Transcript Increased Intracranial Pressure

Increased Intracranial Pressure
Mary Ann Reilly
BSN, MS, CRRN
Santa Clara Valley Medical Center, Rehab
Nurse Manager
• In 2004 the SJ Mercury wrote: "As he was giving
his speech he stumbled slightly and then he started
to perspire a bit. I thought almost immediately that
something is not right.“
• His repeated vomiting prompted paramedics to
treat him with oxygen and monitor his heart for
half an hour -- routine care for a sudden foodborne illness
• The initial suspicion that Mayor Ron Gonzales had food
poisoning Wednesday night shows just how difficult some
strokes are to detect -- and experts say it offers a warning
to people who might find themselves with similar
symptoms.
• Gonzales' type of stroke is called an intraventricular
hemorrhage.
• This means that a blood vessel had broken and was leaking
into the ventricle, which carries spinal fluid.
So what’s the big deal?
• Skull
• Components of Cranial
Vault
– Meninges
• Dura
• Arachnoid
• Pia
– Brain
• Brain tissue 80-88%
– Blood
• Blood 2-11%
– CSF
• CSF 9-10%
http://learntech.uwe.ac.uk/neuroanatomy/neuro4_1.htm
Blood
– 15-20 of the cardiac output
– 20-25% of all oxygen inspired
– 750cc/min
• 80% from carotid arteries
• 20% from vertebral
• Circle of Willis is collateral circulation
– No sugar/fat/oxygen storage
Autoregulation
•When intra-cranial pressure
begins to rise, the body’s own
compensatory mechanisms
include decreasing the production
of CSF and restricting the blood
flow to the brain(by
vasoconstriction).
Autoregulation
• Self Regulated
– PCO2 (carbon dioxide) vasodilator
• For every 1mmHg change in PCO2 there is a 1-2cc
change in blood flow per 100 GMs of brain
– (1300-1400Gms avg. wt.) =s [750 +65] or [750 + 130]
• Diameter of vessels
– Hypercapnia: Increases CBF
– Hypocapnia: Decreases CBF
Intercrainial Pressure Regulation
• When BP increases, cerebral arterioles
constrict to keep blood entering brain at
steady rate.
• When BP falls, cerebral arterioles dilate to
increase blood flow to brain
Intercrainial Pressure Regulation
• Metabolic regulation—changes in O2 and
CO2: Low O2 and increased CO2 cause
vasodilation CSF regulation—decreased
production or increased reabsorption
decreases ICP.
Factors Affecting CBF
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Viscosity of the blood
Seizures
Anemia
Drugs
CSF
• 125-150 cc clear fluid
– 500cc produced per day
– 20cc per hour
– Replaced 4-7 times per day
• Function
– Protection, cushions
– Waster disposal
– Nutritional support (2/3 bodies BS)
CSF Pressure
• Norm
– 1-15 mmHg or <200mm H2O
• Low pressure
– Dehydration
• Increased pressure
– Val Salva,Tumor, Subdural Hematoma,
Subarachnoid Hemorrhage, Infections,
Hydrocephalus
Symptoms of Increasing ICP
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Headache
Visual changes
Nausea
Vomiting
Behavior changes
Changes in LOC
Seizures
Symptoms
• Aniscoria
• Hemiparesis
• Vital sign
changes
– Cushing
Triad
Pulse
Cardiac center is located in the medulla –
compression may affect heart rate
Temperature
Raised indicates infection
Hypothermia seen in drug overdose
Blood Pressure
Increase associated with sympathetic
stimulation. Decrease rarely attributed to brain
injury
Respiration
Increase may indicate damage to the midbrain.
Decrease may indicate damage to lower pons
and upper medulla
Pupils
One reacting the other not may indicate
pressure on the to the 3rd cranial nerve caused
by I-ICP or a lesion
http://learntech.uwe.ac.uk/neuroanatomy/neuro4_4.htm
Cushing’s Triad
• Vital Sign Changes in ICP—
• Systolic pressure increases (widened pulse
pressure results).
• Slowing of heart occurs—bradycardia
(occurs as result of reflexive slowing in
response to increased systolic pressure)
• Respiration changes—becomes slowed
Could it be?
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Difficulty speaking
Blurred vision
Hypertension
Shallow rapid breathing
Visual disturbances
Paresthesia
• Hypoglycemia
OR?
- Confusion
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Lethargy
Nausea & Vomiting
Coma
Seizures
• Syndrome of Inappropriate ADH
OR?
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Changes in LOC
Nausea & Vomiting
Irritability
Disorientation
Personality changes
Seizures
• Fluid Overload
OR?
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Street drug
Alcohol withdrawal
Over dose
Diabetic ketoacidosis
Hypervitiaminosis A
• Drug
• www.merck.com/mrkshared/mmanual/section1/chapter3/3c.jsp
Diagnosis of Increased
Intracranial Pressure
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Overt symptoms
Papilledema
Nuchal rigidity
Lumbar Puncture***
Lumbar Puncture
• Contraindicated
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Focal signs
Intracranial mass
Papilledema
Cardiorespiratory compromise
Infection of skin
Rational for Contraindication
• A simple analogy
Performing a LP in the
presence of I-ICP,
may result in herniation
Herniation
• Tentorium
– Midbrain and diencephalon
through the tentorium
• Uncal
• Tonsillar
– Cerebellar tonsils
through the foramen
magnum
Diencephalic Stage
• Confused and drowsy
• Constricted pupils
• Gaze palsies
Mesencephalic Stage:
• Unconscious
• Decerebrate
posturing
• Dilated pupils
• Hyperventilation
Pontine Stage
• Unconscious
• Decerebrate
posturing
• Constricted pupils
• Irregular breathing
Decorticate posture
• Indicated by rigidity, flexion of the arms,
clenched fists, and extended legs. The arms
are bent inward toward the body with the
wrists and fingers bent and held on the
chest. Presence of this type of posturing
implies severe damage to the brain with
immediate need for medical attention.
Decerebrate Posturing
• Internal rotation and extension of the arms
& lower limb extension
• Due to midbrain compression as the
brainstem is further compressed
Medullary Stage
• Unconscious
• Flaccid
• Loss of homeostatic
control:
• Increase heart rate
• Decrease blood pressure
• Hyperthermia
• Cheyne-Stokes breathing
Cheyne-Stokes
• Breathing describes a waxing and waning
ventilation, sometimes with periods of
apnea, that occur in cycles.
• It is due to a delay in the medullary
chemoreceptor response to blood gas
changes
89
3
http://thediagram.com/3_6/
Common Causes of I-ICP
• Vascular abnormalities
– AV malformations, aneurisms, stroke
• Diffuse cerebral ischemia
– Closed head trauma, shaken baby, vasospasm
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CNS infections
Tumors
Trauma
Obstruction of CSF flow
Hydrochepalus
Intra
Cerebral
Hemorrhage
AV Malformation
Crainal Defect
Crainial defect with
midline shift
• The Monroe-Kelle Hypothesis states that
an increase in the volume of one component
(blood, brain tissue, CSF) must be accompanied
by a decrease in another component if intracranial
pressure is to remain constant. The CSF and blood
volume are the compartments that most easily
change to accommodate changes in
pressure. Interventions to prevent secondary brain
injury follows these principles and focuses
primarily on cerebral blood flow and drainage.
Management / Trauma
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Rapid transportation
Early intubation
Aggressive resuscitation
Immediate CT
ICP monitoring
CAT Scans
• Sensitivity for visualizing blood
approximately 96%
• Visualizes
– Fractures
– Hematomas
Operative Management
• Burr holes
• Intra-operative ultra sound
• Surgical evacuation of mass lesion
– Craniotomy
– Craniectomy
• Ventricular drainage
http://www.trauma.org/neuro/neuromonitor.html
Medical Management
• Adequate cerebral perfusion
– Dehydration
– Hypovolemia
– Hypoxia
• Hyperventilation
– Sepsis
– Normal or hypothermia
• Hyperthermia causes increased cellular metabolism (10-13%),
increased lactic acid production, increased CO2 (vasodilatation)
Osmotic Diuretics
Mannitol
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Reduces ICP in 5-10 min. trough osmotic gradient
BBB must be intact
Removes H2O not Na
Caution with
– Hypotension
– Coagulopathy
– CHF
Duiretics
• Furosemide (lasix)
– Loop of Henle, blocks transport of Cl & Na
– Reduced CSF production 40-70%
– Postssium depletion
Other Medications
• Corticosteroids
• H2 Blockers
• Sedation to control agitation, reduces
metabolic needs
• Analgesia
• Barbiturates to suppress seizures, decreases
metabolic needs, vasoactive effects
Hypothermia
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Decreased cellular metabolism
Brain temp is ~ 2.0o F higher than body
Reduces inflammatory process
Reduces cerebral metabolism
Limits secondary brain injury
Nutrition
• Energy requirement 125-200% ABOVE
normal
• Early feeding has a favorable effect on
survival
• TPN & PPN
Nursing Care
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Assessment
Touch
Oxygen
Control pain
Medicate prior to administering care
Break up activities
Care
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Decrease stimulation
Positioning
Bowel
Bladder
Glascow Coma Scale
Verbal
Eye opening
Motor
Score
Score
Score Finding
5
4
3
2
1
Finding
Normal fluent
appropriate
Confused but
fluent
Mumbling
occasional word
recognizable
Vocalizations
but no words
No vocalizations
or verbalizations
Finding
6
5
4
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Eyes open without
stimulation
Eyes open to loud
noise
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2
Eyes open to pain
only
2
1
No eye opening
1
Follows commands
Locates pain
stimulus
Pulls away from
pain
Flexion posture to
pain
Extension posture
to pain
No motor response
1.
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8.
www.rad.usuhs.mil/rad/herniation
www.thridage.com/health/adam/ency/article
www.homestead.com/emguidemaps/files/coma.html
www.classes.kuma.edu/sm/nurs420
www.emguidemaps.homestead.com/files/anisocoria.html
www.annals.org/cgi/content/full/130 /5/427/F1
www.med.harvard.edu/AANLIB/home.html
http://thediagram.com/3_6/
http://www.sophysa.com/patient/hydrocephalus/hydrocephalus3.htm
Lumbo-Peritoneal Shunt
LEONARDO DA VINCI - Drawing of the cerebral
ventricles after they have been injected with a dye
Speech arrest
Fluent Aphasia
This large cerebral infarct occurred in the
setting of atrial fibrillation and caused a
dense fluent aphasia. The CT scan shown
here was obtained 5 days after the onset of
stroke symptoms. View the temporal movie
of this slice to see the evolution of the lesion
over the 5 day period. Significant swelling in
the infarcted area produces obvious shift of
the midline by day 5. This corresponded
clinically to a diminished level of arousal,
which resolved after 2 days.
Can’t read
Hesitating Speech
Loss of sensation
Chronic Subdural
Cavenous angioma
AV Malformation with MRA
Acute Stroke
sudden onset of right body weakness and
trouble speaking
Diffusion-weighted MR showed a large area of
abnormal signal in the region clinically suspected:
the portion of left hemisphere supplied by the
middle cerebral artery.
Normal aging brain
Normal aging
Normal Aging coronal plane
http://www.med.harvard.edu/AANLIB/home.html
Cerebral Hemorrhage
MS
Look at the large round white spot in the right frontal region. This is
a relatively new lesion, and you can see how it enlarges very rapidly
over the next weeks. Look at the timeline cine. With time, the lesion
enlarges, there is a "halo" of white (high) signal which surrounds
the lesion. This probably represents the edema which forms in
reaction to the acute damage. At the end of the movie, you can see
that the lesion has nearly disappeared, with another lesions
appearing
http://www.neuroland.com/default_old.htm
http://www.neuroland.com/nm/neuropathic_pain.htm
Burst arteries cause Increased ICP by
• Increased Intracrainal PressureNormal
intracrainal pressure—less than 15mm Hg
or 180mm H20. ^ICP considered when
pressure ^than this. When ICP^ ischemia
and hypoxia results and damages neural
tissue. If ICP^ continues—can cause
herniation syndrome.
• Causes of ICPBrain tumors, abscesses,
cerebral edema from injuries. CSF
obstruction—produces hydrocephalus
Communicating vs. non-communicating
Cerebral vasodilation—compensatory
mechanism for conditions of hypoxia (when
pCO2 ^, cerebral vasodilation will occur).
• Head InjuriesSkull fractures—linear,
comminuted, depressed or basilar Basilar
(occurs at base of skull)—produces
hemorrhage from nose, pharynx, ears
Bruising over mastoid bone—Battle’s sign
May cause CSF leaking from ears, nose
Brain Injuries--Concussion vs. Contusion
Intracranial Hemorrhage—Epidural vs.
Subdural Hematoma
• Epidural HematomaBlood collects in the
epidural space Expanding hematoma causes
rapid symptoms of I.C.P. and is considered
medical emergency Treatment—surgical
openings through skull (burr holes) to
decrease I.C.P., craniotomy may be
necessary to remove clot and control
bleeding
• Subdural HematomaCollection of blood between
dura and the brain May be venous in origin, may
be acute, subacute, or chronic depending on size
of vessel and amount of bleeding Acute—cause is
major head injury, symptoms develop over 24-48
hrs. Subacute—less severe trauma, symptoms
develop over 48 hrs. to 2 weeks Chronic—cause is
minor trauma, seen in elderly, symptoms develop
over 3 weeks to 3 months
• Treatment of ICPHyperventilation—blow
off CO2. Osmotic diuretics--^serum
osmolarity Mannitol (Osmitrol) Hypertonic
Glucose Loop diuretics Steroids—IV or p.o.
Dexamethosone (Decadron)
Methylprednisolone (Solu-Medrol)
• Treatment of ICP cont.Anticonvulsants—
prevent seizures IV fluids—keep
moderately dehydrated GIVE 0.45% to
0.9% NaCl AVOID 5% Dextrose
Barbiturates may be used in extreme cases
in order to induce coma and decrease
metabolic demands on brain.
• Brain tumors Classified by site, histologic cell
type, degree of malignancy Gliomas—arise from
neuroglia tissue Medulloblastoma—malignant
tumor of cerebellum Menigiomas—arise from
meniges, slow growing Acoustic neuromas—arise
from 8th cranial nerve Pituitary—arise from
pituitary gland, slow growing Location of tumors
(in cerebral lobes) account for specific symptoms
• Symptoms of Brain Tumors Classic
symptoms of I.C.P. Headache may be worse
in A.M. Seizures are common with all types
of brain tumors Other symptoms depends
on location of tumor within the cerebral
lobes (occipital, frontal, parietal, temporal,
cerebellar)
• Treatment of brain tumorsTumor
reduction—surgery, radiation,
chemotherapy Manage and prevent
symptoms of I.C.P. Crainotomy
Supratentorial approach—above the
tentorium (fold of dura separating cerebral
cortex from cerebellum and brainstem
Infratentorial approach---below the
tentorium
• Pre-op Nursing CareShaving head—permit
needed, save hair, provide cap Teach deep
breathing and leg exercises (no coughing)
Pre-op enema is controversial Excellent
baseline assessments necessary pre-op
• Post-op Nursing Care—Supratentorial
ApproachH.O.B. 30-45 degrees Pillow
under head and shoulder, align neck Avoid
positioning on operative side Monitor for
cranial nerve dysfunction II-visual deficits
III-ptosis IV, V—deficits in extraocular
movements
• Post-op Nursing Care for Infratentorial
ApproachH.O.B. flat, keep client off back
Small pillow under head, neck alignment
Monitor for cranial nerve dysfunction III,
IV, VI—ocular movements VII—absent
corneal reflex, paralysis of facial muscles
VIII—decreased hearing, nystagmus IX,
X—gag and swallowing reflex decreased
• Nursing Care Common to both surgical
approachesContinuous neuro assessments,
especially for I.C.P. Anticonvulsants,
seizure precautions Body temperature
regulation, prevent hyperthermia Turn, deep
breath q. 2 hrs. Reinforce dressings—check
for CSF on drainage Pain management—
use of Codeine
• S.I.A.D.H. Posterior pituitary secretes ADH
to regulate water balance Too much ADH
causes S.I.A.D.H. where kidneys will retain
H2O and blood serum will be hypotonic
Signs and symptoms: Changes in L.O.C.,
headache, nausea and vomiting Decreased
urinary output
• Treatment of S.I.A.D.H.Fluid restriction
500cc or less in 24 hrs. IV fluids 3% or 5%
saline with appropriate electrolyte
replacements (K, Mg) Diuretics (Lasix)
Lithium Carbonate
• Diabetes InsipidusFailure of ADH secretion
and failure of kidneys to store H2O. Signs
and symptoms: Urinary output increased
with specific gravity of urine decreased
Client will have dehydration Treatment: Use
of Vasopressin (Pitressin), given I.M. or s.c.
http://academic.luzerne.edu/aisaacs/webversion/nur204-2003/03increasedintracrainalpressure_files/frame.htm