Intracranial pressure waveform analysis: clinical and research implications.

Assessment of intracranial adaptive capacity is vital in critically ill individuals with acute brain injury because there is the potential that nursing care activities and environmental stimuli to result in clinically significant increases in intracranial pressure (ICP) in a subset of individuals with decreased intracranial adaptive capacity. ICP waveform analysis provides information about intracranial dynamics that can help identify individuals who have decreased adaptive capacity and are at risk for increases in ICP and decreases in cerebral perfusion pressure, which may contribute to secondary brain injury and have a negative impact on neurologic outcome. The ability to identify high-risk individuals allows nurses to initiate interventions targeted at decreasing adaptive demand or increasing adaptive capacity in these individuals. Changes in the ICP waveform occur under various physiologic and pathophysiologic conditions and may provide valuable information about intracranial adaptive capacity. Simple visual assessment of the ICP waveform for increased amplitude and P2 elevation is clinically relevant and has been found to provide a rough indicator of decreased adaptive capacity. Advanced ICP waveform analysis techniques warrant further study as a means of dynamically assessing intracranial adaptive capacity.

Accuracy of continuous jugular bulb oximetry in the intensive care unit.

OBJECTIVE: To address the accuracy of a bedside jugular bulb oxygen saturation (SjO2) catheter monitor (Baxter-Edwards, Santa Ana, CA) versus in vitro co-oximetry measurements in the intensive care unit (ICU). METHODS: By prospective protocol, we compared blood gas measurements with simultaneously recorded continuous bedside oximetric monitor values for 31 ICU patients with traumatic brain injury undergoing jugular bulb catheter monitoring. For suboptimal fiberoptic light signal quality indices, the catheter was repositioned, flushed, or both before drawing the sample for in vitro measurement. Laboratory and bedside monitor data were examined for association using the chi2 and paired t tests and a linear regression model. RESULTS: We assessed 195 samples (median, 5 per patient; range, 1-14) who were monitored an average of 3.4 (range, 1-6) days. The in vivo monitor (range, 32-94%) and in vitro co-oximetry (range, 38-93%) values had acceptable correlation (y = 0.94x + 4.4, r2 = 0.80). For bedside monitor detection of jugular bulb desaturation (SjO2 < 50% for 10 min), the kappa statistic was 0.35, the sensitivity was 45 to 50%, and the specificity was 98 to 100%. CONCLUSION: Continuous ICU SjO2 monitoring correlates significantly with in vitro values, but less so than previously described during intracranial surgery. Although sensitivity of the bedside monitor to detect confirmed desaturations remains an issue, the high specificity indicates that it is less of a concern that patients may be misdiagnosed as having desaturations resulting in unnecessary interventions. Nonetheless, suspected jugular bulb desaturation should be verified before taking therapeutic actions.

Thrombotic, infectious, and procedural complications of the jugular bulb catheter in the intensive care unit.

OBJECTIVE: An assessment of the thrombotic, infectious, and technical complications of continuous jugular bulb catheter monitoring in the intensive care unit (ICU) was made. METHODS: Over a 1-year period, 44 patients suffering from traumatic brain injury, subarachnoid hemorrhage, or stroke received jugular bulb catheter monitoring in the ICU. They were followed for catheter insertion complications and the development of bacteremia. In 20 patients chosen randomly, an ultrasonographic evaluation was performed after removal of the catheter for an assessment of internal jugular vein thrombosis. RESULTS: Of the 44 patients, 1 became bacteremic; the source was identified as a thoracostomy site. Among the complications related to the 44 catheter insertions, there were 2 instances of carotid artery puncture (4.5%), 1 misplaced catheter (thoracic placement), and 1 clinically insignificant hematoma. Of the 20 patients investigated with ultrasonography, 8 (40%) had nonobstructive, subclinical internal jugular vein thrombi after jugular bulb catheter monitoring (95% confidence interval, 19-61%). The median monitoring duration was 3 days (range, 1-6 d). No clinical factor was identified to be associated with thrombus formation. CONCLUSION: We conclude the following: 1) the risk of bacteremia related to the jugular bulb catheter was negligible; 2) complications related to catheter insertion were rare and clinically insignificant; and 3) the incidence of subclinical internal jugular vein thrombosis after jugular bulb catheter monitoring is considerable. Although it is worthy to note this complication, no patient with a thrombus became symptomatic in the present series. The risk-benefit assessment of this monitoring technique must include consideration of subclinical thrombosis.