Archives: Divers Blog Posts

Immersion pulmonary edema (IPE) or swimming-induced pulmonary edema (SIPE) manifests with coughing, blood in sputum, difficulty breathing and a drop in the oxygen content of arterial blood.

Studies describing gas in the portal veins of animals has enabled researchers to develop a model that predictably reproduces portal vein embolization. The decompression stress in the model is severe enough to cause many bubbles all over the body, including the portal vein and liver tissue.

Brain injuries in divers may be more prevalent than previously thought and could potentially occur without a manifestation of acute decompression illness. Read more about this study and its findings.

The findings of study authors proves the hypothesis that breath-hold diving may generate venous gas bubbles. The true relationship of VGE and post-dive neurological symptoms is not known.

The dive profile may be the key in figuring out why some dives result in decompression sickness and others do not. This study also shows that the effect of depth-time on outcome of decompression is overshadowing possible effects of other observed factors.

The entire story of endothelial dysfunction and decompression sickness (DCS) sometimes is similar to the dilemma of chicken and egg: what is first, the bubbles that cause injury of endothelium, or the endothelial dysfunction that enhances occurrence of bubbles?

Normal Eustachian tube (ET) function is important for fitness to dive. Eustachian tube dysfunction may result with ear injury during diving.

Historically, alcohol was used to treat bends in Greek sponge divers. In the late 1980s attempts to verify the possible beneficial effects of ethanol on prevention of decompression sickness (DCS) led to prevailing opinions that there was no proven benefit and that divers should not drink and dive.

Survival of sudden cardiac arrest (SCA) is very low. According to DAN data, nearly 1/3 of reported scuba fatalities may be caused by SCA.