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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.
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