ICP---PHYSIOLOGY AND

PATHOPHYSIOLOGY
MODERATOR: Dr VENKATESH
PRESENTED BY: DR KHAWER
MUNEER

Intracranial pressure
Intracranial pressure refers to the pressure within the
intracranial vault (skull).
It is the pressure exerted by the total volume from
the brain tissue, blood, and CSF.
Intracranial pressure is important as it affects
cerebral perfusion pressure and cerebral blood flow.
Normal ICP is between 5 and 15mmHg.
Because it is very dependant on posture, the external
auditory meatus is usually used as the zero point.

Intracranial pressure
Constituents within the skull include the brain (80%/1400ml), blood
(10%/150ml) and cerebrospinal fluid (CSF 10%/150ml)
The skull is a rigid box so if one of the three components increases
in volume, then there must be compensation by a decrease in the
volume of one or more of the remaining components otherwise the
ICP will increase (Monro-Kellie hypothesis).
The term compliance is often used to describe this relationship, but
it is more accurately elastance (change in pressure for unit change
in volume)

ICP elastance curve

ICP elasta curve

Stage 1/2 = compensation phase. As one of the intracranial
constituents increases in volume, the other two constituents
decrease in volume in order to keep the intracranial pressure
constant.
Stage 3/4 = decompensated phase. When compensatory
mechanisms are exhausted, small increases in the volumes of
intracranial constituents cause large increases in ICP.
The slope of the curve is dependent on which intracranial
constituent is increasing. If it is blood or CSF, both of which are
poorly compressible, then the slope is steeper. If it is brain
tissue, such as from a tumour, the curve is less steep as the
tissue is compressible.

Factors that influence ICP

Arterial pressure
Venous pressure
Intraabdominal and intrathoracic pressure
Posture
Temperature
Blood gases (CO2 levels)

CONTROL OF ICP--There are many ways that ICP is controlled.

VOLUME BUFFERING (pressure-volume relationship)

Blood and CSF provide the main protection to the brain when the
intracranial volume increases.
Cerebral blood volume (CBV) can be increased by increasing the
amount of blood flow that enters the cranium (e.g. by vasodilation,
or by hindering its venous drainage, e.g. head down position, jugular
vein obstruction, increase right heart or intrathoracic pressures)

 CSF plays an important role in compensating for increases

in
ICP by spatial compensation whereby an increase in the
volume of an intracranial constituent will cause a decrease
in intracranial CSF volume by displacing CSF into the
spinal canal. Spatial compensation occurs slowly and is
significant in tumours which expand gradually but
provides limited compensation for acute and sudden
increase in ICP (e.g. in haematomas as it gets exhausted
rapidly).

CONTROL OF CBF AND CBV--Various factors discussed below affect CBF and CBV which in
turn control ICP

Autoregulation (myogenic , hydrostatic pressure)

Arterial carbon dioxide tension
Arterial oxygen tension
Flow-metabolic coupling
Neurogenic control
Temperature
Viscosity of blood

Increased Intracranial Pressure

Can occur due to pathological Conditions Causing a
Rise in Volume of Intracranial Constituents
Any of the three intracranial constituents (tissue,
blood or CSF) can increase in size and volume.

Increased Intracranial Pressure

Brain Tissue
Tumours
Cerebral oedema secondary to trauma, infection, infarction,
hyponatraemia, hypertensive encephalopathy, acute liver
failure, Reyes syndrome
Cerebral abcesses
Cerebral contusions

Increased Intracranial Pressure

Blood
Intracerebral, subarachnoid, subdural, extradural
haematomas
Arteriolar dilatation secondary to hypoxaemia, hypercarbia,
anaesthetic drugs, hyperthermia, seizures, hypotension
Venous dilatation secondary to venous obstruction from
high PEEP, coughing, straining, heart failure, venous sinus
thrombosis, head-down tilt, tight neck ties

Increased Intracranial Pressure

CSF
Hydrocephalus
Meningeal diseases
Choroid plexus tumours

Presentation: Symptoms
Headache
Visual changes
Nausea
Vomiting
Behavior changes
Altered consciousness: irritability to obtundation or
coma.
Seizures
Nuchal rigidity
Focal neurologic deficit

Presentation: Symptoms
Infants may present with less specific
symptoms

Irritability
Bulging fontanel
Lethargy
Poor feeding

Presentation: signs
Papilledema
Retinal haemorrhages
Dilated pupil: usually on the side of the lesion
Cranial nerve palsies of the third, fourth, and sixth cranial
nerves
Hemiparesis, hyperreflexia, and hypertonia: are late signs
Cushing triad: another late sign, and may be a preterminal
event

Presentation: signs
Infants may develop

Macrocephaly
Split sutures
Bulging fontanel
Hydrocephalus: Sun setting" appearance of the eyes may
appear

Cushings Triad
Systolic pressure increases (widened pulse pressure
results).
Slowing of heart occursbradycardia (occurs as result
of reflexive slowing in response to increased systolic
pressure)
Respiration changesbecomes slowed

Effects of raised icp

As ICP rises, CPP falls eventually to a point when there is no cerebral blood flow, no
cerebral perfusion and brain death.
Prior to this, brain structures begin to herniate (protrude through an opening).
- Temporal lobe herniation beneath tentorium cerebelli (uncal herniation) causes
cranial nerve III palsy (dilatation of pupil followed by movement of eye down and
out).
- Herniation of cerebellar peduncles through foramen magnum (tonsillar
herniation).
- Subfalcine herniation occurs when the cingulate gyrus on the medial aspect of
the frontal lobe is displaced across the midline under the free edge of the falx
cerebri and may compress the anterior cerebral artery

herniation

MANAGEMENT OF RAISED ICP

Maintenance of adequate ventilation and blood pressure are the
cornerstones of management of elevated intracranial pressure
Techniques that can be employed to reduce ICP are aimed at reducing the
volume of one or more of the contents of the skull.

Reduce brain size: osmolar therapy (mannitol, hypertonic saline)

Reduce CSF: drainage (EVD)
Reduce blood volume (hyperventilation, avoid hypercarbia, hypoxia)
Surgical removal of pathology (bleed, tumor)
Alternatively can expand skull by decompressive craniotomy

ENLS- emergency neurological life support

Tier Zero:
HOB > 30 degrees
ensure adequate sedation
correct hyponatremia, hyperthermia, and vasogenic
edema
keep CPP > 60-70 mm Hg
**normocarbia (PaCO2 35-45)
**good oxygenation (PaO2 >100)

 Tier One:

secure airway
mannitol0.5-1 gm/kg IV bolus
start3% saline10-20 cc/hr
CSF drainage

Tier Two:
hypertonic salinebolus (3%-23.4%)
considerpropofolbolus and infusion
considerdecompressive craniotomy

 Tier Three:

pentobarbitalbolus and infusion titrated for ICP goal

inducehypothermia
hyperventilationif used with cerebral oxygen monitor
raise MAPto improve CPP

BRAIN TRAUMA FOUNDATION

GUIDELINES- The guidelines address treatment interventions , monitoring , and treatment thresholds that
are specific to TBI or that address a risk that is greater in patients with TBI Like raised ICP

Blood pressure thresholds Level III

Maintaining SBP at 100 mm Hg for patients 50 to 69 years old or
at 110 mm Hg or above for patients 15 to 49 or > 70 years old may
be considered to decrease mortality and improve outcomes.

Intracranial pressure thresholds-- Treating ICP > 22 mm Hg is recommended because values above this level are
associated with increased mortality (Level IIB).

A combination of ICP values and clinical and brain C T findings may be used to
make management decisions (Level III).
Cerebral perfusion pressure thresholds--
The recommended target CPP value for survival and favorable outcomes is
between 60 and 70 mm Hg. Whether 60 or 70 mm Hg is the minimum optimal CPP
threshold is unclear and may depend upon the autoregulatory status of the patient
(Level IIB).

Avoiding aggressive attempts to maintain CPP > 70 mm Hg with fluids and pressors
may be considered because of the risk of adult respiratory failure (Level III)

 Advanced cerebral monitoring thresholds

Jugular venous saturation of ,50% may be a
threshold to avoid in order to reduce mortality and
improve
outcomes (level III).

Monitoring Recommendations ---

Intracranial pressure monitoring

Management of severe TBI patients using information from ICP monitoring is
recommended to reduce inhospital and 2-week post-injury mortality (LevelIB)
ICP should be monitored in all salvageable patients with a TBI (GCS 3-8 after
resuscitation) and an abnormal CT scan. An abnormal C T scan of the head is one that
reveals hematomas, contusions, swelling, herniation, or compressed basal cisterns
ICP monitoring is indicated in patients with severe TBI with a normal C T scan if 2
of the following features are noted at admission: age >40 years, unilateral or bilateral
motor posturing, or SBP <90 mm Hg.

 Cerebral perfusion pressure monitoring

Management of severe TBI patients using guidelines-based recommendations

for CPP monitoring is recommended to decrease 2-wk mortality (Level IIB).
Advanced cerebral monitoring-- Jugular bulb monitoring of AVDO2, as a source of information for management
decisions, may be considered to reduce mortality and improve outcomes at 3 and 6
mo post-injury (Level III)

Treatment Recommendations
Prophylactic hypothermia ----

Early (within 2.5 h), short-term (48 h post-injury), prophylactic hypothermia is not
recommended to improve outcomes in patients with diffuse injury.
Hyperosmolar therapy-----

Mannitol is effective for control of raised ICP at doses of 0.25 to 1 g/kg body
weight. Arterial hypotension (systolic blood pressure < 90 mm Hg) should be avoided.
Restrict mannitol use prior to ICP monitoring to patients with signs of transtentorial
herniation or progressive neurologic deterioration not attributable to extracranial
causes

 Cerebrospinal fluid drainage --An EVD system zeroed at the midbrain with continuous drainage of CSF
may be considered to lower ICP burden more effectively than
intermittent use
Use of CSF drainage to lower ICP in patients with an initial GCS ,6
during the first 12 h after injury may be considered.

Ventilation therapies-----(Level IIB)

Prolonged prophylactic hyperventilation with PaCO2 of 25 mm

Hg is not recommended.

Hyperventilation is recommended as a temporizing measure for

the reduction of elevated ICP

Hyperventilation should be avoided during the first 24 h after

injury when CBF often is reduced critically. If hyperventilation is
used, SjO2 or BtpO2 measurements are recommended to monitor
oxygen delivery.

SjO2, jugular venous oxygen saturation:BtpO2, brain tissue O2

Anesthetics, analgesics, and sedatives

(Level IIB)

Administration of barbiturates to induce burst suppression measured by EEG as

prophylaxis against the development of ICH is not recommended
High-dose barbiturate administration is recommended to control elevated ICP refractory
to maximum standard medical and surgical treatment. Hemodynamic stability is
essential before and during barbiturate therapy.
Although propofol is recommended for the control of ICP, it is not recommended for
improvement in mortality or 6-month outcomes. Caution is required as high-dose
propofol can produce significant morbidity.

Steroids---
The use of steroids is not recommended for improving outcome or reducing ICP. In
patients with severe TBI, high dose methylprednisolone was associated with
increased mortality and is contraindicated.
Nutrition
Feeding patients to attain basal caloric replacement at least by the fifth day and
at most by the seventh day post-injury is recommended to decrease mortality.

Transgastric jejunal feeding is recommended to reduce the incidence of ventilatorassociated pneumonia

 Seizure prophylaxis
Prophylactic use of phenytoin or valproate is not recommended for preventing late PTS.
Phenytoin is recommended to decrease the incidence of early PTS (within 7 d of injury),
when the overall benefit is thought to outweigh the complications associated with such
treatment. However, early PTS have not been associated with worse outcomes
At the present time there is insufficient evidence to recommend levetiracetam compared
with phenytoin regarding efficacy in preventing early post-traumatic seizures and toxicity.

Indications for ICP monitori ng

The Brain Trauma Foundation (BTF) recommends ICP

monitoring to guide ICP/CPP-directed therapy after
severe TBI in all salvageable patients with an abnormal
cranial computed tomography (CT) scan, and in those
with a normal scan if two or more of the following
features are present:
Aged >40 yr;
Unilateral or bilateral motor posturing; or
Systolic blood pressure <90 mm Hg

ICP waveform--

Lundberg first classified ventricular pressure fluctuations in humans in 1960

A waves or plateau wavesThese comprise a steep rise in

ICP from near normal values to 50 mm Hg or more, persisting for 520

minutes and then falling sharply. These waves are always pathological
and indicate greatly reduced compliance. They are frequently
accompanied by neurological
deterioration.

B wavesThese rhythmic oscillations occur every 12 minutes. ICP

rises in a crescendo manner to levels 2030 mm Hg higher than

baseline and then falls abruptly. These waves were originally always
associated with Cheyne-Stokes respiration. However, they also occur in
ventilated patients and are probably related to changes in
cerebrovascular tone and cerebral blood volume. B waves are also
indicative of failing intracranial compensation

 C wavesThese oscillations occur with a frequency

of 48 per minute and are of smaller amplitude than B
waves. They are synchronous with spontaneous TraubHering-Meyer type variations
in blood pressure and are probably of limited
pathological significance.

Measurement of icp
Ventriculostomy
Intraparenchymal monitor
Epidural/subdural catheter
Subarachnoid screw

ventriculostomy
The ventriculostomy is also referred to as the
intraventricular catheter or ventriculostomy drain.
It is a soft tube placed through a burr hole into the
lateral ventricle of the brain. The tubing connects to a
standard transducer set which is never pressurized.
It is the most accurate way to receive and monitor an
ICP.
The ventriculostomy also allows for the therapeutic
drainage of CSF.

Intraparenchymal monitor
The intraparenchymal or a fiberoptic transduced
tipped catheter is seen very often in the ICU.
It is the second most accurate way to obtain an ICP.
There is no way to drain CSF, but infection and
hemorrhage rates are low.

Epidural/subdural catheter
The subdural/epidural catheter is another method to
monitor ICP.
It is less invasive but also less accurate.
It cannot be used to drain CSF.
The catheter has a lower risk of infection or hemorrhage

Subarachnoid screw
The subarachnoid screw, also known as a bolt,
connects to an external traducer via tubing.
It is placed into the skull abutting the dura. It is hollow
screw which allows CSF to fill the bolt, allowing the
pressures to become equal.
The positives of this method are that infection and
hemorrhage risks are low.
The negative aspects include the possibility of errors
from ICP underestimation, misplacement of the screw,
and occlusion by debris

COMPLICATIONS OF ICP
MONITORING
Infection

intracranial haemorrhage or haematoma

CSF Leakage
Mechanical failure or blockage
Over drainage of CSF

EFFECT OF ANAESTHETIC AGENTS ON CBF

AND ICP
VOLATILE ANAESTHETICS---

Cause dose related increase in CBF and a decrease in CMRO2

Cerebral autoregulation is preserved at 1 MAC Concentration of almost all volatile

anaesthetics

in CBF at Doses higher than 1 MAC could reflect uncoupling of flow and metabolism

LUXURY PERFUSION.. The combination of a decrease in neuronal metabolic demand

with an increase in CBF (metabolic supply) has been termed luxury perfusion. A
detrimental circulatory steal phenomenon is possible with volatile anesthetics in the
setting of focal ischemia

The order of vasodilating potency is approximately halothane enflrane > desflrane

isoflrane > sevoflrane.

EFFECT OF INTRAVENOUS AGENTS ON CBF/ICP

BARBITURATES
Dose dependent in CMR and CBF until EEG becomes
isoelectric
Unlike isoflurane, barbiturates reduce metabolic rate
uniformly throughout the brain.
Barbiturates also seem to facilitate absorption of CSF.
Their anticonvulsant properties are also advantageous in
neurosurgical patients who are at increased risk of seizures.

PROPOFOL--Effect on CBF/CMR are similar to those of barbiturates

Although it has been associated with dystonic and
choreiform movements, propofol seems to have signifi cant
anticonvulsant activity.
Both co2 responsiveness and autoregulation are preserved
Its short elimination half-life makes it a useful agent for
neuroanesthesia. Propofol infusion is commonly
used for maintenance of anesthesia in patients with
or at risk of intracranial hypertension

ETOMIDATE---effect similar to barbiturates, greater hemodyamic stability in unstable

pts .Also decreases production and enhances absorption of csf. Concerns with adrenal
suppression and myoclonus limits its use in neuroanesthesia and icu.
KETAMINE-----only intravenous anesthetic that dilates the cerebral vasculature and
increases CBF (50% to 60%) and does not alter much the global CMR02
BZD-----lower CBF and CMR, but to a lesser extent than barbiturates, etomidate, or
propofol
OPOIDS--- have minimal effect on CBF ,CMR and ICP, unless PaCo2 rises secondary to
respiratory depression.

 NEUROMUSCULAR BLOCKING AGENTS---histaminemediated cerebral vasodilation increase ICP, whereas

systemic hypotension (from histamine release or
ganglionic blockade) lowers CPP. Succinylcholine can
increase ICP, possibly as a result of cerebral activation
associated with enhanced muscle spindle activity, but
the increase is generally minimal and clinically
unimportant, if an adequate dose of propofol is given
and hyperventilation is initiated at induction.

Agent

CMR

CBF

CSF
CSF
CBV
Productio Absorptio
n
n

ICP

Halothane

Isoflurane

Desflurane

Sevoflurane

Nitrous
Oxide

Barbiturate
s

Etomidate

Propofol

BZD

Ketamine

, increase; ,
unknown; CMR,
rate;
Opoids
decrease;, little or no
change; ?,
cerebral metabolic

CBF, cerebral blood fl ow; CSF, cerebrospinal fluid; CBV, cerebral blood volume; ICP,
intracranial pressure.

thankyou