A 23-year-old male with no past medical history was brought to the emergency department following a motor vehicle collision (MVC). He was an unrestrained driver T-boned by another vehicle at approximately 50 mph. Extrication from the vehicle was required. He was unresponsive in the field and immediately intubated upon arrival of EMS in the field for airway protection. Trauma scans revealed a right tentorial subdural hematoma with mild mass effect, a right pontine/midbrain intraparenchymal hemorrhage, fracture of the right occipital condyle, and fracture of the eighth tooth. No other injuries were identified. An external ventricular drain (EVD) and intraparenchymal ICP monitor, temperature, and brain tissue oxygen probes via a triple lumen intracranial bolt were placed. He was admitted to the Neuro ICU in hemodynamically stable condition. Proper positioning, sedation, analgesia, and seizure prophylaxis were immediately implemented. Because of ICP elevations to 55 mmHg sedation was increased; a paralytic administered, and 3% hypertonic saline was started. The patient subsequently had a temperature spike and surface cooling with a goal of normothermia was initiated. Acetaminophen was given and empiric antibiotics began to prevent further fever. The paralytic was gradually weaned off. Over the course of a week, his ICP was maintained <20 mmHg and the intracranial bolt was removed. EVD was removed on hospital day 13.

It is the role of the neurocritical care clinician to recognize physiologic signs of elevated ICP and take any necessary steps to prevent secondary brain injury and herniation. Initial evaluation should include baseline vital signs and a complete neurologic exam. Symptoms to be evaluated include changes in vital signs, mental status, and pupil size; in addition to headache, visual disturbances, vomiting and motor function abnormalities (see Table 11.2). If there is sudden or unexplained ICP elevation, the patient must be examined immediately. Interventions to lower the ICP must be initiated urgently prior to any diagnostic studies. Head CT should be repeated to rule out new mass lesion that may require surgical evaluation such as new subdural hematoma, epidural hematoma, or hemorrhagic transformation of stroke.

Most ICP lowering therapies are effective for variable amounts of time and early management goals should include placement of an ICP monitoring device. The purpose of ICP monitoring is to improve the clinician’s ability to maintain adequate cerebral perfusion pressure and oxygenation to the brain. The diagnosis of elevated ICP is made from clinical findings based on the patient’s exam, imaging, and past medical history.

Any patient that is suspected to be at risk for elevated ICP should be considered for placement of an ICP monitoring device. There are four common sites used for ICP measurements; intraventricular, intraparenchymal, subarachnoid, and epidural. Intraventricular monitors are the gold standard of ICP monitoring catheters. They are placed through the skull into the ventricular system and attached to a pressure transducer with collection bag (See Fig. 11.3 for example). The major advantage of an intraventricular system is that CSF can be drained. Disadvantages are infection and potential hemorrhage during placement. Intraparenchymal devices are built around a thin cable with a fiber optic transducer at the tip. These devices are inserted through the skull directly into the brain parenchyma. Their main disadvantage is the lack of ability to drain CSF; advantages include ease of placement and lower risk of infection. Subarachnoid bolts are fluid filled systems within a hollow screw that are placed through the skull adjacent to the dura. The dura is punctured and the CSF communicates with the fluid column and the transducer. Advantages of subarachnoid monitors are low rates of infection and hemorrhage. The major disadvantage is frequent clogging of the system, which renders the measurements unreliable. Epidural ICP monitors contain and optical transducer that rests against the dura once passed through the skull. They are often inaccurate and have limited use clinically.

Once ICP monitors are in place, the waveforms can be easily accessed to help the clinician evaluate intracranial compliance. There are three peaks to the waves that are referenced for clinical significance. P1 is the percussion wave, which reflects arterial pulsation. P2 (tidal wave) represents intracranial compliance and P3 is the dicrotic wave signaling closure of the aortic valve [1, 2]. Normal intracranial compliance is depicted by a sharp, high P1, followed by a P2 that is lower than P1, followed by an even lower P3 wave. Poor intracranial compliance is seen as a P2 wave that is equal to or higher than that of P1 (See Fig. 11.4).