Once the airway is below the surface of a liquid voluntary breath-holding occurs. This is then followed by involuntary laryngospasm as liquid enters the oropharynx and larynx. During both of these periods, the victim is not breathing gas and develops hypercapnia, hypoxaemia and acidosis. Once the arterial oxygen partial pressure drops sufficiently, laryngospasm stops and liquid is then actively aspirated. It is the hypoxaemia which leads to unconsciousness and apnea.
Once aspirated, water leads to several severe side effects:
- One of the most significant is surfactant dysfunction and washout which reduces lung compliance and leads to atelectasis.
- Water also interferes with the normal osmotic gradient in the alveolar-capillary membrane thus directly injuring the pulmonary epithelium. Damage to these cells has several effects including the release of inflammatory mediators and increased membrane permeability worsening fluid accumulation in the lung parenchyma.
It was once believed that the type of water (salt versus fresh water) was a more important determinant of outcome than the volume aspirated, however, more recent studies have found this to be untrue. This is because it’s the volume of water which affects surfactant function regardless of the type aspirated. Pool water is interesting because it typically contains agents to limit bacterial growth so secondary pneumonia is uncommon with this type of aspiration.
The temperature of the water aspirated can also play a role in survival. Cold water is associated with higher rates of survival. This is because it reduces cellular metabolism (and thus oxygen consumption) and activates the diving reflex (leading to bradycardia, hypertension, shunting of blood to the cerebral and coronary circulations).
The history of a drowning episode is usually known. Common tests performed in these cases include:
- Blood gas analysis (ideally arterial) – most cases have a mixed respiratory and metabolic acidosis
- Thoracic radiography:
- Pulmonary oedema is likely
- In some cases, where the volume of water aspirated wasn’t large but they suffered a choking-like episode, non-cardiogenic pulmonary oedema (NCPO) may be identified. This is suspected where the pulmonary oedema is predominantly in the caudodorsal lung field.
- In cases which don’t go on to develop pneumonia, there is usually radiographic resolution of oedema within 7-10 days.
The focus should be on controlling the patient’s hypoxaemia.
The risk of pneumonia is low (estimated at 12% in humans) so empirical antibiotics are not recommended. In general, it is much more likely for these cases to develop pneumonia if they undergo mechanical ventilation.
Steroids also have not been shown to increase survival and their use is not recommended.
Similarly, there is little evidence supporting the use of diuretics in cases of NCPO. Diuretics are most useful for hydrostatic oedema which is associated with congestive heart failure. In cases of NCPO, the oedema is due to changes in pulmonary epithelium permeability (permeability oedema). Fluid can still leak into the parenchyma despite diuretic use. And since diuretics have systemic effects, they put patients at risk of dehydration and potential renal compromise.
There are several criteria that we can use to help identify those patients who could benefit from mechanical ventilation. The main indications are as follows:
- Arterial partial pressure of carbon dioxide > 60 mmHg
- Arterial partial pressure of oxygen < 60 mmHg despite non-invasive oxygen supplementation
- Excessive respiratory effort with impending respiratory fatigue
Prognosis is not known in veterinary medicine. In general, animals showing more organ systems negatively affected and those requiring positive pressure ventilation have a worse prognosis.