Divers who aspirate small quantities of sea water may develop a respiratory disorder with generalized symptoms mimicking those of an acute viral infection. Severe cases merge into near drowning.
The symptoms develop soon after the dive and usually persist for some hours, and they are aggravated by activity and cold exposure.
Superficially, there are similarities between the salt water aspiration syndrome and other diving disorders, but the characteristics and natural history differentiate it from pulmonary barotrauma, decompression sickness, Key West scuba divers’ disease, immersion pulmonary oedema, hypothermia, infections and asthma.
Treatment includes rest and oxygen inhalation.
A common diving illness in the Royal Australian Navy (RAN) in the 1960s was the salt water aspiration syndrome (SWAS)1. Its frequency may have been the result of the strenuous training imposed on novice divers, the absence of purge valves in second stage regulators or the extreme buddy breathing trials in which increasing numbers of trainees shared the one mouthpiece until finally one diver broke for the surface. In the RAN series, most patients with SWAS presented after night diving, when the influence of a cool environment may have aggravated the clinical situation.
In another entirely different diving environment, the professional abalone divers were almost routinely suffering from a brief, overnight affliction that they called ‘salt water fever’, which they correctly attributed to excessive water intake through the mouthpiece. The mouthpiece was connected to the surface-supplied air compressor, via an upstream or tilt valve. This simple piece of equipment was not very efficient in maintaining a water-free air supply and was recognized as a ‘wet’ breathing system. The air intake was sited below the exhaust valves, thus ensuring a nebulized water inhalation. It was replaced by the current first and second stage regulators in the 1980s by most professional divers.
The divers aspirated small quantities of sea water and developed a respiratory disorder, but with generalized symptoms mimicking those of an acute viral infection. More severe cases merged into near drowning.
A prospective survey was carried out on 30 consecutive patients who presented for treatment1. In none of these dives was the depth or duration exposure sufficient to implicate decompression sickness. The symptoms were documented and investigations were performed. To validate the cause, a simple experiment was performed on ‘volunteers’, who were both medical practitioners and divers, in which ‘doctored’ demand valves (second stage regulators) were used with the face immersed in sea water and the line pressure progressively reduced. Various respiratory measurements were monitored that replicated those in the survey. Unfortunately, more formal investigations were not pursued, and this experiment still awaits a more disciplined and sophisticated approach to define the degree and type of aspirate required.
The degree to which the same findings can be applied to fresh water aspirations and quantification of the influence of environmental factors on symptoms, also await clarification.
The frequency of SWAS has diminished somewhat with improved equipment and more lenient demands placed on novice divers, but it is still frequent enough among trainees to cause problems and diagnostic difficulties. Other seafarers to present with a similar disorder, but possibly not as frequently, are snorkellers, surfers and helicopter water rescuees.
The importance of SWAS lies in the understanding of near drowning cases and in its confusion with other diving or infectious diseases.