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