Brain parenchyma, cerebrospinal fluid (CSF), and blood are the three components of the intracranial cavity (Table 215.1). The durability of the skull protects the brain from outside insults, but cannot accommodate an increase in the amount of intracranial contents. Increased ICP is, therefore, a medical emergency that requires careful diagnosis, monitoring, and management.

The Cushing triad is classically associated with increased ICP but is a relatively late finding. It consists of hypertension, bradycardia, and hypopnea. Hypertension occurs as the body attempts to maintain cerebral perfusion pressure (CPP). CPP can be calculated by subtracting the mean arterial pressure (MAP) from ICP (CPP = MAP – ICP). Because CPP is interdependent on MAP, an acute fall in blood pressure in patients with increased ICP places them at risk for cerebral hypoperfusion and long-term neurologic damage. Hypertension associated with increased ICP causes a compensatory bradycardia. Decreased respiratory rate is a late finding, signaling impending herniation and is secondary to compression of brainstem respiratory centers from the increased pressure. Ideally, increased ICP should be identified and treatment started before these findings arise (Table 215.2).

Evacuation of a fluid (CSF or blood) collection or mass removal are the surgical interventions for increased ICP. Medical management of increased ICP includes elevation of the head of the bed, osmotic diuretics, hypertonic saline, hyperventilation, sedation, and hypothermia. Varying amounts of evidence exist for the effectiveness of these interventions in decreasing ICP. Elevating the head of the bed to 30 degrees is one of the simplest interventions for patients with suspected increased ICP. It improves venous outflow from the brain and can be an effective measure at preventing increased ICP from escalating.