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Spinal Cord Injury (SCI)and
Intracranial Disorders
Background
1. Usually due to trauma
2. Most common in the 16 – 30 age group
Causes
1. Motor vehicle accidents
2. Falls, violence, sport injuries (diving)
Physical Description
Concussion, contusion, laceration, transection, hemorrhage, damage to blood vessels supplying spinal cord.
Fractured vertebrae damage cord
Injuries are identified by vertebral level
Risk Factors
1. Age
a. Youth (take risks)
b. Older adults (age-related vertebral degeneration)
2. Gender: males more than females
3. Alcohol or drug use
Pathophysiology
• Primary injury causes microscopic hemorrhages in gray matter of cord and edema of white matter of cord
• Microcirculation of cord is impaired by edema and hemorrhage; further impaired by vasospasm
Pathophysiology
• Necrosis of gray and white matter occurs and function of nerves through injured area is lost
• Acceleration and deceleration as occurs in motor vehicle accidents and falls and is most common cause of abnormal spinal column movements
Pathophysiology
• Other causes include penetration by bullets or foreign objects
Sites of Pathology: Most common areas of involvement
1. Cervical (C1, C2, C4 - C6)
2. T11 to L2
ClassificationsCompleteness
• Complete SCI: motor and sensory neural pathways are completely transected resulting in total loss of motor and sensory function below level of injury
• Incomplete SCI: motor and sensory neural pathways are only partially interrupted resulting with variable loss of function below level of injury function below level of injury
Classifications
• Cause of injury: specific as to trauma
• Level of injury: area of spinal cord affected
Manifestations
General
• Depend upon degree and level spinal cord is injured
• Affects every body system
Manifestations
Spinal Shock
• Temporary loss of reflex function (areflexia) below level of injury beginning immediately after complete transection of spinal cord
Manifestations
1. Bradycardia and hypotension2. Flaccid paralysis of skeletal muscles distal
to injury3. Loss of all sensation of distal to injury4. Absence of visceral and somatic
sensations5. Bladder and bowel dysfunction 6. Loss of ability to perspire
Manifestations
• Spinal shock begins within hour of injury and lasts from few minutes up to several months; ends with return of reflex activity: hyperreflexia, muscle spasticity, reflex bladder emptying
Manifestations
Client with cervical cord injuries may have persistent cardiovascular changes after spinal shock resolves
• Orthostatic hypotension, bradycardia• Decreased peripheral resistance and loss of
muscle tone leading to sluggish circulation and decreased venous return
• Client at risk for thrombophlebitis
Manifestations
Motor Neuron Involvement • Upper motor neuron involvement includes spastic
paralysis, hyperreflexia, inability to carry out skilled movementLower motor neuron involvement: flaccid muscle and extensive muscle atrophy, loss of voluntary and involuntary movement
• Partial motor neuron movement: partial paralysis• All motor neurons affected: complete paralysis • Client may be treated with antispasmodics such as
baclofen (Lioresal) or diazepam (Valium)
Manifestations
Paraplegia
• Paralysis of lower portion of body involving injury to thoracic, lumbar, or sacral portion of spinal cord
• Impairment of sensory and/or motor function
Manifestations
Tetraplegia (formerly quadriplegia)
• Injuries affecting the cervical segments of cord
• Impairment of upper extremities as well
Manifestations
Autonomic Dysreflexia (autonomic hyperreflexia) • Exaggerated sympathetic response occurring in
clients with cord injuries at T6 or higher and after resolution of spinal shock
• Because of lack of control of autonomic nervous system by higher centers, a stimuli such as full bladder results in mass reflex stimulation of sympathetic nerves below level of injury
Manifestations
• Client develops bradycardia and severe HPT, flushed, warm skin with profuse sweating above the lesion and dry skin below and anxiety; if sustained could result in stroke, myocardial infarction or seizures
• Stimuli include• Abdominal discomfort: full bladder• Stimulation of pain receptors: pressure
ulcers• Visceral contractions: fecal impaction
Collaborative Care
Prompt intervention is required• Elevate client’s head and remove any support hose:
this will immediately decrease the blood pressure since client has orthostatic hypotension
• Monitor blood pressure while assessing for causative factor: relief of full bladder, impacted stool, skin pressure
Collaborative Care
– If there is a history of autonomic dysreflexia, client may be able to warn of occurrence
– Notification of physician and administration of medication to lower blood pressure
Collaborative Care
• Care must start at scene of injury to reduce injury, preserve function
• Rapid assessment of ABC (airway, breathing, circulation)
• Immobilize and stabilize head and neck • Use cervical collar before moving onto backboard• Secure head and maintain client in supine position
Collaborative Care
• Care with all transfers not to complicate original injury
• Fractures at C1 – C4 levels result in respiratory paralysis but advances in trauma care allow clients to survive (will require ventilator assistance)
• Address other injuries that may necessitate immediate care
Collaborative Care
Care in emergency department.• Assessment of level of injury• Manifestations of injury at cervical level• Paralysis or weakness of all extremities• Respiratory distress• Pulse < 60; blood pressure < 80• Decreased peristalsis
Collaborative Care
• Manifestations of injury at thoracic or lumbar level: Paralysis or weakness of lower extremities
Collaborative Care
• Findings indicative of spinal shock
• Loss of skin sensation
• Areflexia, flaccid paralysis
• Absent bowel sounds
• Bladder distention
• Decreasing blood pressure
• Loss of cremasteric reflex in male
Collaborative Care
• Interventions
• Address respiratory status
• Oxygen administration
• Ventilator support to those in distress
• Continuous monitoring of cardiovascular status
Collaborative Care
• Monitor fluid status and prevent bladder overdistention; insert indwelling urinary catheter
• Paralytic ileus: insertion of nasogastric tube and connect to suction
• Administration of high-dose corticosteroid to prevent secondary cord damage from edema and ischemia (within 8 hours of injury and continued for 23 hours)
Diagnostic Tests
• Xrays of cervical spine to establish level and extent of vertebral injury
• T scan and MRI: changes in vertebrae, spinal cord, tissues around cord
• Arterial blood gases to establish baseline
Medications
• Corticosteroids
• Vasopressors to treat bradycardia and hypotension
• Histamine H2 antagonists to prevent stress ulcers
• Anticoagulation if not contraindicated
Treatments
• Surgery may be indicated early, if there is evidence of spinal cord compression by bone fragments or hematoma; surgeries include decompression laminectomy, spinal fusion, insertion of metal rods
Treatments
Stabilization and Immunization
• Application of traction (Gardner-Wells tongs)
• External fixation (halo external fixation device): allows for greater mobility, self care, participation in rehabilitation program
Health Promotion
• Education regarding prevention of injuries including use of seat belts
Nursing Diagnoses
Impaired Physical Mobility
• Intervention to maintain joint mobility, prevent contractures
• Maintain skin integrity; use of special beds
• Prevention of deep venous thrombosis
Nursing Diagnoses
Impaired Gas Exchange
• Ventilator support often indicated in cervical injuries
• T1- T7 injuries impair intercostal muscles
• Assist client to cough by splinting lower chest region
Nursing Diagnoses
• Ineffective Breathing Pattern
• Dysreflexia
Altered Urinary Elimination and Constipation
• Long-term client usually requires intermittent catheterization procedure
• Use of stool softeners and bowel training program
Nursing Diagnoses
Sexual Dysfunction• Males have different abilities to have
erections depending on injuries (reflexogenic or psychogenic)
• Females usually do not have sensation but pregnancy is possible
• Discuss client concern, referral for counseling
Nursing Diagnoses
Low Self-esteem
• Client has sustained threat to body image, self-esteem, role performance
• Promotion of self-care, independent decision making
Home Care
• Client moves from intensive care, intermediate care to rehabilitation to home care
• Client needs continued support home health agency, physical therapy, support groups for client and family
Client with Herniated Intervertebral Disk
Definition
• Rupture of cartilage surrounding intevertebral disk with protrusion of nucleus pulposus
• Occurs more often as persons enter middle age and affects males more than females
• Site most commonly affected: L4, L5, S1; if herniated disk occurs in cervical region C6, C7are affected
Pathophysiology
• Protrusion occurs spontaneously or as result of trauma; pressure on adjacent spinal nerves causes manifestations
• Abrupt herniation causes intense pain and muscle spasms
• Gradual herniation occurs with degenerative changes, osteoarthritis and develops as slow onset of pain and neurologic deficits
Manifestations
Herniated disk in lumbar disk• Recurrent episodes of pain in lower back
with radiation across buttock • Sciatica: lumbar pain following sciatic
nerve down posterior leg• Motor deficits: weakness, difficulties with
sexual function and urinary elimination • Sensory deficits: paresthesia and numbness
Manifestations
• Herniated disk in cervical area
• Pain in shoulder, arm, neck
• Paresthesias, muscle spasms
Diagnostic Tests
• Xray: lumbosacral and cervical area to identify deformities and narrowing of disk spaces
• CT scan and MRI• Myelography: used to rule out tumors• Electromyography (EMG): measures electrical
activity of skeletal muscles at rest; identification of muscles affected by pressure of herniated disk
Medications
• Management of pain with analgesics, NSAIDs
• Management of muscle spasms with muscle relaxants
Treatment
Conservative treatment is utilized for 2 – 6 weeks• Decrease activity level• Avoid flexion of spine• Adequate support (corset, cervical collar)• Firm mattress• Prescribed exercise program• Take analgesics, NSAIDs, muscle relaxants• TENS units
Treatment
Surgery (may be combination of different procedures• Laminectomy: removal of part of vertebral lamina to
relieve pressure on nerve• Diskectomy: removal of nucleus pulposus of
intervertbral disk; • Microdiskectomy: use of microscopic procedure
through very small incision• Spinal fusion: insertion of wedge-shaped piece of
bone or bone chips between vertebrae to stabilize them; results in limited movement
Nursing Care
• Emphasis on prevention: proper body mechanics, proper lifting techniques
Nursing Diagnoses
• Acute Pain
• Chronic Pain
• Constipation
Home Care
• Adequate pain control to enable client to be able to participate in ADL
• Utilization of nonpharmacological methods
Client with spinal cord tumor
Definition
• Tumors may be benign or malignant, primary or metastatic
• Occur most often in thoracic area; also cervical and lumbarsacral areas
• Affect clients in age group 20 – 60
Classifications
• Intramedullary tumors arise from tissues of spinal cord
• Extramedullary tumors develop from tissues outside spinal cord
Pathophysiology
• As tumors grow neural deficits result from further compression, invasion, or ischemia, secondary to vascular obstruction
Manifestations
• Depend on area of tumor and anatomic level of involvement
Pain
• Locally at site of tumor
• Radicular pain: involving nerve that is compressed
Manifestations
• Motor deficits: paresis, paralysis, hyperactive reflexes
• Sensory deficits
• Changes in bowel and bladder elimination, sexual function
Diagnostic Tests
• Flat plate xray of spine
• CT scan, MRI :site of cord compression
• Myelogram: clarify area of tumor involvement
• Lumbar puncture: CSF when tumors are present is often xanthochromic (yellow in color)
Medications
• Analgesics and NSAIDs to control pain
• Steroids (dexamethasome (Decadron): to decrease tumor size and inflammation
Treatment
• Surgery: procedures include microsurgery, laser surgery for excision; then laminectomy and fusion to stabilize spine
• Radiation therapy: used to treat metastatic tumors reduce pain, stop progression of neurologic deficits
Nursing Care: similar in aspects to care of client with SCI
• similar in aspects to care of client with SCI
Altered Cerebral Function occurs with illness and injury
Brain Function Deterioration
• Follows a predictable rostral to caudal progression
• Higher levels of function progress to more primitive function
Altered Level of Consciousness (LOC)
Consciousness• Condition in which person is aware of self
and environment and able to respond to stimuli appropriately
• Requires-Arousal: alertness; dependent upon
reticular activating system (RAS); system of neurons in thalamus and upper brain stem
Altered Level of Consciousness (LOC)
• Cognition: complex process involving all mental activities; controlled by cerebral hemispheres
• Components depend on normal physiologic function and connection between 2 systems
Altered Level of Consciousness (LOC)
Pathophysiology
• Lesions or injuries affecting cerebral hemisphere directly or that compress or destroy neurons in RAS
• Metabolic disorders
Altered Level of Consciousness (LOC)
Arousal affected by• Destruction of RAS: stroke, demyelinating diseases• Compression of brain stem producing edema and
ischemia: tumors, increased intracranial pressure, hematomas or hemorrhage, aneurysm
• Cerebral hemisphere function depends on continuous supply or oxygen and glucose
-Most common impairment caused by global ischemia, hypoglycemia
-Localized masses: hematoma, cerebral edema
Altered Level of Consciousness (LOC)
Processes within brain that destroy or compress structures affect LOC:
• Increased intracranial pressure
• Stroke, hematoma, intracranial hemorrhage
• Tumors
• Infections
• Demyelinating disorders
Altered Level of Consciousness (LOC)
Systemic conditions affecting brain function• Hypoglycemia• Fluid and electrolyte imbalances
-Hyponatremia-Hyperosmolality-Acid-base alterations: hypercapnia-Accumulated waste products from liver or renal
failure-Drugs affecting CNS: alcohol, analgesics,
anesthetics• Seizure activity: exhausts energy metabolites
Altered Level of Consciousness (LOC)
Client assessment results with decreasing LOC• Increased stimulation required to elicit response
from client• More difficult to rouse; client agitated and confused
when awakened• Orientation changes: loses orientation to time first;
then place; finally person• Continuous stimulation required to maintain
wakefulness• Client has no response, even to painful stimuli
Patterns of breathing As respiratory center are affected: predictable changes in
breathing patternsTypes of respirations and brain involvement• Diencephalon: Cheyne-Stokes respirations (as with
acidosis)• Midbrain: neurogenic hyperventilation; may exceed
40/minute; due to uninhibited stimulation of respiratory centers
• Pons: apneustic respirations: sighing on mid inspiration or prolonged inhalation and exhalation; excessive stimulation of respiratory centers
• Medulla:ataxic/apneic respirations (totally uncoordinated and irregular); loss of response to CO2
Pupillary and oculomotor responses: Predictable
progression • Localized lesion effects ipsilateral pupil (same
side as lesion)• Generalized or systemic processes pupils affected
equally• Compression of cranial nerve III at midbrain,
pupils become oval and eccentric (off center); progress to pupils become fixed (no response to light); progress to dilation
Pupillary and oculomotor responses: Predictable
progression
• With deteriorating LOC, spontaneous eye movement is lost and reflexive ocular movements are altered
• Loss of simultaneous eye movement
Pupillary and oculomotor responses: Predictable
progression Loss of normal reflex functioning:• Doll’s eye movements: eye movement in opposite
direction of head rotation (normal function of brain stem)
• Oculocephalic reflex: eyes move upward with passive flexion of neck; downward with passive neck extension (normal function)
• Oculovestibular response (cold caloric testing): instillation of cold water in ear canal cause nystagmus (lateral tonic deviation of eyes) toward stimulus (normal function)
Motor Function Predictable progression Assessment of level of brain dysfunction and side of brain
affected• Client follows verbal commands• Pushes away purposely from noxious stimulus• Movements are more generalized and less purposeful
(withdrawal, grimacing)• Reflexive motor responses:
-Decorticate movement: flexion of upper extremities accompanied by extension of lower extremities-Decerebrate posturing: adduction and rigid
extension of upper and lower extremities• Flaccid with little or no motor response
Coma States
• Outcome of altered LOC
• Comas range from full recovery, without any residual effects, to persistent vegetative state (cerebral death) or brain death
Coma StatesStages• Irreversible coma (vegetative state)
-Permanent condition of complete unawareness of self and environment; death of cerebral hemispheres with continued function of brain stem and cerebellum
-Client does not respond meaningfully to environment but has sleep-wake cycles and retains ability to chew, swallow, and cough
-Eyes may wander but cannot track object -Minimally conscious state: client aware of
environment, can follow simple commands, indicate yes/no responses; make meaningful movements (blink, smile)
-Often results from severe head injury or global anoxia
Coma States
Locked-in syndrome• Client is alert and fully aware of environment; intact
cognitive abilities but unable to communicate through speech or movement because of blocked efferent pathways from brain
• Motor paralysis but cranial nerves may be intact allowing client to communicate through eye movement and blinking
• Occurs with hemorrhage or infarction of pons; disorders of lower motor neurons or muscles (polyneuritis, myasthenia gravis, amyotrophic lateral sclerosis (ALS)
Coma States
Brain death• Cessation and irreversibility of all brain functions• General criteria
-Absent motor and reflex movements-Apnea-Fixed and dilated pupils-No ocular responses to head turning and
caloric stimulation-Flat EEG
Prognosis
• Outcome varies according to underlying cause and pathologic process
• Young adults can recover from deep coma
• Recovery within 2 weeks associated with favorable outcome
Collaborative Care
• Management includes identifying cause, preserve function and prevent deterioration
• Involves total system maintenance in many cases
Diagnostic Tests • Blood glucose: cerebral function declines rapidly when <
40 – 50 mg/dL• Serum electrolytes: hyponatremia: coma and convulsions
when Na < 115 mEq/L• ABG: hypoxemia frequent cause of altered LOC;
increased levels CO2 especially if acute• BUN and creatinine: renal function• Liver function tests: tests determine liver function; high
ammonia levels interfere with cerebral metabolism• Toxicology screening of blood and urine (acute drug or
alcohol)
Diagnostic Tests• CBC: anemia or infectious cause of coma• CT, MRI: identification of neurologic damage• EEG: evaluate electrical activity of brain, unrecognized
seizure activity• Radioisotope brain scan: identify abnormal brain lesions• Cerebral angiography: visualization of cerebral vascular
system including aneurysms, occluded vessels, tumors• Transcranial Doppler: assess cerebral blood flow• Lumbar puncture: CSF to assess infection, possible
meningitis
Medications
IV fluids normal saline, lactated Ringer’s
Specific medications to address specific problems• 50% glucose: hypoglycemia• Naloxone for narcotic overdose• Thiamine:Wernicke’s encephalopathy• Regulation of osmolality with diuretics• Antibiotics: infections
Surgery
• May be indicated if cause of coma is tumor, hemorrhage, hematoma
Other Measures (as indicated)
• 1. Airway support and mechanical ventilation if indicated; controlled hyperventilation to promote vasoconstriction to reduce cerebral edema
• 2. Maintenance of nutritional status with enteral feedings
Nursing Diagnoses
• Ineffective Airway Clearance: limit suctioning to < 10 – 15 seconds; hyperoxygenate before
• Risk for Aspiration
• Risk for Impaired Skin Integrity: preventative measures, continual inspection
Nursing Diagnoses
• Impaired Physical Mobility: maintain functionality of joints, physical therapy
• Risk for Imbalanced Nutrition: Less than body requirements
• Anxiety (of family)-Extremely stressful time-Reinforce information from physician-Encourage to speak with client who is in
coma
Increased Intracranial Pressure
Intracranial Pressure (ICP)
• Pressure within cranial cavity measured within lateral ventricles
• Transient increases occur with normal activities coughing, sneezing, straining, bending forward
Intracranial Pressure (ICP)
Sustained increases associated with• Cerebral edema• Head trauma• Tumors• Abscesses• Stroke• Inflammation• Hemorrhage
Monro-Lellie hypothesis
Within skull there are 3 components that maintain state of dynamic equilibrium
• Brain (80%)• Cerebrospinal fluid (10%)• Blood (10%)If volume of any one increases the volume of
others must decrease to maintain normal pressure
Normal intracranial pressure
• 5 – 15 mm Hg, with pressure transducer with head elevated 30 degrees
• 60 – 180 cm water, water manometer with client lateral recumbent
Background regarding regulation of ICP
Cerebral blood flow and perfusion account for twice the amount of increase as CSF does
• Cerebral blood vessels respond to changes in arterial oxygen and carbon dioxide
• Cerebral perfusion pressure (CPP) is pressure needed to perfuse brain cells
-Difference between mean arterial pressure (MAP) and ICP
-Normal pressure is 80 – 100 Hg; to maintain blood flow CPP must be 50 mm Hg
Background regarding regulation of ICP
Autoregulation: compensatory mechanisms in which cerebral arterioles change diameter to maintain cerebral blood flow when ICP increases
• Pressure autoregulation: receptors within small vessels respond to changes in arterial pressure
-Vasodilation: in response to elevated blood pressure
-Vasoconstriction: in response to low blood pressure• Chemical (metabolic) autoregulation
-Vasodilation: carbon dioxide, increased hydrogen ion concentration, low oxygen
-Vasoconstriction: fall in carbon dioxide
Background regarding regulation of ICP
• There is limited ability of brain to respond to ICP; ability for autoregulation is severely limited
Increased ICP
• Increased ICP must be recognized early when interventions can be instituted to stop its progress
• Medical emergency requiring intensive nursing care
Increased ICPManifestations• Changes in LOC: initially behavior and
personality changes and progresses in predictable pattern to coma and responsiveness
• Pressure affects motor functioning: initially hemiparesis on contralateral side and if not effectively treated progresses to decorticate and decerebrate positioning
• Altered vision (blurred vision, diplopia, decreased acuity) pupillary response (gradual dilation, sluggish response)
Increased ICP• Headache on rising; common with slowly
developing increased ICP
• Papilledema noted on fundoscopic exam
• Projectile vomiting
• CNS ischemic response: occurs late in course of increased ICP; Cushing‘s response (triad): increased MAP, increased pulse pressure, bradycardia
• Changes in respiratory pattern and dramatic rise in temperature
Increased ICPCauses• Space occupying lesions• Cerebral edema: increase in volume of brain
tissue due to abnormal accumulation of fluid; local process or affecting entire brain
• Hydrocephalus: increase in volume of CSF within ventricular system, which becomes dilated
-Noncommunicating: obstruction in CSF drainage from ventricular system
Increased ICP
-Communicating: CSF is not effectively reabsorbed through arachnoid villi
-Normal pressure hydrocephalus: occurs in persons > 60 in which ventricles enlarge causing cerebral tissue compression
-Manifestations depend on rate of onset: progressive cognitive dysfunction, gait disruptions, urinary incontinence
• Intracranial hemorrhage
Brain herniation
• Cerebral tissue can be displaced to more compliant area, if ICP is not treated
• Displacement of brain tissue results in further increased ICP and brain damage including lethal brain damage
Brain herniation
Brain herniation syndromes are categorized according to location
• Cingulate herniation
• Central or transtentorial herniation
• Uncal or latral transtentorial herniation
• Infratentorial herniation
Collaborative Care
• Identify and treat underlying condition
• Control ICP to prevent herniation syndromes
Diagnostic Tests
• Diagnosis is made on observation and neurological assessment
• Measures to control pressure are instituted while identifying underlying cause
Diagnostic Tests
Tests for underlying cause• CT scan and MRI: identify possible cause and
evaluate therapeutic options• Serum osmolality: used as indicator of hydration
status; usually maintained slightly elevated to draw excess fluid into vascular system from brain tissue
• Arterial blood gases: monitor pH, CO2, pO2 levels and effect on cerebral circulation; hydrogen ions and carbon dioxide are potent vasodilators; hypoxemia also causes vasodilation but to lesser degree
Medications Diuretics• Osmotic diuretics increase osmolarity of blood and
draw fluid from edematous brain tissue into vascular bed where it can be eliminated by kidneys
• Mannitol is commonly used• Loop diuretics such as furosemide are used, in
addition, to further promote diuresis• Serum electrolytes and osmolality are monitored• Urine specific gravity may also be monitored at
intervals
Medications• Antipyretics or hypothermia blanket: used to control
hyperthermia, which increases cerebral metabolic rate• Anticonvulsants to manage seizure activity• Histamine H2 receptors to decrease risk of stress ulcers• Barbiturates: may be given as continuous infusion to
induce coma and decrease metabolic demands of injured brain; controversial
• Vasoactive medications may be given to maintain blood pressure to support cerebral perfusion
Surgery
• May be indicated to treat underlying cause of increased ICP
• Include removal of brain tumors, burr holes, insertion of drainage catheter or shunt to drain excessive CSF
ICP Monitoring • Continuous intracranial pressure monitor is used for
continual assessment of ICP and to monitor effects of medical therapy and nursing interventions
• Allows for more precise manipulation of therapeutic measures to maintain adequate cerebral perfusion while controlling ICP
• Systems include intraventricular catheter, subarachnoid bolt or screw and epidural catheters; can be used to drain CSF and measure ICP
• Risk for infection exists with invasive procedure
Mechanical Ventilation:
• Involves airway management and prevention of hypoxemia and hypercapnia , which both increase intracranial pressure
Nursing Care
• Protect client from sudden increases in ICP and decrease in cerebral blood flow
• Clients are often critically ill and are in special neurological intensive care unit for constant observation and continuous treatment
Nursing Diagnoses
Ineffective Tissue Perfusion: Cerebral
• Frequent neurologic assessment based on client baseline and changing status
• Early signs are LOC and breathing patterns
• Measures in place to limit increases in intracranial pressure; limit stimulation
Nursing Diagnoses
• Risk for Infection: open head wounds and intracranial monitoring device require meticulous aseptic technique
• Anxiety (of family): need for teaching to maintain restful environment, emotional support
Client with a Headache
Pain within cranial vault and occuring commonly
• May be due to benign or pathological condition
• Majority are mild
Pathophysiology
• Multiple pain-sensitive structures within cranial vault, face, and scalp
Types of Headaches
Tension• Most common• Characterized by sensation of tightness
around head and may have specific localized painful areas
• Caused by sustained contraction of muscles of head and neck
• Precipitated by stress and anxiety
Types of Headaches
Migraine• Recurring vascular headache often initiated by
triggering event and accompanied by neurologic dysfunction
• More common in females between ages 25 -55• Cause not understood but related to abnormalities
in cerebrovascular blood flow, reduction in brain activity, or increase release of sensory substances (e.g. serotonin)
Types of Headaches
• Stages include-Aura: visual disturbances; lasts 5 – 60
minutes-Headache: throbbing pain often with
nausea and vomiting; hypersensitive to light and sound; lasts hours to 1– 2 days
-Postheadache: area of headache is sensitive; client exhausted
• Triggers include stress, fluctuating glucose levels, fatigue, hormones, bright lights
Types of Headaches
Cluster
• Common with middle-aged men
• Typically awakens client with unilateral pain around eye accompanied by rhinorrhea, lacrimation, flushing
• Attacks occur in clusters of 1 – 8 days for weeks
Collaborative Care
• identification of underlying cause and therapeutic management
Diagnostic Tests
• may involve neurodiagnostic testing depending on client history and assessment
Medications: According to type of headache
Migraine headache may require prophylactic therapy including serotonin antagonist or beta blocker
Management of migraine may include• Ergotamine tartrate (Cafergot)• Sumatriptan (Imitrex)• Zolmitriptan (Zomig)• Narcotic analgesic and anti-emetics
Medications: According to type of headache
• Cluster headaches are often treated with same medications as migraines
• Tension headaches are treated with aspirin, acetaminophen
Complementary Therapies
• Supplements
• Relaxation techniques
• Herbal therapy
• Osteopathic manipulation
Nursing Care
• Teach client to manage discomfort effectively, identify any triggers (headache diary), stress management
• Use of medications, and effective use of heat and cold
Client with Seizure Disorder
Seizures:• paroxysmal motor, sensory, or cognitive
manifestations of spontaneous abnormal discharges from neurons in cerebral cortex
• May involve all or part of brain: consciousness, autonomic function, motor function, and sensation
• Epilepsy: any disorder characterized by recurrent seizures
• Affects 2.3 million Americans; increased incidence in children and elderly
Cause • may be idiopathic or associated with birth injuries,
infection, vascular abnormalities, trauma, tumors • Theories propose causes related to altered permeability
of ions, neuron excitability, imbalances of neurotransmitters
• When seizure threshold exceeded, a seizure may result; neurons that initiate seizure activity are called epileptogenic focus
• Unprovoked seizures have no known cause; provoked seizure are related to another condition such as fever, rapid withdrawal from alcohol, electrolyte imbalance, brain pathology
Affects of seizure on brain tissue
• Increased metabolic demand: fourfold requirement of additional glucose and oxygen, resulting in increased cerebral blood flow
• If unmet, cellular destruction can result
Categorization of seizures
Partial seizures: activation of part of one cerebral hemisphere
• Simple partial seizure: no altered consciousness; recurrent muscle contraction; motor portion of cortex affected
• Complex partial seizure: impaired consciousness; may engage in automatisms (repetitive nonpurposeful activity such as lip smacking); preceded by aura, originates in temporal lobe
Categorization of seizuresGeneralized seizures: involves both brain hemispheres;
consciousness always impaired• Absence seizures (petit mal): characterized by sudden
brief cessation of all motor activity, blank stare and unresponsiveness often with eye fluttering
• Tonic-clonic seizures-Most common type in adults-Preceded by aura, sudden loss of consciousness -Tonic phase: rigid muscles, incontinence-Clonic phase: altered contraction, relaxation;
eyes roll back, froths at mouth-Postictal phase: unconscious and unresponsive to
stimuli
Status epilepticus
• Continuous seizure activity, generally tonic-clonic type
• Client at risk to develop hypoxia, acidosis, hypoglycemia, hyperthermia, exhaustion
Status epilepticus
Life threatening medical emergency requiring immediate treatment
• Establish and maintain airway• Diazepam (Valium) and lorazepam (Ativan)
intravenously at 10-minute intervals• 50% Dextose intravenously• Phenytoin (Dilantin) intravenously• Possibly Phenobarbital
Collaborative Care
• Control seizure
• Establish cause
• Prevent further seizures
Diagnostic Tests
• Neurologic exam• EEG to confirm diagnosis and locate lesion• Xray, MRI, CT scan identify any neurologic
abnormalities• Lumbar puncture may be done if infection
suspected• CBC, electrolytes, BUN, blood glucose• ECG to determine cardiac dysrhythmias
Medications Anticonvulsants
• Manage but do not cure seizure
• Actions
-Raise seizure threshold
-Limit spread of abnormal activity within brain
• Try to use lowest dose of single medication to control seizures if possible; may need to try different medications and use combinations
Medications
Medications
• Carbamazepine (Tegretol)
• Phenytoin (Dilantin)
• Valproic acid (Depakote)
• Tiagabine (Gabitril)
Surgery: if all attempts to control seizures are not successful
• May attempt to excise tissue involved in seizure activity
• EEG done during surgery to identify epileptogenic focus
Care of client during a seizure
• Protect client from injury and maintain airway
• Do not force anything into client’s mouth
• Loosen clothing around neck
Health Promotion: Stress the following to clients
• Importance of medical follow-up, taking prescribed medications
• Driving privileges are prohibited in clients with seizure disorders; driver’s licenses are reinstated after seizure free period and statement from health care practitioner
• Client needs proper identification• Family members need to be educated in
preventing injury if seizure occurs
Nursing Diagnoses
• Risk for Ineffective Airway Clearance
• Anxiety
Home Care
• Education of client and family regarding seizure disorder; safety measures, avoidance of alcohol and caffeine
• Referral to support group, national organizations
Client with traumatic brain injury
Traumatic brain injury:
• a leading cause of death and disability; any traumatic insult to brain causing physical, intellectual, emotional, social, or vocational changes
• Includes penetrating head injury (open) and closed head injury
• Estimates of 1 million persons are treated and released with head injuries yearly in USA
Traumatic brain injury:
Risk Factors
• Motor vehicle accidents
• Elevated blood alcohol levels
• Greatest risk: males aged 15 – 30 and those over 75
Mechanisms of trauma
• Acceleration injury: head struck by moving object• Deceleration injury: head hits stationary object• Acceleration-deceleration (coup-contrecoup
phenomenon): head hits object and brain rebounds within skull
• Deformation: force deforms and disrupts body integrity: skull fracture
Types of injuries
Skull fracture: break in continuity of skull usually resulting in brain trauma
Classifications• Linear: dura remains intact; subdural or epidural
hematoma may occur underneath• Comminuted and depressed skull fractures:
increase risk for direct injury to brain tissue from contusion (bruise) and bone fragments; risk for infection
Types of injuries
• Basilar:
-Involves base of skull and usually involve extension of adjacent fractures
-If dura disrupted may have leakage of CSF occurring as
-Rhinorrhea: through nose
-Otorrhea: through ear
Types of injuries
May appear on xray; signs of basilar skull fracture
• Hemotypanum: blood behind tympanic membrane
• Battle’s sign: blood over mastoid process
• “Raccoon eyes”: bilateral periorbital ecchymosis
Types of injuries
Test clear fluid from ear or nose for glucose by using glucose reagent strip: if positive indicates CSF
CSF leakage: increased risk of infection• Keep nasopharnyx and external ear clean• No blowing nose, coughing or hard
sneezing• Prophylactic antibiotic
Collaborative Care
• All require minimal bed rest and observation of underlying injury
• Depressed skull fractures require surgical intervention to debride wound and remove bone fragments embedded in brain tissue
• Basilar fractures with CSF leakage may require surgery
Nursing Care/Home Care
• Client must be monitored for signs of increased intracranial pressure
• Observe in hospital
• Educate family regarding changes in LOC: wake up every 2 hours during first 24 hours home
• Follow–up care
Client with focal or diffuse brain injury
Primary and secondary mechanism occur with brain
injury
• Primary: impact of injury
• Progression of initial injury affecting perfusion and oxygenation of brain cells: intracranial edema, hematoma, infection, hypoxia, ischemia
Focal brain injuries
• Specific observable brain lesion confined to one area of brain; includes epidural hemorrhage, subdural and intracerebral hematoma
• Depending on site and rate of bleeding, manifestations may occur within hours to weeks
• Client may develop increased ICP with altered level of consciousness and potential for brain herniation
Specific types of brain injuries
• Contusion: bruise of surface of brain; manifestations and degree of impairment depend on size and location of injury; slow recovery of consciousness
Specific types of brain injuries
Epidural hematoma (extradural hematoma): blood collects in potential space between dura and skull
• Occurs more often in young to middle aged adults• Occurs with skull fracture from torn artery, tend to
occur rapidly• May have brief lucid period after injury and then
rapid decline from drowsiness to coma with neurological deficits
• Require rapid treatment to prevent complications
Specific types of brain injuriesSubdural hematoma• Localized mass of blood collects between dura mater
and arachnoid mater• More common than epidural hematoma• Types
-Acute subdural hematomas develop within 48 hours of injury
-Chronic subdural hematomas develop over weeks to months
• Manifestations of neurologic deficits develop at the same rate of the hematomas
Specific types of brain injuries
• Intracerebral hematomas: occur more often in older clients because cerebral blood vessels are more fragile and easily torn
• Diffuse brain injury (DBI): affects entire brain and is caused by shaking motion with twisting movement
Specific types of brain injuries
Mild concussion • Momentary interruption of brain function with or
without loss of consciousness• Manifestations: • Retrograde and antegrade amnesia• Headache• Drowsiness, confusion, dizziness• Visual disturbances
Specific types of brain injuriesClassic cerebral concussion• Diffuse cerebral disconnection from brain stem RAS • Has manifestations as with mild concussion but
immediate period of loss of consciousness is less than 6 hours; client may have exhibited seizure and respiratory arrest with bradycardia and hypotension
• May have postconcussion syndrome
Diffuse axonal injury: high speed acceleration-deceleration injury causing widespread disruption of axons in white matter; Poor prognosis: death or persistent vegetative state
Treatment
Concussion• Client should be observed for 1 – 2 hours in
emergency department• Discharged home with instruction for
observations, if loss of consciousness only a few minutes
• Longer period of unconsciousness, admit to hospital for observation
Treatment
Acute TBI
• Recognition and management begins at scene with transport to emergency department
• Hospitalization with critical care and specific neurologic observation and interventions as indicated
Diagnostic Tests:
• same tests as increased ICP
Treatments
• Management of increased ICP
• Surgery: epidural and subdural hematomas; surgical evacuation of clot through burr holes
Health Promotion:
• Injury prevention: use of seat belts, bicycle and motorcycle helmets, gun safety
Client CNS infection
CNS infections
• Most common is bacterial meningitis
• Mortality rate 25% in adults
• Meningococcal occurs in epidemics with people living in close contact
• Pneumococcal effects very young and very old
Risk Factors
• High risk for old and young
• High risk for clients with debilitating diseases, or immunosuppressed
Pathophysiology
• Pathogens enter CNS and meninges causing inflammatory process, which leads to inflammation and increased ICP
• May result in brain damage and life-threatening complications
Meningitis
• Inflammation of pia mater, arachnoid, and subarachnoid space
• Spreads rapidly through CNS because of circulation of CSF around brain and spinal cord
• May be bacterial, viral, fungal, parasitic in origin • Infection enters CNS though invasive procedure
or through bloodstream, secondary to another infection in body
Bacterial meningitis
• Causative organisms: Neisseria meningitis, meningoccus, Streptococcus pneumoniae, Haemophilus influenzae, E. Coli
• Risk factors: head trauma with basilar skull fracture, otitis media, sinusitis, immunocompromised, neurosurgery, systemic sepsis
Bacterial meningitis
Manifestations• Fever chills• Headache, back and abdominal pain• Nausea and vomiting• Meningeal irritation: nuchal rigidity, positive
Brudzinski’s sign, Kernig’s sign, photophobia• Meningococcal meningitis: rapidly spreading
petechial rash of skin and mucous membranes• Increased ICP: decreased LOC, papilledema
Bacterial meningitis
Complications
• Arthritis
• Cranial nerve damage (deafness)
• Hydrocephalus
Viral meningitis
• Less severe, benign course with short duration
• Intense headache with malaise, nausea, vomiting, lethargy
• Signs of meningeal irritation
Encephalitis
• Acute inflammation of parenchyma of brain or spinal cord
• Usually caused by virus • Inflammation occurs with manifestations similar
to meningitis• LOC deteriorates and client may become
comatose• Arboviruses are agents including West Nile virus
Brain abscess
• Infection with a collection of purulent material within brain tissue usually in cerebrum
• Causes include open trauma and neurosurgery; infections of ear, sinuses
• Common pathogens are streptococci, staphylococci, bacteroids
• Becomes space-occupying lesion• At risk for infection and increased ICP
Brain abscess
Manifestations • General symptoms associated with acute
infectious process• Client develops seizures, altered LOC, signs of
increased ICP• Specific neurologic symptoms are related to
location
May be drained surgically, if considered feasible
Collaborative Care
• Bacterial meningitis: requires immediate treatment and isolation of client
• Viral meningitis: supportive treatment and management of client symptoms
• Brain abscess treatment focuses on antibiotic therapy
Diagnostic Tests
• Lumbar puncture: definitive test for bacterial meningitis demonstrating infection: turbid cloudy appearance, increased WBC, gram stain, culture
• CT scan, MRI
Medications
• Meningitis: immediate treatment with effective antibiotics for 7 – 21 days; according to culture results; dexamethasone to suppress inflammation
• Encepahlitis: viral treated with anti-viral medications
• Brain abscess: antibiotic therapy, which may include intraventricular administration; anticonvulsant medications, antipyretics
Health Promotion
• Vaccinations for meningococcal, pneumococcal, hemophilic meningitis
• Prophytlactic rifampin for persons exposed to meningococcal meningitis
• Mosquito control• Prompt diagnosis and treatment of clients with
infections• Asepsis care for clients with open head injury or
neurosurgery
Nursing Diagnoses
• Ineffective Protection
• Risk for Deficient Fluid Volume
Home Care
• Client education for future prevention
• Complete medications and treatment plan
Client with a brain tumor
Description • Growths within cranium including tumors of brain
tissue, meninges, pituitary gland, blood vessels• May be benign or malignant, primary or metastatic• May be lethal, due to location (inaccessible to
treatment) and capacity to impinge on CNS structures • In adults most common tumor is glioblastoma followed
by meningioma and cytoma• Cause is unknown: factor associated include heredity,
cranial irradiation, exposure to some chemicals
Description
Tumors within brain• Compress or destroy brain tissue• Cause edema in adjacent tissues• Cause hemorrhage• Obstruct circulation of CSF, causing
hydrocephalusEstimated 25% persons with cancer develop brain
metastasis, often multiple sites throughout the brain
Manifestations: Multiple depending on location of lesion
and rate of growth • Changes in cognition and LOC
• Headache usually worse in morning
• Seizures
• Vomiting
• Manifestations associated with cerebral edema, increased ICP, cerebral ischemia leading to brain herniation syndromes
Collaborative Care
• Effective treatment includes chemotherapy, radiation therapy, and/or surgery
• Treatment depends on size and location of tumor, type of tumor, neurologic deficits, and client’s over all condition
Diagnostic Tests
• CT scan or MRI: determine tumor location and extent
• Arteriography
• EEG: information about cerebral function, seizure data
• Endocrine studies if pituitary tumor suspected
Treatment
Medications: Chemotherapy, corticosteroids, anticonvulsants
Surgery• Purposes include tumor excision, reduction, or for
symptom relief• Craniotomy: location according to approach to
tumorRadiation: Alone or as adjunctive therapySpecialty procedures: Stereotaxic techniques and use
of laser beam
Nursing Care
• Support during diagnosis and management through selected treatment
• Nursing care involves interventions to deal with altered LOC, increased ICP, and seizures
Nursing Diagnoses
• Anxiety
• Risk for Infection
• Ineffective Protection
• Acute Pain
• Disturbed Self-esteem
Home Care
• Education, support to client and family
• Instructions for treatment plan and follow-up care
• Referral to home care agencies
• Referrals to therapies, community resources, support groups as appropriate
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