Accidental calcium, magnesium, potassium and sodium oxybates (Xywave) overdose: mistiming of a single night's narcolepsy medication leading to respiratory failure requiring mechanical ventilation.

While typically thought of as an illicit substance, oxybate salts or gamma-hydroxybutyrate (GHB) has more recently been prescribed to treat narcolepsy by enhancing night-time sleep resulting in decreased daytime drowsiness. This case involves a college-aged female with prescribed GHB for narcolepsy who took her second nightly dose too early. This resulted in mental depression, respiratory failure, intubation and mechanical ventilation. The patient was successfully extubated in the intensive care unit several hours later with no residual morbidity. We were unable to identify any prior reports of mixed-salt oxybate toxicity following mistimed drug administration. This case should serve as a warning to emergency physicians to be on the lookout for GHB as part of the differential diagnosis for patients with narcolepsy presenting with altered mental status. It should also serve as a warning to patients and prescribers that this medication can have outcomes that require immediate medical intervention.

Accuracy of bedside point of care testing in critical emergency department patients.

BACKGROUND: Point-of-care (POC) testing reduces laboratory turn-around having the potential to improve timely diagnosis and management. We compared the accuracy of nurse performed POC and core laboratory testing and determined whether deviations between the two were clinically meaningful. METHODS: We performed a prospective, observational study on a convenience sample of 50 critical care ED patients in whom a POC chemistry and hematocrit was ordered. Blood samples were divided into 2 aliquots; one sample was tested by the treating nurse using a handheld POC device and the other sample was tested in the core laboratory. Paired comparisons of test results were performed using Pearson's correlation coefficients, Lin concordance coefficients, and Bland Altman plots. RESULTS: Mean patient age was 67, 50% were male, 82% were admitted. Pearson's correlation and Lin concordance coefficients were excellent (0.84-1.00) for all 8 analytes. Mean (95%CI) paired differences between POC and core laboratory measurements were Na+ 0.30 (-0.22 to 0.82) mmol/L, K+-0.12 (-0.14 to - 0.09) mmol/L, Cl- 2.10 (1.41 to 2.78) mmol/L, TCO2-1.68 (-2.06 to -1.30) mmol/L, glucose 2.46 (1.46 to 3.46) mg/dL, BUN, 1.69 (0.95 to 2.42) mg/dL, creatinine 0.13 (0.08 to 0.17) mg/dL, and hematocrit -0.39 (-0.93 to 0.15) %. In 3 of 400 measurements, the difference between POC and core lab exceeded the maximal clinically acceptable deviation based on physician surveys. CONCLUSIONS: Bedside POC by ED nurses is reliable and accurate and does not deviate significantly from core laboratory testing by trained technicians.

Compressive preload reduces segmental flexion instability after progressive destabilization of the lumbar spine.

STUDY DESIGN: Biomechanical human cadaveric study. OBJECTIVE: We hypothesized that increasing compressive preload will reduce the segmental instability after nucleotomy, posterior ligament resection, and decompressive surgery. SUMMARY OF BACKGROUND DATA: The human spine experiences significant compressive preloads in vivo due to spinal musculature and gravity. Although the effect of destabilization procedures on spinal motion has been studied, the effect of compressive preload on the motion response of destabilized, multisegment lumbar spines has not been reported. METHODS: Eight human cadaveric spines (L1-sacrum, 51.4 ± 14.1 yr) were tested intact, after L4-L5 nucleotomy, after interspinous and supraspinous ligaments transection, and after midline decompression (bilateral laminotomy, partial medial facetectomy, and foraminotomy). Specimens were loaded in flexion (8 Nm) and extension (6 Nm) under 0-N, 200-N, and 400-N compressive follower preload. L4-L5 range of motion (ROM) and flexion stiffness in the high-flexibility zone were analyzed using repeated-measures analysis of variance and multiple comparisons with the Bonferroni correction. RESULTS: With a fixed set of loading conditions, a progressive increase in segmental ROM along with expansion of the high-flexibility zone (decrease of flexion stiffness) was noted with serial destabilizations. Application of increasing compressive preload did not substantially change segmental ROM, but did significantly increase the segmental stiffness in the high-flexibility zone. In the most destabilized condition, 400-N preload did not return the segmental stiffness to intact levels. CONCLUSION: Anatomical alterations representing degenerative and iatrogenic instabilities are associated with significant increases in segmental ROM and decreased segmental stiffness. Although application of compressive preload, mimicking the effect of increased axial muscular activity, significantly increased the segmental stiffness, it was not restored to intact levels; thereby suggesting that core strengthening alone may not compensate for the loss of structural stability associated with midline surgical decompression. This suggests that there may be a role for surgical implants or interventions that specifically increase flexion stiffness and limit flexion ROM to counteract the iatrogenic instability resulting from surgical decompression. LEVEL OF EVIDENCE: N/A.