NURS 265 EXAM 3 STUDY GUIDE
45: NEUROLOGIC PROBLEMS
MONITORING FOR INCREASED INTRACRANIAL PRESSURE
• Most at risk for increased ICP resulting
... [Show More] from edema during the first 72 hr. after onset of a stroke
• May have worsening neuro changes starting within 24-48 after their endovascular procedure from increased ICP
• Assess these pt. Q 1-4 hr.
CHART 45-6 KEY FEATURES
• Decreased LOC (lethargy to coma)
• Behavior changes: restlessness, irritability, and confusion
• HA
• N/V (may be projectile)
• Change in speech pattern/slurred speech:
o Aphasia
• Change in sensorimotor status:
o Pupillary changes: dilated and nonreactive (“brown pupils”) or constricted and nonreactive
o Cranial nerve dysfunction
o Ataxia
• Seizures (usually within first 24 hr. after stroke)
• Cushing’s triad:
o Severe HTN
o Widened pulse pressure
o Bradycardia
• Abnormal posturing:
o Decerebrate
o Decorticate
>> INTERVENTIONS
• For increased ICP experiencing a stroke:
o Elevate HOB – sitting them up is very important
o O2 therapy (for O2 < 94%)
o Maintain head in midline, neutral position – promotes venous drainage from the brain
o Avoid sudden and acute hip or neck flexion during positioning
o Avoid the clustering of RN procedures – can elevate ICP even more
▪ Not for neuro pt.
o Hyperoxygenate before and after suctioning
o Provide airway management to prevent unnecessary suctioning and coughing that can increase ICP
o Maintain quiet environment if pt. has a HA
o Keep the room lights low to accommodate and photophobia
o MT BP, heart rhythm, O2 sat, blood glucose, and body temp to prevent secondary brain injury and promote positive outcomes after stroke
▪ MD usually like BP to be slightly elevated after a stroke (SBP = 140-150)
• CRITICAL RESCUE!! – Be alert for S/S of increased ICP in the head injury and report any neuro deterioration to the MD or Rapid Response Team immediately!
o The 1st sign of increased ICP is a declining LOC
TRAUMATIC BRAIN INJURY (TBI)
>>> PATHO
• Can lead to temporary and permanent impairment in cognition, mobility, sensory perception, and psychosocial function
• Direct injury: blow directly to the head
• Indirect injury: force applied to another
body part with a rebound effect to the brain
• Sheared: rebound or rotated on the brain stem
• Bruised: contusion of the brain
• Torn: laceration of the brain as it moves
across the inner surface of the cranial
• Acceleration injury: caused by n external force contacting the head, suddenly placing the head in motion
• Deceleration injury: occurs when the moving head is suddenly stopped or hits a stationary object
•
PRIMARY BRAIN INJURY
• Occurs at the time of injury -- Dives and hits head
• Can be focal or diffuse
o Focal: confined to a specific area of the brain and causes localized damage that can often be detected with a CT scan or MRI
o Diffuse: damage throughout many areas of the brain
▪ Usually too small to detect with CT scan at first but cn worsen to a detectable size
▪ MRI can see microscopic injuries
• Classified as open or closed
o Open: when the skull is fractured or pierced by a penetrating object
o Closed: the integrity of the skull stays intact
• Further defined as mild, moderate, or severe – usually determined by the Glasgow coma scale immediately after resuscitation, presence of brain damage shown in CT scan or MRI, estimation of force of the trauma, and S/S
SECONDARY BRAIN INJURY
• Any processes that occur after the initial injury and worsen or negatively influence pt. outcomes.
o Increased swelling due to primary brain injury
• Result form physiologic, vascular, and biochemical events that are an extension of the primary injury.
o Most common secondary injuries result from hypotension and hypoxia, intracranial HTN, and cerebral edema.
o Damage to the brain tissue occurs primarily because the delivery of O2 and glucose to the brain is interrupted from cerebral edema and increasing pressure.
> HYPOTENSION AND HYPOXIA
• Hypotension = MAP < 70
o r/t shock or clot formation
• Hypoxemia = PaO2 < 80
o r/t resp. failure, asphyxiation, or loss of airway and impaired ventilation
o leads to decreased cognition
• These restrict the flow of blood to vulnerable brain tissue
> INCREASED INTRACRANIAL PRESSURE
• Normal level of ICP = 10 – 15 mm Hg
• A sustained ICP of 20 is detrimental to the brain because neurons begin to die
• As a result of brain injury, the increase in the volume of one component must be compensated for by a decrease in the volume of one of the other components
o Cerebral edema
• The brain can compensate for increased ICP by sending blood volume into the sinuses or jugular veins.
• Increased ICP is the leading cause of death from head trauma in pt. who reach the hospital alive
o Happens when the brain can no longer compensate for the increased ICP
o As ICP increases, cerebral perfusion decreases, leading to brain tissue ischemia and edema
o Brain herniation syndrome: when the brain is forced downward thru the Forman of Monro
> HEMORRHAGE
• Causes a brain hematoma (collection of blood) or clot, may occur at the primary injury or arise later from vessel damage
• All hematomas are potentially life threatening because they act as space-occupying lesions and are surrounded by edema
• 3 types of hemorrhage:
o Epidural hematoma: arterial bleeding into the space between the dura and inner skull.
▪ Caused by a fracture of the temporal lobe
▪ “lucid intervals” awake and talking and a momentary moment of
unconsciousness
o Subdural hematoma (SDH): venous bleeding into the space beneath the dura and above the arachnoid
▪ From a tearing of the bridging veins and within the cerebral hemispheres
or from a laceration of brain tissue
▪ Bleeding from this occurs more slowly than from an epidural hematoma
▪ Acute – presents within 48 hr.
▪ Subacute – between 48 hr. and 2 weeks
▪ Chronic – from 2 weeks to several months
o Traumatic intracerebral hemorrhage (ICH): the accumulation of blood within the brain tissue caused by the tearing of small arteries and veins in the subcortical white matter
▪ From a blow to the back of the head or fractures
> BRAIN HERNIATION
• In the presence of increased ICP, the brain tissue may shift and herniate downward, trying to go thru the foramen magnum
• S/S
o Cheyne-Stokes respirations
o Pinpoint
o nonreactive pupils
o potentially hemodynamic instability
• Any of these S/S are life-threatening and you must call the MD immediately!
ETIOLOGY
• Most common causes of TBI are falls and motor vehicle accidents
• Alcohol and drugs are a significant contributing factor
• Summer and spring months, evenings, nights, and weekends have the greatest number
of injuries
• More common in males than females
>>> COLLABORATIVE CARE
>>> ASSESSMENT
> HISTORY
• May be hard to obtain a hx. from the pt. due to amnesia from injuries
o May be obtained from first responders or witnesses in this case
• Did the pt. lose consciousness? For how long?
• Differentiate confusion from head trauma and intoxication
• Determine whether the pt. had fluctuating consciousness or seizure activity and whether there is a hx. of a seizure disorder.
> PHYSICAL ASSESSMENT
• Assess for:
o S/S of increased ICP, hypotension, hypoxemia, hypercarbia (PaCO2 > 40-45), or hypocarbia (PaCO2 < 40-45)
o Hypercarbia can contribute to ICP
o Hypocarbia is caused by hyperventilation and can lead to vasoconstriction resulting in ischemia
o EtCO2 or a capnography is used to detect CO2 levels in intubated pt.
TABLE 45-4 DIFFERENCES AMONG MILD, MODERTE, AND SEVERE TBI’S
TYPE CAUSED BY S/S
MILD (MTBI)
-- concussion ▪ A blow to the head, transient confusion or
feeling dazed or disoriented and 1 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 neuro deficits that may or not be transient
▪ LOC does not have to occur for a person to be
dx. w/ MTBI
▪ No evidence of brain damage on a CT or MRI imaging scan ▪ HA
▪ Dizziness
▪ Changes in behavior
▪ Usually resolve within 72 hr.
▪ Lasting longer than 72 hr. Is
considered “post-concussion syndrome”
MODERATE ▪ A period of LOC for 30 min. – 6 hr. and a GCS
score of 9 – 12.
▪ Often but not always, focal or diffuse brain injury can be seen with a dx. CT or MRI scan
▪ Post-traumatic amnesia may last up to 24 hr. may occur with either closed or open brain
injury ▪ Short acute or critical care
stay may be needed to prevent secondary injury from brain edema, intracranial bleeding, or inadequate cerebral perfusion
SEVERE ▪ GCS score of 3-8 and LOC for longer than 6 hr.
▪ Focal and diffuse damage to the brain, cerebrovascular vessels or ventricles is common. Both open and close head injuries can cause TBI, and injury can be focal or diffuse
▪ CT and MRI scans can capture images of tissue
damage quite early in the course of this illness. ▪ Require management in
critical care
▪ MT hemodynamics, neuro status, and ICP
▪ At high risk for secondary brain injury from cerebral edema, hemorrhage, reduced perfusion, and the
biomolecular cascade.
CHART 45-8 MILD TBI KEY FEATURES
PHYSICAL COGNITIVE SLEEP EMOTIONAL
▪ Appears dazed or stunned
▪ LOC < 30 min. (unresponsive after injury)
▪ HA
▪ Nausea
▪ Vomiting
▪ Balance or gait problems
▪ Fatigue
▪ Sensitivity to light
▪ Sensitivity to noise ▪ Feeling mentally foggy
▪ Feeling slowed down
▪ Difficulty concentrating
▪ Difficulty remembering
▪ Amnesia about the events around the time of injury ▪ Drowsiness
▪ Sleeping less than usual
▪ Sleeping more than usual
▪ Trouble falling asleep ▪ Irritability
▪ Sadness
▪ Nervousness
▪ More “emotional”
▪ depression
> AIRWAY AND BREATHING PATTERN ASSESSMENT
• PRIORITY – assessment of ABCs
• All pt. with head injuries are treated as though they have cord injury until radiography
proves otherwise
• Assess for indicators of spinal cord injury:
o Loss of mobility and sensory perception
o Tenderness along the spine
o Abnormal head tilt
• Cheyne-Stokes respirations and/or apnea may indicate a brainstem injury
o Artificial airway and vent may be needed
> SPINE PRECAUTIONS
• Pt. with blunt trauma to the head or neck is transported with a cervical collar and a long spine board.
• Long spine board is removed ASAP once at the ER or ICU
• The rigid cervical collar is maintained until definitive dx. Studies to rule out cervical spine injury are completed.
• Once the spine board is removed, spinal precautions are maintained until the provider indicates that it is safe to bend or rotate the spine.
• Spinal precautions include:
o Bedrest
o No neck flexion with a pillow or roll
o No thoracic or lumbar flexion with head of bed elevation/bed controls (reverse Trendelenburg is acceptable)
o Manual control of the cervical spine anytime the rigid collar is removed
o Using a “roll log” to reposition
• MT for skin breakdown under the collar
> VITAL SIGNS ASSESSMENT
• The mechanisms of autoregulation are often impaired due to TBI
• Pt. may have hypotension or hypertension
• Cushing’s triad: a classic but late sign of increased ICP, is manifested by severe hypertension, a widened pule pressure, and bradycardia.
o Usually indicates imminent death
> NEUROLOGIC ASSESSMENT
• A change of 2 points on the GCS is important, notify the MD
• The most important variable to assess with any brain injury is LOC
o Decreased or change in LOC is typically the first sign of deteriorating neuro status
▪ Decrease in arousal, increased sleepiness, increased restlessness and combativeness
• Early indicators of a change in LOC:
o Behavior changes (restlessness, irritability)
o Disorientation
o Report any of these S/S to the MD ASAP!
• Use a bright light to assess pupillary size and reaction to light.
o Facial trauma may swell eyelids, making this assessment difficult
• Pinpoint and nonresponsive pupils are indicative of brainstem dysfunction at the level of the pons.
• Asymmetrical pupils, loss of light reaction, or dilated pupils are treated as herniation of the brain from increased ICP until proven otherwise.
• Pupils that are fixed (nonreactive) and dilated are a poor prognostic sign.
o Known as “blown” pupils
o Atropine causes fixed/dilated pupils
• Late S/S of increased LOC:
o Severe HA
o Nausea
o Vomiting (often projectile)
o seizures
• pt. with a brain injury is at risk for potentially devastating ICP elevations during the first hours after the event and up to 3-4 days after injury when cerebral edema can occur.
• Assess for bilateral motor responses
• The pt. motor loss or dysfunction usually appears contralateral (opposite side) to the site of the lesion
• S/S of brainstem or cerebellar injury:
o Ataxia (loss of balance)
o Decreased or increased muscle tone
o Weakness
• Assess ears and nose for any signs of CSP leaks
o Fluids are sent to the lab to be tested for glucose and electrolyte content
• CSF placed on a white absorbent paper or linen can be distinguished from other fluids by the “halo” sign, a clear or yellowish ring surrounding a spot of blood
• Raccoon’s eyes can mean a fracture of the skulls base
> PSYCHOSOCIAL ASSESSMENT
• Pt. may have personality changes after a TBI
• May have memory loss or altered ability to communicate and understand language
> LABS
• No serum test to dx. a primary brain injury
• Detection of the protein S-100B in serum may indicate some kind of injury to the brain
> IMAGINING ASSESSMENT
• CT
• MRI
• Functional MRI
>>> ANALYSIS
• Top problems for TBI
o 1. Decreased cerebral tissue perfusion
o 2. Decreased memory, sensation, and mobility
>>> INTERVENTIONS
> MAINTAINING CEREBRAL TISSUE PERFUSION
GOAL: maintain adequate cerebral tissue perfusion with no evidence of secondary brain injury from cerebral edema and increased ICP
• Cerebral perfusion is not usually affected by a mild TBI
INTERVENTIONS:
• Nonsurgical –
o PRIORITY = ABC’s and then preventing secondary injury
o Interventions are directed towards preventing or detecting secondary brain injury or the conditions that contribute to secondary brain injury such as:
▪ increased ICP
▪ promoting fluid and electrolyte balance
▪ monitoring the effects of treatments and drug therapy
o Health teaching
o Emotional support
o VS 1-2 hr.
o Report dysrhythmias, hypotension, and hypertension to the MD
o Therapeutic hypothermia may be started, regardless of the presence of fever
▪ This is to rapidly cool the pt. to a core temp of 89.6*F and 93.2*F for 24- 48 hr. after the primary injury – this stops dead tissue from dying
▪ Rewarming must be done carefully, doing it too rapidly can cause cardiac dysrhythmias
▪ Goal = to reduce brain metabolism and prevent the cascade of molecular and biochemical events that contribute to secondary brain injury in moderate-to-severe TBI
o Check ABG’s
o Hyperventilation for the intubated pt. during the first 24 hr. after brain injury is usually avoided because it may produce ischemia by causing cerebral vasoconstriction
o CO2 is a very potent vasodilator that can contribute to increases in ICP
o Prevent intermittent and sustained hypoxemia
o PaO2 levels are maintained between 80-100 to prevent secondary injury
o If the pt. is intubated, provide 100% O2 before and after each pass of the endotracheal suction catheter.
o Lidocaine given IV or endotracheally may be used to suppress the cough reflex; coughing increases ICP [Show Less]