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