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Notes module 11: Neurosensory: Traumatic Brain Injury (tbi) Marnie Quick, rn, msn, cnrn etiology/Pathophysiology of tbi

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Module 11: Neurosensory: Traumatic Brain Injury (TBI)

Marnie Quick, RN, MSN, CNRN
Etiology/Pathophysiology of TBI

  1. Normal brain physiology as it relates to traumatic brain injury

    1. Brain is protected by skull, meninges, CSF (p. 1293 Fig 40-3)

  2. Risk factors

    1. Motor vehicle accidents (MVA)

    2. Elevated blood alcohol level

    3. Contact sports

  3. Mechanisms of craniocerebral trauma

    1. Acceleration injury- head struck by moving object- as swinging bat.

    2. Deceleration injury- head hits stationary object- as concrete wall.

    3. Coup-countrecoup phenomenon(p.1373 Fig 42-5)

      1. Brain rebounds within the skull, hitting both sides of the skull

      2. Usually the countrecoup injury (opposite side of initial impact) causes more severe brain injury

    4. Blunt or penetrating injury to the brain

    5. Closed head injury- potentially more dangerous due to the enclosed space of the skull.

  4. Skull fracture (p. 1373 Table 42-6)

    1. Linear fracture- simple break, dura intact (80% of all skull fractures)

    2. Comminuted- fragmented- have increase chance for infection

    3. Depressed- inward displacement

    4. Basilar-

      1. Any of the above fractures along the base of the skull

      2. Battle’s sign: blood over the mastoid process (ecchymosis behind the ear)

      3. Raccoon eyes: bilateral periorbital ecchymosis

      4. If dura is disrupted may have leakage of CSF occurring as rhinorrhrea (nose) or otorhrea (from ear)

  1. Primary brain injury- Focal brain injuries (p. 1373 Fig 42-6)

    1. Most commonly caused by the coup-contracoup, causing brain injury to a specific part of the brain.

    2. Peek effect 18-36 hrs after impact.

    3. Contusion

      1. Bruising of the surface of the brain is usually the result of the movement of the brain hitting the rough inner surfaces of the skull.

    4. Epidural hematoma

      1. Bleeding into the potential space between the dura and the skull. Normally dura and skull adhere to each other.

      2. More arteries are located in this area; therefore bleeding occurs quickly.

      3. Most common artery torn- middle meningeal artery from a fracture of the temporal bone.

      4. Characteristic symptoms- initial loss of consciousness followed by a lucid period, before the expanding hematoma causes a decrease level of consciousness to coma.

      5. Symptoms of increased intracranial pressure.

      6. Emergency situation due to fast bleed

    1. Subdural Hematoma

      1. Bleeding between dura mater and the arachnoid of the meninges.

      2. More veins located in this area; therefore tends to be a slow bleed

      3. More common than epidural

      4. Acute- bleed that develops within 48 hrs after injury.

      5. Chronic- bleed that develops over weeks or months. Often associated with older adults, alcoholics or individuals with bleeding disorders. Maybe misdiagnosed as dementia.

    2. Intracerebral hematoma

      1. Single or multiple bleeds within the brain.

      2. Usually deep blood vessels are affected by the shearing force of the head injury.

  1. Primary Brain Injury- Diffuse brain injury

    1. Affects the entire brain and is caused by the swirling or twisting movement of the brain within the cranium.

    2. This category includes concussion and diffuse axonal injury.

    3. Concussion (p. 1377 box at bottom)

      1. Temporary axonal injury that results in an interruption of brain function.

      2. Concussions are graded (I-V) from mild to severe

      3. May be discharged home- teach signs of IICP

      4. Post Concussion Syndrome may persist for several weeks or months. Only closest friends may notice the change in behavior, which include headache, general tiredness, dizziness, irritability, memory and concentration difficulties, learning difficulty, insomnia, etc. May occur after other brain injuries, and severity of symptoms are not related to severity of brain injury.

    4. Diffuse axonal injury

      1. Caused by high speed acceleration-deceleration injury resulting in widespread disruption of axons and generally causing a very poor prognosis.

  2. Secondary brain injury

    1. Cerebral edema-

      1. Localized edema around the primary brain injury or diffuse edema throughout the whole brain.

      2. Peaks 24-72 hrs after brain injury

      3. May in itself cause death by herination

      4. May be the result of closed head injury (CHI), open head injury with or without bleeding in the brain, or anoxia resulting from an MI or near drowning.

    2. Increased intracranial pressure (IICP) (Refer to Module #10)

    3. Herniation syndromes (Refer to Module #10)

Common Manifestations/Complications

  1. Comparsion of intracranial hematomas- manifestations (p. 1376 Table 42-7)

  2. Increased intracranial pressure symptoms.

  3. Restlessness may occur as a result of hypoxia, increase intracranial pressure or the client is trying to wake up.

  4. Manifestations of concussion and post concussion syndrome (p. 1377 box at bottom)

  5. Systemic effects of acute brain injury (p.1375 Box 42-3)

  6. CSF leak from nose (rhinorrhea)/ ear (otorrhea)– may be seen with basal skull fractures.

  7. ‘Brainstorming’ is hypothalamic stimulation with autonomic nervous system and adrenals increasing circulation corticoids and catecholamines. Ambiguous symptoms such as hyperthermia (neurogenic temperature), hypertension, diaphoresis, etc.

  8. Post concussion Syndrome (refer to Patho 6 and p. 1377)

  9. May sustain spinal cord injury with head injury, especially cervical

Therapeutic Interventions

  1. Diagnostic tests

    1. Skull X-ray, spinal X-ray (R/O spinal injury) CT/MRI, EEG

    2. ABG’s, CBC, glucose, electrolytes

  2. Treatment of increased intracraninal pressure

    1. Airway management- possible ventilator, O2

    2. Fluid resuscitation

    3. Positing- head of bed 30 degrees, no flexion of neck/hips

    4. Temperature regulation

    5. Medications- Osmotic diuretics

  3. Prevention of complications

    1. Medications to treat/prevent IICP; prevent/treat seizures; to treat other complications such as stress ulcer, stool soltners to prevent straining, and to treat ‘brainstorming- such as Morphine, thorazine, haldol, Inderal, antipyretics (also cooling individual with fans)

    2. Diet/calories- TBI causes a hypermetoblic state. Initially the GI tract may not absorb feedings, swallow/gag reflexes maybe lacking. May need TPN, progressing to NG tube feedings to oral with supplements. Calorie count essential.

    3. CSF leak- assess for glucose (not found in mucous drainage)/ assess for ‘halo’ affect on linens or a pad. Treat- HOB 30 degrees, do not blow nose/sniff, no nasal suctioning, do not pack, lightly cover- change when wet, prophylactic antibiotics. Physician may insert lumbar drain to decrease pressure, or surgically plug the leak with a piece of muscle.

    4. Other systemic effects (p. 1375) including SIADH a self-limiting syndrome the causes hyponatremia.

  4. Surgery

    1. Depressed and comminuted fractures- remove bone fragments. Basilar with CSF leakage may require surgery.

    2. Evacuation of the clot through burr holes (p. 1379 Fig 42-7)

    3. Craniotomy usually necessary for chronic subdural because of the normal changes that blood goes through with time- calcification.

    4. Intracerebral bleed may bleed diffusely throughout the brain, rather than a formed hematoma. This makes it difficult to remove.

    5. Placement of intracranial pressure monitoring devices. (refer to ICP module)

Nursing Assessment Specific to Traumatic Brain Injury (TBI)

  1. Health history

    1. Description of the accident, past medical history.

    2. Description of the neuro vital signs- esp. level of consciousness changes.

  1. Physical exam

    1. Neuro Vital Signs- describe the level of consciousness, pupils, movement of extremities. How often done depends on potential for developing ICP.

    2. Glasgow Coma Scale-(p. 1299 Table 40-4) Scale works best with traumatic brain injured individuals. Allows health care workers to communicate what the patient is like by a number. Based on eye opening, verbal, and motor response. Scores range from lowest level of 3 to highest functioning level of 15. Coma = 8.

    3. Brainstem reflexes- cornea, cough, gag, pupil, extra ocular movements (EOM’s)

    4. Vital signs- late sign- Systolic BP rising causing widen pulse pressure; Pulse decreasing- called Cushing reflex

    5. Skull and face; assess for spinal cord injury

  2. Take into consideration the assessment findings in the older adult (p. 1379 Box 42-4) when evaluating the assessment findings.

Pertinent Nursing Problems and Interventions

      1. Decreased intracranial adaptive capacity

        1. Assess/prevent IICP (refer to IICP module)

        2. Monitor fluid status

      2. Ineffective airway clearance

      3. Ineffective breathing pattern

      4. Home care

    1. Home evaluation, may need rehabilitation, nursing home placement

    2. Teaching about post concussion syndrome

    3. Community agencies/support groups

RNSG 2432 

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