Recovery and pharmacokinetic parameters of desflurane, sevoflurane, and isoflurane in patients undergoing urologic procedures.

STUDY OBJECTIVE: To compare the pharmacokinetics and the speed of recovery after inhalation anesthesia with desflurane, sevoflurane, and isoflurane in elective surgery. DESIGN: Prospective, randomized study. SETTING: University medical center. PATIENTS: 30 ASA physical status I and II adults presenting for elective surgery. INTERVENTIONS: Anesthesia was induced with etomidate and maintained with desflurane (n = 10), sevoflurane (n = 10), or isoflurane (n = 10) and nitrous oxide. The inhalation drugs were titrated until an adequate clinical depth of anesthesia was reached. At the end of anesthesia, the patients breathed oxygen via the endotracheal tube and after extubation via a face mask. MEASUREMENTS AND MAIN RESULTS: The groups were similar with respect to age, weight, duration of anesthesia, and mean arterial pressure. Mean end-tidal concentration (FA = FA0) at the end of anesthesia was 6.34 +/- 1.15% after desflurane, 1.85 +/- 0.42% after sevoflurane, and 1.10 +/- 0.24% after isoflurane. FA/FA0 decreased significantly faster with desflurane than with isoflurane, while there was little difference between desflurane and sevoflurane. As for the terminal half-life (t1/2), there were no differences among the groups (8.16 +/- 3.15 min after desflurane, 9.47 +/- 4.46 min after sevoflurane, and 10.0 +/- 5.57 min after isoflurane). The time until a command was followed for the first time was the same in all three groups (13.0 +/- 4.7 min after desflurane, 13.4 +/- 4.4 min after sevoflurane, and 13.6 +/- 3.4 min after isoflurane). There was no significant correlation between duration of anesthesia and the time until recovery. CONCLUSIONS: There are only minor differences with regard to the recovery phase in premedicated patients who receive clinically titrated inhalation anesthesia with desflurane, sevoflurane, or isoflurane.     

In vitro low-speed side collisions cause injury to the lower cervical spine but do not damage alar ligaments

Whether injuries to the alar ligaments could be responsible for complaints of patients having whiplash injury in the upper cervical spine is still controversially discussed. It is known that these ligaments protect the upper cervical spine against excessive lateral bending and axial rotation movements. The objective of the present in vitro study was therefore to examine whether the alar ligaments or any other structures of the cervical spine are damaged in side collisions. In a specially designed acceleration apparatus, six human osteoligamentous cervical spine specimens were subjected to incremental 90° side collisions from the right (1 g, 2 g, 3 g, etc.) until structural failure occurred. A damped pivot table accounted for the passive movements of the trunk during collision, and a dummy head (4.5 kg) ensured almost physiological loading of the specimens. For quantification of functional injuries, the three-dimensional flexibility of the specimens was tested in a spine tester before and after each acceleration. In all six specimens, structural failure always occurred in the lower cervical spine and always affected the facet joint capsules and the intervertebral discs. In four specimens, this damage occurred during the 2 g collision, while in the other two it occurred during the 3 g and 4 g collision, respectively. The flexibility mainly increased in the lower cervical spine (especially in lateral bending to both sides) and, to a minor extent, in axial rotation. In vitro low-speed side collisions caused functional and structural injury to discoligamentous structures of the lower cervical spine, but did not damage the alar ligaments. Since the effects of muscle forces were not taken into account, the present in vitro study reflects a worst-case scenario. Injury thresholds should therefore not be transferred to reality.     

Thoracolumbar fracture stabilization: comparative biomechanical evaluation of a new video-assisted implantable system

Minimally invasive techniques for spinal surgery are becoming more widespread as improved technologies are developed. Stabilization plays an important role in fracture treatment, but appropriate instrumentation systems for endoscopic circumstances are lacking. Therefore a new thoracoscopically implantable stabilization system for thoracolumbar fracture treatment was developed and its biomechanical in vitro properties were compared. In a biomechanical in vitro study, burst fracture stabilization was simulated and anterior short fixation devices were tested under load with pure moments to evaluate the biomechanical stabilizing characteristics of the new system in comparison with a currently available system. With interbody graft and fixation the new system demonstrated higher stabilizing effects in flexion/extension and lateral bending and restored axial stability beyond the intact spine, as well as having comparable or improved effects compared with the current system. Because of this biomechanical characterization a clinical trial is warranted; the usefulness of the new system has already been demonstrated in 45 patients in our department and more than 300 cases in a multicenter study which is currently under way.     

Lumbar interbody fusion: a parametric investigation of a novel cage design with and without posterior instrumentation

Introduction  

A finite element model of the L4-L5 human segment was employed to carry out a parametric biomechanical investigation of lumbar interbody fusion with a novel “sandwich” cage having an inner stiff core and two softer layers in the areas close to the endplates, with and without posterior fixation.     

Vasopressin-independent regulation of collecting duct aquaporin-2 in food deprivation

BACKGROUND: Humans and animals are frequently subjected to food deprivation or starvation. However, the adaptation of the kidney to this condition is not well understood. The purpose of these studies was to examine the effects of food deprivation on water handling by the kidney, the expression levels of collecting duct (CD) water channel aquaporin-2 (AQP2), and to determine the role of vasopressin in the adaptation of AQP2 to food deprivation. METHODS: Sprague-Dawley (SD) and Brattleboro rats were placed in metabolic cages and deprived of food but had free access to water for 72 hours. Water balance and urine osmolality were measured daily. Kidney tissues were isolated and examined for the expression of AQP2 using semiquantitative immunoblotting and Northern hybridization. The circulating level of vasopressin and the mRNA expression levels of its precursor were determined by radioimmunoassay and Northern hybridization, respectively. RESULTS: In SD rats, the first 24 hours of food deprivation is associated with a significant polyuria and decreased urine osmolality (Uosm). This correlated with a significant down-regulation of AQP2 in the cortex and outer medulla. After 72 hours of food deprivation, Uosm increased above baseline, and urine volume dropped to a lower value. This was associated with a rebound increase in AQP2 expression in the cortex and OM and its up-regulation in the inner medulla. Interestingly, vasopressin mRNA expression and plasma levels were unchanged during food deprivation. Further, in homozygous Brattleboro rats, in which endogenous vasopressin is absent, food deprivation caused changes in urine volume, urine osmolality, and AQP2 expression, which are qualitatively similar to those observed in normal rats. CONCLUSION: Food deprivation impairs water handling by the kidney by causing dual changes in urine volume and urine osmolality. This effect is associated with parallel alterations in the expression of AQP2 and is independent of vasopressin activity. It is concluded that the increase in water reabsorption in the CD is an adaptive response of the kidney to a long period of food deprivation and is mediated via a vasopressin-independent mechanism.     

Grading of degenerative disk disease and functional impairment: imaging versus patho-anatomical findings

Degenerative instability affecting the functional spinal unit is discussed as a cause of symptoms. The value of imaging signs for assessing the resulting functional impairment is still unclear. To determine the relationship between slight degrees of degeneration and function, we performed a biomechanical study with 18 multisegmental (L2-S2) human lumbar cadaveric specimens. The multidirectional spinal deformation was measured during the continuous application of pure moments of flexion/extension, bilateral bending and rotation in a spine tester. The three flexibility parameters neutral zone, range of motion and neutral zone ratio were evaluated. Different grading systems were used: (1) antero-posterior and lateral radiographs (degenerative disk disease) (2) oblique radiographs (facet joint degeneration) (3) macroscopic and (4) microscopic evaluation. The most reliable correlation was between the grading of microscopic findings and the flexibility parameters; the imaging evaluation was not as informative.     

Morphological changes of cervical facet joints in elderly individuals

To better understand the role of facet joint degeneration in chronic neck and back pain epidemiological and morphological data are needed. For the cervical spine, however, such data are rare. Therefore, the aim of this study was to determine the degree of cartilage degeneration of cervical facet joints with respect to spinal level and age, to investigate whether any region of the joint surface is more often affected by degeneration and to determine the localisation of osteophytes. A total of 128 left-sided facet surfaces from 15 fresh frozen cervical spine specimens (59-92 years) including in maximum C2-C7 were inspected in a way to ensure a direct comparability to data reported for the lumbar spine. First, the macroscopic degree of cartilage degeneration was determined and correlated to spinal level and age. Then, each facet surface was divided into five regions (anterior, posterior, lateral, medial and central) to check whether cartilage degeneration occurs more often in any of these regions. Finally, the localisation of osteophytes was determined. The results showed that the mean degree of cartilage degeneration was 2.8 (+/-0.6) on a scale from Grade 1 (no degeneration) to 4 (severe degeneration). None of all 128 facet surfaces was classified as Grade 1. All spinal levels had about the same degree of degeneration (in mean 2.5-3.0). The youngest age group (<70 years) had a somewhat lower degree of degeneration (2.6) than the oldest (> or = 90 years) (3.1). Cartilage defects were found all over the joint surfaces, none of the five regions was more often affected than the others. Least osteophytes were found on the medial border of the facet joints. In conclusion, the prevalence of cervical facet joint degeneration is probably very high in individuals aged 50 years and more, with a tendency to increase in severity with age. All levels of the middle and lower cervical spine were affected to almost the same degree, whereas in the lumbar spine an increase in degeneration towards the lower levels was reported. Also, in the cervical spine in most cases the cartilage was evenly degenerated all over the joint surface while in the lumbar spine certain regions were reported to be affected predominantly.     

The phenotype of early-onset retinal degeneration in persons with RDH12 mutations

PURPOSE: To describe the retinal dystrophy phenotype associated with mutations in RDH12, the gene encoding a retinoid dehydrogenase/reductase expressed in the photoreceptor cells. METHODS: Sixteen persons from 12 families with pathogenic RDH12 mutations on both alleles were studied. Retinal phenotypes were characterized by ophthalmic examination, including psychophysical and standardized electrophysiological methods and multifocal electroretinography (mfERG). RESULTS: The retinal disease in persons with RDH12 mutations in the homozygous (p.G127X, p.Q189X, p.Y226C, p.A269GfsX1, and p.L274P) or compound heterozygous state (p.R65X/p.A269GfsX1, p.H151D/p.T155I, p.H151D/p.A269GfsX1) was diagnosed initially as Leber congenital amaurosis (LCA) or early-onset retinitis pigmentosa. These individuals appeared to share a common clinical picture, independent of the type of mutation, characterized by poor, yet useful visual function in early life, followed by progressive decline due to both rod and cone degeneration. Marked pigmentary retinopathy, including bone spicules in the peripheral retina, was present in all persons older than age 6, and pronounced maculopathy was evident in persons older than 7 years. A unique view into the progressive nature of the disorder was achieved by evaluation of seven affected persons from three consanguineous families, all carrying the homozygous p.Y226C mutation. CONCLUSIONS: Ophthalmic findings in persons with RDH12 mutations suggest that RDH12 loss-of-function results in a characteristic form of early and progressive rod-cone degeneration distinct from that caused by mutations in other LCA genes. From our data, it seems likely that various clinical designations appropriately describe the diagnosis in these persons, including early-onset retinitis pigmentosa, LCA type II, and childhood retinal dystrophy.