Evidentiary table: PbtO₂ monitoring

Reference	Patient number	Study design	Patient group	Technique assessment	End-point	Findings	Quality of evidence
Hoffmann, 1997	32	Retrospective	Cerebrovascular surgery	PbtO2	Definition of normal PbtO2 thresholds	Normal PbtO2 of controls: 31 ± 8 mmHg; normal PbtO2 of cerebrovascular surgery subjects was 70 % lower (~23 mmHg)	Low
Dings, 1998	101	Observational	TBI	PbtO2	Definition of normal PbtO2 thresholds	Normal PbtO2 values varied depending on probe distance below the dura: 7–17 mm = 33.0 ± 13.3 mmHg; 17–22 mm = 25.7 ± 8.3 mmHg; 22–27 mm = 23.8 ± 8.1 mmHg	Low
Pennings, 2008	25	Observational	Brain surgery	PbtO2	Definition of normal PbtO2 thresholds	Normal PbtO2 = 22.6 ± 7.2 mmHg in the frontal white matter. In 11 patients, measurements were continued for 24 h: PbtO2 was 23.1 ± 6.6 mmHg	Low
Doppenberg, 1998 Acta Neurochir Suppl	24	Observational	TBI	PbtO2 and PET	Definition of ischemic PbtO2 thresholds	Ischemic threshold (CBF = 18 mL/100 g/min) was PbtO2 = 22 mmHg. The critical value for PbtO2 was 19–23 mmHg	Low
Sarrafzadeh, 2000	35	Retrospective	TBI	PbtO2 and CMD	Definition of ischemic PbtO2 thresholds	PbtO2 < 10 mmHg is critical to induce metabolic changes seen during hypoxia/ischemia (increased cerebral microdialysis glutamate and lactate/pyruvate ratio)	Low
Kett-White, 2002a	46	Observational	Aneurysm surgery	PbtO2	Definition of ischemic PbtO2 thresholds	Temporary clipping caused PbtO2 decrease: in patients in whom no subsequent infarction developed in the monitored region, PbtO2 was ~11 mmHg; PbtO2 < 8 mmHg for 30 min was associated with infarction	Low
Doppenberg, 1998 Surg Neurol	25	Observational	TBI	PbtO2 with regional CBF (Xenon CT)	Correlation between PbtO2 and CBF	PbtO2 strongly correlated with CBF (R = 0.74, p < 0.001); CBF < 18 mL/100 g/min was always accompanied by PbtO2 ≤ 26 mmHg	Low
Valadka, 2002	18	Observational	TBI	PbtO2 with regional CBF (Xenon CT)	Correlation between PbtO2 and CBF	PbtO2 varied linearly with both regional and global CBF	Low
Jaeger, 2005b	8	Observational	Mixed (TBI, SAH)	PbtO2 with regional CBF (TDP)	Correlation between PbtO2 and CBF	Significant correlation between PbtO2 and CBF (R = 0.36); in 72 % of 400 intervals of 30 min duration with PbtO2 changes larger than 5 mmHg, a strong correlation between PbtO2 and CBF was found (R > 0.6)	Low
Rosenthal, 2008	14	Observational	TBI	PbtO2 with regional CBF (TDP) and SjvO2	Correlation between PbtO2 and CBF	PbtO2 = product of CBF and cerebral arterio-venous O2 tension difference	Low
Longhi, 2007	32	Prospective observational	TBI	PbtO2	Probe location: normal versus peri-contusional	PbtO2 lower in peri-contusional (19.7 ± 2.1 mmHg) than in normal-appearing tissue (25.5 ± 1.5 mmHg); median duration of PbtO2 < 20 mmHg was longer in peri-contusional versus normal-appearing tissue (51 vs. 34 % of monitoring time)	Low
Hlatky, 2008	83	Observational	TBI	PbtO2	Probe location: normal versus peri-contusional	PbtO2 response to hyperoxia in normal (n = 20), peri-contusional (n = 35) and abnormal (n = 28) brain areas: poor response to hyperoxia when Licox was in abnormal brain	Low
Ponce, 2012	405	Prospective observational	TBI	PbtO2	Probe location: normal versus peri-contusional	Average PbtO2 lower in peri-contusional (25.6 ± 14.8 mmHg) versus normal (30.8 ± 18.2 mmHg) brain (p < .001). PbtO2 was significantly associated to outcome in univariate analyses, but independent linear relationship between low PbtO2 and 6-month GOS score was found only when the PbtO2 probe was placed in peri-contusional brain	Low
Ulrich, 2013	100	Retrospective	SAH	PbtO2	Likelihood of PbtO2 monitoring to be placed in vasospasm or infarction territory	The probability that a single PbtO2 probe was situated in the territory of severe vasospasm/infarction was accurate for MCA/ICA aneurysms (80–90 %), but not for ACA (50 %) or VBA aneurysms (25 %)	Low
Johnston, 2004	11	Prospective, interventional	TBI	PbtO2 and PET	Effect of CPP augmentation (70 → 90 mmHg) on PbtO2	Induced hypertension resulted in a significant increase in PbtO2 (17 ± 8 vs. 22 ± 8 mmHg, p < 0.001) and CBF (27.5 ± 5.1 vs. 29.7 ± 6.0 mL/100 g/min, p < 0.05) and a significant decrease in oxygen extraction fraction (33.4 ± 5.9 vs. 30.3 ± 4.6 %, p < 0.05)
Jaeger, 2010	38	Prospective observational	TBI	PbtO2	Identification of ‘‘optimal’’ CPP	Optimal CPP could be identified in 32/38 patients. Median optimal CPP was 70–75 mmHg (range 60– 100 mmHg). Below the level of optimal CPP, PbtO2 decreased in parallel to CPP, whereas PbtO2 reached a plateau above optimal CPP. Average PbtO2 at optimal CPP was 24.5 ± 6.0 mmHg
Schneider, 1998	15	Prospective	TBI	PbtO2	Effect of moderate hyperventilation	Hyperventilation (PaCO2: 27–32 mmHg) significantly reduced PbtO2 from 24.6 ± 1.4 to 21.9 ± 1.7 mmHg	Low
Imberti, 2002	36	Prospective	TBI	PbtO2 and SjvO2	Effect of moderate hyperventilation	20-min periods of moderate hyperventilation (27– 32 mmHg) in most tests (79.8 %) led to both PbtO2 and SjvO2 decrease.	Low
Raabe, 2005	45	Retrospective	SAH	PbtO2	Effect of induced hypertension and hypervolemia	During the 55 periods of moderate hypertension, an increase in PbtO2 was found in 50 cases (90 %), with complications occurring in three patients (8 %); During the 25 periods of hypervolemia, an increase in PbtO2 was found during three intervals (12 %), with complications occurring in nine patients (53 %)	Low
Muench, 2007	10	Prospective	SAH	PbtO2 and TDP	Effect of induced hypertension and hypervolemia	Induced hypertension (MAP ≈ 140 mmHg) resulted in a significant (p < .05) increase of PbtO2 and regional CBF. In contrast, hypervolemia/hémodilution induced only a slight increase of regional CBF while PbtO2 did not improve	Low
Al-Rawi, 2010	44	Prospective	SAH	PbtO2	Osmotherapy with HTS to treat ICP > 20 mmHg	(2 mL/kg) of 23.5 % HTS resulted in a significant increase in PbtO2 (P < 0.05). A sustained increase in PbtO2 (>210 min) was associated with favorable outcome	Low
Francony, 2008	20	RCT	Mixed (17 TBI, 3 SAH)	PbtO2	Osmotherapy with MAN versus HTS to treat ICP > 20 mmHg	A single equimolar infusion (255 mOsm dose) of 20 % MAN (N = 10 patients) or 7.45 % HTS (N = 10 patients) equally and durably reduced ICP. No major changes in PbtO2 were found after each treatment	High
Smith, 2005	35	Prospective	Mixed (TBI, SAH)	PbtO2	Effect of RBCT	RBCT was associated with an increase in PbtO2 in most (74 %) patients	Low
Leal-Noval, 2006	60	Prospective	TBI	PbtO2	Effect of RBCT	RBCT was associated with an increase in PbtO2 during a 6h period in 78.3 % of the patients. All patients with basal PbtO2 < 15 mmHg showed an increment in PbtO2 versus 74.5 % of patients with basal PbtO2 ≥ 15 mmHg	Low
Zygun, 2009	30	Prospective	TBI	PbtO2	Effect of RBC transfusion	RBCT was associated with an increase in PbtO2 in 57 % of patients	Low
Menzel, 1999b	24	Retrospective	TBI	PbtO2 and CMD	Effect of normobaric hyperoxia	N = 12 patients in whom PaO2 was increased to 441 ± 88 mmHg over a period of 6 h by raising the FiO2 from 35 to 100 % versus control cohort of 12 patients who received standard respiratory therapy (mean PaO2 136 mmHg): the mean PbtO2 increased in the O2-treated patients up to 360 % of the baseline level during the 6-hour FiO2 enhancement period, whereas the mean CMD lactate levels decreased by 40 % (p < 0.05)	Low
Nortje, 2008	11	Prospective	TBI	PbtO2 and CMD	Effect of normobaric hyperoxia	Hyperoxia (FiO2 increase of 0.35–0.50) increased mean PbO2 from 28 ± 21 to 57 ± 47 mmHg (p = 0.015) and was associated with a slight but statistically significant reduction of CMD lactate/pyruvate ratio (34 ± 9.5 vs. 32.5 ± 9.0, p = 0.018)	Low
Meixensberger, 2003b	91	Retrospective	TBI	PbtO2 therapy versus standard ICP/CPP management	Effect on outcome	N = 52 versus N = 39 pts; PbtO2 threshold 10 mmHg → no difference in 6-month-GOS (65 vs. 54 %, p < 0.01)	Low
Stiefel, 2005	53	Retrospective	TBI	PbtO2 therapy versus standard ICP/CPP management	Effect on outcome	N = 28 versus → = 25 pts; PbtO2 threshold 25 mmHg → reduced mortality at discharge (25 vs. 44 %, p < 0.05)	Low
Martini, 2009	629	Retrospective	TBI	PbtO2 therapy versus standard ICP/CPP management	Effect on outcome	N = 123 versus N = 506 pts; PbtO2 threshold 20 mmHg → lower functional independence score (FIM) at discharge (7.6 vs. 8.6, p < 0.01)	Low
Adamides, 2009	30	Prospective	TBI	PbtO2 therapy versus standard ICP/CPP management	Effect on outcome	N = 20 versus N = 10 pts; PbtO2 threshold 15 mmHg → no difference in 6-month GOS	Low
McCarthy, 2009	111	Prospective	TBI	PbtO2 therapy versus standard ICP/CPP management	Effect on outcome	N = 63 versus N = 48 pts; PbtO2 threshold 20 mmHg → trend towards better 3-month GOS (79 vs. 61 %, p = 0.09)	Low
Narotam, 2009	168	Retrospective	TBI	PbtO2 therapy versus standard ICP/CPP management	Effect on outcome	N = 127 versus N = 41 pts; PbtO2 threshold 20 mmHg → better 6-month GOS (3.5 vs. 2.7, p = 0.01)	Low
Spiotta, 2010	123	Retrospective	TBI	PbtO2 therapy versus standard ICP/CPP management	Effect on outcome	N = 70 versus N = 53 pts; PbtO2 threshold 20 mmHg → better 3-month GOS (64 vs. 40 %, p = 0.01)	Low
Green, 2013	74	Retrospective	TBI	PbtO2 therapy versus standard ICP/CPP management	Effect on outcome	N = 37 versus N = 37 pts; PbtO2 threshold 20 mmHg → no difference in mortality (65 vs. 54 %, p = 0.34)	Low
Fletcher, 2010	41	Retrospective	TBI	PbtO2 therapy versus standard ICP/CPP management	Effect on outcome	N = 21 versus N = 20 pts; PbtO2 threshold 20 mmHg → higher cumulative fluid balance, higher rate of vasopressor use and pulmonary edema	Low