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124 Cards in this Set
- Front
- Back
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CN I
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Olfactory- smell
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CN II
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Optic- vision (retina of eyes)
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CN III
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Occulomotor-levator palpebrae muscle
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CN IV
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Trochlear- superior oblique (down and lateral)
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CN V
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Tigeminal- chewing (jaw, teeth, mucosa, face and mouth touch and pain, forehead)
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CN VI
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Abducens- lacteral rectus of eye (moves lateral)
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CN VII
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Facial- facial muscles of expression and cheek muscle, taste of anterior 2/3 of tongue
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CN VIII
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Vestibulocochlear- hearing and equilibrium
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CN IX
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Glossopharyngeal- superior pharynx, post of tongue- movement and taste
- senses carotid pressure |
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CN X
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Vagus- Viscera of thorax and abdomen, larynx and middle pharyngeal muscles
- parasympathetic |
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CN XI
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Accessory- sternocleidomastoid and trapezius
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CN XII
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hypoglossal- muscles of tongue
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Hydrostatic pressure
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pushes water out of vasculary system
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Oncotic pressure
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pulls water from tissues to vascular space
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Normal ICP
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0-15 mm Hg
(Can be measured in ventricles, subarachnoid space, subdural space, epidural space r brain tissue ussing pressure transducers) |
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Increased ICP
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> 20 mm Hg
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ICP can increase due to increased..
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- brain tissue volume (cerebral edema, mass)
- CSF (hydrocephalus) - blood (vasodilation) |
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Initial compensatory mechanism
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- changes in CSF absorption or displaceing it into spinal arachnoid space
- Collapse of cerebral veins and dural sinuses, regional cerebral vasoconstriction or dilation, changes in venous outflow - distention of dura or compression of brain tissue (limited-->decompensation) |
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Decompensation S/S
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Decompensatino results in compression and ischemia --> tissue death and necroti tissue damage
- cool, clammy, not pink, perfusion down |
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Autoregulation of Cerebral blood flow
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- automatic adjustment in the diameter of the cerebral vessels by the brain to maintain a constant blood flow during changes in arterial BP
- in order to provide metabolic needs of brain tissue and maintain normal cerebral perfusion WNL |
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Lower limit of mean arterial pressure (MAP)
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50 mm Hg
- below this cerebral flow decreases and will have symptoms |
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More symptoms of cerbreal ischemi
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syncope, blurred vision
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Upper limit of MAP in which autoregulation is effective
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150 mm Hg
- if exceeds, the vessels are maximally constricted and further vasoconstricor response is lost |
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MAP =
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Diastolic BP + 1/3 PP
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CPP (Cerebral Perfussion) =
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MAP-ICP
CPP is the flow times the resistance - when vascualr resistance is high, blood flow to brain tissue is impaired - may not reflect CPP in all areas of brain (could be swelling limiting to areas) |
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As CPP decreases...
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autoregulation fails and cerebral blood flow decreases
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Normal CPP
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60-100 mm Hg
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CPP associated with ischemia and neuronal death
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<50 mm Hg
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CPP associated with ischemia and death
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<30 mm Hg
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When ICP is elevated it is important to maintain the...
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MAP (may have to keep BP higher than normal for this)
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Stage 1 of ICP
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- high complaince
- total compensation of brain - accomadation and autoregulation intact - An increase in volume doesn't increased ICP * usually no signs and symptoms, may be subtle according to ms n. |
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Stage 2 of ICP
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- increase in volume places pt at risk for increased ICP
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Stage 3 ICP
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- any small addition of volume causes a great increase in ICP
- failure of compensatory mechanisms, loss of autoregulation - pt will manifest with S/S of ICP (HA, change in mentation, pupil changes) |
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ICP S/S
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- HA
- change in level on consciousness/mentation - pupil changes ** watch pt closely for 24-48h, could get worse before getting better, like with a stroke, with swelling |
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With loss of autoregulation there is...
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- rise in systolic BP to try and maintain cerebral perfusion (don't be quick with meds, want this)
- monitor BP closely - means that decompensation is coming |
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Cushing's triad
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- systolic HTN
- widening pulse pressure - bradycardia - full bounding pulse - altered respirations *** Neurologic emergency!** |
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Stage 4 of ICP
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ICP increaed to lethal levels with little increase in volume
- herniation (to sides or down to brain stem) - can cause brain stem death if continues |
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Co2 and its affect on CBF (Cerebral blood flow)
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- increase PaCO2 (a vasoactive agent) --> relaxes smooth muscle --> dilates cerebral vessels, decreases cerebrovascular resistance and increased cerebral blood flow
- decrease in PaCo2 constricts cerebral vessels, increases cerebrovascular resistance and decreases cerebral blood flow |
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Oxygen's effect on CBF
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- O2 tension (concentration of O2 at a specific pressure) < 50 mm Hg --> cerebrovascular dilation --> decreases cerebral vascular resistance--> increases CBF --> O2 tension
- If O2 tension is not increased, lactic acid can accumulate with low PaO2 and high hydrogens (acidosis) (both are cerebral vasodilators) = loss of autoregulation and compensatory mechanisms fail to meet metabolic demands |
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An increase in ICP is significant because it
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- decreases CPP
- increases risk for brain ischemia and infarction - is associated with poor prognosis |
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A cerebral insult may result in
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- hypercapnia
- cerebral acidosis - impaired autoregulation - systemic HTN (promotes formation and spread of cerebal edema) |
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Result of edema on brain tissue (edema originally caused by insult to brain)
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- distorts brain tissue and further increases the ICP --> further tissue hypoxia and acidosis--> then more edema around necrotic tissue --> increased ICP more --> brainstem and respiratory center compression --> accumulation of CO2 --> vasodilation --> increased blood volume --> increased ICP --> death
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Definition of edema
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accumulation of fluid in extravascular spaces of brain tissue
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3 types of edema
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- vasogenic
- cytotoxic - interstitial - more than one type can occur on one pt |
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What is the most common type of edema
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vasogenic cerebral edema
- changes in endothelial lining of cerebral capillaries - osmotic gradient that promotes flow of fluid from intravascular to extravascular |
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Symptoms of vvasogenic cerebral edema
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HA, change in consciousness, neuro deficits
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Cytotoxic cerebral edema
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- from lesions or trauma to brain tissue --> cerebral hypoxia, anoxia, sodium depletion, SIADH
- directly into cells, from fluid and protein shift |
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Interstitial Cerebral edema
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hydrocephalus, water intoxication, hyponatermia, brain surgery
- increase in CSF or inability to reabsorb it - treatment is ventriculostomy or chunt |
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Main causes of cerebral edema
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- mass lesions
- head injuries and brain surgery - cerebral infection - vascular insult (ischemia, infarction, thrombosis) - toxic or metabolic encephalopathic conditions (lead, arsenic, uremia, hepatic encephalopathy) |
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Drug Treatment of ICP
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- mannitol
- hypertonic solution - corticosteroids (vasogenic only, not head injury) - control increased metabolic demands (fever, shivers, pain, seizures) |
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Consciousness sign of increased ICP
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- decreased level of consciousness (most sensitive indicator of neurologic function!), can be dramatic or subtle
- it is from ischemia --> reticular activating system has no oxygen |
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AVPU
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A- is patient ALERT?
V- does patient respond to VOICE (but not alert)? P- does pt respond to only pain (not alert and does not respond to voice) U- is pt Unresponsive to all of the above |
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Vital sign changes with ICP
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- Changes in vitals
-HTN first, Cushing's triad late, -with increased pressure on hypothalamus changes in body temp |
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Ocular signs of ICP
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- cranial nerve III
- dilation of pupil ipsilateral of mass lesion - sluggish or no response to light - inability to move eye upward and ptosis of eyelid ***a fixed and dilated pupil is associated with a bad outcome and is considered a neuro emergency*** - may also affect CN IV and CN VI (blurred vision, diplopia, changes in extraocular eye movements) |
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Dilated fixed pupil (one) =
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compressed cranial nerve III
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bilateral dilated, fixed pupils =
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ominous sign
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Decrease in motor function with increased ICP
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- contralateral to lesion
- may be a subtle arm drift first - weakness or paralysis (focal sign) - abnormal posturing from noxious stimuli |
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Decorticate
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hands up on chest
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Decerebrate
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hands straight to sides with hands curves
* more severe * - CAN HAPPEN ON ONE SIDE, WITH OTHER SIDE BEING DECORTICATE, ETC. |
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Consciousness sign of increased ICP
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- decreased level of consciousness (most sensitive indicator of neurologic function!), can be dramatic or subtle
- it is from ischemia --> reticular activating system has no oxygen |
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AVPU
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A- is patient ALERT?
V- does patient respond to VOICE (but not alert)? P- does pt respond to only pain (not alert and does not respond to voice) U- is pt Unresponsive to all of the above |
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Vital sign changes with ICP
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- Changes in vitals
-HTN first, Cushing's triad late, -with increased pressure on hypothalamus changes in body temp |
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Ocular signs of ICP
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- cranial nerve III
- dilation of pupil ipsilateral of mass lesion - sluggish or no response to light - inability to move eye upward and ptosis of eyelid ***a fixed and dilated pupil is associated with a bad outcome and is considered a neuro emergency*** - may also affect CN IV and CN VI (blurred vision, diplopia, changes in extraocular eye movements) |
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Dilated fixed pupil (one) =
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compressed cranial nerve III
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bilateral dilated, fixed pupils =
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ominous sign
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pinpoint pupils
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(pons damage or drugs)
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Decrease in motor function with increased ICP
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- contralateral to lesion
- may be a subtle arm drift first - weakness or paralysis (focal sign) - abnormal posturing from noxious stimuli |
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Decorticate
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hands up on chest
-flexor |
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Decerebrate
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hands straight to sides with hands curves
* more severe * - extensor - CAN HAPPEN ON ONE SIDE, WITH OTHER SIDE BEING DECORTICATE, ETC. |
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HA with increased ICP?
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- compression of OTHER intracranial stuctures around the brain (brain is insensitive to pain!)
* contuous but worse in AM - straining or moving makes it more intense |
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Vomiting with increased ICP
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- NOT preceded by nausea
- possibly projectile |
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Ventriculostomy
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- Gold standard for measuring ICP
- catherter inserted into right lateral ventricle and couples to an external transduce allows removal or sampling of CSP - allows for med admin |
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Complication of Ventriculostomy
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**** INFECTION****
- sometimes will have prophylactic antibx - monitor vital signs **MONITOR for change in drainage color or clairty, dx CSF organism if needed |
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Controbuting factors for infection with ICP monitoring
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- ICP monitoring > 5 days
- use of ventriculostomy - CSF leak - concurrent systemic infection |
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If pt has a ventricular catheter for CSF removal
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there should be a sign above pt's bed
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Nursing care for ICP pt
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- head of bed elevated to 30 degrees
- head in neutral position - possible intubation/mech vent - ICP monitoring - cerebral oxygen monitoring - Maintenance of PaO2 > or equal to 100 mm Hg - Maintenance of systolic pressure between 100-160 mm Hg *Maintenance of CPP > 60 mmHg - reduction of cerebral metabolism (barbituates, pento barbitol or propofol for sedation) - quiet, low stimulating environment - |
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Additional drug therapy for ICP
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- osmotic diuretic, loop diauretics (furosemide)
- antiseizure meds - corticosteroids (dexamethasone) - histamin H2 receptors or PP inhibitor |
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If pt on mannitorl or hypertonic saline
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frequent monitoring of BP and serum sodium levels with hypertonic saline!
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Corticosteroids for ICP
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- not for head injury pts
- watch increase in glucose |
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ICP pt and nutrition
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- pt is in a hypermetabolic state and needs increased glucose
- if can't have PO, enteral or parenteral feedings - higher success with earlier feedings - should start within 3 days after injury and full replacement reached by 7 days *malnutrition promotes more cerebral edema |
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Even though concern is brain, have to also implement...
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measure to prevent immobility complications (DVT, respiratory, falls, confusion)
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Respiratory assessment and nursing care of unconscious pt
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- patent airway
- any pt with glascow <8 is unable to maintain airway and needs intubation - elevate HOB to 30 degrees - limt suction to 2-3 passess, < 10 sec. (increases ICP, make sure to preoxygenate!) - monitor ABCs - Avoid abdominal distention (pushes organs up a decreases breathing) - no noxious stimuli - sedation - treat pain - treat anxiety (makes HR and everything fight against each other) |
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Gloscow coma scale measure
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eyes open
best verbal response best motor response (a command and pain) |
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HOP elevation
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15-30 degrees unless cervical injury
- may need to be flat to maintain CPP - avoid neck flexion (obstruct venous outflow) |
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Moving pt
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- when posturing, minimize stimulation
- turn with slow, gentle movements, continuous lateral rotational therapy - no extreme hip flexion |
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Most common causes of head injury
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motor vehicle crash and fall
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death occurs at 3 points of brain injury
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- immediately after injury
- within 2 hours after the injury - 3 weeks after the injury |
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Predictors of poor outcome from head injury
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- if have intracranial hematoma
- older pt - abnormal motor responses - impaired or absent eye movement or pupillary light reflexes - early sustained hypotension, hypoxemia, hypercapnai - ICP > 20 mm Hg **Glasgow coma scale on arrival is good indicator <8 is 30-70% chance of survival >8 is 90% survival |
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Skull fracture signs (especially basilar)
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- cranial nerve deficits (facial paralysis)
- Battles sign (postaurical ecchymosis) - periorbital ecchymosis (raccoon eyes) Basilar: Rhinorrhea or Otorrhea (CSF leakage, showing break in dura), check post nasal drip as well! - deviation in gaze (to side of lesion) |
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2 types of testing for clear CSF drainage
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- Dextrostix (or Tes Tape strip)
- Halo or ring sign * would be positve for glucose - make sure there is no blood in test cause that can give a false positive for glucose presence |
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Concussion
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- sudden, transietn
- brief loss in LOC - amnesia - HA - short duration ** don't have to do the only wives tale of not letting them go to sleep, just have to make sure they don't lose consciousness - usually no loss in LOC or < 5 min is d/c |
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Post concussion syndrome
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- 2 weeks- 2 months
- HA, lethargy, personality or behavioral changes, shortened attention span, decreased short term memory - changes in intellectual ability - ADL's |
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Contusion
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common in coup- contrapcoup
- maintained integrity of pia mater and arachnoid layers - hemorrhage, infarction, with focal edema |
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Can a cerebral laceration be surgical fixed?
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not really, they can try but poor outcome
- poor prognosis |
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Epidural hematoma
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between dura and inner surface of (dura is normall attached to skull, epidural space is between dura and skull)
- emergency--> rapid surgical intervention |
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Subdural hematoma
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between dura and arachnoid layer (covers brain)
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layers of skull to brain
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skin
skull epidural space Dura mater (actually attached to skull) Arachnoid membrane Pia Mater |
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S/S of Acute subdural hematoma
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24-48 hours of the injury
- similar signs to tissue compression and increased ICP - pt feels drowsy and confused - Ipsilateral pupil dilated and fixed |
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S/S of subacute subdural hematoma
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- occur within 2-14 days of injury
- after initial bleeding, subdural hematoma may appear to enlarge over time |
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S/S of chronic subdural hematoma
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- develops over weeks or months after a seemingly minor head injury
- peak incidence in sixth and seventh decade of life (because of more brain atrophy and larger subdural space, same with alcoholics) |
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Manifestations of subdural hematoma are often misinterpreted for...
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vascular disease (stroke, TIA) and dementia
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Best Dx for craniocerebral trauma
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- CT scan
- non-contrast CT for bleeds |
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Is an MRi or CT scan more sens in detecting small lesions?
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MRI
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Treatment principles for head injury
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- Prevent secondary injury (ABC's first!!)
- timely diagnosis - surgery if necessary |
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Emergency management for head injury
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- ensure patent airway
- stabilize c-spine - admin O2 with non rebreather - establish IV access with 2 large bore cathetrs for NS or LR - control external bleeding with sterile pressure dressing - assess for rhinorrhea, ortorrhea, scalp wounds - remove pts clothing |
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Ongoing management of head injury
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- maint patient warmth (blankets, warm IV fluids, overhead warming lights, warm humidified O2)
- monitor vitals (LOC, O2 sat, cardaic rhythm, GCS, pupil size and reactivity) - anticipate for intubation if gag reflex is impaired or absent - assume neck injury with a head injury - admin fluids cautionsly to prevent fluid overload and increasing ICP |
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Craniotomy
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for depressed fractures and loose fragments, to remove free fragments
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Craniectomy then cranioplasty
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craniotomy to remove a piece of skull and craniplasty to replace later
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4 main things with acute intervention of head injuries
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- maintain cerebral perfusion
- prevent secondary cerebral ischemia - monitor for neurologic changes - treat life threatenind conditions initially!! this is the priority! |
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eye problems
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may need lubrication if loss of corneal reflex
cold then warm compress for periorbital ecchymosis and edema, patch for diplopia |
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hyperthermia
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avoid (increases metabolic demands and increases CBF and increases ICP
- damage to hypothalamus |
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if there is rhinorrhea or otorrhea
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** INFORM MD IMMEDIATELY
****NO NG TUBES!!!!! or nasal suctioning*** |
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Family care
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- keep hope
- outward appearance is deceiving - may have unrealistic expectations for pt - family may expect full recovery to pretrauma status |
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Most common brain tumor
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Glioblastoma multiforme
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Clinical manifestations of brain tumor
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- HA (worse at night)
- usually dull and constant but occasionally throbbing - seizures (any kind) - N/V from increased ICP - cognitive dysfunction - muscle weakness, sensory loss, aphasia, visual-spatial - increaed ICP, cerebral edema |
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chemotherapy and brain tumors
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limited use due to BBB
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Frontal lobe tumors
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- can cause behavioral and personality changes
- loss of emotional control, confusion, disorientation, memory loss, impulsivity, depression - often not perceived by pt but can be frightening to family - assist family in understanding - protect from self and self protection - like seizure precautions - minimize stimuli, create routine, use reality orientation |
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Dilantin
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therapeutic levels are 10-20 mcg.mL
- no grapefruit juice - decrease oral contraceptives - stevens johnson syndrome - nystagmus is sign of toxicity - taper - no pregnancy |
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Tegretol
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therapeutic level 4-12 mcg.mL
- hematologic S/E - photsens - no pregnancy - no grapejuice |
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Valproic acid
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therepeutic dose 40-100 mcg/mL
- teratogenic, hepatotoxic |
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Signs of stroke
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- altered level on consciousness
- weakness, numbness, paralysis - speech or visual disturbances - HA - increased or decreased HR - respiratory distress - unequal pupils - HTN - facial drooping - difficult swallowing - seizures - bladder or bowel incontinence - N/V - vertigo F- face (facial droop) A- arm (arm droop) S- speech T- time (when did it happen?) |
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left hemisphere stroke
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in right handed people and most left handed this is language side --> aphasia
- cautious |
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right hemisphere stroke
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- impulsive, deny or minimize problems, imapired judgement
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Homonymous Hemianopsia
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visual cut, can't see food on once side of tray for example
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