Intracranial pressure and cerebral blood flow. A pathophysiological and clinical perspective

Cerebral ischaemia (and ultimately infarction) occurs when cerebral blood flow cannot meet the metabolic demands of brain tissue. Understanding the relationships between intracranial pressure, mean arterial blood pressure and cerebral blood flow is fundamental to the effective management of the neurosurgical patient. Following traumatic brain injury (TBI), hypotension, hypoxia and raised intracranial pressure result in diminished oxygenation to cerebral tissue, compounding the deleterious effects of the primary injury to the brain. These secondary insults to the brain result in a worse outcome at long-term follow- up. Various techniques can be used to monitor brain function. Transcranial Doppler, PET, jugular venous oxygen, brain tissue oxygenation and cerebral microdialysis help assess the adequacy of cerebral perfusion and/or brain metabolism. These techniques have improved the understanding of cerebral blood flow and brain metabolism, but significant limitations in the acquisition and interpretation of measurements have led to the limited use of several of these modalities. Monitoring of intracranial pressure is the mainstay parameter to assess brain physiology in cerebral trauma. Raised intracranial pressure causes a reduction in cerebral perfusion pressure and leads to the shift of intracranial structures within the cranial cavity. Whatever the primary brain injury (eg. tumour, haemorrhage, neurosurgical operation, trauma) simple measures are routinely taken to optimise cerebral blood flow and reduce the risk of secondary brain injury. These manoeuvres and the therapeutic approaches to the management of elevated intracranial pressure are reviewed.