ASSIGNMENT ON

RAISED INTRACRANIAL

PRESSURE

SUBMITTED TO: SUBMITTED BY:

DR. K. SENTHIL DARSHIKA VYAS

MPT II YEAR

One of the commonest pathological phenomena encountered by the neurosurgeon

is that of increased intracranial pressure (ICP) and it has profound influence on the

outcome of many intracranial problems. If raised intracranial pressure is not

recognised promptly and managed appropriately, there is alwaysaconsiderable risk

in all such patients of secondary brain damage and long term severe disability.

Physiology

The cranium can be thought of as a hollow, rigid sphere of constant volume. There

are three main components within the intracranial space:

brain (1400 ml)

cerebrospinal fluid (CSF) (75 ml) and

blood (app. 75 ml)

All these components are essentially non-compressible. The rigid cranial sphere

provides the premise of the Monro-Kellie doctrine which states that a change in the

volume of brain causes a reciprocal change in the volume of one of the intracranial

components i. e. either blood or CSF.

Intracranial pressure is a result of at least 2 factors, the volume of the brain (about

1400ml in an adult) being constant. 

(a) CSF which is constantly secreted & after circulating absorbed at an equal rate.

CSF circulation is slow (500 to 700 ml/day). At a given time the cranium contains

75 ml of CSF.

(b) Intracranial circulation of blood which is about 1000 litres per day delivered at

a pressure of 100 mmHg and at a given time, the cranium contains 75 ml. Any

obstruction to venous outflow will entail an increase in the volume of intracranial

blood and ICP. As the ICP increases, the cerebral venous pressure increases in

parallel so as to remain 2 to 5 mm higher or else the venous system would collapse.

Because of this relationship CPP (mean art pressure - venous pressure or mean

ICP) can be satisfactorily estimated from mean art pressure - ICP.

Normal ICP is between 0- 10 mm Hg with 15 mm being the upper limit of normal.

Normal intracranial pressure in adults is 8 to 18mm Hg and in babies the pressure

is 10-20mm less when measured through a lumbar puncture. Resting ICP

represents that equilibrium pressure at which CSF production and absorption are in

balance and is associated with an equivalent equilibrium volume of CSF. CSF is

actively secreted by choroid plexus at about 0.35 mllminute and production

remains constant provided cerebral perfusion pressure is adequate.

ICP is not a static state, but one that is influenced by several factors. The recording

of ICP shows 2 forms of pressure fluctuations:

There is a rise with cardiac systole (due to distention of intracranial

arteriolar tree which follows ) and a slower change in pressure with

respiration, falling with each inspiration and rising with expiration.

Straining, compression of neck veins can also cause sudden, considerable

rise in pressure.

Lundberg has described 3 wave patterns ICP waves (A, B, and C waves). 

A waves are pathological. There is a rapid rise in ICP up to 50-100 mm Hg

followed by a variable period during which the ICP remains elevated followed by a

rapid fall to the baseline and when they persist for longer periods, they are called

'plateau' waves which are pathological. 'Truncated' or atypical ones, that do not

exceed an elevation of 50 mm Hg, are early indicators of neurological deterioration

associated with clinical signs of acute brain stem dysfunction.

B  waves are related to respiration and 'Traube-Hering-Mayer' waves respectively.

Is related to various types of periodic breathing with a frequency of 1/2 to 2 per

minute and are of little clinical significance.       

C Wave is related to Traube-Heting-Mayer waves of systemic blood pressure and

has a frequency of 6 per minute.

Both Band C waves are of low amplitude and are not harmful.

CAUSES OF RAISED ICP

Head Injury Intracranial haematoma (EDH, SDH, intracerebral)Diffuse brain swelling, Contusion.

Cerebrovascular Subarachanoid haemorrhage, Cerebral venous thrombosis,Major cerebral infarcts, Hypertensive encephalopathy.

HydrocephalusCrania cerebral disproportion

Congenital or acquired (Obstructive or communicating).

Brain Tumour (Cysts; benign or malignant tumour)Secondary HydrocephalusMass effectOedema

Benign Intracranial HypertensionCNS Infection

Meningitis, Encephalitis, Abscess.

Metabolic Encephalopathy Hypoxic-ischaemic, Reyes syndrome, Hepatic coma,Renal failure, Diabetic ketoacidosis, Hyponatraemia,Burns, Near drowning.

Status epilepticus

Pathophysiology of increased intracranial pressure

Increased ICP is defined as a sustained elevation in pressure above 20mm of

Hg/cm of H20. 

The craniospinal cavity may be considered as a balloon. During slow

increase in volume in a continuous mode, the ICP raises to a plateau level at

which the increase level of CSF absorption keeps pace with the increase in

volume.

Intermittent expansion causes only a transient rise in ICP at first. When

sufficient CSF has been absorbed to accommodate the volume the ICP

returns to normal. Expansion to a critical volume does however cause

persistent raise in ICP which thereafter increases logarithmically with

increasing volume (Volume - pressure relationship).

The ICP finally raises to the level of arterial pressure which it self begins to

increase, accompanied by bradycardia or other disturbances of heart rhythm

(Cushing response). This is accompanied by dilatation of small pial arteries

and some slowing of venous flow which is followed by pulsatile venous

flow.

The rise in ICP to the level of systemic arterial pressure extinguishes

cerebral circulation which will restart only if arterial pressure raises

sufficiently beyond the ICP to restore CBF. If it fails, brain death occurs.

The cause of raise in ICP and the rate at which it occurs are also important.

Many patients with benign ICT or obstructive hydrocephalus show little or

no ill effect, the reason being the brain it self is normal and auto regulation is

probably intact.

In patients with parenchymal lesion (tumor, hematoma and contusion),

because of the shift of brain and disturbed auto regulation, CBF may by

compromised with relatively low levels of ICP.

In acute hydrocephalus, there is rapid deterioration as  there

is no time for compensation. 

Mass Lesions Haematoma, abscess, tumor.

CSF Accumulation Hydrocephalus (obstructive and communicating) and including contralateral ventricular dilatation from supratentorial brain shift.

Cerebral Oedema Increase in brain volume as a result of increased water content:I. Vasogenic-Vessel damage (tumour, abscess, contusion).2. Cytotoxic--<:ell membrane pump failure (hypoxaemia, ischaemia,toxins).3. Hydrostalic-high vascular transmural pressure (loss of autoregulation, postintracranial decompression)4. Hypo-osmolar-hyponatraemia.5. Interstitial-high CSF pressure (hydrocephalus).

Vascular (congestive) brain

swelling

Increased cerebral blood volume.-arterial vasodilatation (active, passive).

Mechanisms involved in raised ICP

CLINICAL FEATURES OF RAISED ICP

Raised ICP causes arterial hypertension, bradycardia (Cushing's response)

and respiratory changes.

It is traditionally accepted that hypertension and bradycardia are due to

ischaemia or pressure on the brainstem. There is also a suggestion that they

could be due to removal of supratentorial inhibition of brainstem

vasopressor centers due to cerebral ischaemia and that bradycardia is

independent of the rise in blood pressure.

The respiratory changes depend on the level of brainstem involved. The

midbrain involvement result in Chyne-Stokes respiration. When midbrain

and pons are involved, there is sustained hyperventilation. There is rapid and

shallow respiration when upper medulla involvement with ataxic breathing

in the final stages.

Pulmonary edema seems to be due to increased sympathetic activity as a

result of the effects of raised ICP on the hypothalamus, medulla or cervical

spinal cord.  

In the non-trauma patient, there may or may not be a clear history of

headache, vomiting and visual disturbances suggestive of papilloedema or a

VI nerve palsy.

The absence of papilloedema does not exclude raised lCP in patients with

acute or chronic problems.

Fifty percent of head injury patients who have raised lCP on monitoring will

exhibit optic disc swelling in only 4% cases. "So fundoscopy may not be of

much use in acute head injuries to detect raised ICP"  

ICP monitoring (INDICATIONS)

HEAD INJURY

(a) being artificially ventilated:

- Coma with compression of3rd ventricle and/or reduction in perimesencephalic

cistern on CT

- Coma following removal of intracranial haematoma.

- Coma with decorticate/decerebrate motor response.

- Coma with mid line shift/unilateral ventricular dilatation.

- Early seizures not easily controlled.

- Refractory hyperpyrexia.

(b) Uncertainty over surgery for small haematoma/multiple lesions.

INTRACEREBRAL AND SUBARACHONOID HAEMORRHAGE

- coma.

- postoperatively following intra operative complications.

- hydrocephalus.

COMA WITH BRAIN SWELLING

- metabolic.

- hypoxiclischaemic.

- infective.

ICP monitoring (METHODS)

Non invasive methods:

(1) Clinical deterioration in neurological status is widely considered as sign of

increased ICP. Bradycardia, increased pulse pressure, pupillary dilation are

normally accepted as signs of increased ICP. The clinical monitoring is age old and

time tested.

 (2) Transcranial doppler, tympanic membrane displacement, and ultrasound 'time

of flight' techniques have been advocated. Several devices have been described for

measuring ICP through open fontanel. Ladd fiber optic system has been used extra

cutaneously.

(3) Manual feeling the craniotomy flap or skull defect, if any, give a clue.

Invasive methods:

(1) Intraventricular monitoring remains one of the popular techniques, especially in

patients with ventriculomegaly. Additional advantage is the potential for draining

CSF therapeutically. Insertion of ventricular catheter is not always simple and can

cause hemorrhage and infection (5%).

(2) Other most commonly used devices are the hollow screw and bolt devices, and

the sub dural catheter. Richmond screw and Becker bolt are used extra durally. A

fluid filled catheter in the subdural space, connected to arterial pressure monitoring

system is cost effective and serves the purpose adequately.

(3) Ladd device is currently in wide use. It employs a fibre optic system to detect

the distortion of a tiny mirror within with balloon system. It can be used in the

subdural , extradural and even extra cutaneously.

(4) A mechanically coupled surface monitoring device is the 'cardio search

pneumatic sensor' used subdurally or extradurally. These systems are not widely

used.

(5) Electronic devices (Camino & Galtesh design) are getting popular world over.

Intraparenchymal probes, the measured pressure may be compartmentalized and

not necessarily representative of real ICP. In addition to ICP monitoring, modern

intraparenchymal sensors help study the chemical environment of the site of

pathology.

(6) Fully implantable devices are valuable in a small group who requires long term

ICP monitoring for brain tumors, hydrocephalus or other chronic brain diseases.

Cosmon intrcranial pressure telesensor can be implanted as a part of shunt system.

Ommaya reservoir is an alternative which can be punctured & CSF pressure

readings are obtained.

(7) Lumbar puncture and measurement of CSF pressure for obvious reasons is not

recommended.

Benefits of ICP monitoring

There is no doubt that ICP monitoring helps in management of conditions where

one expects prolonged intracranial hypertension. Monitoring is the only means by

which therapy can be selectively employed and the effectiveness of therapy can be

accurately studied.

1) Where ever clinical monitoring is not possible, such as during hyper ventilation

therapy and high dose barbiturate therapy, ICP monitoring helps.

2) Pre op monitoring helps in assessment of NPH before a shunting procedure.

3) Cerebral perfusion pressure (CPP), regulation of cerebral blood flow, and

volume, CSF absorption capacity, brain compensatory reserve, and content of

vasogenic events can be studied with ICP monitoring. Some of these parameters

help in prediction of prognosis of survival following head injury and optimization

of' 'CPP guided therapy'.

4) It can provide additional assessment of brain death. Brain perfusion effectively

ceases in nearly all, once ICP exceeds diastolic blood pressure.

The problems of ICP monitoring are cost, infection, and hemorrhage.

The effective maintenance requires a dedicated team effort.  

Potential Problems Exacerbating Raised ICP

 

(1) Calibration of Iep transducers and monilOrs particularly to check the zero

reference point.

(2) Neck vein obstruction:

- Inappropriate position of head and neck - avoid constricting tape around neck.

(3) Airway obstruction:

- Inappropriate PEEP. secretions. bronchospasm etc.

(4) Inadequate muscle relaxant:

- Breathing against ventilation.

- Muscle spasms.

(5) Hypoxia/hypercapnia

(6) Further mass lesion - rescan.

(7) Incomplete analgesia. incomplete sedation and anaesthesia.

(8) Seizures.

(9) Pyrexia.

(10) Hyponatraemia , hypovolaemia

Treatment of increased ICP

There is no doubt the best treatment for increased ICP is the removal of the

causative lesion such as tumors, hydrocephalus, and hematomas.

Post operative increased ICP should be uncommon these days with increased use

of microscope and special techniques to avoid brain retraction. As we so often see,

a basal meningioma once completely removed, has a smooth post op period,

whereas a convexity or even falx meningioma may be easily removed but post

operative period may be stormy, mainly due to impairment of venous drainage,

either due to intraoperative injury to veins and post operative diuretic therapy as

practiced in some centers.

There is still a debate whether increased ICP is the cause or result of the brain

damage. Many feel both compliment each other. There is one school which

questions the very existence of increased ICP. Not all the midline shift seen in CTs

indicate increased ICP. It just means ICP was high during the shift. The shift takes

longer to reverse even after ICP returns to normal . It is widely accepted the

increased ICP is a temporary phenomenon lasting for a short time unless there is a

fresh secondary injury due to a clot, hypoxia or electrolyte disturbance.

Treatment is aimed at preventing the secondary events. Clinical and ICP

monitoring will help.

The following therapeutic measures are available.

1) I line of management:

General measures form the I line of treatment essentially making the patient

comfortable and ABC of trauma management are effectively instituted. Careful

attention to nutrition and electrolytes, bladder and bowel functions and appropriate

treatment of infections are instituted promptly.

Adequate analgesia is often forgotten; it is a must even in  unconscious patients.  

2) II line of management 

Induced cerebral vasoconstriction - Hyperventilation, hyper baric O2, hypothermia

Osmotherapy - Mannitol, glycerol ,urea

Anesthetic agents - Barbiturates, gamma hydroxybutyrate, Etomidate, 

Surgical decompression -Many do not recommend decompressive surgery.

This aims at combating increased ICP which is assumed when there is neurological

deterioration or if ICP monitoring is available and the ICP goes above 25 cm of

H2O.

There is a small group of surgeons who start the II line in conditions where ICP is

expected to raise without waiting for a rise. Many feel that institution of measures

to reduce ICP invariably compromises CBF and wait for the raise in ICP before

starting the II line of management. 

Debate continues in the II line of management as well. Some prefer osmotherapy

alone as the II line. Some prefer measures to induce cerebral vasoconstriction,

thereby reducing CBF and reduce ICP. Some go for both.

a) Hyperventilation aims at keeping the pCO2 down to 30-25 mm Hg so that CBF

falls and cerebral blood volume is reduced and thereby reducing the ICP.

Prolonged hyperventilation should be avoided and becomes in- effective after

about 24 hrs. In addition it causes hypo tension due to decreased venous return . It

is claimed a pCO2 under 20 results in ischemia, although there is no experimental

proof for the same. 

The present trend is to maintain normal ventilation with pCO2 in the range of 30 -

35 mmHg and pO2 of 120 - 140 mmHg. When there is clinical deterioration such

as pupillary dilatation or widened pulse pressure, hyperventilation may be

instituted (preferably with an Ambu bag) until the ICP comes down.

Hyper baric O2, hypothermia are still in experimental stage, especially in Japan .

They basically induce cerebral vasoconstriction and reduce the cerebral blood

volume and the ICP.

b) Osmotherapy is useful in the cytotoxic edema stage, when capillary

permeability is intact, by increasing the serum osmolality. Mannitol is still the

magic drug to reduce to ICP, but only if used properly: it is the most common

osmotic diuretic used. It may also act as a free radical scavenger.

Mannitol is not inert and harmless. Glycerol and urea are hardly used these

days. Several theories have been advanced concerning the mechanism by which it

reduces ICP.

    1) It increases the erythrocyte flexibility, which decreases blood viscosity and

causes a reflex vasoconstriction that reduces cerebral blood volume and decreases

ICP and may reduce CSF production by the choroids plexus. In small doses it

protects the brain from ischemic insults due to increased erythrocyte flexibility. 

    2) The diuretic effect is mainly around the lesion, where blood brain barrier

integrity is impaired and there is no significant effect on normal brain. As one

would have observed, intraaxial lesions respond better than extra axial lesions.

    3) Another theory is, mannitol with draws water across the ependyma of the

ventricles in a manner analogous to that produced by ventricular drainage.

The traditional dose is 1 gm/kg/24 hr of 20% to 25% i.v. either as a bolus or more

commonly intermittently. 

There is no role for dehydration. Mannitol effect on ICP is maximal 1/2 hr after

infusion and lasts for 3 or 4 hrs as a rule. The correct dose is the smallest dose

which will have sufficient effect on ICP. When repeated doses are required, the

base line serum osmolality gradually increases and when this exceeds 330 mosm/1

mannitol therapy should cease. Further use is ineffective and likely to induce renal

failure. Diuretics such as frusemide, either alone or in conjunction with mannitol

help to hasten its excretion and reduce the baseline serum osmolality prior to next

dose. Some claim, that frusemide compliments mannitol and increases the output.

Some give frusemide before mannitol, so that it reduces circulatory overload. The

so called rebound phenomenon is due to reversal of osmotic gradient as a result of

progressive leak of the osmotic agent across defective blood brain barrier, or is due

to recurrence of increased ICP.

c) Barbiturates can lower the ICP when other measures fail; but have no

prophylactic value. They inhibit free radical mediated lipid peroxidation and

suppress cerebral metabolism; cerebral metabolic requirements and thereby

cerebral blood volume are reduced resulting in the reduction of ICP. 

Phenobarbital is most widely used. A loading dose of 10mg/kg over 30 minutes

and 1-3mg/kg every hour is widely employed. Facilities for close monitoring of

ICP and hemodynamic instability should accompany any barbiturate therapy.

d) High dose steroid therapy was popular some years ago and still used by some. It

restores cell wall integrity and helps in recovery and reduce edema. Barbiturates

and other anesthetic agents reduce CBF and arterial pressure thereby reducing ICP.

In addition it reduces brain metabolism and energy demand which facilitate better

healing.

Prevention of intracranial hypertension

(a) The position of patient should minimize any obstruction to cerebral venous

drainage by headup tilt while avoiding any fall in cardiac output. Direct

measurement of global CBF (cerebral blood flow) and CPP (cerebral perfusion

pressure) suggests that head-up tilt of up to 30° is safe.

(b) Hypovolaemia should be avoided especially in subarachanoid haemorrhage

(SAH) . Dehydration, when coupled with hyponatraemia, increases risk of cerebral

infarction.

(c) A stable circulation must be maintained if necessary with colloids and inotropes

(dobutamine or dopamine for its renal sparing action).

(d) Systemic hypertension, if seen, in craniocerebral trauma, should not be treated

directly with agents such as sodium nitroprusside. This drug impairs auto-

regulation and increases risk of boundary zone infarction. The cause of

hypertension like pain or retention of urine should be looked for.

(e) Majority of neurosurgical patients with hyponatraemia don't have syndrome of

inappropriate secretion of antidiuretic harmone (SIADH) and it is unwise to use

fluid restriction to treat these.

(f) Seizures must be recognized in patients who are paralysed and on ventilators.

Episodes of pupillary dilatation with increases in arterial blood pressure and ICP

are suggestive.

(g) Pyrexia not only increases cerebral metabolism and cerebral vasodilatation but

also cerebral edema. Severe hypothermia was used historically, to treat raised ICP.

But now it is not used, as mild hypothermia of few °c only reduces cerebral

ischaemia because of reasons that are still unclear.

(h) Hyperglycaemia should be avoided. There is considerable evidence that

cerebral ischaemia and infarction is made worse by hyperglycaemia. Use of high

glucose solutions is contra indicated unless it is hypoglycaemic encephalopathy

SURGICAL MANAGEMENT

Continuous CSF drainage and surgical decompression

External ventricular drainage (EVD) is a rapid procedure in emergency in a patient

with acute hydrocephalus. In all cases of external drainage, CSF should be drained

gradually against a postive pressure of 15-25 cm H,O. It is an optimal method of

controlling ICP in patients with SAH where cause is disturbed CSF circulation.

Removal of bone flaps or subtemporal decompression are performed much less

routinely.

Benign intracranial hypertension (ElH) can be treated by optic sheath fenestration

and theco-peritoneal

shunting.

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