Diabetic KetoAcidosis / DKA
- 1. Acute Complication of Diabetes Diabetic Ketoacidosis (DKA) By : Najihah
- 2. • DKA is a medical emergency and remains a serious cause of morbidity, principally in people with type 1 diabetes. • It has a mortality of 6-10%. • DKA also is often the presenting problem in newly diagnosed patient. (usually known NIDDM patient)
- 3. • DKA may be precipitated by an intercurrent illness because of failure to increase insulin to compensate for the stress response. - Infections (pneumonia, UTI, URI, meningitis, cholecystitis, pancreatitis) - Vascular disorder (MI, CVD) - Endocrine disorders (hyperthyroidism, cushing’s, acromegaly, pheochromocytoma) - Trauma - Pregnancy - Emotional stress - Drugs- cocaine
- 4. • In these conditions, there will be activation of sympathetic stimulation which will release epinephrine, cortisol, glucagon and growth hormone. • In 25% of patients, there is no precipitating cause.
- 5. • Cardinal biochemical features are: - Plasma glucose >250mg/dl - Arterial pH <7.30 - Serum bicarbonate level <15 mEq/l - Hyperketonemia >3mmol/L - Ketonuria >2+ on std urine sticks
- 6. Pathophysiology a. Insulin deficiency leads to hyperglycemia causes a profound osmotic diuresis leading to dehydration and electrolyte loss. b. Ketosis results from insulin deficiency + elevated catecholamines and other stress hormones. Catecholamines + Stress hormones Effects EN , cortisol, GH Inhibit insulin mediated glucose uptake by muscle peripheral utilization. EN, glucagon, cortisol Activating glycogenolysis and gluconeogenesis EN, GH Activating lipolysis EN, GH Inhibit residual insulin secretion
- 7. - These effects of inadequate insulin + catecholamines and stress hormones lead to unrestrained lipolysis and release FFA for hepatic ketogenesis. - Ketogenesis produce ketone bodies in excess resulting in ketonemia. - This condition further depletes the electrolytes and cause further hypovolemia. - Underperfused tissues start producing lactic acid (due to anaerobic metabolism). - These along with keto-acids create a metabolic acidosis.
- 8. Clinical Assesment Symptoms : - Polyuria, thirst - Leg cramps - Weight loss - Blurred vision - Weakness - Abdominal pain - Nausea, vomitting Signs : - Dehydration - Hypotension (postural/supine) - Cold extremities/peripheral cyanosis - Tachycardia - Air hunger ( Kussmaul breathing ) - Smell of acetone - Hypothermia - Hyporeflexia ( decreased potassium ) - Confusion, drowsiness, coma (10%)
- 9. Investigation • Venous blood : - urea, electrolytes, glucose and bicarbonate (severe acidosis plasma bicarbonate <12mmol/L) • Urine or blood analysis for ketones. • ECG • Infection screen : - CBC, blood and urine culture, C-reactive protein, chest X-ray
- 10. Management 1. Replacement of fluids losses. 2. Correction of hyperglycemia / metabolic acidosis. 3. Replacement of electrolyte loss. 4. Detection and treatment of precipitating cause.
- 11. 1. Replacement of fluids losses. • Isotonic saline (0.9%) or RL solution should be used. • The average fluid deficit in DKA is 6L (3L- extracellular, 3L-intracellular) • Initial fluid replacement is at a rate 5-10ml/kg/hr over first 1-3hrs. • In later stage, when serum sodium >155 mEq/L , 0.45% NS may be substituted. • Rate of infusion is reduced to 150-200ml/hr depending on clinical status and ongoing fluid losses.
- 12. 2. Correction of hyperglycemia / metabolic acidosis. • Insulin given in a dose of 10-15 units as a bolus or 0.15 U/kg IV as an infusion is the treatment of choice in DKA. • Continuous infusion is given in a dose of 125 units regular insulin/250 ml NS at a rate of 0.1 unit/kg/hr. • Insulin infusion should be given until DKA is resolved (usually 8-24 hrs)
- 13. • If no suitable veins are obtainable, IM injection can be given. • Loading dose of 10-20 units regular insulin in deltoid and then 5-10 units/hr q1h - until the blood glucose concentration fall by 55- 110 mg/dL or blood ketone concentrations fall by at least 0.5 mmol/L/hr. • Later insulin can be given every 2-4 hours.
- 14. • When serum glucose lowers to 250 mg/dl, add 5% dextrose to IV solution. • If there is presence of insulin resistance, the dose of hourly insulin can be increased by 50-100% to achieve proper glycemic control. • Excessive rapid correction of hyperglycemia (>100mg/dl/hr) has a risk of inducing osmotic encephalopathy (especially in children).
- 15. 3. Replacement of electrolyte loss. • Potassium - Careful monitoring of potassium is essential because both hyper and hypo can occur and are potentially life threatening. - Wait for serum K+ level before adding KCl to the drip. Serum K+ Dose of KCl (mmol/l of infused fluid >5.5 mmol/l No KCl 3.5-5.5 mmol/l 20 <3.5 mmol/l 40
- 16. • Bicarbonate - Adequate fluid and insulin should resolve the acidosis. - It is currently not recommended - Indications to use : a) Life threatening hyperkalemia b) Lactic acidosis complicating DKA c) Severe acidosis
- 17. 4. Detection and treatment of precipitating cause. • a/microbial iv • Reduce stress • Hyperthyroidism • Cessation of drugs – cocaine • MI
- 18. Complications of DKA • Metabolic - Severe acidosis, hypokalemia, hypoglycemia, hypocalcemia. • Non metabolic - Infection, septic shock, vascular thrombosis, pulm edema, cerebral edema, lactic acidosis, arterial thrombosis, rebound ketoacidosis (premature cessation of insulin therapy).
- 19. Reference • R Alagappan Manual of Practical Medicine , Fifth edition. • Davidson’s principles and practice of medicine, 22nd edition. Thank You
Editor's Notes
- #15: Insulin resistance = failure of blood glucose to fall w/in 1 hr Osmotic encephalopathy = cerebral edema, it is fatal.