Skin Lesions in Swine with Decompression Sickness: Clinical Appearance and Pathogenesis

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Endothelial dysfunction has been considered as pivotal in the pathogenesis of decompression sickness (DCS) and contributes substantively to subsequent inflammatory responses. Escin is well known for its endothelial protection and anti-inflammatory properties, and its protection against DCS has been proved in a rat model. This study aimed to further investigate the protection of escin against DCS in swine. Sixteen swine were subjected to a two-stage experiment with an interval of 7 days. In each stage, 7 days before a simulated air dive, the swine were treated with escin or saline. The first group received a successive administration of escin for 7 days prior to the first dive and saline for 7 days prior to the second; the second group was treated with saline and then escin. After decompression, signs of DCS and circulating bubbles were monitored, and blood was sampled for platelet count and determination of inflammatory and endothelial related indices. The death rate of DCS was markedly decreased in swine treated with escin compared with that in animals treated with saline, though not statistically significant due to the limited number of animals. Escin had no effect on bubble load but significantly ameliorated platelet reduction and endothelial dysfunction, as well as oxidative and inflammatory responses. The results further suggest the beneficial effects of escin on DCS by its endothelia-protective properties, and escin has the potential to be a candidate drug for DCS prevention and treatment.

Section: Methodsmentioning

confidence: 99%

“…Skin lesions were thoroughly examined after surfacing following the rules developed in our previous study (Qing et al, 2017). Briefly, the latency was recorded, and the dimensions of stage III lesions were measured by the palm of a single experimenter.…”

Section: Methodsmentioning

confidence: 99%

Benefits of Escin for Decompression Sickness in Bama Pigs by Endothelial-Targeting Protection

Qing¹,

Meng²,

Zhang³

et al. 2019

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“…Moreover, a recent study from Qing et al, investigated skin lesions in swine with DCS. The authors suggest that skin lesions may result from local occlusion of dermis capillaries with gas bubbles and not from central nervous system (CNS) injuries or arterial bubbles, although arterial bubbles could not be excluded as a cause (Qing et al, 2017). It should be noted that in this study the pigs were decompressed so fast that DCS due to supersaturation was triggered.…”

Section: Theory Of Brain Stem Strokementioning

confidence: 79%

Livedo Racemosa – The Pathophysiology of Decompression-Associated Cutis Marmorata and Right/Left Shunt

Härtig¹,

Reider²,

Sojer³

et al. 2020

Decompression sickness and arterial gas embolism, collectively known as decompression illness (DCI), are serious medical conditions that can result from compressed gas diving. DCI can present with a wide range of physiologic and neurologic symptoms. In diving medicine, skin manifestations are usually described in general as cutis marmorata (CM). Mainly in the Anglo-American literature the terms cutis marmorata, livedo reticularis (LR), and livedo racemosa (LRC) are used interchangeably but actually describe pathophysiologically different phenomena. CM is a synonym for LR, which is a physiological and benign, livid circular discoloration with a netlike, symmetric, reversible, and uniform pattern. The decompression-associated skin discolorations, however, correspond to the pathological, irregular, broken netlike pattern of LRC. Unlike in diving medicine, in clinical medicine/dermatology the pathology of livedo racemosa is well described as a thrombotic/embolic occlusion of arteries. This concept of arterial occlusion suggests that the decompression-associated livedo racemosa may be also caused by arterial gas embolism. Recent studies have shown a high correlation of cardiac right/left (R/L) shunts with arterial gas embolism and skin bends in divers with unexplained DCI. To further investigate this hypothesis, a retrospective analysis was undertaken in a population of Austrian, Swiss, and German divers. The R/L shunt screening results of 18 divers who suffered from an unexplained decompression illness (DCI) and presented with livedo racemosa were retrospectively analyzed. All of the divers were diagnosed with a R/L shunt, 83% with a cardiac shunt [patent foramen ovale (PFO)/atrium septum defect (ASD)], and 17% with a non-cardiac shunt. We therefore not only confirm this hypothesis but when using appropriate echocardiographic techniques even found a 100% match between skin lesions and R/L shunt. In conclusion, in diving medicine the term cutis marmorata/livedo reticularis is used incorrectly for describing the actual pathology of livedo racemosa. Moreover, this pathology could be a good explanation for the high correlation of livedo racemosa with cardiac and non-cardiac right/left shunts in divers without omission of decompression procedures.

“…Autochthonous or circulating bubbles formed after rapid decompression play an important role in the progress of DCS (Qing et al, 2017;Zhang et al, 2017). The bubbles can not only cause mechanical damages and blockage, but also act as foreign bodies that trigger a cascade of inflammatory responses (Levett and Millar, 2008).…”

Section: Discussionmentioning

confidence: 99%

Ulinastatin: A Potential Alternative to Glucocorticoid in the Treatment of Severe Decompression Sickness

Meng¹,

Qing²,

et al. 2020

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Inflammatory reaction is the crux in various clinical critical diseases including decompression sickness (DCS). Ulinastatin (UTI), a potent anti-inflammatory agent, has been used clinically, including as a substitution for steroids. This study aimed to explore the potential effects of UTI upon DCS in a rabbit model. Eighty-eight rabbits were subjected to simulated diving to 6 atmospheres absolute (ATA) for 60 min with 2.5minute decompression. Three doses of UTI (15/7.5/3.75 × 10 5 U/kg) or saline were intravenously administered immediately following decompression. Circulating bubbles were monitored for 3 h following decompression and DCS signs were evaluated for 24 h. Blood was sampled 8 times during 72 h after decompression for inflammatory, endothelial, oxidative and routine blood indices. Lung tissues were also sampled for evaluating endothelial function. Another six rabbits were used as Normal controls. In the high dose UTI group the mortality, general morbidity and incidence of severe DCS was decreased from 31.25 to 9.38% (P = 0.030), 84.38 to 62.50% (P = 0.048) and 46.88 to 21.88% (P = 0.035), respectively. The high dose of UTI significantly postponed the occurrence of DCS (P = 0.030) and prolonged survival time (P = 0.009) compared with the Saline group, and significantly ameliorated inflammation responses, endothelial injuries and oxidative damage. The results strongly suggest the benefit of UTI on DCS, especially for severe cases. Large doses are needed to achieve significant effects. UTI may be a potential ideal pharmacological candidate for the treatment of severe DCS.