Serum Biomarkers and Clinical Outcomes in Traumatic Spinal Cord Injury: Prospective Cohort Study.

BACKGROUND: A plethora of reactive cellular responses emerge immediately after a traumatic spinal cord injury (SCI) and may influence the patient's outcomes. We investigated whether serum concentrations of neuron-specific enolase, interleukin-6, glial-derived neurotrophic factor, and neurotrophic growth factor reflect the acute-phase responses to different etiologies of SCI and may serve as predictive biomarkers of neurologic and functional outcomes. METHODS: Fifty-two patients were admitted to the intensive care unit after SCI due to traffic accidents, falls, and firearm wounds and had blood samples collected within 48 hours and 7 days after SCI. Thirty-six healthy subjects with no history of SCI were included as controls. Neurologic and functional status was evaluated on the basis of American Spinal Injury Association and Functional Independence Measure scores over a period of 48 hours and 6 months after SCI. RESULTS: Serum NSE increased significantly 48 hours and 7 days after SCI compared with controls, while interleukin-6 increased only at 48 hours. In contrast, the neurotrophic growth factor level significantly decreased 48 hours and 7 days after SCI. Serum glial-derived neurotrophic factor level did not differ from control at any time point. Also, there was no significant difference in biomarker concentrations between the etiologies of SCI or the level of spinal injury. There were no correlations between biomarker levels at 48 hours with neurologic or functional outcomes 7 days and 6 months after SCI. CONCLUSIONS: Our results suggest expansive axonal damage coupled with an acute proinflammatory response after SCI. However, in our study biomarker concentration did not correlate with short- or long-term prognosis, such as survival rate or sensory and motor function.

Influence of FIO2 on PaCO2 during noninvasive ventilation in patients with COPD.

BACKGROUND: The administration of a high FIO2 to COPD patients breathing spontaneously may result in hypercapnia, due to reversal of preexisting regional hypoxic pulmonary vasoconstriction, resulting in a greater dead space. Arterial blood gas trends have not been reported in these patients. In a 31-bed medical ICU in a teaching hospital we prospectively investigated the response of 17 CO2-retaining COPD patients, after acute respiratory crisis stabilization with noninvasive ventilation, to an FIO2 of 1.0 for 40 min, after having been noninvasively ventilated with an FIO2 of ≤ 0.50 for 40 min. RESULTS: The mean ± SD baseline findings were: PaO2 101.4 ± 21.7 mm Hg, PaCO2 52.6 ± 10.4 mm Hg, breathing frequency 17.8 ± 3.7 breaths/min, tidal volume 601 ± 8 mL, and Glasgow coma score of 14.8 ± 0.3. PaO2 significantly increased (P < .001) when FIO2 was increased to 1.0, but there was no significant change in PaCO2, breathing frequency, tidal volume, or Glasgow coma score. CONCLUSIONS: During noninvasive ventilation with an FIO2 sufficient to maintain a normal PaO2, a further increase in FIO2 did not increase PaCO2 in our CO2-retaining COPD patients.