INTRACRANIAL PRESSURE

By

Iskandar

INTRODUCTION

The cranium-vertebrae is a rigid structure.The major intracranial content :

- Brain (include neuroglial &

interstitial fluid).

- Blood (arterial & venous).

- Cerebrospinal fluid.Intracranial volume is constant.Normal ICP : 10-15 mmhg (136-204 mmH2O).

INTRACRANIAL CONTENTS

CONTENT VOLUME PERCENTAGE

- Brain 1400 ml 80%(Brain 70%, Interstitial

fluid 10%)

- Blood 150 ml 10%

- CSF 150 ml 10%

TOTAL 1700 ml 100%

MONRO-KELLIE-BURROWS DOCTRINE

A. Physiologic state with normal ICP.

B. Intracranial mass with compensation (normal ICP) :

- Small-moderate SOL.

- Increasing volume is compensated by decrease intracranial content. Venous volume decreases through egress of venous blood from the intracranial cavity into the jugular vein and CSF volume decreases through egress of CSF into the spinal canal.

- Below pressure-buffer capacity of venous blood and CSF.

C. Large Intracranial mass with decompensation and elevated ICP (beyond the pressure-buffer capacity of venous blood and CSF.

PRESSURE-VOLUME CURVE

Compliance (dV/dP) : Change in volume observed for a

given change in pressure. Represent the accomodative

potensial of intracranial space. High when cranial cavity will permit

the accomodation of a large mass with very little change in pressure.

Elastance (dP/dV) : Inverse the compliance. Change in pressure observed for a

given change in volume. Represent the resistence to outward

expansion of an intracranial mass.

BLOOD BRAIN BARRIER Not all substances that are carrier in the blood reach neural tissue, a barrier

blocks entry of many substances into the brain. Function : to regulate the flow of biologically active substances into the brain

and protect the sensitive neural tissue from toxic materials. Two mechanism by which material may be transported across the

endothelial cells : - Lipid soluble : in a passive manner. - Amino acid and sugar : by specific carrier- mediated mechanism. BBB : important in certain clinical setting : - Disruption by any cause, plasma components easily cross the barrier into

neural tissue, causing vasogenic edema. - Tight junction can be transiently opened artificially by intraarterial injection

of a bolus an osmotic agent, such as manitol, which dehydrates the endothelial cells. During this interval, whuch lasts for a few hours, certain chemoterapeutic or other agent can be administered that would not otherwisw cross the barrier.

- When manitol is given intravenously, the consentration in the cerebral capillary is quite low;however, it is sufficient to create an osmotic gradient between the cerebral tissue and the capillary, allowing withdrawal of interstitial fluid into the capillary lumen. An intact tight junction is necessary for this to occur. If the tight junction are not intact, manitol will permeate the neural tissue, preventing the formation of an osmotic gradient.

BLOOD BRAIN BARRIERDifferences between somatic and brain

capillaries : Somatic cap : - Fenestration between endothelial cells allow

free flow of plasma component into the tissue.

- There is bulk flow of plasma component across endethelial cells via pinocytotic vesicles.

Brain capillary : - The endotelial cells are attached to each

other by tight junctions. This junctions act as barrier to the passive movement of many substances across the endothelium.

- There are no intervening fenestrae. - Certain selected plasma component cross

the endothelial membrane if they are lipid soluble;others, such as amino acid and sugars, are transported across the endothelial cells through carrier mediated mechanism.

- The larger of mitichondria in the brain endothelial cells generate energy for active transport.

CEREBRAL EDEMAVasogenic Edema (extracellular)

Cytotoxic Edema (Intracellular)

Interstitial Edema

(Extracellular)

Pathogenesis Increased capillary permeability

Cellular swelling (neuronal, glial & endothalial cells)

Increased brain water due to impairment of absorption of CSF

Location Mainly white Matter Gray and white matter Transependymal flow of CSF and interstitial edema in the periventricular white matter in HCP

Composition Plasma filtrate containing plasma protein

Increased intracellular water and sodium due to failure of membrane transport

CSF

Extracellular Fluid Volume Increased Decreased Increased

Cause of Edema Primary or metastatic tumor, abscess,trauma, late stage of infarction

Early stage of infarction, water intoxication, hypoxia of neural tissue

Obstructive or communicating HCP

Effect of Steroid Effective Not effective Not effective

Effect of Mannitol Effective Effective Questionable

CEREBRAL EDEMA

Normal : the intercellular tight junction are intact.

Vasogenic edema : The tight junction are not competent, allowing leakage of plasma into the interstitial space.

Cytotoxic edema : There is a primary failure of ATP-dependent sodium pump mechanism resulting in intracelular accumulation of sodium and secondarily water.

CEREBRAL BLOOD FLOW Normal : 55-60 ml/100 gr brain tissue/mnt. In Gray matter : 75 ml/100 gr/mnt. In White matter : 45 ml/100 gr.mnt. The most significant factor that determines CBF

at any given time is CPP. CPP = MABP-ICP. MABP = SBP+2DBP or DBP+1/3PP 3 The ability to maintain blood flow to the brain at

a constant level over a wide range of mean arterial pressure (50-160 mmhg) is called autoregulation.

EFFECTS OF ARTERIAL BP, PaCO2 AND PaO2 ON CBF

Three major factor regulate CBF under physiologic conditions :

Systemic blood pressure.

PaCO2. PaO2.

PATHOLOGIC EFFECT OF INCREASED ICP

Increased ICP can cause deleterious effect on the brain in two ways :

Brain ischemia, may occur when the CPP is reduced to critical level.

Focal masses, can cause distortion and herniation of the brain, resulting in compression of critical brainsteam structures.

BRAIN HERNIATION

Supratentorial Herniation : - Cingulate Herniation (Subfalxin Herniation). - Uncal Transtentorial Herniation. - Central Transtentorial Herniation. Infratentorial Herniation : - Tonsilar Herniation. - Upward Cerebellar Herniation.

CINGULATE HERNIATION

A focal mass lesion in the supratentorial compartment exerts progressive pressure locally on the ipsilateral hemisphere.

A supratentorial mass lesion may displace the cingulate gyrus, which is next to the free edge of the falx cerebri, and cause it to herniate under the falx to the opposite side.

The anterior cerebral artery may be compromised by the tight, sharp edge of the falx cerebri.

There are no clinical sign and symptom specific to a cingulate herniation unless ACA kinks and occludes causing bifontral infarction.

Usually warns of impending transtentorial herniation.

UNCAL TRANSTENTORIAL HERNIATION Most commonly herniation syndrome observed

clinically. Often seen with lesions of the middle cranial

fossa. Uncus, the most inferomedial structure of the

temporal lobe, herniate between the rostral brain steam and the tentorial edge into the posterior fossa.

Clinical syndromas : Progressively impaired consciousness, dilated ipsilateral pupil, contralateral hemiparesis.

The PCA may be compromised, causing secondary infarction of the occipital lobe on one or both side.

CENTRAL TRANSTENTORIAL HERNIATION

AKA : Transtentorial herniation. Cause : Mass lesions far from the tentorial

incisura, such as in frontal, parietal or occipital, ex : Bilateral SDH, acute hydrocephalus, etc.

There is a downward displacement of the diencephalon and midbrain centally through the tentorial incisura.

Clinical syndromas : Tend to have bilaterally small reactive pupils, exhibits cheyne-stokes respiration, is quite obtunded, and may show loss of vertical gaze

TONSILAR HERNIATION Cause : acute expansion of posterior fossa lesions, or

result from an ill-advesed lumbar puncture in a patient with a mass lesion within thr cranial cavity.

The tonsil of cerebellum herniates through the foramen magnum into tha upper spinal canal, compressing the medulla.

Manifestations of acute medullary compression : cardiorespiratory impairment, hypertension, high pulse pressure, cheyne-stokes respiration, neurogenic hiperventilation and impaired consciousness.

Cerebellar tonsil ‘cone’ through the for. Megnum, compressing the medulla respiratory arrest.

UPWARD CEREBELLAR HERNIATION

Occasionally seen with posterior fossa masses, may be exacerbated by ventriculostomy.

Cerebellar vermis ascends above tentorium, compressing the midbrain.

Posisibly occluding SCA cerebellar infaction.

May compress sylvian aqueduct obstructive hydrocephalus.

SIGNS AND SYMPTOMS

Cardinal signs : - Headache. - Vomiting. - Papiledema. Symmtoms increased ICP vary depending on whether the increased

ICP : - Chronic (Slowly progressive). - Acute (rapidly evolving lesion). Cushing’s triad : - Hypertension. - Bradycardia. - Respiratory irregularity. The full triad is only seen in about 33% of cases Increased

ICP.

TREATMENT OF INCREASED ICP

The most direct way to normalize raised ICP to the physiologic range is eliminate the cause.

The algorithm for treating intracranial hypertension

The Algorithm for Treating Intracranial Hypertension

TREATMENT OF INCREASED ICP

Patient Position :Head up 30° and neck straight.Reducing ICP (by enhancing venous

outflow and by promoting displacement of CSF from the intracranial compartment to the spinal compartment), and CBF is unaffected by elevating the head to 30°.

The onset of action : Immediate.

TREATMENT OF INCREASED ICP

Hyperventilation :Reducing ICP by reducing CBF and blood

volume through vasocontriction.Generally initiated for acute management

of increased ICP.Should be moderate, bringing the PCO2

down to 28-32 mmhg.Reducing the PCO2 much further will

decrease blood flow to critically low level.

TREATMENT OF INCREASED ICP

Manitol : It has many pharmacologic effects, but the most significant one is osmotic

effect, increase serum osmolality, helps to draw fluid from the brain parenchyma into the vascular space.The others effect : Decrease CSF production, increase CBF and cerebral oxygen consumption, decrease blood viscosity, thereby improving perfusion.

Normal serum osmolality : 275-290 mOs/kg. Not metabolized. Not cross the BBB. Usual doses : 0,25-1 gr/kg at 4-6 hour interval, given in repeated bolus. An increase in serum osmolality of as little…………is enough to have a

significant effect on cerebral edema. Generally effective for 48-72 hours, beyond 72 hours is ineffective because

manitol slowly leaks out of the blood vessel, especially in areas of BBB breakdown, with loss of osmotic gradient.

Should be carefully monitored during therapy : serum osmolality and electrolytes.

TREATMENT OF INCREASED ICP

Ventricular Drainage : Simplest, most effective and quickest method of

decreasing ICP. Advantages : Reducing ICP and ICP monitor. This modalityis particularly effective in patients with

cerebral edema. Experimental : The vasogenic edema fluid that has

extravasated into the interstitial space is cleared by diffusion into either the ventricular system or subarachnoid space.

Draining the ventricular fluid and decreasing the intraventricular pressure promotes rapid diffusion of edema fluid from the side of pathology.

TREATMENT OF INCREASED ICP

Dexametahsone :

TREATMENT OF INCREASED ICP

Barbiturat Coma :