Download 04.13 VV Heat Stroke by DD - Aspen Meadow Vets

Heat Stroke
As it warms up, more and more owners take their dogs out to enjoy the warm weather
and heat stroke becomes more of a concern. Besides ambient temperature, excessive
exercise, seizures, hypothalamic lesions, thyrotoxicosis, and malignant hyperthermia can
also lead to heat stroke.
The core body temperature is maintained within a narrow range by a balance between
heat generation and heat dissipation. Heat is generated by, but not limited to,
shivering, piloerection, catecholamine release, and peripheral vasoconstriction. Heat is
dissipated by loss through the body’s surface, movement of cool air around the body,
direct contact to cool surfaces, and evaporation from the body (panting, sweating).
Dogs lose the majority of their heat through their body surface and panting. Dogs also
lose more heat than human by laying on cool surfaces. Physiologic changes, including
water conservation through activation of aldosterone and ADH, increased cardiac
output, salt conservation, increased GFR, and plasma volume expansion, allow the body
to adjust to environmental changes. It can take up to 60 days for full acclimation.
Heat stroke is a complex pathophysiological state resulting from direct thermal injury to
body tissues exposed to excessive temperature. Heat stroke causes enzymatic
alteration and inactivation, denaturing of proteins, loss of cell membrane integrity, and
mitochondrial dysfunction leading to multiorgan dysfunction in which encephalopathy
predominates.
There are exogenous and endogenous predisposing factors that can lead to inadequate
heat dissipation and generation. Exogenous causes of inadequate heat dissipation
include lack of acclimatization (7-21 days), water deprivation, getting locked in
car/clothes dryer, excessive humidity, broken heat pipes (hot water/steam immersion),
and drug administration (furosemide, negative inotropes, phenothiazines).
Endogenous causes include excessive environmental humidity, obesity, cardiovascular
disease, laryngeal disease, brachycephalic airway syndrome, CNS disease, age, prior
heat stroke, and hair coat. Exogenous causes of increased heat production include
amphetamines, strychnine, organophosphates, pyrethrin, and mycotoxins. Endogenous
causes include exercise, seizures, hyperthyroid, and eclampsia.
DIC is the most common complication of heat stroke and some say it should be assumed in
all cases of heat stroke. Extensive thermal damage to endothelium and cellular necrosis leads
to activation and consumption of platelets and activation of coagulation cascade. Multiple
organ failure is the most serious complication of heat stroke and may include any
combination of circulatory collapse, encephalopathy, ARF, DIC, rhabdomyolysis,
myocardial injury, hepatic failure, intestinal ischemia, ARDS, endothelial dysfunction,
and acid/base disturbances.
Animals presenting with heat stroke may have hyperthermia, petechiae, cortical
blindness, weak or irregular pulses, excessive panting and salivating, dark/brick red
mucous membranes, collapse, tachycardia, hypoperfusion, vomiting, diarrhea, seizures,
abnormal mentation, seizures, pigmenturia, stridorous respirations, cyanosis, and/or a
swollen tongue. Animals can also present deceased. Clinical signs can help to differentiate
pyrogenic and non-pyrogenic hyperthermia. Pyrogenic hyperthermia is due to altered set
point so these animals may not ‘act’ hot (no panting, hypersalivation, seeking cool
places).
Common laboratory abnormalities include:

Biochemical Panel
 Azotemia, increased LES, increased CK, hypoglycemia

CBC


Coagulation Panel


Hemoconcentration, thrombocytopenia, nRBC, schistocytes
Increased FDPs, PT, PTT, D-dimers
Urinalysis

Renal casts, myoglobinuria, glucosuria with normal or low blood glucose
Heat stroke treatment should include active cooling. The mortality rate of dogs is 49%
for those not cooled before presentation vs. 19% for those cooled by owners! The g oal
is to reduce the body temperature to 39C/103F within 30-60 minutes, keeping in mind that this
can start prior to presentation. Cooling too fast will cause vasoconstriction slowing down
heat dissipation and shivering and overcooling is associated with increased morbidity
and mortality. Cool, not cold, water should be used. Soaked blankets/towels changed
frequently (radiant heat loss), and fans to increase evaporative heat loss and convective
loss can also be used. Treatment should also include cardiovascular support with
intravenous fluids (crystalloids/colloids). If abnormal airway structure or function may
require oxygen therapy, endotracheal intubation. Antibiotics are used to help treat bacterial
translocation and decreased activity of reticuloendothelial system. GI protectants are
used to help treat GI ulceration. Depending on the patient, treatment may also need
dextrose supplementation, plasma, blood, sedation, anti-seizure medication, antiarrhythmic medication, and/or mannitol. NSAIDs are contraindicated with this disease
process and use may result in iatrogenic hypothermia, platelet dysfunction, GI ulceration,
and decreased renal perfusion. Corticosteroid use is generally not indicated as use may
result in worsen GI ulceration and renal ischemia.
Body temperature, ECG, urine output, neurologic status, and repeat blood work to
follow abnormal laboratory values (electrolytes, blood gas, CBC, coagulation panel,
biochemistry panel), should be monitored closely during treatment.
The prognosis of animals with heat stroke is guarded to grave. Mortality is proportional
to the duration and intensity of hyperthermia. Dogs that survived the first 48 hours
have a better chance of survival but survivors may have permanent damage to
thermoregulatory center and kidneys. Negative prognostic indicators include coma,
neurologic deterioration, hypothermia, persistent hypoglycemia, worsening of
azotemia, oliguria, DIC, refractory hypotension, pulmonary edema, ventricular
arrhythmias, and an elevated total bilirubin.
The pathophysiology of heat stroke is very similar to that of sepsis and many patients
develop SIRS and die of multiple organ failure. Educating owners on how to prevent
heat stroke and how to initiate treatment prior to presentation will lead to the best
outcome for our patients.