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Introduction: Jugular oxygen saturation monitoring was introduced in neurointensive care after severe traumatic brain injury (TBI) to explore the adequacy of brain perfusion and guide therapeutic interventions. The brain was considered homogeneous, and oxygen saturation was taken as representative of the whole organ. We investigated whether venous outflow from the brain was homogeneous by measuring oxygen saturation simultaneously from the two jugular veins., Methods: In 32 comatose TBI patients both internal jugular veins (IJs) were simultaneously explored using intermittent samples; hemoglobin saturation was also recorded continuously by fiber-optic catheters in five patients. In five cases long catheters were inserted bilaterally upstream, up to the sigmoid sinuses., Main Findings: On average, measurements from the two sides were in agreement (mean and standard deviation of the differences between the saturation of the two IJs were respectively 5.32 and 5.15). However, 15 patients showed differences of more than 15 % in hemoglobin saturation at some point; three others showed differences larger than 10 %. No relationship was found between the computed tomographic scan data and the hemoglobin saturation pattern., Discussion/conclusion: Several groups have confirmed differences between oxygen saturation in the two jugular veins. After years of enthusiasm, interest for jugular saturation has decreased and more modern methods, such as tissue oxygenation monitoring, are now available. Jugular saturation monitoring has low sensitivity, with the risk of missing low saturation, but high specificity; moreover it is cheap, when used with intermittent sampling. Monitoring the adequacy of brain perfusion after severe TBI is essential. However the choice of a specific monitor depends on local resources and expertise.

Objective: We compared brain tissue oxygen tension (PtiO2) measured in peri-focal and in normal-appearing brain parenchyma on computerized tomography (CT) in patients following traumatic brain injury (TBI)., Design: Prospective observational study., Setting: Neurointensive care unit., Patients and Participants: Thirty-two consecutive TBI patients were subjected to PtiO2 monitoring., Interventions: Peri-focal tissue was identified by the presence of a hypodense area of the contusion and/or within 1 cm from the core of the contusion. The position of the tip of the PtiO2 probe was assessed at follow-up CT scan., Measurements and Results: Mean PtiO2 in the peri-contusional tissue was 19.7+/-2.1 mmHg and was lower than PtiO2 in normal-appearing tissue (25.5+/-1.5 mmHg, p < 0.05), despite a greater cerebral perfusion pressure (CPP) (73.7+/-2.3 mmHg vs. 67.4+/-1.4 mmHg, p < 0.05). We observed both in peri-focal tissue and in normal-appearing tissue episodes of brain hypoxia (PtiO2 < 20 mmHg for at least 10 min), whose median duration was longer in peri-focal tissue than in normal-appearing tissue (51% vs. 34% of monitoring time, p < 0.01). In peri-focal tissue, we observed a progressive PtiO2 increase from pathologic to normal values (p < 0.01)., Conclusions: Multiple episodes of brain hypoxia occurred over the first 5 days following severe TBI. PtiO2 was lower in peri-contusional tissue than in normal-appearing tissue. In peri-contusional tissue, a progressive increase of PtiO2 from pathologic to normal values was observed over time, suggestive of an improvement at microcirculatory level.

Aim: The aim of this study was to evaluate the arterio-venous difference in carbon dioxide tension (DPCO2) and the ratio between DPCO2 and arterio-jugular oxygen difference (AJDO2) as indicators of compensated or uncompensated cerebral hypoperfusion., Methods: Cerebral blood flow (CBF) was reduced stepwise in 6 pigs by inducing intracranial hypertension with consequently cerebral perfusion pressure (CPP) reduction: CBF 100%, 50-60 % of baseline, 20-30% of baseline. Intracranial pressure (ICP), mean arterial pressure (MAP), CPP and CBF (laser-Doppler method) were continuously recorded. Superior sagittal sinus was punctured for the determination of AJDO2 and DPCO2., Results: CBF impairment was accompanied by changes in AJDO2 from 6.03 +/- 1.21 vol% to 7.32 +/- 1.30 vol%, up to 8.07 +/- 1.32 vol% (P < 0.01), in DPCO2 from 12.17 +/- 3.25 mmHg to 16 +/- 4.12 mmHg, up to 26.5 +/- 6.41 mmHg (P < 0.01), and DPCO2/AJDO2 ratio from 2.05 +/- 0.39 to 2.06 +/- 0.72 up to 3.41 +/- 1.09 in the 3 phases (P < 0.05)., Conclusions: When CBF declines AJDO2 increases, indicating greater extraction of O2 to satisfy aerobic metabolism. However, this mechanism can no longer compensate once a critical CBF threshold is reached. DPCO2 rises slowly during moderate CBF reduction because of defective washout; the rise is steeper during marked CBF impairment when anaerobic metabolism takes place. During cerebral hypoperfusion the venous blood gases and acid base variables mirror the degree of cerebral perfusion. In particular the DPCO2, and the DPCO2/ AJDO2 ratio may be useful markers of critical brain hypoperfusion.

Background: The authors propose that for a moderate reduction of perfusion during progressive irreversible ischemia, oxygen extraction increases to maintain aerobic metabolism, and arteriojugular oxygen difference (AJDo2) increases. Because of reduced carbon dioxide washout, venoarterial difference in carbon dioxide tension (DPco2) increases, with no change in the DPco2/AJDo2 ratio. With further reduction of cerebral perfusion, the aerobic metabolism will begin to decrease, AJDo2 will decrease while DPco2 will continue to increase, and the ratio will increase. When brain infarction develops, the metabolism will be abated, no oxygen will be consumed, and no carbon dioxide will be produced., Methods: The authors studied 12 patients with acute cerebral damage that evolved to brain death and collected intermittent arterial and jugular blood samples., Results: Four patterns were observed: (1) AJDo2 of 4.1 +/- 0.7 vol%, DPco2 of 6.5 +/- 1.9 mmHg, and a ratio of 1.55 +/- 0.3 with cerebral perfusion pressure of 62.5 +/- 13.4 mmHg; (2) a coupled increase of AJDo2 (5.8 +/- 0.7 vol%) and DPco2 (10.1 +/- 1.0 mmHg) with no change in ratio (1.92 +/- 0.14) and cerebral perfusion pressure (57.9 +/- 5.8 mmHg); (3) AJDo2 of 4.7 +/- 0.4 vol% with an increase in DPco2 (11.8 +/- 1 mmHg) and correspondingly higher ratio (2.7 +/- 0.2); in this phase, cerebral perfusion pressure was 39.7 +/- 10.5 mmHg; (4) immediately before diagnosis of brain death (cerebral perfusion pressure, 17 +/- 10.4 mmHg), there was a decrease of AJDo2 (1.1 +/- 0.1 vol%) and of DPco2 (5.3 +/- 0.6 mmHg) with a further ratio increase (5.1 +/- 0.8)., Conclusions: Until compensatory mechanisms are effective, AJDo2 and DPco2 remain coupled. However, when the brain's ability to compensate for reduced oxygen delivery is exceeded, the ratio of DPco2 to AJDo2 starts to increase.

Background: Postischaemic pyrexia exacerbates neuronal damage. Hyperthermia related cerebral changes have still not been well investigated in humans., Objective: To study how pyrexia affects neurochemistry and cerebral oxygenation after acute brain injury., Methods: 18 acutely brain injured patients were studied at the onset and resolution of febrile episodes (brain temperature > or = 38.7 degrees C). Intracranial pressure (ICP), brain tissue oxygen tension (PbrO2), and brain tissue temperature (Tbr) were recorded continuously; jugular venous blood was sampled intermittently. Microdialysis probes were inserted in the cerebral cortex and in subcutaneous tissue. Glucose, lactate, pyruvate, and glutamate were measured hourly. The lactate to pyruvate ratio was calculated., Results: Mean (SD) Tbr rose from 38 (0.5) to 39.3 (0.3) degrees C. Arteriojugular oxygen content difference (AJD(O2)) fell from 4.2 (0.7) to 3.8 (0.5) vol% (p < 0.05) and PbrO2 rose from 32 (21) to 37 (22) mm Hg (p < 0.05). ICP increased slightly and no significant neurochemical alterations occurred. Opposite changes were recorded when brain temperature returned towards baseline., Conclusions: As long as substrate and oxygen delivery remain adequate, hyperthermia on its own does not seem to induce any further significant neurochemical alterations. Changes in cerebral blood volume may, however, affect intracranial pressure.

This study investigated AJDO2 (arterio-jugular difference of oxygen content) in a large sample of severely head-injured patients to identify its pattern during the first days after injury and to describe the relationship of AJDO2 with acute neurological severity and with outcome 6 mo after trauma. In 229 comatose head-injured patients, we monitored intracranial pressure, cerebral perfusion pressure, and AJDO2. Outcome was defined 6 mo after injury. Jugular hemoglobin oxygen saturation (SjO2) averaged 68%. The mean AJDO2 was 4.24 vol% (SD, 1.3 vol%). There were 80 measurements (4.6%) with SjO2 <55% and 304 (17.6%) with saturation >75%. AJDO2 was higher than 8.7 vol% in 8 measurements (0.4%) and was lower than 3.9 vol% in 718 (42%) measurements. AJDO2 was higher during the first tests and decreased steadily over the next few days. Cases with a favorable outcome had a higher mean AJDO2 (4.3 vol%; SD, 0.3 vol%) than patients with severe disability or vegetative status (3.8 vol%; SD, 1.3 vol%) and patients who died (3.6 vol%; SD, 1 vol%). This difference was significant (P < 0.001). We conclude that low levels of AJDO2 are correlated with a poor prognosis, whereas normal or high levels of AJDO2 are predictive of better results.

We investigated the changes in brain oxygen tension (ptiO2) after ventilation with pure O2 in order to (1) clarify the pathophysiology of O2 exchange in the cerebral microcirculation; and (2) investigate the relationship between brain O2 tension, O2 delivery, and consumption in steady-state conditions during stepwise cerebral blood flow (CBF) reductions. A swine model was developed to reduce CBF in three stable steps: (1) baseline (CBF 100%), (2) CBF of 50-60% of baseline, and (3) CBF of <30% of baseline. CBF was reduced by infusing saline into the left lateral ventricle through a catheter connected with an infusion pump. At each step, hyperoxia was tested by increasing the inspired oxygen fraction up to 100%, PtiO2 reflected the CBF reductions, since it was respectively 27.95 (+/-10.15), 14.77 (+/-3.58), and 3.45 (+/-2.89) mm Hg during the three CBF steps. Hyperoxia was followed by an increase in ptiO2, although the increase was significantly lower when hyperoxia was applied during progressive ischemia. O2 supply to the brain did not change during hyperoxia. Arteriovenous oxygen difference (AVDO2) decreased during the phases of intact CBF and moderate impairment, but not during the phase of severe CBF reduction. In conclusion, ptiO2 reductions closely reflect the imbalance between oxygen delivery and demand; this implies a link between low ptiO2 and defective O2 supply due to impaired CBF. However, this relation is not necessarily reciprocal, since manipulating brain oxygen tension does not always influence brain oxygen delivery, as in the case of ventilation with pure oxygen.