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Adult 2 Test 1 > Neurological alterations pt 2 > Flashcards

Neurological alterations pt 2 Flashcards

1
Q

TIA v. CVA

A

TIA – Transient Ischemic Attack
A brief stroke-like attack that, despite resolving within minutes to hours, still requires immediate medical attention to distinguish from an actual stroke.

CVA – Cerebrovascular accident
Rupture of an artery with bleeding into the brain (hemorrhage) is called a CVA, too.

If the symptoms of a CVA are temporary, usually lasting less than an hour without permanent brain damage, the event is called a transient ischemic attack (TIA).

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2
Q

Stroke

A

Abrupt or rapid onset of a neurological deficit resulting from the interference of blood supply to the brain

Also known as a cerebrovascular accident (CVA)

TIAs are a serious warning sign

2 main classifications
Ischemic and hemorrhagic

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3
Q

Ischemic stroke

A

85% of all strokes in the US

Two types
Thrombotic – blood clot formed in the brain
Embolic – blood clot formed elsewhere and travels to brain

Severity depends on rapidity of onset, size of damage area, & presence of collateral circulation

Usually change in consciousness in first 24hr, but progression in 72 hr as infarction & edema develop

Partial or complete arterial occlusion
>1/3 of ischemic strokes are secondary to a large vessel occlusion

Etiologies

i. Large artery atherosclerosis
ii. Cardioembolic
iii. Lacunar - blood flow to one of the small arteries deep within the brain becomes blocked

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4
Q

hemorrhagic stroke

A

Bleeding into the brain tissue

Intracerebral hemorrhage- HTN is the most common etiology
Bp in 200’s means chance of stroke increases!

Subarachnoid hemorrhage- most common etiology is a ruptured aneurysm

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5
Q

Stroke risk factors

modifiable and non-modifiable

A

Many risk factors are modifiable

Non-modifiable
Gender, age (older adults) , race, heredity

Potentially modifiable
Hypertension, cardiac disease, DM, obesity, blood lipid abnormalities, lifestyle habits such as smoking, alcohol use, diet

risk factor reduction:
Smoking cessation, weight loss, exercise, glucose/BP control

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6
Q

What happens to the brain with a stroke?

A

When blood flow to brain is interrupted

  1. Neuronal metabolism altered within 30 seconds
  2. Metabolism ceases in 2 minutes
  3. Cellular death occurs in 5 minutes

**Brain does NOT hold onto sugar -> so perfusion important!!!

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7
Q

What does treatment focus on?

A

Treatment focuses on maintaining blood flow to area surrounding the infarct

Early recognition is critical to preserving cerebral blood flow and limiting damage

Time IS Tissue!! (for strokes and shock)

If your patient is exhibiting stroke like symptoms, call a Rapid Response and the physician, and encourage them to consider calling a stroke alert!

30-50% survivors are left with moderate to severe disabilities

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8
Q

Hemorrhagic conversion vs Ischemic penumbra

A

Hemorrhagic conversion

i. reperfusion of blood into ischemically injured tissue
ii. brain tissue that has died (due to ischemic stroke) loses its ability to retain blood inside of the arteries, increasing the risk that a large hemorrhage will occur if blood flow were to be returned. This type of bleeding into dead tissue is called a hemorrhagic conversion

ischemic penumbra

i. a rim of tissue lying just outside the core ischemic region (area most severely damaged by stroke or ischemic event).
ii. in the ischemic penumbra, cells are viable for a short amount of time.

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9
Q

CVA clinical manifestations

A

Common findings

  1. Motor deficits: akinesia or hypokinesia, hypo or hyperreflexia
  2. Communication problems:
    i. Aphasia
    ii. Dysphasia
    iii. Dysarthria
  3. Changes in affect and intellectual function
  4. Spatial-perceptual alterations
  5. Changes in elimination

BEFAST - Balance, Eyes, Face, Arm and Speech Test

Location, Location, Location
You’re going to see very different signs and symptoms, depending on where an insult or injury occurs in the brain.

Right-sided stroke:

  1. Left hemiplegia/hemiparesis
  2. Left neglect
  3. Spatial-perceptual deficits
  4. Denial
  5. Short attention span
  6. Impulsive
  7. Impaired judgment
  8. Impaired time sense

Left-sided stroke:

  1. Right hemiplegia/hemiparesis
  2. Impaired language
  3. Impaired right-left discrimination
  4. Slow, cautious behavior
  5. Depression, anxiety
  6. Impaired comprehension
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10
Q

CVA Diagnostic tests:

CT vs MRI

A
  • *CT Scan (preferred)
    a. < 5 minutes
    i. Faster than an MRI in unstable patients
    ii. Patients can be scanned with metal implants, clips
    b. Diagnostic or prognostic
    c. Per the 2018 AHA/ASA guidelines, brain imaging studies should be performed within 20 minutes of arrival.

MRI

a. 30 minutes
b. Soft tissue evaluation (ex: tendons), spinal cord
c. Better at reading ischemic changes quickly in tissue (ischemic strokes) in the first 12 hours of the initial S/S
d. Contrast agents do not include iodine
e. Not preferred bc must go through screening process (for metal etc) and test takes a while

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11
Q

Anticoagulants

A

heparin, warfarin

are not clot busters, but prevent new formation of clots

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12
Q

Antiplatelets

A

ASA, dipyridamole, ticlopidine, clopidogrel

AC: Anti-Clot, Aspirin & Clopidogrel

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13
Q

tPA (Thrombolytics)

A

CLOT BUSTERS: The Big Guns!
tPA works to break down the clot and restore blood flow to the affected area

The only FDA-approved medical therapy for patients with acute ischemic stroke

Demonstrated, improved outcomes when given within 3 hours of first onset of S/S: very small window of usefulness
must be used within 3 - 4.5 hours of exhibiting symptoms

Per the 2018 AHA/ASA guidelines, SBP should be lowered below 185 and DBP below 110 before initiation of tPA

Absolute contraindications

i. thrombopenia
ii. Active internal bleeding, acute trauma
iii. Recent head injury (3 months)
iv. Recent surgery
v. Recent LP (7 days)
vi. Age - <18yrs

Relative contraindications
Pregnancy, large MI, known AVM (arterial venous malformation), concerning labs

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14
Q

tPA parameters for administration

A

ischemic stroke only

within 3 hours of first onset of s/s

Systolic BP below 185
Diastolic BP below 110

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15
Q

Acute Phase Medical Interventions

Ischemic stroke

A

ASA

Statins

Anticoagulants are contraindicated in the emergency phase, but may be ordered once the patient has been stabilized

Permissive hypertension

  1. Allows pt who normally has high bp to stay at elevated levels to a point
  2. Bringing pts too low (for them) had negative results

Blood sugar control

  1. According to the 2013 and 2018 AHA/ASA guidelines, blood glucose levels should be kept within 140-180 mg/dL
  2. Again too low showed with neg results (hypoglycemia)
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16
Q

Acute Phase Medical Interventions

Hemorrhagic stroke

A

HTN management

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17
Q

Acute Phase Medical Interventions

Surgical interventions

A

Angioplasty stents

Endarterectomy

  1. Opening the artery surgically to remove the plaque
  2. Prevents future strokes by removing the plaque
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18
Q

Post-CVA Care

Core Measures

A

Developed by the American Stroke Association for use by primary stroke centers

Implemented during hospitalization and prior to discharge

Hospitals must comply with them for accrediting and certifying bodies

Measures

  1. STK-1: Venous thromboembolism prophylaxis
  2. STK-2: Discharged on anti-thrombotic therapy
  3. STK-3: Anticoagulation therapy for Afib/Aflutter
  4. STK-4: Thrombolytic therapy
  5. STK-5: Anti-thrombotic therapy by the end of Day 2
  6. STK-6: Discharged on a statin medicine
  7. STK-8: Stroke education
  8. STK-10: Assessed for rehabilitation
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19
Q

Post-CVA Care

Goals of care

A

After stabilization in the first 12-24 hours, the goals of care shift to lessening disability and attaining optimal function

If muscles are still flaccid weeks after a stroke, the prognosis for regaining function is poor

Most patients show signs of muscle spasticity with exaggerated reflexes within 48 hours after a stroke (usually a good sign of possibly regaining function): Spasticity-> small voluntary movements/involuntary movements-> voluntary movement of isolated muscle groups

Acute care interventions are continued in this phase as well

20
Q

Post-CVA Care

Interprofessional care

A
  1. Nurses
  2. Physicians
  3. Psychiatrists/psychologists
  4. PT/OT
    a. Physical and occupational therapy begins during the acute phase
  5. Speech therapists
  6. Dietician
  7. RT
  8. Social worker
  9. Pharmacists
21
Q

Post-CVA Care

Inpatient rehabilitation

A

Physical therapy
a. Focus on mobility, progressive ambulation, transfer techniques, and equipment training

Occupational therapy

a. Focus on ADLs like eating, dressing, hygiene, and cooking
b. Also work on cognitive and perceptual evaluations and training

Speech/swallow therapy
a. Focus on speech, communication, cognition, and eating abilities
b. Make recommendations on diet
Food: Regular vs. chopped vs. mechanical soft vs. strictly NPO
Liquid: Regular consistency vs. nectar-thick vs. honey-thick vs. strictly NPO

22
Q

seizures:

seizure vs epilepsy, etiology

A

Seizure= transient, uncontrolled electrical discharge of neurons in the brain that interrupts normal function

Epilepsy: a pre-disposition disorder that causes recurring seizures

Patho:
i. An injury, infection, or medical condition disrupt the normal chemical and/or structural environment of brain neuronsabnormal electrical discharge of neurons

Common etiologies:

  1. Severe birth injury,
  2. congenital CNS defects,
  3. infections,
  4. trauma,
  5. stroke,
  6. metastatic brain tumors,
  7. alcohol withdrawal,
  8. hypoglycemia.
23
Q

seizure classifications

A

General (entire brain affected)

  1. Tonic-clonic
  2. Absence

Focal

Psychogenic – no evidence of a seizure, but pt displays seizure like activity

Status epilepticus: Continuous seizure activity or rapid succession without return of consciousness between seizures

24
Q

Seizures:

Pharmacologic treatment

A

Benzodiazepines

  1. Ativan ,
  2. Valium , and
  3. Versed

Anti-epileptics

  1. Dilantin ,
  2. Keppra ,
  3. Lamictal >)

Intubated if necessary for status epilepticus, or if patient is unable to protect their airway

25
Q

Seizures:

Nursing management

A

i. Aspiration precautions: suction
ii. O2
iii. Vital signs, blood sugar
iv. Padded siderails
v. Bed in lowest position
vi. Positioning (side lying)
vii. Medication administration

Documentation- what preceded the event, what occurred, how long did it last, how was it resolved

  1. Prodromal symptoms
  2. Aura: light, smell, thoughts
  3. Ictal: From the beginning symptoms to the end
  4. Post-ictal: Period after w/ drowsiness, disorientation, headache, nausea
26
Q

Cranial nerve disorders

A

Known as peripheral neuropathies

Etiologies: tumors, trauma, infection, inflammatory disorders, and idiopathic causes

Includes Trigeminal neuralgia, Bell’s palsy, Gullian-Barre Syndrome

27
Q

Trigeminal neuralgia

A

Patho: Compression of the trigeminal nerve (CN V) by superior cerebellar artery

S/S:

a. Classic sign Sudden, unilateral, severe, stabbing episodic pain
b. **Intense unilateral pain (classic sign),
c. facial twitching,
d. frequent blinking

Diagnosis: Purely history, CT/MRI to r/o other causes

Treatment:

a. Anti-seizure meds,
b. Baclofen,
c. antidepressants,
d. nerve blocks,
e. neuroablative surgeries (very painful!)
f. craniotomy if r/t area swelling.

Nursing management:

a. Assess triggers,
b. discuss alternative pain therapies

28
Q

Bell’s Palsy

A

Acute facial paresis r/t inflammation of facial nerve (CN VII) on one side of the face in the absence of a CVA;

etiology of inflammation is unknown

S/S:
Facial droop, numbness of the face/tongue/ear, tinnitus, headache, hearing deficit, drooling

Patients recover spontaneously in 3 week-9 months, with 1/3 having residual effects

Diagnosis: Diagnosis by exclusion

Treatment:

a. Steroids,
b. nerve stimulation,
c. heat & massage,
d. analgesics,
e. hot packs

Nursing management: Educate patient to eat with other side of mouth, facial sling

29
Q

Guillain-Barre Syndrome

A

Acute autoimmune neuropathy after a viral or bacterial infection. Demyelination of nerve cells

Patho:

i. Not well understood,
ii. but infection triggers edema and inflammation of the nerves
iii. Most recover after 1 month

S/S:

a. Numbness and tingling,
b. areflexia,
c. weakness or paralysis of the limbs,
d. autonomic dysfunction

Diagnosis:

a. History & physical,
b. EMG & nerve conduction studies

Treatment:

a. Ventilator if needed,
b. plasmapheresis and IV Ig,
c. vasopressors/fluids if needed

Nursing management: Supportive care, education, parental/enteral nutrition

30
Q

Tetanus Pathology

A

severe infection affecting the spinal and cranial nerves

Patho: Clostridium tetani enters the body through a wound-> low O2 environment allows organisms to mature and produce a potent neurotoxin

Common etiologies:

  1. IV drug use,
  2. human and animal bites,
  3. puncture from nails or other metal objects,
  4. burns,
  5. frostbite,
  6. open fractures,
  7. GSWs
31
Q

Tetanus manifestations

A
  1. ***Trismus “lock jaw” (Classic sign)
  2. Fever
  3. ***As the disease progresses, there is rigidity in the neck, back, abdomen, and extremities (Classic sign)
  4. Tonic, clonic seizures with arching of the back and retraction of the head
  5. Laryngeal and bronchial spasming->apnea and anoxia - usually ***intubated if this occurs
  6. Hypersensitivity to light can trigger a seizure
32
Q

Tetanus treatment and nursing interventions

A

Treatment

  1. Administration of tetanus toxoid, diphtheria toxoid, and pertussis (Tdap) booster
  2. Administration of tetanus immunoglobulin (TIG) before or after the onset of symptoms to neutralize circulating toxins
  3. Intubation if symptomatic
  4. Control of spasms with Valium, barbiturates, and neuromuscularblockers (if needed)
  5. Continuous and prn narcotics for pain management
  6. 10-14 day course of Penicillin, Metronidazole (Flagyl), Tetracycline, or Doxacycline
  7. ***Tracheostomy is usually needed
33
Q

Tetanus nursing interventions

A

Nursing interventions:

  1. Medication administration,
  2. monitoring for signs of decompensation,
  3. focus on prevention of wounds -> turning (can be hard if muscles are rigid)
  4. pain management (using vital signs),
  5. prevention of VAP (ventilator associated pneumonia)
  6. tracheostomy care,
  7. range of motion exercises
34
Q

Botulism patho

A

the most serious type of food poisoning

Patho: GI absorption of neurotoxin produced by Clostridium botulinum->destruction of inhibition of the neurotransmission of Acetylcholine at the myoneural junction

Etiologies:
Improper home canning of foods, contamination of canned foods produced in a factory

35
Q

Botulism manifestations

A

Manifestations (develop rapidly to over a course of days)

  1. ***Descending paralysis (classic sign)
  2. ***Muscle incoordination and weakness (classic sign)
  3. ***Dysphagia (classic sign)
  4. ***Respiratory muscle weakness->respiratory arrest (classic sign)
  5. Seizures
  6. N/V
  7. Abdominal pain
  8. Constipation
  9. Headache
  10. Diplopia
36
Q

Botulism treatment and nursing care

A

Treatment

  1. **Ventilatory support
  2. Tracheostomy (if needed)
  3. Polyvalent anti-toxin
  4. Guanidine hydrochloric acid (enhances Acetylcholine release)

Nursing interventions

  1. Monitoring for signs of decompensation (organ failure)
  2. Supportive care
  3. Tube feeds
  4. Prevention of wounds
  5. Range of motion exercises
  6. Pain management (using vital signs)
  7. Prevention of VAP
  8. Tracheostomy care
37
Q

Spinal cord injury:

Spinal cord injury def

A

temporary or permanent alteration in the function of the spinal cord

38
Q

Spinal cord injury:

Primary injury

A

Cord compression by bone displacement, interruption of blood supply to the cord, or traction from pulling on the cord; penetrating trauma from a GSW, stab wounds, or car accidents can cause tearing or transection.

39
Q

Spinal cord injury:

Secondary injury

A

ongoing progressive damage that occurs after the primary injury

Vascular changes due to hemorrhage, vasospasm, thrombosis, loss of autoregulation, breakdown of the BBB, or infiltration of inflammatory cells

Similar to ischemic penumbra

40
Q

Spinal cord injury:

Spinal shock

A

temporary shock characterized by decreased reflexes, loss of sensation, absent thermoregulation, and flaccid paralysis below the lesion of injury; lasts days to weeks.

41
Q

Spinal cord injury:

Neurogenic shock

A

results from the loss of vasomotor tone caused by injury and characterized by hypotension and bradycardia; loss of sympathetic nervous system innervation causes peripheral vasodilation, venous pooling, and decreased cardiac output. Associated with cervical or high thoracic injury.

42
Q

Classification of Spinal Cord Injury is based on:

A

Mechanism of injury
Level of Injury
Degree of Injury

43
Q

Spinal cord injury:

Level of Injury

A

Is the vertebral level (cervical, thoracic, lumbar, or sacral) with the most damage to vertebral bones and ligaments

If the cervical level is involved, tetraplegia (AKA quadriplegia) occurs
The lower the level, the more function is retained in the arms.

If the thoracic, lumbar, or sacral spinal cord is damaged, the result is paraplegia.

Cervical and lumbar injuries are most common because they are associated with the greatest flexibility and movement

44
Q

Spinal cord injury:

Manifestations

A

Motor and sensory deficits

  • **Respiratory complications r/t injuries above C4
    1. because of the loss of signaling along the phrenic nerve->respiratory muscle dysfunction
    2. Hypoventilation, apnea
  • **Cardiovascular system: Any injury above T6
    1. can lead to dysfunction of the sympathetic nervous system.
    2. Bradycardia, peripheral vasodilation, and hypotension (neurogenic shock)

Urinary system:

  1. Neurogenic bladder occurs in the majority of patients following spinal cord injuries.
  2. Neurogenic bladder: urinary urgency, frequency, incontinence, inability to void, reflex of urine into the kidneys

GI system:

  1. Decreased GI motility->gastric distention and development of paralytic ileus
  2. Delayed gastric emptying, stress ulcers from excess release of hydrochloric acid, dysphagia, constipation, neurogenic bowel

Integumentary system:
1. Skin breakdown related to decreased or absent sensation, immobility, and thermodysregulation

Peripheral vascular system/pain:

  1. Venous thromboembolism related to immobility;
  2. nociceptive and neuropathic pain
45
Q

Spinal cord injury:

Medical care

A

• If respiratory compromise intubation and ventilation->tracheostomy
• If cardiac compromise-> fluids or vasopressors; temporary or permanent pacemaker
• If neurogenic bladder-> Foley catheter, or suprapubic catheter (Watch for CAUTIs which can lead to neurosepsis)
• GI complications: G or J tube placement and tube feeds if they have dysphagia, stool softeners/laxatives
• Integumentary system: Nursing care to prevent and treat wounds
• Peripheral vascular system/pain:
1. Subcutaneous anticoagulants,
2. nerve pain medication
a. **gabapentin
b. **opioids DO NOT work on nerve pain!!!
3. antispasmodics
• Spinal cord decompression surgery

46
Q

Spinal cord injury:

Nursing care

A
  • Frequent assessment to monitor for complications and response to medications
  • Collect and monitor labs
  • Maintaining immobilization of the spine with C-collars or traction, while still turning the patient and performing nursing care
  • O2/ventilatory support/tracheal suctioning
  • Trach care
  • Frequent vital signs
  • Fluid/vasopressor administration
  • Nutritional administration
  • Urinary catheterization
  • Pain medication administration
  • Protection of bony prominences, frequent turning, wound care
  • Surgical wound assessment and care

Adult 2 Test 1 (6 decks)

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