Literature DB >> 28816837

Individualizing Thresholds of Cerebral Perfusion Pressure Using Estimated Limits of Autoregulation.

Joseph Donnelly1, Marek Czosnyka, Hadie Adams, Chiara Robba, Luzius A Steiner, Danilo Cardim, Brenno Cabella, Xiuyun Liu, Ari Ercole, Peter John Hutchinson, David Krishna Menon, Marcel J H Aries, Peter Smielewski.   

Abstract

OBJECTIVES: In severe traumatic brain injury, cerebral perfusion pressure management based on cerebrovascular pressure reactivity index has the potential to provide a personalized treatment target to improve patient outcomes. So far, the methods have focused on identifying "one" autoregulation-guided cerebral perfusion pressure target-called "cerebral perfusion pressure optimal". We investigated whether a cerebral perfusion pressure autoregulation range-which uses a continuous estimation of the "lower" and "upper" cerebral perfusion pressure limits of cerebrovascular pressure autoregulation (assessed with pressure reactivity index)-has prognostic value.
DESIGN: Single-center retrospective analysis of prospectively collected data.
SETTING: The neurocritical care unit at a tertiary academic medical center. PATIENTS: Data from 729 severe traumatic brain injury patients admitted between 1996 and 2016 were used. Treatment was guided by controlling intracranial pressure and cerebral perfusion pressure according to a local protocol.
INTERVENTIONS: None. METHODS AND MAIN
RESULTS: Cerebral perfusion pressure-pressure reactivity index curves were fitted automatically using a previously published curve-fitting heuristic from the relationship between pressure reactivity index and cerebral perfusion pressure. The cerebral perfusion pressure values at which this "U-shaped curve" crossed the fixed threshold from intact to impaired pressure reactivity (pressure reactivity index = 0.3) were denoted automatically the "lower" and "upper" cerebral perfusion pressure limits of reactivity, respectively. The percentage of time with cerebral perfusion pressure below (%cerebral perfusion pressure < lower limit of reactivity), above (%cerebral perfusion pressure > upper limit of reactivity), or within these reactivity limits (%cerebral perfusion pressure within limits of reactivity) was calculated for each patient and compared across dichotomized Glasgow Outcome Scores. After adjusting for age, initial Glasgow Coma Scale, and mean intracranial pressure, percentage of time with cerebral perfusion pressure less than lower limit of reactivity was associated with unfavorable outcome (odds ratio %cerebral perfusion pressure < lower limit of reactivity, 1.04; 95% CI, 1.02-1.06; p < 0.001) and mortality (odds ratio, 1.06; 95% CI, 1.04-1.08; p < 0.001).
CONCLUSIONS: Individualized autoregulation-guided cerebral perfusion pressure management may be a plausible alternative to fixed cerebral perfusion pressure threshold management in severe traumatic brain injury patients. Prospective randomized research will help define which autoregulation-guided method is beneficial, safe, and most practical.

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Mesh:

Year:  2017        PMID: 28816837      PMCID: PMC5595234          DOI: 10.1097/CCM.0000000000002575

Source DB:  PubMed          Journal:  Crit Care Med        ISSN: 0090-3493            Impact factor:   7.598


  35 in total

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Authors:  D K Menon
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5.  Influence of cerebrovascular resistance on the dynamic relationship between blood pressure and cerebral blood flow in humans.

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6.  Critical thresholds for cerebrovascular reactivity after traumatic brain injury.

Authors:  E Sorrentino; J Diedler; M Kasprowicz; K P Budohoski; C Haubrich; P Smielewski; J G Outtrim; A Manktelow; P J Hutchinson; J D Pickard; D K Menon; M Czosnyka
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8.  Continuous monitoring of cerebrovascular pressure reactivity allows determination of optimal cerebral perfusion pressure in patients with traumatic brain injury.

Authors:  Luzius A Steiner; Marek Czosnyka; Stefan K Piechnik; Piotr Smielewski; Doris Chatfield; David K Menon; John D Pickard
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10.  The association between early impairment in cerebral autoregulation and outcome in a pediatric swine model of cardiac arrest.

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