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Diabetic Ketoacidosis (DKA)
IntroductionDiabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes. DKA is defined: Clinically as an acute state of severe uncontrolled diabetes that requires emergency treatment with insulin and intravenous fluids. Biochemically as an increase in the serum concentration of ketones greater than 5 mEq/L, a blood glucose level of greater than 250 mg/dL (although it is usually much higher),blood pH of less than 7.2, and a bicarbonate level of 18 mEq/L or less.
PathophysiologyDKA is characterized by hyperglycemia, acidosis, and ketonuria.DKA is consequence of absolute or relative insulin deficiency with increase in counter-regulatory hormones .Insulin and counter-regulatory hormoneGluconeogenesis and glycogenolysis Hyperglycemia .Lipolysis Free Fatty Acids Ketogenesis Ketonemia and ketonuria pH and bicarbonate serum levels Metabolic acidosis Ketoacidosis.
Pathophysiology cont.Hyperglycemia Glycosuria Osmotic diuresis dehydration and tissue hypoperfusion.Hyperglycemia, osmotic diuresis, serum hyperosmolarity, and metabolic acidosis concentration disturbance.Osmotic diuresis Potassium Sodium loss in the urine.
Causes and Precipitating FactorsThe most common precipitantsInfections (3050%): pneumonia, urinary tract infections, sepsis, gastroenteritis Inadequate insulin treatment (2040%): includes noncompliance, insulin pump failure
Other precipitants
Clinical FeaturesSymptoms:Polydypsia.Polyuria.Hyperglycemia.Nausea, lethargy, anorexia, weakness.Abdominal pain.Reduced motility of GI.Vomiting.Signs:Dehydration: Dry skin and mucous .Orthostatic hypotension. Tachycardia. Reduced JVP.Reduced mental functionKetosis: Sweet odor Kussmaul breathing
InvestigationsGlucose level.Serum Ketones.Acid-base status: pH, Serum bicarbonate.Electrolytes: Na +K+ Mg +2ECGCBC, WBC.Urinalysis.Cardiac markers, Liver enzymes and Amylase.Chest X-Ray.Blood and urine culture.
ManagementAssess:Serum electrolytes, Acid-base status and Renal function.Replace fluids: 23 L of 0.9% saline over first 13 h (1015 mL/kg per hour) subsequently, 0.45% saline at 150300 mL/hchange to 5% glucose and 0.45% saline at 100200 mL/h when plasma glucose reaches 250 mg/dL (14 mmol/L).
Management cont.Administer short acting insulin: IV (0.1 units/kg) or IM (0.3 units/kg), then 0.1 units/kg/hour by continuous IV infusion; increase 2- to 3-fold if no response by 24 h. If initial serum K+ is < 3.3 mmol/L ,do not administer insulin until the potassium is corrected to > 3.3 mmol/L.Assess patient: What precipitated the episode (noncompliance, infection, trauma, infarction, cocaine)? Initiate appropriate workup for precipitating event (cultures, CXR, ECG).Measure capillary glucose every 12 h; measure electrolytes (especially K+, bicarbonate, phosphate) and anion gap every 4 h for first 24 h.
Management cont.Monitor vital signs, mental status, fluid intake and output every 14 h.Replace K+: 10 mEq/h when plasma K+ < 5.5 mEq/L, ECG normal, urine flow and normal creatinine documented; administer 4080 mEq/h when plasma K+ < 3.5 mEq/L or if bicarbonate is given.Continue above until patient is stable, glucose goal is 150250 mg/dL, and acidosis is resolved. Insulin infusion may be decreased to 0.050.1 units/kg per hour.
ComplicationsCerebral edemaCardiac dysrhythmiaPulmonary edemaNonspecific myocardial injury may occur in severe DKAMicrovascular changes consistent with diabetic retinopathy