Traumatic brain injury (TBI) is classified as mild (GCS 13–15), moderate (GCS 9–12), or severe (GCS ≤8) based on the post-resuscitation GCS. Severe TBI is an ICU diagnosis by definition and accounts for a significant proportion of neuro-ICU admissions. The primary injury — the mechanical disruption of brain tissue at the moment of impact — is not reversible. ICU management is therefore focused entirely on preventing and treating secondary brain injury.

Secondary Brain Injury

Secondary brain injury refers to the additional neuronal damage that occurs after the initial insult as a result of physiological derangements that are potentially preventable and treatable. The major causes of secondary injury are hypoxia, hypotension, raised ICP, hyperthermia, hyperglycaemia and hypoglycaemia, and seizures. Each episode of secondary brain injury adds to the cumulative burden of neuronal loss and worsens outcome. The ICU team’s primary responsibility in severe TBI is to prevent these secondary insults from occurring.

Hypotension is particularly damaging — even a single episode of SBP below 90 mmHg in the first 24 hours after severe TBI doubles mortality. This has led to a target of maintaining SBP above 100 mmHg (some guidelines suggest 110 mmHg) in all patients with severe TBI, with MAP targets of 70–80 mmHg to ensure adequate CPP. Hypoxia — defined as SpO2 below 90% or PaO2 below 8 kPa — is equally detrimental.

ICP Monitoring and CPP Targets

ICP monitoring is indicated in patients with severe TBI (GCS ≤8) and an abnormal CT scan, and should be considered in those with a normal CT who have two or more of the following risk factors: age over 40, unilateral or bilateral motor posturing, or SBP below 90 mmHg. The Brain Trauma Foundation guidelines recommend treating ICP above 22 mmHg and targeting a CPP of 60–70 mmHg. Values above 70 mmHg are not beneficial and may cause harm through the systemic effects of the required vasopressors.