Cerebral Multimodal Monitoring in Sepsis: An Experimental Study.

Acute brain dysfunction is a complication of sepsis, and its pathophysiology remains poorly understood. We studied the brain metabolism in a resuscitated animal model of sepsis. Twelve anesthetized, mechanically ventilated, and invasively monitored pigs were allocated to a sham procedure (N = 5) or sepsis (N = 7). Sepsis was induced through fecal inoculation in the peritoneum. Fluid resuscitation was maintained during the entire study period. Animals were observed until spontaneous death or for a maximum of 24 h. In addition to global hemodynamic and laboratory assessment, intracranial pressure and cerebral microdialysis (MD) were evaluated at baseline, 6, 12, 18, and 24 h after sepsis induction. After euthanasia, the brain was rapidly removed and a fragment from the frontal cortex was analyzed for markers of neuroinflammation, metabolism, and neurotransmission. Septic animals developed a hyperdynamic state associated with increased arterial lactate. Cerebral microdialysis showed unchanged levels of lactate/pyruvate ratios and brain glucose between the groups. Brain/serum glucose ratios were increased in the septic animals during the study period despite a progressive decrease in serum glucose. Moreover, extracellular glutamine levels were elevated starting at 6 h after sepsis. Tissue analysis showed elevated glutamate, glutamine, and glutamine synthetase in the sepsis group. However, C-Fos, a marker of neuronal activity, was unchanged between groups. In this animal model of resuscitated sepsis, we found increased oxidative stress and alterations in neuroenergetics characterized by exacerbated activity of the glutamate/glutamine cycle and increased glucose utilization by the brain, however without any evidence of decompensated energy metabolism.

Effects of positive end-expiratory pressure on brain tissue oxygen pressure of severe traumatic brain injury patients with acute respiratory distress syndrome: A pilot study.

PURPOSE: To verify whether high positive end-expiratory pressure levels can increase brain tissue oxygen pressure, and also their effects on pulse oxygen saturation, intracranial pressure, and cerebral perfusion pressure. MATERIAL AND METHODS: Twenty traumatic brain injury patients with acute respiratory distress syndrome were submitted to positive end-expiratory pressure levels of 5, 10, and 15 cm H2O progressively. The 3 positive end-expiratory pressure levels were used during 20 minutes for each one, whereas brain tissue oxygen pressure, oxygen saturation, intracranial pressure, and cerebral perfusion pressure were recorded. RESULTS: Brain tissue oxygen pressure and oxygen saturation increased significantly with increasing positive end-expiratory pressure from 5 to 10 and from 10 to 15 cm H2O (P=.0001 and P=.0001 respectively). Intracranial pressure and cerebral perfusion pressure did not differ significantly with increasing positive end-expiratory pressure from 5 to 10 and from 10 to 15 cm H2O (P=.16 and P=.79 respectively). CONCLUSIONS: High positive end-expiratory pressure levels increased brain tissue oxygen pressure and oxygen saturation, without increase in intracranial pressure or decrease in cerebral perfusion pressure. High positive end-expiratory pressure levels can be used in severe traumatic brain injury patients with acute respiratory distress syndrome as a safe alternative to improve brain oxygenation.

Alveolar recruitment maneuver in patients with subarachnoid hemorrhage and acute respiratory distress syndrome: a comparison of 2 approaches.

PURPOSE: The purpose of the study was to compare 2 alveolar recruitment maneuvers (ARMs) approaches in patients with subarachnoid hemorrhage (SAH) and acute respiratory distress syndrome (ARDS). MATERIAL AND METHODS: Sixteen SAH patients with ARDS were randomized in 2 similar groups. One received ARM with continuous positive airway pressure (CPAP) of 35 cm H(2)O for 40 seconds (CPAP recruitment), whereas the other received pressure control ventilation with positive-end expiratory pressure of 15 cm H(2)O and pressure control above positive end-expiratory pressure of 35 cm H(2)O for 2 minutes (pressure control recruitment maneuver [PCRM]). Intracranial pressure (ICP) and cerebral perfusion pressure (CPP) were measured before and after ARM. The ratio of arterial oxygen tension to fraction of inspired oxygen was measured before and 1 hour after the ARM. RESULTS: After ARM, ICP was higher in CPAP recruitment (20.50 ± 4.75 vs 13.13 ± 3.56 mm Hg; P = .003); and CPP was lower in CPAP recruitment (62.38 ± 9.81 vs 79.60 ± 6.8 mm Hg; P = .001). One hour after the ARM, the ratio of arterial oxygen tension to fraction of inspired oxygen increased significantly only in PCRM (108.5 to 203.6; P = .0078). CONCLUSION: In SAH patients with ARDS, PCRM did not affect ICP and decreased CPP in safe levels, besides improving oxygenation.