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Patient with Neurologic Problems

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Title: Patient with Neurologic Problems


1
Patient with Neurologic Problems
  • By Linda Self

2
Rapid Neurologic Assessment
  • Glasgow Coma Scale
  • Response to painful stimulisternal rub,
    trapezius squeeze
  • Level of consciousnesseven a subtle change is
    the first indicator of a decline in neurologic
    status
  • Decorticationabnormal posturing seen in the
    client with lesions that interrupt the
    corticospinal pathways. The patients arms,
    wrists, and fingers are flexed with internal
    rotation and plantar flexion of the legs.

3
Rapid Neurologic Assessment cont.
  • Decerebration-abnormal posturing and rigidity
    characterized by extension of the arms and
    legs,pronation of the arms, plantar flexion and
    opisthotonos (kind of spasm with head and feet
    bent backward and body bowed forward). Indicates
    dysfunction of the brainstem.

4
Rapid Neurologic Assessment cont.
  • Pupillary assessment, mental exam
  • Cranial nerve exam
  • Olfactory
  • Optic
  • Oculomotor
  • Trochlear
  • Trigeminal
  • Abducens
  • Facial
  • Acoustic
  • Glossopharyngeal
  • Vagus
  • Spinal accessory
  • hypoglossal

5
Brain DisordersMigraines
  • Caused by a phenomenon called cortical spreading
    depression whereby neurological activity is
    depressed over a specific area of the
    cortexformerly felt to be related to dilation of
    cerebral blood vessels
  • Results in release of inflammatory mediators
    leading to irritation of the nerve roots,
    especially the trigeminal nerve
  • Serotonin release involved in the causation
  • Diagnosis is based on HP, neurologic exam and
    imaging.

6
Migraines
  • Triggers
  • Tyramine-containing food and beverages such as
    beer, wine, aged cheeses, chocolate, yeast, MSG,
    nitrates, artificial sweeteners, smoked fish
  • Medicationsestrogens, nitroglycerine,
    nifedipine, cimetidine
  • Other fatigue, hormonal fluctuations, missed
    meals, sleeping problems, varying altitudes

7
Commonly Used Drugs for Migraines
  • NSAIDs
  • Beta blockers such as inderal
  • Calcium channel blockers-verapamil
  • Abortive drugs such as ASA, acetaminophen
  • Ergotamine preparations
  • Triptans
  • Opioids
  • Investigationaldroperidol (Inapsine)

8
Seizures
  • Abnormal, sudden, excessive, uncontrolled
    electrical discharge of neurons within the brain.
    May cause change in LOC, motor or sensory
    ability, and/or behavior.
  • Epilepsychronic disorder characterized by
    recurrent, unprovoked seizure activity

9
Types of Seizures
  • Generalized
  • Absencepetit mal
  • Tonic-clonicgrand mal. Muscle stiffening
    followed by jerking
  • Myocloniccontractions of body muscles
  • Atonicgo limp, drop attacks
  • Partialsimple partial, complex partial
  • others

10
Antiepileptic Drugs
  • Tegretolpartial or generalized seizures
  • Klonopinabsence, myoclonic and akinetic seizures
  • Valiumstatus epilepticus
  • Depakoteall types
  • Zarontin-absence seizures
  • Neurontinpartial seizures
  • Dilantin-all types
  • Topamaxfor intractable partial seizures
  • Keppraadjunct in partial seizures

11
Common side effects of anti-epileptics (AEDs)
  • Teratogenic potential
  • Medication interactions
  • Blood dyscrasias
  • Altered liver function
  • Effects on renal function
  • Wt. gain or loss
  • Sometimes sedation

12
Surgical options
  • Identify seizure area by EEG, insert electrodes,
    surgically excise
  • corpuscallostomy

13
Characteristics of Seizures
  • Important to observe and document
  • How often?
  • Description
  • Progression
  • Duration
  • Last time occurred
  • Preceded by aura?
  • What does patient do post-seizure?
  • Time elapsed before returns to baseline

14
Seizure Precautions
  • Stay with patient
  • O2
  • Airway
  • Suction
  • IV access
  • Siderails up, padded
  • Bed in lowest position
  • Turn patient to side
  • Loosen restrictive clothing
  • Do not force anything into the mouth
  • Following seizuredo neuro checks

15
Status Epilepticus
  • Characterized by prolonged seizures lasting more
    than 5 minutes or repeated seizures over the
    course of 30 minutes
  • Is a medical emergency. Brain damage and death
    can ensue.
  • Untreated can cause hypoxia, hypotension,
    hypoglycemia, dysrhythmias and lactic acidosis.
    Rhabdomyolysis can occur with effects on the
    kidneys.

16
Treatment of Status Epilepticus
  • Lorazepam is the drug of choice due to rapid
    onset of action and long duration of action
  • Valium
  • Phenobarbital
  • Dilantin
  • Supportive/safety care

17
Meningitis
  • Inflammation of the meninges or brain covering
  • Entry is via the bloodstream at the blood-brain
    barrier. May be direct route or via skull
    fracture. Exudate will develop.
  • Viral is most common
  • Fungal-Cryptococcal. Can be caused by sinusitis
  • Bacterial-mortality rate25. Most commonly
    caused by Neisseria meningitidis and
    Streptococcus pneumoniae.

18
MeningitisS/S
  • LOC
  • Disorientation
  • Photophobia
  • Nystagmus
  • hemiparesis
  • CN dysfunction
  • Personality changes
  • N/V
  • Fever and chills
  • Red macular rash
  • Nuchal rigidity, positive Kernigs (hamstring
    pain w/extension) and Brudzinskis (flexion of
    the hips when the neck is flexed)

19
Review of CSF findings
  • Pressure lt20cm of H2O
  • Clear, colorless. Cloudy indicates infection.
    Pink to orangeRBCs
  • Cells 0-5 lymphocytes normal.
  • Glucose50-75mg/dL normal, less than 50 indicates
    infection
  • Proteins 15-45 normal, 45-100 paraventricular
    tumor, 50-200 viral, more than 500bacterial
    infection

20
Meningitis cont.
  • CSF findings
  • Bacterialcloudy, increased WBCs, increased
    protein, decreased glucose, elevated CSF pressure
    gt180mm h20
  • Viralclear, increased WBCs, slighly elevated
    protein, normal glucose, variable CSF pressure

21
Meningitis
  • May display s/s of increased ICP ( see following
    slide)
  • Left untreated, can result in brain herniation or
    damage

22
Meningitis
  • Treatment according to causative pathogen as
    found by LP (lumbar puncture)
  • Bedrest
  • IV fluids, analgesics for pain and fever
  • Anticonvulsants
  • Corticosteroids
  • Pathogen specific abxmeningococcus penicillin or
    cephalosporins, contacts rifampin or cipro
    pneumococcalPCN, cephalosporins and also
    vancomycin

23
ICP
  • Pressure-volume relationship between ICP, volume
    of CSF, blood, brain tissue and cerebral
    perfusion pressure (Monroe-Kellie Hypothesis)
  • Cranial compartment is incompressible and cranial
    contents should have a fixed volume
  • Equilibrium must be maintained. Increased volume
    will result in downward displacement of the brain

24
Key Features of Increased Intracranial Pressure
  • Lethargy to coma
  • Behavioral changes
  • Headache
  • N/V
  • Change in speech pattern
  • Aphasia
  • Pupillary changes--papilledema
  • Cranial nerve dysfunction
  • Seizures
  • Abnormal posturing
  • Cushings Triadelevated BP, decreased pulse and
    decreased respirations

25
Treatment of increased ICP
  • Maintain airway
  • Hyperventilate patient to blow off CO2 (CO2
    dilates blood vessels)
  • Raise HOB to allow for venous drainage
  • Decrease metabolic demands by paralyzing and
    sedating patient
  • Mannitol
  • corticosteroids
  • Pain management
  • Intracranial monitoring (in ventricle)
  • Craniotomies
  • Decompressive craniectomy

26
Brain Attacks (Strokes or CVAs)
  • Affects over 550, 000 Americans per year
  • Two major typesischemic and hemorrhagic
  • Caused by disruption of the normal blood supply
    to the brain
  • May be preventable if causes discovered early

27
Risk Factors for Brain Attacks
  • Obesity
  • Heart disease
  • Diabetes mellitus
  • Hypercholesterolemia
  • Hypercoagulable states
  • Cocaine, illicit drug use
  • Atrial fibrillation

28
Differential Features of the Types of Stroke
  • Thromboticonset is gradual
  • Usually related to ASHD and hypertension
  • Intact LOC
  • May have speech and visual changes
  • Slight HA
  • No seizures
  • Deficits may be permanent

29
Differential of strokes
  • Embolic
  • Abrupt
  • Steady progression
  • Awake
  • May be associated with cardiac disease
  • Maximal deficits at onset
  • No seizures
  • Rapid improvements

30
Differentials of strokes
  • Hemorrhagic
  • Sudden onset
  • Deepening stupor or coma
  • May have hypertension
  • Focal deficits
  • Seizures possible
  • Permanent deficits possible
  • May result from an aneurysm, rupture of an AV
    malformation or severe hypertension

31
Ishemic Stroke
  • Caused by a blockage of a blood vessel
  • Generally caused by atherosclerosis
  • Early warning signs include transient loss of
    vision, transient ischemic attack (called silent
    strokes)
  • Risk factors atrial fibrillation, ASHD, cocaine
    use/abuse, hx of blood clots
  • Treatmentclot buster TPA, streptokinase,others

32
Transient ischemic attack vs. reversible ischemic
neurologic deficit
  • Ischemic strokes are often preceded by warning
    signs such as TIAs or RINDs
  • Both cause transient focal neurologic dysfunction
    from a brief interruption in cerebral blood flow
  • TIAs last minutes to lt24h
  • RINDs last gt24h but less than a week

33
Hemorrhagic strokes
  • If survive event, recovery from hemorrhagic
    stroke better than ischemic
  • Caused by vascular disruption e.g. aneurysms, AVM
  • Surgical decompression

34
Assessment of patient with brain attack
  • Neurologic exam
  • Motor examhemiplegia vs. hemiparesis
  • Sensory changes-neglect syndrome (most notable in
    right cerebral hemispheric injuries)
  • Amaurosis fugaxtemporary loss of vision in one
    eye
  • Hemianopsiablindness in one half of visual field
  • Cranial nerve function
  • Cardiovascular assessmentabrupt reduction of BP
    not advised

35
Assessment
  • Baseline CT, MRI even better (want to ensure that
    the stroke is not hemorrhagic)
  • ECG
  • Echocardiogram
  • Cardiac enzymes

36
Interventions
  • Depending of type of brain attack
  • Anticoagulants (assuming not a bleed)
  • Catheter directed thrombolytic therapymay use if
    systemic tx not effective
  • Endarterectomy
  • Craniotomy
  • Systemic thrombolytic txmust meet strict
    criteria. Must give within 3hours of onset of s/s
  • Wire coils in aneurysmsseals the area

37
Key considerations
  • Impaired physical mobility self care deficit
  • Disturbed sensory perception
  • Unilateral neglectin rt cerebral stroke. May
    have lack of proprioception and failure to
    recognize their impairment
  • Impaired verbal communicationexpressive aphasia
    (Brocas), receptive aphasia (Wernickes)

38
Parkinsons disease
  • Genetic and environmental contributors
  • Associated with four cardinal s/s tremor,
    rigidity, akinesia (slow movements), and postural
    instability
  • Degeneration of substantia nigradecreased
    dopamine. Acetylcholine will predominate. Also
    with norepinephrine loss thus the postural
    hypotension.

39
Parkinsons Key Features
  • Stooped posture
  • Slow and shuffling gait
  • Pill-rolling, mask-like facies, uncontrolled
    drooling, rare arm swinging with walking
  • Change in voice, dysarthria and echolalia
  • Labile and depressed, sleep disturbances
  • Oily skin, excessive perspiration, orthostatic
    hypotension

40
Parkinsons Disease
  • Stages
  • Initial-hand and arm trembling, weakness,
    unilateral involvement
  • Mild-masklike facies, shuffling, bilateral
    involvement
  • Moderateincreased gait disturbances
  • Severeakinesia, rigidity
  • Complete dependence

41
Interventions
  • Eldepryl (MAO inhibitor which decreases the
    breakdown of dopamine)
  • Dopamine agonistsstimulate dopamine receptors
    but have side effects such as nausea, drowsiness,
    postural hypotension and hallucinations. Mirapex
    and Requip mimic the actions of dopamine.

42
Interventions cont.
  • Levodopa/carbidopa. Used as disease progresses.
    Wearing off phenomenon.
  • Amantadineused to treat the wearing off s/s.
  • Stavelo(carbidopa/levodopa/entacapone).
    Dopa-decarboxylase inhibitor/dopamine
    precursor/COMT inhibitor. Useful in end-stage
    disease.

43
Drug toxicity/tolerance in PD
  1. Reduce medication dosage
  2. Change of medications or in the frequency of
    administration
  3. Drug holiday up to 10 days

44
Nursing considerations
  • Maintain mobility and flexibility by ROM
  • Encourage self-care as much as possible
  • Monitor sleep patterns to avoid injury
  • Nutrition-may need soft or thickened foods.
  • Constipation
  • Speech therapy may be needed
  • Psychosocial supportimpaired memory cognition

45
Surgical Management in PD
  • Stereotactic pallidotomy
  • Deep brain stimulation when meds no longer work.
    Electrode is implanted and connected to a
    pacemaker in chest.
  • Fetal tissue transplantation using fetal
    substantia nigra (implanted in the caudate
    nucleus of the brain).

46
Alzheimers Disease
  • Chronic progressive degenerative disease usually
    seen in individuals older than 65
  • Characterized by loss of memory, judgment, and
    visuospatial perception and by a change in
    personality
  • Progressively physically and cognitively impaired
    resulting ultimately in death

47
AD
  • Increased amount of beta amyloid
  • Neurofibrillary tangles throughout the neurons
  • Neuritic plaques
  • Granulovascular degeneration
  • Reduced levels of acetylcholine
  • ? Increased levels of glutamate

48
Key Features of AD
  • Early-forgets names, misplaces household items,
    mild memory loss, short attention span, subtle
    changes in personality, wanders, impaired
    judgment
  • Middlecognition vitally impaired disoriented to
    time, place and event agitated unable to care
    for self, incontinent
  • Severe-incapacitated motor and verbal skills lost

49
Physical Assessment of AD
  • Observe for stage of progression
  • Observe for changes in cognitionattention,
    judgment, learning and memory, communication/langu
    age
  • Observe for changes in behavior
  • Changes in self-care skills
  • Psychosocial assessment
  • Dx of exclusion. Check CMP, CBC, B12, folate,
    TSH, RPR, drug toxicities and levels, alcohol
    screening
  • PET or MRI to r/o pathology

50
  • Mini-mental state examinationorientation,
    registration (repeat three words), naming,
    reading and following directions.
  • Good one is to have them draw a clock with an
    indicated time

51
Interventions for AD
  • Provide environmental stimulation through contact
    with people, provide a clock and calendar,
    present change gradually, allow for rest periods,
    use repetition
  • Be concrete
  • Limit information
  • Prevent overstimulation and provide structure

52
Interventions cont.
  • Promote independence in ADL
  • Be consistent
  • Promote bowel and bladder contenence fy offering
    rest room breaks q2h daytime, limit fluids at hs
  • Administer cholinesterase inhibitors such as
    Aricept, Reminyl and Exelon. Maintains
    functionality for a few more months.

53
Interventions cont.
  • Provide ID band
  • Monitor to ensure safety from wandering
  • Walk patient to reduce restlessness
  • Involve in activities
  • Restraints only as last resort

54
Multiple Sclerosis (MS)
  • Also called disseminated sclerosis or
    encephalomyelitis disseminata
  • Chronic, inflammatory disease of CNS
  • Causes gradual destruction of myelin sheath of
    neurons. Results in scars or sclerosis on the
    myelin sheaths.
  • Results from autoimmune process
  • Between attacks, s/s may resolve but permanent
    injury occurs as disease progresses

55
MS
  • Usually affects adults 20-40 years of age
  • More common in women than men
  • Occurs in more temperate climates
  • No cure

56
MS signs and symptoms
  • Changes in sensation
  • Muscle weakness
  • Incoordination, loss of balance
  • Dysarthria
  • Dysphagia
  • Visual problems (diplopia)
  • Fatigue
  • Bladder and bowel problems
  • Cognitive impairment
  • Heat intolerance
  • indicates initial or presenting symptoms

57
Diagnosis of MS
  • MRI
  • CSF testing will show oligoclonal bands
  • Visual evoked potentials and somatosensory evoked
    potentials (sensory and visual nerves respond
    less actively in MS)
  • Antibody testing for myelin oligodendrocyte
    glycoprotein and myelin basic proteinin
    formative stages for testing at this time

58
Types
  • Relapsing-remitting--charac. by remissions and
    relapses
  • Secondary progressive
  • Primary progressiveno remissions, gradual
    decline
  • Progressive relapsingsteady decline with
    superimposed attacks

59
  • ---Copaxone (immunomodulator that targets
    T-cells, decreases inflammation), Avonex
    (interferon beta), Betaseron (interferon beta),
    Tysabri (immunotherapy)
  • Avoidance of over-heating (Uththoffs phenomenon)

60
Spinal Cord Injury
  • Force applied to spinal cord will result in
    neurologic deficits
  • Injury may be direct insult to the spinal cord or
    may be secondary to a contusion, compression or
    to a concussion (loss of function resulting from
    a blow)

61
Primary mechanisms of injury
  • Hyperflexion injury occurs when the head is
    suddenly and forcefully accelerated forward,
    causing extreme flexion of the neck. Often occurs
    in head-on collisions and diving accidents

62
Primary mechanisms of Injury
  • Hyperextension injuries occur most often in
    automobile accidents in which the clients
    vehicle is struck from behind or during falls
    when the clients chin is struck. The head is
    accelerated and decelerated. Results in
    stretching or tearing longitudinal ligament,
    fractures or subluxates vertebrae and may rupture
    the disc.

63
Primary mechanisms of injury cont.
  • Axial loading (vertical compression) occurs from
    diving accidents, falls on the buttocks, or a
    jump in which a person landed on their feet. The
    blow may cause the vertebrae to shatter. Pieves
    of bone enter the spinal canal and damage the
    cord.

64
Secondary Injury
  • Neurogenic shock
  • Vascular insult
  • Hemorrhage
  • Ischemia
  • Fluid and electrolyte imbalance

65
Extent of Injury
  • Most spinal cord injuries are incomplete lesions
  • Specific syndrome result from incomplete lesions

66
Cervical Injuries
  • May produce
  • Anterior cord syndrome
  • Posterior cord syndrome
  • Brown-Sequard syndrome
  • Central cord syndrome
  • Cauda equina syndromes are associated with
    injuries to the lumbar and sacral cord

67
Cervical Injuries
  • Anterior cord syndrome results from damage to the
    anterior portion of both gray and white matter of
    the spinal cord, generally 2ndary to decreased
    blood supply. Motor function, pain and
    temperature sensation are lost below the level of
    injury but touch, position and vibration remain
    intact.

68
  • Posterior cord lesionrare. Results from damage
    to the posterior gray and white matter of the
    spinal cord. Motor function remains intact but
    the patient loses the sense of position
    sensation, of crude touch and of vibration.

69
  • Brown-Sequardresults from a penetrating injury
    that causes hemisection of the spinal cord or
    injuries that affect half of the spinal cord.
    Motor function, proprioception, vibration and
    deep touch sensations are lost on the same side
    of the body as the lesion. On the opposite of the
    lesion, the sensations of pain, temperature and
    light touch are affected.

70
  • Central cord syndromeresults from a lesion of
    the central portion of the sc. Loss of motor
    function is more pronounced in the upper
    extremities than in the lower extremities.
    Sensation varies.

71
  • Lumbosacral Injuriesdamage to the cauda equina
    or conus medullaris produces a variable pattern
    of motor or sensory loss as the peripheral nerves
    have the potential for recovery and regrowth.
    This injury generally results in a neurogenic
    bowel and bladder.

72
Vital statistics of spinal cord injuries
  • Primary cause is trauma secondary to MVA
  • Unmarried male between 16-30
  • Generally are Causcasian
  • Most injuries are cervical

73
Assessment
  • Thorough history including mechanism of injury,
    any changes since initial responder, previous
    medical history, hx of osteoporosis,
    osteomyelitis or previous neck or back injuries
    or surgeries

74
Assessment
  • First priority for the client with a SCI is
    assessment of the respiratory pattern and airway
  • Ensure neck is stabilized
  • Assess for evidence of abdominal hemorrhage or
    other sites of injury/hemorrhage
  • Glasgow Coma Scale
  • Detailed assessment of the clients motor and
    sensory status

75
Spinal Shock
  • Occurs immediately after injury as a result of
    disruption of pathways between upper motor
    neurons (lie in cerebral cortex) and lower motor
    neurons (lie in spinal cord).
  • Characterized by
  • Flaccid paralysis
  • Loss of reflex activity below level of lesion
  • Bradycardia
  • Possible paralytic ileus
  • Hypotension.
  • May last days to weeks reversal indicated by
    return of reflex activity

76
Assessment
  • Sensory function
  • C4-5 can shrug
  • C5-6 can pull up arms against resistance
  • C7 can overcome resistance with arms flexed
  • C8 can grasp objects
  • L2-4 can raise legs straight up against
    resistance
  • L5 apply resistance when patient dorsiflexes
  • S1apply resistance while the client plantar
    flexes his feet

77
Cardiovascular
  • Dysfunction r/t disruption of the autonomic
    nervous system, especially if above T-6
  • Bradycardia, hypotension and hypothermia may
    result from disruption of sympathetic input
  • BP lt 90 torr requires intervention to ensure
    satisfactory perfusion of the spinal ccord

78
Respiratory
  • Can develop from both immobility and from
    interruption of spinal innervation to the
    respiratory muscles
  • C3-5 innervate the diaphragm

79
Gastrointestinal and Genitourinary assessment
  • Must assess the patients abdomen for indications
    of hemorrhage, distention or paralytic ileus
  • Ileus may develop within 72h of the injury. Can
    cause areflexic bladder which can lead to urinary
    retention and a neurogenic bladder.

80
Musculoskeletal Assessment
  • Assess muscle tone and size
  • Muscle wasting is 2ndary to long-term flaccid
    paralysis seen in lower motor neuron lesions
    (cell body lies in ant. gray column of spinal
    cord. Innervates striated muscles).
  • Upper motor neuron lesions (neuron body lies in
    cortex, axon synapses with lower motor neuron).
    Causes spasticity.

81
Interventions for Patients with Spinal Cord
Injuries
  • Immobilization for cervical injuriesfixed
    skeletal traction such as halo fixation or tongs
  • Maintain proper alignment of head, neck and body
  • Turn using the log roll technique
  • Monitor skin integrity
  • Traction pin insertion site care
  • If thoracic or lumbosacral injuryimmobilize with
    corset or brace
  • Medicationssupportive, may use steroids,
    baclofen, other meds under investigation

82
Interventions for patients with SCIs
  • Surgical decompression and stabilizationspinal
    fusion, insertion of Harrington rods, laminectomy
    (excision of a posterior vertebral arch)
  • Prevent complications of immobility
  • Promote self-care
  • Bladder retrainingspastic (UMN) or flaccid (LMN)
    may be able to initiate voiding or may need IO
    catherterizations

83
Interventions cont.
  • Bowel retrainingLMN may have to have manual
    disimpactions, see p. 993.
  • Rehab, involve community resources
  • Home care management
  • Psychosocial implications

84
Autonomic Dysreflexia or Hyperreflexia
  • Commonly seen in patients with injury to the
    upper spinal cord (T5 and above). Caused by
    massive sympathetic discharge of stimuli from the
    autonomic nervous system.
  • Stimulus sends nerve impulses to sc, travel
    upward until blocked by lesion at level of
    injury. Cant reach brain so reflex is activated
    that increases activity of sympaathetic portion
    of ANS.

85
Autonomic dysreflexia cont.
  • Increased activity of sympathetic portion of ANS
    results in spasms and a narrowing of blood
    vessels with resultant rise in BP. Brain
    perceives elevated BP, sends message to heart
    which slows down and dilates vessels above level
    of injury to dilate. Brain cannot send messages
    below level of injury so BP cannot be regulated.

86
Autonomic Dysreflexia
  • Precipitated by distension of the bladder or
    colon catheterization of or irrigation of the
    bladder
  • Is a medical emergency

87
Key Features of Autonomic Dysreflexia
  • Sudden onset of severe, throbbing headache
  • Severe, rapidly occurring hypertension
  • Bradycardia
  • Flushing above the level of the lesion
  • Pale extremities below the lesion
  • Nausea
  • Blurred vision
  • Piloerection
  • Feeling of apprehension

88
Care of Patient experiencing Autonomic Dysreflexia
  • Place in sitting position
  • Notify physician
  • Loosen tight clothing
  • Assess for cause
  • Check foley cath
  • If no cath, check bladder for distention
  • Place anesthetic ointment on tip of catheter
    before insertion

89
Care of Patient with Autonomic Dysreflexia cont.
  • Check for fecal impaction, disimpact with
    anesthetic ointment if present
  • Check room to ensure not too cool
  • Monitor BP q15 minutes
  • Give nitrates or hydralazine as ordered

90
Myasthenia Gravis (MG)
  • Autoimmune disease of neuromuscular junction.
    Characterized by flare-ups and remissions. Caused
    by auto antibody attack on the acetylcholine
    receptors. May be related to hyperplasia of the
    thymus.
  • Presents with muscle weakness that improves with
    rest, poor posture, ocular palsies, ptosis,
    diplopia, respiratory compromise, bowel and
    bladder problems

91
MG
  • Diagnosis based on HP, labs which include
    thyroid studies, tests to R/O inflammatory
    illnesses, (RA, SLE, polymyositis), acetylcholine
    receptor antibodies (positive confirms but
    negative does not rule out)

92
MG
  • Testing with cholinesterase inhibitors
    (Tensilon). Baseline muscle strength tested then
    injection given. Within 30-40 seconds, most
    myasthenic patients show a marked improvement in
    muscle tone that lasts several minutes.
  • May be used to distinguish between myasthenic
    crisis and cholinergic crisis.

93
Myasthenic Crisis
  • Undermedicated with anticholinesterase drugs.
  • Increased pulse and respirations
  • Rise in BP
  • Anoxia
  • Cyanosis
  • Bowel and bladder incontinence
  • Absence of cough and swallowing reflex

94
Cholinergic crisis
  • Like being tx with chemical weapons
  • Too much acetylcholine
  • Nausea, vomiting, diarrhea
  • Abdominal cramps
  • Muscle twitching
  • Hypotension
  • Blurred vision

95
Treatment of MG
  • Immunosuppression with steroids, Imuran or
    Cytoxan
  • Plasmapheresis
  • Resp. support
  • Nutritional support
  • Eye protection if unable to close eyes completely
  • Thymectomy
  • Maintanancecholinesterase inhibitor drugs such
    as Mestinon
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