NEUROLOGICAL ALTERATIONS

NUR 203 Module C

Terms
Define Terms associated with neurological
alterations:
Headaches Tension, migraines, cluster Tumors benign, cancerous Infections-meningitis, encephalitis Head injury contusions, concussions, fractures, intracranial hemorrhage

Terms (cont)
Transient ischemic attacks Cerebrovascular accidents
Thrombotic Hemorrhagic Embolic

Spinal Cord dysfunctions

Spinal cord injuries Herniated disc

Terms
Spinal Cord dysfunctions
Spinal Shock

Paralysis
Quadriplegic (tetraplegia) Paraplegic

Autonomic Dysreflexia Spasticity Neurogenic bladder/bowel

Terms
Spinal Cord dysfunctions
Respiratory Sexual Infection

Neuromuscular dysfunction
Multiple Sclerosis Parkinsons Guillian-Barre Amyotrophic Lateral Sclerosis

Neuromuscular Dysfunctions

Myasthenia Gravis Trigeminal Neuralgia Bells Palsy Muscular Dystrophy Cerebral Palsy Neural tube defects

VASCULAR HEADACHES
Tension Headache
Results from muscle contraction Tight, band-like discomfort that is unrelenting Pain builds slowly in severity Triggered by fatigue and stress Diagnosis confirmed when they occur more than 15 days a month

 Treatment:
Stress reduction techniques (bio-feedback, psychotherapy and other methods of stress reduction). Also, correction of poor posture.

Cluster Headaches (sometimes classified as a form of migraine)

Cyclical pattern of periorbital pain lasting
form 4 8 weeks and usually occurring in the spring or fall
Headache lasts from 15 minutes to hours and may occur several times a day and may awaken from sleep. Unilateral in nature.

 Pain is described as deep, boring, intense

pain of such severity that the patient has trouble staying still. May develop Horners syndrome
Constricted pupils Unilateral lacrimation Rhinorrhea

Triggered by consumption of alcohol Treated with 100% oxygen via mask Intranasal Lidocaine may be used

Migraine Headache
Typically a true vascular headache Pain results from vasospasm and ischemia of intracranial vessels. Unilateral pain, but may alternate sides Throbbing, pulsatile pain Photophobia, phonophobia, anorexia, nausea, vomiting and focal neurogenic signs may be present

 Aura may precede the event scintillating scotoma (flashing lights), euphoria, fatigue, yawning, and/or craving for sweets Can be triggered by relief of intense stress, missing meals, or tyramine rich foods Patient tries to find relief in a quiet, dark environment Treatment: avoid precipitating factors Meds: propranolol, amitriptyline, valporate, verapamil, phenelzine and methysergide taken daily

 If medical treatment is sought at the time of

the event:
Ergotamine Dihydroergotamine Sumatriptan Chlorpromazine Prochlorperazine

 Patient teaching for migraines:

Identify triggers Avoid alcohol Avoid tyramine rich foods Avoid low blood sugars Reduce stress

INFECTIOUS / INFLAMMATORY DISORDERS

MENINGITIS
Inflammation of the meninges of the brain
and spinal cord
Bacterial Aseptic (other infective agentsusually viral)

CLINICAL MANIFESTATIONS
Classic symptoms:
Nuchal rigidity Brudzinskis sign Kernigs sign Photophobia

Other: fever, tachycardia, h/a, prostration, chills,

nausea, vomiting May be irritable at first with progression to confusion, stupor, and semiconsciousness

 Seizures may occur Petechial or hemorrhagic rash may develop CSF is cloudy with bacterial

BRUDZINSKIS SIGN

KERNIGS SIGN

DIAGNOSIS
Lumbar puncture:
Bacterial: increased protein, decreased glucose, cloudy, increased leukocytes Viral: increased protein, normal glucose, clear, increased lymphocytes

May culture other areas: blood, wounds,

sinuses, etc.

TREATMENT
Isolate until results of CSF analysis are
obtained.
Bacterial is very contagious

ABX Anticonvulsants Fluid and electrolyte replacement Monitor for increased ICP Provide quiet environment Analgesics may be avoided if they have CNS depressant actionswill mask CNS changes

ENCEPHALITIS
Inflammation of the parenchyma of the
brain and spinal cord. Usually caused by a virus.
Arbovirus encephalitis (transmitted by ticks and mosquitoes) Herpes simplex virus encephalitis may occur as a complication of measles, chickenpox, or mumps.

CLINICAL MANIFESTATIONS

Fever Headache Seizures Nuchal rigidity Altered LOC Disorientation Agitation Restlessness or lethargy Drowsiness Photophobia N/V

BRAIN ABSCESS
A collection of either encapsulated or free
pus within brain tissue arising from a primary focus elsewhere (ear, mastoid process, sinuses, heart, distal bones, lungs, bacteremia, etc).

MANIFESTATIONS

Headache Lethargy Drowsiness Confusion Depressed mental status Symptoms of infection
Fever Chills

Traumatic Brain Injuries

Over 2 million traumatic brain injuries occur each
year with approximately 500,000 injuries severe enough to cause hospitalization. Approximately 50% of all trauma deaths associated with head injury More than 60% of all vehicular trauma deaths are a result of heat injury

Traumatic Brain Injury -Mechanism of Injury

Penetrating trauma Blunt trauma
Acceleration Deceleration Rotational forces

Traumatic brain Injury Patho

Primary injury Secondary injury Goals of care include efforts to reduce morbidity &
mortality from primary & secondary injuries

Traumatic Brain Injury Patho. Primary Injury

Occurs at moment of impact May be mild or severe Types of primary injuries:
Contusion, laceration, shearing injuries, and hemorrhage

Traumatic Brain Injury Patho. Secondary Injury

The biochemical & cellular response to the initial
trauma
Can exacerbate the primary injury & cause loss of brain tissue not originally damaged

Ischemia is the primary culprit in secondary brain

injury

Traumatic Brain Injury - Patho Secondary Injury (cont.)

Hypercapnia is a powerful vasodilator
Results in cerebral vasodilatation & increased cerebral blood volume & ICP

Significant hypotension causes inadequate perfusion

to neural tissue
*Not typical to be hypotensive with TBI If hypotensive, need to rule out internal injuries

Traumatic Brain Injury - Patho Secondary Injury (cont.)

Cerebral edema Initial hypertension with severe TBI is common Must control HTN to prevent secondary injury
caused by increased ICP Effects of increases in intracranial pressure may be varied.

BRAIN INJURY CEREBRAL HEMATOMAS

Extravasation of blood produces a spaceoccupying lesion on the brain and leads to increased ICP Epidural & subdural
Extraparenchymal (outside of brain tissue)

Produce injury by pressure effect and displacement

of intracranial contents.

Epidural Hematoma
A collection of blood between the inner table of the
skull & the outermost layer of the dura Most often associated with:
Skull fractures Middle meningeal artery laceration

Epidural Hematoma
Incidence relatively low Can occur as a result of low-impact injuries (falls)
or high-impact injuries (MVAs) Occurs from trauma to the skull & meninges rather than from the acceleration-deceleration forces seen in other types of head trauma

Epidural Hematoma (cont.)

Clinical manifestations:
Brief loss of consciousness followed by period of lucidity This lucid period is followed by a rapid deterioration in LOC Dilated, fixed pupil on the same side as the impact area is a hallmark of EDH May c/o severe, localized H/A & may be sleepy

Epidural Hematoma (cont.)

Diagnosis:
Based on clinical symptoms & evidence of a collection of epidural blood identified on CT scan

Treatment:
Involves surgical intervention to remove the blood and to cauterize the bleeding vessels

Subdural Hematoma
The accumulation of blood between the dura and
underlying arachnoid membrane. Most often is related to a rupture in the bridging veins between the brain and the dura. Acceleration-deceleration & rotational forces are the major causes. Often associated with cerebral contusions & intracerebral hemorrhage

Subdural Hematoma (cont.)

Three types:
Acute, subacute, and chronic

Based on the time frame from injury to clinical

symptoms:

Subdural Hematoma - ACUTE

Hematoma that occurs after a severe blow to the
head. Clinical presentation determined by
the severity of injury to the underlying brain at the time of impact & the rate of blood accumulation in the subdural space.

Subdural Hematoma ACUTE

Observe for deterioration in level of
consciousness or lateralizing signs,
such as inequality of pupils or motor movements.

Deterioration may be rapid Surgical intervention may include

craniectomy, craniotomy, or burr hole evacuation

Subdural Hematoma -SUBACUTE

Develop symptomatically 2 days to 2 weeks after
trauma. Expansion of the hematoma occurs at a rate slower than that in acute SDH. Takes longer for symptoms to become obvious. Clinical deterioration with subacute SDH usually is slower than that with acute SDH Surgical intervention, when appropriate, is the same

Subdural Hematoma CHRONIC

This term is used when symptoms appear days or
months after injury. Most patients usually are elderly or in late middle age. Patients at risk include:
Patients with coordination/balance disturbances, Elderly, Those receiving anticoagulation therapy

Subdural Hematoma CHRONIC

Clinical manifestations are insidious Patient may report a variety of symptoms:
Lethargy, absent-mindedness, headache, vomiting, stiff neck, and photophobia, and show signs of TIA, seizures, pupillary changes, or hemiparesis

Often not seen as initial diagnosis CT scan can confirm diagnosis of SDH

Subdural Hematoma CHRONIC

If surgical intervention required, evacuation of the
chronic SDH may occur by:
Craniotomy, burr holes, or catheter drainage

Outcome variable Return of neurologic status variable Recovery slow Recurrence frequent

Subarachnoid Hemorrhage (SAH)

Described as bleeding into the subarachnoid space Usually caused by rupture of a cerebral aneurysm or
arteriovenous malformation (AVM). Accounts for 6% to 7% of all strokes
Non-traumatic SAH affects more than 30,000 people in US each year Incidence > in women & increases with age

Subarachnoid Hemorrhage (cont.)

Overall mortality rate is 25% with most patients
dying on first day after injury. Approximately 2 million people in the US are believed to have an unruptured cerebral aneurysm, the congenital anomaly responsible for most cases of SAH.

Subarachnoid hemorrhage (cont.)

Known risk factors include: **Hypertension, Smoking, Alcohol use, and Stimulant use

SAH Patho
Pathophysiology of two most common causes is
distinctly different:
Cerebral Aneurysm Arteriovenous (AV)Malformation

SAH CEREBRAL ANEURYSM

As individual with a congenital cerebral aneurysm
matures,
BP rises & more stress placed on vessel wall

Saccular or berry-like & most occur at the

bifurcation of blood vessels

SAH CEREBRAL ANEURYSM

Vessel wall becomes thin & ruptures,
Sending arterial blood at a high pressure into the subarachnoid space.

In other situations, the unruptured aneurysm

expands and
places pressure on surrounding structures.

SAH ARTERIOVENOUS MALFORMATION

Pathologic features related to the size & location of
the malformation. One or more cerebral arteries, known as feeders feed an AVM Feeder arteries enlarge and increase the volume of blood shunted through the malformation. Large, dilated, tortuous draining veins develop

SAH ARTERIOVENOUS MALFORMATION

The enlarged veins rupture easily Cerebral atrophy is sometimes also present.
It is the result of chronic ischemia because of the shunting of blood through the AVM and away from normal cerebral circulation

SAH ASSESSMENT
Characteristically has an abrupt onset of pain,
described as the worst headache of my life. Brief loss of consciousness, nausea, vomiting, focal neurologic deficits, and a stiff neck may accompany the headache. The SAH may result in coma or death.

SAH ASSESSMENT
May have warning leaks which go undetected. Symptoms of unruptured AVM may be found in the
history
Headaches with dizziness or Syncope or Fleeting neurologic deficits

SAH - DIAGNOSIS
Based on:
Clinical presentation, CT scan, **Noncontrast CT is the cornerstone of definitive SAH
diagnosis

Lumbar puncture

SAH DIAGNOSIS (cont.)

CT
In 92% of cases, CT can demonstrate a clot in the subarachnoid space, if performed within 24 hours of the onset of the hemorrhage

Lumbar puncture if initial CT negative

CSF after SAH bloody in appearance with a RBC > 1000/mm3.

SAH Cerebral Angiography

Cerebral angiography necessary once SAH has been
documented
To identify exact cause of the SAH

If a cerebral aneurysm rupture is the cause,

angiography essential for identifying exact location of aneurysm in prep. for surgery.

If AVM rupture the cause,

angiography necessary to identify the feeding arteries & draining veins

SAH Medical Management

Is a medical emergency! Preservation of neurologic function is the goal Initial treatment must always support vital
functions Early diagnosis is essential Ventriculostomy is performed to control ICP if the patients LOC is depressed.

SAH Medical Management

Factors attributing to deaths: 19% - related to direct effects of the initial
hemorrhage 22% - rebleeding 23% - cerebral vasospasm 23% non-neurologic medical complications

SAH Re-bleeding
The occurrence of a second SAH in an unsecured
aneurysm With conservative therapy, 20 30% likelihood of re-bleeding in first month, with highest occurrence on first day after initial bleed Mortality with aneurysmal re-bleeding is 48% to 78%

SAH Rebleeding CONS. MEASURES FOR PREV

BP control:
Maintain SBP no greater than 150 mm Hg (individualized based on previous values): Nitroprusside, metoprolol, Hydralazine *Rebleeding more associated with variations in BP

Prophylactic anticonvulsant therapy

SAH Rebleeding Surgical Aneurysm Clipping

Definitive treatment is surgical clipping

w/complete obliteration of aneurysm. Timing is key issue Usually within first 48 hours of rupture Eliminates risk of rebleeding Allows more aggressive therapy post-op Allows for flushing out excess blood & clots to reduce risk of vasospasm

SAH Rebleeding Surgical Aneurysm Clipping

Classification of Subarachnoid Hemorrhage Early surgery recommended for patients with Grade
I or Grade II SAH & some patients with Grade III Careful consideration of patients clinical situation is necessary in determining if candidate for surgery & optimal time

SAH - Rebleeding
Surgical procedure involves a craniotomy Requires skill of an experienced neurosurgeon Complications

SAH Rebleeding Surgical AVM Excision

Decision for surgical excision depends on the
location & size of the AVM Surgical excision of large AVMs includes risk of reperfusion bleeding Postop low BP maintained to prevent further reperfusion bleeding In large AVMs, 2 4 stages of surgery may be required over 6 to 12 months

SAH Rebleeding Embolization

Used to secure a cerebral aneurysm or AVM that is
surgically inaccessible because of size, location, or medical instability of the patient. Several techniques available All use a percutaneous transfemoral approach in a manner similar to an angiogram

SAH Rebleeding Pharmacologic Therapy

In the Past,
antifibrinolytic agents were suggested (aminocaproic acid)

TODAY,
Antifibrinolytic agents are NOT recommended for routine use in SAH

SAH CEREBRAL VASOSPASM

Presence or absence of cerebral vasospasm
significantly affects the outcome of aneurysmal SAH Estimated that 50% of all SAH patients develop vasospasm
32% resulting in symptomatic vasospasm & 15% - 20% result in ischemic stroke or death

SAH CEREBRAL VASOSPASM

Onset usually 3 5 days after initial bleed & can
last for 3 to 4 weeks. Treatment:
Induced hypertensive, hypervolemic, hemodilution therapy Oral nimodipine; and Transluminal cerebral angioplasty

TRANSIENT ISCHEMIC ATTACKS (TIA)

Sudden, brief episodes of neurologic
dysfunction caused by temporary, focal cerebral ischemia Lasts less than 24 hours, often as little as 5 20 minutes Warning sign of impending CVA

CLINICAL MANIFESTATIONS
Carotid artery occlusion: weakness or
numbness in an arm or leg, aphasia, and visual field cuts Vertebrobasilar circulation: vertigo, diplopia, dysphagia, dysarthria, and ataxia

DIAGNOSIS

Carotid bruit CT Doppler Cerebral angiogram ECG (looking for A fib if site of emboli formation TEE (looking for site of emboli formation)

TREATMENT
Antihypertensives Antiplatelet drugs Surgery

 Neurological deficits occur as a result of

CEREBROVASCULAR ACCIDENT (CVA OR STROKE)

decreased blood flow to a localized area of the brain. Risk factors:

Hypertension Diabetes Mellitus CV disease, a-fib Hyperlipidemia Cigarette smoking, alcohol consumption, cocaine use Obesity

ISCHEMIC CVA
Occurs when blood supply to a part of the
brain is interrupted or occluded. Causes:
Spasm: caused by irritation Thrombosis: platelets adhere to irregular plaque surfaces Embolism: traveling clot which becomes lodged in a narrow lumen

HEMORRHAGIC CVA
Occurs in only 10 % of cases, usually
women Results from rupture of a cerebral blood vessel that results in bleeding into the brain tissue or the subarachnoid space

CLINICAL MANIFESTATIONS

H/A Vomiting Seizures AMS Fever ECG changes Manifestations related to area of injury

 Motor deficits:
Hemiplegia Hemiparesis Flaccidity Spasticity Rigidity Dysphagia

Elimination disorders
Bowel bladder

 Sensory perceptual deficits

Hemianopia Agnosia Apraxia

Language disorders
Aphasia Dysarthria

Cognitive and behavioral changes Intellectual: memory and judgment changes

 Right sided CVA

Impulsive Over estimate their abilities Have decreased attention span Left sided weakness

 Left sided CVA

Slow, cautious, and disorganized Right sided weakness

Spatial perceptual defects: denial of illness

or non functioning body parts; erroneous perception of self; agnosia; apraxia

DIAGNOSIS

CT MRI Doppler ultrasound Cerebral angiogram Lumbar puncture if not contraindicated

TREATMENT
Acute phase (first 12 72 hours):
If not hemorrhagic: anticoagulant Thrombolytics, if not hemorrhagic Calcium channel blockers Hyperosmolar solutions Diuretics Anticonvulsants Decadron Antipyretics

NURSING DIAGNOSIS
ALTERED CEREBRAL TISSUE PERFUSION
Monitor respiratory and airway patency Suction only as needed Lateral low Fowlers position ( HOB 30 to cerebral edema, head in neutral position improves venous drainage) If risk for hemorrhage or IICP, no coughing, deep breathing If no risk of hemorrhage, cough and deep breathe Oxygen as ordered

 Monitor Neurologic Status

LOC Pupilary response Movement, strength of extremities Babinski Decorticate/decerebrate posturing Changes in LOC

 Monitor CV status
Assess for fluid overload (rales, SOB, dyspnea) Fluid restriction (if CO is low, increase fluid based on ADH and aldosterone levels) Prevent thrombosis of lower extremities (ROM, antiembolic hose, pneumatic compression sleeves

Monitor Neuro status

Monitor temp (risk for hyperthermia Monitor for seizures (place on precautions)

 Impaired mobility:
Prevent contractures Passive/active ROM TQ2H Prone position 15 30 minutes several times daily Monitor for thrombophlebitis Self Care deficit Encourage use of unaffected side Teach to dress affected side first

 Sensory perceptual
Keep environment clutter free Well lighted environment Bed in low position Wheels locked Side rails up Keep needed objects of the unaffected side

 Elimination
Bladder Offer bedpan/urinal every 2 hours Encourage bladder training Teach Kegel exercises Use positive reinforcement Bowel Encourage fluids (2000 cc/day unless CI) High fiber diet Stool softeners Establish bowel evacuation routine

 Swallowing
Sit upright when eating and for 30 minutes after Make sure neck is slightly flexed Pureed or soft diet initially Place food/drink on unaffected side When finished eating, assess mouth for absence of food Maintain suction at bedside Minimize distractions so they can concentrate

PROGNOSIS
Assessment
Neurologic Urinary Orthopedic Bowel

Acute Spinal Cord Injury

Diagnosis begins with:
a detailed history of events surrounding incident, precise evaluation of sensory & motor function, & radiographic studies of the spine

Majority occurs in males between 16 & 30

Mechanism of injury

Hyperflexion Hyperextension Rotation Axial loading Penetrating injuries

Mechanism of injury
Hyperflexion
Most often seen cervical area at level of C5 to C6. Sudden deceleration motions

Hyperextension
Involve backward & downward motion of the head Often seen in rear-end collisions or diving accidents

Mechanism of Injury
Rotation Often occur in conjunction with a flexion or
extension injury Axial loading
Vertical compression Falls & lands on feet

Penetrating injuries
Bullet, knife, etc. Cause permanent damage by anatomical transection

SCI Patho
Result of a mechanical force that disrupts
neurologic tissue or its vascular supply or both. Injury process includes both primary & secondary injury mechanism

SCI Patho
Primary injury
The neurologic damage that occurs at moment of impact

Secondary Injury
The complex biochemical processes affecting cellular function Can occur within minutes of injury and can last for days to weeks

SCI Patho
Several events after a spinal cord injury lead to
spinal cord ischemia & loss of neurologic function Leads to:
Ischemia, elevated intracellular calcium Inflammatory changes

Current research focused on inhibiting secondary

processes & preserving functional neurons.

SCI
Functional Injury of the spinal Cord
The degree of disruption of normal spinal cord function Depends on what specific sensory & motor structures within the cord are damaged

Classified as:
Complete or Incomplete

SCI
Complete Injury
Results in a total loss of sensory & motor function below the level of injury

Incomplete Injury
Results in a mixed loss of voluntary motor activity & sensation below the level of the lesion

SCI - Complete Injury

Quadriplegia
Injury occurs from the C1 to T1 level Also known as Tetraplegia

Paraplegia
Injury occurs in the thoracolumbar region (T2 to L1) May have full use of arms

SCI Incomplete Injury

Brown-Sequard Syndrome
Damage to one side of the cord Loss of voluntary motor movement on same side as injury, with loss of pain, temperature & sensation on opposite side

Central Cord Syndrome

Motor & sensory deficit more pronounced in upper extremities than in lower.

SCI Incomplete Injury

Anterior Cord Syndrome
Loss of motor function, as well as loss of sensations of pain & temperature below level of injury Below injury, position sense & sensations of pressure & vibrations remain intact.

Posterior cord Syndrome

Loss of position sense, pressure & vibration below the level of the injury. Motor function & sensation of pain & temperature remain intact

Spinal Shock
The complete loss of all normal reflex activity
below the level of injury. Manifestations include:
Bradycardia & hypotension

Intensity is influenced by level of injury & duration of this shock state can persist for up to 1
month after surgery *Be careful with positioning

Assessment for SCI

Airway Breathing Circulation Neurologic Diagnostic Procedures

AUTONOMIC DYSREFLEXIA
A life threatening complication that may occur
with SCI. Caused by a massive sympathetic response to a noxious stimuli such as:
Full bladder, line insertions, fecal impaction

Results in:
Bradycardia, hypertension, facial flushing, and headache

AUTONOMIC DYSREFLEXIA
Treatment aimed at alleviating noxious stimuli If symptoms persist, anti-hypertensive agents can
be administered to reduce blood pressure Prevention is imperative and can be accomplished through use of a good B & B program

AUTONOMIC DYSREFLEXIA
Clinical algorithm for treatment of autonomic
dysreflexia
Positioning Constrictive devices Look for cause BP Catheter/Bowel

Medical Management
Primary treatment is to preserve remaining
neurologic function Interventions Divided into:
Pharmacologic Surgical nonsurgical

Medical Management
Pharmacologic Management Methylprednisolone
Bolus followed by continuous infusion for at least 24 hrs & preferably 48 hrs. Prevents post-traumatic spinal cord ischemia Improves energy metabolism Restores extracellular calcium Improves nerve impulse conduction

Surgical Management
Laminectomy Spinal fusion Rodding

Non-surgical Management
Cervical Injury
Gardner-Wells and Crutchfield tongs Halo Vest

Thoracolumbar

Nursing Management

CV Astute assessment of fluid volume Inotropic or vasopressor support Hypotension/hypertension Bradycardia DVT Loss of thermoregulation (poikilothermy)

Nursing Management

CV Astute assessment of fluid volume Inotropic or vasopressor support Hypotension/hypertension Bradycardia DVT Loss of thermoregulation (poikilothermy)

Nursing Management
Pulmonary complications are most common cause
of mortality Observe rate, rhythm, pattern ABGs Watch for paralysis/weakness of respiratory muscles airway

Nursing management
Musculosketal
ROM, PT, OT Splints

Integumentary Elimination

Rehabilitation & Maximizing Psychosocial Adaptation

Provide dedicated emotional support four D syndrome
Dependency, depression, drug addiction, and, if married, divorce.

Further support given by:

Social workers, occupational therapists, psychiatric clinical nurse specialists, pastors, physical therapists, long-term rehab, support groups.

Disc Herniation
An intervertebral disc is a pad composed of three
parts that rests between the centers of two adjacent vertebrae. Discs provide cushions for spinal movement. Strenuous activity or degeneration of the disc or vertebrae can allow the disc to move from its normal location.

Disc Herniation (cont.)

Displacement of intervertebral disc material may
be referred to as:
Prolapse, herniation, rupture, or extrusion

Disc Herniation (cont.)

Ruptured intervertebral discs may occur at any
level of the spine. Lumbar discs are more likely to rupture than cervical discs because of the:
Force of gravity; continual movement in this region; and improper movements of the spine, as with lifting or turning

Description
Thoracic disc disorders are the least common More than half of patients give a hx of a previous
back injury. Heavy physical labor, strenuous exercise, & weak abdominal and back muscles increase risk Repeated stress progressively weakens the disc, resulting in bulging and herniation

Clinical Manifestations
Lower back pain that radiates down the sciatic nerve
into the posterior thigh. Typically begins in the buttocks & extends down the back of the thigh and leg to the ankle. Can also lead to groin pain Muscle spasms & hyperesthesia (numbness & tingling) in areas of distribution of affected nerve roots

Clinical Manifestations (cont.)

Pain exacerbated by
straining (coughing, sneezing, defecation, bending, lifting, & straight-leg raising) or prolonged sitting &

Is relieved by
side-lying with the knees flexed.

Clinical Manifestations (cont.)

Any movement of lower extremities that stretches
the nerve causes pain & involuntary resistance Straight-leg raising on the affected side is limited Complete extension of the leg is not possible when the thigh is flexed on the abdomen. May have depression of deep tendon reflexes

Diagnostic Findings
X-Ray Studies
May show spinal degenerative changes Usually do not show a ruptured disc

Magnetic resonance imaging (MRI)

May show extrusion of disc material into the spinal canal and impingement of a spinal nerve root

Diagnostic Findings
Discography
Injection of a water-soluble imaging material into the nucleus pulposus Used to determine internal changes in the disc.

Electromyography of the peripheral nerves

To localize the site of the ruptured disc

Outcome Management
Goals include:
Reducing pain & spasms Improving mobility Repairing any structural problems in the spine or discs

Control Pain & Spasms

Pain usually managed with
Non-steroidal anti-inflammatory drugs (NSAIDS), muscle relaxants, and at times, narcotics Ice may be used for the first 48 hrs After that heat may be used

Control Pain & Spasms- Positioning

Semi-sitting position (in a recliner chair)
More comfortable, reduces back strain promotes forward lumbar spine flexion

Supine with pillows under the legs Lateral with thin pillow between knees with
painful leg flexed AVOID:
prone position sleeping w/thick pillows under the head

Control Pain & Spasms

Physical Therapists
may be able to relieve pain & spasm with stretching exercises & ultrasonic heat treatments

Spinal manipulation
Use of the hands on the spine to stretch, mobilize, or manipulate the spine

Work space or equipment modifications may be

necessary Progressive muscle relaxation exercises For severe lumbar disc problems with leg pain
2 to 4 days of bed rest on a firm mattress

Improve Mobility
Most clients do not require bed rest
> 4 days of BR can be debilitating & slow recovery

Client taught use of proper body mechanics If have to sit, should change positions often Aerobic activities prescribed to help avoid
debilitation Walking, stationary bicycling, & back strengthening
Begin within first 2 weeks after injury (perform for 20 to 30 minutes, 2 or 3 times per week)

Improve Mobility
Work activities individualized Back brace or corset may be prescribed
Usually not recommended once clinical manifestations are relieved

Exercise to strengthen the back and abdominal

muscles
helps prevent further problems if the exercises are done daily throughout life

Surgical Management
Surgery indicated in clients with spinal disc
problems when
Sciatica is severe & disabling Manifestations of sciatica persist without improvement or worsen, and Physiologic evidence of specific nerve root dysfunction

Also used to stabilize spinal fractures

Surgical Management (cont.)

Chemonucleolysis
Chymopapain - a proteolytic enzyme isolated from papaya latex - is used as a meat tenderizer. Injected into the disc, it digests the protein in the disc & shrinks it. Contraindicated in people with multiple allergies & in people allergic to papaya. Immediate & delayed (after 15 days) allergic responses Use abandoned by most practitioners

Percutaneous Disectomy
Herniated disc material can be excised with a
trocar to remove the center of the disc. The laser also is used to destroy the damaged disc.

Microdisectomy
The use of microsurgical instruments to remove the
herniated fragment of disc. Results in less trauma to the surgical site compared with stand surgery & more tissue integrity is preserved.

Decompressive Laminectomy
Term laminectomy is confusing & is used loosely. Laminectomy
Describes complete removal of the bone between the spinous process & the facet; This is seldom necessary.

Laminotomy
More correct term for what is usually done Describes the creation of a hole in the lamina.

Decompressive Laminectomy (cont.)

Surgical removal of the posterior arch, of a
vertebra, exposing the spinal cord. This procedure gives access to the spinal canal for
Removing a spinal cord tumor Removing portions of the facets Decompressing bone infringement on the spinal cord

Decompressive Laminectomy (cont.)

Foraminotomy
Sometimes is performed to enlarge the intervertebral foramen if it is narrowed & osteophytic processes (overgrowth of bone) entrap the nerve root & impinge on neural structures

Spinal Fusion/Arthrodesis
Spinal fusion
Describes the placement of bone grafts (bone chips) between vertebrae New bone that grows fuses the two vertebrae & immobilizes them to reduce the pain. Usually no more than 5 vertebrae are fused Fusing more than five vertebrae causes considerable loss of
movement in the spine

Spinal Fusion/Arthrodesis (cont.)

Bone graft may be obtained from a bone bank or the
anterior-superior iliac crest. During healing, the graft gradually grows into the vertebrae & forms a bone union This bone union causes permanent stiffness in the area.

Spinal Fusion/Arthrodesis
Lumbar Fusion
Stiffness hardly noticed in the lumbar area after a while

Cervical Fusion
Stiffness usually noticeable in the cervical area

The client cannot be guaranteed that back pain will

be relieved permanently or that further surgery will not be required.

Spinal Fusion with Instrumentation

Metal rods may be used to straighten & fuse the
spine in disorders such as scoliosis or multiple vertebral fractures. Other devices also can be used to provide additional support while the bones heal in a fused manner

Complications
General potential complications after spinal disc
surgery at any level include:
Infection and inflammation, injury to nerve roots, dural tears, and hematoma

Complications (cont.)
Non-union of the surgical area also is a risk
Is associated with smoking Some surgeons assess serum nicotine levels prior to surgery to
reduce risk of non-union & validate statements of smoking cessation

Prognosis
Patients with severe and disabling leg pain:
Lumbar disectomy often relieves manifestations of pain faster than continued medical management

Patients w/o leg pain,

little difference in medical vs surgical relief of symptoms

Client preference plays a big role in the technique

chosen

Preoperative Nursing Care

Explain post op limitations, positioning, etc. If fusion is to be done:
Encourage clients who smoke to stop. Clients need to be evaluated for autologeous blood donation. 2 3 units should be donated, the last one at least 1 week
before the surgery

Inform client of bone graft site & the additional pain associated it.

Post Op
Assess:
Dressings, drains Level of pain & response to analgesia Neurologic function compare to baseline

Post Op
BR for post fusion -Risk for DVT
Compression devices Observe for & report S/S

Assess Wound Site:

Bulging or clear drainage May indicate cerebrospinal fluid leakage Anterior approach Usual care for abdominal surgery is required

Positioning
After lumbar fusion
Bed is generally kept flat

Log-rolling
Usually beginning about 4 hrs after surgery, then q 2 4 hrs thereafter Ensure safety Common to have spasms & pain w/turning Analgesics & anti-spasmodics

PostOp Urinary Retention

Common after spinal surgery
because of pain & spasms & as a side effect of narcotics.

Assess for retention

Cath prn as ordered

Post Op Paralytic Ileus

Most common bowel problem after laminectomy & spinal
fusion
Due to lack of peristalsis from a sudden loss of parasympathetic function innervating the bowels & manipulation of the intestines in anterior approaches

Assessment findings
N & V, hard abdomen, absence of bowel sounds

Paralytic Ileus - Intervention

NGT to low intermittent suction NPO Assess at least q 4 hrs

HERNIATION SYNDROMES
**TO PREVENT HERNIATION:
The goal of neurologic evaluation, ICP monitoring, and treatment of increased ICP

Herniation Syndromes
Herniation results in shifting of tissue Places pressure on cerebral vessels & vital function
centers of the brain. If unchecked, herniation rapidly causes death as a result of the cessation of cerebral blood flow & respirations

HERNIATION SYNDROMES (cont.)

Supratentorial Herniation
Uncal Central, or Transtentorial Cingulate Transcalvarial

Infratentorial Herniation
Upward transtentorial herniation Downward cerebellar herniation

Herniation Syndromes UNCAL

Most often noted herniation syndrome Unilateral, expanding mass, usually of the
temporal lobe, increases ICP, causing lateral displacement of the tip of the temporal lobe. Clinical S/S:
Ipsilateral pupil dilation, decreased LOC, respiratory pattern changes/arrest, contralateral hemiplegia (decorticate/decerebrate)

Herniation Syndromes CENTRAL

Often preceded by uncal and cingulate herniation Expanding mass lesion of the midline, frontal,
parietal, or occipital lobes S/S
Similar to Uncal in late stages

Herniation Syndromes CINGULATE

Occurs often Not in itself life-threatening, but if the expanding
mass lesion is not controlled, uncal or central herniation will follow.

Herniation Syndromes Transcalvarial

The extrusion of cerebral tissue through the
cranium In the presence of severe cerebral edema, transcalvarial herniation occurs through an opening from a skull fx or craniotomy site

Herniation Syndromes Upward Transtentorial Herniation

Deterioration progresses rapidly Compression of 3rd cranial nerve & diencephalon
occurs Blockage of central aqueduct Distortion of 3rd ventricle obstruct CSF flow

Herniation Syndromes Downward Cerebellar Herniation

Compression & displacement of the medulla
oblongata occur Rapidly results in respiratory & cardiac arrest

CHRONIC DISORDERS

AMYOTROPHIC LATERAL SCLEROSIS (ALS)

Also known as Lou Gehrigs Disease A progressive degenerative neurologic disease
characterized by weakness and wasting of the involved muscles, without any accompanying sensory or cognitive changes. Unknown cause Affects men more than women, usually between the ages of 40 60.

CLINICAL MANIFESTATIONS
Musculoskeletal:
weakness and fatigue heaviness of the legs fasciculations (focal muscle twitching) Uncoordinated movements Loss of motor control in the hands Spasticity Paresis

 Hyperreflexia Atrophy Problems with articulation

Respiratory
Dyspnea Difficulty clearing the airway

Nutrition
Difficulty chewing Dysphagia

 Emotion
Loss of control, liability

Cognitive
Intellect is not affected Remains alert and mentally intact throughout the course of the disease

Death is usually resultant from pneumonia Diagnosis is made with an EMG

TREATMENT
Supportive Riluzole (Rilutek): drug which extends the
life by a few months Respiratory compromise usually results within 2 5 years of diagnosis

INTERVENTIONS
Mobility
ROM Stretching exercises Splints Ankle boots Wheelchair Frequent rest periods to decrease fatigue

 Nutrition
Suction at bedside Rest before meals Upright to eat and 30 minutes after Semisolid food Frequent meals Soft cervical collar to keep head upright Enteral feedings Syringe with short, small bore tubing (placed on anterior aspect of tongue, used for giving liquids)

 Breathing
Mechanical ventilation as necessary Elevate HOB TQ2H Oxygen Breathing exercises Incentive spirometry Suctioning as needed

 Communication
Speech therapy Hand held computers Pointer held with teeth and use of a picture board Word charts Eye blinks

MULTIPLE SCLEROSIS

Chronic, progressive disorder of the CNS. Weakness Remission Progression Glial scar tissue (hard, sclerotic plaque) Loss of function

CLINICAL MANIFESTATIONS
musculoskeletal
Fatigue (most common and often most disabling) Limb weakness ( loss of muscle strength) Ataxia Intention tremors Spasticity Muscular atrophy Dragging of the foot Foot drop

 Urinary
Hesitancy Frequency Retention Recurrent UTIs Incontinence

 Gastrointestinal
Difficulty chewing Dysphagia Diminished or absent sphincter control Bowel incontinence Constipation

Respiratory
Diminished cough reflex Respiratory infections

 Sensory
Blurred vision Optic neuritis Diplopia Nystagmus Eye pain Visual field defects Vertigo/ loss of balance and coordination Nausea Numbness Parasthesias (numbness or tingling) Diminished sense of temperature/ desensitized touch sensation

 Neurologic

Emotional lability/ mood changes/ depression Forgetfulness Apathy Irritability Impaired judgment Dysarthria (speech problems)
History CSF evaluation MRI Optic/Auditory testing (shows slowed nerve conduction)

Diagnosis

TREATMENT

Corticosteroids Interferon Plasmapheresis Surgery Diet therapy

INTERVENTIONS
Respiratory
CDB Q 2 4 H Elevate HOB 90o to eat

Immobility
PT for walking and hydrotherapy

Gastrointestinal
Stool softeners Encourage activity Maintain fluid intake

 Skin
Assess every shift TQ2H Keep linen clean and dry Massage around bony prominences

Vision
Assess acuity SR elevated, bed in low position, wheels locked Eye patch with diplopia

 Urinary
Administer appropriate meds Intermittent catheterization Assess for infection Increase fluids to 3000 cc/day if allowed

Teaching
Factors which cause exacerbation Hyperthermia Stress Infection pregnancy

MUSCULAR DYSTROPHY
A group of genetic disorders involving gradual
degeneration of muscle fibers Progressive weakness and skeletal muscle wasting, accompanied by disability and deformity Types: 1. Pseudohypertrophic MD (Duchene MD) 2. Facioscapulohumeral MD (LandouzyDejerine)

CLINICAL MANIFESTATIONS
Evidence of muscle weakness usually
appears at 3-4 yrs May have history of delayed motor development, especially walking First symptom may be : difficulties in running, riding a bike Develop characteristic rising from squatting or sitting position on floor (Gowers sign)

TREATMENT
Supportive measures
Physical therapy Orthopedic procedures Use of braces for spine and lower extremities Breathing exercises

MYASTHENIA GRAVIS
A chronic, progressive autoimmune disease
characterized by fatigue and severe muscle weakness of the skeletal muscles, that worsens with exercise and improves with rest Manifestations result from a loss of Ach receptors in the postsynaptic neurons of the neuromuscular junction

CLINICAL MANIFESTATIONS
Primary feature: increasing weakness with
sustained muscle contraction Ptosis (drooping of upper eyelid) Diplopia (double vision) Facial weakness (snarls when smiling) Dysphagia dysarthria

 Weakness and fatigue Decreased function of hands, arms, legs,

and neck muscles Weakening of intercostals Decreased diaphragmatic movement Breathlessness and dyspnea Poor gas exchange Inability to chew and swallow Decreased ability to move tongue

DIAGNOSIS
Based on clinical presentation and response
to anticholinesterase drugs TENSILON TEST

TREATMENT
Anticholinesterase drugs
Pyridostigmine (mestinon) Neostigmine (Prostigmine)

Immunosuppressive therapy
(corticosteroids) Plasmaphoresis Thymectomy

COMPLICATIONS
Myasthenic crisis: caused by
undermedication
Sudden marked rise in B/P due to hypoxia Increased heart rate Severe respiratory distress and cyanosis Absent cough and swallow reflex Increased secretions, increased diaphoresis, increased lacrimation Restlessness, dysarthria Bowel and bladder incontinence

 Cholinergic Crisis: caused by excessive

medication
Weakness with difficulty swallowing, chewing, speaking and breathing Apprehension N/V/D/abdominal cramps Increased secretions and saliva Sweating, lacrimation, fasciculations, and blurred vision

NURSING CARE

Airway management Suction at bedside ABGs Endotracheal intubation if ventilatory support is needed Administer edrophonium chloride (Tensilon) to determine type of crisis Monitor electrolytes, I&O, daily weight Tube feeding if unable to eat

CEREBRAL PALSY
Impaired muscular control due to abnormality in
the brain resulting in abnormal muscle tone and coordination. Physical signs:
Poor head control after 3 months Stiff or rigid arms or legs Pushing away or arching back Floppy or limp body posture Cannot sit up without support by 8 months Use of only one side of body, or only the arms to crawl Clenched fists after 3 months

BEHAVIORAL SIGNS
Extreme irritability or crying Failure to smile by 3 months Feeding difficulties
Persistent gagging or choking when fed After 6 months of age, persistent tongue thrusting

CLINICAL MANIFESTATIONS
Delayed gross motor movement (universal
manifestation) Abnormal motor performance Altered muscle tone Abnormal posture Abnormal reflexes Associated disabilities and problems

INTERVENTIONS

Mobilizing devices Surgery Speech therapy Dental care Hearing aids Physical therapy

PARKINSONS DISEASE
Progressive, degenerative disease
characterized by disability from tremor and rigidity
Depletion of dopamine

CARDINAL FEATURES

Tremor at rest Rigidity Bradykinesia (slow movement) Flexed posture of neck, trunk, and limbs Loss of postural reflexes Freezing movement

OTHER CLINICAL MANIFESTATIONS

Skin problems Heat intolerance Postural hypotension Constipation Dementia Anxiety Depression

TREATMENT
Dopaminergics
Levodopa Carbidopa-levodopa (Sinemet)

Anticholinergics
Trihexphenidyl (Artane) Benztropine (Cogentin)

Dopamine Agonists
Bromocriptine (Parlodel Pergolide (Permax)

 Surgery:
Pallidotomy Sterotaxic thalamotomy Autologous adrenal medullary transplant (doesnt work well) Fetal tissue transplant (better results)

INTERVENTIONS
Mobility
ROM PT (individualized) Ambulate qid Assistive devices Provide for safety

 Communication
Allow time to speak Encourage deep breathing before speaking Speech therapy Alternative methods of communication

Sleep
Quiet environment Position of comfort ROM to decrease rigidity Stay awake during day (meds may interrupt normal sleep cycle)

 Nutrition
Calorie count/weekly weight Assess swallowing ability Soft, solid food appropriate for the individual Massage facial and neck muscles before eating Sit upright for feeding and 30 minutes after Suction at bedside Adequate roughage/fiber Small, frequent meals

 Elimination
Drink 3000 cc/day if possible Increased fiber Increase mobility to stimulate peristalsis Stool softeners/suppositories

Self care:
Encourage independence but set time limits Keep items in reach Give a time frame to allow the patient to do their own care

Bells Palsy Patho & Etiology

Affects motor aspects of the facial nerve, (7th

cranial nerve). Most common type of peripheral facial paralysis. Affects women & men in all age groups Most common between ages 20 & 40 yrs. Results in a unilateral paralysis of the facial muscles of expression.

Bells Palsy Patho & etiology

No evidence of a pathologic cause. Facial paralysis central or peripheral in origin. Central facial palsy is an upper motor neuron
paralysis or paresis.
Client cannot voluntarily show teeth on paralyzed side but can show them with emotional stimulation. Called voluntary emotional dissociation

Bells Palsy Clinical Manifestations

Typical findings on affected side include:
Upward movement of the eyeball on closing the eye (Bells phenomenon) Drooping of the mouth Flattening of the nasolabial fold Widening of the palpebral fissure Slight lag in closing the eye

Eating may be difficult

Bells Palsy Outcome Management

No known cure. Palliative measures include:
Analgesics if discomfort occurs from herpetic lesions Corticosteroids to decrease nerve tissue edema Physiotherapy, moist heat, gentle massage, & stimulation of the facial nerve Corneal protection w/artificial tears, sunglasses, eye patch

Neurological Clinical Assessment

History Physical examination components
Level of consciousness (LOC) Motor function Pupillary function & eye movement Respiratory patterns Vital signs

Bells Palsy Recovery/Prognosis

Clients experiencing Bells Palsy often think they
have had a stroke.
Reassure client

Prognosis
Most clients recover within a few weeks w/o residual manifestations.

If permanent facial paralysis occurs, surgery may

be necessary.
Anastomosis of the peripheral end of the facial nerve with the spinal accessory or hypoglossal nerve may allow closure of the eye & restore tone to face

Trigeminal Neuralgia
Chronic irritation of the fifth cranial nerve Trigeminal nerve has 3 division & neuralgia may
occur in any one or more of these divisions
Opthalmic, maxillary, & mandibular

Trigeminal Neuralgia Etiology

Causes can be intrinsic or extrinsic lesions within
the nerve itself
Ex: multiple sclerosis

Extrinsic lesions are outside the trigeminal root &

include mechanical compression by
Tumors, vascular anomalies, dental abscesses, or jaw malformation

Trigeminal Neuralgia Clinical Manifestations

Characterized by intermittent episodes of intense

pain of sudden onset. Pain is rarely relieved by analgesics Tactile stimulation, such as touch & facial hygiene, & talking may trigger an attack More prevalent in the maxillary and mandibular distributions & on the right side of the face. Bilateral trigeminal neuralgia is rare

Trigeminal Neuralgia Diagnosis

None of the current diagnostic studies identify
trigeminal neuralgia CT scan, MRI, & angiography can identify a causative lesion. Diagnosis made on basis of in-depth history, w/attention paid to triggering stimuli & nature & site of the pain.

Trigeminal Neuralgia Nursing Considerations

Careful history is obtained regarding triggering
stimuli Dental hygiene & nutritional intake are evaluated

Trigeminal NeuralgiaOutcome Mgt

Anticonvulsant agents often prescribed as initial treatment
Carbamazepine (Tegretol) phenytoin

These drugs may dampen the reactivity of the neurons

within the trigeminal nerve For some clients, these medications are all the treatment that is needed Monitor liver enzymes before & during therapy Use caution if hx of alcohol abuse

Trigeminal NeuralgiaOutcome Mgt

Baclofen (Lioresal)
An antispasmodic that may be used alone or in conjunction with anticonvulsants.

Narcotics are not particularly effective Help client use & improve any pain control strategy
they have developed. Provide emotional support

Trigeminal NeuralgiaOutcome Mgt

Surgery includes
Nerve blocks with alcohol & glycerol Peripheral neurectomy & Percutaneous radio-frequency wave forms

Relief obtained not always permanent 0ften better tolerated by elderly or debilitated clients
Therefore, present later with symptoms

Trigeminal Neuralgia Outcome Mgt

More invasive techniques involve major surgical
procedures (craniotomy): Microvascular decompression
Removing the vessel from the posterior trigeminal root

Rhizotomy
Actual resection of the root of the nerve

TN Outcome Mgt Surgical Complications

Same as with any surgical procedure Facial weakness & paresthesias If facial anesthesia present after surgery
Test food before placing in mouth Assess for aspiration & advance diet slowly Water jet device instead of toothbrush Visit dentist soon

If corneal reflex impaired

Eye care

Guillian-Barre Syndrome (GBS)

Once thought to be single entity characterized by
inflammatory peripheral neuropathy Now understood to be a combination of clinical features with varying forms of presentation & multiple pathologic processes.

GBS (cont.)
Most cases do not require admission to CCU Prototype of GBS, known as acute inflammatory
demyelinating polyradiculoneuropathy (AIDP) involves rapidly progressive, ascending peripheral nerve dysfunction leading to paralysis & maybe respiratory failure

GBS (AIDP)
Because of the need for ventilatory support, AIDP is
one of the few peripheral neurologic diseases that necessitate a critical care environment. Annual incidence of GBS is 1.6 1.9 per 100,000 persons. Occurs more often in males Most commonly acquired demyelinating neuropathy. Clusters of cases reported following 1977 swine flu vaccinations

GBS - Etiology
Precise cause unknown Syndrome involves an immune-mediated response Most patients report a viral infection 1 to 3 weeks
before the onset of clinical manifestations, usually involving upper respiratory tract.

GBS - Etiology
Numerous triggering events include:
Viral infections Bacterial infections Vaccines Lymphoma Surgery Trauma

GBS - Pathology
Affects:
motor & sensory pathways of the peripheral nervous system, as well as the autonomic nervous system functions of the cranial nerves.

Believed to be an autoimmune response to antibodies

formed in response to a recent physiologic event. Once temporary inflammatory reaction stops, myelinproducing cells begin the process of re-insulating demyelinated portions of PNS. Degree of axonal damage is responsible for the degree of neurologic dysfunction.

GBS Assessment & DX

Symptoms include:
Motor weakness Paresthesias & other sensory changes Cranial nerve dysfunction (especially oculomotor, facial, glossopharyngeal, vagal, spinal
accessory, and hypoglossal); and

Some autonomic dysfunction

GBS Assessment & DX

Abrupt onset of lower extremity weakness that
progresses to flaccidity and ascends over a period of hours to days. Motor loss usually symmetric, bilateral, and ascending In the most severe cases, complete flaccidity of all peripheral nerves, including spinal and cranial nerves, occurs.

GBS Assessment & DX

Admitted to hospital when lower extremity
weakness prevents mobility Admitted to CCU when progression of weakness threatens respiratory muscles. DX based on clinical findings plus CSF analysis & nerve conduction studies. Diagnostic finding is elevated CSF protein with normal cell count

GBS Assessment & DX

Frequent assessment of respiratory system Most common cause of death is from
RESPIRATORY ARREST As disease progresses & respiratory effort weakens, intubation & MV are necessary Continued, frequent assessment of neurologic deterioration is required until the patient reaches the peak of the disease & plateau occurs.

GBS Medical Mgt

No curative treatment available Disease must run its course, which is characterized
by ascending paralysis that advances over 1 to 3 weeks & then remains at a plateau for 2 to 4 weeks. Plateau stage followed by descending paralysis & return to normal or near-normal function.

GBS Medical Mgt

Main focus is the support of bodily functions &
prevention of complications Plasmapheresis often used in attempt to limit severity & duration
Contraindicated if hemodynamically unstable

IV imunoglobulin may be used Steroids may be used

GBS Nursing Mgt (cont.)

Support all normal body functions until the patient
can do so on his or her own Requires extensive long-term care,
recovery can be a long process

GBS Nursing Mgt (cont.)

Focuses on:
Maintaining surveillance for complications Initiating rehabilitation Facilitating nutritional support, Providing comfort & emotional support

GBS Monitor for Complications

Once intubated and on MV
Observe for pulmonary complications (ie: atelectasis, pneumonia, pneumothorax

Autonomic dysfunction, dysautonomia

Can produce variations in HR & BP Hypertension and tachycardia may require beta-blocker therapy

GBS Initiating Rehabilitation

Immobility may last for months Usual course of GBS involves:
average of 10 days of symptom progression 10 days of maximal level of dysfunction Followed by 2 to 48 weeks of recovery

Patient requires physical & occupational

rehabilitation because of the problems of long-term immobility.

GBS Rehab (cont.)

Facilitating Nutritional Support
Usually accomplished through use of enteral feeding

Patient education Participation in a neurologic rehabilitation program

(if necessary)

GBS Providing Comfort & Emotional Support

Pain control
A safe, effective, long-term solution to pain management must be identified.

Extensive psychologic support *GBS does not affect the LOC or cerebral function
Patient interaction & communication are essential elements of the nursing management plan.

Clinical Manifestations
Using the Glasgow Coma Scale Coma, Persistent Vegetative State Other Complications

Glasgow Coma Scale (GCS) A tool for assessment

For LOC only Not a complete neurological exam Evaluation of 3 categories
Eye opening Verbal response Motor response

Rapid Neurologic Examination

Organized, thorough, & simple. Performed accurately & easily at each assessment
point Conscious Patient Unconscious Patient

Rapid Neurologic Assessment Conscious Patient

Exam should take less than 4 minutes LOC Facial Movements Pupillary function & eye movements Motor assessment Sensory VS Change in status

Rapid Neurologic Assessment Unconscious Patient

Assessment takes 3 to 4 minutes Initial efforts are directed at achieving maximal
arousal of the patient LOC Pupillary assessment Motor examination Respiratory pattern VS

Neurologic changes Associated with Intracranial Hypertension

Increasing ICP can be identified by changes in: LOC (*1st Sign of deterioration in a conscious
patient)
Increased restlessness, confusion, agitation, decreased responsiveness

Pupillary Reaction Motor Response Vital Signs Respiratory Patterns

Diagnostic Procedures

Computerized tomograpy (CT Scan) Magnetic resonance imaging (MRI) Cerebral Angiography Myelography Cerebral Blood Flow Studies Electrophysiology Studies Lumbar Puncture

COMA
A state of unconsciousness in which both
wakefulness and awareness are lacking A symptom, rather than a disease
Occurs as a result of some underlying process

Can be produced by a wide variety of both

neurologic & non-neurologic conditions Comprises a continuum of many levels

COMA - Etiology
Structural neurologic lesions Metabolic and toxic conditions Psychiatric disorders

COMA Structural Lesions

Vascular lesions
Ischemic & hemorrhagic strokes

Trauma
Loss of consciousness may occur immediately or may develop several daysweeks after injury

Brain tumors and brain abscesses

Compression of neurologic structures Often accompanied by motor paralysis

COMA Metabolic & Toxic Conditions

Accounts for more than half of all cases of
coma

COMA Cardiopulmonary Decompensation

Any cardiopulmonary condition can precipitate a state of coma by threatening the state of oxygenation of cerebral tissue

COMA Poisoning & Alcohol

May occur as the result of self-administration,
accidental ingestion, industrial exposure, or homicidal administration Drug overdose 30% of cases in ED Symptoms depend on substance ingested Alcohol may not be cause of coma in inebriated patient
Trauma, cerebral hemorrhage, subdural hematoma

Thiamine deficiency

COMA Hypertensive Encephalopathy/HTN Crisis

Sudden onset, usually following hx of kidney
disease, severe HTN, or both

COMA - Meningitis
Common cause of coma Fever or signs of meningeal irritation Abrupt onset, severe HA followed by loss of
consciousness Hx of infectious process affecting middle ear or paranasal sinuses should raise suspicion of meningitis.

CLINICAL MANIFESTATIONS
Classic symptoms:
Nuchal rigidity Brudzinskis sign Kernigs sign Photophobia

Other: fever, tachycardia, h/a, chills, nausea,

vomiting, seizures May be irritable at first with progression to confusion, stupor, and semiconsciousness

COMA

Encephalitis Post-convulsion Other Metabolic Disturbances Hyper/hypoglycemia Hepatic coma Pneumonia Ecclampsia, various endocrine disorders; hyperthermia, & electrolyte, acid-base, or water imbalance.

COMA Patho.

Slight or moderate cortical depression Complete cortical suppression Midbrain depression Brain stem depression

COMA Assessment & DX

Detailed serial neurologic examinations CT or MRI
Usually readily identify structural causes

Lumbar Puncture (unless contraindicated by signs of

increased ICP)
Analysis of CSF pressure & content **CT precedes Lumbar Puncture to identify patients at risk for brain herniation

Laboratory studies to identify metabolic or

endocrine abnormalities

Medical Management
Identification & tx of underlying cause Emergency measures to support vital functions &
prevent further neurologic deterioration Protection of airway & ventilatory assist If cause not known
Thiamine (at least 100 mg), glucose, & a narcotic antagonist suggested

Medical Mgt (cont.)

Prognosis depends on
cause of the coma & length of time unconsciousness persists.

Best prognosis is associated with early arousal Metabolic coma - better prognosis than coma caused
by a structural lesion Traumatic coma - better outcome than non-traumatic

COMA
Clinical Manifestations of Metabolically &
Structurally Induced Coma

COMA Nursing Mgt

**Patient is totally dependent on the health care
team Interventions directed toward:
Assessment changes in neurologic status & clues to the origin of the coma Supporting all body functions Maintain surveillance for complications Providing comforting and emotional support Initiating rehabilitation measures

COMA Eye Care

Blink reflex is often diminished or absent
Results in drying & ulceration of the cornea

Interventions to protect the eyes

Instill saline or methyl cellulose lubricating drops & taping eyelids shut Instilling saline drops q 2 hr & applying a polyethylene film over the eyes

Coma Stimulation Therapy

Based on the belief that structured brain
stimulation fosters brain recovery

PERSISTENT VEGETATIVE STATE (PVS)

State of unconsciousness in which wakefulness is
present but awareness is lacking Absence of any ascertainable cerebral cortical function Complete or partial hypothalmic & brain stem autonomic functions are present, Sleep-wake cycles are present There is complete unawareness of self & the surrounding environment

Diagnostic Criteria for PVS

No evidence of awareness of self or environment Inability to interact with others No evidence of sustained, reproducible,
purposeful, or voluntary behavioral response to visual, auditory, tactile, or noxious stimuli No evidence of language comprehension or expression

Diagnostic Criteria for PVS(cont.)

Intermittent wakefulness manifested by presence
of sleep-wake cycles Sufficiently preserved hypothalmic & brain stem autonomic functions to permit survival with medical & nursing management Bowel & bladder incontinence Variably preserved cranial nerve reflexes and spinal reflexes

PVS - Assessment & DX

Differentiating feature between PVS & coma is the
wakefulness of the PVS patient Most difficult differential diagnosis is between PVS & a locked-in state
Locked-in state patient is conscious but unable to communicate because of severe paralysis

Differentiating characteristics of PVS & other related conditions

PVS - Assessment & DX

Diagnosis must be made by a specialist with
expertise in this area. Moral, ethical & legal issues pertaining to PVS are the subject of much debate Positron-emission tomography (PET) & electroencephalography (EEG) are used to support diagnosis

PVS - Medical Mgt

No treatment to reverse PVS is known Coma sensory stimulation is being studied Prognosis depends on the cause of the underlying
brain disease For patient in a PVS that resulted from degenerative or metabolic brain disease
No chance for recovery is possible

Average life expectancy is 2 to 5 years

PVS - Medical Mgt

Collaboration between physicians & family to
determine appropriate level of medical management Decisions must be made regarding:
Resuscitation status Medications (including antibiotics & O2) Hydration, nutrition, and Long-term placement

PVS - Nursing Management

Primarily comprised of:
Performing a detailed neurologic assessment Providing supportive & hygienic measures, and Preventing complications of immobility Psychosocial & informational support of the family

REYE SYNDROME (RS)

A disorder defined as toxic encephalopathy
associated with other characteristic organ involvement. Very uncommon now- review from PEDS

ASSESSMENT OF INTRACRANIAL PRESSURE

INTRACRANIAL PRESSURE
Intracranial space comprises 3 components:
brain substance (80%), cerebrospinal fluid (CSF) (10%), and blood (10%).

Under normal conditions, the ICP is maintained

below 15 mm Hg mean pressure

INTRACRANIAL PRESSURE
Monroe-Kellie hypothesis proposes that
an increase in volume of one intracranial component must be compensated by a decrease in one or more of the other components so that total volume remains fixed

ICP
As ICP rises, small increases in volume may
cause major elevations in ICP. Cerebral blood flow (CBF) corresponds to the metabolic demands of the brain & is normally 50 ml/100 g of brain tissue/minute. Brain requires 15% to 20% of the resting cardiac output & 15% of the bodys O2 demands

ICP
MAP of 50 150 does not alter CBF when
autoregulation is present Acidosis (causes cerebrovascular dilation)
Hypoxia, hypercapnia, ishcmia

Alkalosis (causes cerebrovascular constr.)

hypocapnia

Changes in metabolic rate

Increases increase CBF Decreases decrease CBF

Operative Terms
Burr hole Craniotomy Craniectomy Cranioplasty Supratentorial Intratentorialy

Mgt of Intracranial Hypertension

Once identified, therapy must be prompt Most current evidence suggests that ICP generally
must be treated when it exceeds 20 mmHg All therapies are directed toward reducing the volume of one or more of the components (blood, brain, CSF) that lie within the intracranial vault.

ICP
Major goal of therapy is to determine the cause of
the elevated pressure, and if possible, to remove the cause In absence of a surgically treatable mass lesion, intracranial hypertension is treated medically.

ICP Nsg Interventions for intracr. HTN

Patient positioning Maintaining normothermia Controlled ventilation to ensure normal PaCO2 Administering meds
Keep CPP near 80 mmHg to provide adequate blood supply to the brain CPP = MAP ICP

Performing ventricular drainage

ICP Nursing Interventions POSITIONING

Head elevation increases venous return
May place some patients at risk for intracranial HTN & cerebral ischemia caused by increases of CPP

Recent trend is to individualize head position to

maximize CPP & minimize ICP measurements

ICP Nursing Interventions POSITIONING

Obstruction of jugular veins or an increase in
intrathoracic or intrabdominal pressure is seen as increased pressure through the open venous system,
impeding drainage from the brain and increasing ICP.

ICP Nursing Interventions POSITIONING

Positions that decrease venous return from the
head must be avoided if possible. Examples of positions to avoid:
Trendelenburg, prone, extreme flexion of the hips, angulation of the neck

ICP Nursing Interventions POSITIONING

If have to place in Trendelburg
Monitor ICP & VS closely

May use mechanisms to reduce intracranial pressure

Sedation and/or ventricular drainage

ICP Nsg Interventions

Associated with increased ICP:
Use of PEEP > 20 cm H20 pressure Coughing, suctioning Tight tracheostomy tube ties Valsalva maneuver Care activities performed one after another

Associated with decreased ICP:

Family contact & gentle touch

ICP BP control
Maintenance of arterial BP in the high normal range
is essential in the brain-injured patient. Inadequate perfusion pressure decreases the supply of nutrients & O2 requirements for cerebral metabolic needs. A blood pressure too high increases cerebral blood volume and may increase ICP

ICP BP Control MEDICATIONS

Sedatives small, frequent doses Antihypertensive agents
Avoid use of nitroprusside & NTG (potent peripheral & cerebral vasodilators)

To reduce vasodilating effect of anti-hypertensives,

co-treatment with beta-blockers
Metoprolol, Labetalol

SEIZURES
Episodes of excessive and abnormal
discharges of electrical activity within the CNS Epilepsy is a syndrome of recurrent, paroxysmal episodes of seizure activity
Partial Generalized

PARTIAL (FOCAL, LOCAL) SEIZURES

Simple partial seizures
Seizure activity occurs in a specific body part Jacksonian March Sensory phenomena Autonomic manifestations Psychic manifestations

GENERALIZED SEIZURES
Absence: sudden, brief sensation of motor
activity accompanied by a blank stare and unconsciousness Myoclonic:sudden, uncontrollable jerking movements of either a single muscle group or multiple groups, sometimes causing the patient to fall. Patient loses consciousness for a moment and is then confused postictally

TONIC CLONIC SEIZURE

May or may not have an aura Sudden loss of consciousness Tonic phase Clonic phase

 Tonic-clonic phase Clonic seizures: rhythmic muscular

contraction and relaxation lasting several minutes Tonic seizures: an abrupt increase in muscular tone and muscular contraction Tonic-Clonic Grand Mal

STATUS EPILEPTICUS
Continuous seizing activity and may have
brief periods of calm. Because the patient is in a constant state of seizing, they may develop hypoxia, acidosis, hypoglycemia, hyperthermia, and exhaustion

 Complex Partial Seizures

With automatisms: purposeless repetitive activities Complex partial evolving to secondary generalized

PHARMACOLOGY
Phenytoin (Dilantin)
Therapeutic level: 10 20 mcg SE: nystagmus, diplopia, ataxia, slurred speech, insomnia, dizziness, gingival hyperplasia, n/v/c, measles like rash, rust colored urine, Steven Johnsons syndrome

 Phenobarbital
Therapeutic range: 10 40 mcg/ml SE: drowsiness, dizziness, h/a, n/v/d, jaundice, mild rash Nursing Interventions No abrupt withdrawal Use caution No alcohol, CNS depressants, other barbiturates Medic alert identification No calcium products Deep IM

 Nursing interventions for Dilantin:

Dont give IM Incompatible with dextrose Not faster than 50 mg/min IV Monitor for hypotension, bradycardia, bradypnea Do not give po with milk, calcium, antacids, MOM Hold tube feeding Teaching

Neural Tube Defects

Neurological Dysfunctions

HYDROCEPHALUS
Blockage of the drainage of cerebrospinal
fluid from the ventricles of the brain or from impaired absorption of CSF within the subarachnoid space Many causes

CLINICAL MANIFESTATIONS
Bulging fontanels with or without head

enlargement Dilated scalp veins Frontal protrusion (Bodding) Eyes rotated downward (setting sun sign) Sluggish pupils, unequal response to light Irritability Poor feeding

Lower extremity spasticity Difficulty swallowing, feeding Shrill, high pitched cry seizures

TREATMENT
Preferred procedure: ventriculoperitoneal shunt Preoperative
Elevate HOB Prevent crying which increases intracranial pressure Avoid jarring, bouncing or any activity that will increase intracranial pressure Head measured daily Monitor fontanels for bulging

 Ventriculoperitoneal shunt Post op care

Position flat, on unoperative side Monitor for increased ICP (indicates obstruction of shunt) NPO restriction for 24 48 hours IV fluid caution to prevent overload

Revised as child grows Complications

Infection Malfunction due to obstruction

SPINA BIFIDA OCCULTA

A neural tube defect that is not visible
externally Skin depression or dimple, port wine angiomatous nevi, or dark tufts of hair may be the only visible sign No treatment is necessary unless neurologic problems develop (abnormal weight gain, problems with bowel or bladder, etc.)

SPINA BIFIDA CYSTICA

Neural tube defect with external sac-like
protrusion
Meningocele: encases meninges and spinal fluid but no neural elements Myelomeningocele: contains meninges, spinal fluid and nerves

MYELOMENINGOCELE
Located anywhere on the neural tube May be covered with a fine membrane, the
dura, meninges, or skin Most frequently occurs in the lumbar or lumbar sacral area 80-85 % have associated hydrocephalus

PATHOPHYSIOLOGY
Failure of the neural tube to close during the
first 28 days of pregnancy Can also occur due to splitting of the already closed tube due to increase in cerebrospinal fluid pressure during the first trimester

CLINICAL MANIFESTATIONS
Usually not uniform on both sides Affects bowel and bladder sphincters
(constant dribbling or overflow incontinence; lack of bowel control or rectal prolapse no rectal temps for these children) May have lower joint deformities (from contractures in utero)

DIAGNOSIS

MRI CT Ultrasound Elevated maternal alpha fetoprotein level (done at 16 18 weeks gestation)

PREOPERATIVE CARE
Warm incubator without clothing (clothing may irritate
sac) Moist dressing changes every two hours (0.9% Normal Saline) Cleanse carefully if soiled Keep prone Diapering is contraindicated until repaired ROM (restricted to foot, ankle and knee) Prone position when held by parents (may not be able to do) Tactile stimulation (caressing, stroking, other comfort measures)

POSTOPERATIVE CARE

Maintain prone or side lying position Frequent vital signs and daily weights Measure head circumference daily Examine fontanels for signs of tension or bulging Catheterization for urinary retention Monitor for infection

PROGNOSIS
Assessment
Neurologic Urinary Orthopedic Bowel

Complications

Increased intracranial pressure Unconsciousness Systemic Infections Neurogenic Shock Seizure disorders Others

INCREASED ICP
Risk factors: head injury, brain tumors,
cerebral bleeding, hydrocephalus, and edema from surgery or injury Most often associated with a space occupying lesion

PATHOPHYSIOLOGY
The skull is a hard, bony vault filled with
brain tissue, blood, and CSF. A balance b/w these 3 maintains the pressure w/in the cranium B/C the bony skull cant expand, when one of the 3 components expands, the other 2 must compensate by decreasing in volume in order for the total brain volume to remain constant

INCREASED INTRACRANIAL PRESSURE

Decreased LOC is the first sign
Alert Lethargic Obtunded Stuporous Semicomatose

DECORTICATE POSTURING

DECEREBRATE POSTURING

MORE CLINICAL MANIFESTATIONS

Pupillary responses:
Early: diplopia, blurring, decreased acuity

Changes in motor function:

Early: progressive muscle weakness Late: decorticate, decerebrate, flaccid

Headache
Early: vague but present Late: accompanied by projectile vomiting without nausea

 B/P and Pulse:

Early: relatively stable Late: increased SBP while DBP stays the same (widened pulse pressure); bradycardia

Temperature:
Early: normal, then increases hyperthermia followed by hypothermia as CSF increases

Respirations:
Early: normal Late: decreased at first together with increased SBP and decreased pulse. As ICP increases, the character changes: deeply yawning, signing, Cheyenne Stokes.

DOLLS EYES

Unconscious patients only Hold eyes open Briskly turn head side to side If eyes move in the opposite direction than the way the head is turned, then the patient has positive dolls eyes. This is normal If they stay fixed at midline, this is negative. Do not perform on a patient with a cervical fracture

TREATMENTS

Mannitol Corticosteroids Antipyretics Barbiturates to induce coma Anticonvulsants Antibiotics IV fluids (NS is best but NS may be used) Surgery

SEIZURES
Episodes of excessive and abnormal
discharges of electrical activity within the CNS Epilepsy is a syndrome of recurrent, paroxysmal episodes of seizure activity
Partial Generalized

PARTIAL (FOCAL, LOCAL) SEIZURES

Simple partial seizures
Seizure activity occurs in a specific body part Jacksonian March Sensory phenomena Autonomic manifestations Psychic manifestations

 Complex Partial Seizures

With automatisms: purposeless repetitive activities Complex partial evolving to secondary generalized

STATUS EPILEPTICUS
Continuous seizing activity and may have
brief periods of calm. Because the patient is in a constant state of seizing, they may develop hypoxia, acidosis, hypoglycemia, hyperthermia, and exhaustion

ACTIONS DURING SEIZURES

Airway
Loosen clothing around neck Turn to side if possible Do not force anything into the mouth Oxygen as ordered via mask Suction as needed

 Injury
Bed in low position with wheels locked Side rails up Padded side rails If standing, lie down; place padding under head protect the head from injury Remove potentially harmful objects Teaching Dont smoke alone or in bed, avoid alcohol, avoid being tired, grab the bars in the bathroom, dont lock doors, avoid excessive caffeine