Inner-ear decompression sickness in nine trimix recreational divers.

INTRODUCTION: Recreational technical diving, including the use of helium-based mixes (trimix) and the experimentation of new decompression algorithms, has become increasingly popular. Inner-ear decompression sickness (DCS) can occur as an isolated clinical entity or as part of a multi-organ presentation in this population. Physiological characteristics of the inner ear make it selectively vulnerable to DCS. The inner ear has a slower gas washout than the brain thus potentially making it more vulnerable to deleterious effects of any bubbles that cross a persistent foramen ovale (PFO) and enter the basilar artery, whilst the inner ear remains supersaturated but the brain does not. METHODS: A questionnaire was made widely available to divers to analyse the incidence of inner-ear DCS after technical dives. One-hundred-and-twenty-six divers submitted completed questionnaires, and we studied each incident in detail. RESULTS: Nine (7.1%) of the 126 responders reported to have had at least one episode of inner-ear DCS, of which seven occurred without having omitted planned decompression stops. Of these seven, four suffered from DCS affecting just the inner ear, while three also had skin, joint and bladder involvement. Five of the nine divers affected were found to have a PFO. All affected divers suffered from vestibular symptoms, while two also reported cochlear symptoms. Three divers reported to have balance problems long after the accident. CONCLUSIONS: This small study is consistent with a high prevalence of PFO among divers suffering inner-ear DCS after trimix dives, and the pathophysiological characteristics of the inner ear could contribute to this pathology, as described previously. After an episode of DCS, vestibular and cochlear injury should always be examined for.

Skeletal muscle lactate overproduction during metformin intoxication: An animal study with reverse microdialysis.

Lactic acidosis during metformin intoxication is classically mainly attributed to diminished lactate clearance through liver gluconeogenesis. Here we studied 6 healthy, sedated and mechanically ventilated pigs to clarify whether high dose of metformin also increases skeletal muscle lactate production. Each animal had two microdialysis catheters inserted in gluteus muscles, one per side. One catheter was infused with saline (control) while the other one was infused with metformin diluted in saline (1M), both at a rate of 0.3µl/min. Dialysate lactate concentration and lactate-to-pyruvate ratio, a marker of the balance between anaerobic glycolysis and aerobic (mitochondrial) metabolism, were measured every 3h, for 12h. Continuous infusion of metformin caused a progressive rise in dialysate lactate level (p=0.007) and lactate-to-pyruvate ratio (p<0.001) compared to that of saline, as for mitochondrial "poisoning". These findings suggest that skeletal muscle lactate overproduction contributes to the development of metformin-induced lactic acidosis.