Patients in<unk>  are almost always K+ depleted despite initially fairly normal K+.
This is due to extracellular shift of K+ due to acidosis as well as insulin infusion, which increases uptake of K+ intracellularly.
This is due to extracellular shift of K+ due to acidosis as well as insulin infusion, which increases uptake of K+ intracellularly.
Mortality rate approximately 2-5%
Defining features include hyperglycemia (glucose > 250mg/dl), acidosis (pH < 7.3), and ketonemia
Leads to osmotic diuresis and depletion of electrolytes including sodium, potassium, magnesium, calcium and phosphorus.
Further dehydration impairs glomerular filtration rate (GFR) and contributes to acute renal failure
Hypokalemia may inhibit insulin release
Due to insulin deficiency -> lipolysis / accumulation of of ketoacids (represented by increased anion gap)
Compensatory respiratory alkalosis (i.e. tachypnea and hyperpnea - Kussmaul breathing)
Breakdown of adipose creates first acetoacetate leading to conversion to beta-hydroxybutyrate
Causes activation of RAAS in addition to the osmotic diuresis
The initial serum values for electrolytes such as K+ may be higher than actual body stores
Cation loss (in exchange for chloride) worsens metabolic acidosis
Diabetic ketoacidosis
Insulin or oral hypoglycemic medication non-compliance 
Alcoholic ketoacidosis
Infection
Starvation ketoacidosis
Cardiac Ischemia
Cerebral edema in DKA
Intra-abdominal infections