Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are the two most serious metabolic complications of diabetes mellitus (DM). These disorders can occur in both type 1 and type 2 DM. DKA is characterized by hyperglycemia, ketone body formation and metabolic acidosis. Precipitating causes are usually infection or insulin omission. Over the past 20 years, there has been no reduction in the DKA mortality rates, which remain between 3.4% and 4.6%. HHS is manifested by marked elevation of blood glucose, hyperosmolality and little or no ketosis. Precipitating causes of HHS are infection, undiagnosed diabetes and substance abuse. The mortality rates of the HHS remain high at approximately 15%. Basic common pathophysiological mechanisms in both conditions, which differ only in the magnitude of dehydration and degree of ketoacidosis, are the reduction in the effective insulin action combined with increased counterregulatory hormones (glucagon, catecholamines, cortisol, and growth hormone). While in DKA the lack of insulin combined with increased catecholamines results in accelerated lipolysis and thus production of excess fatty acids, leading to beta-oxidation and ketogenesis, in HHS residual beta-cell function is adequate to prevent lipolysis but not hyperglycemia. The prognosis of both conditions is substantially worsened in patients > 65 years of age and in the presence of coma and hypotension. Mainstays of therapy are intravenous insulin and fluid replacement as well as the concomitant treatment of the precipitating factors. Improved patient education and implementation of measures such as home glucose and ketone monitoring might decrease the number of hospital admissions due to DKA and HHS, which are, in their majority, preventable).