DIABETIC KETOACIDOSIS (DKA): A state of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia, dehydration, and acidosis-producing derangements in intermediary metabolism, including production of serum acetone. Can occur in both Type I Diabetes and Type II Diabetes – In type II diabetics with insulin deficiency/dependence The presenting symptom for ~ 25% of Type I Diabetics. Hyperosmolar Hyperglycemic State (HHS): An acute metabolic complication of diabetes mellitus characterized by impaired mental status and elevated plasma osmolality in a patient with hyperglycemia. Occurs predominately in Type II Diabetics – A few reports of cases in type I diabetics. The presenting symptom for 30-40% of Type II diabetics. Not commonly associated with ketonaemia and acidosis Classic Triad of DKA: Hyperglycemia - blood glucose greater than 11.1 mmol/L Ketosis - ketones present in blood and/or urine Acidosis - pH less than 7.3 and/or bicarbonate less than 15 mmol/L DKA is generally categorized by the severity of the acidosis. MILD – Venous pH less than 7.3 and/or bicarbonate concentration less than 15 mmol/L MODERATE – Venous pH less than 7.2 and/or bicarbonate concentration less than 10 mmol/L SEVERE – Venous pH less than 7.1 and/or bicarbonate concentration less than 5 mmol/L Risk factors for DKA at onset: Age <12 yrs No first degree diabetic relative Lower socioeconomic status High dose glucocorticoids, atypical antipsychotics, diazoxide and some immunosuppresive drugs Poor access to medical care Uninsured Usage of SGLT-2 inhibitor – euglycaemic DKA SGLT2 inhibitors blunt insulin production in the face of stress hormones leading to increased ketotic metabolism Why do ketones develop? No carbohydrate intake fasting gastroenteritis Atkins diet, neonates fed high-fat milk Prolonged exercise, pregnancy Lack of insulin activity onset of diabetes (insufficient secretion) interruption of insulin delivery in established pt Increase in insulin resistance infection, illness, surgery, stress Alcohol, salicylate ingestion, inborn metabolic errors Causes of DKA/HHS: Stressful precipitating event that results in increased catecholamines, cortisol, glucagon. Infection (pneumonia, UTI) Alcohol, drugs Stroke Myocardial Infarction Pancreatitis Trauma Medications (steroids, thiazide diuretics) Non-compliance with insulin DKA is a complex metabolic state of: hyperglycemia, ketosis, and acidosis Symptoms include: Deep, rapid breathing Fruity breath odor Very dry mouth Nausea and vomiting Lethargy/drowsiness DKA is life-threatening and needs immediate treatment Symptoms of DKA/HHS Polyuria Polydypsia Blurred vision Nausea/Vomiting Abdominal Pain Fatigue Confusion Obtundation Physical Examination in DKA/HHS: Hypotension, tachycardia Kussmaul breathing (deep, labored breaths) Fruity odor to breath (due to acetone) Dry mucus membranes Confusion Abdominal tenderness Treatment of DKA: Fluids and Electrolytes Fluid replacement –Restores perfu