MANAGEMENT OF PX WITH NEUROLOGIC Toxicologic

DYSFUNCTION
- Drug overdose, ETOH intoxication
 Aletered LOC
Metabolic
 Inc ICP
 Intracranial sx - Hepatic/ renal failure, diabetic
 Seizure disorders ketoacidosis
 Headache - Metab waste cannot excrete

ALTERED LOC Assessment & diagnostic findings. Altered LOC:

- Not oriented, does not follow - GCS, neuro check & assessment
commands/ needs persistent stimuli to - CT scan, MRI
maintain state of alertness - Labs:
- Less responsive to/ less aware of o Glucose
environmental stimuli o Electrolytes
o Ammonia
ASSESSMENT OF LOC
o BUN
Level I – alert o ABG
o Drug levels
II- Lethargy (delirium, confused state)
o Alcohol/ ETOH
III- Stupor
GCS SCALE
IV- Coma (gcs = 7-3)

 Level or responsiveness + consciousness

(important gauge)

Coma

- Prolonged state of unconsciousness

- Not responsive

Akinetic mutism

- Unresponsiveness to env; no
movement/sound but @ times opens
eyes Pathophysiology of altered LOC

Persistent vegetative state  Causes of altered LOC

- Wakeful but no conscious content, no
cognitive functioning/ affective function
- Cannot carry conversation, cannot talk
Causes of Altered LOC
Neurologic
- Head injury, CVA
  EDEMA , pressure up / decrease in
blood/ CSF
  Disruption in neuron /
neurotransmitter functioning
 Disruptions in anatomic structures
  faulty impulse transmission
  impede communication within brain/
brain to other parts of body
   s/s
Complications : + Mgt
 Resp failure (brainstem affected)-
intubate
o Aspiration/pneumonia happens
o We intubate the px,
nebulization, antbx if with
infection
o Pneumonia – strict aspiration
precaution, elevate HOB
 Immobility
o Pressure ulcers (Vit C & zinc for
wound healing), venous stasis
(host, stockings, foot pumps,
ankle flexion exercises, SCD),
MS deterioration, disturbed GI
functions - paralytic, aspirations
o Every 1-3 days, bowel , inc fiber
if not CI, inc fluids if not CI
o Aspiration – precautions, take
in by mouth should sit up 90
deg during before & 45 min
after ; chin tuck and double
swallow like for stroke/
paralysis
MGT of altered LOC
 Patent airway
o Suction PRN
o No deep suctioning may induce
vagal stimulation
May down LOC
 Oral care
o Toothete (any liquid is being
suctioned)
o 3-4x a day oral care
Easy to have fungal infection
yung px
 Eye care (corneal integrity)
o Artificial tears (gentil eyedrops),
eye patches (alternating)
o Px may have infx, always open
ang eyes
 Circulatory status (BP, PR)
 Hydration (IVF, TF)
 Skin care
o Skin barrier on the genital area
o pericare
o Petroleum jelly
o Px may have incontinence
 Fall & safety precautions
o Raise side rails
 Nutritional support (TPN, TF)
o IV nutrition
 Provide sensory stimulation (reality
reorientation, pictures)
o Pic of immediate family
 Precautions: fall & safety, skin,
aspiration
 DVT precautions
 Bowel, bladder programs
o Laxatives
o Make sure voiding every 4 hrs
and not beyond that to prevent
urinary retention, infection
o Palpate bladder
o Bladder scan, ICP, condom cath
o 150 ml or more urinary
retention; in and out
catheterization
 Determine & treat causes
 Prevent complications
 Deconditioning
o If not moving, pathologic fx
o Muscles – weak
o So do ROM exercises several
times a day
 Padded side rails, restraint free as much
as possible (socks sa hands/mittens)
INC ICP
Causes:
- Trauma, hemorrhage, tumors,
hydrocephalus, edema or inflammation,
 infx, S/P brain sx, CVA, TRAUMATIC
brain injury (head trauma and
personality changed)
Intracranial contents:
- Brain tissue 1400 gm
- Blood 75 ml
- CSF 75 ml
- Any deviation in the number affects ICP
Normal ICP : 10-20 mm Hg
INCREASED ICP
- Pressure exerted by cranium on brain
ICP PATHOPHYSIOLOGY
tissue, CSF, brain’s circulating blood
volume
Compensatory mechanism by the brain:
(Monro- Kellie Hypothesis)
 Displacing / shifting CSF
 Decreasing cerebral blood flow/ volume
 Up or diminishing CSF absorption
INCREASED ICP
Leads to : (+) compensation
 Dec cerebral blood flow
o Stimulation of vasomotor
 Up blood flow
o Up paCO2
 Vasodilation  up blood flow
 Cerebral edema
o Dec production & flow of CSF
o Auto regulation mechanism
 ABILITY of the body to Change
diameter of blood vessels
 control blood flow
 Cerebral response to up ICP
o Cerebral perfusion rate
 Maintain steady perfusion pressure
o Movement of blood is
dependent on the pressure
o When arterial SBP 110-140
mmHg & ICP is less 40 mmHg
o Cerebral perfusion pressure
( CPP) = arterial pressure minus
ICP
o Normal cerebral perfusion
pressure CPP : 70 -100 mmHg
o CPP: less 50 mm Hg
 Irreversible brain
damage (ischemia &
necrosis happen)
o If ICP = arterial SBP
 Cerebral circulation
ceases
 UP ICP
 Attempt at normal ICP
regulation
 Slight up in cerebral perfusion
pressure (so blood flow in)
 If ICP remains high (dec LOC,
headache): loss of auto
regulatory mechanism
 Cerebral vasodilation
 Up blood flow; decreased
venous outflow
 Venous congestion = further up
in ICP
 Cellular hypoxia >= cushing’s
response (stimulate vasomotor)
 Cerebral ischemia (up SBP, slow
bounding HR, widening PP)
Cerebral infarction (HTN, Dec
RR, HR < CUSHING’S TRIAD > ) =
brain death
(brain herniation already happen)
Assessment angiography
- Cerebral angiography
- Ct scan/ MRI/ pet/ spect
- Transdoppler studies
o Cerebral blood record X
 - Evoked potential studies
LP is avoided to inc ICP
- May release pressure if punctured, may
induce brain herniation (movement of
brain tissue)
Early signs of inc ICP
 Disorientation, restlessness, confusion
 Pupillary changes, impaired extraocular
movements (CN oculomotor, optic)
 Unilateral body weakness
 Constant worsening headache
o Worse with movement,
straining
Late signs:
 Deteriorating LOC
 Dec / erratic HR, RR, widening PP
(cushing triad)
 Up BP, up temp
 Projectile vomiting
 Decorticate/ decerebrate positioning
 Loss brain stem reflexes
o Pupillary, gag, swallowing
Complications of inc ICP
 Brain stem herniation
 Diabetes insipidus
o DEC antidiuretic hormone
(Vasopressin) (pituitary gland)
o Excess diluted urine output
 SIADH
o Up secretion of ADH
o Fluid overload, hypoNa
MGT
 Elevate HOB 15-30 deg ; avoid
trendelenburg
 Keep head in neutral position (cervical
collar to maintain this position)
- if u move the head dec blood supply to
the brain –> (hypothesis) will try to inc
blood flow to the brain -> inc icp
 Avoid flexion/ rotation of neck; avoid
flexion more 60 deg
o Up intra ABD , up intrathoracic
pressure
 Restrict fluids
 Monitor VS, electrolyte balance, neuro
status
 Keep environment quiet
 Schedule procedures to coincide with
sedation  cluster care
o Anticonvulsant 30 min prior
 IV access gauge 18-19, ICP monitoring
 Maintain oxygenation
 Reduce metabolic demands
o Sedatives
 Avoid straining, coughing
 Inc fluids
 Avoid Valsalva maneuver
o Stool softeners + high fiber diet
 Ventricular drainage of CSF
o VP shunt
 Medication
o Sedatives/barbiturates,
osmotic/ loop diuretics,
corticosteroids
o Anticonvulsants
 Hyperventilation ( vasoconstriction)
with mechanical ventilator
o Maintain paCO2 at 35-45 mm
Hg
 Control fever, prevent shivering
 Maintain BP, O2
 Limit fluids
 Prevent infection (meningitis)
 Avoid isometric exercises
 Accurate I & O (foley cath)
Mgt for Inc ICP
  Surgery  Transphenoidal
o VP shunt - Incision beneath upper lip into nasal
o Craniotomy cavity
o Craniectomy
Pre op:
 Used post-supratentorial approach
craniotomy - Diagnostic test
o Tentorium = folds of dura - Fluid restriction
matter - NPO, written consent, clearances
 Halo sign or ring sign - Meds
o Csf leak, bleeding o Hyperosmotic (Mannitol) +
o Let the fluid drop in 4x 4 if may diuretic (furosemide)
red in the middle and less red o IV antibx
arround – we have csf leak o Antiseizure meds (phenytoin
 Check drainage for glucose (CSF <Dilantin> / fosphenytoin <
leakage) cerebyx>)
 Use aseptic tech in cleaning post-op o Diazepam (antianxiety)
wound o Corticosteroids
(dexamethasone)
Site for ICP Monitor Implant
o Mannitol – warm first with
- Reading position: towel
Supine, manometer 1 inch above ear
Post op:

INTRACRANIAL SX - Maintain airway, VS monitoring , neuro

check
Craniotomy
- Cerebral edema peak 24-36 hrs post op
Indications: - Increased ICP mgt & prevention
 Tumor removal - Log rolling; skin care
 Relieve up ICP - Regulate temp
 Blood clot evacuation - Monitor for complications
 Control bleeding - Jackson pratt @ + pressure
o First few days after sx , if u
pinch it, there will be sudden
Intracranial Sx Incision outflow of drainage and sudden
down of ICP and can induce
Tentorium = infolding of dura , forms tough brain herniation
membrane shelf o So not in neg pressure
 Supratentorial - If anterior fossa incision (supratentorial)
- Above tentorium; incision above o Position on back/ side with 30
hairline degrees HOB as ordered by
 Infratentorial neurosurgeon
- Below tentorium, brain stem - If infratentorial incision = position on
- Incision @nape of neck / around side depending on neurosx
occiput
 - If transphenoidal approach = HOB - Genetic/ developmental defects
raised; nasal packing maintained ( si - No known cause
surgeon ang kukuha)  Secondary/ acquired seizure
- Hypoxemia (HI, HTN, CNS infections)
Complications Intracranial SX
- Metabolic & toxic conditions (RF,
Immediate : hypoglycemia, hypoCa, hypoNa)
- Brain tumor, drug & ETOH withdrawal ,
 Up ICP ( 24-36 hrs) allergies
 Bleeding
 Hypovolemic shock PATHOPHYSIOLOGY
 Altered fluid & electrolyte balance  Electrical disturbance within nerve cells
 Infection (cephalasphorine, ceftriaxone   nerve cells emit abnormal, recurring,
– can pass bbb) uncontrolled electrical discharges
 Seizures   excessive neuronal discharge
o Gaba agonist  Leads to s/s of seizure:
o Phenytoin o Loss of consciousness
Do not use tongue depressor = may break o Excess movement/ loss of
muscle tone / movement
Late complications: o Disturbances in behavior,
 DVT/PE mood, sensation & perception
o Blood thinners/ SCD Seizures : 3 phases + Mgt
 Pulmonary infx/ UTI
 Pressure ulcers Prodromal / preictal phase

- Produces aura (sensory signals)

SEIZURE DISORDERS: - Flash of light, mood or behavior
changes, sudden sensation of smell or
Definitions: taste
Epilepsy - They know na magkakaseizure na sila/
yung aura kasi
- Collection of diff syndrome - Side lying position
characterized by seizures
Ictal phase
Seizure
- Seizure itself
- Excessive electrical discharge of energy - Amnesia, confusion, inability to be
from nerve cells in brain aroused, sleepiness
- Let the seizure happen , do not restrain,
Convulsion
do not take VS
- Tonic –clonic muscular reaction to - Do not do anything, just make sure put
excessive electrical energy arising from an oral airway before seizure, place to
nerve cells in brain side
- But if seizure is happening, do not place
CAUSES:
na
 Primary seizure idiopathic
 - Time the seizure, document, duration, o Jerking, may bite tongue /
lost of consciousness, eye inside cheeks
- Monitor for VS, any recurrence  Absence seizure / petit mal
- Brief (3-5 sec) abrupt loss of
consciousness
Postictal  Myoclonic seizures
- Short, sporadic muscle contractions last
- After seizures
several minutes
- Amnesia, confusion, inability to be
 Febrile seizure
aroused, sleepiness
- 2ndary high fevers + convulsions
- Don’t reappear
 Status epilepticus (“E”)
DX TESTS:
- Seizure rapidly recur again and again
- Ct scan, mri, eeg, pet, cerebral - Most dangerous
- Cerebral Angiography, medical HX & - Longer
neuro exam - Phenytoin
- LP to rule out infectious cause
(meningitis)
- Blood labs
o Electrolytes, chemistry profile
Parial seizures / Focal
Classification of Seizures
 Simple
 Generalized seizure: affects 1 side of - Single muscle contraction or sensory
brain & both hemispheres alteration
- Tonic- clonic (grand mal)  Complex
- Absence seizures (petit mal blank - Complex sensory changes
space) o Hallucination, personality
- Myoclonic seizure changes
- Febrile o Loss of consciousness, loss
- Status social inhibitions
 Partial seizures (local or focal): affects 1 - Motor changes
side of brain but do not spread o Loss of b/b functions, chewing
throughout entire= motions, etc

Precautions:
GENERALIZED SEIZURES
 Tonic clonic / grand mal seizures
- Tonic clonic muscle contraction
- Loss of consciousness
- Recovery period (confusion +
exhaustion)
o Tonic = muscle contraction,
stiffening, loss of b/b functions
o Clonic = follow tonic phase;
quick succession of muscle
 Padded side rails
 Disposable oral airway @bedside
 Dec stimulation (dim light), quiet
environment
 Saline lock (IV access)
 Suction , O2, airway @ bedside
 No padded tongue depressor @
bedside
During seizure:
 Note time, duration of seizure
 If patient standing, place on floor
- Protect head, body
 Protect patient during seizure
 Maintain patent airway
 Don’t insert tongue blade during active
seizure
 Do not restrain, loosen tight clothing
 Turn to side
After the seizure:
 Monitor VS, neuro check neuro check
 Document observations
 Keep on side
 Administer O2 PRN; prepare to suction,
monitor for incontinence
 Provide rest, sleep
 Document seizures/ recurrences
Anticonvulsant therapy
- Importance of adherence to
maintaining serum levels
- Status epilepticus may occur if suddenly
stopped med
- Avoid alcohol, nicotime
Drug TX for grand mal seizures
 Stabilize overexcited nerve membranes
& or up effects of GABA
 Kinds:
o Hydantoins
o Barbiturates & barbiturate –
like drugs
o Benzodiazepines
TX for grand mal seizures: Hydantoins
Less toxic; hepatotoxic; highly CHON bound
 Phenytoin (Dilantin)
o IV oral; 10-20 mcg/ml
 Fosphenytoin (cerebyx) anticonvulsant
o Short term TX Status epilepticus
o s/p neurosx
o peak levels 10-20 mins
 Mephenytoin (Mesantoin)
- Severe liver toxicity
Adverse effects:
- Gingival hyperplasia
- CNS depression, liver toxicity
- Bone marrow suppression
- Cardia arrhythmias, BP changes
- Urinary retention, libido changes
- Hyperglycemia (long term use)
NURSING CONSIDERATIONS: Hydantoins
 Oral care = use soft bristled toothbrush
 IV route:
- Not mix woth D5%W; only with NSS
- Check VS
- Avoid give IVP into veins @back
hand ,may cause permanent
discoloration
- Phenytoin : only slow IVP
  Avoid IM route if possible
 Monitor CBC, serum phenytoin (may
cause immunosuppression, anemia, low
cbc)
 Fall & safety precautions
 Alert: sound alike, look alike meds
o Celebrex (celecoxib), cerebyx
(fosphenytoin)
Drug TX for grand mal seizures: Valproic Acid
- GABA agonist
- A/E: hepatoxic, pancreatitis
Drug TX for grand mal seizures: Valproate
Sodium
 Valproate Na, Divalproex Na (Depakote)
- GABA agonist (uses: mania, Seizure)
- A/E: hepatoxic, pancreatitis
- Depakote sprinkles
Drug TX for petit mal seizures: Succinimides
Suppress abnormal brain electrical activity, up
effects of GABA
Examples:
- Ethosuximide (Zarontin)
- Methsuximide (Celontin)
 Do not abruptly stop medication
o Causes status epilepticus
Management for seizures:
 Avoid oral thermometers
 Seizure precaution
o Raise side rails
o Plastic oral airway at bedside
o Salinelock, IV access
o Suction, O2,
o No padded
 Fall, safety precaution
Emergency condition
Status epilepticus
- Series of generalized seizures that occur
without full recovery of consciousness
bet attacks
- Prolonged >5 mins or repeated seizures
> 30 min
- Cerebyx (fosphenytoin)
 Converts to phenytoin in body
 150 mg fosphenytoin = 100 mg
phenytoin
 Can deliver 100-150 mg/min IVPB
 Diazepam, lorazepam

Drug-drug interactions: Causes Status Epilepticus

- Primidone (mysoline) - Sudden withdrawal from antiepileptic

o Decreased effect of this drug drugs
- Infx
- Acute ETOH withdrawal
- HI
Patient teaching: anticonvulsant
- Cerebral edema
 Take prescribed dosage to maintain
blood levels
 Consult doc if unable to take meds HEADACHES / CEPHALGIA
because of illness
Kinds:
 Observe for side effects, adverse
reactions Primary
 Notify doctor if seizure is not controlled
- No organic cause
 Don’t take over the counter drugs
o Migraine
 Wear medic-alert bracelet
 o Cluster - NSAIDS (diclofenac, naproxen)
o Tension
Cluster Headache
Secondary
- After waking up
With organic cause (brain tumor/ aneurysm) - Histamine cephalalgia
- 20 yrs (men); 50 yrs (women
- Pain unilateral, oculotemporal/
MIGRAINE HEADACHE oculofrontal ; non throbbing,
excoriating
 Unilateral, frontotemporal, throbbing - Pain intense in/ around eye
pain behind eye/ear with sensitive - Pain q 8-12 hrs for 24 hrs for 6-8 wks
scalp, photophobia, n/v, anorexia (cluster)
 Last for hours-days - Cause unknown: hypotahalamus
 May have aura (sensory signals) hyperacticity
Pathophysio: - Severe form vascular headache
 Onset during relaxation, nap, REM
 Triggering event  arterial vasospasm sleep
 dec cerebral blood flow  Headache:
  rebound vasodilation o Ipsilateral
o Rhinorrhea (runny nose)
Triggering factors:
o Ptosis
 Menstrual cycle/ menopause/ o Miosis (pupil constriction)
pregnancy  Mgt:
 Bright lights Same as migraine
 Depression
Tension headache
 Sleep deprivation
 Stress  Neck, shoulder muscle ache + bilateral
 Fatigue pain @base of skull, forehead
 Tyramine foods  Skeletal muscle tension by physical/
- (ETOH, aged cheese, caffeine, yeast, emotional stress
nuts, artificial sweeteners-aspartame_  May occur:
 Meds (Tagamet, Nitroglycerin,  n/v, photophobia, activity aggravates
estrogen) pain
 Foods – MSG, overuse of caffeine  Mgt:

Analgesics (Tylenol, ASA), muscle relaxants

Migraine Headache TX:

Drug therapy MANAGEMENT OF PATIENTS WITH CVA

- Ergotamine prep Brain attack or CVA Cerebrovascular accident
- Triptans
o Imitrex (Sumatriptan)  Destruction of brain cells due to sudden
o Zomig (Zolmitriptan) dec in cerebral blood flow
- Analgesic (asa, acetaminophen)
  Cerebral anoxia lasting than 10 mins
causes cerebral infarction with
irreversible damage
 Diagnosis:
 CT scan, MRI, LP, Doppler flow studies,
EEG, cerebral arteriography
Types:
Ischemic
- Thrombotic (atherosclerotic clot)
o Accounts for more than 50 %
o Common carotid art, vertebral
basilar junction (site)
- Embolic (blood clot)
o Middle cerebral artery (site)
Hemorrhagic
- Bleeding
- Blood vessel has ruptured secondary to
aneurysm (circle of willis)
- In deep coma already
- Sudden onset
Stroke continuum: Time course classification
 TIA (“silent stroke”)
o Sudden loss of motor, sensory,
visual functions
o Few sec-mins less than 24 hrs
 Reversible Ischemic Neuro Deficit
o More pronounced than TIA,
more than 24 hrs
o Resolves in few days with no
neuro deficit
 Stroke in evolution
o Worsening neuro s/s over
several mins – hrs
o Progressing stroke
 Completed stroke
o Stabilized neuro s/s
- TIA ( only one with warning)
Neuro deficits of Stroke
Visual
 Hemianopsia (loss ½ visual field)
 Peripheral vision loss
 Diplopia (double vision)
Motor
 Hemiparesis (weakness)
 Hemiplegia (paralysis)
 Ataxia (unsteady gait)
 Dysarthria (word forming)
 Dysphagia
Sensory
 Paresthesia
Verbal
 Expressive aphasia
 Receptive aphasia
 Global (mixed) aphasia
Cognitive
 Short & long term memory loss
 Decreased attention span
 Impaired concentration
 Altered judgmental/ abstract reasoning
Emotional
 Loss of self control
 Emotional lability
  Dec tolerance to stress o improves neurologic
 Depression functioning for thrombotic
 Fear, hostility, anger (grieving stage) stroke
 Feelings of isolation o dissolves existing clot
o risk for bleeding
COMPARISON OF LEFT AND RIGH HEMISPHERIC
 PT, OT consults
STROKES
o To maintain muscle, joint
Left Hemispheric Stroke function
 ST consult (SLP)
1. Paralysis of R side of body
o Aphasia, swallowing problems
2. Right visual field defects
3. Aphasia
4. Altered intellectual activity
CVA NURSING INTERVENTIONS
5. Slow cautious behavior
6. Nice and afraid to fall  Provide emergency care; administer O2
7. Slurred speech, always want to follow  Patent airway, suction PRN
Right Hemispheric Stroke  Bedrest to prevent re-bleeding
o Common in 1st 2 weeks
1. Paralysis of left side of the body  Position px to prevent contractures;
2. Left visual field defects turn every 2 hours
3. Spatial-perceptual deficit  Speak slowly & simply; establish form of
4. Inc distractibility communication (expressive/ receptive
5. Impulsive behavior & poor judgment aphasia)
6. Lack of awareness of deficits  Monitor for increasing ICP
7. Always shouting, wants to get out of o 1st 72 hrs of stroke
bed  Monitor VS; assess LOC & neurologic
CVA Treatment status ; I & O
 Nutritional support
 Carotid endarterectomy (thrombotic)  Bowel & bladder programs
o Removal of the affected area  Teach the use of assistive devices
o Atherosclerotic plaque removal  Fall & safety precautions
 Surgical evacuation of clot or
hematoma (embolic)
 Anticoagulants
o For non-hemorrhagic strokes
o Enoxaparin Na
o Heparin
o Warfarin Na
 Anticonvulsants, diuretics, anti HTN,
analgesics
 Thrombolytic IV tx: (embolic)
o tPa (Tissue Plasminogen
Activator)