Cerebrovascular pressure reactivity and brain tissue oxygen monitoring provide complementary information regarding the lower and upper limits of cerebral blood flow control in traumatic brain injury: a CAnadian High Resolution-TBI (CAHR-TBI) cohort study

Intensive Care Medicine Experimental

Table 2 Performance of various multivariable logistic regression models to predict 6-month post-injury outcomes

Model	Favorable vs unfavorable outcome			Alive vs dead
Model	AUC (95% CI)	AIC	Nagelkerke R²	AUC (95% CI)	AIC	Nagelkerke R²
TBI-IMPACT	0.86 (0.76–0.96)	66.00	0.51	0.78 (0.66–0.90)	68.37	0.27
TBI-IMPACT + % Time CPP < 60 mmHg + % Time CPP > 70 mmHg	0.86 (0.76–0.96)	68.81	0.53	0.81 (0.69–0.93)	69.44	0.33
TBI-IMPACT + % Time CPP < 60 mmHg + % Time CPP > 70 mmHg + % Time PbtO₂ < 20 mmHg	0.87 (0.77–0.96)	69.83	0.54	0.81 (0.70–0.93)	71.15	0.34
TBI-IMPACT + % Time CPP < LLR	0.86 (0.76–0.96)	65.81	0.53	0.80 (0.68–0.93)	65.85	0.32
TBI-IMPACT + % Time CPP > ULR	0.86 (0.77–0.96)	66.66	0.52	0.81 (0.69–0.92)	67.40	0.28
TBI-IMPACT + % Time CPP < LLR + % Time CPP > ULR	0.87 (0.77–0.96)	67.77	0.53	0.80 (0.68–0.93)	67.48	0.33

The TBI-IMPACT model included age, admission GCS, admission pupil exam, and Marshall score
AIC Akaike Information Criterion, AUC Area under the curve, CPP cerebral perfusion pressure, GCS Glasgow Coma Scale, LLR lower limit of reactivity, PbtO₂ brain tissue oxygenation, ULR upper limit of reactivity