Page 467 - Clinical Small Animal Internal Medicine

44 Disorders of Heat and Cold 435

be necessary. Broad‐spectrum antibiotics are recom- heat damage. NSAIDs upregulate HSPs and may confer
VetBooks.ir mended if a bacterial infection is suspected and when protection against heat stroke in patients that are on
NSAIDs at the time of the heat stroke incident. In fact,
possible, antibiotic therapy should be deescalated based
on culture results. Prolonged fever with no response to
prevention during heat waves although there is no pub-
antimicrobials and a thorough, inconclusive work‐up in humans, NSAIDs may be indicated for heat stroke
may indicate an immune‐mediated process that requires lished research on this in dogs. Importantly, NSAIDs
immunosuppression, a viral process that requires con- are contraindicated after a heat stroke event has
tinued monitoring and supportive care, or a neoplastic occurred due to the risk of negative effects on the kidneys,
process that has yet to be identified. Treatment with coagulation system, and gastrointestinal tract.
antipyretics that inhibit prostaglandin synthesis, such as The clinical signs of heat stroke depend on the degree
nonsteroidal antiinflammatory drugs (NSAIDs), is con- and duration of temperature elevation, as well as a signifi-
troversial as inhibiting the fever may allow continued cant contribution by individual patient factors. Diagnosing
propagation of an infectious agent. Possible side‐effects heat stroke is often based on a history of confinement or
of these medications in each individual patient should exertion on a hot, humid day. Most animals will present
also be considered carefully prior to their administra- with an elevated body temperature although it may be
tion. Although uncommon, true fevers exceeding 41 °C normal or low, especially if external cooling has been initi-
(106 °F) require more aggressive intervention with active ated prior to presentation or the patient is in the advanced
cooling to prevent organ damage and other systemic stages of shock. On initial physical exam, tachycardia,
effects. panting, and injected mucous membranes may be noted.
Cardiac arrhythmias may be ausculted or suspected due
to the presence of pulse deficits. Neurologic deficits rang-
Heat Stroke ing from obtundation to coma and seizure may occur.
Skin and mucous membranes should be examined for
Heat stroke is probably the most common cause of life‐ evidence of petechiae and ecchymosis and venipuncture
threatening hyperthermia (>40 °C/104 °F) encountered sites should be monitored for appropriate hemostasis.
in veterinary medicine and results from inadequate heat Initial work‐up includes an electrolyte panel (including
dissipation from the body. Classic heat stroke is caused blood glucose), packed cell volume (PCV) with total
by exposure to high environmental temperatures, which solids (TS), complete blood count, chemistry profile, and
overwhelm the body’s ability to offload heat by means of coagulation assays. Common abnormalities include
convection and radiation. The most common situation hemoconcentration with elevations in PCV and TS, ele-
causing classic heat stroke occurs when an animal is vations in liver enzymes (ALT, AST, alkaline phosphatase,
locked in an enclosed vehicle where the temperature can bilirubin), renal and prerenal azotemia, elevated creatine
rapidly increase past the outside ambient temperature kinase, prolonged clotting times, and hypoglycemia.
due to solar heat and poor interior ventilation. This situ-
ation develops more rapidly in larger dogs that produce Treatment
greater body heat and have less relative surface area for
heat dissipation than smaller dogs. The initial therapy for heat stroke should be aimed at
Exertional heat stroke is the result of physical activity rapidly returning body temperature to normal and
in a hot and/or humid environment and is often seen correcting hypovolemia and acid–base and electrolyte
in working dogs. Increased environmental humidity derangements. Immediately upon recognition of a heat
decreases respiratory evaporative heat loss while stroke crisis, owners should be instructed to thoroughly
increased work of breathing promotes heat production wet a patient with tepid water. Support staff should be
and further exacerbates this condition. Many cases of trained to instruct owners in this crucial step provided it
exertional heat stroke occur early in the warm weather will not unnecessarily delay transport to a veterinary
season due to lack of acclimatization to the change of hospital. Upon presentation, the previously described
temperature. Dogs with altered means of respiratory active cooling techniques should be initiated. At least
evaporative heat loss, such as brachycephalic dogs and one peripheral IV catheter should be placed and room‐
dogs suffering from laryngeal paralysis, may be more temperature fluids administered to increase effective
vulnerable to exertional and classic heat stroke. Obesity circulating volume and improve perfusion, enhancing
and a thick hair coat can further decrease the ability to peripheral heat loss.
dissipate heat from the body in both forms of heat stroke. During fluid resuscitation, heart rate, blood pressure,
Some dogs may have a genetic resistance to heat stroke lactate, PCV/TS, and urine production should be moni-
due to increased levels of heat shock proteins (HSP), tored to guide therapy. A description of goal‐directed resus-
which protect and repair essential cellular proteins from citation targets is found in Chapter 41. If hypoproteinemia