Case Study: Heat Stroke in Canine Patient

Signalment: 2-year-old, male neutered, Labrador Retriever

History: Patient presented in July after a hike, laying down and not wanting to get back up. His owner suspected he overheated so put him in a pool to cool him off. The dog vomited once. He was first brought to an Urgent Care where his temperature was elevated at 104 F and his blood glucose was low at 57 mg/dL.

Physical Exam: Upon presentation to AVES Emergency department, the dog was found to be weakly ambulatory, with a temperature of 98.3° F, and he was found to be approximately 5% dehydrated.

Initial Treatment: Labwork performed by the emergency doctor at AVES showed mild hypoglycemia (73 mg/dL) and mild azotemia (Creatinine 2.7 mg/dL and BUN 31 mg/dL). Hospitalization was recommended based on the physical exam findings, initial lab work and knowledge that illness from heat stroke has the potential to worsen over the first few days after the initial heat  injury. He was started on IV fluids at 120 ml/kg/day and maropitant. His blood sugar decreased further to 68 ml/dL so he was started on 2.5% dextrose. While hospitalized he developed several sequelae of heat stroke.

Problems developed secondary to heat stroke:

  1. Acute Kidney Injury
    Date Creatinine (mg/dL) BUN (mg/dL) Urine Output Weight
    7/14 2.7 31 38 kg
    7/15 4.6 69 40.7 kg
    7/16 9.7 87 1.2 mL/kg/hr 42.8 kg
    7/17 13.5 110 1.4 mL/kg/hr 43.4 kg
    7/18 10.5 >130 2.6 mL/kg/hr 42.5 kg
    7/19 am 12.6 >130 1.8 mL/kg/hr 40.7 kg
    7/19 pm 13.1 >130
    7/20 am 12.8 >130 4 mL/kg/hr 40.4 kg
    7/20 pm 12.9 >130
    7/21 13 >130 5.2 mL/kg/hr 40.1 kg
    7/22 12 >130 8.3 mL/kg/hr 37.2 kg
    7/23 10.9 114 15 mL/kg/hr 37.6 kg
    7/24 4.7 77 8 mL/kg/hr 36 kg
    7/25 3.9 75 5.7 mL/kg/hr 35.3 kg
    7/30 2.3 53
    8/5 1.6 31 35.5 kg

    While the patient was hospitalized for heat stroke he developed a progressive acute kidney injury. His azotemia peaked 4 days after the heat stroke incident and did not start to improve until 10 days after. He was initially treated with 120 ml/kg/day LRS  to help correct dehydration and protect his kidneys from pre-renal injury. Based on physical exam findings (chemosis, skin turgor, weight gain) we did suspect he became fluid overloaded and a urinary catheter was placed to carefully monitor his “ins and outs”, which allowed us to more specifically tailor his fluid therapy to his urine production. The patient developed profound polyuria which was likely driven by the recovery phase of his kidney injury and the IV fluids he was receiving. Once his azotemia started to improve we suspected his polyuria was being driven by a combination of IV fluids and the recovery phase of his kidney injury. In order to determine how much of a role IV fludis were playing into his polyuria, his IV fluids were decreased by about 20 ml/hr every 4 hours  and his urine production did start to decrease in response. The patient did have a nasogastric tube for food and did start to eat and drink on his own so he was able to help maintain his hydration orally.  After several days of the urinary catheter his urine became cloudy and a urine culture confirmed a multi drug resistant infection. Based on culture results we treated him with chloramphenicol. A recheck urine culture after 2 weeks of therapy was negative. The patient was discharged after 12 days of hospitalization and at subsequent recheck appointments his kidney values had completely normalized.

  2. Hypoglycemia
    Upon presentation to AVES, the patient’s blood sugar was slightly low at 73 ml/dL and decreased further to 68 ml/dL. At that point he was treated with IV dextrose added to his IV fluid. His blood glucose normalized after 2 days of treatment and he did not require further supplementation.
  3. Disseminated Intravascular Coagulation
    On presentation the patient had mildly decreased platelets, about 128,000 platelets/uL. The following day his platelet count had dropped to 8,000 platelets/uL and he developed ecchymosis on his ventrum. His PT/PTT were slightly prolonged on presentation but did not worsen. His platelet count was rechecked 6 days later and had improved to 130,000 platelets/uL and his ecchymosis resolved. Based on these results, his mildly prolonged PT/PTT and thrombocytopenia was likely secondary to Disseminated Intravascular Coagulation which is common in severe heat strokes.
  4. GI upset
    During early hospitalization the patient developed regurgitation, hematochezia and melena. Understandably he was not interested in eating. He was treated with pantoprazole, entyce, maropitant and ondansetron. A nasogastric tube was placed and enteral nutrition started with Royal Canine Gastrointestinal Low Fat liquid diet. It was started at ¼ resting energy rate and increased daily until the dog was receiving his full calorie amount. The dog started eating on his when his kidney values began to improve.  His hematochezia and melena resolved on their own after a few days. By the time of discharge pantoprazole, maropitant and ondansetron were discontinued and Entyce was prescribed to go home in case it was needed for appetite stimulation.

Follow up: The patient returned to AVES 4 days after discharge for a recheck appointment. At this time a kidney panel was checked which showed improved but still mild azotemia (creat 2.3 mg/dL and BUN 53 mg/dL). Clinically he was eating well with no GI upset and a good energy level. He was rechecked again 9 days after discharge, a kidney panel showed resolution of azotemia (creat 1.6 mg/dL and BUN 31 mg/dL). His final recheck at AVES was 20 days after discharge for a CBC since he was being treated with chloramphenicol for his MDR UTI which was all within normal limits. A recheck urine culture was submitted and was negative for infection.

Discussion: Heat injury occurs on a spectrum from heat injury to heat stroke. More severe instances of heat stroke can affect every body system, resulting in MODS, DIC and death. The patient had many risk factors for mortality in heat stroke including hypoglycemia, prolonged PT, and creatinine >1.5. As this case shows, dogs with severe heat stroke and subsequent progressive AKI can recover with careful management.