Pathophysiology The underlying cause of death in patients with EDHs is the volume of blood that constitutes them as well

as the rapidity in which this blood accumulates. In most fatal cases the volume of blood is between 75 to 120 ml, with some showing greater volumes. When epidurals reach this volume rapidly, as occurs in arterial bleeds, they exert what is referred to as mass effect, which in turn increases intracranial pressure (ICP). Within the skull there is a normal ICP, which is usually between 0-10 mm Hg, which is found in the brain itself and cerebrospinal fluid (CSF). This ICP in turn exerts pressure on the blood vessels within the cranium. Any change in ICP is due to a change in volume of one of these components, the brain, CSF or the blood in the vessels. This pressure volume relationship within the cranial vault is referred to as the Monro-Kellie hypothesis. In essence what it says is that in order to maintain normal ICP any increase in volume of one of these components, such as an EDH, must be compensated for by a decrease in the volume of the other components. Thus, the mass effect induced by the expanding EDH must give rise to a decrease in volume within the brain, the ventricles with its contained CSF and the volume of blood within the vessels in order to try and maintain normal ICP. These compensatory mechanisms can maintain an ICP up to 20-25 mm Hg, which is considered the upper range of normal, for any change in volume of less than 75 to 120 ml. However, once the volume of EDH exceeds the range of 75 to 120 ml, these compensatory mechanisms can no longer maintain even the upper limits of a normal ICP. Once a pressure of 25 mm Hg is reached any continued expansion of the EDH will lead to marked life threatening increases in ICP. At this point the continued expansion of the EDH will cause the underlying cerebral hemisphere to shift toward the opposite side. This shifting of the cerebral hemisphere is referred to as a midline shift and or subfalcine herniation. Since subfalcine herniation is the most common type and believed to be the precursor of all other types of herniation I will give a brief description of this form of herniation. Subfalcine herniation is also referred to as cingulated herniation. It is due to displacement of the frontal lobe of the shifting cerebral hemisphere toward the opposite side. This results in its most medial part, that which is adjacent to the flax cerebri, the cingulated gyrus, to pass beneath the inferior border of the falx. In the process this can cause compression of the anterior cerebral artery, which in turn decreases blood supply to the frontal lobe. Such shifting is also associated with collapse of the shifting cerebral hemispheres ventricles with displacement of its contained CSF into the spinal canal. The compromise of blood supply of the anterior cerebral artery can lead to edema of the parenchyma supplied by that artery, which in turn causes an increase in volume of that portion of the brain due to the accumulation of edema fluid, and in turn is followed by further increase in ICP. Thus, a vicious cycle is created, which if not addressed quickly and adequately will lead to other severe forms of herniation leading to pressure on the brainstem through its downward displacement into the foramen magnum and its consequent compression by the cerebellar tonsils. Such pressure will ultimately lead to hemorrhages within the midbrain (Duret hemorrhages) with compromise of the reticular activating system and subsequent coma and compromise of the cardiac and respiratory control centers within the medulla, which leads to death.