Heat stroke: when a dog’s temperature control system fails
Any disruption to the temperature control mechanisms in dogs can lead to heat stroke (HS).
Temperature control in dogs
Under normal conditions, the thermoregulatory centre, which is located in the anterior hypothalamus, maintains body temperature within a narrow range of limits. This is achieved through a balance between the body’s heat production and dissipation mechanisms.1 With respect to elevated temperatures in dogs, it is essential to know how to differentiate between fever and hyperthermia. In the case of fever, body temperature rises because the hypothalamus increases the body’s internal temperature setting in response to the release of pyrogens. Thus, in a febrile patient, endogenous physiological mechanisms are activated to preserve heat (vasoconstriction or shivering) and reach the new temperature set by the thermoregulatory centre. In nonfebrile hyperthermia, on the other hand, the patient’s organism is trying to reduce its body temperature.1
At temperatures below 32 °C, over 70% of body heat is dissipated from the body’s surface via radiation and convection mechanisms, but as ambient temperature increases, temperature control is achieved through evaporation (by means of panting in dogs). Unfortunately, as ambient humidity increases, evaporation becomes less efficient, and it is virtually nonexistent when humidity reaches 80%.2
Heat stroke: aetiopathogenesis
Whether it is heat stroke caused by overexposure to a hot, humid environment (classic HS) or extreme physical activity (exertional HS), the patient suffers an imbalance in their intrinsic/extrinsic heat production and heat dissipation mechanisms.
In veterinary medicine, HS is characterised by a nonpyrogenic, rectal temperature > 41 °C and nervous system dysfunction, bearing in mind that some animals can be normothermic or even hypothermic at the time of admission if their owners have been trying to cool them or if they are in an advanced state of shock.3 Heat stroke is a very serious situation with a mortality rate of up to 50%, even when appropriate technical and human resources are available for intensive treatment.4
Although it can affect any dog, Labradors (given their playful character and predisposition for obesity), Belgian Malinois (on account of the intense training they undergo), and of course, brachycephalic breeds (due to their anatomical complications) are all predisposed to heat stroke.3,4
- The body’s inability to dissipate excess heat causes dehydration, decreased cardiac output, hypotension and vascular collapse. The accumulation of blood in the spleen and liver contributes to the development of shock and intestinal ischaemia.
- Patients with heat stroke suffer a systemic inflammatory response syndrome that usually progresses to multiple organ dysfunction syndrome. The combination of the direct damage caused by the heat, hypovolaemic and distributive shock, metabolic acidosis, neurological dysfunction, endotoxaemia and DIC results in decreased organ perfusion, tissue necrosis and haemorrhagic diathesis.
- The most common complications include rhabdomyolysis, neurological damage and dysfunction, acute kidney injury (AKI), acute respiratory distress syndrome, hepatobiliary damage, sepsis, and acute pancreatitis. Massive haemorrhagic diarrhoea and haematemesis can occur, which is believed to be accompanied by bacterial translocation.3
Laboratory abnormalities in dogs with HS
The most frequent changes include a rise in CK, ALT, AST, GGT and alkaline phosphatase concentrations, as well as elevated haematocrit and metarubricytosis in the absence of anaemia and polychromasia (a very characteristic sign of heat stroke), and haemoglobinuria.3
AKI is thought to affect all patients with HS, but may initially have a subclinical course and pass undetected based on normal markers of renal function.5
Treatment
The goals of HS treatment are to control the hyperthermia, provide cardiovascular support and treat any complications.
- The first measures to normalise a dog’s temperature include placing the animal in a cool area away from direct sunlight, spraying with cool water (not freezing) and placing cooling packs (not frozen) on the axillae and groin. The aim is to achieve a temperature of 39.4 °C in the first 30–60 minutes, but without provoking overcooling that could further stimulate the thermoregulatory centre.
- Intravenous fluids should be administered according to each patient’s needs, as should oxygen in the event of respiratory failure.
- The use of glucocorticoids is recommended if pulmonary oedema is suspected, but not as a routine measure.
- Broad-spectrum antibiotics should be combined with fluoroquinolones (and sometimes metronidazole) to combat bacteraemia. The use of potentially nephrotoxic antibiotics and antipyretics is not recommended.6
Conclusions
Heat stroke is a common clinical situation with a high mortality rate. It is therefore important to give owners sound advice on how to avoid it. They must be aware of the importance of avoiding exposure to high temperature and relative humidity conditions, especially in predisposed dogs and those which practice intense exercise. If this is not possible, at the very least exposure time must be minimised, with the dog allowed to cool off periodically and maintained well hydrated. If owners must travel with their dog, it is best done at cooler times of the day, keeping the temperature in the vehicle at 20–24 °C and with frequent stops to give the animal a chance to drink.
