Pathophysiology of Raised Intracranial Pressure

In this article, we will discuss the Pathophysiology of Raised Intracranial Pressure. So, let’s get started.

Pathophysiology

The volume of the intracranial contents (brain + CSF + blood) is constant regardless of the pressure generated within it.
[V intracranial = Vbrain + Vcsf + Vblood = Constant]
Any changes in volume of one of its contents occurs at the cost of other two (Monro-Kelly principle). This is not applicable to the pliable skull of infants.

The brain being dependent mainly on
oxygen, suffer during hypotension and hypoxia the two major factors for secondary damage to the brain. Initially when the volume of the intracranial content increases, there is no increase in CSF pressure due to buffering mechanisms such as shift of CSF and then venous blood flow from the cranial cavity, followed by a minimal compression of the parenchyma. Once the buffering capacity is exhausted, the ICP starts rising. When the expansion of the mass lesion is slow, e.g. tumor, the compensatory mechanisms can mask the rise in ICP. Fast expanding mass lesion shift the midline structures to opposite side.

The effects of raised ICP are:

(i) Herniation syndrome

(ii) Fall in cerebral perfusion pressure.

Cushing’s reflex is a protective mechanism that leads to increase in blood pressure and fall in the pulse rate in an effort to increase cerebral perfusion pressure in patients with raised ICP.

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