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Introduction: Decompression sickness (DCS) has traditionally been categorized as type I DCS, affecting joints and skin, and type II affecting the nervous system. In the present study, we wanted to examine whether divers with a history of neurological DCS demonstrated a pattern of symptoms and clinical neurological and neurophysiological signs different from divers with other manifestations of DCS or no history of DCS., Methods: Up to 1990, 365 Norwegian offshore divers worked in the North Sea. Two hundred and eight divers who had performed saturation diving, bounce diving or both, were included in this study. They filled in a questionnaire for registration of diving experience and health complaints, and episodes of DCS were registered. All participants had a clinical neurological and neurophysiological examination (ERP- P300)., Results: One hundred and sixty three of the 208 divers (78.4%) reported episodes of DCS. Neurological DCS was reported by 41 (19.7%) divers. Forty-five divers (21.6%) reported no episodes of DCS. Divers who reported episodes of DCS reported significantly more symptoms compared with divers who reported no DCS. Divers who reported neurological DCS had significantly more neurological findings on motility tests, sensory tests and coordination/cerebellar tests. The P300 motor reaction times were significantly longer in divers reporting DCS, but there was no significant difference between divers with neurological DCS and divers with other forms of DCS., Conclusions: This study indicates that DCS is associated with long-term effects on the nervous system independent of the symptomatology in the acute stage., (Copyright © 2022 Elsevier B.V. All rights reserved.)

Background: Capillary leak syndrome is a rare type of decompression sickness (DCS) that may be responsible for hypovolemic shock with edema., Clinical Case: A 21-year-old amateur diver suffered from an inner ear DCS following air diving to 96msw. He presented subsequent deterioration with hypovolemia and facial edema secondary to capillary leak syndrome., Discussion: In DCS, bubbles formation alters the wall of blood vessels and activates complex biochemical mechanisms inducing extravascular protein leakage. The clinical expression of this syndrome is variable, ranging from simple hemoconcentration to hypovolemic shock. Close clinical-biological monitoring of patients with elevated hematocrit with or without hypoalbuminemia is advisable. Early vascular filling with albumin infusion may prevent the occurrence of hypovolemic shock and improve the prognosis., (Copyright © 2018 Société Nationale Française de Médecine Interne (SNFMI). Published by Elsevier Masson SAS. All rights reserved.)

Patent foramen ovale (PFO) is associated with an increased risk of decompression sickness (DCS) in divers that results from a paradoxical embolization of nitrogen bubbles. The number of scuba divers worldwide is estimated in the millions, and the prevalence of PFO is 25%-30% in adults. It is interesting that despite these numbers, many important issues regarding optimal screening, risk stratification, and management strategy still remain to be resolved. Recently published data suggest the possible effectiveness of both PFO closure and conservative diving measures in preventing arterial gas embolization. This review aims to introduce the basic principles of physiology and the pathophysiology of bubble formation and DCS, summarize the current literature on PFO and diving, and review the possibilities of diagnostic workup and management., (Copyright © 2015 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.)

Diving exposes a person to the combined effects of increased ambient pressure and immersion. The reduction in pressure when surfacing can precipitate decompression sickness (DCS), caused by bubble formation within tissues due to inert gas supersaturation. Arterial gas embolism (AGE) can also occur due to pulmonary barotrauma as a result of breath holding during ascent or gas trapping due to disease, causing lung hyperexpansion, rupture and direct entry of alveolar gas into the blood. Bubble disease due to either DCS or AGE is collectively known as decompression illness. Tissue and intravascular bubbles can induce a cascade of events resulting in CNS injury. Manifestations of decompression illness can vary in severity, from mild (paresthesias, joint pains, fatigue) to severe (vertigo, hearing loss, paraplegia, quadriplegia). Particularly as these conditions are uncommon, early recognition is essential to provide appropriate management, consisting of first aid oxygen, targeted fluid resuscitation and hyperbaric oxygen, which is the definitive treatment. Less common neurologic conditions that do not require hyperbaric oxygen include rupture of a labyrinthine window due to inadequate equalization of middle ear pressure during descent, which can precipitate vertigo and hearing loss. Sinus and middle ear overpressurization during ascent can compress the trigeminal and facial nerves respectively, causing temporary facial hypesthesia and lower motor neuron facial weakness. Some conditions preclude safe diving, such as seizure disorders, since a convulsion underwater is likely to be fatal. Preventive measures to reduce neurologic complications of diving include exclusion of individuals with specific medical conditions and safe diving procedures, particularly related to descent and ascent., (© 2014 Elsevier B.V. All rights reserved.)

Background: Post-decompression shock with plasma volume deficit is a very rare event that has been observed under extreme conditions of hypobaric and hyperbaric exposure in aviators and professional divers., Case Report: We report a case of severe hypovolemic shock due to extravasation of plasma in a recreational scuba diver presenting with inner ear decompression sickness. Impaired endothelial function can lead to capillary leak with hemoconcentration and hypotension in severe cases. This report suggests that decompression-induced circulating bubbles may have triggered the endothelial damage, activating the classic inflammatory pathway of increased vascular permeability., Conclusion: This observation highlights the need for an accurate diagnosis of this potentially life-threatening condition at the initial presentation in the Emergency Department after a diving-related injury. An elevated hematocrit in a diver should raise the suspicion for the potential development of capillary leak syndrome requiring specific treatment using albumin infusion as primary fluid replacement., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Deep diving is defined as diving to depths more than 50 m of seawater (msw), and is mainly used for occupational and military purposes. A deep dive is characterized by the compression phase, the bottom time and the decompression phase. Neurological and neurophysiologic effects are demonstrated in divers during the compression phase and the bottom time. Immediate and transient neurological effects after deep dives have been shown in some divers. However, the results from the epidemiological studies regarding long term neurological effects from deep diving are conflicting and still not conclusive. Prospective clinical studies with sufficient power and sensitivity are needed to solve this very important issue., (Copyright © 2010 Elsevier B.V. All rights reserved.)

Introduction: Dysbaric osteonecrosis is a rare illness in professional divers and compressed-air workers. The correlation between dysbaric osteonecrosis and previous decompression sickness with osteoarthromuscular pain (type 1 decompression sickness) remains a controversial subject. The probability for ischemic lesions detected with MRI to turn into osteonecrosis after decompression sickness is still not established., Exegesis: The authors report the case of a military diver declared definitely medically unfit to dive after the occurrence of advanced dysbaric osteonecrosis of the shoulder, eight months after decompression sickness treated with hyperbaric oxygen, in the same area. A close link between those two events and the requirement for monitoring the follow-up of acute type 1 decompression sickness are discussed., Conclusion: Every decompression sickness with osteoarthromuscular pain should be early examined with MRI in order to screen osteomedullar damages liable to worse with diving and change subsequently in bone necrosis.

A 42-year-old patient was admitted to our ICU for severe decompression illness with tetraplegia. He presented an acute respiratory distress syndrome (ARDS), following a very long hyperbaric oxygen therapy (using a US. Navy Treatment Table 7). The ARDS resulted in pulmonary fibrosis, and the patient died despite maximal support in ICU. The risk of pulmonary toxicity of oxygen must be considered when using a prolonged recompression treatment table.

Patient salvage rates depend on the extent of injury, speed and appropriateness of treatment, and the patient's age and state of health in addition to other variables. Undertreatment of DII may result in significant morbidity and associated costs. If there is any doubt regarding whether a patient might benefit from treatment, a trial at pressure is indicated. Among those with AGE who reach recompression within 5 minutes, the death rate may be only 5%, and those who survive have little morbidity. Among those whose recompression delay increases to 5 hours, however, mortality approaches 10%, and more than 50% of the survivors experience residua. All dive accidents should be thoroughly investigated by professionals. Sport divers who manifest any symptoms of DII should refrain from further diving because response to therapy for future episodes is generally relatively poor. Victims of DII must have long-term follow-up.

We have evaluated the contribution of extravascular gas bubbles to spinal cord injury in decompression sickness. For this purpose, a model of decompression sickness was developed by subjecting rats to simulated dives using compressed air. Various diving profiles were tested and the presence of spinal cord injury was demonstrated by electrophysiologic measurements. To evaluate the space occupying lesions induced by gas bubbles in the white matter, the spinal cord was fixed by perfusion with 10% buffered formalin. Tissue blocks from cervical, thoracic, and lumbar spinal cords were embedded in paraffin. Tissue sections were double stained with luxol fast blue and hematoxylin and eosin. The space occupying lesions were quantified with a digitizer tablet. The fractional area of the lesions was 0.009% in controls and 0.026% in rats subjected to diving. We conclude that the volume of extravascular free gas present in the cord of rats with spinal decompression sickness is small and that artifacts of tissue preparation contribute to the volume estimate. As far as can be judged from the results in this animal model, the contribution of extravascular gas bubbles to spinal cord decompression injury is minor.

The prevalence of right-to-left interatrial shunts was determined by contrast echocardiography in a blind comparison of 61 divers who had had decompression sickness, divided into four predetermined clinical subgroups, and a control group of 63 who had not. The prevalence of shunt was 15/63 in the controls and did not differ significantly in 24 divers with onset of neurological symptoms more than 30 minutes after surfacing (4/24) or 6 with joint pain only (1/6). In divers who had neurological symptoms within 30 minutes of surfacing the prevalence of shunt was 19/29, significantly higher. Rashes soon after surfacing were related to shunts but late rashes were not.

The purpose of the study was to determine if a near-maximum exposure to air at increased atmospheric pressure causes gross fetal malformations, decreased birth weight, or death when administered to pregnant sheep during peak development of the embryo. Twenty-eight timed-pregnant sheep were alternately assigned to a series of 25- or 30-minute exposures at either 4.6 atmospheres absolute or surface pressure between days 12 and 40 of gestation. About day 130 of pregnancy, 11 experimental and eight control fetuses were recovered, weighed, measured, fixed, and examined for defects. No major structural malformations were present. One minor variation, an undescended testis, occurred in a treated fetus. The results indicate that a series of short, marginally tolerated "dives" by pregnant sheep during peak development does not affect fetal health or survival.

A modified alpha pattern activity occurred in the EEG of a 21-year-old man during recovery from a diving injury. It persisted for 10 days but finally the EEG became normal. There was clinical and neurophysiological evidence of additional separate lesions in the cervical and mid-thoracic spinal cord. The latter resulted in spastic paraplegia but the patient made an otherwise good recovery.