Influence of hyperventilation on brain tissue-PO2, PCO2, and pH in patients with intracranial hypertension.

A harmful effect of prolonged hyperventilation on outcome has been shown in comatose patients after severe head injury. The purpose of this study was to assess the acute effect of moderate hyperventilation for treatment of intracranial hypertension (ICP < 20 mmHg) on invasively measured brain tissue-PO2 (PtiO2), PCO2 (PtiCO2) and pH (tipH) in severely head injured patients. 15 severely head injured patients (GCS < or = 8) were prospectively studied. Intracranial pressure (ICP), mean arterial blood pressure (MABP), cerebral perfusion pressure (CPP), endtidal CO2 (ETCO2), PtiO2, PtiCO2 and tipH (Paratrend or Licox microsensors) were continuously recorded using multimodal monitoring. Following a baseline period of 15 minutes, patients were hyperventilated for 10 minutes. Arterial blood gas analysis was done before, during and after hyperventilation. At least three hyperventilation maneuvers were performed per patient. For statistical analysis the Friedman test was used. Hyperventilation (paCO2: 32.4 +/- 0.6 to 27.7 +/- 0.5 mmHg) significantly reduced ICP from 25.3 +/- 1.5 to 14.2 +/- 1.9 mmHg (p < 0.01). As a consequence, CPP increased by 9.6 +/- 3.4 mmHg to 76.8 +/- 3.2 mmHg. Brain tissue PCO2 decreased from 37.5 +/- 1.3 to 34.6 +/- 1.2 while tipH increased from 7.13 to 7.16. In all patients, hyperventilation led to a reduction of brain tissue PO2 (PtiO2/Licox: 24.6 +/- 1.4 to 21.9 +/- 1.7 mmHg, n.s.; PtiO2/Paratrend: 35.8 +/- 4.3 to 31.9 +/- 4.0 mmHg, n.s.). In one case hyperventilation even had to be stopped after 7 min because the drop in brain tissue PO2 below 10 mmHg signalized imminent hypoxia. As well known, hyperventilation improves CPP due to a reduction in ICP. However, this does not ameliorate cerebral oxygenation as demonstrated by the decrease in PtiO2. This underlines that hyperventilation should only be used with caution in the treatment of intracranial hypertension.

Monitoring of brain tissue PO2 in traumatic brain injury: effect of cerebral hypoxia on outcome.

This study investigates the effect of hypoxic brain tissue PO2 on outcome, and examines the incidence of possible causes for cerebral hypoxia. We studied 35 patients with severe head injury (GCS < or = 8). Age was 33.2 (+/- 11.3) years. Total time of monitoring of PtiO2, intracranial pressure (ICP), cerebral perfusion pressure (CPP), and endtidal PCO2 (ETCO2) was 119.3 (+/- 65.7) hours. Data were continuously recorded by a computer system. Outcome was assessed at discharge and after 6 months post injury. 56% of the patients with more than 300 minutes of PtiO2 < 10 mm Hg died, 22% had an unfavourable outcome, 22% had a favourable outcome. Cerebral hypoxia was associated with intracranial hypertension (ICP > 20 mm Hg) in 11.5 (+/- 15.1)%. CPP was compromised below 60 mm Hg in 16.8 (+/- 23.4)%. Hypocarbia (ETCO2 < 28 mm Hg) was present in 48.0% of the time of PtiO2 < 10 mm Hg. No obvious cause for cerebral hypoxia was found in 45% of the data. These result underscore the association of cerebral hypoxia with poor neurological outcome and stress the meaning of monitoring of PtiO2 as an independent parameter in patients following TBI.

Bifrontal measurements of brain tissue-PO2 in comatose patients.

The purpose of this study was to compare brain tissue-PO2 (PtiO2) in lesioned vs. non-lesioned brain tissue. PtiO2 was monitored bifrontally with a "Clark"-type microcatheter in patients following severe head injury (n = 6) and subarachnoid hemorrhage (SAH) (n = 1) from day 2 to day 12 posttrauma/post SAH. Mean arterial blood pressure, intracranial pressure (ICP), cerebral perfusion pressure and end-tidal CO2 were monitored. Data were stored and analyzed by a multimodal cerebral monitoring system. The CT of five patients was classified as "diffuse injury" and of one patients as "evacuated mass lesion". The patient with SAH (Hunt and Hess IV) had a concomitant intracerebral hematoma which was removed. In all cases, one catheter was placed close to the lesion, while the other was situated in an area with no visible pathology. For analysis, bifrontal PtiO2 data were taken from both on-line monitoring and O2 reactivity tests (FiO2 1.0 for 10 min). Two different patterns were identified: periods of concordance (22% of recordings) and periods in which PtiO2 was lower in lesioned cerebral white matter (78%) but always running parallel. In the latter case, O2-reactivity response was markedly reduced on the lesioned side. Our findings demonstrate a decreased PtiO2 and a reduced O2 reactivity in contused or infarcted brain tissue. Future studies have to clarify which PtiO2 is more important to be used as a guide for therapy.

Cerebral oxygenation in contusioned vs. nonlesioned brain tissue: monitoring of PtiO2 with Licox and Paratrend.

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 (delta Licox/Paratrend: mean PtiO2 < 5 mm Hg) after 20 hours post insertion. In pericontusional tissue PtiO2 was reduced relative to non lesioned tissue (delta lesioned/non lesioned: mean PtiO2: 10.3 mm Hg). In contusioned brain tissue PtiO2 was always below the "hypoxic threshold" of 10 mm Hg, independent of the type of microsensor used. During a critical reduction in cerebral perfusion pressure (< 60 mm Hg), 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.

Multimodal cerebral monitoring in comatose head-injured patients.

Monitoring of comatose patients in the neurosurgical intensive care unit (NICU) is constantly extended by the development of new methods for monitoring of cerebral function, metabolism and oxygenation. To simplify the interpretation of the rising number of parameters, and to avoid data overflow, a multimodal cerebral monitoring (MCM) system has been developed for the acquisition, display, on-line analysis and recording of physiological parameters from multiple bedside data sources. This article describes the technical details and the design of this computerized data acquisition system for variable applications in clinical patient monitoring and research. A Windows (Microsoft Corporation, Redmont, Washington) platform was equipped with an analog/digital converter board. Software for multimodal cerebral monitoring was developed using LabVIEW for Windows (National Instruments, Austin, Texas), a graphical programming system. Two software modules were created: One for the automatic acquisition of data, display of time dependent trend graphs, processing of on-line histograms, special functions for research, and storage of data in compatible format. The other module serves as an off-line monitor to display recorded data in various modalities. The MCM system has been used in 30 comatose patients with severe head injury. Mean time of MCM is 5.3 days (+/- 2.8 days), resulting in a total running time of the system of about 3800 hrs. Hardware and software proved to run stable and safe. The MCM system has become a valuable tool for monitoring of comatose patients. The simultaneous display of trend graphs of various monitoring parameters and the online processing of histograms improved the survey of the patient's condition in the ICU. Recorded data were analysed offline and contribute to a consecutively increasing data bank.

Mannitol decreases ICP but does not improve brain-tissue pO2 in severely head-injured patients with intracranial hypertension.

Little is known about the effect of post-traumatic mannitol infusion on cerebral metabolism and oxygenation. The purpose of this study was to investigate the effects of mannitol in comatose patients on PtiO2, PtiCO2 and brain tissue pH using Clark-type electrodes implanted into cerebral white matter. In the neurosurgical intensive care unit PtiO2, PtiCO2, brain tissue pH, arterial blood pressure, intracranial pressure (ICP), cerebral perfusion pressure (CPP) and jugular bulb oxygen saturation (SjvO2) were prospectively studied in eleven patients with severe traumatic brain injury (TBI) during a total of 30 mannitol administrations (125 ml of 20% Mannitol infused over 30 min through a central vein). When the initial ICP before mannitol infusion was below 20 mmHg neither ICP nor any of the other parameters changed significantly during or after mannitol infusion. With a pre-infusion ICP above 20 mmHg a significant effect was seen on ICP (decrease from 23 +/- 1 to 16 +/- 2 mmHg at 60 min) and CPP (increase from 68 +/- 2 to 80 +/- 3 mmHg at 120 min). These effects were not reflected in PtiO2 or SjvO2, which were 29 +/- 4 mmHg and 61 +/- 3%, respectively, at the beginning of mannitol injection and remained unchanged during the observation period. PtiCO2 and brain tissue pH were not affected by mannitol infusion. Future studies should focus on the identification of ICP or CPP thresholds where infusion of mannitol may actually improve O2-supply to the brain.

Monitoring of cerebral oxygenation in patients with severe head injuries: brain tissue PO2 versus jugular vein oxygen saturation.

Monitoring of cerebral oxygenation is considered to be of great importance in minimizing secondary hypoxic and ischemic brain damage following severe head injury. Although the threshold for cerebral hypoxia in jugular bulb oximetry (measurement of O2 saturation in the jugular vein (SjvO2)) is generally accepted to be 50% oxygen saturation, a comparable value in brain tissue PO2 (PtiO2) monitoring, a new method for direct assessment of PO2 in the cerebral white matter, has not yet been established. Hence, the purpose of this study was to compare brain PtiO2 with SjvO2 in severely head injured patients during phases of reduced cerebral perfusion pressure (CPP) to define a threshold in brain PtiO2 monitoring. In addition, the safety and data quality of both SjvO2 and brain PtiO2 monitoring were studied. In 15 patients with severe head injuries, SjvO2 and brain PtiO2 were monitored simultaneously. For brain PtiO2 monitoring a polarographic microcatheter was inserted in the frontal cerebral white matter, whereas for SjvO2 measurements were obtained by using a fiberoptic catheter placed in the jugular bulb. Intracranial pressure was monitored by means of an intraparenchymal catheter. Mean arterial blood pressure, CPP, end-tidal CO2, and arterial oxygen saturation (pulse oximetry) were continuously recorded. All data were simultaneously stored and analyzed using a multimodal computer system. For specific analysis, phases of marked deterioration in systemic blood pressure and consecutive reductions in CPP were investigated. There were no complications that could be attributed to the PtiO2 catheters, that is, no intracranial bleeding or infection. The "time of good data quality" was 95% in brain PtiO2 compared to 43% in SjvO2; PtiO2 monitoring could be performed twice as long as SjvO2 monitoring. During marked decreases in CPP, SjvO2 and brain PtiO2 correlated closely. A significant second-order regression curve of SjvO2 versus brain PtiO2 (p < 0.01) was plotted. At a threshold of 50% in SjvO2, brain PtiO2 was found to be within the range of 3 to 12 mm Hg, with a regression curve "best fit" value of 8.5 mm Hg. There was a close correlation between CPP and oxygenation parameters (PtiO2 and SjvO2) when CPP fell below a breakpoint of 60 mm Hg, suggesting intact cerebral autoregulation in most patients. This study demonstrates that monitoring brain PtiO2 is a safe, reliable, and sensitive diagnostic method to follow cerebral oxygenation. In comparison to SjvO2, PtiO2 is more suitable for long-term monitoring. It can be used to minimize episodes of secondary cerebral maloxygenation after severe head injury and may, hopefully, improve the outcome in severely head injured patients.