Chain of events analysis in diving accidents treated by the Royal Netherlands Navy 1966-2023.

Introduction: Diving injuries are influenced by a multitude of factors. Literature analysing the full chain of events in diving accidents influencing the occurrence of diving injuries is limited. A previously published 'chain of events analysis' (CEA) framework consists of five steps that may sequentially lead to a diving fatality. This study applied four of these steps to predominately non-lethal diving injuries and aims to determine the causes of diving injuries sustained by divers treated by the Diving Medical Centre of the Royal Netherlands Navy. Methods: This retrospective cohort study was performed on diving injuries treated by the Diving Medical Centre between 1966 and 2023. Baseline characteristics and information pertinent to all four steps of the reduced CEA model were extracted and recorded in a database. Results: A total of 288 cases met the inclusion criteria. In 111 cases, all four steps of the CEA model could be applied. Predisposing factors were identified in 261 (90%) cases, triggers in 142 (49%), disabling agents in 195 (68%), and 228 (79%) contained a (possible-) disabling condition. The sustained diving injury led to a fatality in seven cases (2%). The most frequent predisposing factor was health conditions (58%). Exertion (19%), primary diver errors (18%), and faulty equipment (17%) were the most frequently identified triggers. The ascent was the most frequent disabling agent (52%). Conclusions: The CEA framework was found to be a valuable tool in this analysis. Health factors present before diving were identified as the most frequent predisposing factors. Arterial gas emboli were the most lethal injury mechanism.

Modern assessment of pulmonary function in divers cannot rely on old reference values.

INTRODUCTION: Pulmonary function testing (PFT) is an important part of dive medical examinations. Depending on the standard used to assess fitness to dive, different reference sets and fixed cut-off points are used. Reference values are part of an ongoing debate regarding the validity and accuracy related to different age groups, sex and ethnic backgrounds. The Global Lung Initiative (GLI) has provided an all-age reference set which corrects for sex and ethnicity (GLI-2012); this has had substantial impact on pulmonary medicine. METHOD: We present an algorithm that can be used to standardise analysis of PFT in divers using the GLI-2012 reference set. Differences in the analysis of PFT between the ECSC/ERS-1993 and the GLI-2012 reference values are illustrated by means of three case reports. CONCLUSION: Using a valid database of reference values increases accuracy and might prevent additional medical investigations and/or incorrect assessment of fitness to dive. Although our algorithm needs further evaluation to ensure its validity, the preliminary results are promising. Whatever algorithm is used, we urge dive medical physicians to consider using valid reference sets when analysing PFT for assessment of fitness to dive.

Toll-like receptors in human chondrocytes and osteoarthritic cartilage.

BACKGROUND AND PURPOSE: Degenerating cartilage releases potential danger signals that react with Toll-like receptor (TLR) type danger receptors. We investigated the presence and regulation of TLR1, TLR2, and TLR9 in human chondrocytes. METHODS: We studied TLR1, TLR2, TLR4, and TLR9 mRNA (qRT-PCR) and receptor proteins (by immunostaining) in primary mature healthy chondrocytes, developing chondrocytes, and degenerated chondrocytes in osteoarthritis (OA) tissue sections of different OARSI grades. Effects of a danger signal and of a pro-inflammatory cytokine on TLRs were also studied. RESULTS: In primary 2D-chondrocytes, TLR1 and TLR2 were strongly expressed. Stimulation of 2D and 3D chondrocytes with a TLR1/2-specific danger signal increased expression of TLR1 mRNA 1.3- to 1.8-fold, TLR2 mRNA 2.6- to 2.8-fold, and TNF-α mRNA 4.5- to 9-fold. On the other hand, TNF-α increased TLR1 mRNA] expression 16-fold, TLR2 mRNA expression 143- to 201-fold, and TNF-α mRNA expression 131- to 265-fold. TLR4 and TLR9 mRNA expression was not upregulated. There was a correlation between worsening of OA and increased TLR immunostaining in the superficial and middle cartilage zones, while chondrocytes assumed a CD166(×) progenitor phenotype. Correspondingly, TLR expression was high soon after differentiation of mesenchymal stem cells to chondrocytes. With maturation, it declined (TLR2, TLR9). INTERPRETATION: Mature chondrocytes express TLR1 and TLR2 and may react to cartilage matrix/chondrocyte-derived danger signals or degradation products. This leads to synthesis of pro-inflammatory cytokines, which stimulate further TLR and cytokine expression, establishing a vicious circle. This suggests that OA can act as an autoinflammatory disease and links the old mechanical wear-and-tear concept with modern biochemical views of OA. These findings suggest that the chondrocyte itself is the earliest and most important inflammatory cell in OA.