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NEUROTRAUMA

 

 

Cerebral Perfusion Pressure

Cerebral Perfusion Pressure (CPP) is defined as the difference between the Mean Arterial Pressure (MAP) and the Intracranial Pressure (ICP).

CPP = MAP - ICP

This represents the pressure gradient driving cerebral blood flow (CBF) and hence oxygen and metabolite delivery. The normal brain autoregulates its blood flow to provide a constant flow regardless of blood pressure by altering the resistance of cerebral blood vessels.

These homeostatic mechanisms are often lost after head trauma (cerebral vascular resistance is usually increased), and the brain becomes susceptible to changes in blood pressure. Those areas of the brain that are ischaemic, or at risk of ischaemia are critically dependent on and adequate cerebral blood flow, and therefore cerebral perfusion pressure.

Key Recommendations

Maintenance of CPP reduces mortality in severe head injury.

 

CPP should be maintained above 70-80mmHg

 

Systemic hypotension is associated with poor prognosis

 


Maintenance of an adequate Cerebral Perfusion Pressure is a cornerstone of modern brain injury therapy.

After brain injury, and especially in the multiply injured patient, cerebral blood flow may be lowered to the ischaemic threshold. To prevent further neuronal death (the secondary brain injury), this flow of well oxygenated blood must be restored. There is no class I evidence for the optimum level of CPP, but 70-80mmHg is probably the critical threshold. Mortality increases approximately 20% for each 10mmHg loss of CPP. In those studies where CPP is maintained above 70mmHg, the reduction in mortality is as much as 35% for those with severe head injury.

Cerebral Perfusion Pressure may be maintained by raising the Mean Arterial Pressure or by lowering the Intracranial Pressure. In practice ICP is usually controlled to within normal limits (<20mmHg) and MAP is raised therapeutically. It is unknown whether ICP control is necessary providing CPP is maintained above the critical threshold.

Control of intracranial hypertension is discussed on the pages on intracranial pressure.

There is substantial evidence now that early hypotension (BP < 90mmHg) is associated with increased morbidity and mortality following severe brain injury. Even patients with one episode of hypotension during their ICU stay have a significantly reduced prognosis. Maintenance of an adequate MAP requires primarily a normovolaemic patient. Control of other sites of haemorrhage has the highest priority (with oxygenation). These patients should NOT be kept 'dry' with fluid restriction, but maintained in zero balance. Further elevation of MAP, once normovolaemia is achieved, is usually accomplished with norepinephrine, though dopamine may be used. There is little evidence to recommend any one agent over another.

trauma.org 5:1 2000


References

Bouma GJ, Muizelaar JP: Relationship between cardiac output and cerebral blood flow in patients with intact and with impaired autoregulation. J Neurosurg 73:368-374, 1990

Bouma GJ, Muizelaar JP, Bandoh K et al: Blood pressure and intracranial pressure-volume dynamics in severe head injury: relationship with cerebral blood flow. J Neurosurg 77:15-19, 1992

Marion DW, Darby J, Yonas H: Acute regional cerebral blood flow changes caused by severe head injuries. J Neurosurg 74:407-414, 1991

Rosner MJ, Daughton S: Cerebral perfusion pressure management in head injury. J Trauma 30:933-941, 1990

Changaris DG, McGraw CP, Richardson JD et al: Correlation of cerebral perfusion pressure and Glasgow Coma Scale to outcome. J Trauma 27:1007-1013, 1987

Chesnut RM, Marshall SB, Pick J et al: Early and late systemic hypotension as a frequent and fundamental source of cerebral ischaemia following severe brain injury in the Traumatic Coma Data Bank. Acta Neurochir Suppl (Wien) 59:121-125, 1993

Marmarou A, Anderson RL, Ward JD et al: Impact of ICP instability and hypotension on outcome in patietns with severe head trauma. J Neurosurg 75:S59-S66, 1991