INTRACRANIAL PRUSSER

Done by: Murad Aamar

Hashemite University

Skull has three essential components:

- Brain tissue = 78%

- Blood = 12%

- Cerebrospinal fluid (CSF) = 10%

Any increase in any of these tissues causes increased ICP

Normal ICP = 4 -15 mmHg

Factors that influence ICP:

Arterial pressure

Venous pressure

Intraabdominal and intrathoracic pressure

Posture

Temperature

Blood gases (CO2 levels)

*The degree to which these factors ICP

depends on the ability of the brain to

accommodate to the changes

ICP and the Monro Kellie doctrine

Alexander Monro observed in 1783 that the cranium is a ‘rigid box’

containing a ‘nearly incompressible brain’. Therefore any expansion in

the contents, especially haematoma and brain swelling, may be

initially accommodated by exclusion of fluid components, venous

blood and cerebrospinal fluid (CSF). Further expansion is associated

with an exponential rise in intra-cranial pressure The result is

hypoperfusion and herniation.

Regulation and Maintenance

Normal intracranial pressureThe pressure exerted by the total volume from the brain tissue, blood, and CSF

If the volume in any one of the components increases within the cranial vault and the volume from another component is displaced, the total intracranial volume will not change

Normal compensatory adaptations

-Alteration of CSF absorption

-Displacement of CSF into spinal subarachnoid

space

Cerebral Blood Flow

Definition

The amount of blood in milliliters passing

through 100 g of brain tissue in 1 minute

About 50 ml/min per 100 g of brain tissue

Importance of ICP to BP and CPP

Brain needs constant supply O2 and Glucose

BP: heart delivers blood to brain at an average BP of 120/80 (Mean BP = 100); this mean arterial pressure (MAP) must be higher than ICP

CPP (Cerebral Perfusion Pressure): is the pressure needed to overcome ICP in order to deliver O2 & nutrients

MAP is the DRIVING FORCE

ICP is the RESISTENCE

Cerebral Perfusion Prusser = MAP – ICP

= 100 mmHg – 15 mmHg

= 85 mmHg (Normal)

CPP < 50 mmHg→ cerebral ischemia

CPP < 30 mmHg → brain death

Regulatory Mechanisms of Cerebral Blood Flow

Autoregulation of cerebral blood flow

Metabolic Regulation of cerebral blood flow

Autoregulation

The automatic alteration in the diameter of the cerebral blood vessels to maintain a constant blood flow to the brain

Maintains CPP regardless of changes in BP

Problem: Autoregulation is limited

If BP and/or ICP rises: Autoregulation fails

When autoregulation fails, blood flow to brain increases or deceases → poor perfusion and cellular ischemia or death

Metabolic Regulation of cerebral blood flow

Factors affecting cerebral blood flowPCO2

PO2

Acidosis

Mechanisms of Increased ICP

Causes

Mass lesionCerebral edema

Head injury

Brain inflammation

Metabolic insult

Sustained increases in ICP result in brainstem

compression and herniation of the brain from one

compartment to another

CSF pathway:

GENERAL PRENCEPLES

A few basic principles concerning intracranial dynamics, CSF, CBF,

and ICP are essential to grasp at the outset and are sum- marized

here.

1-The first principle is obvious. The cranial cavity has a fixed

volume comprised of

(1) brain tissue (parenchyma),

(2) CSF, and

(3) blood vessels and intravascular blood.

According to the Monro-Kellie doctrine, the sum of these

components within the fixed volume of the cranial cavity

implies that an increase in one component must be

accompanied by an equal and opposite decrease in one or both

of the remaining components.

If this does not occur, the ICP will rise to levels close to the systemic

blood pressure, producing a reverberating blood flow pattern with no

net flow.

For each intracranial component, there is a family of pathologic

conditions of excess volume and a means to improve that excess

See the next slide:

-Brain tissue: brain edema due to inflammation , tumer, cyst,

abscess or hematoma.

-Vascular: elevated Pco2; hyperperfusion rate with loss of

autoregulation as in sever hepertention after a truma; venous

return obstructon

-CSF: impaired absorption with congenital, posthemorrhagic or

postinfectious hydrocephalus.

A consequence of this principle is that if there is an elevation in the

volume of any one compartment, there is a stage of compensation in

which the volume of one or more other compartments can be

reduced to avoid elevations in the ICP.

2-The second principle is not obvious, and may seem coun- terintuitive.

-Spinal fluid is produced at a constant rate (≈15 to20 mL/hr),

by an energy-dependent, physicochemical process, mainly by the choroid

plexus of the ventricles.

It is essential to understand that production is little affected by any

intracranial backpressure; thus, CSF production continues unabated, even to

lethal elevations of intracranial pressure.

Because production is almost always constant, it follows that

derangement of CSF dynamics almost always involves some aspect of

impeding CSF absorption through obstruction along the CSF pathways

inside the brain, subarachnoid spaces at the basal cisterns or

cerebralconvexity, or arachnoid granulations from which most absorp-

tion occurs.

The only exceptions to the almost constant CSF production are the

excess production associated with the rare choroid plexus papilloma

tumor and the occasional decreased CSF production seen with some

gram-negative bacte- rial meningitis with ventriculitis, usually in

neonates.

3-The third basic principle is that the CBF normally varies over a wide

range (30 to 100 mL/100 g brain tissue/min), depending on metabolic

demand from neuronal activity within a particular area of the brain.

The CBF may be considered in aggregate or of specific small regions,

pathologic or normal.

The blood flow to any brain area is generally abundant, exceeding

demand by a wide margin, so that O2 extraction ratios are often low.

The brain vasculature matches the blood flow to tissue metabolic

demand and the CBF generally maintains what is needed, despite wide

variations in systemic blood pressure, by a phenomenon known as

autoregulation. .

Factors such as an elevated or decreased arterial PCO2 shift the

curve as indicated. In the setting of traumatic brain injury, the

curve becomes more pronounced (i.e., smaller changes in blood

pressure or PCO2) and affects the CBF dramatically.

* If tissue demand exceeds autoregulation, or if CBF declines for

pathologic reasons, the first defense is that the O2 extraction will

increase (i.e., arteriovenous O2 difference, AVDO2) An important

implication is that if brain dysfunction is occurring clinically

because compensatory mechanisms (e.g., autoregulation changing

the vascular resistance, capacity to elevate mean systemic arterial

pressure, ability to increase O2 extraction) have been exceeded, the

tolerance for further decline in blood flow is low, and tissue damage

is seriously threatened. Therapy to increase blood pressure or

decrease ICP may be urgently needed.

A fourth principle derives from the other three and the fact that

injured tissue swells, making obvious the potential for a cascading

injury by a vicious cycle mechanism (next figure).

If the stage of compensation (see earlier), even with therapy, is

exceeded, and ICP is elevated high enough by some mechanism so that

cerebral perfusion pressure (CPP) declines, CBF can decline to levels

at which tissue injury occurs.

CPP = mean arterial pressure (MAP) − ICP

Brain edema swelling within the closed cranium will lead to further

increases in ICP with even further decreases in CPP in a stage of

decompensation. When the capacity for autoregulation is exceeded

or damaged so that it can no longer play a role, CBF is linked

directly to the CPP.

A fifth principle concerns focal mass effect and its progression in

regard to the complex anatomy of the cranial cavity. The cranial

cavity is not just a hollow spherical space but contains several

almost knifelike projections of folded dura, the falx and tentorium,

which divide the cavity into right and left supratentorial

compartment and an infratentorial compartment, the posterior

fossa. The sphenoid wing is a prominent, mostly bony ridge that

separates the anterior fossa containing the frontal lobe from the

middle fossa containing the temporal lobe.

it is unusual for focal mass effects not to be accompanied by an

overall increase in ICP. The point at which focal mass effect evolves

to include a rise in overall ICP depends largely on the compliance

within the cranial cavity. Young patients with so-called tight brains

can develop raised ICP, even with relatively small volumes of mass

that produce only effacement of the cortical gyri. On the other

hand, patients with advanced cerebral atrophy can, for example,

tolerate large frontal intracerebral hematomas or chronic subdural

hematomas with compression of the lateral ventricle and midline

shift while maintaining a tolerable ICP and a surprising degree of

intact neurologic function.

A sixth principle concerns the separateness of the phenomenology of

the following: (1) focal mass effect (as described earlier); (2) diffuse

raised ICP; and (3) ventriculomegaly (enlargement of the cerebral

ventricles).

Although these three processes often occur in combination, the

notion that they are separable comes from the observation that there

is a pure form of each

. The pure form of raised ICP—without focal mass lesion, trauma or

enlargement of the ventricular system—is a condition known as

idiopathic intracranial hypertension or pseudotumor cerebri.

The pure form of ventriculomegaly is a condition known as

adult chronic idiopathic or normal-pressure hydro- cephalus

(NPH).

The pure form of the focal mass lesion without increased ICP or

ventriculomegaly is common; it occurs with tumors too small to

raise ICP on their own that are not in a location to interfere with

CSF pathways. Instead, there focal mass lesions are typically

discovered incidentally or because of symptoms from a focal

neurologic deficit or seizure disorder.

CLINICAL POINT OF VIEW

Normal ICP varies over a wide range, with generally accepted

values between 0 and 20 mm Hg. Diffuse raised ICP, in the fully

evolved pure form, results in a clinical picture that may include

symptoms of headache, nausea and vomiting, double vision, and

obscuration of vision

The accompanying clinical signs may include papilledema and sixth

cranial nerve palsy with lateral rectus weakness and side by side

diplopia,

initially worse on far vision or gaze directed toward the side of the

palsy. The papilledema is a mostly chronic phenomenon and is not

seen acutely.

Papilledema (or papilloedema) is optic disc swelling that is caused by

increased intracranial pressure. The swelling is usually bilateral and can

occur over a period of hours to weeks. Unilateral presentation is

extremely rare

sixth cranial nerve palsy with lateral rectus weakness

. With raised ICP, there may also be obscurations of vision, in which

patients report that their vision temporarily fades or becomes gray,

visual loss, sometimes even to permanent blindness in combination

with headache. these obscurations are caused by the effect of

diffusely increased ICP on the sensitive optic nerves.

Pure ventriculomegaly—specifically, enlargement of the lateral

ventricles—is characterized by gait disturbance and incontinence

early in the clinical picture. As the process worsens, cognitive

disturbances may be added on. The early appearance of gait

disturbance and urinary incontinence is attributed to dysfunction

of the medial cerebral hemispheres in which the leg area of the

primary motor cortex and bladder control area reside

Parinaud’s syndrome results from dorsal midbrain com- pression, and its

features include a loss of upgaze known as

‘sun-setting’ . In infants, the fontanelle is tense and bulging, with an increase

in head circumference and bulging scalp veins.

The next table summarizes the relationships among ICP, mass

lesions, and ventriculomegaly.