Traumatic Brain Injury

Increased ICP

- dec LOC - behavioral changes: restlessness, irritability, & confusion - HA - nausea & vomiting - changes in speech pattern: aphasia, slurred speech - change in sensorimotor status: pupillary changes, cranial nerve dysfunction, ataxia - seizures - Cushing' triad: severe hypertension, widened pulse pressure, bradycardia - abnormal posturing: decerebrate (extensor), decorticate(flexion) LATE: HA, nausea, vomiting & seizures

1st priority

ABCs

Intracerebral hemorrhage

Accumulation of blood within the brain tissue caused by the tearing of small arteries & veins in the subcortical white matter. Acts like a tumor & can be devastating depending on location.

Secondary brain injury

Any process that occurs after the initial injury & worsen or negatively influence pt outcomes. Result from hypotension & hypoxia, intracranial hypertension, & cerebral edema. Damage occurs primarily bc the delivery of oxygen & glucose to the brain is interrupted.

Maintain fluid & electrolyte balance

At risk for DI & SIADH Fluid overload can occur & cerebral edema can worsen from rapid admin of IV fluids

Vital sign assessment

BP & pulse. Hypo or hypertension. Cushings triad is a LATE sign of increased ICP- usually indicate imminent death.

Mild TBI

CONCUSSION: characterized by a blow to the head, transient confusion or feeling dazed or disoriented, & one or more of these conditions: (1) loss of consciousness for up to 30 min (2) loss of memory for events immediately before or after the accident (3) focal neurological deficit(s) that may or may not be transient. No evidence of brain damage on MRI or CT - appears dazed or stunned - loss of consciousness <30 min - headache - nausea - vomiting - balance or gait problems - dizziness - visual problems - fatigue - sensitivity to light & noise - feeling mentally foggy - feeling slowed down - difficulty concentrating - difficulty remembering - amnesia about the events around the time of injury - drowsiness - sleeping more or less than usual - trouble falling asleep - Irritability - sadness - nervousness - more "emotional" Symptoms usually resolve within 72 hrs but may persist days, weeks, or months. For some, severe physical & cognitive problems remain despite relatively mild initial symptoms & normal diagnostic test findings. Persistent symptoms following MTBI is referred to as post-concussion syndrome.

Closed TBI

Caused by blunt trauma. Can lead to contusions & lacerations of the brain. CONTUSION: a bruising of the brain tissue & is most commonly found at the site of impact (coup injury) or in a line opposite the site if impact (contrecoup injury). Contusions & lacerations are most commonly located at the base of the frontal & temporal lobes. LACERATION: actual tearing of the cortical surface vessels, which may lead to secondary hemorrhage & significant cerebral edema & inflammation. DIFFUSE AXONAL INJURY: when damage to the brain is severe but w/o local injury injury or widespread injury to the white matter of the brain. R/t high speed acceleration/deceleration. Causes shearing of large nerve fibers & stretching if blood vessels in many areas of the brain. Can cause visual field loss or weakness on one side of the body. Manifestations: impaired cognitive function, resulting in disorganization, impaired memory, & varying degrees of inattentiveness. Most survivors require long-term care.

Hemorrhage

Causes a brain hematoma( collection of blood) or clot, may occur as part of the primary injury & begin at the moment of impact. May also arise later from vessel damage. All hematomas are potentially life threatening bc they act as space occupying lesions & are surrounded by edema.

Spine precautions

Cervical collar & long spine board. Precautions include: (1) bedrest (2) no neck flexion w/ a pillow or roll (3) no thoracic or lumbar flexion w/ hob elevation (4) manual control of the cervical spine anytime the rigid collar is removed (5) log roll to reposition. Neurological function must be assessed after each position change.

Moderate TBI

Characterized by a period of loss of consciousness for 30 min - 6 hrs & a GCS score or 9-12. Sometimes focal or diffuse brain injury can be seen w/ MRI or CT. Memory may last up to 24hrs. Closed or open TBI. Acute care stay may be needed for close monitoring & to prevent secondary injury from brain edema, intracranial bleeding, or inadequate cerebral perfusion.

Brain death

Coma of known cause as established by history, clinical exam, lab testing, & neuroimaging Normal or near normal core body temp Normally systolic BP At least one neurological exam

Increase ICP

Cranial contents include: brain tissue, blood, & cerebrospinal fluid. Normal ICP: 10-15 mmHg. The increase in the volume of one component must be compensated for by a decrease in the volume of any of these components. CSF is easiest to displace.. to the spinal subarachnoid space or rate of absorption is increased. Increased ICP is the leading cause of death from head trauma in pts who reach the hospital alive... when compensation no longer takes place ' the brain cannot accommodate further volume changes. As ICP increases, cerebral perfusion decreases, leading to brain tissue ischemia & edema.. if edema remains untreated, the brain my herniate downward toward the brain stem or laterally from an unilateral lesion within one cerebral hemisphere, causing irreversible brain damage & possibly death (brain herniation syndromes)

TBI

Damage to the brain from an external mechanical force & not caused by neurodegeneearive or congenital conditions.

Severe TBI

GCS 3-8 & loss of consciousness for longer than 6hrs. Focal & diffuse damage to the brain, cerebrovascular vessels, &/or ventricles are common. Open or closed TBI. When the damage is present in a localized area of the brain, it is usually extensive. CT and MRI scans can capture images of tissue damage quite early in the course of this illness. Require management in critical care, including monitoring of hemodynamics, neurologic status, & possibly ICP. At high risk for secondary brain injury from cerebral edema, hemorrhage, reduced perfusion, & the biomolecular cascade.

Neuro assessment

GCS.. 2 point deterioration is considered clinically important- notify provider. LOC!! EARLY: behavior change & disorientation Pupils. Pinpoint & nonresponsive- brainstem dysfunction. Asymmetric, loss of light reaction or unilateral or bilateral dilated pupils are tested a herniation. Fixed nonreactive & dilated are poor prognosis. Bilateral motor response. Motor loss or dysfunction usually appears contralateral to the site of the lesion. Posturing?? Ears & nose for CSF leak. Palmate head for fractures & hematoma. Battles sign (indicate feature to middle cranial fossa) Raccoon eyes (skull base fracture)

Hypotension & hypoxia

Hypotension <70 mm Hg & hypoxemia Pao2 <80 mm Hg restrict blood flow to vulnerable brain tissue. May occur as a direct result of moderate to severe brain injury or secondary due to systemic injuries. Low blood flow & hypoxemia contribute to cerebral edema, creating a cycle of deteriorating perfusion & hypoxic damage. Pts w/ hypoxic damage r/t moderate to severe brain injury face a poor prognosis & typically experience memory impairment & reduce cognitive function.

Open TBI

LINEAR: simple, clean break in which the impacted area of bone bends inwards & the area around it bends outward. Most common type. DEPRESSED: bone is pressed inward into the brain tissue to at least the thickness of the skull. OPEN: the scalp & dura are lacerated.. creating a direct opening to the brain tissue. COMMINUTED: involves fragmented bone w/ depression into the brain tissue. BASILAR: occurs at the base of the skull & can result in CSF leakage from the nose or ears. CSF leak increases the risk for a CNS infection. Associate w/ an increased risk for hemorrhage caused by damage to the internal carotid artery. Can also damage cranial nerves I, II, VII, & VIII PENETRATING: at high risk for infection from the object that pierced the skull & from other environmental contaminants.

Manifestations

No two brain injuries are alike. Increase ICP, hypotension, hypoxemia or hypercarbia Subtle changes in BP, consciousness, & pupillary reaction to light can be very informative about neurological deterioration.

Primary brain injury

Occurs at the time of injury & results from physical stress (force) within the tissue caused by blunt force. Focal- confined to a specific area of the brain & causes localized damage that can often be detected w/ a CT scan or MRI. Diffuse- characterized by damage throughout many areas of the brain. May not be able to be detected until necrosis occurs. Open Or Closed

Increased ICP treatment

Provide oxygen to decrease ischemic injury, sustaining MAP or systolic BP within a therapeutic range, & draining CSF, manage ICP pressure with attention to balancing fluid I&o & promoting normal serum electrolyte values. Maintain cerebral perfusion pressure (CPP). CPP= ICP-MAP. Maintenance of a CPP >70 mmHg is generally accepted as an expected outcome of therapy.

Epidural hematoma

Results from arterial bleeding into the space between the dura & the inner skull. Pts have lucid intervals that last for minutes during which time the pt is awake & talking, this is followed by a momentary unconsciousness that occurs within minutes in the injury. Occurs w/ a fracture of the temporal bone which houses the middle meningeal artery.

Subdural hematoma

Results from venous bleeding into the space beneath the dura & above the arachnoid. Occurs w/ a tearing of the braiding veins within the cerebral hemispheres or from a laceration of brain tissue. More slow bleed. Acute SDH: 48hrs after impact Subacute SDH: 48hrs-2wks Chronic SDH: 2wks-several mo Highest mortality rate bc they are often unrecognized until the pt presents w/ severe neurological compromise.

Barbiturate coma

Used for increased ICP that cannot be controlled by other means. Requires mechanical ventilation, sophisticated hemodynamic monitoring,& ICP monitoring Complications include: decreased GI motility, cardiac dyrhythmias from hypokalemia, hypotension, & fluctuations in body temp.

Mild, moderate, or severe

Usually determined by the Glasgow coma scale score immediately following resuscitation, the presence or absence of brain damage imaged by CT or MRI following the trauma, an estimation of the force of the trauma, & symptoms of the injured person.

Preventing & detecting secondary brain injury

VS q 1-2 hr IV fluids or drug therapy to prevent severe hypo or hypertension Cooling for temp. Therapeutic hypothermia- core temp of 89.6-93.2 for 24-48 hrs Hyperventilation may be used. Carbon dioxide is a very potent vasodilator that can contribute to increases in ICP Maintain Paco2: 35-38 mm Hg Pao2: 80-100 HOB 30 degrees, head midline & neutral position. CPP >70 mm Hg

Nutrition

Weigh daily

Drug therapy

mannitol (Osmitrol)- osmotic diuretic is used to treat cerebral edema by pulling water out of the extra cellular spaces of the edematous brain tissue. Most effective when given w/ Lasix.. reduces rebound Give mannitol through a filter, check for crystals Monitor for i&o, severe dehydration, indications of AKI, weakness, edema, & changes in UO. Serum osmolarity of 310-320 Foley for strict i&o. Sedatives like propofol (Diprivan) manage agitation Antiepileptics such as phenytoin (Dilantin) for seizures