Management of Raised Intracranial Pressure
The management of raised intracranial pressure is undergoing rapid change. The choice of medical treatments to reduce intracranial pressure varies between institutions and regions of the world. The mainstay of therapy, however, continues to be the infusion of a hyperosmolar solution to achieve an osmotic gradient to force the exit of water from the brain. This review introduces the basic concepts of raised intracranial pressure, summarises several recent studies that have challenged dogma in the field, and provides practical advice on hyperosmolar treatment, based on personal experience and a critical reading of the literature.
Forty years after the inception of the specialty of neurological critical care, its central tenets regarding the treatment of raised intracranial pressure (ICP) have been challenged. Recent clinical trials have dashed many closely held notions about ICP monitoring and the use of hyperosmolar agents to reduce ICP. The deconstruction of our ideas regarding ICP measurement and treatment are interesting but leave a gap that requires guidance. What follows is applicable to most of the commonly encountered causes of intracranial hypertension, including intracerebral haemorrhage, brain swelling from cerebral infarction, traumatic brain injury, intracerebral and extracerebral haematoma, brain tumour and acute hydrocephalus. Figure 1 gives an imaging example of such a mass. This review provides advice on the main methods for reducing ICP, with emphasis on the use of hyperosmolar solutions to reduce the volume of the brain.
(Enlarge Image)
Figure 1.
MRI showing a large right middle cerebral artery stroke with brain swelling that rerquired treatment with hyperosmolar therapy.
Any recommendations on this subject first require an explanation of the reasoning behind the treatment of elevated ICP. The fundamentals are:
In counterpoint, several problems limit the clinical application of these axioms. A relationship between elevated ICP and poor outcome is supported mainly by retrospective studies of patients with traumatic brain injury. While seemingly self-evident, there is sparse confirmation that reducing ICP improves clinical outcome. Furthermore, several clinical trials have shown no benefit from monitoring ICP as a means of directing treatment.
Abstract and Introduction
Abstract
The management of raised intracranial pressure is undergoing rapid change. The choice of medical treatments to reduce intracranial pressure varies between institutions and regions of the world. The mainstay of therapy, however, continues to be the infusion of a hyperosmolar solution to achieve an osmotic gradient to force the exit of water from the brain. This review introduces the basic concepts of raised intracranial pressure, summarises several recent studies that have challenged dogma in the field, and provides practical advice on hyperosmolar treatment, based on personal experience and a critical reading of the literature.
Introduction
Forty years after the inception of the specialty of neurological critical care, its central tenets regarding the treatment of raised intracranial pressure (ICP) have been challenged. Recent clinical trials have dashed many closely held notions about ICP monitoring and the use of hyperosmolar agents to reduce ICP. The deconstruction of our ideas regarding ICP measurement and treatment are interesting but leave a gap that requires guidance. What follows is applicable to most of the commonly encountered causes of intracranial hypertension, including intracerebral haemorrhage, brain swelling from cerebral infarction, traumatic brain injury, intracerebral and extracerebral haematoma, brain tumour and acute hydrocephalus. Figure 1 gives an imaging example of such a mass. This review provides advice on the main methods for reducing ICP, with emphasis on the use of hyperosmolar solutions to reduce the volume of the brain.
(Enlarge Image)
Figure 1.
MRI showing a large right middle cerebral artery stroke with brain swelling that rerquired treatment with hyperosmolar therapy.
Any recommendations on this subject first require an explanation of the reasoning behind the treatment of elevated ICP. The fundamentals are:
As intracerebral volume expands, ICP increases at a greater than linear rate, approximating an exponential function.
The skull and its underlying inelastic dura restrict the expansion of its contents (brain, intravascular blood and cerebrospinal fluid). Any increase in the volume of one component occurs only at the expense of a reduction in the volume of the others.
As ICP rises, it opposes cerebral blood flow sufficiently to cause global brain ischaemia and brain death. This is reflected in cerebral perfusion pressure, which approximates blood pressure minus ICP.
Medical and surgical treatments that lower ICP act either by reducing the volume of one of the components listed in no. 2 above, removing a mass, or by opening the closed cranium to the atmosphere.
Except for headache, vomiting, and papilloedema, the signs of an intracranial mass are due to secondary tissue shifts induced by the mass, and not to raised ICP. Clinical signs only approximately reflect the level of ICP.
In counterpoint, several problems limit the clinical application of these axioms. A relationship between elevated ICP and poor outcome is supported mainly by retrospective studies of patients with traumatic brain injury. While seemingly self-evident, there is sparse confirmation that reducing ICP improves clinical outcome. Furthermore, several clinical trials have shown no benefit from monitoring ICP as a means of directing treatment.
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