Diabetic ketoacidosis is an all too frequent and sometimes preventable complication of Type I diabetes mellitus, responsible for significant morbidity and mortality within the diabetic population. Precipitating diseases account for the majority of deaths occurring in patients admitted in diabetic ketoacidosis, but some deaths are still attributable to ketoacidosis alone, despite recent advances in therapy and management. Recognition of the ketoacidotic state is paramount to optimal therapy, and often hinges on the diagnostic acumen of the physician. Since 20 to 30% of patients presenting in diabetic ketoacidosis do so as the initial manifestation of their previously undiagnosed disease, physicians must maintain a high level of suspicion for this condition. Understanding the pathogenetic mechanisms leading to and prevailing in diabetic ketoacidosis will allow physicians to intervene in a rational manner, approaching therapy with specific end-points in mind: (a) restoration of optimal volume status; (b) reversal of acidosis; (c) reduction of serum glucose levels; (d) replacement of specific electrolytes in a timely manner; (c) institution of appropriate therapy for any precipitating cause; and, (f) careful monitoring of the patient's biochemical, physical and mental parameters to allow adjustment in therapy as necessary. The mainstay of treatment for diabetic ketoacidosis is appropriate fluid and insulin therapy. Low-dose intravenous infusion is now the accepted mode of insulin delivery for patients with this condition. Potassium replacement is almost always necessary, often requiring massive amounts of this ion due to the total body depletion seen with the development of ketoacidosis. Controversy still surrounds routine use of phosphate in diabetic ketoacidosis but replacement may be needed if serum levels fall toward the lower limits of normal values, to avoid the potential adverse effects of phosphate depletion. Administration of bicarbonate is also controversial and should be reserved for patients whose pH is less than 7.0 to 7.1 and then it should be added to intravenous fluids, not given as an intravenous bolus. Efforts toward preventing diabetic ketoacidosis should be of prime importance to physician and patient alike. Preventive measures should include patient education about diabetes mellitus, precipitating factors of diabetic ketoacidosis, signs and symptoms of early metabolic decompensation, rational insulin therapy during minor illness and appropriate timing of physician contact to help avoid this serious and sometimes fatal complication of diabetes mellitus.