38 Heatstroke
A spectrum of severity is seen in dogs suffering from heat-induced illness in terms of both pathophysiological derangements and clinical consequences. It may therefore be more accurate to employ a gradation of severity from heat stress to heat exhaustion to heatstroke. Nevertheless, the general term ‘heatstroke’ will be used here.
Heatstroke results from severe hyperthermia, although a specific threshold above which heatstroke occurs has not been defined in dogs. Cellular injury may occur above 41°C and permanent brain damage is reportedly possible. Enzyme dysfunction, protein denaturation and severe organ damage may occur above 43°C and are associated with a significant increase in mortality. Further information regarding the prognosis in dogs with heatstroke is provided in Box 38.1.
BOX 38.1 Prognostic considerations in dogs with heatstroke
The prognosis in heatstroke depends on a number of factors including:
Unfavourable prognostic indicators include:
In fatal cases, death usually occurs within 24 hours. Death is unlikely to occur in patients surviving more than 48 hours.
Heatstroke occurs when heat gain markedly exceeds heat loss and this is predominantly due to the cooling mechanisms stimulated by the hypothalamus becoming overwhelmed. These mechanisms include:
Heatstroke may occur more readily in dogs suffering from a lack of acclimatization to warmer weather. The acute phase response and heat shock proteins may also be involved in the pathogenesis of heatstroke.
A variety of predisposing factors exist that may be classified as endogenous or exogenous. Most of these factors impair heat loss and include:
Some factors affect heat gain, for example exercise, pyrexia, and especially external ambient temperature. Measures designed to try to prevent heatstroke are summarized in Box 38.2.
BOX 38.2 Preventative measures for heatstroke in dogs
Heatstroke can be avoided in the majority of cases if appropriate preventative measures are employed. Preventative measures are especially important in dogs predisposed to heatstroke (e.g. brachycephalic breeds, dogs with laryngeal dysfunction, obese dogs) and include:
Heatstroke may be divided into two types. Classic heatstroke occurs due to exposure to high environmental temperature, for example being locked in a car with shut windows on a warm day, or being tied up outside without shade/water. Exertional heatstroke is the result of strenuous exercise. Many pathophysiological derangements are possible in heatstroke due to both direct heat-induced cytotoxicity and acute physiological changes due to hyperthermia. These are summarized in Box 38.3. Multiple organ dysfunction syndrome (MODS) (Box 38.4) is the most serious potential sequela of heatstroke.
Nursing Aspect
On an emergency basis, nurses are often the first members of staff to speak to owners ringing about dogs with suspected heatstroke. While telephone diagnosis is generally to be avoided, the history in these cases is often very suggestive and early intervention can be crucial to a positive outcome. Advice includes:
The possible effect of cooling measures implemented by the owner prior to presentation must be borne in mind as some dogs with heatstroke may be normothermic at presentation as a result.
Presenting Signs and Case History
A 2-year-old male neutered Newfoundland dog presented collapsed in the mid-afternoon on a warm summer’s day. The dog had been out for a relatively long period of exercise in the middle of the day and had started to pant excessively on the way home. On returning home he had drunk a large volume of water, vomited a short while after, and then collapsed. Following a telephone conversation with the practice, the dog had been hosed down with cool water and then driven immediately to the practice with the air conditioning on maximum in the car. No other significant preceding history was reported.
On presentation the dog was recumbent, markedly depressed and panting excessively. Cardiovascular examination revealed a heart rate of 160 beats per minute but it was very difficult to hear the heart sounds clearly due to the panting. Dorsal pedal pulses could not be palpated and femoral pulses were weak; pulse deficits were suspected. Mucous membranes were markedly hyperaemic with a rapid capillary refill time. Rectal temperature was 41.8°C and digital rectal examination revealed fresh blood. Pupillary light reflexes (direct and consensual) and menace responses were intact bilaterally.
Clinical Tip
The clinical findings in this case are relatively typical for dogs presenting with heatstroke. However, clinical findings depend on factors such as the severity and duration of hyperthermia, cooling measures performed prior to presentation, and the delay in presentation. As such a variety of clinical findings are possible.
The dog was assessed as suffering from severe hyperthermia due to heatstroke with evidence of cardiovascular, intestinal and possible neurological compromise. Given that cooling measures had already been started, it was suspected that rectal temperature would have been higher prior to presentation.
A short large bore intravenous catheter was placed in each cephalic vein and blood obtained via one of the catheters for an emergency database. This revealed haemoconcentration (manual packed cell volume 64%, reference range 37–55%; serum total solids 90 g/l, reference range 49–71 g/l), hypoglycaemia (blood glucose 2.0 mmol/l, reference range 3.3–6.1 mmol/l) and mildly raised blood urea nitrogen concentration (13.0 mmol/l, reference range 2.5–8.9 mmol/l). Blood smear examination at initial presentation was unremarkable.
Flow-by oxygen supplementation was provided and intravenous volume resuscitation was commenced using an isotonic replacement crystalloid solution. Hartmann’s solution (buffered lactated Ringer’s solution) was administered into each cephalic vein (total 40 ml/kg bolus) using pressure infusors (see Figure 4.1) and glucose supplementation (0.5 g/kg slow i.v. diluted) provided. The dog was soaked in cool water and multiple fans applied. Electrocardiography was performed and revealed predominantly sinus rhythm with intermittent ventricular premature complexes (VPCs) (see Figure 12.4).
The dog’s cardiovascular status and mentation showed satisfactory improvement on this initial management. A further 15 ml/kg bolus of Hartmann’s was administered and as the dog continued to pant excessively, butorphanol (0.2 mg/kg i.v.) was administered with good effect. Cooling measures were discontinued when the rectal temperature reached 39.5°C to avoid rebound hypothermia (see Ch. 16). The dog was maintained on intravenous fluid therapy with glucose supplementation (2.5% glucose/Hartmann’s solution) and blood glucose monitored intermittently. Continuous electrocardiographic monitoring was performed but no antidysrhythmic therapy was indicated. Free catch urinalysis revealed moderate proteinuria, marked haemoglobinuria, no detectable glucosuria and an absence of urinary casts.
The dog remained clinically stable but developed widespread petechiation (see Ch. 21). Repeat peripheral blood smear examination performed several hours after presentation revealed marked thrombocytopenia, an increase in nucleated red blood cells and a mild subjective neutrophilia with some toxic change (see Ch. 3). Given the concerns regarding coagulopathy, and the lack of both a coagulation analyser and access to fresh frozen plasma (FFP), it was decided to refer the dog for more specialist management.
Follow-up information from the referral centre confirmed coagulopathy with marked prolongation of both prothrombin time (PT) and activated partial thromboplastin time (APTT). Multiple units of FFP were administered and intravenous glucose supplementation was required for a further 24 hours. A biochemistry profile revealed abnormalities consistent with muscle and hepatic parenchymal damage. No further complications were identified and the dog went on to make a complete recovery with intensive supportive care.
As demonstrated by this case, a variety of clinicopathological findings may be identified in dogs suffering from heatstroke. These are summarized in Table 38.1. In the author’s experience petechiation is relatively common in dogs with heatstroke, not all of which are thrombocytopenic. This suggests probable vasculitis or platelet dysfunction as the cause of the petechiation.
Table 38.1 Possible clinicopathological findings in dogs with heatstroke
| Test | Possible findings |
|---|---|
| Packed cell volume (PCV) | Increased (haemoconcentration) or decreased (haemorrhage) |
| Serum total solids (TS) | Increased (haemoconcentration) or decreased (haemorrhage, leakage through inflamed vessel walls) |
| Blood glucose | Low, normal or high |
| Electrolytes | Hypernatraemia (dehydration); hyperkalaemia (muscle breakdown) |
| Venous acid–base status | Respiratory alkalosis, metabolic acidosis, hyperlactataemia |
| Arterial blood gas analysis | Hyper- or hypocapnia, hypoxaemia |
| Peripheral blood smear | Increased nucleated red blood cells, thrombocytopenia, neutrophilia or neutropenia |
| Biochemistry | Azotaemia (prerenal, renal), increased liver enzymes, hyperbilirubinaemia, increased creatine kinase (CK) |
| Urinalysis | Haematuria, haemoglobinuria, myoglobinuria, inappropriate glucosuria and casts (indicate renal damage) |
| Coagulation | Prolonged prothrombin time (PT), prolonged activated partial thromboplastin time (APTT) |