Adult Health Exam 3

Neuro

central nervous system (CNS)

CN 1-2

brain and spinal cord

peripheral nervous system (PNS)

CN 3-7

spinal nerves

autonomic nervous system (ANS) components (nerve fibers, ganglia)

meninges

3 protective layers/membranes that surround brain and spinal cord

1. dura mater (outer)

2. arachnoid mater

3. pia mater (inner)

nervous system gerontological considerations

1. gradual loss of neurons, ventricles in brain widen (decrease in cerebral blood flow)

2. changes in myelin sheath leads to decrease in conduction

3. autonomic nervous system changes (makes them more likely to have orthostatic hypotension)

4. decrease in taste, smell, balance, and response to temperature changes

neurological diagnostic studies

CSF

tissue biopsy (nerve, muscle, brain, artery tissue)

head CT (plain or with angiography)

MRI

EEG (seizures)

PET scan (look for cancer)

carotid artery ultrasound (presenting stroke like symptoms)

CSF

cerebrospinal fluid

normal CSF - clear, no red blood cells are present, small amount of protein present, glucose present

get CSF from lumbar puncture or ventriculostomy (in head)

if glucose low - possible bacterial meningitis

protein high - possible tumor, multiple sclerosis

lumbar puncture

spinal tap

can rule out certain issues

pre and post of lumbar puncture or ventriculostomy

pre: coagulation labs, vital signs, check neuro status

post: vital signs, lie flat for 1 hr***, asses for numbness/tingling and in extremities or inability to void

dyskinesia

movement problem

dysphasia

inability to generate speech or comprehend speech (aphasia)

diplopia

double vision

ataxia

balance/coordination issue

aphasia

inability to generate speech or comprehend speech

expressive or receptive

dysarthria

difficulty speaking/slurred speech

primary spinal cord injury

direct physical trauma

secondary spinal cord injury

ongoing progressive injury post trauma

body response to injury (ex. swelling)

spinal shock

loss of deep tendon and sphincter reflexes

occurs shortly after acute spinal cord injury

loss of sensation

flaccid paralysis below level of injury

lasts days/weeks but can recover

autonomic dysreflexia

life threatening

can occur after return of reflexes post spinal shock

massive, uncompensated cardiovascular reaction

autonomic dysreflexia s/s

hypertension

throbbing headache

diaphoresis above level of injury

bradycardia

piloerection (goosebumps)

flushing above level of injury

anxiety

nausea

blurred/spots vision

nasal congestion

causes of autonomic dysreflexia

distended bladder/rectum

pain or stimulation of skin (clothes rubbing on skin)

autonomic dysreflexia nursing interventions

elevated HOB 90 degrees

fix cause (distended bladder - do straight cath)

manage BP/frequent vitals

neurogenic shock

level of injury - C spine and T6 + above

s/s: hypotension, bradycardia, temperature dysregulation

worsens cord ischemia (can’t recover)

above C3 injury to spinal cord

total loss of respiratory function

mechanically ventilated and intubated

C3-C5 injury to spinal cord

respiratory insufficiency

below T2 injury to spinal cord

paraplegia (partial/complete loss of lower limbs)

C1-T1 injury to spinal cord

tetraplegia (loss of function of all four limbs)

systems affected from spinal cord injury

motor/sensory (can end up with sacral wounds due to this)

respiratory

cardiovascular

urinary

GI

integumentary

metabolism

peripheral vascular

spinal cord injury diagnostics

CT

MRI (give more info)

spinal cord injury treatment

VTE prophylaxis

surgical stabilization

skeletal traction (tongs/halo ring)

spinal cord injury nursing considerations

respiratory status in newer onset typically

cardiovascular instability

skin care

bowel and bladder managemnet (can self cath/bowel regimen)

pain management

stress ulcers (if inpatient, prophylactic in ICU to avoid ICU stress ulcers)

spinal immobilization

fluid/nutritional management

intracranial pressure (ICP)

normal range: 5-15 mmHg

increased ICP from:

1. primary (initial injury)

2. secondary (hypoxia, ischemia, hypotension, edema in brain tissue)

what’s in the skull?

brain tissue

blood

CSF

the brain autoregulates/compensates until it can’t

cerebral edema causes (increased ICP)

1. infections (meningitis, encphalitis)

2. head injury/brain surgery

3. brain abscess

4. brain tumors

5. metabolic issues (DKA, hepatoencephalopathy)

6. vascular problems (stroke)

cerebral edema clinical manifestations

1. changes in LOC

2. cushing’s triad

3. pupillary changes (ex. fixed dilated pupils)

4. decreased motor function

5. headache

6. vomiting

7. posturing

cushing’s triad

1. bradycardia

2. hypertension w widened pulse pressure

3. irregular respirations

sign of pending brain herniation (brain goes downward)

types of posturing

1. decorticate

2. decerebrate

BOTH BAD

decorticate posturing

everything goes towards core

abnormal flexion on glascow scale

decerebrate posturing

worse of the two

everything goes outward

abnormal extension in glascow scale

cerebral edema diagnositcs

1. CAT scan

2. MRI

3. EEG (to check seizure activity)

4. ICP measurement: ventriculostomy (drill a hole in brain, risk for infection, monitor CSF)

5. glascow coma scale (assess neuro status)

NO LUMBAR PUNCTURES (may cause herniation, changes pressure)

cerebral edema treatment

drug therapy

1. osmotic diuretics (mannitol)

2. hypertonic saline (monitor BP and sodium levels***)

3. corticosteroids (dexamethasone)

cerebral edema nutritional therapy

increased glucose requirements due to hypermetabolic state

GCS

look at slideshow

less than 8 - intubate

cerebral edema goals

1. airway (GCS less than 8 - intubate)

2. normal ICP

3. fluid/electrolyte/nutritional balance

4. decrease complications from immobility

cerebral edema considerations

HOB 30 degrees (improves jugular venous outflow)

head midline (helps with outflow and pressure)

head injuries

1. scalp lacerations (bleed a lot, skin around head is very vascular)

2. skull fractures (takes a lot of force)

3. concussions (rest brain, no electronics)

4. diffuse axonal injury (can have normal CAT scan, sheering of brain tissue BAD)

5. contusions (bruising of brain)

6. epidural hematoma (bleeding between dura and inner skull surface, bleeding typically arterial)

   1. ****goes from initial unconsciousness to lucency (seems fine) to quick decrease in LOC

7. subdural hematoma (dura and arachnoid space, common in geriatric pts)

skull fractures

1. basilar skull fracture (takes substancial amount of force, bottom part of skull, cradles brain)

2. battle’ sign (bruising behind ears)

3. raccoon eyes (bruising under eye)

4. CSF from nose/ears (otorhhea, rhinorhea)

   1. can test with glucose strip (don’t block from CSF coming out)

acute subdural hematoma

bleed from occurence

subacute subdural hematoma

slow bleed, 2-14 days post injury, might have s/s then

chronic subdural hematoma

always have area that bleeds

never healed

concussion teaching

s/s of neurologic emergency

limit screen time

do not return to sports the same day

may require someone to stay overnight (not about someone waking them up, want to know if they are arousable)

no driving until cleared by HC provider

nursing considerations

frequent neuro checks

no nose blowing

don’t block nose/ears if have CSF leak

health promotion (wear helmets, follow concussion protocol)

meningitis

acute inflammation of the meninges surrounding the brain and spinal cord

associated with fall/winter/early spring (viral in nature)

can be viral or bacterial

bacterial meningitis

50-100% fatality rate if untreated (give antibiotics quickly)

common agents: streptococcus pneumoniae, neisseria meningitidis

gets in from respiratory tract/bloodstream, penetrating skull injuries, and fractured sinuses/fracture skull bones

bacterial meningits clinical manifestations

fever

headache

N/V

nuchal rigidity (stiff neck, can not touch chin to chest, very painful)

photophobia and decreased LOC (not as common)

bacterial meningitis complications

1. elevated/increased intracranial pressure

2. residual neurological dysfunction

3. waterhouse-friderchesen syndrom (very rare)

   1. DIC

   2. petechiae

   3. adrenal hemorrhage (glands)

   4. CV collapse

bacterial meningitis diagnostics

1. H and P

2. CAT scan/CT scan (rule out other reasons due to headache, if bleeding in brain and did lumbar puncture, can cause herniation)

3. blood cultures

4. lumbar puncture (after CAT scan)

5. increased neutrophils

bacterial meningitis treatment

medical emergency until proof it’s not bacterial

antibiotics prior to confirmation via lumbar puncture

pain management (head and neck pain)

IVF

rest

maybe mannitol (if increased cranial pressure)

maybe antiseizure meds

viral meningitis

treatment with antibiotics while waiting confirmation from LP

enterovirus - most common pathogen

self limiting (has to run it’s course)

symptom management (treat symptoms, can send home from hospital)

CSF has decreased glucose, bacteria consuming glucose

characteristics of parkinson’s

bradykinesia (slow execution of movement)

rigidity

tremor at rest

gait changes (shuffling)

parkinson’s mnemonic: TRAP

tremor

rigidity

akinesia (absent of movement)

postural instability

who gets parkinson’s and why?

males>females

increase risk with age

possbile genetic link?

secondary parkinson’s (like parkinsons) related to environmental exposures (ex. copper, psychiatric meds (lithium, haloperidol), manganese, carbon monoxide poisoning)

parkinson’s complications

dementia

psychosis

aspiration (big one)

falls (big one)

parkinson’s diagnostics

no real test

H and P

clinical features (symptoms that point to parkinson’s)

CT/MRI (rule out stroke or tumor)

parkinson’s drug therapy overview

problem is with neurotransmitter imbalance

goals:

1. enhance release or supply of dopaminergic neurotransmitters (dopamine)

2. block effects of overactive cholinergic neurons (acetylcholine)

effects of giving parkinson’s drugs late

administer medications on time so symptoms don’t come back

drug therapy

levodopa/carbidopa

enhances release/supply of dopaminergics

give with food

may abruptly stop/start working

delayed med effects (give med on time)

dyskinesia

N/V

lightheadedness

parkinson’s surgical therapy

when patient is having zero response to medications

types:

1. deep brain stimulation

2. ablation (burn off part of tissue)

3. transplantation of fetal neural tissue

parkinson’s nutritional therapy

6 small meals a day

spread protein out throught the day

reduce constipation by increasing fiber and fluids

guillane-barre syndrome

autoimmune process that occurs days or weeks after a bacterial or viral illness

guillane-barre clinical manifestations

acute, ascending, rapidly progressive symmetric weakness of the limbs

autonomic nervous system dysfunction (fluctuating BP and HR)

pain

diaphragm is affected (most serious complication)

guillaine barre treatment

ventilator if diaphragm is affected (supportive treatment)

plasmapheresis (take plasma out, filter out antibodies, put plasma back in)

high dose immunoglobulin (IVIG)

guillaine barre outcomes

most recover spontaneously in about 28 days

80% walk independently in 6 months

60% make a full recovery in a year

guillaine barre worse outcomes

people with GI infection

older in age

poor upper extremity strength

those who need mechanical ventilation

stroke

ischemia or bleeding that results in brain cell death

2 main categories: ischemic and hemorrhagic

ischemic strokes

1. thrombotic - injury to vessel, clot forms (most common)

2. embolic - embolus lodges and blocks flow, sudden onset

embolic ischemic stroke examples

blood embolus

fat embolus

air embolus

associated with a-fib, infective endocarditis, MI, and other heart conditions

hemorrhagic strokes

1. intracerebral - prognosis is poor

2. subarachnoid hemorrhage - usually caused by ruptured aneurysm

stroke risk factors

hypertension (most important modifiable risk factor)

age

race

obesity

diabetes (multiplies risk by 5)

family history

heart disease (a fib multiplies risk of stroke by 5)

smoking (doubles risk)

transient ischemic attack

ischemia without infarct (brain tissue doesn’t die)

transient (short lived)

s/s last less than an hour

1/3 of people with a TIA go on to have a stroke

right brain damage

impulsivity

impaired judgement

left-sided deficit

minimize/deny they are having a stroke

left brain damage

decrease speech/language ability

aware of deficits

impaired comprehension related to math and language

stroke clinical manifestations

motor deficits (can’t move arm or leg)

communication deficits (aphasia, dysarthria)

affect

intellectual function

spatial-perceptual problems

aphasia

expressive (trouble speaking) and receptive (trouble understanding)

dysarthria

gurgly speech

stroke diagnostics

onset of symtpoms is VERY IMPORTANT****

CT to rule out bleed

MRI (better than CT to identify ischemic stroke)

BP management (220/110 is okay for ischemic stroke (acute phase) if no fibrinolytic given

if fibrinolytic given, BP < 185/110 to start and BP 180/105 max for 24 hrs post fibrinolytic

TPA (tissue plasminogen activator)/fibrinolytic

3-4.5 window post onset of symptoms to give it

careful screening: no recent GI bleed, stroke, head trauma, no major surgery within 14 days, no internal bleeding within 22 days

frequent vital signs and neuro assessment using NIHSS

important to have accurate patient weight

no anticoagulation during acute phase due to risk of bleeding

stroke treatments

TPA/fibrinolytic

endovascular therapy (balloon/stent/clot retrieval)

hemorrhagic treatment (surgical decompression, clip/coil ruptured anurysm)

physical therapy

occupational therapy

speech therapy

stroke medications

statins for high cholesterol and TIA (transient ischemic stroke) history

anticoagulation for a-fib

antithrombolitics for ischemic stroke: either anticoagulants or antiplatelet meds (can be 1 or 2)

stroke nursing management

assessment using NIHSS every couple of hours

decrease modifiable risk factors (health promotion)

NPO until swallow eval/study performed

ASSESS GAG REFLEX BEFORE ATTEMPTING TO FEED

communicate with patient (be aware of possbile deficits)

dementia

cognitive disorder with decline in 1 or more cognitive domains:

1. complex attention (able to focus on a lot of things)

2. executive function (higher level thinking)

3. language

4. learning and memory

5. perceptual (motor)

6. social cognition

types of dementia

1. alzheimer’s disease

2. vascular dementia

3. lewy body dementia

alzheimer’s diseae

no cause

contributing factors include:

1. age (greatest risk factor)

2. family history

3. genetic link

4. cardiovascular factors (brain health related to heart)

5. diabetes (high blood sugars can damage brain)

6. head trauma

alzheimers clinical manifestations

changes in brain occur 15 years before symptoms

early warning signs (word finding difficulties, poor recent memory, misplacing objects)

stages include mild, moderate, and severe

alzheimer’s diagnostics

diagnosis of exclusion

CT/MRI (may show changes in late stages (ex. atrophy (shrinking brain)))

PET scan (can detect amyloid plaques)

biomarkers (CSF (lumbar puncture)/imaging)

neuropsychologic testing

alzheimer’s treatment

drug therapy:

1. namenda (memantine)

2. aricept (donepezil)

3. exelon (rivastigmine transdermal patch)

4. antidepressants

5. antispychotics for behaviors

6. sleep aids

alzheimer’s patient goals

1. maintain functional ability

2. safe environment/minimize injury

3. personal care needs

4. maintain dignity

alzheimer caregiver goals

1. decrease stress

2. maintain their own health

managing behavioral problems

1. avoid extremes (temperature, noise)

2. cover up their tubes and lines

3. distraction

other considerations for alzheimers

1. pain management

2. swallowing issues/aspiration

3. infection prevention

4. scheduled toileting

5. caregiver support

6. safety

do’s and don’ts

DO:

1. treat with respect/dignity

2. simplify requests

3. use distraction

4. reassure

DON’T

1. ask them to recall things

2. reorient

3. rush them

4. scold them

5. attempt to rationalize