complications CRITICAL CARE

Lisa L. Powell, DVM, Diplomate ACVECC, University of Minnesota

Canine Heatstroke

Heatstroke is defined as a state of extreme hyperthermia (106109 F)

resulting in thermal injury to tissues, which occurs when heat generation
exceeds the bodys ability to dissipate heat.
eat dissipation occurs through 4 mecha-

H nisms: radiation, convection, conduc-

tion, and evaporation. Heat loss through
radiation and convection occurs by cutaneous
vasodilatation and increased cardiac output.
Conductive heat loss occurs through contact
with cool surfaces. Evaporation occurs through
sweating in humans, horses, and cows, and by
panting in dogs.

When the ambient temperature is below 89.5 F,

heat loss may occur through conduction, radia-
tion, and convection. As the ambient tempera-
ture increases and approaches body temperature,
evaporative heat loss becomes much more
important. In addition, evaporative heat loss
becomes less efficient with increased ambient
humidity.

Pathophysiology Severe ecchymosis on the ventral abdomen of a dog with disseminated intravascular coagulation secondary
Inability to dissipate heat may result from to heatstroke caused by a grooming dryer
endogenous or exogenous sources. Endogenous
factors that contribute to a decrease in the abili-
ty to dissipate heat include obesity, brachy- sipation include water deprivation, confinement fasciculations. In addition, malignant hyperther-
cephalic conformation, laryngeal paralysis/ in a poorly ventilated area, lack of acclimatiza- mia due to abnormal calcium metabolism may
upper airway obstruction, cardiovascular or tion, and high humidity. occur in predisposed breeds exposed to specific
respiratory disease, extremes in age, and central anesthetic drugs. Often, heatstroke is caused by
nervous system disease. Animals with a history Increased heat production leading to heatstroke a combination of a decreased ability to dissipate
of heatstroke tend to be predisposed to further may be caused by exercise, febrile disease, heat and increased heat production.
episodes, even at lower temperatures and hormonal hyperthermia (hyperthyroidism,
humidity. Exogenous factors that limit heat dis- pheochromocytoma), seizures, or severe muscle c o n t i n u e s

co m p l i c a t i o n s . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . N AV C c l i n i c i a ns b r i e f . a u g u s t . 2 0 0 8 . . . . . 1 3
complications CONTINUED

In the initial stages of heat stress, cardiac output nia and at least 2 of the following: prolonged PT, demand for ATP in hyperthermic patients. Hypo-
increases due to peripheral vasodilatation and prolonged aPTT, and clinical signs compatible glycemia on presentation was associated with a
decreased vascular resistance. As hyperthermia with DIC (petechiae, ecchymoses, hematochezia, poorer outcome.2
progresses, splanchnic blood pooling occurs hematemesis, hematuria). Dogs with a diagnosis
and causes a decrease in circulating blood vol- of DIC, based on these parameters, were also Gastrointestinal System
ume, resulting in hypotension. Cardiac output more likely to die.2 Hypotension and thermal injury contribute to
then starts to decline due to decreased vascular severe gastrointestinal epithelial damage and
resistance and hypovolemia. With a decrease in Renal System necrosis, resulting in hemorrhagic diarrhea,
circulating blood volume, heat loss through the In the kidney, direct thermal injury damages the hematemesis, gastric ulceration, and potential
mechanisms of radiation and convection fail, renal tubular epithelium. Decreased renal blood for bacterial translocation into the bloodstream.
causing an elevation in body temperature and flow from hypoperfusion and microthrombosis In hypoperfused states, blood supply to the
then heatstroke. secondary to DIC also contributes to the patho- intestinal villus is shunted from the arteriole to
genesis of renal failure. Depending on the sever- the venule, thus decreasing oxygen delivery to
Global thermal injury causes multisystem organ ity of renal damage, oliguric or anuric renal the villus tip and intestinal mucosa. This results
dysfunction; organ damage occurs at tempera- failure may ensue. in significant hypoxia to the villi and mucosal
tures above 109 F. At these higher tempera- lining, causing enterocyte death and intestinal
tures, uncoupling of oxidative phosphorylation Elevated creatinine levels were significantly asso- mucosal sloughing.
occurs, enzymes are denatured, and cell mem- ciated with decreased survival in 2 studies.1,2
brane functions are distrupted. The coagulation, Azotemia may worsen for the first 24 to 48 Gastrointestinal ulceration and decreased
renal, hepatic, gastrointestinal, and central nerv- hours, despite aggressive fluid therapy due to absorptive capacity occur as a result of villus
ous systems may all be affected, with mortality continued renal damage from excretion of hypoxia. In addition, the gastrointestinal mucosa
rates reported in dogs from 36% to 50%.1,2 excessive myoglobin, produced from thermal is an important barrier to significant bacterial
injury to muscle tissue. This derangement is translocation into the portal circulation. With
Types of Complications manifested by elevations in serum creatinine intestinal mucosal damage, bacterial and endo-
Coagulation System kinase levels, which have been documented in toxin translocation is enhanced, increasing the
Thermal injury to the endothelium causes wide- many cases of canine heatstroke. risk for sepsis in these critically ill patients.
spread vascular damage and initiates coagula-
tion to help repair the injured vessels. In Hepatic Effects Central Nervous System
addition, extensive cell necrosis in multiple The liver sustains direct thermal damage, caus- Dysfunction in the central nervous system may
organs stimulates the release and consumption ing widespread hepatic cellular necrosis. result from low cerebral perfusion, cerebral
of coagulation factors and platelets. The severity Hypoperfusion and microthrombosis from coag- edema, or direct thermal injury to neurons,
of the thermal injury contributes to development ulation abnormalities may also contribute to causing neuronal degeneration. Dogs often pres-
of DIC in dogs with heatstroke. Direct thermal hepatic dysfunction. Elevations in hepatic ent in an altered mental statedisorientation,
injury to bone marrow causes early release of enzymes are so common that 1 author suggests stupor, seizures, muscle tremors, and coma are
nucleated red blood cells, which elevates the that, in humans, normal levels of liver enzymes common presenting signs.2 In humans, the defi-
number of these cells in circulation. should place a diagnosis of heatstroke in nition of heatstroke includes hyperthermia with
doubt.3 the presence of neurologic dysfunction; howev-
Thrombocytopenia is a common result of ther- er, it has been shown that the central nervous
mal injury and may be due to direct heat dam- Levels of ALT, AST, and ALP were elevated in system in dogs is intrinsically resistant to ther-
age to platelets or may be associated with DIC. 79% to 83% of dogs in 1 study.2 Hepatic dys- mal injury, allowing for higher core body tem-
In 2 retrospective studies of canine heatstroke, function may progress, evidenced by persistently peratures before manifestation of central
thrombocytopenia was a common finding, but it elevated liver enzymes, elevated bilirubin, hypo- nervous system abnormalities.4
was not associated with a worse outcome. In 1 glycemia, and hypocholesterolemia. Hypo-
study, elevated PT and aPTT were associated glycemia is commonly found on presentation Prevention of Complications
with increased mortality.2 In this study, DIC was and may be due to hepatic dysfunction or Multiorgan dysfunction and failure are the
diagnosed in dogs that also had thrombocytope- increased use in response to an increased sequelae to heatstroke in dogs, and the severity
of organ malfunction is related to the degree

aPTT = activated partial thromboplastin time; ALP = alkaline phosphatase; ALT = alanine aminotransferase; AST = aspartate aminotransferase; ATP = adenosine triphosphate;
DIC = disseminated intravascular coagulation; PT = prothrombin time

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 Cooling Methods
Methods of cooling include soaking with luke-
warm water, covering the patient with towels
soaked with lukewarm water, and placing a fan
in front of patients to maximize heat loss
through radiation and convection. Cool- and
cold-water enemas have fallen out of favor, as
further constriction of vascular beds of the gas-
trointestinal tract can worsen gastrointestinal
ischemia and bacterial translocation.

Fluids & Blood Products

In every case of heatstroke, the goal of treatment
is to increase organ perfusion. This is best
accomplished through administration of intra-
venous fluids. Large doses of crystalloid fluids
should be avoided in patients with altered men-
tation, as these dogs may be more prone to
cerebral edema. However, cerebral perfusion
must be maximized. To achieve perfusion while
preventing tissue edema, both crystalloids and
A dog with multiple organ failure, including hepatic and oliguric renal failure, in a semicomatose state sec-
colloids can be used together.
ondary to heatstroke
The administration of fresh frozen plasma can
and duration of the hyperthermic state. Heat- dogs on presentation were significantly lower help provide needed coagulation factors in the
stroke most often occurs in the warm summer than those in dogs that were not cooled.1 Owners treatment and prevention of DIC. Many heat-
months and is especially common when humidi- should be instructed to use lukewarm water, as stroke patients require multiple doses of plasma
ty is high. cold water or ice will cause peripheral vasocon- over several days to treat coagulation abnormali-
striction and lead to a decreased ability to lose ties. A dose of 10 to 20 mL/kg/day should be
Owners of active dogsincluding those heat through convective mechanisms. If severe used. PT, aPTT, and platelet levels should be
involved in hunting, field trials, and scheduled signs of heatstroke are present, the owners checked on a daily basis.
runsand working dogs should be educated should wet the dog down and immediately pres-
about warning signs of heat exhaustion and ent it to a veterinary clinic for further therapy. Blood Pressure Support
heatstroke. Most owners are aware of the possi- Blood pressure should be supported and
bility of overheating and the need to rest their Factors associated with a poorer outcome checked to assure maximum tissue perfusion.
dogs when appropriate, provide plenty of fresh include hypoglycemia, elevated PT and aPTT, Vasopressors may be necessary in volume-resus-
water, and cool them with shade and water delayed presentation (> 90 minutes after signs citated patients to maintain normal blood pres-
hoses. Other preventable causes of heatstroke are evident), and elevated serum bilirubin and sure. Dopamine, norepinephrine, dobutamine,
include prolonged exposure to cage dryers; con- creatinine levels.1,2 Efforts should therefore be and vasopressin are examples of medications
finement in a closed, unventilated area (such as directed at preventing these complications, used to support blood pressure in hypotensive,
a car); and extended muzzling. through aggressive cooling measures and opti- volume-resuscitated patients (Table).
mizing organ perfusion.
Cooling the dog with possible heatstroke before Antibiotics
presentation to a veterinarian is imperative. In 1 Treatment of Complications If signs of gastrointestinal compromise are
study, only 38% of dogs died when cooled The progress of multiorgan failure depends on present (vomiting, hemorrhagic diarrhea,
before presentation compared with 61% that the duration of hyperthermia. Cooling measures ileus), broad-spectrum antibiotics may be
died if not cooled.2 In another study, 16 of 42 should be aimed at lowering core body temper- administered to help prevent sepsis from bacterial
dogs presenting with heatstroke were cooled by ature while preventing hypothermia. translocation and may include a combination
their owners, and rectal temperatures of these of antibiotics effective against gram-positive,
c o n t i n u e s

co m p l i c a t i o n s . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . N AV C c l i n i c i a ns b r i e f . a u g u s t . 2 0 0 8 . . . . . 1 5
complications CONTINUED

COMING
Table. Medications for Blood Pressure Support

Drug Dose Comments

SOON
Dobutamine 2.510 g/kg/min Selective -1 agonist
Use with caution in cats
Dopamine Renal perfusion enhancement (dogs): Dopaminergic agonist at
2.5 g/kg/min lower doses
Vasoconstriction: 510 g/kg/min -1 and -1 agonist at
higher doses
Norepinephrine 0.051 g/kg/min Potent -1 agonist
Vasopressin 0.0010.004 U/kg/min Vasoconstriction via V-1
receptors on vascular
smooth muscle cells

gram-negative, and anaerobic bacteria. Exam-

ples include ampicillin and cefazolin (gram-
positive and some anaerobes), enrofloxacin TAKE-HOME MESSAGES
Heatstroke may develop due to envi-
(gram-negative bacteria), and metronidazole
ronmental or endogenous factors, is
(for anaerobes). Nonsteroidal antiinflammatory most commonly seen in the warmer
drugs and glucocorticoids should be avoided months, and is often associated with CONSULTANT ON CALL: Cranial
because of the potential for gastrointestinal higher humidity. However, exertional Cruciate Ligament Rupture
ulceration and effects on renal perfusion. activity, confinement in an unventilat-
ed space, or prolonged exposure to PROCEDURES PRO: Gastrointestinal
dryers or other heating units can Anastomosis
Urine Output cause heatstroke at any time.
Monitoring urine output is important in dogs COMPLICATIONS: Hypoxia During
Aggressive cooling measures should
with signs of oliguria or anuria accompanied by be instituted immediately, while Anesthesia
azotemia. A urinary catheter and closed-collec- avoiding hypothermia, as duration of APPLIED BEHAVIOR: Update on
tion system should be placed, and urine should hyperthermia is associated with a
worse outcome and progression of
Veterinary Research
be collected and measured aseptically every 4
to 6 hours. If oliguria or anuria is present in a
organ failure. COMPARATIVE IMAGERY: Urine
Prevention of complications of heat- Crystals
volume-resuscitated patient (urine output < 2
stroke include client and community
mL/kg/H), diuretics, such as furosemide or education about avoiding situations WHATS THE TAKE-HOME?:
mannitol, can be administered as a constant-rate associated with development of Nutritional Supplement Toxicity
infusion to help stimulate urine production. hyperthermia, and if heatstroke is
present, maximizing tissue perfusion DEVICES: Laparoscopic Equipment
In summary, complications of heatstroke through the use of intravenous fluid
therapy.
include DIC, acute renal failure, altered menta- Plus, of course, Capsules, Applied
tion, hepatic failure, and gastrointestinal dys- Cytology, Diagnostic Tree, Make Your
function. Mortality ranges from 36% to 50%, Diagnosis, Patient Support, and much
highlighting the importance of early, aggressive more!
therapy in dogs presenting with heatstroke.

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DIC = disseminated intravascular coagulation

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