The following report describes a ten-year-old castrated-male Jack Russell te1Tier, who was presented to Cornell University's Emergency service in May, 2016 for evaluation of anorexia, lethargy, vomiting, and diarrhea. The patient had a tlu·ee-month history of waxing and waning inappetence and intermittent periods of lethargy. At the time of presentation he had a four-day history of inappetence progressing to anorexia, vomiting, dial1'hea and lethargy. Diagnostics performed included ·a complete blood count, serum chemistry panel, disseminated intravascular coagulation panel, thoracic and abdominal radiographs, full abdominal ultrasound, urine culture, and urinalysis. Three view thoracic radiographs and two view abdominal radiographs revealed no abnormalities. Blood work revealed a severe metabolic acidosis (pH 7.158), high anion gap (32.1), with no respiratory compensation (pCO2 34.1 mmHg), hyperglycemia (568 mg/dL), ketonemia (5.9 mmol/L), and elevated creatinine, hyponatremia, hypochloremia, hypocalcemia, and hypokalemia. Urine was collected via cystocentesis revealing USG of 1.028, glucosuria (>2g/dL), and ketonuria ( 40-80). Based on the findings of significant hyperglycemia coupled with ketoacidosis and ketonuria a diagnosis of diabetic ketoacidosis was made and treatment was initiated. The diagnosis, stabilization, approach and rationale for treatment of a patient presenting in diabetic ketoacidosis, and discussion of the progression of diabetes mellitus to diabetic ketoacidosis will be the focus of this case.