The cranium and the vertebral canal, along with the relatively inelastic dura, form a rigid container, such that the increase in any of its contents; brain, blood, or CSF, will tend to increase the ICP. In addition, any increase in one of the components must be at the expense of the other two; this relationship is known as the Monro-Kellie doctrine. Small increases in brain volume do not lead to immediate increase in ICP because of the ability of the CSF to be displaced into the spinal canal, as well as the slight ability to stretch the falx cerebri between the hemispheres and the tentorium between the hemispheres and the cerebellum. However, once the ICP has reached around 25 mmHg, small increases in brain volume can lead to marked elevations in ICP; this is due to failure of intracranial compliance.
Traumatic brain injury is a devastating problem with both high subsequent morbidity and high mortality. Injury to the brain occurs both at the time of the initial trauma (the primary injury) and subsequently due to ongoing cerebral ischemia (secondary injury). Cerebral edema, CSF hypertension, circulatory hypotension, and hypoxic conditions are well recognized causes of this secondary injury. In the intensive care unit, raised intracranial pressure (intracranial hypertension) is seen frequently after a severe diffuse brain injury (one that occurs over a widespread area) and leads to cerebral ischemia by compromising cerebral perfusion.
Cerebral perfusion pressure (CPP), the pressure of blood flowing to the brain, is normally fairly constant due to autoregulation, but for abnormal mean arterial pressure (MAP) or abnormal ICP the cerebral perfusion pressure is calculated by subtracting the intracranial pressure from the mean arterial pressure: CPP = MAP ? ICP . One of the main dangers of increased ICP is that it can cause ischemia by decreasing CPP. Once the ICP approaches the level of the mean systemic pressure, cerebral perfusion falls. The body’s response to a fall in CPP is to raise systemic blood pressure and dilate cerebral blood vessels. This results in increased cerebral blood volume, which increases ICP, lowering CPP further and causing a vicious cycle. This results in widespread reduction in cerebral flow and perfusion, eventually leading to ischemia and brain infarction. Increased blood pressure can also make intracranial hemorrhages bleed faster, also increasing ICP.
Severely raised ICP, if caused by a unilateral space-occupying lesion (e.g. a hematoma) can result in midline shift, a dangerous sequela in which the brain moves toward one side as the result of massive swelling in a cerebral hemisphere. Midline shift can compress the ventricles and lead to hydrocephalus. Prognosis is much worse in patients with midline shift than in those without it. Another dire consequence of increased ICP combined with a space-occupying process is brain herniation (usually uncal or tonsilar). In uncal herniation, the uncus hippocampus becomes compressed against the free edge of the tentorium cerebelli, frequently leading to brainstem compression. If brainstem compression is involved, it may lead to respiratory depression and is potentially fatal. This herniation is often referred to as “coning”.
Major causes of morbidity due to raised intracranial pressure are due to global brain infarction as well as decreased respiratory drive due to brain herniation.
Traumatic brain injury is a devastating problem with both high subsequent morbidity and high mortality. Injury to the brain occurs both at the time of the initial trauma (the primary injury) and subsequently due to ongoing cerebral ischemia (secondary injury). Cerebral edema, CSF hypertension, circulatory hypotension, and hypoxic conditions are well recognized causes of this secondary injury. In the intensive care unit, raised intracranial pressure (intracranial hypertension) is seen frequently after a severe diffuse brain injury (one that occurs over a widespread area) and leads to cerebral ischemia by compromising cerebral perfusion.
Cerebral perfusion pressure (CPP), the pressure of blood flowing to the brain, is normally fairly constant due to autoregulation, but for abnormal mean arterial pressure (MAP) or abnormal ICP the cerebral perfusion pressure is calculated by subtracting the intracranial pressure from the mean arterial pressure: CPP = MAP ? ICP . One of the main dangers of increased ICP is that it can cause ischemia by decreasing CPP. Once the ICP approaches the level of the mean systemic pressure, cerebral perfusion falls. The body’s response to a fall in CPP is to raise systemic blood pressure and dilate cerebral blood vessels. This results in increased cerebral blood volume, which increases ICP, lowering CPP further and causing a vicious cycle. This results in widespread reduction in cerebral flow and perfusion, eventually leading to ischemia and brain infarction. Increased blood pressure can also make intracranial hemorrhages bleed faster, also increasing ICP.
Severely raised ICP, if caused by a unilateral space-occupying lesion (e.g. a hematoma) can result in midline shift, a dangerous sequela in which the brain moves toward one side as the result of massive swelling in a cerebral hemisphere. Midline shift can compress the ventricles and lead to hydrocephalus. Prognosis is much worse in patients with midline shift than in those without it. Another dire consequence of increased ICP combined with a space-occupying process is brain herniation (usually uncal or tonsilar). In uncal herniation, the uncus hippocampus becomes compressed against the free edge of the tentorium cerebelli, frequently leading to brainstem compression. If brainstem compression is involved, it may lead to respiratory depression and is potentially fatal. This herniation is often referred to as “coning”.
Major causes of morbidity due to raised intracranial pressure are due to global brain infarction as well as decreased respiratory drive due to brain herniation.
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