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.