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ISU Student Experience

Heat Stroke in Dogs

Written by: Natalie Allen, 3rd year veterinary student • 2019 Scholar

History and Physical Exam

Titan is a 7 year old pit bull who presented to IVS unresponsive after being on a run. The patient was in lateral recumbency with an initial temperature of 108.4. Upon physical exam, Titan had hyperthermia, tachycardia (abnormally high heart rate), tachypnea (Increase respiratory rate), as well as petechiation (pinpoint bruising) on his gums and ventral midline. The patient also vomited and had bloody diarrhea, which later became frank blood.

Heat Stroke Pathophysiology

In heat stroke cases, the body’s thermoregulation center cannot correctly dissipate heat resulting in an increase in body temperature. As the temperature elevates, tissue inflammation occurs leading to damage and necrosis (cellular death) in multiple organs, especially the liver since it is the shock organ in dogs. Necrosis causes further vascular damage, which leads to disseminated intravascular coagulation (DIC).  Widespread coagulation results in decreased amounts of platelets since the body is using all that are available. As a result, patients are unable to clot blood appropriately, hence increased PT and PTT (clotting) times with subsequent petechiation.

Additionally, heat stroke can cause GI sloughing and potential sepsis. Sepsis is indicated if the patient has low blood glucose because the bacteria utilize all the sugar. Other potential complications involve liver damage, kidney damage, cerebral edema (brain swelling), seizures, hemorrhage, shock and neurological damage.


Titan was diagnosed with heat stroke and immediately started on cooling methods. These included pouring alcohol on the paw pads to facilitate evaporation, supplementing O2 to cool the airways, and placing wet towels on the torso with a fan adjacent to the patient to allow for convection. The patient was administered 3 liters of IV fluids with hydromorphone for pain. Unfortunately, there is continuous debate regarding which cooling methods are the most effective in cases of heat stroke as there are no studies resolving the issue.


A complete blood count and chemistry panel was run to assess internal organ function, platelet count, and clotting ability. There was a dramatic decrease in platelets indicating DIC and a marked reduction of white blood cells on the slide suggesting sepsis. The patient was started on a fentanyl CRI (constant rate infusion) for pain and a series of medications as well as a plasma transfusion. The plan for Titan was to continue to monitor kidney and platelet values every 24 hours for the next several days with potential additional plasma transfusions. Through the evening, Titan’s condition declined. Bloody urine was noted and the petechiation spread to the ventral thorax and ears. Additionally, Titan’s PT and PTT values were dramatically increased at 32/166 when rechecked, indicating DIC. Unfortunately, in cases of heat stroke, DIC and acute renal (kidney) failure are significant risk factors for guarded prognosis. After sixteen hours of hospitalization and 2 plasma transfusions, Titan was humanely euthanized due to decreased condition and poor improvement.


  • Unasyn to prevent infection (an antibiotic)
  • Dextrose in fluids for hypoglycemia
  • Maropitant for vomiting
  • Metronidazole for diarrhea
  • Pantoprazole for potential GI ulceration

Lab Abnormalities 

  • PCV: 49%
  • PT/PTT: 19/108 seconds
  • Platelets: 41 K/uL
  • Blood Glucose: 34 mg/dL
  • Creat: 1.9 mg/dL
  • BUN: 27 mg/dL
  • Manual WBC count: 20 WBC on slide
  • Manual platelet count: 1 phf


  • Bruchim, Y., Klement, E., Saragusty, J., Finkeilstein, E., Kass, P., & Aroch, I. (2006). Heat stroke in dogs: a retrospective study of 54 cases (1999–2004) and analysis of risk factors for death. Journal of veterinary internal medicine, 20(1), 38-46.
  • Gaudio, F. G., & Grissom, C. K. (2016). Cooling methods in heat stroke. The Journal of emergency medicine, 50(4), 607-616.
  • Leon, L. R., & Helwig, B. G. (2010). Heat stroke: role of the systemic inflammatory response. Journal of applied physiology, 109(6), 1980-1988.

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