Non-invasive estimation of cerebral perfusion pressure using transcranial Doppler ultrasonography in children with severe traumatic brain injury

Abstract

Objective: To identify if cerebral perfusion pressure (CPP) can be non-invasively estimated by either of two methods calculated using transcranial Doppler ultrasound (TCD) parameters.

Design: Retrospective review of previously prospectively gathered data.

Setting: Pediatric intensive care unit in a tertiary care referral hospital.

Patients: Twenty-three children with severe traumatic brain injury (TBI) and invasive intracranial pressure (ICP) monitoring in place.

Interventions: TCD evaluation of the middle cerebral arteries was performed daily. CPP at the time of the TCD examination was recorded. For method 1, estimated cerebral perfusion pressure (CPPe) was calculated as: CPPe = MAP × (diastolic flow (Vd)/mean flow (Vm)) + 14. For method 2, critical closing pressure (CrCP) was identified as the intercept point on the x-axis of the linear regression line of blood pressure and flow velocity parameters. CrCP/CPPe was then calculated as MAP-CrCP.

Measurements and main results: One hundred eight paired measurements were available. Using patient averaged data, correlation between CPP and CPPe was significant (r = 0.78, p = < 0.001). However, on Bland-Altman plots, bias was 3.7 mmHg with 95% limits of agreement of - 17 to + 25 for CPPe. Using patient averaged data, correlation between CPP and CrCP/CPPe was significant (r = 0.59, p = < 0.001), but again bias was high at 11 mmHg with wide 95% limits of agreement of - 15 to + 38 mmHg.

Conclusions: CPPe and CrCP/CPPe do not have clinical value to estimate the absolute CPP in pediatric patients with TBI.

Keywords: Cerebral perfusion pressure; Head injury; Non-invasive monitoring; Transcranial Doppler ultrasound; Traumatic brain injury; Ultrasound.

Fig. 1

Using patient averaged data, correlation between cerebral perfusion pressure (CPP) and non-invasively estimated cerebral perfusion pressure (CPPe = (mean arterial blood pressure × diastolic flow velocity/mean flow velocity) + 14) was significant (r = 0.78, p ≤ 0.001). The Bland-Altman plot of agreement between the two revealed bias of 3.7 mmHg with 95% limits of agreement − 17, + 25 mmHg

Fig. 2

Using patient averaged data, correlation between cerebral perfusion pressure (CPP) and non-invasively estimated CPPe using TCD-derived critical closing pressure (CrCP = intercept point of the regression line between arterial systolic and diastolic pressures and systolic and diastolic flow velocities; CPPe in this scenario = MAP-CrCP) was significant (r = 0.59, p = < 0.001). The Bland-Altman plot of agreement between the two revealed bias of 11 mmHg with 95% limits of agreement − 15, + 38 mmHg

Fig. 3

Linear regression analysis of pressure-flow relationships before [1], during [2], and after [3] use of hypertonic saline to manage intracranial pressure spike. The critical closing pressure (CrCP) is represented by the intercept of the regression line with the x-axis. CrCP for 1 = 19, CrCP for 2 = 39, and CrCP for 3 = 18.8. CrCP likely increased due to ICP increases given that other contributory physiologic variables that contribute to CrCP were unchanged

Fig. 4

Linear regression analysis of pressure-flow relationships during [1], and after [2] use of mannitol, hypertonic saline, and hyperventilation to manage intracranial hypertension. The critical closing pressure (CrCP) is represented by the intercept of the regression line with the x-axis. CrCP for 1 = 60, CrCP for 2 = 72.9. CrCP high due to increased ICP. Increasing CrCP could be partially caused by increased cerebrovascular resistance from reducing partial pressure of carbon dioxide, but a lack of reduction in CrCP is consistent with an ICP that continued to increase despite treatment