4.5 Article

Continuous monitoring of cerebrovascular pressure reactivity in patients with head injury

Journal

NEUROSURGICAL FOCUS
Volume 25, Issue 4, Pages -

Publisher

AMER ASSOC NEUROLOGICAL SURGEONS
DOI: 10.3171/FOC.2008.25.10.E2

Keywords

cerebral perfusion pressure; cerebrovascular pressure reactivity; head injury; intracranial pressure monitoring; static rate of autoregulation

Funding

  1. MRC [G0600986, G0601025, G9439390, G0001237] Funding Source: UKRI
  2. Medical Research Council [G0001237, G0601025, G0600986, G9439390] Funding Source: researchfish
  3. Medical Research Council [G9439390, G0600986, G0001237, ID 65883, G0601025] Funding Source: Medline

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Object. Cerebrovascular pressure reactivity is the ability of cerebral vessels to respond to changes in transmural pressure. A cerebrovascular pressure reactivity index (PRx) can be determined as the moving correlation coefficient between mean intracranial pressure (ICP) and mean arterial blood pressure. Methods. The authors analyzed a database consisting of 398 patients with head injuries who underwent continuous monitoring of cerebrovascular pressure reactivity. In 298 patients, the PRx was compared with a transcranial Doppler ultrasonography assessment of cerebrovascular autoregulation (the mean index [Mx]), in 17 patients with the PET-assessed static rate of autoregulation, and in 22 patients with the cerebral metabolic rate for O-2. Patient outcome was assessed 6 months after injury. Results. There was a positive and significant association between the PRx and Mx (R-2 = 0.36, p < 0.001) and with the static rate of autoregulation (R-2 = 0.31, p = 0.02). A PRx > 0.35 was associated with a high mortality rate (> 50%). The PRx showed significant deterioration in refractory intracranial hypertension, was correlated with outcome, and was able to differentiate patients with good outcome, moderate disability, severe disability, and death. The graph of PRx compared with cerebral perfusion pressure (CPP) indicated a U-shaped curve, suggesting that too low and too high CPP was associated with a disturbance in pressure reactivity. Such an optimal CPP was confirmed in individual cases and a greater difference between current and optimal CPP was associated with worse outcome (for patients who, on average, were treated below optimal CPP [R-2 = 0.53, p < 0.001] and for patients whose mean CPP was above optimal CPP [R-2 = -0.40, p < 0.05]). Following decompressive craniectomy, pressure reactivity initially worsened (median -0.03 [interquartile range -0.13 to 0.06] to 0.14 [interquartile range 0.12-0.22]; p < 0.01) and improved in the later postoperative course. After therapeutic hypothermia, in 17 (70.8%) of 24 patients in whom rewarming exceeded the brain temperature threshold of 37 degrees C, ICP remained stable, but the average PRx increased to 0.32 (p < 0.0001), indicating significant derangement in cerebrovascular reactivity. Conclusions. The PRx is a secondary index derived from changes in ICP and arterial blood pressure and can be used as a surrogate marker of cerebrovascular impairment. In view of an autoregulation-guided CPP therapy, a continuous determination of a PRx is feasible, but its value has to be evaluated in a prospective controlled trial.

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