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July is about trips to the beach, sunbathing and enjoying the sunshine. However, with the hot weather, also comes the increasing concern for heatstroke for our furry friends.

What it is and how it presents

Evaporation, primarily occurring through pant­ing, is the most important mechanism for dissipating body heat in dogs, along with increased salivation.

This system might fail after exposure to a hot, humid environment or strenuous physical exercise, leading to heatstroke.

Predisposing factors for heatstroke include obesity, thick haircoat, geriatric age, brachycephalic anatomy, and upper airways, cardiovascular or neurologic diseases impairing physiologic cooling mechanisms. Certain drugs, such as diuretics or cardiac drugs may also affect heat dissipation. In addition, metaldehyde, amphetamine, and macadamia nut intoxication may induce hyperthermia in dogs.

Heatstroke is usually diagnosed when an acute onset of systemic clinical signs occurs in a previously healthy animal that presents a core body temperature >41°C (105.8°F). However, patients can appear normo- or even hypothermic on presentation, particularly if cooling measures are initiated by the owners or if they are in an advanced stage of shock.

Clinical findings include hyperthermia, tachypnoea, panting, collapse, shock, altered consciousness, seizures, vomiting, diarrhoea, petechiae, and ecchymosis.

There are different degrees of severity and a grading tool like the one used in human medicine has been recently proposed (Hall et al. 2021) and it is reported below.

Pathogenesis and main laboratory abnormalities.

Thermal injury leads to diffuse vascular damage and activation of the coagulation cascade, resulting in hypercoagulability, formation of multiple microthrombi, and diffuse microvascular thrombosis. The terminal result is disseminated intravascular coagulation (DIC), which might be initially subclinical, which is a major factor in the morbidity and mortality of heatstroke patients.

In most dogs, haemostatic analyte abnormalities are noted as early as at presentation and at 4 hours post presentation (PP). Tests should be repeated at 4 hours PP, to avoid delayed intervention in the acute phase of the initiation of DIC as recommended in a recent publication (Bruchim et al. 2017).

Normalization of the body temperature does not decrease the hypercoagulable state.

As DIC may become clinically overt only hours to days after the initial thermal insult, dogs with heatstroke should be monitored closely for haemostatic abnormalities and clinical signs of DIC (i.e., petechiae, ecchymoses, melena, haematochezia, and haematuria) for at least 24 to 48 hours after the thermal insult had occurred.

Bruchim et al. showed that prolonged prothrombin time (PT) and activated partial thromboplastin time (aPTT) at 12 to 24 hours post-presentation and hyperfibrinogenaemia at 24 hrs post-presentation are significantly associated with death.

Typical hematologic abnormalities include pathologic metarubricytosis (i.e., increased counts of nucleated red blood cells in examination of stained blood smears, in absence of anaemia and polychromasia) and increased haematocrit resulting from haemoconcentration, secondary to splenic contraction, compensatory shock and dehydration. The nucleated RBC count at presentation has been shown to be higher in non-surviving dogs compared to the survivors of heatstroke and has proven an excellent prognostic marker for prediction of secondary complications and survival. Some authors (Mastrorilli C et al. 2013) suggest that botryoid nuclei are commonly seen in dogs with heatstroke. Similar findings are reported as being frequent in people with heatstroke.

Rhabdomyolysis is a primary characteristic of heatstroke in dogs, occurring during and following the heat insult, and is exacerbated during the first 24 hrs of hospitalization due to skeletal and cardiac muscular hypoperfusion, resulting from hypovolemic, distributive shock and micro thromboses, secondary to developing DIC. Evidence of rhabdomyolysis and muscle damage, including increased activity of CK, AST, ALT and possibly, presence of myoglobinuria.

Renal thermal injury, decreased renal perfusion due to hypovolemic, distributive shock and dehydration, endotoxemia, myoglobinuria secondary to rhabdomyolysis cause kidney injury, which may be mild and go unnoticed at presentation, but often, rapidly turns into overt renal failure.

Heatstroke is a life-threatening condition in which clinicopathological signs and prognosis of canine heatstroke depend on the duration and severity of hyperthermia. Early diagnosis, rapid initiation of cooling measures, intensive and prolonged treatment, and monitoring, may offer the best chance for survival. Heatstroke can be prevented by not forcing dogs to exercise in hot environments, and providing adequate access to water, shade, and ventilation.


Further readings:



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