Sarah M. Collins, DAVN(Medical), RVN, CertSAN
A patient with heatstroke constitutes an emergency, and so must be seen and dealt with immediately as it is a life-threatening condition.
Heatstroke can be defined as an increased core body temperature (>40°C) caused by a marked increase in environmental temperatures. One of the most common examples is a dog which has been shut in a hot car. This is classed as non-exertional heatstroke and is due to environmental factors. Exertional heatstroke is a much rarer condition where the temperature increases due to over-exercise in warm, humid conditions.
In normal conditions, and without underlying disease, the body is able to maintain a normal (dog 38.3-38.7°C, cat 38.0-38.5°C) core temperature by thermoregulation: a thermostatic feedback mechanism which occurs in the hypothalamus balancing heat production and heat loss. Heat can be produced metabolically or gained from the environment. Heat loss occurs via evaporation, radiation, conduction and convection.
The body's first response to an increased temperature is vasodilation. Blood from organs and muscle is sent to peripheral areas such as the ears, face and feet which have less hair, where it is able to be lost by radiation and convection. If this does not decrease the core temperature then the body responds by increasing the respiratory rate and panting. As the animal pants, large amounts of air move across the tongue, oropharynx and trachea which results in heat loss as saliva evaporates from these mucosal surfaces.
In extreme environmental conditions these mechanisms are unable to maintain the heat gain/ heat loss balance and so core temperature increases. This creates an increase in tissue oxygen demand, and so in response the body increases its metabolic rate, a process which itself creates heat therefore adding to the problem. Unable to cool itself, the body's core temperature continues to rise until clinical signs of heatstroke are displayed.
The initial clinical signs seen with heatstroke include rapid panting, tachycardia, bounding pulses and dry mucous membranes. The longer the patient is exposed to hot, humid conditions, the worse the clinical signs become, and deterioration occurs rapidly. The patient will become dull and depressed with poor peripheral pulses and a marked respiratory effort. As the patient's condition worsens the mucous membranes become pale and respiration actually becomes shallower. In severe cases the patient will have a seizure or become comatose, and death usually follows.
It is therefore important to treat such patients quickly by removing them from the source and cooling them to prevent long-term organ damage.
The following main steps apply to most heatstroke patients:
1. Remove from source and move to cool environment.
2. Begin cooling using ice packs over major central vessels, e.g., jugular, femoral.
3. Place an intravenous catheter. Place extra ones if possible, especially in larger patients.
4. Administer cool fluids intravenously.
5. Place a urinary catheter.
6. Take blood samples.
The extent of cooling depends on the patient's condition on presentation. Gastric lavage with ice-cold water lowers core temperature without causing peripheral vasoconstriction, but can obviously only be performed on an unconscious patient. Instilling cold water into the urinary bladder and removing after approximately 10 minutes also has the same effect and has the advantage of allowing measurement and monitoring of urinary output at the same time--an important parameter for assessing renal function which is likely to become impaired in this condition. Other methods of cooling include the use of fans, cool intravenous fluids and cold water enemas. It is extremely important not to cause peripheral vasoconstriction as this will inhibit heat dissipation from organs and muscle.
Cooling methods should be stopped when the rectal temperature reaches 39-40°C as further decrease will cause shivering and heat production.
Patients having a seizure should receive diazepam or, if this does not stabilise the patient, general anaesthesia should be considered to stop seizure activity, maintain a patent airway and to allow cooling methods to be instigated.
A major complication seen with heatstroke is disseminated intravascular coagulation (DIC). This is caused by thermal damage to endothelial cells and cell necrosis. Clinical signs of DIC include petechial haemorrhages; it is treated by administering fresh plasma to provide coagulation factors.
Nursing of the heatstroke patient is very demanding in both time and effort and the outcome very much depends on the condition of the patient on presentation and the complications which may arise.