The continuum of heat injury begins with heat stress with minimal heat cramp, then heat exhaustion, then heat stroke.
Clinical signs worsen down the continuum and there is no specific time period defining one level from the next. Rather the severity of clinical signs dictates the definition culminating in heat stress, which is “hyperthermia associated with a systemic inflammatory response leading to a syndrome of multiorgan dysfunction in which encephalopathy predominates”.
Thermal homeostasis is regulated by the hypothalamus. When the body senses that it is too cold, it triggers the appropriate of vasoconstriction and shivering. Conversely, when the body is too hot, it enacts heat dissipating mechanisms.
The primary form of heat dissipation in dogs and cats is via EVAPORATION where heat is dissipated via water molecules from the patient, usually via panting and very, very minimally sweat glands on their feet. Radiation and convection follow evaporation in quantity of heat dissipated. Radiation is the loss of heat via conversion to electromagnetic energy. Convection is the dissipation of heat by air flow. Conduction is heat transfer via direct contact.
When patients become too hot, they rely on three mechanisms to help them thermoregulate. First, thermoregulation from the anterior hypothalamus. Secondly, there is an acute-phase response that releases pro- and anti-inflammatory cytokines that help regulate cellular metabolism. Finally, there is the production of intracellular heat shock proteins, which help protect intracellular proteins and help regulate baroreceptors to prevent excessive vasodilation. The really amazing thing about heat shock proteins is that as a dog becomes more acclimated, these proteins are upregulated in production providing more of a buffer to protecting important structures within the cells. However, as heat exposures continue, the pet becomes unable to compensate any further and these regulatory mechanisms fail to work.
RISK FACTORS:
First, we can look at those with environmental risk factors. Pets kept in hot, humid environments without air circulation are at high risk. Additional places near high radiation or convection release (such as airstrips, parking lots) can also expose pets to high temperatures even if the ambient temperature is not very high. Patients kept in small, not well-ventilated kennels or muzzles are also at high risk for heat stress as they are unable to dissipate enough heat.
Exertional risk factors mainly include working dogs that are not properly acclimated with training. These include military or police working dogs, greyhound racing dogs, hunting dogs, or trail dogs. Their risk is exacerbated by overwork and a lack of appropriate rest opportunities.
Other risk factors include patients with pre-existing conditions such brachycephalic breeds, upper airway disease, obesity, are geriatric, have thick or double hair coats, or have concurrent medical conditions predisposing them to increased risk (i.e., cardiac, respiratory, some endocrinopathies, renal disease).
It is important to note that the risk exponentially increases if there are multiple risk factors involved quickly escalating from potential heat stress exposure to fulminant heat stroke.
PREVENTION:
Is the key to heat stress. Advise your clients to HYDRATE their pets/charges. Cool, fresh water should be available at all times and adequate time to access this water should be provided. A cool, shaded, well-ventilated area should be easily accessible. Another important component is recognize is acclimating dogs to their environments. If an owner has recently moved to a new region or area or if the dog has been assigned a specific task or job, there should be a period of time appropriate to slowly introduce the animal to the conditions they will be in consistently.
PRESENTATION:
At triage, the patient may be hyperthermic, normothermic, or hypothermic depending on how far away from the heat insult they are in and what phase of (de)compensation they are in. Pulse rate is usually increased, with a weak quality and there may be pulse deficits. Respiratory rate is usually increased and patients have hyperemic, injected mucous membranes with a shortened capillary refill time. The mentation of these patients can vary significantly ranging from bright and alert to stuporous or even comatose.
PHYSICAL EXAMINATION:
Cardiovascularly, these patients often present with a sinus tachycardia; however, many also have an intermittent ventricular arrhythmia. It is important to do an initial ECG and intermittently monitor heart rate and rhythm to identify progressive arrhythmias that should be treated with lidocaine or other anti-arrhythmic agents. Because of the attempt to dissipate as much heat as possible, these patients are also systemically vasodilated and hypovolemic, which leads to hypotension that should be treated with aggressive fluid therapy but may still require pressor support.
Some of these patients may have pre-existing upper airway disease, which can worsen respiratory signs. Depending on the severity of their heat injury they may develop pulmonary edema or hemorrhage secondary to seizures or disseminated intravascular coagulation (DIC), or they may have vomited during the heat stroke and could have aspiration pneumonia. Listen closely at the initial exam and make sure to continue monitoring throughout resuscitation and recovery.
Depending on the severity of the heat injury, the central nervous system may be affected, manifesting initially as ataxia or head bobbing, possible abnormal mentation, and can progress to seizures or coma. It is important to check a glucose as a cause for these signs as many patients also have loss of glucose regulation during heat injury.
You may also see petechia or ecchymoses as platelets are consumed or become dysfunctional leading to thrombocytopenia and -pathia. As the shock organ of the dog is the GI tract, the patient may have melena or hematochezia as perfusion is shifted away from the GI system. Muscle breakdown and hypoperfusion can lead to pigmenturia from myoglobinuria although this usually occurs as you are resuscitating the patient. Vomiting and/or diarrhea may have been noted by the owner as well.
DIAGNOSTICS:
On CBC, the patient is likely to be hemoconcentrated from dehydration with nucleated red blood cells that were prematurely released from the bone marrow. They may have an inflammatory leukogram or a left shift and a thrombocytopenia is usually present. On chemistry, there is likely to be hypoalbuminemia (or hypoproteinemia depending on the severity of the diarrhea), increased ALT, AST, and CK from muscle damage, hypoglycemia as glucose stores are used up and azotemia from pre-renal and potentially renal causes. One may also note a hypocalcemia associated with the severity of the injury. Coagulation times are also likely to be prolonged with clotting factors being consumed.
Don’t forget to get your point of care diagnostics like lactate, ECG, blood gases, blood pressure, etc. as well.
IMMEDIATE TREATMENTS:
Active cooling should be initiated if the patient’s temperature is >105 Fahrenheit. Remember that we do not want to cool the patient below 104 as the body will continue to cool on its own. Severe brain damage will occur at temperatures >108. To actively cool your patient, go back to your four modes of heat loss:
| Mode of Heat loss | Modifications to increase heat loss |
| Conduction | Cool bedding / surfaces, application of cool water / ice, cool water baths, intravenous fluids, cold water enemas / gastric lavage |
| Convection | Air conditioning, cooling fans, open windows during transport |
| Radiation | Shade, access to outdoors if cooler, cool ambient environment, air conditioned area |
| Evaporation | Sprayers, soakers, misters, gaining patent airway, ice in O2 mask – REDUCING HUMIDITY |
Remember that IV fluids do not need to be chilled as they have been hanging out at room temperature, which is likely to be lower than the patient’s. Your patient may require fresh frozen plasma to help replace lost clotting factors, help maintain oncotic support, and restore perfusion. Additionally, blood pressure medications may be required to help maintain blood pressure while you volume resuscitate your patient.
BE CAUTIOUS OF…
- Hypothermia: due to hypothalamic dysregulation, the patient may not yet be able to regulate their own body temp and may oscillate between hyper- and hypothermia. Remember to monitor it often.
- Ongoing losses: it is so easy to get behind in these patients as they usually come in profoundly dehydrated and hypovolemic with profuse diarrhea. Remember to weigh your patient often, track losses, and measure PCV/TP regularly.
- Acute kidney injury: as stated before, these patients can develop myoglobinuria from muscle breakdown. The myoglobin can cause tubular damage to the kidneys. So it is important to keep up with fluid therapy and monitor urine production and character.
- Perfusion: just because you caught up once doesn’t mean you will stay caught up. Go back and recheck perfusion regularly to make sure that you are not only normovolemic but distributing that volume appropriately.
- Muscle cramping! The ischemic injury to the muscles can significantly impact muscle contraction and range of motion. Massage limbs to help restore blood flow to these areas and improve mobility.
ONGOING SUPPORTIVE CARE
- Continue IV fluids and monitor ins and outs closely
- Early nutrition is vital in helping to restore gut motility and allowing for tissue repair
- Pain medication to aid in pain associated with gut sloughing, thermal burns, etc.
- Oncotic support. Remember large volumes of diarrhea leads to loss of proteins which can predispose your patient to vasculitis and edema.
- Antibiotics if evidence of bacterial translocation or neutropenic
- Thermal monitoring
- NO NSAIDs
- until platelets recover and you have achieved normovolemia and perfusion
There are many negative potential prognostic indicators that are associated with heatstroke. And the more you have, the worse it can be. But remember, some dogs have all of them and they make it so it’s not impossible.
- Hypoglycemia
- Hypocholesterolemia
- Hyperbilirubinemia
- Hypoalbuminemia
- Increased creatinine
- Ventricular arrhythmias
- Secondary hemostatic coagulopathy
- DIC
- Seizures
- Increased nRBCs
- Delay from onset to treatment
- Obesity
Remember that owner awareness is the key to PREVENTING heat injury, which is the best treatment. Educate owners early and often. Advocate on social media platforms and throughout your clinic.
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