Severe head injury 1-Cerebral blood flow and autoregulation

Cerebral blood flow is normally maintained at a constant rate by myogenic and metabolic autoregulation. These homeostatic mechanisms are impaired following head injury. Distinct patterns of CBF have been described following head injury that have direct clinical relevance with regard to management of TBI. (Martin et al. J neurosurg 1997).

1. Hypoperfusion phase

CBF is reduced in the first 72 hours following injury with resultant global and regional ischaemia. Myogenic autoregulation is severely impaired and CBF is directly dependent of systemic BP. Resultant cerebral ischaemia may result in cytotoxic cerebral edema and increased ICP. In this phase systemic BP must be maintained to achieve CPP in between 60-70 mmHg (BTF guideline).

Management: defend ICP, restore MAP, reduce ICP.

2. The hyperaemic phaseFollowing hypoperfusion phase, autoregulatory mechanisms may start to recover with improved blood flow. This phase may persist up to 7-10 days post injury and occurs in 25-30% of patients. Intracranial inflammation and effects of medical therapies directed at maintaining adequate cerebral perfusion may result in cerebral hyperaemia and increased ICP. The consequences of hyperaemia, inflammation and altered blood brain permeability result in vasogenic cerebral edema.Since there is restoration of CBF or increased CBF, a range of CPP recommended is 50-70 mmHg.

Management: optimize CPP, normalize MAP, reduce ICP.

3. The vasopastic phase

In about 10-15% of patients, particularly in those with severe primary and secondary injuries or those with significant traumatic SAH, a vasopastic phase may persist up to 14 days. This phase represents a complex of cerebral hypoperfusion due to arterial vasospasm, posttraumatic hypometabolism and impaired autoregulation.

Management: maintain CPP, maintain MAP.