Treatment of Salt Water Aspiration Syndrome

Most of the clinical manifestations of SWAS respond rapidly to rest and the administration of oxygen. Warming the patient is of symptomatic benefit. In general, no other treatment is required.

There is a possibility that some of the clinical manifestations may not entirely be caused by to the aspiration of water, but by the body’s (and specifically the respiratory tract’s) response to aspirated organisms, foreign bodies or irritants carried to the lungs with the sea water aspiration.

Salt Water Aspiration Syndrome: Differential Diagnosis

In the differential diagnosis of SWAS, the possibility of other occupational diseases of divers must be considered:

Acute infection – The aspiration syndrome may mimic an acute respiratory infection that develops soon after a dive. It is often claimed that a mild upper respiratory infection is likely to be aggravated by diving. This is questionable with the number of divers who continue to dive, uneventfully, despite such infections. Differentiation between SWAS and an acute infection can be made from the history of aspiration, serial chest x-ray studies, spirometry and a knowledge of the natural history of the infectious diseases. In the first few hours of this syndrome, the possibility of both influenza and early pneumonia are often considered – to be dismissed as the symptoms clear within hours.

Decompression sickness with cardiorespiratory or musculoskeletal manifestations – If there is a likelihood of cardiorespiratory symptoms of decompression sickness (‘chokes’), recompression therapy is indicated. Decompression sickness should be considered in patients who conduct deeper, prolonged or repetitive diving. The specific joint pains and abnormal posturing characteristic of the ‘bends’ are quite unlike the vague generalized muscular aches, involving the limbs and lumbar region bilaterally, seen with SWAS. The immediate beneficial response to the inhalation of 100 per cent oxygen in SWAS is of diagnostic value. With decompression sickness, any relief is more delayed. Chest x-ray studies, lung function tests and blood gas analyses may be used to confirm the diagnosis. Decompression sickness responds rapidly to recompression therapy (as does SWAS to hyperbaric oxygenation). Otherwise, except for the occurrence of a latent period, the clinical history of the two disorders is dissimilar.

Pulmonary barotrauma – Serious cases of pulmonary barotrauma result in pneumothorax, air emboli and mediastinal emphysema occurring suddenly after a dive. In minor cases of pulmonary barotrauma, confusion with the SWAS may arise. In these patients, the diagnosis and treatment of the former must take precedence until such time as the natural history, chest x-ray findings, spirometry and blood gas analysis demonstrate otherwise. Oxygen is appropriate first aid treatment for both disorders. Hyperbaric oxygen is also an effective (but unnecessary) treatment for SWAS.

Hypothermia – The effects of cold and immersion are usually maximal at, or very soon after, the time of rescue. The clinical features are likely to be confused with SWAS only when both conditions exist. The body temperature is higher than normal in SWAS and lower than normal in hypothermia.

Key West scuba divers’ disease6 – This and other infective disorders resulting from contaminated equipment may cause some confusion. Fortunately, these illnesses usually take longer to develop (24 to 48 hours) and to respond to therapy. There is thus little clinical similarity in the sequence and duration of the clinical manifestations.

Asthma – Some patients have hyperreactive airways to hypertonic saline (sea water), analogous to an asthma provocation test (see Chapter 55). Such patients have the clinical signs of asthma (expiratory rhonchi, especially with hyperventilation, typical expiratory spirometry findings and positive asthma provocation tests). They respond to salbutamol or other beta agonists.

Immersion pulmonary oedema – This disorder may be either a complication or an initiator of SWAS.

Salt Water Aspiration Syndrome: Discussion

A detailed investigation into the causes of recreational scuba diving deaths4,5 revealed that SWA was part of the sequence leading to death in 37 per cent of the cases – often a consequence of equipment problems or diving technique. In these cases, ‘leaking regulators’ were either observed and commented on by the victim beforehand or were demonstrated during the subsequent diving investigation.

The degree of aspiration increases with the volume of air required (e.g. with exertion, swimming against currents, panic) and/or with a diminished line pressure to the second stage.

SWA often formed a vicious circle with panic and exhaustion.

Hypoxia from SWA aggravated the problems of fatigue and exhaustion and was a precursor to loss of consciousness (with or without dyspnoea) in both near drowning and drowning cases.

In recreational scuba, the diver may attribute SWA-induced post-dive lethargic symptoms to sub-clinical decompression sickness or the unusual physical demands of the dive activity. If the diver is exposed to cold and develops the generalized symptoms characteristic of a feverish reaction, he or she will be unlikely to relate this to an unnoticed aspiration some hours earlier.

Whether the clinical manifestations are entirely caused by the hyper-osmotic sea water or whether there is a contribution to the pulmonary inflammatory response from the various organisms, vegetation and particulate matter in sea water is not known. Extrapolating from the animal experiments on aspiration, it would seem that the required inhaled volume of hyper-osmotic sea water would be more than 100 ml in humans. Small particle nebulization is not essential, but it is possibly relevant in those divers who were not aware of aspiration.

There is no distinct division in the initial presentations among SWAS, near drowning and drowning cases. Aspiration syndromes merge with near drowning – the intensity of the symptoms and the degree of consciousness often depending on environmental circumstances, the activity of the victim and the administration of oxygen.

Clinical Features of Salt Water Aspiration Syndrome

The following observations were made on clinical cases of SWAS1,2:

Immediate symptoms

On specific interrogation, a history of aspiration was given in 90 per cent. Often, the novice diver did not realize the significance of the aspiration as the causal event of the syndrome.

Most divers noted an immediate post-dive cough, with or without sputum. It was usually suppressed during the dive. Only in the more serious cases was the sputum bloodstained, frothy and copious (as seen routinely in near drowning cases).

Subsequent symptoms

The following symptoms were observed:

  1. Rigors, tremors or shivering – 87 per cent
  2. Anorexia, nausea or vomiting – 80 per cent
  3. Hot or cold (feverish) sensations – 77 per cent
  4. Dyspnoea – 73 per cent
  5. Cough – 67 per cent
  6. Sputum – 67 per cent
  7. Headaches – 67 per cent
  8. Malaise – 53 per cent
  9. Generalized aches – 33 per cent

The signs and symptoms usually reverted to normal within a few hours and rarely persisted beyond 24 hours, unless the case was of greater severity.

RESPIRATORY SYMPTOMS

There was often a delay of up to 2 hours before dyspnoea, cough, sputum and retrosternal discomfort on inspiration were noted. In the mild cases, respiratory symptoms persisted for only an hour or so, whereas in the more severe cases, they commenced immediately following aspiration and continued for days. The respiratory rate roughly paralleled the degree of dyspnoea. Physical activity and respiratory stimulants appeared to aggravate the dyspnoea and tachypnoea, as did movement and exercise.

Auscultation of the chest revealed crepitations or occasional rhonchi, either generalized or local, in about half the cases. Rarely, they were high pitched and similar to those observed in obstructive airways disease.

Administration of 100 per cent oxygen was effective in relieving respiratory symptoms and removing any cyanosis.

X-ray study of the chest revealed areas of patchy consolidation, or a definite increase in respiratory markings, in about half the cases. These usually cleared within 24 hours, but they remained longer in severely affected patients. X-ray studies taken after the incident and repeated within a few hours sometimes showed a variation of the site of the radiological abnormality.

Expiratory spirometry performed repeatedly over the first 6 hours showed an average drop of 0.7 litres from the baseline in both forced expiratory volume in 1 second and vital capacity measurements. Even those patients who had no respiratory symptoms had a reduction in lung volumes. Arterial blood gases revealed oxygen tensions of 40 to 75 mm Hg with low or normal carbon dioxide tensions, indicative of shunting (perfusion) defects.

GENERALIZED SYMPTOMS

Patients often complained of being feverish. Malaise was the next most prominent feature. Headaches and generalized aches through the limbs, abdomen, back and chest were important in some cases, but usually not dominant. Anorexia was transitory.

The feverish symptoms were interesting – and are also seen in near drowning cases. Shivering, similar in some cases to a rigor and in other cases to generalized fasciculations, was more common in the colder months. It was precipitated or aggravated by exposure to cold, exercise or breathing 10 per cent oxygen (a research procedure, not recommended clinically). It was relieved by administration of 100 per cent oxygen. It occurred especially in patients exposed to cold because of duration and depth of dive, inadequate thermal clothing and environmental conditions during and after the dive.

The association of shivering with hypoxia and cold had been described previously3. The shivering occurs concurrently with the pyrexia, which also takes an hour or two to develop.

Pyrexia was verified in half the cases, up to 40°C (mean, 38.1°C; standard deviation [SD] = 0.6), and the pulse rate was elevated (mean, 102 per minute; SD = 21), over the first 6 hours.

Some patients obtained relief from these symptoms by either hot water baths or showers or by lying still in a warm bed.

In some patients, there was an impairment of consciousness, including transitory mild confusion or syncope with loss of consciousness on standing. These were clinically approaching the near drowning cases described (see Chapter 22), and they were treated accordingly.

INVESTIGATIONS

Haemoglobin, haematocrit, erythrocyte sedimentation rate and electrolytes remained normal. The white blood cell count was usually normal, although mild leucocytosis (not in excess of 20 000 per cubic millimetre) was observed in a few cases, with moderate polymorphonuclear leucocytosis and a shift to the left.
Lactic dehydrogenase estimations revealed a mild rise in some cases. X-ray and lung volume changes were as described earlier.

Examination of the diving equipment may reveal the cause of the aspiration. Inspection of the second stage regulator, breathing against the regulator with the air supply restricted and having another diver use the equipment under similar conditions all may identify the problem. See the section on re-enactment of a diving incident in Chapter 51.

The Etiology of Salt Water Aspiration Syndrome

Salt water aspiration (SWA) is a ubiquitous consequence of diving in the ocean, as well as among surfers, snorkellers, helicopter rescuees and ocean swimmers, who now recognize SWAS.

With divers, a watertight seal of the demand valve should ensure that water does not enter the spaces that carry the inspiratory and expiratory air.

This depends on the integrity of the mouthpiece, inspiratory valve or diaphragm (rubber or silicone) and the expiratory or exhaust valves. Any damage, wear, perforation, displacement or foreign body can disrupt these seals. This is more likely with increasing pressure gradients across the seals, such as with increasing respiration.

Whether the diver is aware of the ‘leaking’ probably depends on many factors, such as the volume, the site of entry (the proximity of the leak to the air inlet) and the attention paid to other activities. Sometimes the diver will recollect a specific incident leading to the aspiration (often inducing a cough), or he or she may notice a ‘bubbling’ or ‘wet’ sensation in the regulator. Other times, the diver may not notice anything, as occurs with the inhalation of many nebulized particles.

SWA in divers may occur in certain circumstances, namely:

  1. In inexperienced divers because they commonly overbreathe the regulator.
  2. Excessive respiratory flow and volumes, as with exercise and anxiety.
  3. Increasing depth and thus density of the inspired gas.
  4. During buddy breathing or re-inserting the regulator underwater.
  5. From a faulty, corroded or damaged regulator.
  6. Foreign body (salt crystals, weed, sand) interference with the diaphragm or exhaust valve seating.
  7. Failure of the mouthpiece seal, as from tears.
  8. Being towed at speed.
  9. With upstream regulator valves, as in some surface supply units.
  10. Whenever the air intake is below the exhaust outlet – a positional effect.
  11. Removing the regulator on the surface.

As we know from respiratory medicine, larger volumes of fluid in the upper respiratory tract stimulate a laryngeal response varying from coughing to laryngospasm. Nebulized droplets with diameters of 1 to 10 micrometres are distributed to the terminal bronchi, with less deposition in the upper respiratory tract. The aspiration volumes in diving probably depend on the previously listed 10 circumstances.

Salt Water Aspiration Syndrome: History

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.

HISTORY

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.