MARY ANN RODRIGUEZ

Exam 5 Intracranial Review

Intracranial regulation:
NORMAL ICP= 5-15
Risk for imbalance:
 Elderly persons: degenerative patho conditions or injuries (FALLS)= intracranial regulation
imbalance
 Adolescents and young adults: Traumatic injury to head
SEIZURES: (9) Episodes of abnormal motor, sensory, or autonomic activity
 All or part of brain can be involved
Types
Partial (focal): Generalized:
begin in one hemisphere OR in a specific region involve electrical discharges beginning in both
of cortex (temporal, frontal, or parietal, most hemispheres of brain and spreading throughout
often) cortex and down into brainstem: resulting in
 Simple partial: conscious maintains abnormal movements/spasms bilaterally
(dejavue) palpitations, flushing •Absence (petit-mal): blank stare, last few
seconds
 Complex partial: Lose conscious for
•tonic-clonic (grand-mal)
several minutes; lip-smacking, knit &
Tonic=complete stiffness + clonic=jerking
pick, amnesia
4 distinct phases:
1) Prodromal: right before
2) Aural: odor, taste, vision
3) Ictal: seizure taking place=INCONTINENT

4) Post-ictal: immediately following
tonic/clonic= deep sleep>4-6 hours
Monitor: RR & reposition
 Idiopathic: genetic/developmental defects
 Acquired: trauma, infection, hypoglycemia, metabolic disturbances, endocrine dysfunction,
tumors, ETOH, withdraw (doesn’t mean for the rest of life)
 Epilepsy: condition of recurrent seizure activity- different intervals (now > 8months >2years >
6 months for rest of life
RISK FOR SEIZURE: .
•Febrile state: >103-104 GOAL: decrease fever
•Exposure to toxins
•Metabolic disorder
•Hypoxia
•F&E imbalances
•Tumors:
brain triggers:
Flashing lights, excessive caffeine intake, overwhelming fatigue, excessive stress
DRUGS: cocaine, aerosol, glue products

Diagnostics:
 Health history and history of the seizures

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  EEG/CT/MRI > tracing of the brain
EEG: specific order to hold certain meds (follow orders), Restrict caffeine prior to procedure, LIE
very still
 Routine labs: (to rule out.....) > CBC
 Cerebral angiography: DYE to cerebral
MEDS: ATI
Antiseptics: maintenance; prevent seizure activity
Anticonvulsants: STOPS seizure activity
Assessment
Diagnosis (NANDA)
Planning:
 Prevent INJURY, promote optimal mobility function while on med, promote psychosocial while
seizure activity
Interventions:
 Avoid triggers
 Med use
 Follow dr visits
 Turn to side
ACUTE PHASE=when it happens…what to do:
Priority: SAFETY >Risk for injury, clear area, protect head
Record: before event; time it…longer than 5 minutes=exhaust brain
Evaluation

Seizure precaution:

Postictal phase

 Nothing by mouth while seizing

 Pad side rail, pillows, blankets
 IV for new onset seizure or epilepsy (PATENT)

Status epilepticus: Tonic/ clonic (most worrisome  Insufficient ventilation= hypoxemia=dysrhythmias,

hyperthermia= ACIDOSIS
>>>>>Hypoxia, acidosis, Hyperglycemia, hyperthermia, exhaustion<<<<<
Meds to help reverse these conditions: Oxygen, 50% dextrose IV
 Med emergency
 Rapid IV meds needed (ativan/valium); repeated in 10 minutes as needed
 Dilantin IV given for longer-term control of seizures

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  Phenobarbital may be used
DOCUMENT:
 TIMING
 Before
 After: position phase: HA, muscle ache, fatigue
 How long slept?
EDUCATION:
 Avoid:
 Strobe lights
 Flickering lights
 Call if seizure >5minutes
 Do not double up on meds/take within 24 hours
 GOAL: prevent/recurring

MENINGITIS
Infection (bacterial, fungal or viral) involving the meninges which cover the brain and spinal cord.
 Caused by Neisseria meningitis
 Spreads though saliva, spit, cough, kissing
 Bacterial meningitis → medical emergency
Risk factors:
 Infant, teens, young adults
 Outbreaks → high population, crowded areas, college, military (vaccines)
 Medical conditions: HiV, no spleen
 Travels to Africa

Expected manifestation:
 Severe HA → D/T meningeal inflammation
 nuchal rigidity (neck stiffness),
 fever accompanied by chills
 altered mental status tachycardia > disorientation to place, person, year,
 photo-sensitivity, phono phobia
Newborns: slow or inactive, irritable, vomit, feeding poorly
Young children: look at child’s reflexes for s/s of meningitis

Key indicator: trigger pain= positive ⇢ notify provider

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Brudzinski’s sign: (positive)
 Hips and knees flex when neck is flexed

Positive kernigs sign:

 indicate presence of meningeal irritation (flex the hip & extend leg>>>>test is positive if unable
to fully extend the leg
Risk for developing ICP:
 Monitor v/s, neurological status at least q4 hours → if does have meningitis neuro check q2-4
hrs
 Restlessness, confusion, ↓ level of consciousness, presence of Cushing’s triad → severe
hypertension, widened pulse pressure and bradycardia
Health promotions:
1. VACCINES: prevented w/vaccine; keep up-to-date
 Meningococcal conjugate (NCV4) Vaccine:
o School age 11-12 yo (single dose & booster shot @ 16 years old
 Serogroup B meningococcal (Bexsero & trumenba)@ 16-23 yo
2. Acute care:
 Treat pain/fever (104-105) aggressively
 Seizure precaution
 Vitals
 I&O
 Neuro-checks
 Proper position → key: neutral position
 Darken room d/t photosensitivity (cover eyes)
 ↓ environmental stimuli
 Address nutritional needs
 Respiratory isolation ⇢ mask on pt if out of room
3. Ambulatory care:
 Few weeks post-acute phase
 High protein & calorie
 Small meals
Diagnosis of bacterial meningitis: → acute inflammation of the meninges and the CNS
 Priority → antibiotic: everyone in contact ⇢ prophylaxis antibiotic (Cipro)
 ↓ Environmental stimuli
 Maintain seizure precaution → D/T brain edema and meningeal irritation=seizure activity
 Monitor I & 0
 Semi-fowlers → 30-45 degrees will help reduce edema in the brain
 Isolation for 1st 24 hours → highly contagious, ↓ environmental stimuli
 ISOLATION DROPLET PRECAUTION ⇢ mask
 Private room
Meningitis = HIGH fever > risk for febrile seizure

↓ LOC and ability to swallow is at risk for aspiration → bed at 30-45 to promote emptying
 Monitor I/O Q 8HRS
 CHECK residual q4-6 hours
 Observe RR

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Diagnostic test:
 Lumbar puncture
 Blood culture prior to antibiotic → alter results, obtained to identify causative organism
CSF → Lumbar puncture results: ***REPORT TO HEALTH DEPARTEMENT***
 Cloudy CSF (bacterial) clear (virus)
 ↑ WBC
 ↑ Protein
 ↓ glucose (bacterial)
BE AWARE OF ICP: WHY? CNS = Edema= ↑ ICP = Altered intracranial regulation
Lumbar puncture=↑ ICP: #1 Diagnosis = CT SCAN
Post op:
 4-6 hours
 Lie flat & still
 LOG ROLL while lying FLAT WHY? Massive, massive headache
Standard labs:
 CBS
 Chemistry
 Blood work
MED:
 Ceftriaxone or cefotaxime in combo with vancocin
 Prophylactic antibiotics also: ciprofloxacin, rifampin, ceftriaxone ⇢treat family too
 2 weeks’ worth of antibiotic ⇢ start as soon as culture is obtained
 Anticonvulsants
 Corticosteroids
 Antipyretics
 Mild analgesics

PARKINSONS DISEASE: (4) chronic neurological disorder

Manifestations
 Tremor (typically unilateral) (can include hand, diaphragm, tongue, lip & jaw
o Pill-rolling: thumb/index/middle finger
o Resting tremors (hands/arms in a supination-pronation appearance)
 Rigidity ⇢ stiffness in the muscles (unilateral /bilateral)
 Akinesia/Bradykinesia ⇢slow movement
 Postural instability → may complain of being unable to STOP themselves from going forward
(propulsion) or backward (retropulsion)
o Propulsive (standing up leans over), shuffling gait with wider base of support noted; head
bent forward (risk for fall)
 (cogwheel rigidity) ⇢stiffness combined with tremors (stop and go) during range of motion
 Depression, anxiety, dementia
 Hypokinesia ⇢ ↓ movement
 Flat affect ⇢ no emotion
 Dysphonia ⇢ changes in voice, hoarseness’, sore throat

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Management:
GOAL: control symptoms and maintain functional independence
Three priority:
 Maximus neurological function > meds
 Maintain independence
 Optimize social well being
Implementation:
 Safety, promoting mobility, nutrition → monitor BUN/creatinine: dehydration- turgor
 Bowel impaction: stool softner, laxative/enema,
Drug therapy p. 1988
 Exercise and ambulation
o Non-traditional approaches are becoming popular
o Mobile/independent as possible > PT, yoga, stretch
 Self-care
o OT collaboration
 Injury prevention: safety gait
o Assess sleeping pattern ⇢ ties to Injury d/t poor light at night
 Nutrition: Poor nutrition=↓ calcium → Vit/minerals, calcium replacement
o As disease progresses, PEG tube/enteral nutrition may be required
o Risk for aspiration ⇢ small frequent meals 5-6 x/day; D/T dyspagia→ tremors
 Communication
o ST collaboration (speech therapy)
 Psychosocial support
Surgical management includes:
 Stereostatic pallidotomy
 Deep brain stimulation→ awake during surgery; Important; electrode to trigger brain to
↓tremors

HYDROCEPHALIC: (4)
The accumulation of excessive CSF within the ventricular system of the brain. The ventricular system
dilates when CSF flow is obstructed.
 Imbalance being produced and absorption
 ⇡ CSF (Ventricles DILATE and brain compresses against the SKULL
RISK FACTORS:
 Associated with myelomeningocele → Severe form of spinal bifida= sac extend opening in the
spine
 Intrauterine infection (infants) ⇢ spinal cord or canal >>>do not form or do not form or did not
close normally
 Perinatal hemorrhage (infants)
 Meningitis, tumors, hemorrhage (older kids)
 Congenital

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 INFANT: EARLY: LATE: CHILD: EARLY: LATE:
 Rapid head growth  “Setting-sun” sign  Strabismus  Seizures
(measure head  Frontal bone  Frontal headache in  Increased BP
circumference) enlargement am – relieved by  Decreased HR
 Bulging fontanel  Vomiting; emesis or sitting up  Altered resp pattern
---*(rub gently difficulty eating  n/v – projectile  Blindness
anterior/posterior  Altered resp  Ataxia  “posturing” –(head
Bulging=fluid pattern  Diplopia injury)
accum  Shrill, high-pitched  Restlessness
 Irritability cry  Irritable
 Poor feeding  Sluggish pupil confusion
 Distended scalp response
veins
 Cranial sutures
widely separated

OPEN SUTURE = SKULL ENLARGEMENT

CLOSED SUTURE= S/S results in NO enlargement= increased ICP occurs = emergent

Treatment:
Shunting⇢
 shunt in ventricles drains
 subq under the skin
 empty above atrium & ❤ ️or instill peritoneal cavity, fluid reroutes from brain to areas of body>
REABSORBS
Ventriculostomy: insert drain to ventricle to relieve pressure
Medications
Osmotic diuretic (MANNITOL): before/after surgery for a while

Cerebrovascular Accident (CVA): Severe HA ⇢ complete neuro assessment + ⇣FLUIDS (Call physician for order)
Difference in types of stroke:
Hemorrhagic – vessel that bursts and allows bleeding INTO the tissue causing INCREASED PRESSURE.
Thrombus – causes the vessel to narrow, which blocks the passage of blood.
Embolic – a blood clot or other debris circulating in the blood until reaches an artery in the brain that is too narrow
for it to pass so it ends up lodging itself and blocks blood flow
- the brain can make an “alternate route” also called COLLATERAL CIRCULATION to prevent CVA
TIA – transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia. Major
difference is the absence of acute infarction of the brain and symptoms typically last less than 1 hour.

***what they all have in common is that they interrupt blood flow which results in the lack of
oxygen and glucose***
Modifiable Non-modifiable
 HTN → diet, exercise, meds  Age⇢ atherosclerosis (Hardening of
 Smoking the artery)
 Lack exercise/obesity ⇢ maintain  Family HX
daily activity  Gender
 Excessive ETOH  ethnicity
 A-fib→ atria of the ❤️is not contract
good “fibrillation” =allowed blood to

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 clot around leaflet; if breaks
off=embolism=STROKE – oral
anticoagulants like warfarin and
dabigatran
 Diabetes – exercise and nutrition
o 40 mins 3-4 days/week to
reduce risk for stroke
o Low fat, fruits and vegetables
 Cholesterol
 Oral contraceptives high in progestin
and estrogen

ISHEMIC STROKES: (↑B/P needed for perfusion) Check w/provider b/fore giving med
Results from inadequate blood flow to the brain from partial or complete occlusion of an artery
 use of Thrombolytic therapy
 Time frame 3-4 ½ hours of onset of start of s/s (clot buster: aTPA)
 Stable pt →anticoagulant
 Stent placement
Transient ischemic attacks (TIA): Transient episodes (come and go), typically last an hour
afib⇢ oral anticoagulant – MEDICAL EMERGENCY BECAUSE IT CAN LEAD TO STROKE
S/s of TIA depends on the BV that’s involved and the area of the brain that’s ischemic
- Carotid system – temporary loss of vision in 1 eye (amaurosis fugax), transient hemiparesis,
numbness or loss of sensation, or sudden inability to speak.
- Vertebrobasilar system – tinnitus, vertigo, darkened/blurred vision, diplopia, ptosis, dysarthria,
dysphagia, ataxia, unilateral/bilateral numbness or weakness.
ABCD Score used to predict risk for stroke 2 DAYS after a TIA
Hemorrhagic strokes:
Result from bleeding into the brain tissue itself or into the subarachnoid space or ventricles.
 No anticoagulant/thrombolytic = worse bleeding
 Surgery ⇢ bleeding under control →embolectomy

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Ischemic Strokes: INADEQUATE BF TO THE BRAIN FROM PARTIAL OR COMPLETE OCCLUSION OF
ARTERY  CLASSIFIED INTO:
Thrombotic: Embolic:
Occurs from injury to a blood vessel wall & Occurs when an embolus lodges in and occludes a
formation of a blood CLOT= narrowed cerebral artery=in infarction & edema of area
lumen=↓blood to the brain= less oxygen  quick onset MOST LIKELY TO OCCUR
 slow onset DURING ACTIVITY
 OFTEN DURING OR AFTER SLEEP  typical headache
 ⇡ cholesterol, atherosclerosis, ↑ HTN,  embolic is w/in the heart= a-fib, MI,
diabetes endocarditis, valve prosthesis at
 **most thrombotic strokes assoc. higher risk
with HTN or diabetes – both **rheumatic heart disease cause in young-middle
accelerate atherosclerosis age
 Many TIAs happen before thrombotic **embolus from atherosclerotic plaque common
strokes in older adults

HEMMORAGIC strokes: bleeding into the brain tissue intracerebral or subarachnoid

Intracerebral hemorrhage Subarachnoid hemorrhage:
Bleeding within the brain caused by rupture of a Occurs when there is intracranial bleeding into
vessel the cerebral fluid filled-space between the
 rapid onset ⇢ injury to vessel of arachnoid & pia matter membranes
brain=a lot of bleeding  Some warning sign possible, “silent
 often occurs during activity – sudden killer” w/aneurysm d/t no warning
onset, symptoms progress over mins signs
to hrs due to bleeding  ⇣LOC, N/V, seizures, stiff neck
 HA, N/V, ⇣LOC, HTN is the most  NO
common cause thrombolytic/anticoagulated=worse
 Poor prognosis   The most dangerous complications
 Rupture of vessel: cerebral vasospasm ⇢ treat
*HTN ⇢ meds/manage if w/Nimodipine
uncontrolled=aneurysm=bleeding o Release of endothelin (a
*Aneurysm →stop bleeding, clipping potent vasoconstrictor)
procedure, coiling procedure o Pt who are at risk for
 NO vasospasm kept in ICU for up
thrombolytic/anticoagulant=worse to 14 days until threat of
 Trauma, Tumors and use of vasospasm is reduced
o PEAK TIME FOR VASOSPASM
Symptoms: IS 6-10 DAYS AFTER INITIAL
At first, patient experiences SEVERE HAs with BLEED
N/V.  Cause by rupture of cerebral
aneurysm, trauma, drug abuse

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 (cocaine)
 MOST OFTEN CAUSED BY A RUPTURE
OF A CEREBRAL ANEURYSM

Right-brain damage:

- Left side paralyzed

- Tends to deny/minimize problems
- Rapid performance, short attention span
- Impulsive  safety problems
- Impaired judgement and impaired time concepts

Left-Sided damage:

- Right side paralyzed

- IMPAIRED SPEECH/LANGAUGE APHASIAS
- Slow performance, cautious
- Depression and anxiety  aware of deficits
- IMPAIRED COMPREHENSION RT LANGAUGE, MATH
- CAN’T DISTINGUISH FROM RIGHT OR LEFT

Affect: may have difficulty controlling their emotions. Responses may be exaggerated or unpredictable.
Depression & feelings associated with changes in body image and loss of function can make this worse.
They may be frustrated by mobility and communication problems.

Intellectual Function: Memory & judgment maybe impaired. A left-sided stroke is more likely to result in
memory problems related to language. They may be cautious in making judgments. The person with a
right –sided stroke tends to e more impulsive and to move quickly. Patient with either may have
difficulty making generalizations, which interferes with their ability to learn.

Spatial-perception: A stole pm the right-side is more likely to cause problems. There 4 categories. The
first is incorrect perception of self and illness. Patients may deny their illness or body parts. The 2 nd is
the [patient’s erroneous perception of self in space. The patient may neglect all input from the affected
side. The third is agnosia, the inability to recognize an object by sight, touch or hearing. The 4 th is
apraxia, inability to carry out learned sequential movements on command. They can’t brush their hair.

Elimination : may be temporary loss of bowel and urine. If at least partial sensation for bladder filling
remains, then voluntary urination is present. Initially, the patient may experience frequency, urgency,
and incontinence. Constipation may result from immobility, decrease in abdominal strengthen,
dehydration, and diminished response to the defecation reflex. Both may result due to lack of ability to
communicate needs.

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ACUTE CARE:

Initial:

Pt unresponsive  CAB

Pt responsive  ABC

Call Stroke team: RN, Neurologist, Radiologist, Radiologic Tech

Perform pulse ox and maintain adequate O2 above 95 – supplemental O2 if needed

Establish IV access with normal saline

Remove clothing

Obtain CT/MRI

Perform BASELINE lab test  immediately tx BG if HYPOglycemic

POSITION HEAD MIDLINE

HOB 30 degrees if no symptoms of shock or injury

Seizure precautions

Anticipate THROMBOLYTIC therapy for ISCHEMIC STROKE

PT NPO UNTIL SWALLOW REFLEX EVALUATED

Ongoing monitoring: VS, NEURO STATUS, LOC (NIH STROKE SCALE), motor and sensory func, pupil
size/reactivity, SaO2, and cardiac rhythm and reassure pt and family.

Medications:
Antiplatelets:

- Aspirin 81-325mg/day
- Ticlopidine (Ticlid)
- Clopidogrel (Plavix)
- Dipryridamole (Persantine)
- Aggrenox ( combination ASA & Persantine)

PATIENTS WITH AFIB

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↓↓↓↓↓↓↓

Anticoagulants:

- Warfarin (Coumadin)

Direct Factor Xa Inhibitors: DON’T NEED CLOSE MONITORING OR DOSAGE ADJUSTMENTS

- Rivaroxaban
- Dabigatran
- Apixaban

Statins: STROKE PREVENTION FOR HIGH CHOLESTEROL AND HAVE HAD A TIA

- Simvastatin (Zocor)
- Lovastatin (Mevacor

DRUG THERAPY FOR ISCHEMIC STROKE:

tPA (tissue plasminogen activator): for ischemia strokes ONLY not hemorrhagic!
It dissolves the clot within the blood vessel by activating the protein that causes fibrinolysis.
REMEMBER: within 3 hours from the onset of stroke symptoms. It can be given 3 to 4.5 hours after
onset IF strict criteria is met.

Screening for TPA includes:

 NONcontrast CT/MRI – to rule out hemorrhagic stroke

 Blood tests for coagulation disorders
 Screening for recent history of GI bleeding, stroke, or head trauma within the past 3 months
 Major surgery within 14 days
 Active internal bleeding within 22 days
During tPA infusion:
 Monitor VS and neuro status  to assess improvement or for potential deterioration RT to
intracerebral hemorrhage
 Control BP (SBP less than 185 mm Hg) is CRITICAL DURING TX AND FOR 24 HOURS FOLLOWING

Aspirin 325 mg  can be given 24-48 hours after the onset of ischemic stroke; USED CAUTIOUSLY IF
PATEINT HAS A HX OF PUD

**ANTICOAGULANTS IN THE EMERGENCY PHASE AFTER AN ISCHEMIC STROKE  NOT RECOMMENDED

 RISK FOR INTRACRANIAL HEMORRHAGE **’

When patient is stable:

 Anticoagulants and Platelet inhibitors which include aspirin, ticlopidine, clopidogrel, and
dipyridamole
 Patients with Afib  warfarin and direct factor Xa inhibs  -tran, -ban

DRUG THERAPY FOR HEMORRHAGIC STROKE:

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Main drug therapy is the MANAGEMENT OF HYPERTENSION
 Oral and IV agents to maintain BP
 Seizure prophylaxis in the acute period is situation specific and decided among interprofessional
care team

General signs & symptoms:

Cognitive changes:
 LOC changes
 Denial
 Spatial and proprioceptive changes ⇢ more common in R/sided stroke
 Memory, judgment changes, concentration
Motor changes:
 Hypotonia (flaccid paralysis)
 Hypetonia (spastic paralysis)
 Impairment of mobility
 Respiratory function
 Swallowing/speech, gag reflex,
Sensory changes:
 Visual changes
Diagnostic:
Pt with suspected TIA or stroke arrive to ER  rapidly undergo NONcontrast CT or MRI
- Can distinguish b/t ischemic and hemorrhagic stroke
- Determine size, location and treatment options for the stroke
MRI – more effective in ischemic stroke
CT – rules out hemorrhage

 MRI/Contrast CT scan ⇢ confirms (1st scan may not pick up on changes=admitted for follow up
CT
 Doppler: carotid ultrasound ⇢ plaque buildup
 Cardiac imaging (echo): leaflet of valves
 Cerebral angiography
 Swallowing studies: → post stroke d/t aspiration →thick food, pureed
 LABS: CBC, Chemistry, lipid panel ⇢ check status of cholesterol

Prevention:
Health promotion:
 Healthy diet→ ↑ fruits& veg, ⇣ saturated/total fat
 Weight control
 Exercise ⇢ control B/P, weight
 Limit alcohol
 No smoking
 Drug therapy
 Control HTN
 Routine assessment

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ACUTE CARE:
 ABG’S CPR
 Get to ER ⇢ 911: Never drive to ER D/T the need of Oxygen via N/C, Intubation
 Respiratory → maintain oxygenation
 Establish IV (large bore)
 CT/MRI ASAP
 Proper patient position → HOB 30 degrees
 Base labs
 NPO
 Seizure precaution ⇢safety
 Monitor for ↑ ICP (Hemorrhage stroke: ↑ volume going into brain cranium): ICP Normal range
5-15 if ⇡ 1st raise HOB 30 degrees
 Remove denture/clothing
 Mobility (1-sided working)
REHAB:
 MS → Getting back to normal function
 Survivorship
 Sexual function ⇢ regain, live w/changes
Planning:
 Maintain stable LOC
 Attain max physical function
 Attain max self-care → social worker, case manager
 Maintain stable body function
 Maximize communication abilities
 Maintain adequate nutrition
 Prevent complications
 Attain coping skill

Important Stroke Terms:

Aphasia: unable to speak (comprehending or producing it)
 Receptive Aphasia: unable to comprehend speech (Wernicke’s area)
 Expressive Aphasia: comprehends speech but can’t respond back with the correct words, if at
all (Broca’s area)
 Mixed Aphasia: combination of the two types of aphasia.
 Global Aphasia: complete inability to understand speech or produce it.
Dysarthria: unable to hear speech clearly d/t weak muscles (slurred) ⇢ writing tablet, something to
write on
Apraxia: can’t perform voluntarily movements (winking/moving arm to scratch an itch) even though
muscles function is normal.
Agraphia: loss the ability to write
Alexia: loss the ability to read…doesn’t understand or recognize the words
Agnosia: doesn’t understand sensations or recognize known objects or people
Dysphagia: issues swallowing (weak muscles)
Hemianopia: limited vision in half of the visual field

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BRAIN TUMOR: ⇢ chemo/radiation (normal B/P S: 90-135 D: 60-85)
Patho: Tumor grows, expands, and invades and eventually compresses and/or displaces normal brain
tissue → Affecting intracranial regulation
Problems: ICP, cerebral edema, hydrocephalis, pituatary disfunction=SIADH

Cerebral tumors most common

Primary: originate within the CNS or covering of brain ⇢do not spread/not malignant
Secondary: originate from cancer in other parts of body
GENERAL S/S:
 HA In AM
 N/V
 visual CHANGE
 SEIZURE
 PAPIL EDEMA
 Change in personality, mentation
TUMORS IN BRAIN STEM:
 Hearing loss
 Facial pain weakness
 Dysphagia/ ↓ gag reflux
 Nystagmus
 hoarseness
 Ataxia/dysarthria tumors in cerebellum
Pediatric ⇢brain tumor
 ↓ appetite
 Visual disturbance
 Change in personality

MANAGEMENT:
*Drug therapy
 Chemo, radiation, combination OF BOTH
⇢Direct drug delivery: emerging practice: disc shape drug placed in cavity delivers drugs
*Analgesics:
 Codeine/Tylenol for headaches
 Corticosteroids to reduce edema from tumor, helps control pain
*Anticonvulsants
*H2 blockers/PPI.> prophylaxis → ulcers (stress to body)
*Stereotactic approaches
 Gamma knife (high-dose ionized radiation) Precise in treatment

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Collaborative Care
Surgical therapy
 Craniotomy to access tumors
 Ventricular shunts help remove extra fluids
Nursing care
Pre op: (psychosocial support)
 Anxious
 Body image (hair shave)
Post op → (ICU)
 Monitor changes of status
 NEURO Q 15 – 30 min
 ECHYMOSIS Around the eyes common > COLD COMPRESS
 Monitor breathing status
 Wean off ventilator
 Dysrhythmia d/t F/E imbalance
 STRICT I & O
 NPO 24 hours → BRAIN STEM removal to prevent N/V
 CRANIOTOMY for brain stem ⇢ FLAT @ 48 hours = prevent pressure on neck incision
 Proper position is crucial to avoid ↑ ICP
↓ ↓ ↓↓
Neck in neutral position
 Turn side to side slowly if needed
 Large tumor removed: NON-operative side prevent displacement of cranial content by gravity
 No flex /hyper-flex of neck
 No Left/right turn
 Monitor labs
 Corticosteroids
 Osmotic diuretic for edema
Diagnostic:
 Hx/physical
 Assess s/s
 where in brain tumor sitting/affecting?
 MRI/PET SCAN →determine small tumor
 CT BRAIN SCAN ⇢ location
 EEG
 LUMBAR PUNCTURE

Head injury/brain death/organ donation (14)

Head Injury
Risk:
 Elderly d/t falls
 Motor vehicle accidents

Post -concussion syndrome (a closed head injury)

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Closed head injuries:
Contusion:
Bruising to area of impact (coup) or directly in line opposite to site of impact after (contrecoup)
 Most typically in frontal and temporal lobes
 Moderate to severe injury
Loss of consciousness and stupor/confusion →post contusion
Bleeding into tissues of brain can occur; swelling peaks about 18-36 hours after injury
24-48 hours observation depends on s/s

Concussion: a “shaking” movement to the brain with temporary loss of neurologic function with no
apparent structural damage

 Mild: Transient confusion, disorientation, brief disruption in LOC (memory lapse for < 30 min);
headache
 Diffuse axonal injury: d/t shaking
 More widespread injury to white matter
 Loss of consciousness for typically <6 hrs with post-traumatic amnesia
 Often from high-speed acceleration/deceleration events
 Duration of unconsciousness indicates severity of injury ⇢ intensive care unit
 Small areas of hemorrhage may be evident on scans
Post-concussion syndrome = complex disorder in which various symptoms last for weeks and sometimes
months after the injury
 Loss of consciousness does not have to be present to confirm this syndrome
Post-concussion symptoms include: important fam/pt
 Headaches → feels like tension =neck injury
 Dizziness
 Fatigue
 Irritability ⇢ stubborn and argue
 Anxiety
 Insomnia
 Loss of concentration and memory
 Noise and light sensitivity

Open head injury: object penetrates the brain or trauma is so severe that scull/scalp is open.
Traumatic Brain Injury (closed or open)
Primary injury: due to the initial damage
 Contusions, lacerations, damage to blood vessels, acceleration/deceleration injury, or due to
foreign object penetration
 Closed brain injury
 Open brain injury: object penetrates the brain or trauma is so severe that the scalp and skull are
opened
Secondary injury: damage evolves after the initial insult (ex. Fall off ladder)
 Due to cerebral edema, ischemia, or chemical changes associated with the trauma
Manifestations depend upon the severity and location of the injury, but typically include:
 Altered LOC
 Pupillary abnormalities

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  Sudden onset of neurologic deficits and neurologic changes; changes in sense, movement,
reflexes
 Changes in vital signs
 Headache
 Seizures
Scalp wounds
 Tend to bleed heavily, and are also portals for infection (SCALP/FACE bleed heavily)
→ antibiotic
Level of conscious:
 Level of responsiveness & consciousness is the most important indicator of the patient's
condition
 LOC is a continuum (spectrum) from normal alertness and full cognition (consciousness) to coma
 Altered LOC is not the medical diagnosis but the result of a pathology;
LOC is a symptom what is causing it?
 Coma: unconsciousness, unarousable unresponsiveness
 Persistent vegetative state: devoid of cognitive function but has sleep-wake cycles
CONTINUUM

Cerebral Blood Flow (CBF):

 Amount of blood in mL passing through 100g of brain tissue in 1 minute
⇢ Normal: about 50 mL/min per 100g of brain tissue (NOT ON T)
IMPORTANT: Sufficient cerebral perfusion pressure for brain to properly maintain
 Auto-regulation
 Adjusts diameter of blood vessels
 Ensures consistent CSF
 Only effective if mean arterial pressure (MAP) 70 to 150 mm Hg (Autoregulation)
Cerebral perfusion pressure (CPP) 60-100 NORMAL
CPP = MAP – ICP (Normal is 60 to 100 mm Hg. (TEST) ⇢ Optimal blood flow)
<50 mm Hg is associated with ischemia and neuronal death
EX: B/P: 90/42, ICP: 19; D:42X2=84, 84+S/90=174, divide by 3= 58 (MAP) 58-19=39 CPP → VERY LOW

Lewis 1137

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Diagnostic:
 CT scan / MRI / PET
 EEG
 Cerebral angiography
 ICP and brain tissue oxygenation measurement (LICOX catheter)
 Doppler
 NO lumbar puncture- could cause herniation from sudden release of the pressure in skull from
above area of puncture

Basics of Intracranial Pressure: Normal ICP: 5-15mm/hg (>20…treatment)

Skulls has three essential components: brain, cerebrospinal fluid (CSF), Blood
If one ⇡ other has to ↓ to maintain ICP

Factors that ⇡ ICP

 Arterial pressure & venous pressure
 Intraabdominal or thoracic pressure (vomiting/bearing down…)
 Temperature
 CO 2 Pressure
Monro-Kellie doctrine (regulation & maintenance)
 Addresses the pressure-volume relationship between ICP, volume of CSF, blood/brain tissue,
and cerebral perfusion pressure
 The cranial compartment is incompressible, and the volume inside the cranium is a fixed
volume
 If one component ⇡, another must ↓ to maintain ICP.
For example, an ⇡ in lesion volume (e.g. bleeding in brain) will be compensated by ↓ CSF and venous
blood.
Normal ICP 5 to 15 mm Hg (test)
Elevated if >20 mm Hg sustained
Triggers:
 Movement of head ⇢ keep head NEUTRAL
 Position → keep HOB 30 degrees; lower or higher = ICP
 B/P
 Shunt
 Edema

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  Temperature
 Cough/sneeze
 Suction
Normal compensatory (body tries to fix itself) adaptations
 Changes in CSF volume
 Changes in intracranial blood volume
 Changes in tissue brain volume
BUT, the ability to compensate is limited.
 If volume increase continues (i.e.: continued brain bleeding), ICP rises and leads to
decompensation
Stages of increased ICP
 Stage 1: total compensation ⇢ ONE ⇡ other ⇣
 Stage 2: ↓compensation; risk for ↑ICP
 Stage 3: failing compensation (loss of autoregulation); clinical manifestations of ↑ICP
(Cushing’s triad) EMERGENCY
 ⇡ systolic BP
 ↓ pulse (but full, and bounding pulse)
 Widening pulse pressure (an ⇡ in the difference between systolic and diastolic pressures
over time)
🚒 neurologic emergency
 Stage 4: Herniation = imminent death if not corrected

Measurement of ICP:
 Guides clinical care
Indications
 Glasgow Coma Scale of ≤8
 Severe Head Injury ---- GCS score of 8 < 8 intubate
 Moderate Head Injury ---- GCS score of 9 to 12
 Mild Head Injury ---- GCS score of 13 to 15
 Abnormal CT scans or MRI

Monitor site and measurement of ICP:

Ventriculostomy (“gold standard”) ⇢ gold standard
 Catheter inserted into lateral ventricle

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  Coupled with an external transducer
Fiberoptic catheter
 Sensor transducer located within the catheter tip

Subarachnoid bolt or screw

 Between arachnoid membrane and cerebral cortex

Cerebral Edema
 ↑ Extravascular fluid (water content) in brain increase in tissue volume that can increase
ICP
 Variety of causes
Three types of cerebral edema (NEURO ASSESSMENT)
 Vasogenic: white matter (tumor absence), HA, change of LOC
 Cytotoxic: lesion, trauma-cerebral hypoxia → SIADH
 Interstitial: Hydrocephalic ⇢ excess cerebral fluid, shunting
Clinical Manifestations
 Change in LOC ⇢ restless, confused, prob responding to question
 Flattening of affect → coma
 Change in vital signs ⇢ Cheyne stokes, ↓ RR & irregular, hyperventilating
 Cushing’s triad
 Change in body temperature → labial, High or low
Ocular signs
Compression of oculomotor nerve
 Unilateral pupil dilation
 Sluggish or no response to light
 Inability to move eye upward
 Eyelid ptosis
Other cranial nerves
 Diplopia, blurred vision, EOM changes
Headache
 Often continuous
 Worse in the morning
Vomiting
 Not preceded by nausea
 Projectile
↓ in motor function
 Hemiparesis/hemiplegia
 Posturing (2 typess)

Decerebrate posturing (Extensor) E=extend the arms

 Indicates more serious damage

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Decorticate posturing (flexor)
 Flexion “to the core” (AMS TO THE CORE)

Early signs of ICP: Late Signs of ICP:

 Changes in LOC ⇢Restlessness, Respiratory and vasomotor changes
confusion, ↑ drowsiness, ↑  VS: Cushing’s triad: bradycardia,
respiratory effort, purposeless hypertension, bradypnea
movements  Projectile vomiting = ICP
 Pupillary changes and impaired ocular  Further deterioration of LOC; stupor
movements to coma
 Weakness in one extremity or one  Hemiplegia, decortication,
side decerebration, or flaccidity
 Headache—constant, increasing in  Respiratory pattern alterations
intensity or aggravated by movement including Cheyne-Stokes breathing
or straining and arrest
 Loss of brainstem reflexes—pupil,
gag, corneal, and swallowing

CHILDREN signs OF ICP:

 HA, N/V, dizziness, sun setting eye effect

Infant:
 Irritability, SHRILL cry, sensitive to light
Late same as adults
MEDICATIONS:
 Mannitol (Osmitrol) ⇢ Monitor F & E, listen to lungs for rales
 Plasma expansion
 Osmotic effect
 Monitor fluid and electrolyte status.
 Concurrent antacids, H2 receptor blockers, proton pump inhibitors ⇢ prevent stress ulcer
 Anti-seizure medications

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  Antipyretics ⇢ fever
 Sedatives
 Analgesics
 Barbiturates
Hypertonic saline
 Moves water out of cells and into blood.
 Monitor BP and serum sodium levels
Corticosteroids (not recommended for general traumatic head injury)
 Vasogenic edema → tumor abscess
 Monitor fluid intake, serum sodium and glucose levels.
Nutritional Therapy
 Hypermetabolic and hypercatabolic state ↑ need for glucose (metabolism)
 Enteral or parenteral nutrition
 Early feeding (within 3 days of injury)
 Keep patient normovolemic. Important!
 IV 0.9% NaCl preferred over D5W or 0.45% NaCl
Subjective data
 Level of consciousness (LOC)
 Glasgow Coma Scale
 Eye opening
 Best verbal response
 Best motor response
 Pupillary Check for Size and Response
Cranial nerves
 Eye movements
 Corneal reflex
 Oculocephalic reflex (doll’s eye reflex)
 Oculovestibular (caloric stimulation)

Motor strength
 Squeeze hands
 Palmar drift test
 Raise foot off bed or bend knees
Motor response
 Spontaneous or to pain
Vital signs
 Abnormal Respiratory Patterns of Coma
1324 lewis

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Planning:
Maintain:
 Patent airway
 Normal ICP 5-15
 Normal F & E/Normal nutrition balance
 Prevent complications
Interventions:
Respiratory function:
 Tongue fall back = occlusion
 Suctioning: < 10 sec b/c ↑ ICP
F & E:
 Accurate I & O critical
 Diabetic insipidus or
 ISIDH = hyponatremia
Monitoring ICP:
⇡ ICP=
 Valsalva maneuver
 Cough
 Sneezing
 Suctioning → stimulates cough
 NG TUBE – abdominal distention = ↑ ICP
 Hypoxia
 Arousal from deep sleep
Body position:
 Neutral (midline position)
 30 degrees only
 Turn pt q2 hours → turn gently and slowly
 Avoid hip flexion
Protect from injury:
 Restless, irritable, got off ventilator coma= confusion → pad rails
 Psychosocial consideration:
 Waking up state of coma or unconscious= anger, confused → allow family to participate
Traumatic Brain Injury (TBI) with Intracranial bleeding

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Subdural hematoma (between dura matter and Epidural hematoma (between skull and dura
arachnoid layer) matter) →arterial bleed
 Injury to brain tissue and blood  From rupture of meningeal artery;
vessels medical emergency
 Typically, from vessels that drain from  Initial period of unconsciousness
the surface of the brain into sagittal brief lucid interval then followed by
sinus decreased in LOC
 Most often venous in nature.... Treatment:
therefore, slow to develop Rapid surgical intervention to drain hematoma
 Arterial cause would develop more and prevent herniation
rapidly  A lot do not survive
 Acute, subacute, and chronic
 Acute: manifest within 24-48 hrs.; s/s
similar to increased ICP
 Sub-acute: manifest within 48 hrs. to
2 weeks; s/s similar to acute subdural
hematoma
Treatment:
 Craniotomy to drain and/or remove
blood clot
 Mortality rate high for both
secondary to associated brain damage
Chronic
 Typically, in elderly
 Injury to manifestations can be
3weeks to months!
 Often mistaken for stroke

Treatment: same-evacuation of the clot

Skull Fracture:

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Such fractures can cause tears in the membranes surrounding the brain, or meninges with resultant
leakage of the CSF.
 Fluid may accumulate in the middle ear space and dribble out through a perforated eardrum
(CSF otorrhea) or into the nasopharynx via the eustachian tube, causing a salty taste. =RED
FLAG → TEST FOR gluscos
 Check ears/nose for clear drainage=CSF

CSF may also drip from the nose (CSF rhinorrhea) in fractures of the anterior skull base, yielding a halo
sign. HALO=CSF

Raccoon eyes/Battle’s sign

INTRACRANIAL SURGERY
 Craniotomy: opening of the skull (bone flap is returned)
Purposes: remove tumor, relieve elevated ICP, evacuate a blood clot, control hemorrhage
 Craniectomy: excision (removal) of portion of skull (bone flap is not returned)
 Cranioplasty: repair of cranial defect using a plastic or metal plate
 Burr holes: for exploration or diagnosis, to provide access to ventricles or for shunting
procedures, to aspirate a hematoma or abscess, or to make a bone flap

CUSHINGS TRIAD= BRAIN BEING AFECTED, ↑B/P, ↑HR, ↓RR

Preoperative Care: Medical Management

Medications
 Anticonvulsants
 Corticosteroids → tumors/abscess
 Osmolar diuretics (Mannitol)
 Antibiotics
 Diazepam

 Obtain baseline neurologic assessment

 Assess patient and family understanding of and preparation for surgery → consent signed

Postoperative Care
 Patient in ICU

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Postoperative goals:
 detecting and reducing cerebral edema
 relieving pain
 preventing seizures
 monitoring ICP and neurologic status.
The patient may be intubated and have arterial and central venous lines.

Brain Death (ADVOCACY)

Determination of Death Act: determination of brain death; certain test conducted b/fore considered brain death
Presumptive signs of death:
 Unresponsive
 No respirations
 No pulse
 Pupils fixed and dilated
 Body temp indicates hypothermia; skin cold with generalized cyanosis
Conclusive signs of death:
 Livor mortis (venous pooling of blood in dependent body parts causing purple discoloration of
the skin).
 Decapitation (separation from head to body)
 Decomposition ((decay or putrification of the body)
 Rigor mortis (stiffness of the limbs and body that develops 2 - 4 hours after death and may take
up to 12 hours to fully develop).
*LVN may not accept an order that would require the LVN to “pronounce death,
*The law requires that in order for a registered nurse to pronounce death, the facility must have a
written policy that is jointly developed and approved by the medical staff or medical consultant and the
nursing staff, specifying under what circumstances a RN can make a pronouncement of death.

Assessment (3) criteria that must be present for declaring brain death
1. Coma
a. Establish absence of cerebral function
b. Determine that patient is comatose or unresponsive (no cerebral motor response to
pain)
2. Absence of brain stem reflexes
a. No response to bright light in either eye
b. Ocular movements (review handout provided in class)
i. Oculocephalic response is tested (Doll’s eyes- see handout) CN 3, 6, 8
ii. Oculovestibular reflex is tested (see handout) CN 3, 6, 8
iii. Absence of corneal reflex CN 5 & 7
iv. Absence of facial movement to a noxious stimulus
v. Absence of pharyngeal and tracheal reflexes (gag & cough) CN 9 & 10
c. Apnea (done via apnea testing procedures)

Oculocephalic response (dolls eyes) CN III, Oculovestibular reflex CN III, VI, VIII
VI, VIII

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 Absence of corneal reflex CN V & V11 Absence of pharyngeal& tracheal reflexes
CN 9 & 10

Apnea testing

ORGAN DONATION: → becomes a FULL CODE

 Organs that can be donated:
 Kidney, liver, heart, pancreas, intestines, cornea, heart valves, skin bone tendons, cord blood
stem cell, blood, platelets, hands/faces
 Restrictive:
 Active cancer, systemic infection

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ANTISEIZURE MEDS:
carbamazepine:
 Dizziness, drowsiness, blurred vision, double vision, nausea, SKIN RASH, avoid
pregnancy
clonazepam/klonopin:(po, IV)
 Drowsiness, sleepy, fatigue, behavior changes, liver issue, renal failure, suicidal ideation
 Wear med bracelet
 Monitor CBC
diazepam/valium: (sedative) → oral/IV (5-10)
 status epilepticus (not prolonged/daily use; stops Seizure
 Drowsiness, sleepy, fatigue, HYPOTENSION, tachycardia
 Monitor RR
ethosuximide/Zarontin:
 Absent seizure
 Appetite loss → monitor albumin, nausea, HA, dizziness, fatigue, RASH
levetiracetam/Keppra: antiepilectic (TR: 12.0-16.0)
 Combination w/other
 IV, dilute
 Loss of appetite, HA, behavioral changes, irritability, fatigue, dizziness, not driving
 Wear med bracelet
phenobarbitual:
 Drowsiness, irritability, hyperactivity (children), depression, behavior problems, anemia
→ CBC, GI/N/V,
 ↓ ca+
 No alcohol, addictive (take as prescribe)
phenotoin/Dilantin: partial/generalize
 Therapeutic blood level 10-20; < 10= seizure
 Lots of drug interactions
 RASH, SEVERE BLISTER (STEVENS JOHHSON)
 Gum overgrowth → see dentist regularly
 Hairless, insomnia, fatigue, N/
valproic acid/ Kepakene:
 Upset stomache
 Altered bleeding time
 Liver toxicity
 Hair loss
 Weight loss
 Tremors

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Frontal lobe  responsible for verbal EXPRESSION of thoughts
Occipital lobe  vision
Temporal lobe  understanding speech
Limbic  memory and learning

In decorticate rigidity, the upper extremities (arms, wrists, and fingers) are flexed with
adduction of the arms. The lower extremities are extended with internal rotation and
plantar flexion. Decorticate rigidity indicates a hemispheric lesion of the cerebral cortex.

The hypothalamus is responsible for autonomic nervous system functions, such as heart
rate, blood pressure, temperature, and fluid and electrolyte balance (among others).

The 3 categories included are eye opening, best verbal response, and best motor
response

Mannitol is an osmotic diuretic that induces diuresis by raising the osmotic pressure of
glomerular filtrate, thereby inhibiting tubular reabsorption of water and solutes. It is
used to reduce intracranial pressure in the client with head trauma.

Valporic Acid  Gastrointestinal effects from valproic acid are common and typically
mild, but hepatotoxicity, although rare, is serious. To minimize the risk of fatal liver
injury, liver function is evaluated before initiation of treatment and periodically
thereafter. The other options are unrelated to the use of this medication.

Amantadine is an antiparkinson agent that potentiates the action of dopamine in the

central nervous system. The expected effect of therapy is a decrease in akinesia and
rigidity. Leukopenia, urinary retention, and hypotension are all side and adverse effects
of the medication.

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Phenytoin  Phenytoin is an anticonvulsant that can cause gingival hyperplasia, as well
as bleeding, swelling, and tenderness of the gums. The client should use good oral
hygiene and gum massage and have regular dental checkups. Alcohol interferes with
the absorption of phenytoin, so it should be avoided. Change in the color of the urine is
a normal reaction. A sore throat, fever, glandular swelling, or any skin reaction
indicates hematological toxicity and needs to be reported.

Manifestations of secondary injury includes hypoxia, ischemia, hypotension, and

increased ICP that follows primary injury.

Lumbar puncture position is fetal

An altered level of consciousness is an early sign of increased intracranial pressure

(ICP). Late signs of increased ICP include tachycardia leading to bradycardia, apnea,
systolic hypertension, widening pulse pressure, and posturing.

Absence seizures are very brief episodes of altered awareness. There is no muscle
activity except eyelid fluttering or twitching. The child has a blank facial expression.
These seizures last only 5 to 10 seconds but may occur one after another several times
a day. The child experiencing absence seizures may appear to be daydreaming. If the
child is participating in group activities, they sometimes need help catching up with the
group, especially if a seizure occurs. Decreasing grades is a sign of absence seizures, as
well as lowered intellectual processes.

Decerebrate (extension) posturing is an abnormal extension of the upper extremities,

with internal rotation of the upper arm and wrist and extension of the lower extremities
with some internal rotation. Decorticate posturing involves flexion of the upper
extremities and extension of the lower extremities. 

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