A four-year-old female spayed Australian Shepherd was presented to the Cornell University Hospital for Animals (CUHA) Emergency Service for a one-hour history of staggering and rigidity, progressing to suspected seizure activity. On presentation, the patient was laterally recumbent, tachypneic, tachycardic, and hypotensive. Neurologic abnormalities included stupor, miotic pupils, and absent withdrawals in the pelvic limbs. The patient was emergently treated with intravenous (IV) fluids for hypovolemic shock, mannitol for presumptive cerebral edema, and a bolus dose of diazepam following an apparent seizure. Point-of-care blood work revealed a severe metabolic acidosis, hypernatremia, hypokalemia, and hypoglycemia. Clinical evidence of petechiae, prolonged coagulation times, and thrombocytopenia supported the diagnosis of coagulopathy. Many nucleated red blood cells were observed on peripheral blood smear. Treatment was initiated and included levetiracetam, pantoprazole, maropitant, and broad-spectrum antibiotics. Physical examination and diagnostics performed the following day revealed improved neurologic status but evidence of severe liver and muscle damage, as well as mild acute kidney injury, all consistent with exertional heat stroke and subsequent disseminated intravascular coagulation (DIC). Upon further investigation, the patient was believed to have gotten into the neighbor’s compost pile just prior to onset of clinical signs. Tremorgenic mycotoxin ingestion with secondary heat stroke was thus prioritized over an intracranial cause for seizures. Over the next four days, the patient responded well to supportive care. Given her excellent response to medical therapy, the patient was discontinued from all medications and discharged to care of her owner with a good prognosis.