Fig 1.
Flow chart demonstrating the recruitment of pediatric traumatic brain injury patients.
Fig 2.
Example of a 4 hour epoch of multimodality monitoring signals in pediatric TBI.
In this screenshot, CPP is shown in the top panel and the pressure reactivity index in the second panel over a 4 hour period from 06:00 to 10:00. In the third panel is a risk chart whereby a negative PRx (good autoregulation) is denoted by a grey colour, and a disturbed PRx (>0.3) is denoted in black. In two instances, CPP drops below 60 mm Hg. During these drops in CPP, PRx is deranged (black on the risk chart). On the bottom panel, CPP is plotted against PRx and a polynomial curve is fitted. The minimum of this curve is around 65 mm Hg, which would therefore indicate the optimal CPP at time point 10:00.
Fig 3.
Real-time calculation of CPPoptimal in-vivo.
Fig 3A is an example of a pediatric TBI patient. ICP is displayed in the top panel, followed by CPP (both the absolute CPP (line) and the calculated CPPopt (circles)), a risk chart of PRx and finally a histogram indicating the time spent at various distances from the calculated optimal CPP. Although this patients CPP was above 60 mm Hg for the whole of this recording, CPP was consistently below the calculated optimal CPP. This is depicted in the histogram which indicates that over this 2 day period, the patient spent almost 20% of time (expressed as a percentage of the total time CPPopt available) > 10 mm Hg below the instantaneous CPPopt. In the second day of this recording we see persistently disturbed PRx. This patient died three days after admission. Fig 3B shows an analogous example in another pediatric TBI patient. This patient demonstrated multiple plateau waves of ICP and a CPP between 60 and 70 mm Hg. Autoregulation as indicated by the PRx risk chart was mainly good. CPP was mainly close to the calculated optimal CPP as seen in both in the time series view (panel 2) and in the CPP-CPPopt time-histogram (bottom panel). This patient survived.
Table 1.
Table of demographics of patients with traumatic brain injury included in the study.
The statistical tests are all univariate and uncorrected for multiple comparisons.
Fig 4.
Severely impaired pressure reactivity index during refractory intracranial hypertension.
High intracranial pressure was associated with persistently impaired pressure reactivity index as indicated by the solid red line (coded as black in this figure) on the PRx risk chart. In this situation, fluctuations in MAP are transmitted to ICP.
Table 2.
Multimodality monitoring parameters in brain injured patients stratified by outcome at completion of brain monitoring.
ICP–intracranial pressure, MAP–mean arterial pressure, CPP–cerebral perfusion pressure, CPPopt–optimal cerebral perfusion pressure, PRx–pressure reactivity index, RAP–cerebrospinal compensatory reserve.
Fig 5.
Time spent at different distances from CPPopt in non survivors (light grey) and survivors (dark grey).
In those that survived the distribution of time spent across the various CPP-CPPopt (ΔCPP) ranges approximated a normal distribution. Most time was spent in the range between -10 and positive 10 mm Hg, while only a small proportion of time was spent less than -10 mm Hg or greater than 10 mm Hg from CPPopt. In non-survivors (light grey), more time is spent in the extreme CPP–CPPopt (ΔCPP) ranges. This is reflected in Table 2, those who did not survive spent significantly more time with their with their CPP more than 10 mm Hg below CPPopt (Mann-Whitney p = 0.04) and less time with their CPP within 10 mm Hg of the CPPopt (Mann-Whitney U test p = 0.02).