Traumatic brain injury

43 Traumatic brain injury




Overview/pathophysiology


Traumatic brain injury (TBI) can cause varying degrees of damage to the skull and brain tissue. Primary injuries occur at the time of impact and include skull fracture, concussion, contusion, scalp laceration, brain tissue laceration, and tear or rupture of cerebral vessels. Secondary problems that arise soon after and are the result of the primary injury include hemorrhage and hematoma formation from tear or rupture of vessels, ischemia from interrupted blood flow, cerebral swelling and edema, infection (e.g., meningitis or abscess), and increased intracranial pressure (IICP) or herniation, any of which can interrupt neuronal function. These secondary injuries or events increase the extent of initial injury and result in poorer recovery and higher risk of death. Cervical neck injuries are commonly associated with TBIs. Because of the potential for spinal cord injury, all TBI patients should be assumed to have cervical neck injury until it is conclusively ruled out by cervical spine x-ray examination.


Most TBIs result from direct impact to the head. Depending on force and angle of impact, the brain may suffer injury directly under the point of impact (coup) or in the region opposite the point of impact (contrecoup) because of brain rebound action within the skull, or tissue tearing or shearing may occur elsewhere because of the rotational action of the brain within the cranial vault. TBI may be classified by location, severity, extent, or mechanism (contact, acceleration, deceleration, rotational). Common causes include motor vehicle accidents; falls; and sports-related injuries, such as those occurring in football or boxing. Acts of violence, such as gunshot or stab wounds, often result in missile or impalement TBIs.



Health care setting


Acute care (trauma center, intensive care); rehabilitation unit



Assessment


The Glasgow Coma Scale (GCS) standardizes observations for objective assessment of a patient’s level of consciousness (LOC). GCS 13-15 is mild, 9-12 is moderate, and 3-8 is severe. This or some other objective scale should be used to prevent confusion with terminology and to quickly detect changes or trends in patient’s LOC. LOC is the most sensitive indicator of overall brain function.




Concussion:


Mild diffuse TBI in which there is temporary, reversible neurologic impairment may involve loss of consciousness and possible amnesia of the event. No damage to brain structure is visible on computed tomography (CT) scan or magnetic resonance imaging (MRI) examination.


TBI concussions have been given the following grades:


• Grade I: No loss of consciousness


• Transient confusion

• Symptoms resolve in less than 15 min

• Grade II: No loss of consciousness


• Transient confusion

• Symptoms last more than 15 min

• If symptoms last more than 1 wk, imaging may be needed

• Grade III: Any loss of consciousness

After concussion, patients may have headache, dizziness, nausea, lethargy, difficulty focusing, and irritability, especially to bright lights or loud noises. Although full recovery usually occurs in a few days, a postconcussion syndrome with headache; dizziness; irritability; emotional lability; lethargy; sleep disturbance; and decreased attention, judgment, concentration, and memory abilities may continue for several weeks or months.



Diffuse axonal injury:


Diffuse brain injury caused by stretching and tearing of the neuronal projections because of a rotational, shearing type of injury. Diffuse microscopic damage occurs. No distinct focal lesion, such as infarction, ischemia, contusion, or intracerebral bleeding, is noted, but patients have an immediate and prolonged unconsciousness of at least 6-hr duration. CT scan may show small hemorrhagic areas in the corpus callosum, cerebral edema, and small midline ventricles. Brain stem injury may be associated with diffuse axonal injury (DAI), resulting in autonomic dysfunction. Mild DAI is coma lasting 6-24 hr with patient beginning to follow commands by 24 hr. Full recovery is expected. Moderate DAI is coma lasting longer than 24 hr but without prominent brain stem signs. Severe DAI is prolonged coma with prominent brain stem signs, such as decortication or decerebration, and usually predicts severe disability, possible vegetative state, or death.



Contusion:


Bruising of brain tissue, which produces a longer-lasting neurologic deficit than concussion. Size and severity of bruising vary widely, and the bruise or a small, diffuse venous hemorrhage usually is visible on CT scan. Traumatic amnesia often occurs, causing loss of memory not only of the trauma, but also of events occurring before the incident. Loss of consciousness is common, and it is generally more prolonged than that with concussion. Changes in behavior, such as agitation or confusion, can last for several hours to days. Headache, nausea, lethargy, motor paralysis, paresis, and possibly seizures can occur as well. Depending on extent of damage, there is potential for either full recovery or permanent neurologic deficit, such as seizures, paralysis, paresis, or even coma and death.



Brain laceration:


Actual tearing of the brain’s cortical surface, resulting in direct mechanical disruption of neural function and causing focal deficits. Blood vessel tearing causes hemorrhage, resulting in contusion, edema, or hematoma formation. Seizures often occur as well. Brain lacerations usually result from depressed skull fractures, penetrating injuries, missile or impalement injuries, or rotational shearing injury within the skull. Shock waves from a bullet’s high energy produce additional damage. A knife or other impalement object should be supported and left in the wound to control bleeding until it can be removed during surgery. Contusions and lacerations often are found together. The consequences of a laceration usually are more serious than those with a contusion because of the increased severity of trauma.



Skull fracture:


Can be closed (simple, with skin intact) or open (compound), depending on whether the scalp is torn, thereby exposing the skull to the outside environment. Skull fractures are further classified as linear (hairline), comminuted (fragmented, splintered), or depressed (pushed inward toward the brain tissue). A blow forceful enough to break the skull is capable of causing significant brain tissue damage, and therefore close observation is essential. With a penetrating wound or basilar fracture (see below), there is potential for cerebrospinal fluid (CSF) leakage, meningitis, encephalitis, brain abscess, cellulitis, or osteomyelitis.


• Basilar fractures: Fractures of the base of the skull do not show up easily on skull/cervical x-ray examination. Indicators include blood from the nose, throat, ears; serous or serosanguineous drainage from the nose (rhinorrhea), throat, ears (otorrhea), eyes; Battle’s sign (bruising noted behind the ear); “raccoon’s eyes” (bruising around eyes in the absence of eye injury); and bleeding behind the tympanum (eardrum) noted on otoscopic examination. Glucose in serous drainage signals the presence of CSF. CSF leakage indicates a tear in the dura, making the patient particularly susceptible to meningitis. Basilar fractures may damage the internal carotid artery and cranial nerves. Hearing loss also may occur.

• Temporal fractures: May result in deafness or facial paralysis.

• Occipital fractures: May cause visual field and gait disturbances.

• Sphenoidal fractures: May disrupt the optic nerve, possibly causing blindness.


Rupture of cerebral blood vessels



• Epidural (extradural) hematoma or hemorrhage: Usually, bleeding between the dura mater (outer meninges) and skull causes hematoma formation. This creates pressure on the underlying brain and produces a local mass effect, causing IICP and shifting of tissue, which leads to brain stem compression and herniation. Indicators are primarily those of IICP: altered LOC, headache, vomiting, unilateral pupil dilation (on same side as the lesion), and possibly hemiparesis. Although some individuals never regain consciousness, most patients lose consciousness for a short period immediately after injury, regain consciousness, and have a lucid period lasting a few hours or 1-2 days. However, because arterial bleeding causes a rapid rise in intracranial pressure (ICP), a rapid decrease in LOC often ensues. The bleeding site often is the middle meningeal artery or vein because of temporal bone fracture. These patients are at risk for brain stem herniation. A unilateral dilated fixed pupil is a sign of impending herniation and is a neurosurgical emergency. Patients should not be left alone because respiratory arrest may occur at any time.

• Subdural hematoma or hemorrhage: Accumulation of venous blood between the dura mater (outer meninges) and arachnoid membrane (middle meninges) that is not reabsorbed. Hematoma formation creates pressure on the underlying brain and produces a local mass effect, causing IICP and shifting of tissue, leading to brain stem compression and herniation. This type of hematoma is classified as acute, subacute, or chronic depending on how quickly indicators arise. In acute subdural hematomas, indicators appear within 24-48 hr, resulting from focal neurologic deficit (hemiparesis, pupillary dilation) and IICP (decreased LOC, falling GCS score, nausea, vomiting, headache). When indicators occur 2-14 days later, the hematoma is considered subacute. When indicators occur more than 2 wk later, it is considered chronic. Early indicators can include headache, progressive personality changes, decreased intellectual functioning, slowness, confusion, and drowsiness. Later indicators may include unilateral weakness or paralysis, loss of consciousness, and occasionally seizures. Patients with cerebral atrophy (e.g., older persons, long-term alcohol users) are more prone to subdural hematoma formation.

• Intracerebral hemorrhage: Arterial or venous bleeding into the brain’s white matter. Signs of IICP may develop early if the bleeding causes a rapidly expanding space-occupying lesion. If the bleeding is slower, signs of IICP can take 36-72 hr to develop. Indicators depend on hematoma location and size and can include altered LOC, headache, aphasia, hemiparesis, hemiplegia, hemisensory deficits, pupillary changes, and loss of consciousness.

• Subarachnoid hemorrhage: Bleeding into the subarachnoid space below the arachnoid membrane (middle meninges) and above the pia mater (inner meninges next to brain). The patient often has a severe headache. Other general indicators include vomiting, restlessness, seizures, and loss of consciousness. Signs of meningeal irritation include nuchal rigidity and positive Kernig’s and Brudzinski’s signs (see p. 256). This patient may be a candidate for a shunt because of hemorrhagic interference with CSF circulation and reabsorption and is at particular risk of cerebral vasospasm.


Indicators of IICP



• Early indicators: Alteration in LOC ranging from irritability, restlessness, and confusion to lethargy; possible onset or worsening of headache; beginning pupillary dysfunction, such as sluggishness; visual disturbances, such as diplopia or blurred vision; onset of or increase in sensorimotor changes or deficits, such as weakness; onset or worsening of nausea.

• Late indicators: Continued deterioration of LOC leading to stupor and coma; projectile vomiting; hemiplegia; posturing; alterations in vital signs (VS) (typically increased systolic blood pressure [SBP], widening pulse pressure, decreased pulse rate); respiratory irregularities, such as Cheyne-Stokes breathing; pupillary changes, such as inequality, dilation, and nonreactivity to light; papilledema; and impaired brain stem reflexes (corneal, gag, swallowing).

Note: The single most important early indicator of IICP is a change in LOC. Late indicators of IICP usually signal impending or occurring brain stem herniation. Signs generally are related to brain stem compression and disruption of cranial nerves and vital centers. Hypotension and tachycardia in the absence of explainable causes, such as hypovolemia, usually are seen as a terminal event in TBI. IICP usually peaks around 72 hr after initial insult and then gradually subsides over 2-3 wk.



Brain herniation:


Brain herniation occurs when IICP causes displacement of brain tissue from one intracranial compartment to another, resulting in compression, destruction, and laceration of brain tissue. See late indicators of IICP for signs of impending or initial herniation. In the presence of actual brain herniation, patient is in a deep coma, pupils become fixed and dilated bilaterally, posturing may progress to bilateral flaccidity, brain stem reflexes generally are lost, and respirations and VS deteriorate and may cease.



Brain death:


Criteria for determining brain death are not universally agreed upon. Check state and institutional guidelines. General criteria include absent brain stem reflexes (e.g., apnea, pupils nonreactive to light, no corneal reflex, no oculovestibular reflex to ice-water calorics), absent cortical activity (e.g., several flat electroencephalogram [EEG] tracings spaced over time), and coma irreversibility continued over a specific timeframe (e.g., 24 hr). Brain stem auditory-evoked responses and cerebral blood flow studies (e.g., transcranial Doppler, angiography, brain scan with a cerebral perfusion agent) also may be used to help confirm brain death.



Diagnostic tests




Cervical spine and skull x-ray examinations:


To locate neck and skull fractures. Because of the close association between TBIs and spinal or vertebral injuries, cervical immobilization is essential until cervical x-ray examination rules out fracture and potential SCI.



CT scan:


Used with acute injury to identify type, location, and extent of injury, such as accumulation of blood or a shift of midline structure caused by IICP.



MRI scan:


To identify type, location, and extent of injury. Although not usually performed in acute, unstable patients, this test is the study of choice for subacute or chronic TBI. It is superior to CT scan for detecting isodense chronic subdural hematomas or evaluating contusions and shearing injuries, especially in the brain stem area. MRI techniques such as fluid attenuated inversion recovery (FLAIR) are particularly sensitive to detecting DAI and small hemorrhages.



Cerebral blood flow studies (transcranial doppler, xenon inhalation enhanced ct):


To determine focal areas of low blood flow or spasm, possibly indicating ischemic areas, by noninvasively measuring cerebral blood flow velocities.



EEG:


To reveal abnormal electrical activity indicating neuronal damage caused by ischemia or hemorrhage. EEG may be used to establish brain death in conjunction with other tests and may be done serially to assess development of pathologic waves.



Evoked potentials:


To evaluate integrity of the anatomic pathways and connections of the brain. Stimulation of a sense organ, such as an ear, triggers a discrete electrical response (i.e., evoked potential) along a neurologic pathway to the brain. Measurement of the brain’s response to auditory, visual, and/or somatosensory stimulation also aids in predicting neurologic outcome.



Positron emission tomography:


To evaluate tissue metabolism of glucose and oxygen.



Single photon emission CT:


To determine low cerebral blood flow and areas at risk for ischemic tissue perfusion.



Infrared spectroscopy:


To continuously and noninvasively assess cerebral O2 saturation.



Cerebral angiography:


To reveal presence of a hematoma and status of blood vessels secondary to rupture or compression. Angiography usually is performed only if CT scan or MRI scan is unavailable or to evaluate possible carotid or vertebral artery dissection.



Cisternogram:


To identify dural tear site with basilar skull fracture.



CSF analysis:


To evaluate for infection, if indicators are present.



Nursing diagnosis for patients going home with a concussion





Nursing diagnosis:



Deficient knowledge


related to unfamiliarity with caretaker’s responsibilities for observing patient who is sent home with a concussion


Desired Outcomes: Following instruction, caretaker verbalizes knowledge about the observation regimen. Caretaker returns patient to the hospital if neurologic deficits are noted.


















ASSESSMENT/INTERVENTIONS RATIONALES
Assess caretaker’s health care literacy (language, reading, comprehension). Assess culture and culturally specific information needs. This assessment helps ensure that materials are selected and presented in a manner that is culturally and educationally appropriate.
Give the following instructions:  

– Do not give patient anything stronger than acetaminophen to relieve headache.
 A possible exception is codeine for pain control. Otherwise, opioids and other medications that alter mentation are avoided because they can mask neurologic indicators of IICP and cause respiratory depression. Aspirin is usually contraindicated because it can prolong bleeding if it occurs.

– Assess patient at least q1-2h for first 24 hr as follows: awaken patient; ask patient’s name, location, and caretaker’s name; monitor for twitching or seizure activity.
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Jul 18, 2016 | Posted by in NURSING | Comments Off on Traumatic brain injury

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