Management of Raised Intracranial Pressure
Treatments to reduce ICP work in a narrow therapeutic window, perhaps because compression of venous structures by brain displacements rapidly elevates ICP in a self-regenerating cycle. Although this review emphasises hyperosmolar therapies, these comprise but one component of an ensemble of interventions that are undertaken in parallel. One obvious solution to reducing pressure and minimising clinical deterioration from brain compression is to remove a mass surgically. This is feasible only in certain circumstances, mainly of a discrete clot in the subdural or extradural space, and for some tumours. Contused brain tissue, swollen cerebral infarctions, oedema surrounding a tumour and deep haemorrhages are not amenable to removal. Furthermore, in keeping with the earlier-mentioned clinical trials, a study of surgical removal of cerebral haemorrhages gave generally negative results. A recently completed follow-up trial by the same investigators did not alter this conclusion.
A reduction in the volume of the intracerebral contents can also be accomplished by removing cerebrospinal fluid from the ventricles but this requires the insertion of a catheter and the effects are only temporising in most cases. The remaining available treatments may be considered to be 'medical'. Foremost among these is the maintenance of normal body temperature, as fever greatly increases cerebral blood flow and volume, thereby raising ICP. Although several trials have failed to show that hypothermia improves outcome in patients with raised ICP, lowering body temperature does lower pressure, the problem being that rewarming results in a return to elevated levels. Sedation and pharmacological paralysis are part of the regimen for managing critically ill patients with brain masses; there may be a direct effect of some of the drugs used that lowers ICP but their ability to facilitate mechanical ventilation and avoid 'bucking' the ventilator are more important. Hyperventilation quickly lowers ICP through the mechanism of alkalosis in the CSF that causes cerebral vasoconstriction and reduces cerebral blood volume but the effect is transient because homoeostatic production of ammonium ions by the choroid plexus rapidly returns the pH of cerebrospinal fluid (CSF) towards normal (which is 7.37, not 7.40 as in blood). Finally, corticosteroids have a beneficial effect on peritumoural oedema but do not affect other forms of brain swelling and are no longer used except in the situation of brain tumours.
This leaves hyperosmolar treatment, or osmotherapy, as the main means of lowering ICP over long periods of time. All hyperosmolar agents shrink the brain and reduce ICP by creating a gradient for water extraction from the interstitial fluid to the vascular compartment. The agents used in clinical practice have differing capacities to remain on the vascular side of the blood–brain barrier, a characteristic summarised as the reflection coefficient of each substance. Hyperosmolar substances that rapidly cross the barrier, such as glucose, are therefore not effective dehydrating agents for the brain. It follows that solutions such as D5/W (5% dextrose in water) and D5/0.5% normal saline (dextrose 5% in 0.5% normal saline) are also ineffective and have the deleterious effect of forcing water into the brain and raising ICP. Table 1 shows the osmolarities and reflection coefficients of the main agents used for osmotherapy. Those with both an osmolarity above the normal serum value of approximately 287 mOsm/L and a high reflection coefficient have the ability to reduce brain volume and to lower ICP.
Hyperosmolar solutions also induce a rapid but brief change in cerebrovascular tone that results in a transient drop in ICP. Agents such as mannitol that are renally excreted cause a diruresis that raises serum osmolarity and prolongs the favourable effect of an osmotic gradient. Therapy begins with the avoidance of serum hyperosmolarity. This is accomplished by choosing intravenous fluids, typically normal saline, for maintenance and for medication infusions that do not add free water to the circulation. If further reduction in ICP is needed, therapeutic induction of serum hyperosmolarity is required.
Therapeutic Programmes to Reduce Intracranial Pressure
Treatments to reduce ICP work in a narrow therapeutic window, perhaps because compression of venous structures by brain displacements rapidly elevates ICP in a self-regenerating cycle. Although this review emphasises hyperosmolar therapies, these comprise but one component of an ensemble of interventions that are undertaken in parallel. One obvious solution to reducing pressure and minimising clinical deterioration from brain compression is to remove a mass surgically. This is feasible only in certain circumstances, mainly of a discrete clot in the subdural or extradural space, and for some tumours. Contused brain tissue, swollen cerebral infarctions, oedema surrounding a tumour and deep haemorrhages are not amenable to removal. Furthermore, in keeping with the earlier-mentioned clinical trials, a study of surgical removal of cerebral haemorrhages gave generally negative results. A recently completed follow-up trial by the same investigators did not alter this conclusion.
A reduction in the volume of the intracerebral contents can also be accomplished by removing cerebrospinal fluid from the ventricles but this requires the insertion of a catheter and the effects are only temporising in most cases. The remaining available treatments may be considered to be 'medical'. Foremost among these is the maintenance of normal body temperature, as fever greatly increases cerebral blood flow and volume, thereby raising ICP. Although several trials have failed to show that hypothermia improves outcome in patients with raised ICP, lowering body temperature does lower pressure, the problem being that rewarming results in a return to elevated levels. Sedation and pharmacological paralysis are part of the regimen for managing critically ill patients with brain masses; there may be a direct effect of some of the drugs used that lowers ICP but their ability to facilitate mechanical ventilation and avoid 'bucking' the ventilator are more important. Hyperventilation quickly lowers ICP through the mechanism of alkalosis in the CSF that causes cerebral vasoconstriction and reduces cerebral blood volume but the effect is transient because homoeostatic production of ammonium ions by the choroid plexus rapidly returns the pH of cerebrospinal fluid (CSF) towards normal (which is 7.37, not 7.40 as in blood). Finally, corticosteroids have a beneficial effect on peritumoural oedema but do not affect other forms of brain swelling and are no longer used except in the situation of brain tumours.
This leaves hyperosmolar treatment, or osmotherapy, as the main means of lowering ICP over long periods of time. All hyperosmolar agents shrink the brain and reduce ICP by creating a gradient for water extraction from the interstitial fluid to the vascular compartment. The agents used in clinical practice have differing capacities to remain on the vascular side of the blood–brain barrier, a characteristic summarised as the reflection coefficient of each substance. Hyperosmolar substances that rapidly cross the barrier, such as glucose, are therefore not effective dehydrating agents for the brain. It follows that solutions such as D5/W (5% dextrose in water) and D5/0.5% normal saline (dextrose 5% in 0.5% normal saline) are also ineffective and have the deleterious effect of forcing water into the brain and raising ICP. Table 1 shows the osmolarities and reflection coefficients of the main agents used for osmotherapy. Those with both an osmolarity above the normal serum value of approximately 287 mOsm/L and a high reflection coefficient have the ability to reduce brain volume and to lower ICP.
Hyperosmolar solutions also induce a rapid but brief change in cerebrovascular tone that results in a transient drop in ICP. Agents such as mannitol that are renally excreted cause a diruresis that raises serum osmolarity and prolongs the favourable effect of an osmotic gradient. Therapy begins with the avoidance of serum hyperosmolarity. This is accomplished by choosing intravenous fluids, typically normal saline, for maintenance and for medication infusions that do not add free water to the circulation. If further reduction in ICP is needed, therapeutic induction of serum hyperosmolarity is required.
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