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which two major pathways result in brain damage
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ischemia consists of which two categories
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causes of brain damage
- ischemia from heart attach, cardiac arrest
- head trauma - concussions, hematoma
- infection - encephalitis [infection of the brain]
- brain tumor
- stoke, brain attack, or CVA
- hypoxia from drug use, rsp arrest
- seizures
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global brain injury Tx
- oxygen and perfusion
- cooling to dec. metabolic needs
- blood sugar control
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during recovery from a global brain injury, damage can occur from
- exitatory amino acids and calcium cascade - these are changes once the crisis has passed and the brain tissue is trying to get bac kto normal
- brain swelling - vasogenic and cytotoxic
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manifestations of diffuse/global brain injury
- stepwise, it goes from rostral to caudal
- first - LOC
- pupillary changes - tells us which side is affected
- oculomotor response - the way your eyes move around in your head
- motor response - hand grip test
- patterns of breathing, circulation
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your most important assessment is ?
LOC
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Level of consciousness
- alert
- confusion and disorientation
- delirium
- obstundation - pt. is really sleepy but your able to wake them up
- stupor - barely waking up
- coma
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pupillary changes
indicated the presence and level of brain stem dysfunction
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oculomotor response
- eye movement
- nystagmus - uncontrolled side to side rapid movement of the eyes
- doll's eyes - eyes are fixed, and moves away from the direction your're turning their head in
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motor response
- can tell you the level of brain dysfunction
- determines most severely damaged side
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decorticate posturing
sign of Brain injury, a lot of pressure on the brainstem. Their in a coma and will spontaneously develop this flexed position where their arms and hands are pulled in, their feet is fanned out and knees turned inward
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decerebrate posturing
lower level injury within the brain. Hyperextension where the arms and hands are turned out, feet are flexed downward. Can happen before the person is going to die
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patterns of breathing
Rate, rhythm, pattern
Sighing & yawning
Cheyne-Stokes - More rapid deep breathing then slower more shallow breathing
Gasping breath - A neurological reflex before they stop breathing all together
Hyperventilation- Can happen with damage to the lower brain centers
Very irregular - Periods of apnea, etc.
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increased intracranial pressure [ICP] causes
- inc. blood volume
- inc. cerebral spinal fluid
- inc. brain tissue
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high intracranial pressure effects
- obstructs cerebral blood flow
- destroys brain cells
- herniation - where parts of the brain that are normally positioned in certain areas in our head begin to move into compartments it would not normally be
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Cushing's triad
- late signs of increased intracranial pressure
- high BP
- slow pulse
- wide pulse pressure
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early signs of increased intracranial pressure
- LOC: restless, disorientation
- headache: maybe, usually
- VS: HR, BP, RR stable
- Pupils: dilated ipsilaterally [side of injury]
- visual changes: blurring, dec. visual acuity
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increased intracranial pressure late signs
- LOC: coma
- Headache: increasing pain
- VS: cushings triad: inc. BP, slow pulse and wide pulse
- Pupils: dilated bilaterally and fixed
- Visual changes: can't be assessed
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Cerebrovascular attack [CVA] types
- also known as brain attack
- ischemic stroke
- hemorrhagic stroke
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ischemic strokes types
- transient ischemic attack [TIA]
- thrombotic stroke [large vessel]
- Lacunar infarct [small vessel stroke]
- embolic stroke [moving clot]
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temporary ischemic stroke
- focal ischemic cerebral neurological deficits - lack O2 for a short period of time
- usually lasts 1-2 hours
- temporary disturbances in cerebral blood flow - reverses before infarction occur
- can be a warning sign for something more serious
- no damage occurs
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where would embolus be most likely to come from?
left side of heart
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thrombotic CVA
- Presence of earlier TIAs?: frequent
- Onset: acute, hours to days
- Associated headache: occasional, not severe
- Stiff neck: rare
- Loss of consciousness: occasional, not at onset
- Blood in CSF?: rare
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Embolic CVA
- Presence of earlier TIAs?: occasional
- Onset: acute
- Associated headache?: often mod., severe
- Stiff neck: rare
- Loss of consciousness: occasional, brief
- Blood in CSF: rare
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Hemorrhagic CVA
- Presence of TIAs: infrequent
- Onset: acute, progressing
- Associated headache: frequent, severe
- Stiff neck: frequent
- Loss of conspicuousness: frequent
- Blood in CSF: frequent
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CVA clinical manifestation
- sudden in onset, not LOC
- usually one-sided
- most common - weakness of face and arm
- other - unilateral numbness, vision loss, aphasia, dysarthria, and sudden, unexplained imbalance or ataxia
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right brain damage
- paralyzed LEFT side
- behavior: quick, impulsive
- spacial and perceptual deficits
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LEFT brain damage
- paralyzed RIGHT side
- behavior: slow, cautious
- speech and language deficits
- depression
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how much time do you have to treat a brain attack?
- must be immediate [within three hours]- usually early identification, special medical teams
- differentiate the type of stroke b/ each one is treated differently
- Tx with new medications and procedures
- better recovery if area surrounding ischemic areas has circulation restored fast
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what medication is used to treat ischemic stroke first?
thrombolytics - tPA, tissue plasminogen activator
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which type of CVA should NOT use tPA?
hemorrhagic stoke
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seizure disorders
- seizure = sudden, disorderly discharge of a group of cerebral neurons within the brain. sometimes this activates a part of the brain that controls motor function
- convulsion - motor seizures
- not a disease but symptoms
- common is children esp. related to fevers, elders
- epilepsy - seizure disorder without identifiable cause
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seizure threshold is affected by?
- congenital defects: fam his.=more susceptible
- tumors
- vascular lesions
- metabolic abromalities - changes in ph, etc.
- head injury
- fever - related to children
- drug and alcohol use/withdrawal - decreases seizure threshold
- infections
- medications
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manifestation of seizure
- +/- bizarre muscle movements
- +/- unsual sensation. perceptions [tactile, odors, sounds, visual]
- +/- loss of consciousness
- exact manifestations depends on the LOCATION of focus and SPREAD in the brain
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aura
A change in sensation that the person notices shortly before their going to have a seizure. Usually a sensory change, it might be a smell, sound, or feeling
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prodroma
Sensations that people get even a longer period of time before they actually have a seizure and it can even be hours or days leading up to the seizure and kind of more subtle changes
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postictal state
- after seizure
- esp. for seizure that caused loss of consciousness, it's a global change in the entire brain
- pt. can be confused, combative, very sleepy and hard to focus
- time where we as the nurse can intervene and care for the pt.
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partial seizure
starts in one lobe, so no loss of consciousness if simple, or, if complex spreads to both lobes, leading to impaired consciousness
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generalized seizure
- wide spread
- spread widely and fast to both lobes, so loss of consciousness
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absence seizures
- often confused with simple partial
- NOT just a blank stare
- motion [automatisms, eyelid movement]
- lasts a few seconds
- cease in adulthool or evolve into motor seizures
- the medications phenobarbitol and phenytoin worsen seizures
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Atonic or akinetic seizures
- "drop attacks" - sudden loss of muscle tone for a few minutes
- can be familial
- rule out syncope
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generalized motor seizure include which phases
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tonic phase
- simple partial seizure is prodrome
- loss of consciousness
- sharp tonic muscle contractions
- incontinence [bladder]
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clonic phase
- brain fights back, alternating contraction and relaxation, slowing
- postictal: altered LOC, sleepy
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drugs for seizure wont help up to how many percent of the seizure pts.? what other Txs are there?
up to 40%
other treatments include: brain surgery, ketogenic diet, vagal nerve stimulator
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brain surgery for seizures
underutilized as a cure for seizures
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ketogenic diet
high fat and protein w/ no carbs
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vagal nerve stimulator
product that a pt. can control. it shuts down and increase the potentiation threshold for the neurons in the brain so that they don't lead to seizures
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anti epilepic drugs [AEDs]
- lack of adherence is the major reason for poor control due to bad SE
- balance of seizure control and adverse effects of the AEDs
- important to diagnose type of seizure, as it affects choice of AEDs
- may need to adjust doses and add meds
- adjust dosages using plasma drug levels
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why use plasma drug levels to when adjusting AEDs doases.
- seizures may be infrequent, making it hard to monitor effectiveness
- non-compliance may be an issue
- with multiple drugs, hard to know which is causing effect
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4 mechanisms for AEDs
- block sodium channels so that neurons depolarize more slowly and stops rapid firing
- block calcium channels, same
- block glutamate [excitatory neurotransmitter] receptors
- increase GABA [inhibatory neurotransmitter] - by increasing GABA your going to reduce the number of seizures
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common problems with AEDs
- rapid withdrawl can lead to sever aeizures
- most AEDs cause CNS depression, ESP. with other CNS depressants like alcohol
- many AEDs are metabolized by the live, induce liver enzymes, and change metabolism of other meds, including other AEDs
- enzymes induction leads to inactivation of normal dose - oral contraception and warfarin
- most AEDs can have negative effects on the fetus, but seizures have worse effects on the fetus
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traditional AEDs meds include
well known, cheaper, more adverse SE
phenytoin (Dilantin)
carbamazepine
valproic acid
phenobarbitol
ethosuximide
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newer AEDs seizure meds
not as tested, more expensive, but fewer adverse SE
- gabapentin
- lamotrigine
- topiramate
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Phenytoin [Dilantin]
Normalizes sodium flux in neuron
Raises seizure threshold
For partial and tonic clonic seizures, but NOT absence seizures
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Phenytoin adverse effects
CNS: dizziness, sluggishness, confusion (Avoid alcohol, other CNS depressants)
GI: nausea, constipation
If the pt. developed Rash – They must stop he medication!
Gingival hyperplasia [overgrowth of the gums hich can cause bleeding, loss of teeth, etc] (use folate rinse)
Teratogenic (palate, lip, heart)
Folate supplementation REDUCES RISK
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Drug-nutrient interactions of phenytoin
- - INDUCES [increases] hepatic metabolism of
- vitamin
- - B12, folate, vitamin D, vitamin K
- - This causes a lot of the SE
- - DISPLACES folate from plasma proteins
- - Phenytoin metabolism USES UP folate
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monitor phenytoin serum levels
- - highly bound to plasma proteins
- note free, unbound phenytoin levels
- narrow therapeutic range
- liver has limited ability to metabolize - keep 10 - 20 mcg/ml therapeutic range
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phenytoin toxicity
- sedation
- nystagmus
- ataxia - not being able to walk correctly and losing your balance
- diplopia - double vision
- cognitive impairment
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pehnytin DRUG ONLY interactions
- - Many drug incompatibilities
- - (Do NOT mix C/ other parenteral Rxs)
- - INDUCES hepatic p-450 enzymes
- - DISPLACES other drugs, nutrients from plasma proteins
- - BINDS to proteins in enteral feedings
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carbamazepine
- - Similar to phenytoin, but fewer side effects
- - Can cause leukopenia, anemia, thrombocytopenia, even fatal aplastic anemia (bone marrow shut down) - rarely
- - Can cause bad bone marrow suppression that can even be fatal by cutting off production of blood cells
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phenobarbital
- can be used for simple partial
- also used [infreq] for complex-partial, tonic-clonic and febrile seizures
- similar adverse effects as phenytoin but NO EFFECT ON FOLATE, NO GINGIVAL HYPERPLASIA [over growth of gums]
- ling time to stabalize - Stakes
- a while to stabilize in the blood, it has a long half life so you have to add to it gradually and allow it to level out over a couple of weeks
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valproic acid [Depakote]
- - inc. Acts on increasing Gamma aminobutyric acid (GABA), an inhibitory neurotransmitter
- - For ALL generalized seizures
- - 75% of partial seizures controlled also
- - Also used for bipolar disorder
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Valproic acid adverse effects
- - Teratogenic (neural tube defects) - avoid in pregnancy
- - Hepatotoxicity, pancreatitis (avoid infants, elderly)
- - CNS depression (avoid alcohol, etc.)
- - Inhibits platelet aggregation
- - NO BEHAVIORAL EFFECTS
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Benzodiazepines
- - Diazepine receptors potentiate GABA
- - Used for rapid cessation of seizures
- - MONITOR for respiratory depression
In a person who has uncontrolled seizures, people have used benzodiazepine to stop the seizure activity completely right away
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Clonazepam (Klonopin)
A benzodiazepine for maintenance therapy of absence, akinetic seizures
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MAGNESIUM SULFATE
- - For seizures caused by hypomagnesemia (eclampsia, hypothyroidism, alcohol withdrawal)
- - Side effects from hypocalcemia (CNS depression, hypotension, hypothermia, circulatory collapse)
- - Monitor serum magnesium levels
- - Treat magnesium sulfate toxicity with IV calcium gluconate
- - An antisizure medication that is a smooth muscle relaxant that works in situations where hypomagnesaemia are causing the problem
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Best indicators for respiratory depression is
respiratory rate and count RR freq
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STATUS EPILEPTICUS
- - Continuous tonic-clonic seizures that last for over 20 min., unconscious
- - The longer the seizure activity, the more resistant to stopping the seizure, start treatment within 5 min.
- - Seizures using up oxygen and glucose, cause acidosis, brain damage, even death
Goals: maintain ventilation, treat hypoglycemia, stop seizures
- Start IV, draw labs [looking at electrolytes], give benzodiazepine
- - Lorazepam (Ativan), long acting (72 hr), preferred - Will quickly stop the seizure
- - Diazepam (Valium), short acting, need repeat
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