Cerebral Oxygenation in Contusioned vs. Nonlesioned Brain Tissue: Moniting of PtiO2 with Licox and Paratrend

Abstract

Brain tissue PO2 in severely head injured patients was monitored in parallel with two different PO2-microsensors (Licox and Paratrend). Three different locations of sensor placement were chosen: (1) both catheters into non lesioned tissue (n = 3), (2) both catheters into contusioned tissue (n = 2), and (3) one catheter (Licox) into pericontusional versus one catheter (Paratrend) into non lesioned brain tissue (n = 2). Mean duration of PtiO2-monitoring with both microsensors in parallel was 68.1 hours. Brain tissue PO2 varied when measured in lesioned and nonlesioned tissue. In non lesioned tissue both catheters closely correlated (Δ Licox/Paratrend: mean PtiO2 < 5mmHg) after 20 hours post insertion. In pericontusional tissue PtiO2 was reduced relative to non lesioned tissue (Δ lesioned/non lesioned: mean PtiO2: 10.3mmHg). In contusioned brain tissue PtiO2 was always below the "hypoxic threshold" of 10mmHg, independent of the type of micorsensor used. During a critical reduction in cerebral perfusion pressure (<60mmHg), PtiO2 decreased measured with both microsensors. Elevation of inspired oxygen fraction, normally followed by a rapid increase in tissue PO2, only increased PtiO2 when measured in pericontusional and nonlesioned brain. To recognize critical episodes of hypoxia or ischemia, PtiO2-monitoring of cerebral oxygenation is recommended in nonlesioned brain tissue.