Transient and sustained increases in intracranial pressure (ICP)

Elevated intracranial pressure can occur in the form of short-lived ‘plateau waves’ or refractory intracranial hypertension. Plateau waves are thought to occur due to a  cerebral vasodilatory cascade where increased cerebral blood within the skull causes marked increases of intracranial pressure and decreases of cerebral perfusion pressure. The decrease in cerebral perfusion pressure causes further dilation (an auto regulatory response) and aggravates the increased intracranial pressure (Rosner and Beck, 1984). At the peak of the plateau, the brain is hypo-perfused and hypoxic. Hypoperfusion can be monitored on ICM+ with thermodilution probes, transcranial Doppler ultrasound while cerebral hypoxia can be monitored with near infrared spectroscopy (NIRS) or brain tissue oxygenation (Dias et al., 2015, Lang et al., 2014).

Refractory intracranial hypertension also results in decreases in brain oxygenation and disturbed pressure reactivity (Czosnyka et al., 2016, Balestreri et al., 2004). Since severe refractory intracranial hypertension carries a high mortality, identifying early indicators that might predict raised ICP is an active area of research. Disturbed cerebral auto regulation may denote a higher risk of subsequent raised ICP (Czosnyka et al., 2016, Guiza et al., 2013).

Increased ICP is related to unfavourable patient outcome 6-months after the injury (Cabella et al., 2016).