Patricia Ann D.
Canto, MD
Adult Neurology
OBJECTIVES
Review the Ventricular System and CSF
Pathway.
Identify common manifestations of patients
with increased intracranial pressure (ICP).
Evaluate and correlate history and
examination in localization of possible
neurological lesion.
Discuss the pathophysiology of each clinical
condition that result to increased ICP.
OBJECTIVES
Discuss the appropriate ancillary procedures
and lab examination that would aid in
differential diagnoses.
Discuss the treatment and therapeutic/nontherapeutic options including surgical
approach.
Review the pharmacodynamics and
pharmacokinetics of appropriate medicines.
CEREBROSPINAL FLUID
Function:
Mechanical protection by
bouyancy
Provides a constant
chemical environment for
neuronal activity
Important for acid-base
regulation for control of
respiration
Rate of production:
500mL/day (0.30.4mL/min)
CSF formation is
dependent on cerebral
perfusion
VENTRICULAR SYSTEM
THE CSF PATHWAY
INTRACRANIAL PRESSURE (ICP)
Pressure within the skull
Cranium is similar to a closed box with 3 volume
components
Brain Tissue (intra/extracellular fluids): 78%
Blood: 12%
Cerebrospinal fluid: 10%
Each of the 3 components contributes to the total
pressure exerted within the skull ICP
Changes in ICP are attributed to volume changes in
one or more of the constituents contained in the
cranium.
Normal ICP: 0-20 mmHg
THE MONROE-KELLIE HYPOTHESIS
RELATIONSHIP BETWEEN CEREBRAL PERFUSION
PRESSURE AND INTRACRANIAL PRESSURE
FORMULA
NORMAL
ICP
0-20 mmHg (adult)
CPP = MAP - ICP
70-100 mmHg (adult)
CBF = CPP
CVR
20-70 mL/100g tissue/min
MAP = DBP + 1/3 (SBP-DBP)
70-110 mm Hg (adult)
CEREBRAL AUTOREGULATION
CAUSES
Obstructed to CSF flow
and/or absorption
Increase CSF
production/CSF volume
expansion
Generalized Cerebral
Edema
Cytotoxic, Vasogenic or
Interstitial
Cerebral or Extracerebral
mass
Increase in Venous
pressure
OBSTRUCTED CSF
FLOW
Obstruction at ventricles
or in the subarachnoid
space at the base of the
brain
Ventricle closest to the
obstruction enlarges the
most
OBSTRUCTED CSF
ABSORPTION
Obstruction of the
basal cisterns
Extensive meningeal
disease
At absorptive sites
adjacent to cerebral
convexities and SSS:
ventricles are normal
in size
INCREASE CSF PRODUCTION
Rare
Choroid plexus papilloma increased ICP and
hydrocephalus
SPACE OCCUPYING LESIONS
Brain Tumors
Massive Infarction
with edema
Extensive Traumatic
Contusion
Parenchymal,
Subdural or
extradural
hematoma
Abscess
GENERALIZED CEREBRAL EDEMA
Ischemic-anoxic states, acute
hepatic failure, hypertensive
encephalopathy, hypercarbia, Reye
hepatocerebral syndrome
Increased pressure reduces CPP
Cytotoxic
Fluid accumulation within cells
Vasogenic
Proteinaceous fluid leaks into
extracellular space from capillaries
Interstitial
CSF pushed into the extracellular space
in periventricular white matter in
hydrocephalus
INCREASED VENOUS PRESSURE
Impairs CSF Reabsorption
CLINICAL PRESENTATION
Headache
Vomiting
Papilledema
Ocular Palsies
Altered Level of consciousness
Herniation Syndromes
Cushings Triad: increased systolic
BP with widened pulse pressure,
bradycardia and abnormal
breathing pattern
Anisocoria
SUPRATENTORIAL HERNIATION
SYNDROMES
Subfalcine
Herniation of brain tissue under
falx cerebri
Unilateral space occupying
lesion
Central (diencephalic)
Dencephalon is displaced
downward through tentorium
cerebelli resulting in
rostrocaudal deterioration
Duret hemorrhages, pituitary
stalk shearing, bilateral
occipital infarctions
Reduced level of consciousness
appears early
SUPRATENTORIAL HERNIATION
SYNDROMES
Tentorial (Uncal)
Uncus is displaced over
edge of tentorium
cerebelli and traps
ipsilateral CN III
If it continues, central and
tonsillar herniation may
occur
Ipsilateral CN III palsy: 1st
sign
Can compress PCA
INFRATENTORIAL HERNIATION
SYNDROMES
Upward cerebellar
Cerebellar vermis ascends
rostral to tentorium cerebelli
Compressing the midbrain
may compress cerebral
aqueduct
Tonsillar
Herniate through foramen
magnum compressing
medulla
Occur with supratentorial or
infratentorial lesions or with
increased ICP
CASE 1
A 62 year-old male right-handed male was
brought in due to progressive holocranial
headaches with a VAS of 8-9/10 accompanied
by fever, projectile vomiting and diplopia.
Physical Examination findings were
unremarkable.
Pertinent Neurologic Examination findings:
Drowsy and disoriented with bilateral
papilledema, bilateral lateral rectus palsies,
bilateral extensor toe sign and positive
meningeal signs.
LOCALIZATION
Headache
Fever
Projective vomiting
Diplopia
Drowsy
Disoriented
Bilateral papilledema
Bilateral LR palsy
Bilateral Extensor toe sign
(+) Meningeal Sign
LOCALIZATION
Is there a
lesion?
Upper Motor
Neuron
Lower Motor
Neuron
LOCALIZATION
Upper Motor
Neuron
Supratentorial
Cortical
Subcortical
Infratentorial
Brainstem
Spinal Cord
Cerebellum
LOCALIZATION
Lower Motor
Neuron
Anterior Horn
Cell
Peripheral
Nerve
Neuromuscular
Junction
Muscle
LOCALIZATION
1
YES There is a Lesion!!!
Upper Motor Neuron
Supratentorial
Diffuse Cortical and Subcortical
DIFFERENTIAL DIAGNOSIS
Vascular
Intracerebral or epidural
hemorrhage with mass
effect, SAH, large
hemispheric stroke,
venous thrombosis,
jugualr vein ligation, SVC
syndrome
Infectious
Abscess or empyema,
meningitis or encephalitis
Trauma
Autoimmune
Behcets syndrome,
systemic lupus
erythematosus,
sarcoidosis
Metabolic
Endocrine disturbances
(parathyroid, thyroid,
adrenal), hepatic
encephalopathy
Iatrogenic
Vitamin A intoxication,
medications (anabolic
steroids, tetracycline,
cyclosporine)
Neoplastic
Mass lesion, carcinomatous
meningitis
Degenerative
Congenital
DO NOT MISS!!!
Herniation
Acute Hydrocephalus
Surgical Mass Lesions
ANCILLARY PROCEDURES
Neuroimaging
Find the cause!!!
Check for mass effect, midline shift,
effacement of the basal cisterns and sulci,
global or focal edema, acute/subacute
hemorrhage/infarction
10-15% TBI patients have elevated ICP
despite normal CT
33% comatose TBI patients with normal
head CT and 2 of the following will have
increased ICP
>40 years old
Posturing
SBP <90 mmHg
ANCILLARY PROCEDURES
ICP Monitoring indications
GCS < 8 with abnormal CT
GCS < 8 with normal CT if 2/3 of
the following risk factors are
present
Age >40 years
Posturing
SBP <90 mmHg
ICP waveforms can provide
information about compliance.
P1: arterial wave
P2: rebound
P3: Venous outflow
Elevated P2: poor compliance
Compliance = volume
pressure
INTRACRANIAL PRESSURE MONITORS
INTRACRANIAL PRESSURE MONITORS
TYPE OF MONITOR
PRO
CON
Intraventricular
Gold standard, more global ICP
measurement, allows for diagnosis
and treatment
Highest infection rate (5-20%),
risk of hemorrhage (2%)
Intraparenchymal
Infection and hemorrhage rate low
(1%), easy to place
Measures regional ICP, cannot
recalibrate placement, drift
(reading may vary by 3 mmHg)
Subarachnoid/Subdural
Infection and hemorrhage rate low
Unreliable measurements, not
often used
Epidural
Low risk of hemorrhage compared
to Intraventricular and
intraparenchymal monitors,
occasional use with coagulopathic
liver patients
Unreliable measurements
ANCILLARY PROCEDURES
Lundberg Waves
Marker of critically low intracranial compliance
Result from:
Spiral tissue hypoperfusion
Progressive arteriolar dialtion
Increased cerebral blood volume
Termination spike serves to restore brain perfusion and
break cycle of cerebral vasodilation
Pressure gradients between brain compartments can
cause shift and herniation even when the absolute ICP
in any given compartment is <20 mmHg
LUNDBERG WAVES
Lundberg A (plateau waves):
sudden increases in ICP of 20100mm Hg
Minutes to hours
Cause reduced CBF/CPP and brain
ischemia
Treat aggressively by increasing
CPP and decreasing ICP
Lundberg B
Increases of 5-20 mmHg
Lasts 1-5 minutes
Related to respiratory variation
Characterized by sharpened
waveform
ANCILLARY PROCEDURES
Microdialysis technology
Placed intracranially in an at-risk
area
Measure tissue levels of lactate,
pyruvate and glucose
Brain tissue oxygen monitoring
Multimodality monitoring
Combination of microdialysis
technology with a brain tissue
oxygen sensor, ICP and CBF
monitoring
Offers a biochemical profile of the
regional brain environment
PREVENTION OF ELEVATED ICP IN BRAININJURED PATIENTS AT RISK
Elevate the head of the bed
to 30-45 degrees.
Keep head midline to
promote venous drainage
Avoid all free water and
maintain normal or
elevated serum osmolarity
Place a central venous
catheter to infuse
vasoactive or hyperosmolar
medications as needed
Hypotension will
exacerbate increased ICP
PREVENTION OF ELEVATED ICP IN BRAININJURED PATIENTS AT RISK
Avoid fever and treat
shivering
Prevent seizures
Control pain and agitation
Consider lidocaine 1% 10cc
into ETT before suctioning
Maintain Normocarbia
Maintain euvolemia with
normal saline or albumin
TREATMENT OF ELEVATED ICP
Consider Urgent Neurosurgical referral
Evacuation
Ventricular Drainage
Decompressive Hemicraniectomy
Lumbar-Peritoneal Shunting
TREATMENT OF ELEVATED ICP
Optimize CPP
Vasopressors
Isotonic Fluids
Reducing blood pressure
TREATMENT OF ELEVATED ICP: OSMOTIC TX
Hypertonic saline
Loading dose: 30mL 23% saline over 10-20mins via
central line
Maintenance dose: 3% saline 1mg/kg/h titrate to a
serum Na of 150-155 mEq/h
Mannitol 20%
Loading dose: 1g/kg (or 100g if wt unknown)
Maintenance dose: 0.5g/kg ever 4-6 hours titrated
to a serum osmolarity of 300-320 mOsm or
osmololal gap (measure Osm-calculated Osm) of 50
mOsm/kg
Half-life: 0.16 hour
Efficacy: 15-30 minutes
Duration of effect: 90 minutes 6 hours
TREATMENT OF ICP
Mannitol
Major osmotic diuretic
Elevates blood plasma osmolality
flow of water from tissues
into interstitial fluid and plasma
Expands circulating volume and
decreases blood viscosity
increase CBF and cerebral oxygen
delivery
Hypertonic Saline
Dehydration of brain tissue,
reduce viscosity, increase plasma
tonicity and regional brain tissue
perfusion, increase CO and MAP,
decreased inflammatory
response to brain injury,
restoration of normal membrane
potentials, and reduction of
extravascular lung volume
TREATMENT OF ICP
Carbonic Anhydrase
Inhibitors
Acetazolamide 500 mg BID
or TID
Reduce CSF formation
Loop Diuretic
Furosemide 0.5-1.0 mg/kg
alone
0.15-0.30mg/kg in
combination with Mannitol
Block Na/K/Cl symporter in
the ascending limb of the
loop of Henle
OSMOTIC THERAPY
PROS
Hypertonic
Saline
1.
2.
3.
4.
5.
Mannitol
1.
2.
CONS
Can be given as
continuous infusion
Ease of titration
Improves CPP
Volume expands
Effective in lowering ICP in
patients refractory to
Mannitol
1.
2.
3.
4.
Can use through a
peripheral line
Bolus dosing
1.
2.
5.
6.
3.
4.
5.
6.
USE IF
AVOID IF
Volume Overload
Flash pulmonary edema
Extreme hypernatremia
Rebound cerebral edema
upon tapering
Renal insufficiency (less
common )
Single report of CPM
when used in chronic
hyponatremia
Want to
volume expand
or improve CPP
Decompensate
d CHF, care if
baseline
hyponatremia
>24 hours (risk
of CPM
Volume depletion
Must replete UO ml/ml
with saline especially in
TBI and SAH
Hypotension
Rebound cerebral edema
Hypernatremia
Renal insufficiency
(reversible, seen if >200g
used daily or osmolal gap
>60-75 mOsm/kg)
Want to
diurese, no
central line
access
Renal failure,
hypotension
TREATMENT OF ELEVATED ICP
Short-term hyperventilation to PaCO2 of 25-30
mmHg.
Barbiturates
Pentobarbital: 5-20 mg/kg bolus followed by 1-4
mg/kg/h titrated to burst suppression on EEG
Can be used in patients refractory to ICP
treatments
Induced hypothermia to 32 to 340C
Steroids
Paralytics
