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Definition:
Traumatic brain injury (TBI) is physical injury to brain tissue that temporarily or permanently impairs
brain function.
Pathology:
• Closed injuries typically occur when the head is struck, strikes an object,
or is shaken violently, causing rapid brain acceleration and deceleration.
• Acceleration or deceleration can injure tissue at the point of impact
(coup), at its opposite pole (contrecoup), or diffusely.
• The frontal and temporal lobes are particularly vulnerable.
• Axons, blood vessels, or both can be sheared or torn.
• Concussion:
– Concussion is defined as a transient and reversible posttraumatic
alteration in mental status (eg, loss of consciousness or memory,
confusion) lasting from seconds to minutes and not more than 6 h.
– No gross structural brain lesions and serious neurologic residua.
– Temporary disability can occur due to symptoms, such as nausea,
headache, dizziness, memory disturbance, and difficulty
concentrating (postconcussion syndrome) that usually resolve
within weeks.
• Brain Contusions:
– Contusions (bruises of the brain) can occur with open or closed
injuries.
– Contusions can impair a wide range of brain functions, depending
on contusion size and location.
– Larger contusions may cause brain edema and increased
intracranial pressure (ICP).
– Contusions may enlarge in the hours and days following the initial injury and cause
neurologic deterioration
• Hematomas:
– Hematomas can occur with open or closed injuries.
– They may be epidural, subdural, or intracerebral.
– Subarachnoid hemorrhage is common
Pathophysiology :
• Brain function may be immediately impaired by direct damage (eg, crush, laceration) of brain
tissue or occurs shortly thereafter from the cascade of events triggered by the initial injury.
• TBI of any sort can cause cerebral edema and decrease brain blood flow.
• Any swelling from edema or an intracranial hematoma has nowhere to expand and thus
increases ICP.
• The brain becomes ischemic.
• Systemic complications from trauma (eg, hypotension, hypoxia) can also contribute to cerebral
ischemia (secondary brain insults).
• Excessive ICP initially causes global cerebral dysfunction.
• If excessive ICP is unrelieved, it can push brain tissue across the tentorium or through the
foramen magnum, causing herniation and increased morbidity and mortality
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• Transtentorial herniation may result in coma, unilaterally or bilaterally dilated and unreactive
pupils, hemiplegia (usually on the side opposite a unilaterally dilated pupil), and Cushing triad
(hypertension, bradycardia and poor respiration).
Diagnosis:
• Initial measures:
– Perform a rapid, focused neurologic evaluation.
– Assess adequacy of the airway and breathing.
– Perform pupillary light response.
– Assessed before paralytics and sedatives are given.
– Reassessed at frequent intervals (eg, every 15 to 30 min initially, then every 1 h after
stabilization)
• Complete neurologic examination is done as soon as the patient is sufficiently stable.
• CT scan of the head is indicated for the following:
– Patients with impaired level of consciousness.
– GCS score < 15.
– focal neurologic findings.
– persistent vomiting.
– Seizures.
– a history of loss of consciousness.
– clinically suspected fractures.
• CT can detect hematomas, contusions and skull fractures.
• MRI may be useful later in the clinical course to detect more subtle contusions, DAI, and brain
stem injury.
• The vast majority of patients with mild TBI retain good neurologic function.
• With moderate or severe TBI, the prognosis is not good.
• The assessment of TBI outcomes is usually based on the GCS score as follows:
o 14 or 15 - Good recovery (return to previous level of function).
o 9 – 13 - Moderate disability (capable of self-care).
o 3 – 8 - Severe disability (incapable of self-care).
o < 8 - Vegetative (no cognitive function).
• Occurrence and duration of coma after a TBI are strong predictors of disability.
• Of patients whose coma exceeds 24 h, 50% have severe persistent neurologic sequelae, and 2 to
6% remain in a persistent vegetative state at 6 mo.
• Cognitive deficits, with impaired concentration, attention, and memory, and various personality
changes are a more common cause of disability.
• Posttraumatic anosmia and acute traumatic blindness seldom resolve after 3 to 4 mo.
• Hemiparesis and aphasia usually resolve at least partially, except in the elderly.
Treatment:
At The Scene:
• A clear airway is secured and external bleeding is controlled before the patient is moved.
• Avoid displacement of the spine or other bones to protect the spinal cord and blood vessels.
• Proper immobilization should be maintained with a cervical collar and long spine board.
• After the initial rapid neurologic assessment, pain should be relieved with a short-acting
opioid (eg, fentanyl ).
In the hospital:
• After quick initial evaluation, neurologic findings (GCS and pupillary reaction), BP, pulse, and
temperature should be recorded frequently for several hours because any deterioration
demands prompt attention.
• The cornerstone of management for all patients is -
maintenance of adequate ventilation, oxygenation, and brain perfusion to avoid
secondary brain insult.
aggressive early management of hypoxia, hypercapnia, hypotension, and increased
ICP helps avoid secondary complications.
Bleeding from injuries (external and internal) is rapidly controlled.
intravascular volume is promptly replaced with crystalloid (eg, 0.9% saline) or
sometimes blood transfusion to maintain cerebral perfusion.
Hypotonic fluids (especially 5% D/W) are contraindicated because they contain
excess free water, which can increase brain edema and ICP.
1. Mild injury:
• Injury is mild (GCS score 14-15) in 80% of patients.
• If there is brief or no loss of consciousness, vital signs are stable, a normal head CT scan,
and normal mental and neurologic function, they may be discharged home provided
family members or friends can observe them closely for an additional 24 h.
• The patients are brought back to the hospital if any of the following develop:
– Decreased level of consciousness
– Focal neurologic deficits.
– Worsening headache.
– Vomiting
– Deterioration of mental function (eg, seems confused, cannot recognize people,
behaves abnormally)
– Seizures.
4. Seizures:
• Seizures can worsen brain damage and increase ICP and therefore should be treated
promptly.
• In patients with significant structural injury (eg, larger contusions or hematomas, brain
laceration, depressed skull fracture) or a GCS score < 10, a prophylactic anticonvulsant
should be considered.
• Inj phenytoin is commonly used. A loading dose of 20 mg/kg IV is given followed by
maintenance dose of 2 to 2.7 mg/kg tid for adult.
5. Skull fractures:
• Aligned closed fractures require no specific treatment.
• Depressed fractures sometimes require surgery to elevate fragments, manage lacerated
cortical vessels, repair dura mater, and debride injured brain.
• Open fractures may require surgical debridement unless there is no CSF leak and the
fracture is not depressed by greater than the thickness of the skull.
6. Surgery:
• Intracranial hematomas may require urgent surgical evacuation to prevent or treat brain
shift, compression, and herniation.
• Small intracerebral and subdural hematomas rarely require surgery.
• Factors that suggest a need for surgery include -
a midline brain shift of > 5 mm.
7. Rehabilitation:
• When neurologic deficits persist, rehabilitation is needed.
• Rehabilitation is best provided through a team approach that combines physical,
occupational, and speech therapy, skill-building activities, and counseling to meet the
patient's social and emotional needs.
• Brain injury support groups may provide assistance to the families of brain-injured
patients.