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Treatment options
Cooling - whole body cooling prior to admission is
highly recommended. The literature provides different cooling methods (e.g, cold enema, gastric lavage and
ice baths); however, other successful and perhaps more practical methods use evaporative cooling via whole body irrigation with tap water and placement of a fan facing the animal. Animals with thick undercoats may benefit from shaving prior to wetting. A cool environment with low humidity is also beneficial. Cooling with ice directly on body surfaces and/or peripheral blood vessels should be avoided as it may result in cutaneous vasoconstriction and decrease heat loss ability. During cooling, the patient’s temperature should be monitored every 5-15 minutes to avoid hypothermia. Cooling should be terminated when body temperature has reached 39.5oC (103oF). Cooling does not result in suppression
of the inflammatory response, but will prevent further cellular destruction. Most canine heatstroke victims
suffer from distributive shock, as described above. Although the absolute intravascular volume has not changed significantly, vasodilatation and venous pooling of blood lead to a relative hypovolemia. As the animal
is cooled, the vasomotor tone will return to normal. Therefore, judicious fluid therapy is warranted. An initial crystalloid dose of 10-20 ml/kg should be administered and perfusion parameters (HR, MM, CRT, pulse quality, blood pressure, mentation and urine output) continuously reassessed to help guide fluid additional fluid therapy. When perfusion cannot be restored with crystalloids alone, synthetic colloids (hydroxyethyl starch solutions), vasopressor agents (dopamine, vasopressin and norepinephrine) and positive inotropes (dobutamine) should be considered.
Dextrose should be administered to hypoglycemic
dogs as a single bolus (1ml/kg of diluted 50% dextrose not to exceed a maximum of 10 ml) followed by a 2.5- 5% dextrose CRI, with close monitoring of the glucose concentrations. All dogs with heatstroke should be given oxygen therapy during triage. Animals with severe dyspnea or laryngeal edema should be intubated, although this can decrease self-cooling mechanisms inherent with panting. In the most severe cases, general anesthesia with 100% oxygen or positive pressure ventilation may be required. Mannitol therapy may
be beneficial in animals with cerebral edema causing intracranial hypertension, although it can also worsen cerebral hemorrhage, if present. Mannitol administration has beneficial effects on the kidney and will help restore urine output and flush tubular casts out in animals with AKI.A suggested treatment regime might include 0.5-1 gm/kg of mannitol over 10-20 minutes after the initial fluid resuscitation, followed by 1-2 additional boluses over the ensuing 12 hours. Benzodiazepines (diazepam, midazolam) are administered as a bolus followed by a CRIif the animal seizures (about 33% of the cases). Other
causes for seizures such as hypoglycemia or metabolic and electrolyte imbalances should be ruled-out.
Antimicrobial treatment is not warranted in mild to moderate cases. In severe cases, broad spectrum antibiotics are indicated to treat sepsis due to presumed gastrointestinal bacterial translocation. A combination
of antimicrobials effective against gram positive, gram negative and anaerobic bacteria is recommended in severe cases utilizing the “escalation-de-escalation” method. A combination of a potentiated penicillin and
a fluoroquinolone or a third generation cephalosporin could be considered. Gastric protectants such as H2 blockers (e.g famotidine) or proton pump inhibitors (pantoprazole) should be administered to prevent further gastric damage. Antiemetics and promotility agents are essential for prevention of vomiting and consequent aspiration pneumonia. If urine output remains insufficient despite adequate fluid replacement and means arterial blood pressure is > 60 mmHg, medical therapy with furosemide and/or mannitol should be considered. Overhydration must be avoided in anuric/oliguric patients and fluid therapy adjusted based on urine output and intravascular volume status of the patient. Hemodialysis may be indicated in dogs with oligoanuria despite medical therapy, as well as those patients with severe overhydration, uremia or electrolyte derangements.
The treatment of the hemostatic abnormalities due to DIC is based on stabilization of the coagulation system with fresh frozen plasma and concurrent prevention
of thrombosis with anticoagulants. Hemofiltration has been suggested as an effective treatment modality in
an experimental model of severe canine heatstroke, causing early clearance of accumulated serum cytokines, creatinine and BUN. Clinical data is unavailable at this time.
Serial monitoring of the patient’s clinical and clinicopathological parameters is essential for early identification of complications and appropriate intervention. Continuous monitoring of vital signs, including temperature, femoral pulse rate and quality and capillary refill time to assess perfusion, hydration and shock status, is warranted. In addition, PCV/TS, serum glucose, coagulation profile (including TEG or ROTEM when available), CBC, lactate, blood gas (arterial or venous), arterial blood pressure, and urine output should be monitored. The mental status of the patient should be evaluated frequently and continuous ECG monitoring is recommended as arrhythmias may develop during the first 24 hrs after the heatstroke occurs.
Mortality rates in dogs suffering from severe heatstroke are reportedly between 40-50%. Animals with heat- induced illness have a reportedly lower mortality
rate (35%). At the author’s institution, mortality rates decreased to 40 and 43% in 2 recent studies (Bruchim et al. 2016, Cell stress chaperon, Segev et al. Veterinary
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