The authors describe a dedicated therapeutic vertebroplasty technique that uses newly designed instruments, acrylic cement, and dual guidance with ultrasonography and computed tomography for pain control in patients with bone failure, and report their experience. Between 1990 and 2002, they performed 868 percutaneous cementoplasty procedures in patients with severe osteoporosis, vertebral tumors, and symptomatic hemangiomas. In patients with osteoporosis, satisfactory results were obtained in 78% of cases; in patients with vertebral tumors, satisfactory results were obtained in 83% of cases; and in patients with hemangiomas, satisfactory results were obtained in 73% of cases. In the global series of 868 cementoplasties, an epidural leak was observed in 15 cases, which caused neuralgia in only three patients without spinal cord compression. In two patients, an asymptomatic pulmonary embolism was detected. The needle of the new vertebroplasty set is designed with side wings for easier rotation and removal. The screw syringe increases the precision of injection. The risk of leak is substantially reduced. The system is safe, reduces the cement manipulation time, and allows excellent control of the injection. The authors performed 130 vertebroplasties with this system without major complications.
Introduction The risk for decompression sickness (DCS) after hyperbaric exposures (such as SCUBA diving) has been linked to the presence and quantity of vascular gas emboli (VGE) after surfacing from the dive. These VGE can be semi-quantified by ultrasound Doppler and quantified via precordial echocardiography. However, for an identical dive, VGE monitoring of divers shows variations related to individual susceptibility, and, for a same diver, dive-to-dive variations which may be influenced by pre-dive pre-conditioning. These variations are not explained by currently used algorithms. In this paper, we present a new hypothesis: individual metabolic processes, through the oxygen window (OW) or Inherent Unsaturation of tissues, modulate the presence and volume of static metabolic bubbles (SMB) that in turn act as precursors of circulating VGE after a dive. Methods We derive a coherent system of assumptions to describe static gas bubbles, located on the vessel endothelium at hydrophobic sites, that would be activated during decompression and become the source of VGE. We first refer to the OW and show that it creates a local tissue unsaturation that can generate and stabilize static gas phases in the diver at the surface. We then use Non-extensive thermodynamics to derive an equilibrium equation that avoids any geometrical description. The final equation links the SMB volume directly to the metabolism. Results and Discussion Our model introduces a stable population of small gas pockets of an intermediate size between the nanobubbles nucleating on the active sites and the VGE detected in the venous blood. The resulting equation, when checked against our own previously published data and the relevant scientific literature, supports both individual variation and the induced differences observed in pre-conditioning experiments. It also explains the variability in VGE counts based on age, fitness, type and frequency of physical activities. Finally, it fits into the general scheme of the arterial bubble assumption for the description of the DCS risk. Conclusion Metabolism characterization of the pre-dive SMB population opens new possibilities for decompression algorithms by considering the diver’s individual susceptibility and recent history (life style, exercise) to predict the level of VGE during and after decompression.
Commercial saturation diving involves divers living and working in an enclosed atmosphere with elevated partial pressure of oxygen (ppO2) for weeks. The divers must acclimatize to these conditions during compression, and for up to 28 days until decompression is completed. During decompression, the ppO2 and ambient pressure are gradually decreased; then the divers must acclimatize again to breathing normal air in atmospheric pressure when they arrive at surface. We investigated 51 saturation divers’ subjective evaluation of the saturation and post-decompression phase via questionnaires and individual interviews. The questions were about decompression headaches and fatigue; and time before recovering to a pre-saturation state. Twenty-two (44%) of the divers who responded declared having headaches; near surface (44%) or after surfacing (56%). 71% reported post-saturation fatigue after their last saturation, 82% of them described it as typical and systematic after each saturation. Recovery was reported to normally take from 1 to 10 days. The fatigue and headaches observed are compatible with divers’ acclimatization to the changes in ppO2 levels during saturation and decompression. They appear to be reversible post- decompression.
Excessive fluid loss triggered by hyperbaric pressure, water immersion and hot water suits causes saturation divers to be at risk of dehydration. Dehydration is associated with reductions in mental and physical performance, resulting in less effective work and an increased risk of work-related accidents. In this study we examined the hydration status of 11 male divers over 19 days of a commercial saturation diving campaign to a working depth of 74 m, using two non-invasive methods: Bioelectrical impedance analysis (BIA) and urine specific gravity (USG). Measurements were made daily before and after bell runs, and the BIA data was used to calculated total body water (TBW). We found that BIA and USG were weakly negatively correlated, probably reflecting differences in what they measure. TBW was significantly increased after bell runs for all divers, but more so for bellmen than for in-water divers. There were no progressing changes in TBW over the 19-day study period, indicating that the divers’ routines were sufficient for maintaining their hydration levels on short and long term.
A series of dives was carried out to depths of 600 and 800 m seawater (msw) using baboons (Papio papio). Experiments were designed to study the effects of compression and the use of a He-N2-O2 gas mixture on high-pressure nervous syndrome (HPNS). When N2 was added to the He-O2 mixture at the beginning of a linear compression (200 msw/h), the symptoms associated with HPNS were still seen; in addition, the electroencephalogram (EEG) changes were more severe than those seen without N2. By use of an identical mixture, a 2-h exponential compression to 600 msw produced less severe signs of HPNS than the nonexponential profile. By use of a 2-h exponential compression to 600 msw and with addition of N2 at the end of compression, the HPNS that had been started under the He-O2 mixture decreased. Progressive addition of N2 during compression reduced the behavioral signs of HPNS without further EEG changes. These results show that the action of N2 is more complex than can be explained by a simple narcotic pressure antagonism and that the HPNS differed according to the gas mixture used.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.