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.

The Management of Drowning: Prognosis

It is difficult to prognosticate in individual cases because data from the literature, much of it in the paediatric age group, arise from widely different situations. These situations range from childhood bath and pool incidents in fresh water to boating, swimming and diving activities in the open sea. Nevertheless, several reasonably consistent observations emerge.

Factors that negatively affect outcome include submersion time, time to initiation of effective CPR, severe metabolic acidosis, Glasgow Coma Scale (GCS <5), cardiac arrest and the presence of fixed dilated pupils. However, complete recoveries have been reported despite the presence of one or more of these adverse predictors.

Poor prognostic factors

Prolonged submersion.Prolonged time to effective cardiopulmonary resuscitation.Cardiac arrest.Absence of spontaneous respiration.Prolonged coma.

Several pooled series indicate that 90 per cent of patients who arrive at least arousable with spontaneous respiration and purposeful response to pain will survive neurologically intact. In contrast, of the patients in this series who arrived comatose, 34 per cent died, and 20 per cent of the survivors had neurological damage18.

Unresponsive coma, decorticate and decerebrate rigidity, areflexia and fixed dilated pupils are not in themselves diagnostic signs of death, although they are, of course, signs of a poor prognosis. Patients who arrive in hospital in asystole usually have a poor prognosis, and one series reported a 93 per cent mortality rate after cardiac arrest. Current treatment regimens do not alter the outcome.

The rapid development of severe hypothermia, either before or during the final submersion, is probably protective and helps to explain some spectacular recoveries after prolonged periods of submersion. The role of the diving reflex remains controversial.

The Management of Drowning: Hospital (Emergency department/Intensive care)

Hospital management is subdivided into initial emergency department management and continuing therapy in the intensive care unit. All patients should receive oxygen (see Chapter 49) while undergoing evaluation.

Emergency department

On arrival, the emphasis is on evaluation and resuscitation of respiratory failure. Preliminary assessment includes airway, circulation and level of consciousness re-evaluation. Continuous monitoring of pulse, blood pressure, pulse oximetry and electrocardiography are commenced.

The severity of the case determines the appropriate care. If submersion victims show no signs of aspiration on arrival in the emergency department, there may be no need for hospital admission. Patients who are asymptomatic and have normal chest auscultation, chest x-ray findings and arterial blood gases will not subsequently deteriorate7–9. They may safely be discharged after 6 hours. In contrast, patients with mild hypoxaemia, auscultatory rales or rhonchi or chest x-ray changes should be admitted for observation because they may deteriorate.

In moderately hypoxaemic patients who have not lost consciousness and who are breathing spontaneously, the use of non-invasive ventilatory support with face mask or nasal continuous positive airway pressure (CPAP) may be an alternative to sedation and endotracheal intubation, provided adequate gas exchange is achieved.

Seriously affected patients should be admitted to an intensive care unit or a high-dependency unit. Patients with symptomatic hypoxaemia or disturbed consciousness may rapidly deteriorate further as a result of progressive hypoxaemia. Patients who have had a cardiac arrest or are unconscious and/or severely hypoxaemic require ventilatory support and should be intubated using a rapid sequence induction technique. A nasogastric tube should be inserted and the stomach emptied before induction, if possible.

Concurrent with resuscitation measures, a careful search for any other injuries, such as cranial or spinal trauma, internal injuries and long bone fractures, should be undertaken. Initial x-ray studies should include the chest and cervical spine. Cerebrovascular accident, myocardial infarction, seizure or drug abuse should be suspected if the cause of the incident is not readily apparent. One study revealed that 27 per cent of recreational diving deaths appeared to have a cardiac event as the disabling injury11, so a high index of suspicion for myocardial ischaemia should be maintained. A 12-lead electrocardiogram would be advisable early in the evaluation.

Similarly, in the scuba diver, other disorders such as pulmonary barotrauma and cerebral arterial gas embolism may have initiated or complicated the drowning. These conditions may require specific treatment such as recompression, hyperbaric oxygen or drainage of a pneumothorax. Nevertheless, it should never simply be assumed that a diver ‘must have’ suffered pulmonary barotrauma and arterial gas embolism just because the diver was brought to the surface rapidly or unconscious. There have been many unconscious ascents from significant depths in which it appears that pulmonary barotrauma did not occur. Moreover, such an assumption would indicate hyperbaric therapy. Although recompression should not be withheld from a patient who clearly warrants it, it is logistically difficult and more hazardous for an intensive care patient, and recompression should not be used speculatively.

The main goal of therapy is to overcome major derangement of hypoxaemia with its subsequent acidosis. The benchmark should be an arterial oxygen tension (PaO2) of at least 60 mm Hg. This may be achieved by administration of oxygen by mask in milder cases, possibly with CPAP, but some patients will require more aggressive therapy, employing intermittent positive pressure ventilation (IPPV) with a high fractional inspired oxygen concentration (FIO2).

High ventilatory pressures may be required to obtain adequate tidal volumes. Progress should be monitored by serial arterial blood gas determinations and continuous pulse oximetry.

The institution of continuous positive end-expiratory pressure (PEEP) with either IPPV or spontaneous ventilation, (i.e. CPAP) will decrease the pulmonary shunting and ventilation-perfusion inequality and increase the functional residual capacity, thus resulting in a higher PaO2. Nebulized bronchodilator aerosols may be used to control bronchospasm. In sedated patients, fiberoptic bronchoscopy can be used to remove suspected particulate matter, and repeated gentle endotracheal suction will assist in the removal of fluid from the airway.

Early on in the resuscitation sequence, large-bore intravenous access should be established and warmed crystalloid fluids commenced. Moderate volumes may be required initially because of tissue losses, immersion diuresis and dehydration, but care should be taken not to overhydrate. Simultaneously, blood for haematology and biochemistry laboratory work can be drawn for baseline assessment. Testing should include cardiac enzymes. Intra-arterial pressure monitoring is useful and allows frequent arterial blood gas determinations to guide ventilation and acid-base management.

If cardiac arrest is diagnosed, the rhythm should be rapidly determined, and defibrillation and/or intravenous adrenaline (epinephrine) should be administered according to advanced life support protocols (see Figure 23.3). Other arrhythmias should also be appropriately treated if they have not responded to correction of hypoxaemia and restoration of adequate tissue perfusion.

In the past, it was common to attempt to correct metabolic acidosis by giving bicarbonate. The use of bicarbonate in this setting is controversial, and some clinicians may prefer to hyperventilate a patient to create a respiratory compensation for the metabolic acidosis. A more modern alternative intravenous alkalinizing agent is tromethamine acetate (tris-hydroxymethyl aminomethane [THAM]). THAM has the apparent advantage that its action does not result in the generation of carbon dioxide (as occurs with sodium bicarbonate), and as such it may be a better choice in hypercapnic patients who have mixed acidaemia or in patients who are difficult to ventilate. These descriptors may apply to drowning victims.

Some drowning victims have been noted to be markedly hypoglycaemic, and an association with alcohol intoxication, physical exhaustion and hypothermia is relevant. Blood glucose concentrations should be rapidly determined along with blood gases on arrival at hospital, and intravenous glucose therapy should be instituted if appropriate. Untreated hypoglycaemia may aggravate hypoxic brain lesions. However, intravenous glucose must be used with care because hyperglycaemia is also potentially harmful to injured neurons. Hyperglycaemia resulting from massive catecholamine release or other causes may require insulin infusion.

Hypothermia may complicate drowning and pose difficulties with resuscitation end points in the event of cardiac arrest (see Chapter 28). The emergency department management of hypothermia depends on severity, and low-reading thermometers are required because severe hypothermia may otherwise be overlooked. Warmed intravenous fluids and inspired gases, insulation, forced-air warming blankets and radiant heat may be sufficient, but in severe cases, gastric lavage, peritoneal lavage or even cardiopulmonary bypass has been employed. Resuscitation should continue at least until core temperature approaches normal. Care should be taken to avoid hyperthermia because even mild degrees of cerebral hyperthermia can be profoundly disadvantageous to the injured brain.

Hypovolaemia may result from the combined effects of immersion diuresis and pulmonary and tissue oedema. Circulatory support maybe required to provide adequate perfusion of vital tissues. The maintenance of effective cardiac output may require the correction of hypovolaemia, which may be unmasked by the instigation of body rewarming. PPV also decreases venous return to the heart and thus lowers cardiac output. This can usually be overcome by volume restoration or even augmentation. If after volume replacement the patient does not rapidly regain adequate cardiac output, then inotropic support will be required.

Although not studied specifically in the context of drowning, there is compelling evidence from large randomized studies suggesting that resuscitation of intensive care patients with crystalloid fluids results in better outcome (and less requirement for renal replacement therapy) than does resuscitation using colloids. If colloids are used, small volumes of concentrated albumin may be optimal. Care must be taken not to overhydrate drowning patients.

Once intravascular volume is normalized and adequate cardiac output is established, fluid administration should be parsimonious. Diuretics (e.g. frusemide) have also been employed where overhydration is suspected. A urinary catheter with hourly output measurements is essential to determine renal perfusion and function and is a good indication of adequate volume. Electrolyte disturbances are usually not a significant problem in the initial phases, but any abnormality should be corrected.

Antibiotics given prophylactically are of dubious benefit. Antibiotics should be employed only where clearly clinically indicated, guided by sputum and blood cultures. Routine use may encourage colonization by resistant organisms.

Intensive care

The general principles of intensive therapy are followed, but with special emphasis on respiratory function because near drowning is a common cause of the acute respiratory distress syndrome (ARDS).

The following clinical parameters, established on arrival in the emergency department, should be regularly monitored:

  1. Routine clinical observations such as pulse, blood pressure, temperature, respiratory rate, minute volume, inspiratory and PEEP pressures, electrocardiography, pulse oximetry and urine output.
  2. Where indicated, invasive monitoring such as central venous pressure, pulmonary artery wedge pressure and cardiac output by a pulmonary artery catheter.
  3. Blood tests such as arterial blood gas and acid-base status, haemoglobin, packed cell volume, white cell count, serum and urinary electrolytes, serum and urinary haemoglobin and myoglobin levels, serum creatinine, urea, glucose, protein and coagulation status.
  4. Regular chest x-ray examination to detect atelectasis, infection, pneumothorax, pulmonary oedema, pleural effusions and other disorders.
  5. Serial measurement of pulmonary mechanics, by measurement of airway pressures and compliance, which are also useful in monitoring progress. In the less severely ill patient, simple spirometry is a useful guide to recovery.

The optimal method of ventilation aims to produce an adequate oxygen tension at the lowest FIO2 (preferably FIO2 of 0.6 or less to avoid pulmonary oxygen toxicity; see Chapter 17) with the least haemodynamic disturbance and the least harm to the lung. CPAP can be dramatic in improving oxygenation by reducing intrapulmonary shunting. Pressures of 5 to 10 centimetres of water are usual, but greater pressures may be required. Patients receiving PPV tend to retain salt and water, so fluid intake should be reduced to about 1500 ml/day with low sodium content. Fluid overload may have a deleterious effect on pulmonary function.

Various modes of ventilation have been employed. These include spontaneous respiration with CPAP, IPPV with and without PEEP, synchronous intermittent mandatory ventilation, pressure support and high-frequency ventilation. Increasing experience in the management of ARDS has led to the development of so-called ‘lung protective ventilator strategies’ characterized by relatively long inspiratory times, high end-expiratory pressures and relatively small tidal volumes. This may require acceptance of both a degree of ‘permissive hypercapnia’ and mild respiratory acidosis that in the short term may be treated with bicarbonate or THAM, before medium-term compensation through renal retention of bicarbonate. Postural changes (e.g. prone ventilation) are sometimes experimented with in individual patients. There is no universally applicable formula for ventilating these patients, and much individualization of regimens occurs in high-level intensive care units. These types of strategy may be necessary in severely affected drowning victims.

Femoro-femoral or full cardiopulmonary bypass has been employed both for rewarming hypothermic patients and for establishing adequate oxygenation in severe cases12. Severe ARDS has been successfully managed with variable periods (up to weeks) of extracorporeal membrane oxygenation (ECMO).

Because of improvements in cardiorespiratory support, preservation of the central nervous system is now the major therapeutic challenge13. The application of various brain protection techniques including deliberate hypothermia, hyperventilation, barbiturate coma and corticosteroids has not altered cerebral salvage rates in the specific context of drowning14,15. Studies in community cardiac arrest do provide circumstantial support for the use of hypothermia after prolonged resuscitation. Although some intensive care units may try this in drowning victims, it is certainly not considered a standard of care. It is notable that corticosteroids have not been shown to reduce cerebral oedema or intracranial pressure (ICP) and are not recommended.

Central nervous system function is assessed clinically and potentially by electroencephalography. ICP monitoring has been advocated where intracranial hypertension is suspected, with prompt therapy for any sudden elevation.

Serial creatinine estimations often reveal mild renal impairment in patients requiring intensive care. Severe acute renal failure16 requiring dialysis is less common, but it may develop in patients who presented with severe metabolic acidosis and elevated initial serum creatinine levels. Occasional cases of rhabdomyolysis have also been reported.

Hyperpyrexia commonly follows drowning, and its effect may be deleterious, especially to the injured brain. External cooling and antipyretic drugs to prevent shivering and to keep the temperature lower than 37°C may be indicated.

Continuing hyperexcitability and rigidity may require the use of sedative and relaxant drugs.

The Management of Drowning: Advanced Life Support and Transport

A regional organized emergency medical service (e.g. paramedics) that carries specialized apparatus such as oxygen, endotracheal tubes, suction and intravenous equipment should be activated, if available. In any case, the patient should be transferred to hospital as soon as possible. The early administration of oxygen by suitable positive pressure apparatus, by personnel trained in its use, may be the critical factor in saving lives. For this reason, oxygen administration equipment should be carried on all dive boats. Patients who regain consciousness or who remain conscious after drowning events may have significant pulmonary venous admixture with resultant hypoxaemia. All such patients should receive supplementary oxygen and be further assessed in hospital. Respiratory and cardiac arrests have occurred after apparently successful rescue.

Although endotracheal intubation remains the best method for securing an airway and achieving adequate ventilation, the necessary expertise may not be available until the victim is transferred to hospital. In such cases, the use of airway devices such as the laryngeal mask airway may improve ventilation while the patient is being transported to hospital. Other airways such as the pharyngo-tracheal lumen airway and the Combitube tube are alternatives, but they require more training and have their own problems. One potential problem with all supraglottic devices, and with mouth-to-mouth and bag-mask ventilation techniques for that matter, is that the airway pressures required to inflate a ‘wet’, non-compliant lung may be very high and not easily achieved with these devices or methods. Endotracheal intubation may the only way to achieve adequate tidal volumes in such patients.

Properly trained and equipped personnel attending a case in the field may be able to invoke advanced resuscitation techniques such as the airway interventions mentioned earlier and the monitoring methods, drug administration strategies and arrhythmia treatments specified in Figure 23.3.

Advanced life support algorithm. CPR, cardiopulmonary resuscitation; ECG, electrocardiogram; ETT, endotracheal tube; IV, intravenous; IO, intra-osseous; LMA, laryngeal mask airway. (From the Australian Resuscitation Council.)
Advanced life support algorithm. CPR, cardiopulmonary resuscitation; ECG, electrocardiogram; ETT, endotracheal tube; IV, intravenous; IO, intra-osseous; LMA, laryngeal mask airway. (From the Australian Resuscitation Council.)

Advanced life support algorithm. CPR, cardiopulmonary resuscitation; ECG, electrocardiogram; ETT, endotracheal tube; IV, intravenous; IO, intra-osseous; LMA, laryngeal mask airway. (From the Australian Resuscitation Council.)

The Management of Drowning: Rescue and initial resuscitation

In the diving setting, the management of a drowning situation often begins with witnessing a diver become unconscious underwater. Before resuscitation efforts can begin, the victim must be retrieved to the surface. Related considerations were reviewed by the Undersea and Hyperbaric Medical Society (UHMS) Diving Committee1, and their findings are outlined here.

The overarching goal of this initial phase of the rescue is to retrieve the diver to the surface as quickly as possible, even if the victim has a mouthpiece in place and appears to be breathing (which would be a most unusual circumstance). More typically, the victim is found unconscious with the mouthpiece out. No attempt should be made to replace it; however, if the mouthpiece is retained in the mouth, then the rescuer should make an attempt to hold it in place during the ascent. An ascent should be initiated immediately. If there is significant risk to the rescuer in ascending (if the rescuer has a significant decompression obligation), then making the victim buoyant and sending him or her to the surface may be the only option, depending on the degree to which the rescuer wishes to avoid endangering himself or herself.

The committee flagged one exception to the advice to surface immediately. In the situation where a diver is in the clonic phase of a seizure with the mouthpiece retained, then the mouthpiece should be held in place and ascent delayed until the seizure abates. To be clear, however, this does not apply to the more common situation of the seizing diver whose mouthpiece is out. In the latter situation, the ascent should be initiated while the diver is still seizing. This dichotomy arises because of the committee’s perception of the shifting balance of risk between pulmonary barotrauma and drowning in situations where the airway is at least partially protected or not. Thus, where the airway is completely unprotected (mouthpiece not retained), the risk of drowning outweighs the risk of barotrauma imposed by seizure-induced apposition of the glottis tissues. Where the airway is partly protected (mouthpiece retained and held in place), the opposite holds true. This matter is discussed in more detail in the committee report.

At the surface, the victim should be made positively buoyant face-up, and a trained rescuer should attempt to give two mouth-to-mouth rescue breaths. Experience has shown that this is often all that is required to stimulate the victim to breathe. Pausing to give rescue breaths will slightly delay removal from the water for definitive cardiopulmonary resuscitation (CPR) and is therefore a gamble that the victim has not yet having suffered cardiac arrest. However, given the extremely poor outcome expected if a drowning victim suffers a hypoxic cardiac arrest and the time it usually takes to remove a diver from the water, the committee determined that this was a gamble worth taking. The best chance of survival lies in preventing hypoxic cardiac arrest, and establishing oxygenation is the means of such prevention. If the diver has already had a cardiac arrest, then a small extra delay in initiating CPR imposed by performing in-water rescue breaths is not likely to alter the outcome. There is some human evidence suggesting a survival advantage for in-water rescue breathing in non-diving drowning situations2.

Once at the surface and in a situation where the surface support is not immediately to hand, a choice must be made whether to wait for rescue or initiate a tow to shore or nearest surface support. The committee determined that if surface support is less than a 5-minute tow away, then a tow should be commenced with intermittent rescue breaths administered if possible. If surface support or the shore is more than a 5-minute tow away, then the rescuer should remain in place, continuing to administer rescue breaths for 1 minute. If there is no response in this time, then a tow toward the nearest surface support should be initiated without ongoing rescue breaths. These guidelines are summarized in Figure 23.1.

Undersea and Hyperbaric Medical Society Diving Committee guidelines for rescue of an unresponsive diver from depth.
Figure 23.1 Undersea and Hyperbaric Medical Society Diving Committee guidelines for rescue of an unresponsive diver from depth. It is recommended that the interested diver read the original paper which contextualizes these recommendations more thoroughly. CPR, cardiopulmonary resuscitation. (From Mitchell SJ, Bennett MH, Bird N, Doolette DJ, et al. Recommendations for rescue of a submerged unconscious compressed gas diver. Undersea and Hyperbaric Medicine 2012;39:1099–1108.)

It is notable that these guidelines contain no reference to in-water chest compressions. Although techniques for in-water chest compressions have been described3,4, the committee did not consider there was adequate evidence of efficacy to justify the extra difficulty and stress to the rescuer for their inclusion in the rescue protocol.

The victim should be kept horizontal as much as possible during and after removal from the water. The patient should be moved with the head in the neutral position if cervical spine injury is suspected. Scuba divers are most unlikely to have suffered cervical spine trauma. A basic life support algorithm should be initiated immediately, beginning with assessment of the airway (Figure 23.2).

Basic life support algorithm. AED, automatic external defibrillator; CPR, cardiopulmonary resuscitation. (From the Australian Resuscitation Council.)
Figure 23.2 Basic life support algorithm. AED, automatic external defibrillator; CPR, cardiopulmonary resuscitation. (From the Australian Resuscitation Council.)

AIRWAY

Vomiting and regurgitation frequently follow a submersion incident. Foreign particulate matter causing upper airway obstruction should be removed manually or later by suction. Obstruction of the upper airway by the tongue is common in the unconscious patient.

Two methods are used to overcome the obstruction:

Head-tilt/chin-lift is accomplished by pushing firmly back on the patient’s forehead and lifting the chin forward by using two fingers under the jaw at the chin. The soft tissues under the chin should not be compressed, and unless mouth-to-nose breathing is to be employed, the mouth should not be completely closed. This technique should be avoided if cervical spine injury is suspected.

Jaw-thrust describes the technique of forward displacement of the lower jaw by lifting it with one hand on either side of the angle of the mandible. Unless cervical spine injury is suspected, this technique is often combined with head-tilt.

Time should not be wasted in trying to clear water from the lower airways. If airway obstruction is encountered and has not responded to normal airway management, the Heimlich manoeuvre (sub-diaphragmatic thrust) has been suggested5. This manoeuvre, which was proposed as a routine step to clear water from the airway, has not received the widespread endorsement of resuscitation councils around the world. It should be used with caution and only as a last resort because of the risks of regurgitation of gastric contents, rupture of the stomach and causing delay in initiating effective ventilation. Persistent airway obstruction may result from a foreign body, but other causes include laryngeal oedema or trauma, bronchospasm and pulmonary oedema.

BREATHING

Respiration can be assessed by placing one’s ear over the victim’s mouth while looking for chest movement, listening for air sounds and feeling for the flow of expired air. If breathing is detected, oxygen should be administered and the victim maintained in the ‘recovery’ position to avoid aspiration of fluid or vomitus.

If breathing is absent, mouth-to-mouth or mouth-to-nose breathing is instituted. Initially, two full breaths of air, with an inspiratory time (for the victim) of 1 to 1.5 seconds, are recommended. For adults, an adequate volume to observe chest movement is about 800 ml. If no chest movement is seen and no air is detected in the exhalation phase, then head-tilt or jaw-thrust manoeuvres should be revised. Failing that, further attempts at clearing the airway with the fingers (only if the victim is unconscious!) should be undertaken. With mouth-to-mouth respiration, the rescuer pinches the victim’s nose and closes it gently between finger and thumb. Mouth-to-nose rescue breathing may be more suitable in certain situations, such as when marked trismus is present or when it is difficult to obtain an effective seal (e.g. injury to mouth, dentures).

Paramedics or other practitioners with advanced skills are likely to use a bag-mask-reservoir device connected to an oxygen source for manual positive pressure ventilation in the field. Useful adjuncts in resolving upper airway obstruction may include a nasopharyngeal airway, oropharyngeal airway or supraglottic airway device such as a laryngeal mask. Endotracheal intubation in the field should be undertaken only by highly trained and experienced practitioners.

The rate of chest inflation should be about 12 per minute (one every 5 seconds) with increased rate and decreased volume in young children.

It must be made clear that the recent advocacy for ‘compression-only CPR’ in which rescue breathing is omitted and first responders provide only chest compressions to victims of community cardiac arrest is not relevant to CPR in the context of drowning.The cause of cardiac arrest in the community is usually some sort of cardiac disease, whereas it is hypoxia in drowning. Compression-only CPR works in community cardiac arrest because the victim is not hypoxic at the onset of cardiac standstill, and the lungs are filled with air to functional residual capacity. In contrast, hypoxia is usually the cause of cardiac arrest in drowning, and the lungs are frequently compromised by aspirated fluid and alveolar collapse. Failing to ventilate the lungs during resuscitation of a drowning victim is likely to bias against a good outcome.

CIRCULATION

The presence of a carotid or femoral pulse should be sought in the unconscious non-breathing victim. This is often difficult because the patient is usually cold and peripherally vasoconstricted. Although it is possible that external cardiac compression (ECC) could precipitate ventricular fibrillation in a hypothermic patient, if in doubt it is safer to commence ECC than not.

If no carotid pulse is detected, ECC should be commenced after two initial breaths. Higher rates of compression are now recommended, with greater outputs achieved at 100/minute compared with the traditional 60/minute standard. Controversy still exists over the mechanism of flow in external compression, with the evidence for the older ‘direct compression’ model being challenged by the ‘thoracic pump’ theory.

Cardiac compression should be performed with the patient supine on a firm surface. The legs may be elevated to improved venous return. The rescuer kneels to the side of the patient. The heel of the rescuer’s hand should be placed in line with the patient’s sternum. The lower edge of the hand should be about two fingers above the xiphisternum (i.e. compression is of the lower half of the sternum). The second hand should be placed over the first, and the compression of the sternum should be about 4 to 5 centimetres in adults in the vertical plane. To achieve this, the rescuer’s elbow should be straight, with the shoulders directly over the sternum. A single rescuer may be able to achieve rates of only 80/minute because of fatigue, but if several rescuers are present, it may be possible to maintain high rates.

Further help should be sought immediately, by a third person, if possible, without compromising resuscitation efforts.

Survival from Drowning

Treatment at the scene of an accident is sometimes of little ultimate consequence with many disorders, but in drowning it often determines whether the victim lives or dies. The standard of first aid and resuscitation training of the rescuers therefore influences outcome.

In human drowning, deterioration after initial resuscitation is frequently recorded, and this influences management (see Chapter 23).

The temperature of the water and thus the degree of hypothermia may also be factors. Poorer results are achieved in warm water drowning.

In what was previously referred to as ‘dry’ drowning (in which the distal airway remains relatively dry because of early laryngospasm), the patient is hypoxic and, if rescued in time, may– make a rapid recovery. However, when laryngospasm relaxes and fluid aspiration occurs as it eventually does if the victim remains immersed, the result is drowning.

Other factors that influence outcome include the following: the presence of chlorine, other chemicals and foreign bodies; the aspiration of stomach contents; and the subsequent development of pneumonitis, respiratory infection and multi-organ failure.

One likely cause for delayed death is progressive lung injury2. ARDS develops in a significant proportion of drowning cases; usually hours or days after the aspiration. Other causes of death in the days after the event include cerebral hypoxia, secondary infections (usually of the lungs), renal failure and iatrogenic events.

Factors that negatively influence survival have been well documented by Modell:

  • Prolonged immersion.
  • Delay in effective cardiopulmonary resuscitation.
  • Severe metabolic acidosis (pH <7.1).
  • Asystole on admission to hospital.
  • Fixed dilated pupils.
  • Low Glasgow Coma Scale score (<5).

Nevertheless, none of these predictors is infallible, and survival with normal cerebral function has been reported with all the foregoing factors.

Claims of survival after extended duration underwater without ventilation of the lungs have been used to encourage rescuers to persevere with resuscitation efforts. There have been cases reported in victims who have been submerged for between 15 and 45 minutes4–7 and who have survived without neurological sequelae. The explanations given for such prolonged durations of survival are as follows:

1. Hypothermia is protective and develops very rapidly with aspiration of water. In swimmers and divers, hypothermia may be present before the incident.

2. The ‘diving reflex’ is a possible, but contentious, explanation. Within seconds of submersion, the diving reflex may be triggered by sensory stimulation of the trigeminal nerve and by reflex or voluntary inhibition of the respiratory centre in the medulla. This produces bradycardia and shunting of the blood to the areas more sensitive to hypoxia – the brain and coronary circulations. It is independent of baroreceptor or chemoreceptor inputs. The diving reflex is more intense in the frightened or startled animal, compared with animals which dive or submerge voluntarily, but it is not known whether this finding is applicable to humans. Water temperatures higher than 20°C do not inhibit the diving reflex, but progressively lower temperatures augment it.

3. Gas exchange in the lungs can continue after submersion. With or without the effects of laryngospasm, there may be several litres of air remaining within the lungs, thus allowing for continued exchange of respiratory gases. Increased pressure (depth) transiently enhances oxygen uptake by increasing the PO2 in compressed lungs. In an unconscious state, with low oxygen use and the effects of hypothermia, a retained respiratory gas volume could add considerably to the survival time, although it is not often considered in the literature on drowning.

Whether fluid enters the lungs in an unconscious victim depends on many factors, including the spatial orientation of the body. For example, a dependent position of the nose and mouth, facing downward, is not conducive to fluid replacement of the air in the lungs.

Even though spectacular and successful rescue can be achieved after prolonged submersion, it is more frequent that this is not so. Many victims lose consciousness and die after only a few minutes of submersion.

Clinical Features of Drowning

The respiratory manifestations of drowning include the following:

  • Dyspnoea.
  • Retrosternal chest pain.
  • Blood-stained, frothy sputum.
  • Tachypnoea.
  • Cyanosis.
  • Pulmonary crepitations and rhonchi.
  • Hypoxaemia.

Pulse oximetry typically reveals low oxygen saturations, but a pulse oximeter may not read at all on a cold, peripherally shut-down victim. An arterial blood gas determination reveals hypoxaemia (lower limit of the ‘normal’ range for arterial oxygen tension [PO2] is 80 mm Hg [10.5 kPa]). There is often acidaemia that usually has a metabolic component, but that may be mixed and very severe in a respiratory peri-arrest situation. Carbon dioxide levels are frequently elevated in a peri-arrest condition, but they may be normal or even low during spontaneous breathing or manual ventilation.

Initial chest x-ray studies may be normal, or they may show patchy opacities or pulmonary oedema. Significant hypoxia may be present even when chest x-ray changes are subtle or even absent.

Complications may include pneumonitis, pulmonary oedema, bronchopneumonia, pulmonary abscess and empyema. Severe pulmonary infections with unusual organisms leading to long-term morbidity have been reported. Progression to the acute respiratory distress syndrome (ARDS) is not uncommon in drowning situations.

Central nervous system effects of hypoxia include variable impairment of consciousness, ranging from awake to comatose, with decorticate or decerebrate responses. If hypoxia is prolonged, a global hypoxic brain injury can result with cerebral oedema, raised intracranial pressure and sustained coma. Seizure activity is common in this setting.

Cardiovascular manifestations are largely the result of the effects of hypoxaemia on the heart. Progressive bradycardia leading to asystolic cardiac arrest is not uncommon. After rescue and resuscitation, supraventricular tachycardias are frequent, but various other dysrhythmias may occur. When the hypoxic acidotic insult has been severe, hypotension and shock may persist despite re-establishment of a perfusing rhythm. The central venous pressure may be elevated as a result of right-sided heart failure exacerbated by elevated pulmonary vascular resistance, rather than by volume overload. Mixed venous oxygen tension may also be low, indicating tissue hypoperfusion.

Multi-system organ failure may develop secondary to the hypoxaemia, acidosis and resultant hypoperfusion. Decreased urinary output occurs initially and occasionally progresses to acute tubular necrosis and renal failure. Haemoglobinaemia, coagulation disorders and even disseminated intravascular coagulation may complicate the clinical picture.

Laboratory findings include decreased arterial oxygen with variable PaCO2 values, metabolic and respiratory acidosis, haemoconcentration, leucocytosis, increased lactic dehydrogenase, occasional elevated creatinine levels and haemolysis as indicated by elevated free haemoglobin. Serum electrolytes are usually within the normal range.

The arterial oxygen tension is always low, but the carbon dioxide tension may be low, normal or elevated.

Recovery from drowning is often complete in survivors. However, residual neurological deficiencies may persist in the form of either cognitive impairment or extrapyramidal disorders.