Risks/Outcomes/PredictorsRisk factors and treatment outcome in scuba divers with spinal cord decompression sickness
Introduction
Decompression sickness (DCS) encountered by divers results from the formation of intravascular and extravascular inert gas bubbles previously dissolved within tissues after inadequate decompression from hyperbaric exposure. Neurological injuries are predominant in DCS, and spinal cord is the most commonly affected site. The clinical features of spinal involvement are numerous, and neurological symptoms may vary considerably from minimal subjective sensory abnormalities to complete paraplegia with bladder dysfunction that could result in permanent disability. The pathophysiological mechanisms of spinal cord lesions include several hypotheses, that is, arterial, venous, and autochthonous bubble theories, but extravascular bubble growth in spinal white matter and venous cord infarction resulting from bubble embolization of epidural vertebral venous system causing obstruction of venous drainage and subsequent coagulation activation and platelet aggregation are probably the main explanation for the pathogenesis of this myelopathy [1].
By reducing bubble volume and by hastening inert gas elimination, recompression therapy with hyperbaric oxygen (HBO) remains the mainstays of modern treatment of DCS. On the basis of historical experience, recompression to 2.8 atmosphere absolute (ATA) using 100% oxygen (eg, US Navy table 5 or 6) is the most commonly procedure with a high rate of efficiency and a low incidence of side effects [2], [3], [4]. However, published human outcome data comparing these so-called short oxygen tables with other treatment tables using deeper recompression to 4 to 6 ATA with nitrogen-oxygen or helium-oxygen mixtures are limited and conflicting [5], [6], [7], raising some questions regarding the optimal recompression strategy.
Numerous studies have been conducted in the past with the aim on identifying possible determinants of outcome in neurological DCS [8], [9], [10], [11], particularly the clinical presentation before treatment [12], [13], the symptom latency after surfacing [14], [15], [16], [17], and the delay between the onset of symptoms and recompression treatment [11], [16], [18], [19], [20], [21], [22], [23], [24]. However, identification of preponderant factors that could prevent divers from developing severe neurological DCS is still elusive.
From the previously mentioned considerations, the purpose of this study was to investigate the influence of potential risk factors associated with a poor outcome in spinal cord DCS. We also sought the real prognostic value of a simple clinically based scoring system previously developed by Boussuges and coworkers [25].
Section snippets
Study design
From June 2002 to October 2007, we retrospectively reviewed the clinical and diving data on 63 consecutive air divers referred to our hyperbaric center with symptoms indicative of spinal cord DCS.
Clinical diagnosis of spinal cord injury was made when the criteria of bilateral sensory or/and motor deficit were recognized after the diver surfaced. If the need arises, other characteristic signs consistent with involvement of spinal cord in DCS such as acute back pain or bladder dysfunction were
Results
There were 52 (82%) men and 11 (18%) women with a mean (±SD) age of 46 (±12) years who were retained for analysis. Forty-eight (76%) were experienced amateur or diving instructors. Diving profiles were as follows: mean (±SD) maximum depth of 40 (±13) meters of seawater and mean (±SD) dive time of 30 (±12) minutes. Five patients (8%) performed a provocative decompression profile (ie, fast ascent or omitted decompression stops according to their dive computers), and repetitive dive was only
Discussion
The prevalence of injured divers with incomplete recovery after spinal cord DCS is reported between 22% [17] and 61% [21] in the recent literature, supporting our results despite the differences in diving population, treatment procedures, and delay in time to hyperbaric recompression.
The main finding of this study is that initial clinical presentation depicted by the severity score of Boussuges in neurological DCS provides major prognostic information about the clinical outcome and the severity
Acknowledgments
The authors wish to thank the team of the hyperbaric center Sainte Anne for their participation to this study (special appreciation to J.M. Pontier, P. Constantin, and P. Louge).
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The opinions and assertions contained herein are the private's ones of the authors and are not to be construed as the official or as reflecting the views of the French Navy.