral ischemia
  • > 150mmHg =  increased ICP

5) Intracranial pressure (ICP)

  • An increase in ICP can decrease CPP.
  • ICP is dependent on the volume of the following compartments:
  • Brain parenchyma (< 1300 mL)
  • Cerebrospinal fluid (100 – 150 mL)
  • Intravascular blood (100 – 150 mL)
  • Cushing reflex (hypertension, bradycardia, and respiratory irregularity) due to an increase in ICP
  • Normal ICP is age-dependent (adult younger than ten years old, child 3-7 years old, infant 1.5-6 years old)
  • > 20 mm Hg= increased morbidity and mortality and should be treated. It is perhaps more important to maintain an adequate CPP.

Types of

TBI can be classified as primary injury and secondary injury:

Primary Injury

Primary injury includes injury upon the initial impact that causes displacement of the brain due to direct impact, rapid acceleration-deceleration, or penetration. These injuries may cause contusions, hematomas, or axonal injuries.

  • Contusion (bruise on the brain parenchyma)
  • Hematoma (subdural, epidural, intraparenchymal, intraventricular, and subarachnoid)
  • Diffuse axonal injury (stress or damage to axons)

Secondary Injury/Secondary Neurotoxic Cascade

Secondary injury consists of the changes that occur after the initial insult. It can be due to:

  • Systemic hypotension
  • Hypoxia
  • Increase in ICP

After a primary brain injury, a cascade of cellular and biochemical events occurs which include the release of glutamate into the presynaptic space resulting in activation of N-methyl-D-aspartate, a-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid, and other receptors. This ionic shift may activate cytoplasmic and nuclear enzymes, resulting in mitochondrial damage, and cell death and necrosis.

Brain Herniation

Herniation occurs due to increased ICP. The following are the types of herniations.

1) Uncal transtentorial

  • The uncus is the most medial portion of the hemisphere, and the first structure to shift below the tentorium.
  • Compression of parasympathetic fibers running with the third cranial nerve
  • Ipsilateral fixed and dilated pupil with contralateral hemiparesis

2) Central transtentorial

  • Midline lesions, such as lesions of the frontal or occipital lobes or vertex
  • Bilateral pinpoint pupils, bilateral Babinski signs, and increased muscle tone. Fixed midpoint pupils follow along with prolonged hyperventilation and decorticate posturing

3) Cerebellar tonsillar

  • Cerebellar tonsils herniate in a downward direction through the foramen magnum
  • Compression on the lower brainstem and upper cervical spinal cord
  • Pinpoint pupils, flaccid paralysis, and sudden death

4) Upward posterior fossa/cerebellar herniation

  • The cerebellum is displaced in an upward direction through the tentorial opening
  • Conjugate downward gaze with an absence of vertical eye movements and pinpoint pupils

Causes

Traumatic brain injury is usually caused by a blow or other traumatic injury to the head or body. The degree of damage can depend on several factors, including the nature of the injury and the force of impact.

Common events causing traumatic brain injury include the following:

  • Falls. Falls from bed or a ladder, down stairs, in the bath and other falls are the most common cause of traumatic brain injury overall, particularly in older adults and young children.
  • Vehicle-related collisions. Collisions involving cars, motorcycles or bicycles — and pedestrians involved in such accidents — are a common cause of traumatic brain injury.
  • Violence. Gunshot wounds, domestic violence, child abuse and other assaults are common causes. Shaken baby syndrome is a traumatic brain injury in infants caused by violent shaking.
  • Sports injuries. Traumatic brain injuries may be caused by injuries from a number of sports, including soccer, boxing, football, baseball, lacrosse, skateboarding, hockey, and other high-impact or extreme sports. These are particularly common in youth.
  • Explosive blasts and other combat injuries. Explosive blasts are a common cause of traumatic brain injury in active-duty military personnel. Although how the damage occurs isn’t yet well-understood, many researchers believe that the pressure wave passing through the brain significantly disrupts brain function.

Effects

Some brain injuries are mild, with symptoms disappearing over time with proper attention. Others are more severe and may result in permanent disability. The long-term or permanent results of brain injury may need post-injury and possibly lifelong rehabilitation. Effects of brain injury may include:

  • Cognitive deficits
    • Coma
    • Confusion
    • Shortened attention span
    • Memory problems and amnesia
    • Problem-solving deficits
    • Problems with judgment
    • Inability to understand abstract concepts
    • Loss of sense of time and space
    • Decreased awareness of self and others
    • Inability to accept more than one- or two-step commands at the same time
  • Motor deficits
    • Paralysis or weakness
    • Spasticity (tightening and shortening of the muscles)
    • Poor balance
    • Decreased endurance
    • Inability to plan motor movements
    • Delays in getting started
    • Tremors
    • Swallowing problems
    • Poor coordination
  • Perceptual or sensory deficits
    • Changes in hearing, vision, taste, smell, and touch
    • Loss of sensation or heightened sensation of body parts
    • Left- or right-sided neglect
    • Difficulty understanding where limbs are in relation to the body
    • Vision problems, including double vision, lack of visual acuity, or limited range of vision
  • Communication and language deficits
    • Difficulty speaking and understanding speech (aphasia)
    • Difficulty choosing the right words to say (aphasia)
    • Difficulty reading (alexia) or writing (agraphia)
    • Difficulty knowing how to perform certain very common actions, like brushing one’s teeth (apraxia)
    • Slow, hesitant speech and decreased vocabulary
    • Difficulty forming sentences that make sense
    • Problems identifying objects and their function
    • Problems with reading, writing, and ability to work with numbers
  • Functional deficits
    • Impaired ability with activities of daily living (ADLs), such as dressing, bathing, and eating
    • Problems with organization, shopping, or paying bills
    • Inability to drive a car or operate machinery
  • Social difficulties
    • Impaired social capacity resulting in difficult interpersonal relationships
    • Difficulties in making and keeping friends
    • Difficulties understanding and responding to the nuances of social interaction
  • Regulatory disturbances
    • Fatigue
    • Changes in sleep patterns and eating habits
    • Dizziness
    • Headache
    • Loss of bowel and bladder control
  • Personality or psychiatric changes
    • Apathy
    • Decreased motivation
    • Emotional lability
    • Irritability
    • Anxiety and depression
    • Disinhibition, including temper flare-ups, aggression, cursing, lowered frustration tolerance, and inappropriate sexual behavior

    Certain psychiatric disorders are more likely to develop if damage changes the chemical composition of the brain.

  • Traumatic Epilepsy
    • Epilepsy can happen with a brain injury, but more commonly with severe or penetrating injuries. While most seizures happen immediately after the injury, or within the first year, it is also possible for epilepsy to surface years later. Epilepsy includes both major or generalized seizures and minor or partial seizures.

Symptoms of

Traumatic brain injury can have wide-ranging physical and psychological effects. Some signs or symptoms may appear immediately after the traumatic event, while others may appear days or weeks later.

  • Headache that gets worse and does not go away.
  • Weakness, numbness, or decreased coordination.
  • Repeated vomiting or nausea.
  • Slurred speech.
  • Look very drowsy or cannot wake up.
  • Have one pupil (the black part in the middle of the eye) larger than the other.
  • Have convulsions or seizures.
  • Cannot recognize people or places.
  • Are getting more and more confused, restless, or agitated.
  • Have unusual behavior.
  • Lose consciousness.
  • A headache that gets worse or does not go away
  • Repeated vomiting or nausea
  • Convulsions or seizures
  • Not being able to wake up from sleep
  • Larger than normal pupil (dark center) of one or both eyes. This is called dilation of the pupil.
  • Slurred speech
  • Weakness or numbness in the arms and legs
  • Loss of coordination
  • Increased confusion, restlessness, or agitation

Mild traumatic brain injury

The signs and symptoms of mild traumatic brain injury may include:

Physical symptoms

  • Loss of consciousness for a few seconds to a few minutes
  • No loss of consciousness, but a state of being dazed, confused or disoriented
  • Headache
  • Nausea or vomiting
  • Fatigue or drowsiness
  • Problems with speech
  • Difficulty sleeping
  • Sleeping more than usual
  • Dizziness or loss of balance

Sensory symptoms

  • Sensory problems, such as blurred vision, ringing in the ears, a bad taste in the mouth or changes in the ability to smell
  • Sensitivity to light or sound

Cognitive or mental symptoms

  • Memory or concentration problems
  • Mood changes or mood swings
  • Feeling depressed or anxious

Moderate to severe traumatic brain injuries

Moderate to severe traumatic brain injuries can include any of the signs and symptoms of mild injury, as well as these symptoms that may appear within the first hours to days after a head injury:

Physical symptoms

  • Loss of consciousness from several minutes to hours
  • Persistent headache or headache that worsens
  • Repeated vomiting or nausea
  • Convulsions or seizures
  • Dilation of one or both pupils of the eyes
  • Clear fluids draining from the nose or ears
  • Inability to awaken from sleep
  • Weakness or numbness in fingers and toes
  • Loss of coordination

Cognitive or mental symptoms

  • Profound confusion
  • Agitation, combativeness or other unusual behavior
  • Slurred speech
  • Coma and other disorders of consciousness

Children’s symptoms

Infants and young children with brain injuries might not be able to communicate headaches, sensory problems, confusion and similar symptoms. In a child with traumatic brain injury, you may observe:

  • Change in eating or nursing habits
  • Unusual or easy irritability
  • Persistent crying and inability to be consoled
  • Change in ability to pay attention
  • Change in sleep habits
  • Seizures
  • Sad or depressed mood
  • Drowsiness
  • Loss of interest in favorite toys or activities

Diagnosis of

History and Physical

A good history concerning the mechanism of injury is important. Follow advanced trauma life support protocol and perform primary, secondary, and tertiary surveys. Once the patient is stabilized, a neurologic examination should be conducted. CT scan is the diagnostic modality of choice in the initial evaluation of patients with head trauma.

The GCS is used to describe the level of consciousness. Patients who are intubated are only evaluated for motor scores and eye-opening and the suffix T is added to the final score. The maximal GCS score is 10T and the lowest is 2T.

Classification of TBI is as follows:

Clouding of consciousness, where there is a mild deficit in processing by the brain. It may persist for many months and the patient may have a loss of recent memory, but long term memory remains intact.

Lethargy is a state of depressed alertness and can result in an inability to perform tasks that are usually done without any effort. The patient may be aroused by stimuli but then settles back into a state of inactivity. Awareness of the environment is present.

Obtundation is a state of decreased alertness and awareness. The patient will briefly respond to stimuli and only follow simple commands, but will not be aware of the surroundings.

Stupor is when the patient cannot communicate lucidly and requires painful stimuli to be aroused. Once the stimulation is withdrawn, the patient returns to the inactive state.

Coma is when the patient is not able to respond to any type of stimuli

Exam

Initial vitals are important to review. Cushing’s triad, a combination of hypertension, bradycardia, and irregular or decreased respirations may present in patients with increased intracranial pressure.

Assuming that the patient’s airway, breathing, and circulation are intact, the patient should then be evaluated using the Glasgow Coma Scale (GCS), assessing for eye-opening, verbal responses, and motor responses. The minimum score is 3, and the maximum score is 15.

Glasgow Coma Scale:

Eye-opening response

  • Spontaneous (4)
  • To verbal stimuli (3)
  • To pain (2)
  • No response (1)

Verbal response

  • Oriented (5)
  • Confused (4)
  • Inappropriate words (3)
  • Incomprehensible speech (2)
  • No response (1)

Motor response

  • Obeys commands for movement (6)
  • Purpose movement to painful stimuli (5)
  • Withdraws to painful stimuli (4)
  • Flexion response to painful stimuli (decorticate posturing) (3)
  • Extension response to painful stimuli (decerebrate posturing) (2)
  • No response (1)

Evaluation

CT scan is required in patients with head trauma

  • Moderate (GCS score 9 to 12)
  • Severe (GCS score < 8)

For patients who are at low risk for intracranial injuries, there are two externally validated rules for when to obtain a head CT scan after TBI.

It is important to understand that no individual history and physical examination findings can eliminate the possibility of intracranial injury in head trauma patients.

Skull x-rays are only used to assess for foreign bodies, gunshots or stab wounds

New Orleans Criteria

  • Headache
  • Vomiting (any)
  • Age > 60 years
  • Drug or alcohol intoxication
  • Seizure
  • Trauma visible above clavicles
  • Short-term memory deficits

Canadian CT Head Rule

  • Dangerous mechanism of injury
  • Vomiting = two times
  • Age > 65 years
  • GCS score < 15, 2-hours post-injury
  • Any sign of basal skull fracture
  • Possible open or depressed skull fracture
  • Amnesia for events 30 minutes before injury

Level A Recommendation

With the loss of consciousness or posttraumatic amnesia only if one or more of the following symptoms are present:

  • Headache
  • Vomiting
  • Age > 60 years
  • Drug or alcohol intoxication
  • Deficits in short-term memory
  • Physical findings suggestive of trauma above the clavicle
  • Posttraumatic seizure
  • GCS score < 15
  • Focal neurologic deficit
  • Coagulopathy

Level B Recommendation

Without loss of consciousness or posttraumatic amnesia if one of the following specific symptoms presents:

  • Focal neurologic deficit
  • Vomiting
  • Severe headache
  • Age > 65 years
  • Physical signs of a basilar skull fracture
  • GCS score < 15
  • Coagulopathy
  • Dangerous mechanism of injury
  • Ejection from a motor vehicle (such as Pedestrian struck or a fall from a height > three feet or five stairs)

The risk of intracranial injury when clinical decision rule results are negative is less than 1%.

For children, Pediatric Emergency Care Applied Research Network (PECARN) decision rules exist to rule out the presence of clinically important traumatic brain injuries. However, this rule applies only to children with GCS > 14.

Rancho Los Amigos Scale

This scale is used to describe the behaviors, cognitions, and emotional responses in patients who are emerging from a coma.

  • Level I: No Response: Total Assistance – no response to stimuli
  • Level II: Generalized Response: Total Assistance – inconsistent and non-purposeful responses
  • Level III: Localized Response: Total Assistance – inconsistent response
  • Level IV: Confused/Agitated: Maximal Assistance –  bizarre, non-purposeful behavior, agitation
  • Level V: Confused, Inappropriate Non-Agitated: Maximal Assistance – response to simple commands, non-purposeful, and random response to complex commands.
  • Level VI: Confused, Appropriate: Moderate Assistance – follows simple commands, able to understand familiar tasks, but not new tasks
  • Level VII: Automatic, Appropriate: Minimal Assistance for Daily Living Skills – Able to perform daily routine and understands familiar settings. Aware of diagnosis, but not impairments.
  • Level VIII: Purposeful, Appropriate: Stand By Assistance – Consistently oriented to person, place and time, and some awareness of impairments and how to compensate. They can carry out familiar tasks independently but might be depressed, and/or irritable
  • Level IX: Purposeful, Appropriate: Stand By Assistance on Request – Able to complete different tasks, aware of impairments, able to think about consequences with assistance
  • Level X: Purposeful, Appropriate: Modified Independent  – Able to multitask in many different environments. May create tools for memory retention and anticipate obstacles which may result from impairments

Imaging tests

  • Computerized tomography (CT) scan. This test is usually the first performed in an emergency room for a suspected traumatic brain injury. A CT scan uses a series of X-rays to create a detailed view of the brain. A CT scan can quickly visualize fractures and uncover evidence of bleeding in the brain (hemorrhage), blood clots (hematomas), bruised brain tissue (contusions), and brain tissue swelling.
  • Magnetic resonance imaging (MRI). An MRI uses powerful radio waves and magnets to create a detailed view of the brain. This test may be used after the person’s condition stabilizes, or if symptoms don’t improve soon after the injury.

Treatment / Management

Medicines to treat the symptoms of TBI and to lower some of the risks associated with it, such as

  • Anti-anxiety medication to lessen feelings of nervousness and fear
  • Anticoagulants to prevent blood clots
  • Anticonvulsants to prevent seizures
  • Antidepressants to treat symptoms of depression and mood instability
  • Muscle relaxants to reduce muscle spasms
  • Stimulants to increase alertness and attention

The most important goal is to prevent secondary brain injuries. This can be achieved by the following:

  • Maintain airway and ventilation
  • Maintain cerebral perfusion pressure
  • Prevent secondary injuries (by recognizing and treating hypoxia, hypercapnia, or hypoperfusion)
  • Evaluate and manage for increased ICP
  • Obtain urgent neurosurgical consultation for intracranial mass lesions
  • Identify and treat other life-threatening injuries or conditions (if they exist)

A relatively higher systemic blood pressure is needed:

  • Increase in intracranial pressure
  • Loss of autoregulation of cerebral circulation

Priorities remain the same:  the ABC also applies to TBI. The purpose is to optimize perfusion and oxygenation.

Airway and Breathing

Identify any condition which might compromise the airway, such as pneumothorax.

For sedation, consider using short-acting agents having minimal effect on blood pressure or ICP:

  • Induction agents:  Etomidate or propofol
  • Paralytic agents: Succinylcholine or Rocuronium

Consider endotracheal intubation in the following situations:

  • Inadequate ventilation or gas exchange such as hypercarbia, hypoxia, or apnea
  • Severe injury (GCS score of = 8)
  • Inability to protect the airway
  • Agitated patient
  • Need for patient transport

The cervical spine should be maintained in-line during intubation.

Nasotracheal intubation should be avoided in patients with facial trauma or basilar skull fracture.

Targets:

  • Oxygen saturation > 90
  • PaO2 > 60
  • PCO at 35 – 45

Circulation

Avoid hypotension. Normal blood pressure may not be adequate to maintain adequate flow and CPP if ICP is elevated.

Target

  • Systolic blood pressure > 90 mm Hg
  • MAP > 80 mm Hg

Isolated head trauma usually does not cause hypotension. Look for another cause if the patient is in shock.

Intubation

  • Patients should be pre-oxygenated as the risk of hypoxia outweighs the risk of hyperoxia.
  • Historically lidocaine has been used for pre-treatment to blunt sympathetic response to airway manipulation during laryngoscopy, but studies have shown no definitive benefit.
  • Etomidate allows hemodynamic stability and is a commonly used first-line agent for induction, though it has a reported risk of adrenal insufficiency. Propofol may be useful in lowering blood pressure, and thus the intracranial pressure in hypertensive patients. It may also have anti-epileptic effects. Ketamine has a theoretical risk of increasing intracranial pressure, though more recent studies have been mixed on this. It may be useful in hypotensive patients to increase MAP and CPP.
  • Paralytic agents such as rocuronium, vecuronium, or succinylcholine may be a consideration, however, these agents will limit the ability to perform a neurologic exam after administration.

Circulation

  • Maintain normotension with target SBP greater than 90 and less than 140
  • Initiate fluid resuscitation with normal saline with the goal of euvolemia.
  • If the patient has hypotension that is refractory to fluid resuscitation, vasopressor support should be initiated. Phenylephrine may be the best choice for a neurogenic shock as it has pure vasoconstriction effects, and studies have shown that it increases cerebral perfusion pressure (CPP) without increasing intracranial pressure (ICP). In patients who are bradycardic due to Cushing’s reflex, norepinephrine may be a better choice.
  • Packed red blood cells should be transfused for a goal of Hb over 10 mg/dL in severe TBI.
  • Coagulopathy should be corrected.

Increased intracranial pressure

  • Cerebral perfusion pressure (CPP) = mean arterial pressure (MAP) – intracranial pressure (ICP)
  • Elevation of the head of the bed to 30 degrees or reverse Trendelenburg positioning can lower ICP
  • Hyperosmolar therapy via mannitol using a bolus of 1 g/kg and/or hypertonic saline (dosing depends on the concentration available and vascular access) may be given to reduce ICP

Seizures

  • Patients with severe TBI, including GCS less than 10, cortical contusion, depressed skull fractures, subdural, epidural, subarachnoid, or intracerebral hemorrhage, penetrating head injury are at risk for seizures.
  • Seizure activity that is apparent clinically or on EEG should receive management with benzodiazepines and anti-epileptic drugs (AEDs).
  • Propofol may be optimal for post-intubation sedation.
  • AED prophylaxis should also is a viable option in severe TBI patients. Phenytoin or fosphenytoin are first-line, levetiracetam is an alternative that may have fewer side effects. Prophylaxis should last for 7 days.

Increased ICP

Increased ICP can occur in head trauma patients resulting in the mass occupying lesion. Utilize a team approach to manage impending herniation.

Signs and symptoms:

  • Change in mental status
  • Irregular pupils
  • Focal neurologic finding
  • Posturing: decerebrate or decorticate
  • Papilledema (may not be apparent with a rapid elevation of ICP)

CT scan findings:

  • Attenuation of sulci and gyri
  • Poor gray/white matter demarcation

General Measures

  • Head Position: Raise the head of the bed and maintain the head in midline position at 30 degrees: potential to improve cerebral blood flow by improving cerebral venous drainage.
  • Lower cerebral blood volume (CBV) can lower ICP.
  • Temperature Control: Fever should be avoided as it increases cerebral metabolic demand and affects ICP.
  • Seizure prophylaxis: Seizures should be avoided as they can also worsen CNS injury by increasing the metabolic requirement and may potentially increase ICP. Consider administering fosphenytoin at a loading dose of 20mg/kg.
  • Only use an anticonvulsant when it is necessary, as it may inhibit brain recovery.
  • Fluid management: The goal is to achieve euvolemia. This will help to maintain adequate cerebral perfusion. Hypovolemia in head trauma patients is harmful. Isotonic fluid such as normal saline or Ringer Lactate should be used. Also, avoid hypotonic fluid.

Sedation: Consider sedation as agitation and muscular activity may increase ICP.

  • Fentanyl: Safe in intubated patients
  • Propofol: A short-acting agent with good sedative properties, the potential to lower ICP, possible risk of hypotension and fatal acidosis
  • Versed: sedative, anxiolytic, possible hypotension
  • Ketamine: Avoid as it may increase ICP.
  • Muscle relaxants: Vecuronium or Rocuronium are the best options for intubation; Succinylcholine should not be used as ICP may rise with fasciculations.

ICP monitoring:

  • Severe head injury
  • Moderate head injury with increased risk factors such as abnormal CT scan finding
  • Patients who cannot be evaluated with serial neurological examination
  • ICP monitoring is often done in patients with severe trauma with a GCS of less than 9. The reference range for normal CIP is 2-15 mmHg. In addition, the waveform of the tracing is important.

Hyperventilation:

Normocarbia is desired in most head trauma patients. The goal is to maintain PaCO between 35-45 mmHg. Judicious hyperventilation helps to reduce PaCO2 and causes cerebral vasoconstriction. Beware that, if extreme, it may reduce CPP to the point that exacerbation of secondary brain injury may occur. Avoid hypercarbia: PaCO > 45 may cause vasodilatation and increases ICP.

Mannitol:

  • A potent osmotic diuretic with net intravascular volume loss
  • Reduces ICP and improves cerebral blood flow, CPP, and brain metabolism
  • Expands plasma volume and can improve oxygen-carrying capacity
  • The onset of action is within 30 minutes
  • Duration of action is from two to eight hours
  • Dose is 0.25-1 g/kg (maximum: 4 g/kg/day)

Avoid serum sodium > 145 m Eq/L

  • Serum sodium > 145 m Eq/L
  • Serum osmolality > 315 mOsm

Relative contraindication:  hypotension does not lower ICP in hypovolemic patients.

Hypertonic saline:

May be used in hypotensive patients or patients who are not adequately resuscitated.

The dose is 250 mL over 30 minutes.

Serum osmolality and serum sodium should be monitored.

Hypothermia may be used to lower cerebral metabolism but it is important to be aware that hypothermia also makes the patient susceptible to infections and hypotension.

Mild Head Trauma

The majority of head trauma is mild. These patients can be discharged following a normal neurological examination as there is minimal risk of developing an intracranial lesion.

Consider observing at least 4 to 6 hours if no imaging was obtained.

Consider hospitalization if these other risk factors are present:

  • Bleeding disorder
  • Patient taking anticoagulation therapy or antiplatelet therapy
  • Previous neurosurgical procedure

Provide strict return precautions for patients discharged without imaging.

Rehabilitation

Areas covered in brain injury rehabilitation programs may include:

  • Self-care skills, including activities of daily living (ADLs): feeding, grooming, bathing, dressing, toileting, and sexual functioning
  • Physical care: nutritional needs, medicines, and skin care
  • Mobility skills: walking, transfers, and self-propelling a wheelchair
  • Communication skills: speech, writing, and alternative methods of communication
  • Cognitive skills: speech, writing, and alternative methods of communication
  • Socialization skills: interacting with others at home and within the community
  • Vocational training: work-related skills
  • Pain management: medicines and alternative methods of managing pain
  • Psychological testing and counseling: identifying problems and solutions with thinking, behavioral, and emotional issues
  • Family support: assistance with adapting to lifestyle changes, financial concerns, and discharge planning
  • Education: patient and family education and training about brain injury, safety issues, home care needs, and adaptive techniques

Physical Rehabilitation

TBI may result in a decrease in short and long-term global health (physical and behavioral) and put them at an elevated risk for disability, pain, and handicap (i.e., difficulty with a return to work, maintaining peer networks.) Rehabilitation therapies like physical therapy, occupational therapy, speech-language therapy, and assistive devices and technologies may help to strengthen patients to perform their activities of daily living.

Psychotherapy

  • Initial education, long-term support groups (symptom-focused and process groups), family education, and social issues like financial, legal and transportation.
  • Virtual reality and videogaming-based therapy in treating balance, coordination, and cognitive issues like attention and concentration data are under larger scale clinical trials to prove efficacy.

Medications

  • Depakote, NSAIDs, and triptans: May be considered for headaches which are the single most common symptom associated with concussion/mTBI
  • SSRIs: Citalopram 10 mg daily for 1 week, then 20 mg daily if tolerated (up to 80 mg daily if needed). Sertraline 25 mg daily increasing weekly in 25 mg increments to a maximum dose of 200 mg/day for depression
  • Anticonvulsants: mood stabilization and seizure prevention
  • Atypical antipsychotics: for agitation and irritability with beta-blockers in severe cases
  • Dopaminergic agents: for concentration and focus
  • Cholinesterase inhibitors/cognitive enhancers for memory
  • Atypical agents: Buspar for emotional stabilization and Modafinil for focus.

General Guidelines for Using Medications:

  • Start low, go slow, whenever medications are required
  • Rule out social factors first, such as abuse, neglect, caregiver conflict, and environmental issues
  • No large quantities of lethal medications, high suicide rate due to disinhibition
  • Full therapeutic trials, since under treatment is common
  • Minimize benzodiazepines (impairs cognition), anticholinergics (induces sedation), seizure-inducing (impedes neuronal recovery), and antidopaminergic agents
  • No caffeine (due to agitation and insomnia), no diet, herbal, or energy drinks (may precipitate aggression).

Other Considerations in Treating PTSD in Patients with mTBI

  • Present information at a slower rate
  • Use a structured intervention approach with agenda, outline, or handouts
  • In groups, ask “PTSD” to respond first, then ask others to respond
  • Allow free contribution, use refocus/redirection with a clear transition between topics
  • The therapist should avoid frustrating mTBI patients by forcing them to recall incidents that are only partially encoded.

Management of Sleep Dysfunction

Immediately following TBI, the difficulty in falling asleep and frequent waking is common; whereas, after several years excessive somnolence is more typical.

  1. Acute Phase less than 3 months: Provide education about concussion about changes in sleep quality and duration sometimes associated with concussion. Provide information on good sleep habits with specific suggestions to improve the quality and duration of sleep (regularly scheduled bedtime). Sleep medications may be helpful in the short-term. Zolpidem 5 mg at night, if poor results after 3 nights of therapy, increase to 10 mg nightly. Also, prazosin, with 1 mg at bedtime for 3 days, may increase to 2 mg at bedtime through day 7.
  2. Chronic phase: more than 3 months: Review current medications and other current health conditions for factors that might contribute to chronic sleep disturbances, including chronic pain or co-morbid psychiatric conditions. Consider sleep study to provide objective evidence of sleep disturbance and to rule out coexisting sleep apnea or other sleep disorders. Consider a course of cognitive-behavioral therapy (CBT) focused on sleep.

Complications

  • Deep vein thrombosis rates are higher in head trauma patients
  • Neurological deficits
  • CSF leak
  • Hydrocephalus
  • Infections
  • Seizures
  • Cerebral edema
  • Post-traumatic seizures
  • Deep vein thrombosis
  • Hydrocephalus
  • Spasticity
  • Mood and behavior changes
  • Gait abnormalities
  • Cognitive decline
  • PTSD
  • Post-traumatic headache
  • Insomnia

Complications

Several complications can occur immediately or soon after a traumatic brain injury. Severe injuries increase the risk of a greater number and more-severe complications.

Altered consciousness

Moderate to severe traumatic brain injury can result in prolonged or permanent changes in a person’s state of consciousness, awareness or responsiveness. Different states of consciousness include:

  • Coma. A person in a coma is unconscious, unaware of anything and unable to respond to any stimulus. This results from widespread damage to all parts of the brain. After a few days to a few weeks, a person may emerge from a coma or enter a vegetative state.
  • Vegetative state. Widespread damage to the brain can result in a vegetative state. Although the person is unaware of surroundings, he or she may open his or her eyes, make sounds, respond to reflexes, or move.

    It’s possible that a vegetative state can become permanent, but often individuals progress to a minimally conscious state.

  • Minimally conscious state. A minimally conscious state is a condition of severely altered consciousness but with some signs of self-awareness or awareness of one’s environment. It is sometimes a transitional state from a coma or vegetative condition to greater recovery.
  • Brain death. When there is no measurable activity in the brain and the brainstem, this is called brain death. In a person who has been declared brain dead, removal of breathing devices will result in cessation of breathing and eventual heart failure. Brain death is considered irreversible.

Physical complications

  • Seizures. Some people with traumatic brain injury will develop seizures. The seizures may occur only in the early stages, or years after the injury. Recurrent seizures are called post-traumatic epilepsy.
  • Fluid buildup in the brain (hydrocephalus). Cerebrospinal fluid may build up in the spaces in the brain (cerebral ventricles) of some people who have had traumatic brain injuries, causing increased pressure and swelling in the brain.
  • Infections. Skull fractures or penetrating wounds can tear the layers of protective tissues (meninges) that surround the brain. This can enable bacteria to enter the brain and cause infections. An infection of the meninges (meningitis) could spread to the rest of the nervous system if not treated.
  • Blood vessel damage. Several small or large blood vessels in the brain may be damaged in a traumatic brain injury. This damage could lead to a stroke, blood clots or other problems.
  • Headaches. Frequent headaches are very common after a traumatic brain injury. They may begin within a week after the injury and could persist as long as several months.
  • Vertigo. Many people experience vertigo, a condition characterized by dizziness, after a traumatic brain injury.

Sometimes, any or several of these symptoms might linger for a few weeks to a few months after a traumatic brain injury. This is currently referred to as persistent post-concussive symptoms. When a combination of these symptoms last for an extended period of time, this is generally referred to as post-concussion syndrome.

Traumatic brain injuries at the base of the skull can cause nerve damage to the nerves that emerge directly from the brain (cranial nerves). Cranial nerve damage may result in:

  • Paralysis of facial muscles or losing sensation in the face
  • Loss of or altered sense of smell
  • Loss of or altered sense of taste
  • Loss of vision or double vision
  • Swallowing problems
  • Dizziness
  • Ringing in the ear
  • Hearing loss

Intellectual problems

Many people who have had a significant brain injury will experience changes in their thinking (cognitive) skills. It may be more difficult to focus and take longer to process your thoughts. Traumatic brain injury can result in problems with many skills, including:

Cognitive problems

  • Memory
  • Learning
  • Reasoning
  • Judgment
  • Attention or concentration

Executive functioning problems

  • Problem-solving
  • Multitasking
  • Organization
  • Planning
  • Decision-making
  • Beginning or completing tasks

Communication problems

Language and communications problems are common following traumatic brain injuries. These problems can cause frustration, conflict and misunderstanding for people with a traumatic brain injury, as well as family members, friends and care providers.

Communication problems may include:

Cognitive problems

  • Difficulty understanding speech or writing
  • Difficulty speaking or writing
  • Inability to organize thoughts and ideas
  • Trouble following and participating in conversations

Social problems

  • Trouble with turn taking or topic selection in conversations
  • Problems with changes in tone, pitch or emphasis to express emotions, attitudes or subtle differences in meaning
  • Difficulty understanding nonverbal signals
  • Trouble reading cues from listeners
  • Trouble starting or stopping conversations
  • Inability to use the muscles needed to form words (dysarthria)

Behavioral changes

People who’ve experienced brain injury often experience changes in behaviors. These may include:

  • Difficulty with self-control
  • Lack of awareness of abilities
  • Risky behavior
  • Difficulty in social situations
  • Verbal or physical outbursts

Emotional changes

Emotional changes may include:

  • Depression
  • Anxiety
  • Mood swings
  • Irritability
  • Lack of empathy for others
  • Anger
  • Insomnia

Sensory problems

Problems involving senses may include:

  • Persistent ringing in the ears
  • Difficulty recognizing objects
  • Impaired hand-eye coordination
  • Blind spots or double vision
  • A bitter taste, a bad smell or difficulty smelling
  • Skin tingling, pain or itching
  • Trouble with balance or dizziness

References

  1. https://www.ncbi.nlm.nih.gov/books/NBK430854/
  2. https://www.ncbi.nlm.nih.gov/books/NBK549892/
  3. https://www.ncbi.nlm.nih.gov/books/NBK430770/
  4. https://www.ncbi.nlm.nih.gov/books/NBK537017/
  5. https://www.ncbi.nlm.nih.gov/books/NBK537017/
  6. https://www.ncbi.nlm.nih.gov/books/NBK448102/
  7. https://www.ncbi.nlm.nih.gov/books/NBK459300/
  8. https://en.wikipedia.org/wiki/Traumatic_brain_injury
  9. https://www.hopkinsmedicine.org/health/conditions-and-diseases/traumatic-brain-injury
  10. https://www.mayoclinic.org/diseases-conditions/traumatic-brain-injury/diagnosis-treatment/drc-20378561
  11. https://www.aans.org/en/Patients/Neurosurgical-Conditions-and-Treatments/Traumatic-Brain-Injury
  12. https://www.cdc.gov/traumaticbraininjury/symptoms.html
  13. https://medlineplus.gov/traumaticbraininjury.html

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