Heat Stroke in pets
Dogs and cats get rid of their heat in two main fashions, through panting and through convection (air flow over their skin). As core temperature increases they pant more and vasodilate their peripheral vessels to increase heat loss. Any upper airway disease that prevents effective air exchange from the lungs, and any disease/condition that blocks heat loss through the skin, pre-disposes animals to heat stroke (brachycephalics, obesity, heart disease, collapsing trachea, thick hair coat, etc).
As core temperature increases further so much blood is shunted to the peripheral vessels the perfusion of major organs decreases and damage occurs. This leads to other protective mechanisms (acute phase response and heat shock proteins), but when they are overwhelmed the result is a severe systemic inflammatory response throughout the body. This results in shock, SIRS, MODS, permeability of the GI which adds in endotoxin stress, and eventually DIC.
History: Outside in warm weather +/- excessive exercise, humid weather, being trapped in a car/small room with windows and no airflow, upper airway disease, chronic heart disease, etc.
- Shock; usually tachycardia, weak pulse, depending on the time-frame fast or prolonged crt, +/- arrhythmias
- depressed, weak, possibly comatose. Usually will have intact PLRs but can be cortically blind with pupils dilated or pinpoint, signs of cerebral edema may be present
- Gastrointestinal System:
- vomiting and diarrhea and usually with HGE. Gastric ulceration likely.
- Respiratory System:
- Check for signs of upper airway obstruction, intubate if necessary, aspiration pneumonia often occurs, and if DIC present then pulmonary hemorrhage may be present and crackles/harsh sounds may be heard.
- important to monitor urine production with fluid therapy to ensure anuric renal failure not present, ideally place a u-cath.
- A diagnosis of heat stroke can be usually be made based on a history, however initial bloodwork should be performed including:
- Glucose (may be low due to sepsis and require supplementing)
- Coagulation Factors (APTT and PT)
- Urinalysis (preferable urine obtained prior to starting fluids to assess for renal damage)
- Biochemistry including CK, BUN, Electrolytes
- Haematology and smear (looking for RBCs, nucleated RBCs, shistocytes, and platelet numbers)
- COOLING: This needs to be started ASAP and is recommended to advise owners to begin at home. Cool to cold water is recommended as well as fans to remove the heat. Have owners dump water over the animal and blow fans, and have A/C on in the car.
- DO NOT USE ICE-WATER OR PLACE ICE-PACKS ON THESE ANIMALS- this will result in vasoconstriction of the peripheral vasculature and paradoxically prevent cooling.
- Stop cooling when temperature reaches 39.5 C or excessive cooling may occur.
- FLUIDS: These patients often present in hypovolemic shock. If no known or no suspicion of heart disease, give boluses of 25mL/kg dog, 15mL/kg cat over 10-15min, then re-assess parameters.
- If crystalloids cannot establish a maintainable blood pressure consider colloids or vasporessors (Dobutamine, Dopamine, Epinephrine).
- These animals carry a poor prognosis
- OXYGEN: Continuous oxygen support and monitoring of respiration is required as pulmonary function can become impair. Monitor SPO2 and blood gases if you have them and supplement oxygen or respiration (intubation and ventilation) as required.
- ELECTROLYTES/GLUCOSE: Monitoring of these values and correction as indicated is required. Hypoglycemia is not unsual and IV bolus of 0.25-0.5g/kg dextrose should be administered (make fluids to a 2.5% or 5% solution after initial shock boluses are complete).
- MENTATION: If mentation still abnormal after fluid resuscitation then cerebral edema may be present. Avoid jugular compression (neck leads, pressure), elevated head (15-30 degrees on a slope), and Mannitol 0.5-1g/kg over 20min should be considered.
- URINE: urinary catheter should be placed and urine output monitored, should be >2mL/kg/hr
- COAGULATION: APTT and PT should be measured and monitored (or ACT if PT/APTT not available), as well as platelet count. Elevated APTT/PT/ACT and decreasing platelets are indicative of DIC. Consider Plasma transfusion if APTT/PT are prolonged.
- GASTRO: Severe compromise to the GI system will likely be present. Start on gastro-protectants (omeprazole, sucralfate if able to have medications PO), antibiotics (Metronidazole, Amoxicillin), and monitor for development of intussusception.
- This is a spectrum disease, the worse the presentation initially the worse the prognosis. Those patients with evidence of MODS or SIRS or DIC have a guarded prognosis, along with animals displaying severe neurological signs.
- Aggressive and prompt treatment is the best chance of success, and the main two components are COOLING and FLUIDS! Always begin this before transfer to another clinic.
- Earlier commencement of treatment results in a much better prognosis, if owners call unsure about whether or not to have their animal seen, recommend strongly veterinary care immediately. Delayed admission > 90min is associated with decreased prognosis.
- Signs of worse prognosis: coma on presentation or decline of neurological status despite therapy, hypothermia on presentation, persistent or worsening hypoglycemia/hypotension/hypoproteinemia/azotemia, evidence of DIC, VPCs, labored breathing/pulmonary edema, prolonged clotting times on presentation
- Overall 50% survival rate in general.
1.Small Animal Critical Care Medicine, Silverstein and Hopper, 2009
2.Heat stroke in dogs: A retrospective study of 54 cases (1999-2004) and analysis of risk factors for death, J Vet Intern Med. 2006 Jan-Feb;20(1):38-46. Yaron Bruchim, Eyal Klement, Joseph Saragusty, Efrat Finkeilstein, Philip Kass, Itamar Aroch School of Veterinary Medicine, The Hebrew University of Jerusalem, Israel.
3.Heatstroke In Dogs: Clinical Signs, Treatment, Prognosis, and Prevention Compend Contin Educ Pract Vet. June 2003;25(6):422-431. 30 Refs W. Shannon Flournoy, Douglass K. Macintire, James S. Wohl Auburn University