Crystallization of Local Anesthetics When Mixed With Corticosteroid Solutions

OBJECTIVE: To evaluate at which pH level various local anesthetics precipitate, and to confirm which combination of corticosteroid and local anesthetic crystallizes. METHODS: Each of ropivacaine-HCl, bupivacaine-HCl, and lidocaine-HCl was mixed with 4 different concentrations of NaOH solutions. Also, each of the three local anesthetics was mixed with the same volume of 3 corticosteroid solutions (triamcinolone acetonide, dexamethasone sodium phosphate, and betamethasone sodium phosphate). Precipitation of the local anesthetics (or not) was observed, by the naked eye and by microscope. The pH of each solution and the size of the precipitated crystal were measured. RESULTS: Alkalinized with NaOH to a certain value of pH, local anesthetics precipitated (ropivacaine pH 6.9, bupivacaine pH 7.7, and lidocaine pH 12.9). Precipitation was observed as a cloudy appearance by the naked eye and as the aggregation of small particles (300 µm, pH 7.5). Ropivacaine with dexamethasone sodium phosphate also precipitated, but it was only observable by microscope (a few crystals of 10-100 µm, pH 7.0). Bupivacaine with betamethasone sodium phosphate formed precipitates of non-aggregated smaller particles (<10 µm, pH 7.7). Lidocaine mixed with corticosteroids did not precipitate. CONCLUSION: Ropivacaine and bupivacaine can precipitate by alkalinization at a physiological pH, and therefore also produce crystals at a physiological pH when they are mixed with betamethasone sodium phosphate. Thus, the potential risk should be noted for their use in interventions, such as epidural steroid injections.

Pathophysiology of degenerative spinal disease causing lumbar and cervical spinal pain

As degenerative spinal disease among spinal diseases causing lumbar and cervical spinal pain is the endless repetition of "the biological healing of mechanical damage" occurring over a lifetime, spinal pain by degenerative spinal disease occurs as a series of successive changes through the repetitive damage-healing process of various spinal structures including the intervertebral disc rather than a temporary phenomenon of any given pathophysiologic change in one moment. Degenerative spinal disease generally begins with degeneration of the intervertebral disc. Then herniation of the intervertebral disc resulting in subsequent radicular pain occurs when the nucleus pulposus with degeneration located in the intervertebral disc tears and penetrates the annulus fibrosus. Subsequently, disc space narrowing occurs and alters the spinal biomechanics, followed by degenerative changes to the vertebral endplate, vertebra itself, and facet joint. Finally, these changes lead to spinal stenosis, which is the final destination of degenerative spine disease. Although the exact pathogenesis of spinal pain could be still unclear because of some inconsistencies between the degenerative changes in the spine and the clinical manifestations of spinal pain, an accurate understanding of the pathophysiology and future predictions for further mechanical injury as well as thorough history taking and careful attention to the long-term clinical courses and other associated risk factors including daily life posture and work posture are needed for successful treatment of spinal pain.

Ascorbic acid insufficiency induces the severe defect on bone formation via the down-regulation of osteocalcin production / 대한해부학회지

The L-gulono-gamma-lactone oxidase gene (Gulo) encodes an essential enzyme in the synthesis of ascorbic acid from glucose. On the basis of previous findings of bone abnormalities in Gulo-/- mice under conditions of ascorbic acid insufficiency, we investigated the effect of ascorbic acid insufficiency on factors related to bone metabolism in Gulo-/- mice. Four groups of mice were raised for 4 weeks under differing conditions of ascorbic acid insufficiency, namely, wild type; ascorbic acid-sufficient Gulo-/- mice, 3-week ascorbic acid-insufficient Gulo-/- mice, and 4-week ascorbic acid-insufficient Gulo-/- mice. Four weeks of ascorbic acid insufficiency resulted in significant weight loss in Gulo-/- mice. Interestingly, average plasma osteocalcin levels were significantly decreased in Gulo-/- mice after 3 weeks of ascorbic acid insufficiency. In addition, the tibia weight in ascorbic acid-sufficient Gulo-/- mice was significantly higher than that in the other three groups. Moreover, significant decreases in trabecular bone volume near to the growth plate, as well as in trabecular bone attachment to the growth plate, were evident in 3- or 4-week ascorbic acid-insufficient Gulo-/-. In summary, ascorbic acid insufficiency in Gulo-/- mice results in severe defects in normal bone formation, which are closely related to a decrease in plasma osteocalcin levels.