Heat-related illness / Heatstroke

Care Pathway

1. Planning & Triage

Receptionist Telephone Triage

  • Prioritise as an Emergency: Advise the owner that this is a veterinary emergency requiring immediate examination
  • Advise Pre-Hospital Cooling: Instruct the owner to start cooling the pet immediately, as this significantly improves survival
    • Wet the pet thoroughly with cool (not ice-cold) water from a shower, hose or bucket
    • During transport, maximise airflow using a fan, car air conditioning or by opening windows
  • Critical "What Not To Do" Advice: Instruct the owner NOT to cover the pet with wet towels, as this traps heat and prevents evaporative cooling
  • Manage Expectations: Inform the owner that the prognosis is guarded and depends on how quickly treatment is initiated

In-Clinic Triage & Initial Plan

Core Triage Principle

Heatstroke is a multi-organ syndrome driven by hyperthermia. The primary goals are to rapidly but controllably reduce core body temperature while simultaneously treating for shock, CNS dysfunction and impending organ failure.

Prepare for Arrival

  • Prepare a cooling station: move the patient to a cool, well-ventilated area with access to running water and fans
  • Gather equipment for aggressive fluid resuscitation (i/v catheters, fluids, pump, lines)
  • Ready bedside diagnostics (thermometer, ECG, BP monitor, glucometer, lactate meter)
  • Prepare for oxygen supplementation
  • Ensure emergency seizure-control drugs are accessible
  • Consider the VetCompass Clinical Grading Tool for dogs

Immediate Triage Actions

  • Move the patient directly to the prepared cooling area
  • Immediately begin active cooling measures while performing other assessments
  • Perform a rapid ABC assessment, focusing on neurological and cardiovascular status
  • Start continuous rectal temperature monitoring
  • Secure intravenous (i/v) access and start shock-rate fluid resuscitation
  • Run initial bedside diagnostics: PCV/TS, blood glucose, lactate

2. Presentation & Risk Factors

Causes & Risk Factors

  • Exertional: Excessive strenuous exercise without acclimatisation
  • Environmental: Confinement in hot, humid environments with poor ventilation (e.g., cars, conservatories)
  • Endogenous Factors: Brachycephalic breeds, obesity, thick/dark coat, cardiovascular or laryngeal disease
  • Over-represented Breeds: Labrador, Golden Retriever, Chow Chow, Bulldog, French Bulldog, Greyhound, English Springer Spaniel, Cavalier King Charles Spaniel, English Bull Terrier, Weimeraner, Newfoundland, Pomeranian, Pug and Staffordshire Bull Terrier

Key Clinical Features

Hallmark: Core temperature >40-41°C (104.0-105.8°F) with central nervous system dysfunction and varying degrees of organ dysfunction

  • Patient may be normothermic or even hypothermic on presentation due to owner cooling or advanced shock
  • Shock: Hypotension, tachycardia and inadequate organ perfusion
  • Mucous Membranes: Often brick red (hyperaemic)
  • Cardiopulmonary: Arrhythmia, pulmonary oedema, multifocal necrotising pneumonia
  • CNS: Ataxia, altered mentation, stupor or seizures
  • Gastrointestinal: Haematemesis, haematochezia
CRITICAL SAFETY NOTE: Heatstroke can rapidly progress to acute kidney injury (AKI), DIC, systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS). Death is usually due to haemodynamic deterioration and pulmonary lesions

3. Diagnostics

Diagnostic Approach

  • Primary Diagnosis: Based on history of exposure/exertion and compatible clinical signs
  • Do NOT rely on body temperature alone, as pre-hospital cooling or shock can normalise it
  • Supportive Findings: Presence of nucleated RBCs, high CK or botryoid neutrophils may aid diagnosis in cases with a vague history
First-line Investigations

Haematology & Biochemistry

  • Haematology: Nucleated RBCs, raised PCV (haemoconcentration), thrombocytopenia
  • Blood Smear: Schistocytes (suggests DIC), botryoid neutrophils
  • Biochemistry: Azotaemia (pre-renal or renal), marked increase in CK (rhabdomyolysis) and hepatic enzymes (ALT/AST)
  • Glucose: Hypoglycaemia is a common finding
  • Electrolytes: Variable; hyperkalaemia, hypernatraemia, hyponatraemia, hypophosphataemia and hypocalcaemia can occur

Coagulation, Blood Gas & Urinalysis

  • Coagulation: Indicated in all patients. Prolonged PT/aPTT and thrombocytopenia are hallmarks of DIC; perform sequential monitoring
  • Blood Gas Analysis: Metabolic acidosis with a compensatory respiratory alkalosis is typical
  • Lactate: Often elevated due to hypoperfusion
  • Urinalysis: Myoglobinuria, bilirubinuria, glucosuria, casts, proteinuria
Investigations to Consider
  • ECG: Recommended if an arrhythmia is suspected or detected
  • Serum cardiac troponin I: Can be markedly elevated with severe myocardial damage
  • Thoracic radiography: Recommended in any patient with cardiopulmonary dysfunction
Differential Diagnosis for Collapse & Hyperthermia

Toxins & Seizure Activity

  • Toxins: Metaldehyde ('shake and bake'), mycotoxins, illicit drugs (amphetamines)
  • Primary Seizure Disorder: Status epilepticus causing secondary hyperthermia
  • Meningitis/Encephalitis

Metabolic & Systemic Disease

  • Sepsis: Pyrexia from severe infection
  • Immune-mediated disease: e.g., steroid-responsive meningitis-arteritis (SRMA)
  • Metabolic: Diabetic ketoacidosis, hyperthyroidism (rare in dogs)
  • Neoplasia

4. Treatment Protocol

Immediate Active Cooling

  • Goal: Reduce core body temperature to 39.5°C (103.1°F) and then cease active cooling to prevent rebound hypothermia
  • Monitor temperature every 10 minutes during cooling
  • Recommended Methods:
    • Douse the patient with cool (not ice-cold) running water from a hose or shower
    • Use fans to promote evaporative cooling (apply ocular lubricant)
    • Place cold packs on large vessels (axilla, groin, jugular)
    • Place patient on a cool surface in a large, well-ventilated area
CRITICAL SAFETY NOTE: AVOID placing wet towels over the patient (traps heat), using ice-cold water (causes vasoconstriction), placing the patient in a small cage (prevents heat radiation) or using antipyretics like NSAIDs (risk of AKI)
Symptomatic & Supportive Care

Fluid & Oxygen Therapy

  • Fluid Resuscitation: Correct distributive shock with i/v buffered isotonic crystalloid boluses (15–20 ml/kg over 15–30 mins)
  • Reassess perfusion parameters after each bolus; avoid overhydration
  • Early fluid therapy is crucial to protect against AKI
  • Oxygen Therapy: Provide to any hypoxaemic patient
  • AVOID oxygen hoods or cages in hyperthermic patients as they trap heat

Haemodynamic & GI Support

  • Vasopressors: Indicated if patient remains hypotensive despite adequate fluid resuscitation (e.g., noradrenaline CRI)
  • Blood Products: Consider FFP for coagulopathy/DIC or fresh whole blood if also anaemic
  • Gastroprotectants: Use proton pump inhibitors (e.g., omeprazole) for evidence of GI bleeding
  • Anti-emetics: Use maropitant or ondansetron if vomiting or nausea is present

Seizure Control

  • First-line: Benzodiazepines (Diazepam or Midazolam)
  • Second-line: Use one or more of phenobarbitone or levetiracetam
  • A propofol CRI may be necessary if refractory to second-line therapies
  • Repeated neurological examinations are essential

Hypoglycaemia Management

  • Indication: Treat if blood glucose is <3.3 mmol/l
  • Give 1 ml/kg of 50% dextrose as an i/v bolus over 10 minutes
  • Dilute 1:4 with crystalloids before administration
  • Follow with a 2.5–5% dextrose CRI
  • Monitor blood glucose closely

Antibiotic Therapy

  • Indication: Consider if neutropenic or sepsis is suspected
  • Rationale: Decreased GI blood flow may increase intestinal permeability, risking bacterial translocation
  • Protocol: Start with broad-spectrum cover, e.g., Co-amoxiclav + Marbofloxacin

Analgesia

  • Abdominal pain may be present due to gastrointestinal disease
  • Opioids: e.g., Methadone boluses
  • CRI Options: Fentanyl, Ketamine or Lidocaine may be considered
  • AVOID NSAIDs until patient is haemodynamically stable and renal function is confirmed normal

Contextualised Care: Managing Cerebral Oedema

  • Indication: Use mannitol for patients with neurological signs of cerebral oedema
  • Trigger: Recommended if Modified Glasgow Coma Scale < 8 or if neurological status is rapidly deteriorating
  • Dose: 0.5–1 g/kg i/v over 15–20 minutes
  • CRITICAL: Patient must be fully volume resuscitated before mannitol administration to prevent precipitating AKI

5. Monitoring & Complications

Key Monitoring Parameters

  • Temperature: Every 10 minutes during active cooling, then q1-2h to detect rebound hyperthermia or hypothermia
  • Cardiovascular: ECG, blood pressure, heart rate, pulse quality
  • Neurological Status: Mentation, Modified Glasgow Coma Scale
  • Renal: Urine output, serial BUN/creatinine
  • Coagulation: PT/aPTT, platelet count, monitoring for clinical bleeding
  • Lactate: Serial monitoring advised to assess perfusion

Potential Complications

  • Disseminated intravascular coagulation (DIC)
  • Acute kidney injury (AKI)
  • Systemic inflammatory response syndrome (SIRS)
  • Multiple organ dysfunction syndrome (MODS)
  • Acute respiratory distress syndrome (ARDS)
  • Rhabdomyolysis and secondary myoglobinuria
  • Neurological damage (cerebral oedema, haemorrhage)

6. Nursing Care

Key Nursing Considerations

Active Cooling Management
  • Monitor rectal temperature every 5-10 minutes during active cooling
  • Cease all active cooling measures when temperature reaches 39.5°C (103.1°F) to prevent iatrogenic hypothermia
  • Use a combination of cool (not cold) running water and fans to maximise evaporative heat loss
Intensive Monitoring
  • Frequently assess and record all vital signs: HR, RR, pulse quality, CRT, mucous membrane colour and mentation
  • Report any deterioration, particularly in neurological status or perfusion, immediately
  • Continuously monitor ECG for arrhythmias
  • Monitor blood pressure to guide fluid therapy and vasopressor use
Catheter & Fluid Care
  • Ensure i/v catheter is secure, patent and free from contamination
  • Check the leg regularly for any signs of swelling, pain or phlebitis
  • Administer fluid therapy as prescribed via an infusion pump, monitoring closely for signs of fluid overload (increased RR, chemosis, crackles on auscultation)
Neurological Support
  • Nurse in a quiet, dimly lit and low-stress environment to minimise cerebral activity
  • Monitor for seizure activity; have emergency seizure protocol ready
  • Elevate the head 15-30 degrees if cerebral oedema is suspected, ensuring there is no pressure on the jugular veins
Recumbency & Hygiene
  • Turn recumbent patients every 4 hours to prevent decubitus ulcers and atelectasis
  • Provide thick, padded, non-retentive bedding
  • Perform meticulous patient hygiene, cleaning and drying immediately after any urination or diarrhoea to prevent skin scald
Monitoring for Complications
  • Be vigilant for early signs of DIC, such as petechiae, ecchymoses or bleeding from catheter sites
  • Monitor urine output closely to detect early signs of Acute Kidney Injury (AKI)
  • Observe for gastrointestinal signs like haematemesis or haematochezia

7. Prognosis

2–57% Reported Mortality Rate
3 days Median Hospital Stay
  • Prognosis is guarded and depends on severity and speed of treatment
  • The fatality rate using the VetCompass Grading Tool reported as: 2.21% for MILD events, 5.46% for MODERATE events and 56.76% for SEVERE events
  • Most deaths occur within the first 24 hours
  • Patients that survive the first 48 hours have a good chance of long-term survival
  • Negative Prognostic Indicators: Brachycephalic conformation, age >12 years, neurological signs on admission, presence of DIC or AKI and delay in receiving veterinary treatment
  • Patients are at risk for DIC and organ failure for up to 5-7 days after the initial event

8. Drug Dose Tables

Drug Class / Use Drug Dose Notes
Seizure Control Diazepam 0.5–1 mg/kg i/v or per rectum
  • First-line agent for active seizures
  • Give as bolus q10 mins up to 3 times
Midazolam 0.2–0.3 mg/kg i/v, i/m or i/n
CRI: 0.3 mg/kg/h
  • First-line agent, suitable for CRI
  • Give as bolus q10 mins up to 3 times
Cerebral Oedema Mannitol 0.5–1 g/kg i/v over 15-20 mins
  • For neurological signs unresponsive to initial therapy
  • Ensure patient is rehydrated first
Metabolic Support Dextrose 50% 1 ml/kg i/v bolus (diluted 1:4)
  • For blood glucose <3.3 mmol/L
  • Follow with 2.5–5% CRI
  • Monitor glucose closely
Antiarrhythmic Lidocaine 2 mg/kg i/v bolus, repeat up to 8 mg/kg total
CRI: 0.025–0.1 mg/kg/min
  • For sustained or compromising ventricular arrhythmias
  • Rule out electrolyte abnormalities first
Vasopressors Noradrenaline 0.1–2 µg/kg/min CRI
  • First-line vasopressor for refractory hypotension
Adrenaline 0.05–1 µg/kg/min CRI
  • Second-line agent
Vasopressin 0.5–5 mU/kg/min CRI
  • Second-line agent
GI Support Omeprazole 1 mg/kg i/v or p/o q12h
  • Proton pump inhibitor for GI bleeding
Maropitant 1 mg/kg i/v or s/c q24h
  • Anti-emetic
Ondansetron 0.5 mg/kg i/v or p/o q12h
  • Anti-emetic
Metoclopramide 1–2 mg/kg/day CRI
  • Anti-emetic with prokinetic effects
Antibiotics Co-amoxiclav 8.75–25 mg/kg i/v q8h
  • For broad-spectrum cover if sepsis is suspected
Marbofloxacin 2 mg/kg i/v q24h
  • Combine with co-amoxiclav for broad-spectrum cover

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