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INCREASED INTRACRANIAL

PRESSURESupervised By: Prof Dr.WALID S. MAANIPresented by : Rami R. Abusaleh

Def: CSF is a clear, colorless body fluid found

in the brain and spine.

Secretion Absorption

Any obstruction to the flow will lead to increase ICP

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Anatomy

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BloodChoroi

d Plexus

lateral ventricles

foramen of Monro

Third ventric

leAqueduct of Sylvius

fourth ventric

le

foramen of Magendie

subarachnoid space

Granulation Of Pachioni

CSF Circulation

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Histology

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1. Sum of the intracranial volumes of blood, brain, CSF, and other components (for example, tumour, haematoma) is constant.

2. The skull is considered as an enclosed and inelastic container. An increase in the volume of any one of the intracranial contents must be offset by a decrease in one or more of the others or be associated with a rise in ICP. 

3. Intracranial blood (especially in the venous compartment) and CSF are the two components whose volume can adapt most easily to accommodate an increase in the volume of intracranial contents.2

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Monro-Kellie doctrine

THE VOLUME PRESSURE RELATIOSHIP

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Pressure Normally 0-140 mm CSF (0-10 mm

Hg N.B: (Children 3-7 ,Term infants 1.5-6) There are normal regular waves due to pulse

and respiration With increased pressure “pressure waves”

appear

volume : Average intracranial volume = 1700 ml

1. Brain (80%) = 1400 ml2. Blood (10%) = 150 ml3. CSF (10%) = 150 ml

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Normal ICP

Cerebral Perfusion

Pressure CPP = MAP ‑ ICP (Normal = 70 - 100 mm Hg)

MAP = 1/3 Systolic + 2/3 Diastolic BP CEREBRAL BLOOD FLOW (CBF)

PressureFlow = ----------------

Resistance

Cerebral Perfusion Pressure (systemic pressure – intracranial pressure)

Cerebral Blood Flow = --------------------------------------- Cerebral Vascular Resistance

COMPENSATORY MECHANISMS FOR

EXPANDING MASSES: Immediate

Decrease in CSF volume by movement of fluid to the lumbar area.

Decrease in the blood volume by squeezing blood out of sinuses

Delayed Decrease in the extra-cellular fluid.

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COMPENSATORY MECHANISMS

WHEN COMPENSATORY MECHANISMS

FAIL; Pathology OCCURS: Brain Oedema Brain Herniation Ischemia if CPP (< 30‑40 mm Hg)

N.B: After head injury cerebral blood flow depends on SYSTOLIC BP (Stress)

N.B: The ICP finally rises to the level of arterial pressure which it self begins to increase, accompanied by bradycardia or other disturbances of heart rhythm (Cushing response).

COMPENSATORY MECHANISMS FAIL

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Pathology

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Etiology of intracranial hypertension

Increased Volume of

Intracranial Constituents.

Space Occupying

Lesions

Localised mass lesions

Disturbance of CSF circulation

Obstruction to major venous

sinuses

Diffuse brain oedema or

swelling

Idiopathic

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Localised mass

lesions

Traumatic haemato

mas

Neoplasms

Abscess

Focal oedema secondary to trauma,

infarction, tumour

Disturbance of CSF

circulation

Obstructive hydrocephal

us

Communicating

hydrocephalus

Obstruction to major venous sinuses

Depressed fractures overlying

major venous sinusesCerebral venous

thrombosis

Diffuse brain oedema or swelling

Encephalitis, meningitis, diffuse

head injury, subarachnoid haemorrhage,

Reye’s syndrome, lead

encephalopathy, water intoxication,

near drowning

Idiopathic

Benign intracrani

al hypertensi

on

There is no consistent relation between the severity of symptoms and the degree of hypertension.

A) Headache : (Traction on vessels + Compression on dura)

characteristics:1. Throbbing or bursting .2. Worse in the morning3. Exacerbated by any factors that further increase ICP

(ex: coughing, sneezing, or exertion)4. Relived by vomiting & analgesia.

B)Visual Disturbance C) Projectile vomiting

Clinical Presentation

Herniation:

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Herniation of intracerebral

contents•Uncal: most frequently noted herniation

Results in ipsilateral pupil dilatation, decreased level of consciousness, changes in respiratory patterns, respiratory arrest, and contralateral hemiplegia

•Subfalcine which results in affection of the ACA leading to contralateral leg weakness

Supratentorial herniation

•Results in loss of consciousness, small reactive pupils advancing to fixed/dilated pupils, respiratory changes leading to respiratory arrest and decorticate posturing advancing to flacidity

Central/Transtentorial herniation

•Tonsillar: As a result of a downward herniation the medula oblongata is compressed and displaced causing respiratory and cardiac arrest

Infratentorial herniation

Early signs Late signs A) Headache : : increasing with projectile vomiting

A) Headache : increasing with projectile vomiting

B) LOC: restlessness, agitation, lethargy

B) LOC: difficult to arouse, decreasing Glasgow Coma Scale

C)Papilloedema:delayed or sluggish reaction, unilateral changes in size

C)Papilloedema: Loss of vision if severe and prolonged.

D) MOTOR: pronator drift, weakened hand grasp

D) MOTOR: posturing, flaccid muscles

E) MEMORY: mildly impaired

E) VITAL SIGNS: CUSHING’S TRIAD

F) SPEECH: slowed or slurred

F) SPEECH: decreasing, or with groans or moaning

Cushing’s Triad

1. HTN, high pulse pressure, 2. Cheynes-Stoke respiration, 3. Cushing’s response, in 1/3 of cases of tonsillar

herniation.4. Hematoma.

N.B: The most common anatomical locations affected by herniation syndromes include subfalcine, central transtentorial, uncal transtentorial, upward cerebellar, cerebellar tonsillar/foramen magnum, and transcalvarial .

Signs of Herniation:

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Early:

Headache, projectile vomiting and papilloedema.

Late: Change in the level of consciousness, Loss of motor and sensory functions, pupillary

changes (compression of Cranial Nerve III) Vital sign changes, bradycardia and irregular

respirations, Posturing: decorticate(flexion), decerebrate

(extension) or mixed (intermittent) Coma

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Herniation CP

Herniation of intracerebral

contents

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General Management

Resuscitation : A.B.C, Head elevation

IV: Fluid management. mannitol (Osmotic diuretics) Glucocorticoids Propofol  Hypertonic saline bolus (may lower ICP)

Treat the Cause (The best therapy for (ICH))

Sedation : Keeping patients appropriately sedated can decrease ICP by reducing metabolic demand,

Bp control : maintain CPP >60 mmHg.

Position : positioned to maximize venous outflow from the head

INTRACRANIAL PRESSURE MONIRORING .

Control Fever (as it increases brain )

Antiepileptic therapy (if needed)

Barbiturates : ( reduce brain metabolism and cerebral blood flow)

Removal of CSF (ventriculostomy )

Rapid aspiration of CSF should be avoided because it may lead to obstruction of the catheter opening by brain tissue.

Decompressive craniectomy 

General Management

ICP Monitoring

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ICP Monitoring

Non-invasive systems

Tissue resonance

analysis (TRA),

Ocular sonography

Transcranial Doppler

(TCD)

Intraocular pressure

Tympanic membrane

displacement

Invasive systems

Subdural

Subarachnoid

Interparenchymal

Intraventricular

Lumber puncture

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1) Subdural2) Subarachnoid3) Interparenchymal4) Intraventricular5) Lumber puncture

Invasive Systems ICP Monitoring

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ICP MONITORING

Video

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• 1)Simple, Spinal fluid doesn’t reflect the ICP if

there is no communication.• 2)May cause acute brain stem compression.

Lumber puncture

• The "gold standard" of ICP monitoring catheters. •placed into the ventricular system and affixed to

a drainage bag and pressure transducer with a three-way stopcock.

•Advantages: •accuracy, simplicity of measurement, and

the unique characteristic of allowing for treatment of some causes of elevated ICP via drainage of CSF.

•Disadvantages: Infections

Intraventricular

Invasive Systems ICP Monitoring

• consist of a thin cable with an electronic or fiberoptic

transducer at the tip.• The most widely used device is the fiberoptic Camino

system. These monitors can be inserted directly into the brain parenchyma via a small hole drilled in the skull.

• Advantages :• Ease of placement.• A lower risk of infection .• Disadvantages:

•inability to drain CSF for diagnostic or therapeutic purposes.

•mechanical failure due to the complex design of these monitors.

Intraparenchymal :

•Epidural monitors contain optical transducers that rest against the dura after passing through the skull.• Inaccurate, as the dura damps the pressure transmitted to

the epidural space.• They are of limited clinical utility. • Used in the management of coagulopathic patients with

hepatic encephalopathy complicated by cerebral edema.

Epidural 

Subarachnoid

• Subarachnoid bolts are fluid-coupled systems within a hollow screw that can be placed through the skull adjacent to the dura. The dura is then punctured, which allows the CSF to communicate with the fluid column and transducer.

•The most commonly used subarachnoid monitor is the Richmond (or Becker) bolt; other types include the Philly bolt, the Leeds screw, and the Landy screw .

•Advantages:•Low risk of infection and haemorrhage.

•Disadvantages:•Often unreliable; therefore, they are rarely used.

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Non-invasive systems

• an ultrasound-based method, has shown some promise.

Tissue resonance

analysis (TRA)• can provide a noninvasive measure of

optic nerve sheath diameter, which has been found to correlate with intracranial pressure.

Ocular sonography

• measures the velocity of blood flow in the proximal cerebral circulation.

Transcranial Doppler (TCD)

• can be assessed noninvasively using an ultrasonic handheld optic tonometer.

Intraocular pressure

• (measured using an impedance audiometer).

Tympanic membrane

displacement

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ICP monitoringIndication

Bullock and colleagues:

There was sufficient class II and III evidence to support the following recommendations (no class I) :

ICP monitoring is appropriate in patients with severe head injury (GCS 3-8 after CPR) and an abnormal (CT) scan (haematomas, contusions, oedema or compressed basal cisterns)

ICP monitoring is appropriate in patients with severe head injury and a normal CT scan if ≥ 2 of the following features are noted on admission: age > 40 years, unilateral or bilateral motor posturing, systolic blood pressure < 90 mm Hg

ICP monitoring is not routinely indicated in patients with mild or moderate head injury; however, a clinician may choose to monitor ICP in certain conscious patients with traumatic mass lesions.

According to The Department of Neurosurgery,

Faculty of Medicine, Jordan University Hospital, Amman, Jordan.

Objective: This retrospective study was done to evaluate the Intracranial Pressure (ICP) monitoring and its effect on the outcome of multi-trauma patients, including severe head injury, in Jordan University, Hospital, as many studies were published with controversies.

This study was done by Prof Dr. Walid Maani, Dr.Awni Musharbash, Dr. Qussai Saleh, Dr. Ahmed Tamimi & Dr. Moh'd Abu-Elrub.

Intracranial Pressure Monitoring, Experience in

JordanUniversity Hospital

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Methods: A total of 67 patients were included in the

study, and in 42 patients ICP monitoring was used.

Results: It was found that the mortality rate increases with the higher readings in the ICP, reaching up to 100% in patients with an ICP of 60mmHg and above. Although the mortality rate was less in the ICP monitored patients (35.7%), compared to the Non- ICP monitored patients (52%).

Conclusion: The final outcome of severely head injured patients is not truly known especially in multitrauma patients. 36

Intracranial Pressure Monitoring, Experience in

JordanUniversity Hospital

Role of CT up to 1/3 of patients with initially normal scans developed CT scan abnormalities within the first few days after closed head injury .

By Definition, the term ‘IIH’ describes patients with isolated raised (not related to an intracranial disorder, a meningeal process or cerebral venous thrombosi).

Typically affecting young obese women with menstrual irregularities or taking OCPs, roduces a syndrome of increased intracranial pressure without identifiable cause.

Pathophysiology: remain unclear but those proposed classically include :1. increased brain water content.2. excess CSF production.3. reduced CSF absorption and increased cerebral venous

pressure.

Diagnosis : Modified Dandy criteria

Idiopathic intracranial hypertension

Signs and symptoms : of increased ICP .1. No localising focal neurological signs except unilateral or bilateral sixth

nerve paresis.2. CSF opening pressure ≥25 cm H2O* but without cytological or chemical

abnormalities.3. Normal neuroimaging adequate to exclude cerebral venous thrombosis—

that is, MRI of the brain, often with additional sequences (CT or MR venography).

TTT:1. lumber puncture2. weight loss3. Medical treatment:

a) Carbonic anhydrase inhibitors, such as acetazolamide ,are the main medical treatment classically prescribed for IIH. Acetazolamide decreases the production of CSF in humans .

b) Topiramate particularly for the treatment of headaches.c) Oral steroids

Idiopathic intracranial hypertension

Surgery: is required in patients with a fulminant onset of disease or when

other treatments have failed to prevent progressive visual loss.

In patients with papilloedema who have severe visual loss, but minimal or no headache, optic nerve sheath fenestration (ONSF) is often advised, while in those with visual loss, papilloedema and headache, a CSF diversion procedure, such as ventriculo-peritoneal (VP) or lumbo-peritoneal (LP) shunting, is preferred.

Aggressive management with CSF shunting is usually required to prevent catastrophic visual loss in those with acute and rapidly progressive visual loss. 

These patients might benefit from a transient lumbar drain while awaiting a more definite surgical procedure.

Idiopathic intracranial hypertension

MRI findings in idiopathic intracranial hypertension .

Biousse V et al. J Neurol Neurosurg Psychiatry 2012;83:488-494©2012 by BMJ Publishing Group Ltd

Top: Posterior flattening of the globes resulting in

shortening of the eyes and hyperopic shift (arrows). Dilation and tortuosity of

the optic nerve sheath (arrowheads). Bottom left:

Empty sella (arrow) Bottom right: Contrast-

enhanced magnetic resonance venography showing bilateral distal

transverse sinus stenosis (arrows).

Resolution of bilateral transverse sinus stenosis after lumbo-peritoneal shunt in a young obese woman with idiopathic intracranial hypertension.

Biousse V et al. J Neurol Neurosurg Psychiatry 2012;83:488-494

Resolution of bilateral

transverse sinus stenosis after

lumbo-peritoneal shunt in a young

obese woman with idiopathic

intracranial hypertension.

Increased ICP is defined as a sustained elevation in pressure

above 20mm of Hg  

An excess of brain water may occur:1. Around lesions within the brain:

Tumor Abscess

2. In relation to traumatic damage3. In relation to ischemic brain insult

Types of edema:1. Vasogenic (extra cellular): tumors2. Cytotoxic (intra cellular): metabolic states3. Interstitial (extra cellular): increased IVP

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BRAIN OEDEMA

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BRAIN OEDEMA

Thank You

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