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436 Section 5 Critical Care Medicine
is present (albumin <2.0 g/dL, TP <5.0 g/dL), colloid episode when given prior to the incident. There is no evi-
VetBooks.ir therapy with natural colloids may be needed to support dence of any benefit to administering NSAIDs in the face
of an active heat stroke episode and there is warranted
intravascular volume and prevent third spacing of fluids.
If hypoglycemia is present (blood glucose <70 g/dL), an
renal, gastrointestinal, and coagulation systems. Similarly,
initial bolus of 50% dextrose (0.5–1.0 mL/kg, diluted to concern for adverse effects on the already compromised
25% with crystalloids) should be administered, then a there is no supporting evidence for the administration of
constant rate IV infusion of a crystalloid solution with corticosteroids during or after a heat stroke episode.
2.5–5% dextrose initiated for continued glucose support. Additional treatments are indicated based on diagnos-
Blood glucose should be monitored and dextrose supple- tic test results and individual patient needs. For more
mentation titrated to prevent hyperglycemia. If coagula- information on general critical care considerations, see
tion parameters indicate a hypocoagulable condition Chapter 35.
(prolonged prothrombin time [PT] or partial thrombo-
plastin time [PTT]), appropriate blood products (ideally Prognosis
fresh frozen plasma 10–20 mL/kg) may be indicated. If
bleeding is evident or the degree of derangement is great Heat stroke is a serious condition and the prognosis is
enough to raise concern for spontaneous hemorrhage dependent on many factors, including duration of tem-
then plasma is administered as needed until coagulation perature elevation, extent of temperature elevation,
times rechecked 1–2 hours after transfusion are normal. rapidity of initiation of treatment, and development
Continuous ECG monitoring is recommended to allow of complications. Poor prognostic indicators include
rapid identification of the development of cardiac coma or hypothermia at the time of presentation,
arrhythmias. In patients with severe neurologic deficits progressive decline in neurologic status, worsening
or seizure activity, diazepam (0.5 mg/kg IV), phenobarbi- azotemia, hyperbilirubinemia, persistent hypoglyce-
tal (12–16 mg/kg), or levetiracetam (60 mg/kg) should be mia, DIC, cardiac arrhythmias, and pulmonary edema.
administered to achieve seizure control. If neurologic Hypoglycemia has been found to be more profound in
evaluation suggests increased intracranial pressure then nonsurvivors and persistent hypoglycemia despite
mannitol (0.5–1.0 g/kg IV over 15 min) may be consid- treatment with dextrose has been associated with
ered for possible treatment of cerebral edema although increased mortality. Increasing creatinine level despite
hyperosmolar agents should be used with care in animals IV fluid therapy has also been associated with increased
that have acute hypernatremia, as often happens with mortality. The presence of nucleated red blood cells at
heat stroke. Coverage with broad‐spectrum antibiotics is the time of presentation may indicate more severe heat
advised due to the concern for bacterial translocation stroke and correlates with outcome.
from a disrupted gastrointestinal (GI) barrier. If evidence In general, animals with moderate to severe heat stroke
of GI injury is present in the form of hematemesis should be given a guarded to poor prognosis. Animals
or hematochezia then GI protectants, including that survive an episode of heat stroke are expected to
histamine‐2 blockers (famotidine 0.5 mg/kg IV BID) or make a full recovery although lasting neurologic deficits
proton pump inhibitors (omeprazole 1 mg/kg PO BID, or renal dysfunction may occur. Survival of heat stroke
pantoprazole 1 mg/kg IV BID) are indicated. does not confer protection from future events and owners
Nonsteroidal antiinflammatories have been associated should continue to be aware of environmental conditions
with preventing or decreasing the severity of a heat stroke to minimize the chances of occurrence.
Further Reading
Aroch I, Segev G, Loeb E, et al. Peripheral nucleated red Ettinger SJ, Feldman E, eds. Textbook of Veterinary
blood cells as a prognostic indicator in heatstroke in Internal Medicine, 7th edn. St Louis, MO: Saunders
dogs. J Vet Intern Med 2009; 23: 544–51. Elsevier, 2010.
Bruchim Y, Loeb E, Saragusta J, et al. Pathological findings in Silverstein D. Small Animal Critical Care Medicine.
dogs with heatstroke. J Comp Pathol 2009; 140: 97–104. St Louis, MO: Saunders Elsevier, 2009.