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WSV18-0161
VECCS
MANAGEMENT OF HEAT STROKE IN THE DOG
Y. Bruchim1
1Senior Lecturer of Veterinary Medicie, The Hebrew University of Jerusalem, Jerusalem, Israel
Heatstroke is caused by the inability to dissipate accumulated heat. In dogs it is characterized by
core temperatures above 105.8oF (41oC) with CNS dysfunction. It results from exposure to a hot and humid environment or from strenuous physical exercise. Activation of inflammatory and haemostatic pathways initiates a systemic inflammatory response syndrome (SIRS) which often progresses to multi-organ dysfunction syndrome (MODS). Serious complications of heatstroke include rhabdomyolysis, acute kidney injury (AKI), acute respiratory distress syndrome (ARDS), and disseminated intravascular coagulation (DIC). Several factors are associated with the risk of developing heatstroke. These include prior occurrence of heatstroke or heat stress, obesity, breed (brachiocephalic, Golden and Labrador retrievers), body weight (>15kg), high environmental temperature and humidity, and lack of acclimation and fitness. Prior heatstroke may affect the thermoregulatory center in the preoptic zone which is responsible for heat sensation and dissipation. Excess body fat increases
the body’s natural thermal isolation and impairs normal heat dissipation mechanisms in obese people and animals. Large breed dogs are significantly more at
risk of developing heatstroke, particularly exertional heatstroke, suggesting that the ratio between body size and surface area is an important factor of heat dissipation during heat stress. The median body weight of 54 dogs with naturally occurring heatstroke was 31 kg, also -supporting this theory. The most common clinical signs of canine heatstroke include collapse, shock, tachypnea, spontaneous bleeding (e.g. petechie, hematemesis,
and hematochezia), disorientation/stupor, coma and seizures. Although the definition of heatstroke is based on hyperthermia causing shock and hypotension, it
is important to remember that patients can be hyper-, normo- or hypothermic on presentation, particularly if cooling measures were initiated by the owners prior to presentation. Furthermore, in a retrospective study of canine heat related illness, hypothermia upon admission was a poor prognostic indicator. High body temperatures initiate a myriad of inflammatory, coagulation and tissue damage processes, varying in severity and progression between dogs. Thermal endothelial cell injury leads to diffuse vascular damage and initiation of coagulation and subsequent microvascular thrombosis. In addition, multi- organ cellular necrosis further stimulates the coagulation system and results in DIC, an important factor in the morbidity and mortality of heatstroke patients. The injured endothelium releases thromboplastin and factor
XII, which activates coagulation and the complement cascade, inducing SIRS and widespread DIC. Hepatic injury and failure due to hypoperfusion, microembolism and direct hyperthermic damage may exacerbate the haemostatic disorders. In vitro studies have shown that high temperatures (>42°C) lead to platelet aggregation, activation of the coagulation cascade and enhanced fibrinolysis. Normalization of body temperatures inhibit fibrinolysis but not the coagulation cascade or platelet aggregation. In a retrospective study of 54 dogs with naturally-occurring heatstroke, 50% were diagnosed with DIC. In 11 such dogs, severe bleeding and widespread microthrombosis, characteristic of hemorrhagic diathesis were invariably noted at necropsy. As DIC may appear hours to days after the initial hyperthermic insult,
dogs with heatstroke should be monitored closely for coagulation abnormalities and clinical signs of DIC for at least 24 hours after the insult. In a recent study in which serial monitoring of coagulation parameters were followed during the first 36 hours of hospitalization
in 30 dogs with heatstroke, haemostatic analytes
at presentation were not associated with mortality. However prolonged PT and aPTT at 12-24 hours post presentation, lower total protein C activity at 12 hrs and hyperfibrinogenemia at 24 hrs post presentation were significantly associated with mortality. Increased D-dimer concentration and low anti-thrombin activity were common at all time-points, but were not associated with mortality (Figure 1) (Bruchim and Kelmeret al, JVECCS 2016). Interestingly, in that study, which was performed 10 years following the first one at the same institution, DIC was not associated with mortality, the median number of fresh-frozen plasma units administered increased from
2 to 4 units per dog and mortality decreased from 50 to 40%.
Figure 1: Trends in haemostatic parameters throughout hospitalization in 30 dogs with naturally-occurring heatstroke with survivors (n=18) depicted in black and non-survivors depicted in gray. * depicts significant difference between survivors and non survivors. PT – prothrombin time, aPTT – activated thromboplastin time.
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