Transcript Changes in Peripheral Nervous System

Neurosensory:
Altered Cerebral Function and Increased intracranial
pressure (IICP)
Updated Fall 2011 by John Nation, RN, MSN
From the notes of Charlene Morris, RN, MSN
&
Marnie Quick, RN, MSN, CNRN
Overview of Today’s Lecture
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Discuss altered cerebral function
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Anatomy and physiology
Definition of common terms
Neurological assessment techniques
Increased intracranial pressure
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Anatomy and physiology
Clinical manifestations
Interventions
Nursing concerns
Flow of CSF: Produced by filtration of the blood by the choroid plexus of
each ventricle flows inferiorly through the lateral ventricles,
intraventricular foramen, third ventricle, cerebral aqueduct, fourth
ventricle and subarachnoid space and to the blood.
Altered Cerebral Function:
Arousal/cognition (LOC) Patho/assessment
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Reticular Activating System (RAS) – Reticular
Formation - meshwork of gray cell within brainstem
extending to the thalamus.
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Controls wakefulness, arousal and alertness.
Cerebral cortex outer layer of gray cell bodies of
brain. Controls cognition, thought process.
Altered Cerebral Function:
What is Consciousness?
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Consciousness (Merriam- Webster): waking life (as that to
which one returns after sleep, trance, or fever) in which
one's normal mental powers are present “the ether wore
off and the patient regained consciousness”
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Dynamic state
Continuum from awareness of self and
environment to unawareness
Consciousness to deep coma
Coma- prolonged unconsciousness
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Causes of Changes in LOC
Alcohol intoxication
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Drug intoxication (particularly opiates, narcotics, sedatives, and anti-anxiety or seizure
medications)
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Arrhythmia
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Brain disorders
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Central nervous system diseases
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Lack of oxygen (hypoxia)
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Abnormal blood sugars (diabetic coma)
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Electrolyte or mineral imbalance
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Exposure to heavy metals or hydrocarbons
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Extreme fatigue or sleep deprivation
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Ketoacidosis
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Head trauma
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Heart failure
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Hypoglycemia (low blood sugar)
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Increased carbon dioxide levels (hypercarbia) often seen in emphysema
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Infection
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Low blood pressure (hypotension)
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Metabolic disorders
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Thyroid or adrenal gland disorders
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Seizures such as those related to epilepsy
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Shock
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Stroke
Source: National Institute of Health
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Causes of Coma:
Coma can be caused by:
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Traumatic brain injuries. Brain injuries that result from traffic
collisions or acts of violence are the most common cause of
comas.
Stroke. Acute loss of blood flow to the brain followed by
swelling or no blood flow to a major part of the brainstem can
result in a coma.
Diabetes. Blood sugar levels that get too high
(hyperglycemia) and stay too high or get too low
(hypoglycemia) and stay too low can cause coma.
Source: Mayo Clinic: http://www.mayoclinic.com/health/coma/DS00724/DSECTION=causes
Causes of Coma (Cont’d):
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Lack of oxygen. People who have escaped drowning or been
resuscitated after a heart attack may not awaken due to lack
of blood flow and oxygen to the brain.
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Infections. Encephalitis and meningitis are infections that
cause inflammation of the brain, spinal cord or the tissues
that surround the brain. Severe cases of either encephalitis or
meningitis can result in a coma.
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Toxins. Exposure to toxins, such as carbon monoxide or drug
overdoses, can cause brain damage and coma.
Source: Mayo Clinic: http://www.mayoclinic.com/health/coma/DS00724/DSECTION=causes
Altered Levels of Consciousness:
Definitions of Terms
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Lethargy - a slight reduction in alertness, less aware
of what is happening around them and think more
slowly.
Obtundation - a moderate reduction in alertness or
clouding of consciousness.
Stupor - an excessively long or deep sleeplike state.
Arousal is brief by vigorous stimulation, such as
repeated shaking, loud calling, pinching.
Coma - is a state of complete unresponsiveness,
cannot be aroused, in a deep coma lacks avoidance
of pain.
– Some reflexes may be present.
Altered Cerebral Function:
Assessment of arousal/cognition (LOC)
Is the patient alert?
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Assess to person/place/time/event (A&O x 4)
Respond to verbal stimuli?
Respond to painful stimuli?
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Purpose: shows the brain receives the impulse, interprets it, and responds
Types of painful stimuli:
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Trapezius pinch- grasp at least two inches of trapezius muscle. Squeeze and
twist.
Supraorbital pressure- carefully applied upward pressure on the ridge along the
upper portion of the bony orbital structure
Pressure on finger nails
Sternal rub- not considered appropriate
Is the patient unresponsive?
A-----V-----P-----U!
Trapezius Pinch
Injury reported as secondary to sternal rub.
Descending Response to pain stimuli
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Pushes your hand away
Pulls away from pain site
General movement
Flexion
Extension
No response
Decorticate posturing- abnormal flexion
Decerebrate posturing- abnormal extension
Glasgow Coma Scale
A score of 13 to 14 indicates mild deficit. A score between 9 and 12 points
to moderate deficit, and a score of 8 or less indicates severe coma.
Assessment of Vital Signs
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Temperature - hypothalamus pressure can
lead to alterations in body temperature
Cushing’s triad – caused by edema &
increased intracranial pressure
1) Increased systolic BP
2) Decreased pulse rate
3) Irregular respirations
Assessment of arousal/cognition - Respiratory
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Respiratory- changes occur as brainstem is
being compressed
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Yawning & sighing
Cheyne-Stokes – crescendo-decrescendo with apnea
Central Neurogenic hyperventilation
Apneustic breathing – Pauses in inspiration and
expiration
Cluster breathing – irregular deep to shallow with apnea
Ataxic respirations - grossly irregular
Respiratory Irregularities
Cranial Nerves
Assessment of arousal/cognition
Pupillary light reflex
Sensory: CN 2 - Optic
Motor: CN 3 Occulomotor
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Note pupil size; darken
room; shine light in and
note reaction and size
Occipital lobe
Brain stem
Assessment of arousal/cognition
Pupillary light reflex
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PERRLA- “Pupils equal, round, reactive to light
and accommodation”
Anisocoria: The two pupils are not of equal size.
Light-near dissociation, refers to a condition where the light
reflex is absent or abnormal but the near response is intact.
There is no clinical condition in which the light reflex is present
and the near response is absent.
Amaurotic: blind eye still has consensual response
Assessment Arosual/cognition
EOM’S & Brain stem function
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Eye movement- CN 3,4,6
In Deep COMA- test EOM’s by
Oculocephalic reflex
Doll’s eyes- Sensory- CN 8;
Motor- CN 3,4,6
Good Dolls eyes: eyes move in
opposite direction of head
movement – intact brain stem at
Pons & nerves
Bad/negative Dolls eyes: eyes
do not move head turned
How tested with spinal cord injury?
Assessment arousal/cognition Additional Motor
Assessment
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Ability to move, strength, and symmetry
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Coordination
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Grips, arm strength, & drift
Planter flexion, dorsiflexion, & leg strength
Finger to nose, heel up and down shin
Planter Reflex- Babinski testing
Meningeal signs- Brudzinski, nuchal rigidity
Planter Reflex and Babinski testing
Babinski's reflex – present when
the great toe flexes toward the top
of the foot and the other toes fan
out after the sole of the foot has
been firmly stroked.
• Postitive response indicates
damage to nerve paths connecting
the spinal cord and the brain
(corticospinal tract)
• Abnormal after the age of 2.
Meningeal signs- Brudzinski, nuchal
rigidity
One of the physically demonstrable symptoms of meningitis is
Brudzinski's sign. Severe neck stiffness causes a patient's hips and
knees to flex when the neck is flexed.
Meningitis signs- Kernig’s sign
Kernig's sign. Severe stiffness of the hamstrings causes an inability
to straighten the leg when the hip is flexed to 90 degrees.
Neuro assessment - Sensation
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Dull vs. sharp – use broken tongue
depressor or cotton tip applicator
Include face, hands, arms, abdomen, feet,
and legs
Neuro Assessment Videos
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Lewis DVD
Altered cerebral function
Nursing assessment for Cerebral Dysfunction
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Terms used to describe LOC
Description more important than term
Health history- drugs/head injury/metabolic
Physical exam- modify as individual cooperation
Neuro Vital Signs
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LOC, V/S, Pupils, Strength/Movement, Sensation
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Glasgow coma scale
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NIH Stroke Scale – want low score
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NIH Stroke Scale pdf
Common manifestations/Complications
Coma states and brain death
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Irreversible coma- persistent vegetative state
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Locked-in Syndrome (not true coma)
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Does not have functioning cerebral cortex
Caused by anoxia or severe brain injury
Sleep-wake cycles; chew/swallow/cough, no tracking
Functioning RAS & cortex; pons level interference
Aware, communicate with eyes
Brain death
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Loss of all brain function- flat EEG, no blood flow
Prognosis of individual with altered cerebral functioning
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Outcome varies according to underlying cause and
pathologic process
The longer the individual unconscious, the longer
has absent Doll’s eyes; the poorer the cognitive
recovery
Residual mental problems typically outweigh the
physical
Altered Cerebral Function
Therapeutic Interventions
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Diagnostic tests- to R/O & identify cause of altered
cerebral function
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CT, MRI, EEG, blood work
Medications- vary according to problem
Overdose; fluid/electrolyte replacement; antibiotics
Surgery- (Ex. tumors, intracranial bleeds)
Other- airway/vent; treat IICP; enteral feeding
Altered Cerebral Functioning:
Pertinent Nursing problems
Identify the priorities:
 Impaired physical mobility
 Risk for aspiration
 Ineffective coping- Family
 Ineffective tissue perfusion (cerebral)
 Risk for impaired skin integrity
 Ineffective airway
 Risk for imbalanced nurtition
 Alteration in breathing pattern
 Home care
Increased Intracranial Pressure (IICP)
Increased Intracranial PressureOverview
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Normal ICP Control
Autoregulation
Causes of Increased ICP
Clinical Manifestations
Diagnostic Studies
Monitoring Increased ICP
Treatment
ICP
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Skull is a closed box with three essential
components: blood 12%, brain tissue 78%,
and cerebrospinal fluid (CSF) 10%
Normally, arterial pressure, venous pressure,
intraabdominal and intrathoracic pressure,
posture, temperature, and blood gases keep
ICP relatively constant
Monro-Kellie hypothesis
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Brain tissue, blood, and CSF are mostly constant in
volume
If the volume of one component increases, another
component will be displaced
In total, the intracranial pressure will not change
while compensation is possible
(ex. Change in CSF production or absorption,
vasoconstriction or dilation, compression or
distention of brain tissue)
The ability to accommodate change is limited
Measuring Increased ICP
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Normal ICP is 0 to 15 mm Hg
Usually treated once above 20 mm Hg
Cerebral Blood Flow (CBF)
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Cerebral Blood Flow- amount of blood in mls passing
through 100g of brain tissue in 1 minute
Global CBF is 50ml/min
Normal blood flow 25ml/min in white matter
Normal blood flow 75 ml/min in gray matter
Brain requires constant supply of oxygen and
glucose
Brain uses 20% of oxygen and 25% of glucose
Autoregulation
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Autoregulation- the automatic adjustment in
diameter of cerebral blood vessels to
maintain constant blood flow despite
changes in blood pressure
Autoregulation is not effective with a MAP
less than 50 mm Hg
Autoregulation is not effective with a MAP
greater than 150 mm Hg
Autoregulation (Cont’d)
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Cerebral Perfusion Pressure (CPP)pressure needed to ensure blood flow to the
brain
CPP= MAP- ICP
Normal CPP is 70 to 100 mm Hg
CPP < 50 mm Hg causes ischemia and
neural death
CPP< 30 mm Hg is not compatible with life
Factors Affecting Cerebral Blood Flow
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Increased PaCO2 dilates cerebral vessels
Decreased PaCO2 constricts cerebral vessels,
increases cerebrovascular resistance, reduces CBF,
and decreases ICP
Decreased cerebral O2 tension dilates cerebral
vessels
Cardiac or respiratory arrest
Diabetic coma
Infections
Encephalopathies
Cerebral Edema
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Increased accumulation of fluid in extravascular
spaces of brain tissue
Results in increased tissue volume
Caused by brain abscess, brain tumor, hematoma,
hemorrhage, contusion, posttraumatic brain swelling,
meningitis, enephalitis, anoxic and ischemic
episodes, cerebral infarction, venous thrombosis,
lead or arsenic intoxication, hepatic encephalopathy,
uremia
Three types: vasogenic, cytotoxic, and interstitial
(more than one type can occur at the same time)
Cerebral Edema (Cont’d)
Vasogenic Cerebral Edema–
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Most common
Changes in endothelial lining of cerebral
capillaries allow leakage of macromolecules into
extravascular space
Fluid flows to extravascular space due to osmotic
gradient
Can be caused by tumors, abscesses, and toxins
Cerebral Edema (Cont’d)
Cytotoxic Cerebral Edema–
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Occurs most often in gray matter
Lesions or trauma cause cerebral hypoxia,
sodium depletion, and syndrome of inappropriate
antidiuretic hormone (SIADH)
Fluid then shifts from extracellular space directly
into the cells
Cerebral Edema (Cont’d)
Interstitial Cerebral Edema–
Periventricular diffusion of ventricular CSF in a
patient with uncontrolled hydrocephalus
Causes of Increased ICP
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Aneurysm rupture and subarachnoid hemorrhage
Brain tumor
Encephalitis
Hydrocephalus
Hypertensive brain hemorrhage
Intraventricular hemorrhage
Meningitis
Severe head injury
Subdural hematoma
Status epilepticus
Stroke
Source: National Institute of Health
Stages of Compliance with IICP
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Compensation is effective & autoregulation
present – CSF, Blood, and Brain
Compliance less effective & increase risk for
IICP
Any small increase in volume causes great
increase in ICP, loss of autoregulation &
Cushing's triad
Herniation
Increased Intracranial Pressure (IICP)
Cerebral edema/hydrocephalus
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Cerebral edemaIncreases the volume of
brain tissue which can
cause herniation
Hydrocephalus–
Build up of CSF inside the
skull
Increased intracranial pressure (IICP):
Nursing assessment specific to IICP
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Health history- assess brain involvement
Physical exam–
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Altered cerebral function assessment
Frequency depends on potential IICP
Early sign- change in LOC
3rd Cranial nerve compression- pupil dilation, no response to
light, ptosis of the eyelid on ipsilateral side as lesion
Papilledema, projectile vomiting, vision changes, seizures
Late sign- Cushing’s Traid – Widening pulse pressure
(increasing SBP & decreasing DBP) decreased HR, and
irregular respiratory pattern
Increased Intracranial Pressure (IICP):
Therapeutic Interventions
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Diagnostic tests
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CT Scan
MRI
PET
EEG
Angiography
Transcranial doppler studies
ECG
CBC, Coags, BMP, ABGs, drug screen
Increased Intracranial Pressure (IICP):
Therapeutic Interventions (Cont’d)
Medications–
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Osmotic diuretic (Mannitol)
Sometimes loop diuretic (Lasix)
Antiseizure medications (Dilantin)
Corticosteroids (Decadron) (brain tumors, bacterial
meningitis)
Proton pump inhibitor (Protonix) GI prophylaxis
Vasoactive drugs to maintain MAP
Barbituates
Sedation
ICP monitoring
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LICOX cath – brain tissue oxygenation of frontal
white matter PbtO2
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Jugular venous bulb cath SjvO2 indicates brain tissue
removal of O2 from blood
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Normal PbtO2 is 37-47 mmHg
Normal SjvO2 is 60% to 80%
<50 to 55% of O2 in venous blood indicates impairment of
flow and brain taking out more O2 than normal
ICP Waveforms (P1, P2, & P3) see Lewis p. 1474
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P1 arterial pulse wave should be highest
P2 is intracranial compliance – if higher than P1 compliance
is compromised
P3 is the venous pulsation and should be the lowest
Intracranial pressure monitoring can be used to continuously
measure ICP. The ICP tracing shows normal, elevated, and plateau
waves. At high ICP the P2 peak is higher than the P1 peak, and the
peaks become less distinct and plateau.
ICP Monitoring (Cont’d) Pg 1473
Intraventricular Monitoring:
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Considered gold standard of ICP monitoring
Surgically placed into ventricular system
Has drainage bag, pressure transducer, and three
way stopcock
Accurate, can drain CSF
Infection occurs in up to 20% of patients
Risk of hemorrhage during placement (2%)
ICP Monitoring (Cont’d)
Intraparenchymal Monitoring:
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Inserted into brain parenchyma via small hole drilled in skull
Thin cable with fiberoptic transducer at the tip
Easier to place, lower risk of infection, lower risk of bleed
Cannot drain CSF
Not as accurate
Mechanically complex design carries greater risk of failure
ICP Monitoring (Cont’d)
Subarachnoid Monitoring:
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Hollow screw placed through skull into dura
Dura is then punctured, allowing CSF to
communicate with the transducer
Frequently clog and are considered unreliable
Rarely used
ICP Monitoring (Cont’d)
Epidural Monitoring:
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Rest against the dura after passing through the
skull
Often inaccurate and are of limited clinical utility
Used for coagulopathic patients with hepatic
encephalopathy
ICP Monitoring (Cont’d)
Noninvasive Monitoring Tissue resonance analysis (TRA)ultrasound-based method
 Transcranial doppler
 Intraocular pressure
 Tympanic membrane displacement
 None of above have demonstrated
reproducible clinical success at this time
ICP Monitoring
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New Approaches to ICP Monitoring
Intraventricular and subarachnoid monitoring
devices for IICP
Increased intracranial pressure (IICP):
Pertinent Nursing Problems and Interventions
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Ineffective tissue perfusion: cerebral
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Assess/report sign IICP
Adequate airway
Promote venous drainage
Control environment stimuli
Plan nursing care – avoid clustering care
Avoid Valsalva’s maneuver
If bone flap out post op- assess & position
Assess external shunts/drains
VP shunt (a narrow piece of
tubing) is surgically placed in
the ventricle of the brain to
drain CSF to the abdomen
where it is absorbed by the
body.
CSF Shunt
After VP Shunt Surgery
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There is mild pain involved with this surgery. Acetaminophen
(Tylenol ) or ibuprofen may be used for postoperative
discomfort.
You will be in the hospital for 1 - 3 days. Once you are eating
and drinking, and there are no complications, you will be able to
go home.
You will have a follow-up appointment in the neurosurgery clinic
in 7-10 days. Your head dressing and staples will be removed
at that time.
After discharge, you may resume your regular activities unless
you are told otherwise.
In the future, you will need antibiotics before dental work and
other invasive procedures.
After VP Shunt Surgery (Cont’d)
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When to Call your Neurosurgeon or Nurse Practitioner
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Sometimes a shunt malfunctions by becoming clogged, disconnected, or
infected. If this happens, you may experience any of the following signs and
symptoms:
Redness, pain or swelling of the skin along the length of the shunt or at the
incision sites
Drainage from the incision
Fever greater than 101.5° F-usually within the first six months of surgery
Irritability or excessive sleepiness
Nausea or vomiting
Recurring headaches
Blurred or double vision
Sudden or gradual change in personality
Rubbing of the head
Weakness
Balance or coordination problems
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Brain Herniation
Brain Herniation
Cingulated Herniation - a
•Cingulate gyrus slips under
falx cerebri
•Usually caused tumor or
bleed
•Non life threatening
Brain Herniation
Uncal or Lateral Herniation - b
•Uncus of temporal lobe slips
through notch of tentorium and
compresses the ipsilateral CN 3,
brainstem, & vital centers
• Life threatening
Brain Herniation
Central or Transtentorial Herniation - c
•Caused by: downward pressure
on mid structures of cerebrum or
general cerebral edema which
compresses the brainstem
• Life threatening – compresses
RAS & vital centers
•Abnormal heart rhythms,
disturbances or cessation of
breathing, cardiac arrest, and
death
Brain Herniation
Extracranial Herniation - d
•Occurs with displacement of brain
through a cranial defect.
•Usually Non-life threatening
Brain Herniation
Infratentorial (subtentorial or Tonsillar)
Herniation - e
•Downward displacement of
infratentorial structures
through the foramen
magnum
• Life threatening
The End!