Heatstroke hub
Workflow for non-exertional and exertional heatstroke in dogs and cats. Cooling is the single most time-critical intervention; multi-organ complications are the most common cause of death.
- Stop active cooling at 39.4°C / 103°F. Continued cooling causes hypothermic overshoot, which is independently associated with worse outcomes. The thermometer goes in the rectum and stays there.
- Do not use ice or ice water. Causes peripheral vasoconstriction and traps heat centrally. Use cool tap water (room temperature) on the body, fans, alcohol on paw pads.
- The patient is not out of the woods at 39.4°C. Coagulopathy, AKI, GI translocation, and cerebral edema develop over the following 24–72 hours. Monitor aggressively.
- Hypoglycemia is common. Especially in hunting dogs and small breeds. Check BG on arrival and treat if < 60 mg/dL.
Recognition
Working dogs, hunting dogs, agility/sporting dogs in warm weather. Often relatively young, otherwise healthy. Onset during or shortly after exercise. Hypoglycemia common. Often more severe coagulopathy than non-exertional cases.
Confined patient: cars, closed rooms, sun exposure without shade, hair dryer / cage dryer mishaps. Brachycephalic breeds, obese patients, and patients with laryngeal paralysis are over-represented. Cats less commonly affected because of behavioral thermoregulation.
Diagnostic criteria
- Core body temperature ≥ 40.5°C / 105°F (often 41–43°C / 106–110°F at presentation)
- CNS dysfunction (obtundation, ataxia, seizures, coma) OR known heat exposure
- Multi-organ dysfunction in advanced cases: coagulopathy, AKI, hepatic injury, GI signs, cardiovascular collapse
A presentation temperature within reference range does not rule out heatstroke; cooling may have already occurred during transport. The history and clinical picture matter as much as the thermometer.
Treatment checklist
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1
Begin active cooling immediately
Wet the patient with cool tap water (not ice water); apply liberally to body, axillae, groin, paw pads. Place fans to maximize evaporative cooling. Alcohol on paw pads adds modest evaporative effect. Move to a cool environment.
Cooling rate target ~0.05–0.08°C/min (drop ~3°C in 30–45 min). Faster cooling than this risks overshoot and shivering.
Cold water IV fluids (refrigerated) are not standard. Use room-temperature crystalloids. Cold gastric or peritoneal lavage is sometimes described in case reports but is not first-line.
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2
Continuous rectal temperature monitoring
Rectal probe in continuously, ideally with display in line of sight. Stop active cooling at 39.4°C / 103°F. Dry the patient, remove fans. The temperature will continue to drift down for 15–30 minutes after active cooling stops.
Hypothermic overshoot below 37.2°C / 99°F warrants passive warming (blankets) but not active heating.
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3
IV access + initial fluid resuscitation
Place IV catheter as cooling begins (do not delay cooling for IV access). Balanced isotonic crystalloid. Avoid aggressive over-resuscitation; heatstroke patients are at risk for cerebral edema.
Open fluid therapy calculator →Initial bolus (dog): 10–20 mL/kg over 15–20 min, reassess Initial bolus (cat): 10–15 mL/kg over 15–20 min, reassess Maintenance: 2–4 mL/kg/hr after volume status restored -
4
Glucose check + correct hypoglycemia
Blood glucose on arrival. If < 60 mg/dL, give 50% dextrose 0.5–1 mL/kg IV diluted 1:4 with saline. Recheck in 15 min and add dextrose to maintenance fluids (2.5–5%) if persistent.
Open hypoglycemia hub → -
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Baseline diagnostics
Run on arrival, repeat at 6, 12, 24 hr, and as clinically indicated:
- PCV/TS: hemoconcentration on arrival, may drop later from coagulopathy or fluid resuscitation
- Lactate: marker of perfusion; normalize with resuscitation; persistent elevation = poor prognosis
- Glucose, electrolytes, BUN, creatinine: AKI develops over 24–48 hr
- PT/aPTT, platelet count: coagulopathy is the most common cause of death; check at admission and serially
- ALT, total bilirubin: hepatic injury common, peaks at 24–48 hr
- CK: rhabdomyolysis
- Continuous ECG: VPCs, AV blocks common
- Blood gas if available: metabolic acidosis with respiratory compensation typical
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6
Treat coagulopathy / DIC if present
DIC is the leading cause of death in heatstroke. Indicated by prolonged PT/aPTT, thrombocytopenia, schistocytes, or active bleeding (petechiae, melena, hematuria, hemoptysis). Initiate transfusion of fresh frozen plasma if active bleeding or PT/aPTT > 1.5× normal with clinical signs.
Open transfusion calculator →FFP dose: 10–20 mL/kg, may repeat q8–12 hr pRBC if PCV < 20%: Volume per transfusion calculator -
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GI protection
Bloody diarrhea, mucosal sloughing, and bacterial translocation are common as gut perfusion is restored. Empiric coverage may be appropriate.
Antiemetic: Maropitant 1 mg/kg IV q24h GI protectant: Pantoprazole 1 mg/kg IV q12–24h or omeprazole 1 mg/kg PO q12h once eating Empiric antibiotics: Ampicillin/sulbactam 22 mg/kg IV q8h ± enrofloxacin 10 mg/kg IV q24h if bloody diarrhea or sepsis evidence -
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Address cerebral edema if signs present
Persistent obtundation, deteriorating mentation, or seizures after cooling raise concern for cerebral edema. Indications for treatment include declining mentation despite normothermia and hemodynamic stability.
Mannitol: 0.5–1 g/kg IV slow over 15–20 min, may repeat q6h × 3 doses Hypertonic saline (alternative): 3–5 mL/kg of 7.2% over 5–10 min Head elevation: 15–30° to facilitate venous drainage Avoid mannitol if patient is anuric or volume-depleted. Check renal function and volume status first.
Seizure activity: treat with the status epilepticus protocol. Heatstroke + status carries a poor prognosis.
Open status epilepticus hub → -
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Monitor for arrhythmias
Continuous ECG for at least 24 hours. Ventricular premature complexes are most common; hemodynamically significant ventricular tachycardia warrants treatment with lidocaine 2 mg/kg IV bolus followed by CRI 25–80 µg/kg/min if needed. Avoid lidocaine in cats.
Open lidocaine CRI calculator → -
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What NOT to do
- Do not use ice baths or ice packs. Peripheral vasoconstriction traps heat centrally. Cool tap water + fans is more effective.
- Do not give corticosteroids prophylactically. No evidence of benefit; may worsen GI ulceration and immunosuppression.
- Do not give NSAIDs. Worsens AKI risk and GI ulceration in already compromised patient.
- Do not give heparin prophylactically. Evidence does not support routine use; may worsen bleeding in DIC.
- Do not over-resuscitate with fluids. Cerebral edema risk; titrate to perfusion endpoints rather than a fixed volume target.
- Do not stop monitoring at 24 hr. Coagulopathy, AKI, hepatic injury can manifest 48–72 hr post-event.
Prognosis
- Persistently low body temperature on arrival (already in hypothermic phase = worse)
- Hypoglycemia, hypocoagulability, or DIC at admission
- Persistent hyperlactatemia despite resuscitation
- Seizures, persistent obtundation, or coma
- Acute kidney injury with oliguria/anuria
- Time to active cooling > 90 min from event onset
Patients who survive the first 48 hours and avoid AKI generally have a good long-term outcome.
Sources
- Bruchim Y, Klement E, Saragusty J, et al. Heat stroke in dogs: a retrospective study of 54 cases (1999–2004) and analysis of risk factors for death. J Vet Intern Med 2006;20:38–46.
- Hall EJ, Carter AJ, Bradbury J, et al. Establishing risk factors for canine heat-related illness in UK dogs: a VetCompass study. Sci Rep 2020;10:9128.
- Drobatz KJ. Heatstroke. In: Silverstein DC, Hopper K, eds. Small Animal Critical Care Medicine, 3rd ed. Elsevier; 2023.
- Segev G, Daminet S, Meyer E, et al. Characterization of kidney damage using several renal biomarkers in dogs with naturally occurring heatstroke. Vet J 2015;206:231–235.