brain injuries and symptoms

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  1. which two major pathways result in brain damage
    • hypoxia
    • ischemia
  2. ischemia consists of which two categories
    • focal 
    • global
  3. 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
  4. global brain injury Tx
    • oxygen and perfusion
    • cooling to dec. metabolic needs
    • blood sugar control
  5. 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
  6. 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
  7. your most important assessment  is ?
  8. 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
  9. pupillary changes
    indicated the presence and level of brain stem dysfunction
  10. 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
  11. motor response
    • can tell you the level of brain dysfunction 
    • determines most severely damaged side
  12. 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
  13. 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
  14. 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.
  15. increased intracranial pressure [ICP] causes
    • inc. blood volume
    • inc. cerebral spinal fluid
    • inc. brain tissue
  16. 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
  17. Cushing's triad
    • late signs of increased intracranial pressure
    • high BP
    • slow pulse
    • wide pulse pressure
  18. 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
  19. 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
  20. Cerebrovascular attack [CVA] types
    • also known as brain attack
    • ischemic stroke
    • hemorrhagic stroke
  21. ischemic strokes types
    • transient ischemic attack [TIA]
    • thrombotic stroke [large vessel]
    • Lacunar infarct [small vessel stroke]
    • embolic stroke [moving clot]
  22. 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
  23. where would embolus be most likely to come from?
    left side of heart
  24. 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
  25. 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
  26. Hemorrhagic CVA
    • Presence of TIAs: infrequent 
    • Onset: acute, progressing
    • Associated headache: frequent, severe
    • Stiff neck: frequent
    • Loss of conspicuousness: frequent 
    • Blood in CSF: frequent
  27. 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
  28. right brain damage
    • paralyzed LEFT side
    • behavior: quick, impulsive
    • spacial and perceptual deficits
  29. LEFT brain damage
    • paralyzed RIGHT side
    • behavior: slow, cautious
    • speech and language deficits
    • depression
  30. 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
  31. what medication is used to treat ischemic stroke first?
    thrombolytics - tPA, tissue plasminogen activator
  32. which type of CVA should NOT use tPA?
    hemorrhagic stoke
  33. 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
  34. 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
  35. 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
  36. 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
  37. 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
  38. 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.
  39. partial seizure
    starts in one lobe, so no loss of consciousness if simple, or, if complex spreads to both lobes, leading to impaired consciousness
  40. generalized seizure
    • wide spread
    • spread widely and fast to both lobes, so loss of consciousness
  41. 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
  42. Atonic or akinetic seizures
    • "drop attacks" - sudden loss of muscle tone for a few minutes 
    • can be familial 
    • rule out syncope
  43. generalized motor seizure include which phases
    • tonic phase
    • clonic phase
  44. tonic phase
    • simple partial seizure is prodrome
    • loss of consciousness 
    • sharp tonic muscle contractions
    • incontinence [bladder]
  45. clonic phase
    • brain fights back, alternating contraction and relaxation, slowing
    • postictal: altered LOC, sleepy
  46. 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
  47. brain surgery for seizures
    underutilized as a cure for seizures
  48. ketogenic diet
    high fat and protein w/ no carbs
  49. 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
  50. 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
  51. 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
  52. 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
  53. 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
  54. two major types of AEDs
    • traditional 
    • newer
  55. traditional AEDs meds include
    well known, cheaper, more adverse SE

    phenytoin (Dilantin)


    valproic acid


  56. newer AEDs seizure meds
    not as tested, more expensive, but fewer adverse SE

    • gabapentin
    • lamotrigine
    • topiramate
  57. Phenytoin [Dilantin]
    Normalizes sodium flux in neuron

    Raises seizure threshold

    For partial and tonic clonic seizures, but NOT absence seizures
  58. 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
  59. 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
  60. 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
  61. phenytoin toxicity
    • sedation
    • nystagmus
    • ataxia - not being able to walk correctly and losing your balance 
    • diplopia - double vision
    • cognitive impairment
  62. 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
  63. 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
  64. 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
  65. 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
  66. Valproic acid adverse effects
    • - Teratogenic (neural tube defects) - avoid in pregnancy
    • - Hepatotoxicity, pancreatitis (avoid infants, elderly)
    • - CNS depression (avoid alcohol, etc.)
    • - Inhibits platelet aggregation
  67. 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
  68. Clonazepam (Klonopin)
    A benzodiazepine for maintenance therapy of absence, akinetic seizures
    • - 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
  70. Best indicators for respiratory depression is
    respiratory rate and count RR freq
    • - 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
Card Set:
brain injuries and symptoms
2013-12-10 00:17:36
3220 final exam fall
3220 final exam fall
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