MANAGEMENT OF DIABETIC KETOACIDOSIS (DKA) IN ICU MODERATOR - DR. GAURAV CHOPRA SIR (HOD) PRESENTER – DR. V.HEMANT (PG-1)
INTRODUCTION DKA is defined as an a bsolute (or near-absolute) insulin deficiency, resulting in- Severe hyperglycemia Ketone body production Systemic acidosis Most common in type 1 diabetes, but increasingly seen in type 2 diabetes.
PATHOPHYSIOLOGY
UNCHECKED GLUCONEOGENESIS HYPERGLYCEMIA OSMOTIC DIURESIS DEHYDRATION UNCHECKED KETOGENESIS KETOSIS DISSOCIATION OF KETONE BODIES INTO HYDROGEN IONS AND ANIONS ANION GAP METABOLIC ACIDOSIS Often a precipitating event is identified (infection, lack of insulin administration)
ETIOLOGY Infection (pneumonia, UTI, gastroenteritis, sepsis) Failure to take insulin Failure to increase insulin dose (inadequate insulin administration) Unrecognized symptoms of new onset diabetes mellitus Infarction (cerebral, coronary, mesenteric) Acute stress ( trauma, emotional) Pancreatitis Pregnancy Drugs (cocaine)
CLINICAL PRESENTATION OF DKA HISTORY: Thirst Polyuria Abdominal pain Nausea and/or vomiting Profound weakness EXAMINATION: Tachycardia Dry skin, decreased skin turgor Kussmaul breathing “Fruity” breath Altered mental status Hypotension Anorexia Patients with any form of diabetes who present with abdominal pain, nausea, fatigue, and/or dyspnea should be evaluated for DKA.
ESSENTIAL INVESTIGATIONS ABG and Anion Gap Urinalysis and urine ketones by dipstick CBC with differential count Serum ketones ECG, CXR Electrolyte panel Screening for a possible infective cause as a trigger
LABORATORY DIAGNOSTIC CRITERIA OF DKA PARAMETER NORMAL RANGE DKA Plasma glucose (mg/dl) 76-115 >=250* Arterial pH † 7.35-7.45 <=7.30 ß-Hydroxy butyrate (mg/dl) 4.2-5.2 >=31 (children) >=40 (adults) Serum B icarbonate (mmol/L) ‡ 22-28 <=18 Effective Serum Osmolality (mmol/kg) 275-295 <=320 Anion gap (mmol/L) <10 >10 Serum ketones Negative Positive Urine ketones Negative Moderate to High *May occur at lower glucose values, especially under physiologically stressful conditions. ‡ Suggestive, But not diagnostic of DKA † If venous pH is used, a correction of 0.03 must be made
MONITORING Flow sheet maintained tabulating mental status, vital signs, insulin dose, fluids and electrolytes administered and urine output. Capillary glucose 1- 2 hourly, electrolytes especially K+, HCO3- and phosphate) and anion gap every 4 hourly for first 24hrs. Monitor BP, pulse, respiration, fluid intake and output every 1- 4 hrs. * Watch for tachypnoea, decrease in respiratory drive, CO2 retention, decreased sensorium (in severe DKA), be prepared for intubation and mechanical ventilation support.
MANAGEMENT OF DKA Replacement of fluids losses Replacement of electrolytes losses Correction of hyperglycemia/metabolic acidosis Detection and treatment of precipitating causes Conversion to a maintenance diabetes regimen (prevention of recurrence )
FLUID THERAPY IN DKA Normal Saline 1-2 L over 1-2 Hrs Calculate Corrected Serum Sodium High or Normal S. sodium Low S. sodium ½ NS at 250-500 ml/Hr NS at 250-500 ml/Hr (S. Glucose<250 mg/dl) Change to D5, NS or ½ NS
INITIAL RATE OF FLUID REPLACEMENT Hours Volume 1 st Hour 1000-2000 ml 2 nd Hour 1000 ml 3 rd to 5 th Hour 500-1000 ml/Hr 6 th to 12th Hour 250-500 ml/Hr Fluid is usually replaced over 12-24 hrs. Monitors urine output, HR, BP & respiratory status. Care must be taken in cardiac and renal disease patients.
ELECTROLYTE MANAGEMENT POTASSIUM (K + ) K + ≥ 5.5, do not administer K + 4 - 5.4, add KCl 20 mEq /L K + 3 - 3.9, add KCl 40 mEq /L K + < 3, add KCl 60 mEq /L Check q 2 hrs *If initial K + is <3.3 mEq /L, DO NOT give insulin until serum values is supplemented to >3.3 due to risk of severe hypokalemia .
BICARBONATE (HCO3-) Replacement is generally not necessary as insulin will reverse the HCO3- deficit with its inhibition of lipolysis. Consider HCO3- in the following situations: Severe acidosis with pH<7 ( it should be stopped once pH is >7.1) Severe loss of buffering capacity when serum HCO3- <5-10 mEq /L Acidosis induced cardiac or respiratory distress Severe hyperkalemia
SODIUM (Na + ) Hyperglycemia causes an artifactually low serum sodium, and the correct value must be calculated. Corrected Na+ = Measured Na+ +[1.6(Measured blood glucose – 100]/100). OTHERS Hypomagnesemia occurs early in the course of DKA and requires correction. Phosphorus correction is required when it is severely depleted (<1mg/dl).
INTRAVENOUS INSULIN THERAPY IN DKA IV Bolus: 0.1 U/kg body weight IV Infusion: 0.1 U/kg/h body weight IV Infusion: 0.05-0.1 U/kg/h body weight until resolution of ketoacidosis (S. Glucose<250 mg/dl Add 5% Dextrose IVF)
BLOOD GLUCOSE MONITORING Check initial blood glucose (BG) q1h. Goal decrease in BG is 50-70 mg/dl/hr. Once stable (3 consecutive values decreased in target range), change BG monitoring to q2h. Resume q1h BG monitoring for each change in the insulin infusion rate. Add dextrose 5% IVF when BG < 250 mg/dl. Goal BG for DKA is 150-200 mg/dl until anion gap closes.
CHANGING THE INSULIN INFUSION RATE Decrease IV insulin by 50% if BG decreases by >100mg/dl/hr in any 1 hour period. Increase insulin by 50% if change in BG is <50 mg/dl/hr. s. If BG decreases to < 250 mg/dl, insulin infusion may need to be decreased 50% to maintain BG at target level. Start subcutaneous insulin when : Anion gap closed Serum HCO3- increases to >15 mEq /L Patient is able to eat
Stop the insulin infusion after all the following are done : Give short-acting insulin ( aspart or lispro) s/cat twice the hourly IV rate Give long-acting insulin (glargine) s/c at 0.2-0.3 U/kg. Ensure patient has a meal and is eating. *Lowering BG >100 mg/dl/hr may cause osmotic encephalopathy. * Failure to give s/c insulin may result in rebound hyperglycemia and ketosis due to short t1/2 of IV regular insulin.
CAUSES OF MORBIDITY AND MORTALITY IN DKA Shock Hypokalemia during treatment Hypoglycemia during treatment Cerebral edema during treatment Acute renal failure Adult respiratory distress syndrome Vascular thrombosis Precipitating illness, including MI, stroke, sepsis, pancreatitis, pneumonia