NEURO II MEDSURGE test 1

brain is composed of

brain tissue, CSF, and blood

what blood gases need to be managed with brain

acidotic specifically

intracranial pressure def

hydrostatic force measured in the brain CSF compartment

intracranial pressure reasons for increase

hematoma, contusion, abscess, rapidly growing tumor, infection of the meninges

normal brain ICP

5-15 mm Hg

if ICP >20

needs to be txed

if ICP >30

patient will die

complications of increased ICP

inadequate perfusion=brain damage, cerebral herniation=brainstem compression and respiratory arrest

ICP changes present how in patient

change in LOC (d/t dec blood flow), change in vital signs like cushings triad (bradycardia, systolic htn, irregular respirations), ocular signs (CN III compression=dilation, NR, sluggish, cant move eye up, ptosis), fixed pupil, dec motor function, HA, vomiting

how is vomiting different for neuro traumas?

will be unexpected and projectile

Cushings triad

sign of inc ICP, bradycardia, systolic HTN, irregular respiratory pattern

if the patient had a head injury and now has a fixed unilateral dilated pupil, what is this a sign of?

Neuro emergency!

dx for ICP issue

CT and MRI to find cause, lumbar puncture is not done with inc ICP due to possible herniation bc it could cause rapid pressure changes within the cranium

drugs for inc ICP

osmotic (mannitol) and corticosteroid (decadron)

nursing care for inc ICP

respect of patient, HOB 30 degrees, maintain airway and adequate O2, avoid anything that would increase ICP, nutrition, skin integrity, infection

perfusion for ICP

when we talk about neuro trauma its critical to perfuse the brain as top priority, remember the brain does not store O2 and glucose it requires constant supply, so cerebral perfusion is vital in these patients

CPP

cerebral perfusion pressure

CPP normal

60-100mm Hg

if CPP is less than 50

it is critical and need to correct

if CPP is less than 30

patient will not survive

how to calculate CPP?

MAP-ICP=CPP

what happens if brain is perfused?

function fails and homeostasis is lost

scalp lacerations

a lot of bleeding, possibility of infection

basal skull fracture

battle sign (postauricular ecchymosis), behind ear bruising, raccoon eye (periorbital ecchymosis), fx associated with tear in dura-CSF leak, rhinorrhea and otorrhea, halo sign will show if glucose in discharge, never put NG tube blindingly

concussion

a sudden change in LOC with or without loss of consciousness

sx of consussion

HA, amnesia to event, short disruption in LOC

post concussion syndrome

may develop 2 weeks to 2 months after injury, HA, lethargy, personality changes, behavioral changes, dec attention span, dec short term memory, change in intellectual ability

contusion

bruising of the brain usually sue to closed head injury, may have fracture, edema, necrosis at site, coup-contrecoup injury (two for one head hit, forward and back), may have seizures post injury

lacerations

tearing of brain tissues usually due to penetrating injuries, immediate tissue death

epidural hematoma

bleeding between the dura and inner surface of the skull, EMERGENCY

subdural hematoma

bleeding between the dura mater and the arachnoid layer covering the brain

intracerebral hematoma

bleeding within the parenchyma, also deadly

head trauma dx

CT is best

nursing care of head trauma

pain management, observe for fever, neuro check, changes in sensory function, keep ICP down

brain tumors

usually detected with problems, txed with surgery, radiation, and chemo

ischemic stroke

85-87%, thrombotic (clot) and embolic (travels, usually caused by a-fib)

hemorrhagic stroke

13-15%, intracerebral hemorrhage, also subarachnoid hemorrhagic stroke (bleeding into subarachnoid space, deadly)

stroke protocols

1. notice facial drooping, arm tingling on one side, speech problems, time is money, terrible ha

2. do a CT or transcranial doppler to find bleed or cause of stroke

3. if no bleed then give chewable aspirin and tPA

3a. if bleed then OR NO aspirin

4. If bleed then can use a merci retriever and puncture clot and remove it, or drill, tie off bleeder, and evacuate

5. hold BP meds after stroke for 1-2 days to help perfuse brain

what strokes have highest mortality?

hemorrhagic

stroke risk factors

age, HTN, heart disease, DM, family hx, ethnicity/race (AA more strokes), hx of stroke or TIA, use of ETOH, smoking, high fat diet, drug usage, lack of exercise, obesity

subarachnoid hemorrhage

usually caused by an aneurism, sudden onset of worst HA of my life, at risk for vasospasm

tx for subarachnoid hemorrhage

will spend 14 days in ICU on HHH therapy for prevention of cerebral vasospasm (hypertension, hypervolemia, hemodilution and vasodilating calcium ch blocker like nimodipine)

transient ischemic attack def

temporary, sx lasts less than 1 hr, can be motor, sensory, cognitive, warning sign of progressive cerebrovascular disease, no permanent damage just clogged vessels and these pts will be on statin therapy for rest of life

stroke manifestations

neuromotor, communication, Broca's=expressive aphasia, Wernicke's=receptive aphasia, global is receptive and expressive aphasia, affect, intellectual function, spacial and perceptual alteration, elimination functions (cant go pee or poop)

with strokes where will the pupil damage be compared to motor?

ipsilateral (same side) pupil damage but contralateral motor deficits

ex: right brain stroke injury=pupil dilated on right, and motor dysfunction on left

typical stroke signs

Sudden:

onset of numbness or weakness of face, arm, or leg, particularly on 1 side

confusion, trouble talking or comprehending

changes in vision

difficulty with walking, coordination, balance

onset of terrible headache

tPA for stroke guidelines

timing within 3-4.5hrs of sxs onset, get CT first, dont give if hemorrhagic stroke, coagulations disorders, recent hx of GI bleed or stroke, head trauma within past 3 months, major surgery within last 14 days

stroke nursing care

drug therapy with antiplatelet and anticoagulant, never admin a drug that increases bleeding to a pt with a cerebral bleed, OT/PT/speech therapy, respiratory and cardiac monitoring, skin care, educate or on BP control, nutrition, sensory perception, bowel/Bladder regimen, educate or in BP control, family counseling, appropriate environment temp and safety

meningitis dec

acute inflammation of the lining of the brain and spinal cord

sx of menigitis

fever, severe HA, n.v, nuchal rigidity(stiff neck)

if Lumar puncture for meningitis is clear then

its viral and that better

if lumbar puncture for meningitis is cloudy then

its bacterial and a medical emergency, contains wbc/rbcs and can result in residua neurological dysfunction

lumbar puncture process

1. Prepare patient

2. Lay pt in lateral recumbent (side lying) or seated and leaning forward bending over, empty bladder before

3. Assess before or sx of inc ICP like pupillary sxs, HA, stiff neck, vomiting etc

4. Use sterile technique, and take kit and drape them, locally numb area, pain scale, and aspirate with sterile needle in between l3 and l4, or l5 and aspirate CSF

5. Post procedure band aid, sxs of changes in ICP

trigeminal neuralgia sx

sudden pain knifelike often in lips, cheek, forehead, often have twitching, repeated blinking, tearing of 1 eye, precipitated by cold/hot blast air changes, chewing, brushing teeth, unpredictable pain

cause of trigeminal neuralgia

herpes, HSV, post covid

nursing care for trigeminal neuralgia

stress management for unpredictable pain, self image changes, observe for side effects of meds, eating causes tic so worry about total nutritional intake

Bells palsy def

peripheral face paralysis affecting facial nerve in patients without CVA, begin recovery after 6 months, some damage can occur if not txed correctly

cause of bells palsy

unclear, maybe from herpes simplex virus

bells palsy sx

Flaccid face on affected side with drooping mouth and drooling (in pts without CVA)

Unable to close eyelids with an upward movement of eyeball

Flattening of nasolabial folds

Unilateral loss of taste

Decreased ability to chew

nursing management of bells palsy

Gentle massage, moist heat

Pain management

Risk of corneal abrasion

Increased risk of aspiration

depression/body image

tx of bells palsy

Corticosteroids give immediately

Acyclovir if HSV

Can stop permanent paralysis

Guillain Barre syndrome def

rare neurological illness notes by ascending symmetrical paralysis

Guillain Barre cause

unknown (autoimmune destruction of the peripheral myelin)

Guillan Barre sx

1-3 weeks post URI or GI infection s/p vaccination, distal muscles weaker spreads towards diaphragm, paresthesia's usually followed by paralysis

what is most important in tx with Guillan Barre?

respiratory

clinical complications with Guillain Barre

Respiratory infection or UTI

Respiratory insufficiency

DVT, paralytic ileus, PE

Malnutrition

nursing care for Guillain Barre

Monitor for infection

Monitor respiratory status

Observe for thrombophlebitis

Passive ROM

Occupational therapy consult

Most will have full recovery after some time

primary spinal cord injury

Cord compression

Disruption of blood flow to spinal cord

Pulling on spinal cord

Penetrating trauma

secondary spinal cord injury

damage that happens after the initial injury

cervical injury causes

tetraplegia

thoracic or lumbar injury causes

paraplegia

complete spinal cord injury

total loss of motor and sensory below level of injury

incomplete cord lesion

some tracts are spared, so there is partial function restored

brown Sequard syndrome

Damage to ½ of cord, loss of motor, position and vibratory on the side of injury and loss of pain and temperature on the other side of the body

respiratory manifestations of cord injury

Above C4=total loss of respiratory muscle function=mechanical ventilation all the time

cardiovascular manifestations of cord injury

Above T6 there is danger of hypotension and bradycardia

nursing care of spinal cord injuries

Prevent UTI

Prevent respiratory infections

Prevent contractures/skin breakdown

Monitor cardiac status/prevent blood clot

Autonomic dysreflexia

autonomic dysreflexia

Autonomic dysreflexia involves stimulation of sensory receptors below the level of the SCI. The intact SNS below the level of injury responds to the stimulation with a reflex arteriolar vasoconstriction that increases BP. The parasympathetic nervous system cannot directly counteract these responses via the injured spinal cord. Immediate interventions include elevating the head of the bed 45 degrees or sitting the patient upright (to lower the BP) and determining the cause (bowel impaction, urinary retention, UTI, PI, tight clothing).