Intracranial pressure: 

Dr. A. Vincent Thamburaj,   
Neurosurgeon, Apollo Hospitals,  Chennai , India.

It is the term applied to the pressure of CSF with in the cranium.


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. 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. The conception of the cranium acting as a near rigid container of virtually incompressible substances in the form of brain, blood & CSF in known as the Monro Kellie doctrine. CSF can be displaced through the foramen magnum into spinal theca.

The spinal dural sheath can accept a quantity of CSF as it does not fit the canal closely, being surrounded by a layer of loose areolar tissue & plexus of epidural veins. In addition, in states of increased ICP there is increase in passage of blood through venous emissaries. 

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.

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. B & C waves are related to respiration and 'Traube-Hering-Mayer' waves respectively and are of little clinical significance.       

Cerebral blood flow (CBF): 

The brain accounts for only 2% of total body weight, yet its blood flow represents 15% of resting cardiac output and uses 20% total amount of oxygen consumed. Each 24 hours brain requires 1000 liters in order to obtain 71 lit of oxygen and 100 gm of glucose. The CBF remains constant over a wide range of arterial pressures (between 60 to 150 mm hg) when the mean arterial pressure is increased beyond 150 mm hg there is increased blood flow. CBF ceases when art. mean pressure drops to 20mm Hg. In chronically hypertensive this auto regulation limits appear to be reset.

The exact nature of this auto regulation is not known.

(a) myogenic theory suggests direct reaction of the cerebral arterial smooth muscles to the stretch.

(b) The humoral theory involves regulations by the direct effect of by- products of metabolism

(c) Neurogenic theory rests on perivascular nerves.

The auto regulation is influenced by various factors.

With normal cerebrovascular system and BP, even moderate alterations of pCO2 are capable of markedly altering CBF. Within the range of 30 to 60 mm Hg there is a 2.5% change in CBF as the pCO2 changes by 1 mmHg. With less then 20 and more than 80 mmHg there is no further change. In old age and arteriosclerosis, there is marked decrease in pCO2 influence.

The effects of pO2 are not as marked as CO2 Changes. Moderate variation of O2 above and below the normal level do not affect CBF. pO2 causes constriction of a non ischemic brain along with reduction in CBF. In ischemic hemisphere, increasing the pO2 has no effect. Cerebral vaso dilatation begins with pO2 of 50 mm Hg & CBF increases. When pO2 falls to 30 mmHg, CBF may have tripled.

The ICP influences the CBF through the cerebral perfusion pressure (CPP) which is the difference between mean arterial pressure (MAP) and ICP. Raise in  ICP would lead to a fall in CPP and every effort should be taken to maintain the CPP to 50 mm Hg or more during treatment of raised ICP.

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. 

The raise in ICP disturbs brain function by

(1) Reduction in CBF

(2) Transtentorial or foramen magnum herniation resulting in selective compression and ischaemia in the brain stem.

Transtentorial herniation with brainstem compression can lead to clinical deterioration even with adequate CBF. A temporal mass may cause uncal herniation without raised ICP. Similarly a frontal mass can cause axial distortion to impair brainstem perfusion. 

Clinical features if 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.    

ICP monitoring:

ICP monitoring is most often used in head trauma in the following situations:

1) GCS less than 8

2) Drowsy with CT findings (operative or non operative)

3) Post op hematoma evacuation

4) High risk patients  (a) Above 40 yrs. (b) Low BP (c) Those who require ventilation.

There is nothing to achieve in monitoring ICP in the patients with GCS of less than 3.


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.  

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.

Surgical decompression:

Decompressive craniotomies such as sub temporal decompression are recommended only in highly selected patients these days. Herniation of brain thro' defect, cause further injury, further edema and further increased ICP. But in occasional cases, when every other measure has failed, such decompression craniotomy may be justified.

There are occasional reports from few centers  recommending such procedures.

Medicine is an ever changing field. Standard and safety precautions must be followed. But as new research and clinical experience broaden our knowledge, changes in treatment and drugs therapy become necessary or appropriate. Ultimately it is the responsibility of treating surgeon relying on his experience and knowledge of the patient to decide the best for the patient.




















































































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