Major neurological events following foam sclerotherapy

Aim This report describes two complications of severe neurologic alterations (TIA, CVA) after foamed sclerotherapy injection. Methods Using foam sclerotherapy in accepted concentrations, volume, and in standard ratio of air to sclerosant, two serious neurologic complications occurred. Results In both cases described, unknown atrial communications existed resulting in foam emboli. One case involving the vertebral system resolved without treatment. The other involving the cerebral system was treated with hyperbaric oxygen. Conclusions Foam sclerotherapy can cause serious neurologic phenomenon even though the incidence is rarely described. Immediate treatment with 100% O2 and possible hyperbaric O2 therapy should be considered.

Oxygen transport to tissue by persistent bubbles: theory and simulations

Persistent gas bubbles able to traverse capillaries can be prepared from a slowly permeating gas or with a mechanical structure surrounding a gas phase. If they are permeable to gases, such bubbles will carry O2 from the lungs to the tissues via the blood stream. Using a mathematical model based on physical laws, we present simulations of the behavior of bubbles stabilized by a slowly permeating gas (gas X). We show that the bubble persists longer if the tissue and venous blood contain N2 to dilute gas X and slow its outward diffusion. A 6-microns -diam bubble carries 0.11 pl of O2 during the breathing of pure O2, so 4.6 x 10(8) bubbles/ml in the blood will supply a normal arteriovenous difference. In conditions used for hyperbaric O2 therapy, a bubble carries approximately 0.26 pl of O2. Stabilized bubbles have the potential to transport O2 efficiently; they release O2 to tissue at high PO2 and require injection of only small amounts of a foreign substance.

Attenuation of hypoxic ventilation by hyperbaric O2: effects of pressure and exposure time

Hyperoxia affects O2 chemoreception in the highly perfused carotid bodies and causes a reduction of the ventilatory hypoxic drive (HD) as was shown for anesthetized cats and awake rats. We looked for a quantitative description of such an effect on HD as a function of both O2 pressure and exposure duration. Ventilation of rats was measured using the barometric method before and after hyperbaric O2 (HBO) exposure, at either air, 80% O2, or 4% O2. We used three exposure durations: 180, 550 and 900 min. The O2 pressure ranged between 1.2 and 3.0 ATA. At each time duration we used four to five groups of rats at a range of O2 pressures that yielded the full scale of effect on HD but avoided obvious lasting difficulties in breathing. HBO caused a reduction of breathing frequency and elevation of tidal volume in both air and 80% O2 but almost no change in minute ventilation. Hypoxic minute ventilation (4% O2) decreased after HBO, mainly through reduced frequency. HD was described by a power function of O2 pressure for each HBO duration. HD did not decline below 20% of the full control response. Ventilatory HD diminution is pictured as a function of both O2 pressure and HBO duration. The dependency of HD on exposure time and on pressure is similar to other known toxic effects of HBO.

BCNU-induced protection from hyperbaric hyperoxia: role of glutathione metabolism

To explore the role of the glutathione oxidation-reduction cycle in altering the sensitivity of rats to the effects of hyperbaric hyperoxia, we administered N,N-bis(2-chloroethyl)-N-nitrosourea (BCNU) to decrease tissue glutathione reductase activity. We then exposed these animals and their matched vehicle-treated controls to 100% O2 at 4 ATA. Animals that received BCNU and were immediately exposed to hyperbaric O2 showed enhanced toxicity by seizing earlier in the exposure than controls. Animals that received BCNU 18 h before the hyperbaric O2 exposure were paradoxically protected from the effects of the exposure with a prolongation of their time to initial seizure and a marked increase in their survival time during the exposure. Tissue glutathione concentrations were also measured in the various groups and the hyperbaric O2 exposure produced marked decreases in hepatic glutathione levels in all control animals. In animals treated with BCNU 18 h before exposure, hepatic glutathione concentrations also decreased, but the concentrations had significantly increased during the 18-h waiting period, allowing these animals to maintain hepatic levels in the normal range even during their hyperbaric exposures. We conclude that treatment of rats with BCNU 18 h before exposure to hyperbaric hyperoxia results in enhanced protection of the animals during the exposure.