Protocols: cerebral perfusion pressure (CPP)-, intracranial pressure- and ‘optimal CPP’-oriented therapy
He continuous measurement of ICP is an essential modality in brain monitoring systems. After a decade of enthusiastic attempts to introduce newer modalities for brain monitoring (e.g. tissue oxygenation, microdi-alysis, cortical blood flow, TCD and jugular bulb oxygen saturation), ICP monitoring remains a robust clinical tool that provides the core of clinical monitoring in most critical care units. here is, however, increasing recognition of the complex and detailed information provided by the technique regarding compensatory mechanisms intrinsic to the brain as well as information about regulation of CBF.
Fig. 4.9. Example of evaluation of ‘optimal CPP’. This is a plot of pressure reactivity index (PRx) versus cerebral perfusion pressure (CPP) over a period of 4-6 h. The plot shows the typical U-shaped curve found in the presence of preserved autoregulation. The value of CPP associated with the lowest PRx is the ‘optimal CPP’. The bottom graph shows a histogram of CPP over the same period of time. If the peak of the histogram is at the same CPP level as the bottom of the U-shaped curve in the top graph, it indicates that the current CPP is well matched to the optimal level. In this particular case, the optimal CPP was 76 and current modal CPP was 68 mmHg. According to the algorithm suggested by Steiner and colleagues, CPP should be slightly increased in the next step.
The m anagement and control of raised ICP requires its continuous monitoring. For example, most authors agree that ICP should be m onitored in acute states such as head injury, poor-grade subarachnoid haemorrhage and intracerebral haematoma, and that the level of ICP can be used to titrate and select therapy. Cerebral perfusion pressure-oriented protocols and the ‘Lund protocol’ cannot be conducted correctly without guidance from real-time ICP recordings.
More sophisticated use of the technique recognizes that autoregulation of CBF is one of the most important mechanisms of brain protection following head injury. he relationship between PRx (or autoregula-tion assessed using TCD) and CPP shows a U-shaped curve (Fig. 4.9). he curve indicates that CPPs that are too low or too high are associated with autoregulation failure. herefore, the ‘optimal CPP’ in which cerebral autoregulation is strongest may be identified by plotting PRx against CPP in individual cases (from the moving time window of the last few hours). Patients with a greater distance between their averaged CPP and post-hoc assessed ‘optimal CPP’ have worse outcomes after head trauma. An algorithm has been proposed by Steiner and colleagues to modify CPP-oriented therapy to maintain CPP close to ‘optimal CPP’. However, it remains to be demonstrated prospectively whether such a strategy is able to improve outcome .
Refractory intracranial hypertension
When secondary cerebral insults lead to ‘refractory intracranial hypertension’, mean ICP rises above 80 mmHg as a result of brain swelling. he term ‘refractory intracranial hypertension’ implies that ICP increases over a few hours to very high values and leads to death of the patient unless aggressive ICP treatment is installed. his increase in ICP is commonly accompanied by a reduction in pulse amplitude and a gradual increase in ABP (the Cushing reflex). he moment of brainstem herniation through the foramen magnum is commonly marked by a rapid decrease in ABP, a rise in heart rate and a terminal decrease in the cerebral perfusion. When all pressure-volume compensatory reserves are exhausted, any further increase in intracranial volume produces fast and often fatal elevations in ICP. Decompressive craniectomy is often seen as a last resort in this setting. However, its greatest benefit may require that the decision about surgery be undertaken well before uncontrollable elevations in ICP occur -with the intervention optimally being employed at ICP values that do not exceed 25 mmHg. However, several patients with ICP at this level will not develop refractory ICP elevations, and we need better early markers of subsequent refractory intracranial hypertension. In this context, some measures of cerebrovascular physiology may predict refractory intracranial hypertension – one being early loss of cerebrovascular reactivity (PRx) (Fig. 4.10).
Fig. 4.10. Refractory intracranial hypertension. The second half of this graph shows intracranial pressure (ICP) increasing above 60 mmHg, while cerebral perfusion pressure (CPP) falls well below 40 mmHg. The patient died. The earlier part of the graph shows a rise in ICP from 20 to 40 mmHg, associated with a decrease in CPP below 50 mmHg. This period of progressive ICP elevation is preceded by a 60 min phase during which the pressure reactivity index (PRx) increases (note the change of colour of a bar from greenish to red within the critical period indicated by a grey background). See colour plate section.
