Neuron-specific enolase and S100B protein levels in recreational scuba divers with neurological decompression sickness.

INTRODUCTION: Neuron-specific enolase (NSE) and S100B protein are brain-origin proteins commonly described to assess the presence and severity of neurological injury. To date, there are limited data examining the influence of scuba diving on these biomarkers, particularly when symptoms of decompression sickness (DCS) occur. The purpose of this controlled study was to determine whether these serum neurochemical markers could be used as 1) indicators of neurological DCS and 2) predictors of incomplete recovery. METHODS: Fifty-nine divers with neurological DCS and 37 asymptomatic divers admitted for inadequate decompression, serving as controls, were consecutively enrolled between 2010 and 2012. Blood samples were collected at initial presentation up to 6 hours after dive completion (controls) or onset of symptoms (DCS divers). Biomarkers were quantified in nonhaemolysed samples only. Clinical outcome was assessed at 6 months post-injury. RESULTS: The two groups did not differ regarding the variables examined, except for the total dive time which was slightly shorter in the control group. NSE, but not S100B protein, was higher in the DCS group than in controls (P < 0.0001). An NSE level > 15.9 µg L⁻¹ determined by ROC analysis predicted DCS development with a specificity of 100% (95% confidence interval (CI) 90 to 100) and a sensitivity of 24% (95% CI 14 to 36). There was a trend towards a higher likelihood of residual neurological deficits above this cut-off value (P = 0.08). CONCLUSIONS: Early determination of NSE was found to be useful for the diagnosis of neurological DCS with a high specificity. However, its clinical applicability in decision making for determining treatment as well as its prognostic value remains to be established. Reliability of S100B protein was not demonstrated in the present study.

Neurological decompression illness and hematocrit: analysis of a consecutive series of 200 recreational scuba divers.

Neurological complications are common in recreational divers diagnosed with decompression illness (DCI). Prior reports suggest that hemoconcentration, with hematocrit values of 48 or greater, increase the risk for more severe and persistent neurological deficits in divers with DCI. Herein we describe our experience with neurological DCI and hematocrit values in a large series of consecutively treated divers. We performed a retrospective chart review of 200 consecutive recreational divers that received treatment for DCI. Standard statistical analyses were performed to determine if there were any significant relationships between diving-related or demographic parameters, neurological manifestations, and hematocrit. In 177 of the 200 divers (88.5%), at least one manifestation of neurological DCI (mild, moderate, or severe) was present. The median hematocrit value was 43, for both male and female divers, with a range of 30 to 61. Hematocrit values did not correlate with diver age or level of diving experience. In male divers, the hematocrit did not correlate with neurological symptoms, including the sub-group with values of 48 or greater. In contrast, female divers with hematocrit values of 48 or greater were significantly more likely to develop motor weakness (p=0.002, Fisher's exact test) and an increased number of severe sensory symptoms (p=0.001, Kendall's tau statistic). Neurological complications are common in recreational divers treated for DCI. Hematocrit values of 48 or higher were correlated with the presence of motor weakness and severity of sensory symptoms in female divers. The hematocrit did not correlate with neurological DCI in male divers.

Complement activation during saturation diving.

In this study, the levels of activated complement fragments C3a and C5a were measured on 11 U.S. Navy divers as they performed a 28-day saturation dive to a pressure equivalent of 1,000 feet of seawater (fsw, 31.3 atm abs). Two subjects developed symptoms consistent with the high pressure nervous syndrome (HPNS) and three were treated for type I DCS (joint pain only). These events allowed us to test two hypotheses: a) alterations in C3a or C5a levels during compression are related to the occurrence of HPNS and b) increases in complement fragments are an indicator of decompression stress associated with type I DCS. There was no correlation between changes in C3a and C5a levels during compression and the diagnosis of HPNS. Our results suggest that an increase in C3a and C5a levels during saturation diving correlates with decompression stress and the clinical diagnosis of type I DCS.