Relationship between right-to-left shunts and cutaneous decompression illness

• Published in: Clinical science (1979) Vol. 100; no. 5; p. 539
• Main Authors: Wilmshurst, P T, Pearson, M J, Walsh, K P, Morrison, W L, Bryson, P
• Format: Journal Article
• Language: English
• Published: England 01-05-2001
• Subjects: Case-Control Studies; Decompression Sickness - etiology; Female; Heart Septal Defects, Atrial - complications; Heart Septal Defects, Atrial - diagnostic imaging; Heart Septal Defects, Atrial - surgery; Humans; Male; Retrospective Studies; Skin Diseases - etiology; Ultrasonography; Valsalva Maneuver - physiology
• ISSN: 0143-5221
• DOI: 10.1042/CS20000296

The presence of a large right-to-left shunt is associated with neurological decompression illness after non-provocative dives, as a result of paradoxical gas embolism. A small number of observations suggest that cutaneous decompression illness is also associated with a right-to-left shunt, although an embolic aetiology of a diffuse rash is more difficult to explain. We performed a retrospective case--control comparison of the prevalence and sizes of right-to-left shunts determined by contrast echocardiography performed blind to history in 60 divers and one caisson worker with a history of cutaneous decompression illness, and 123 historical control divers. We found that 47 (77.0%) of the 61 cases with cutaneous decompression illness had a shunt, compared with 34 (27.6%) of 123 control divers (P<0.001). The size of the shunts in the divers with cutaneous decompression illness was significantly greater than in the controls. Thus 30 (49.2%) of the 61 cases with cutaneous decompression illness had a large shunt at rest, compared with six (4.9%) of the 123 controls (P<0.001). During closure procedures in 17 divers who had cutaneous decompression illness, the mean diameter of the foramen ovale was 10.9 mm. Cutaneous decompression illness occurred after dives that were provocative or deep in subjects without shunts, but after shallower and non-provocative dives in those with shunts. The latter individuals are at increased risk of neurological decompression illness. We conclude that cutaneous decompression illness has two pathophysiological mechanisms. It is usually associated with a large right-to-left shunt, when the mechanism is likely to be paradoxical gas embolism with peripheral amplification when bubble emboli invade tissues supersaturated with nitrogen. Cutaneous decompression illness can also occur in individuals without a shunt. In these subjects, the mechanism might be bubble emboli passing through an 'overloaded' lung filter or autochthonous bubble formation.