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.