Name
ALCOHOLIC KETOACIDOSIS
DESCRIPTION
DETAIL
OCCURS IN CHRNOCALLY MALNOURISHED ETHANOL ABUSERS AFTER ADRINKING BINGE WHICH CULMINATES IN SEVERE VOMITING, DEHYDRATION, AC STARVATION & KETOACIDOSIS. SOME HAVE WITHDRAWAL SYMPTOMS & OTHERS HAVE GASTRITIS, PANCREATITIS OR INFECTIONS. * ARTERIAL PH < 7.3 & SERUM BICARBONATE LEVELS < 15 MEQ / L * CALCULATED ANION GAP > 14 MMOL/L * PARTIAL PRESSURE OF CO2 IS DECREASED SECONDARY TO COMPENSATED HYPERVENTILATION * IN AKA, THE AVERAGE RATIO OF HYDROXYBUTYRIC ACID TO ACETOACETIC ACID( 5:1) TENDS TO BE HIGHER THAN IN DIABETIC KETOACIDOSIS ( 3:1 ). * USE REAGENT STRIPS FOR MEASURING KETONE BODIES IN URINE THAT MEASURE BETA-HYDROXYBUTYRATE. * THE HALLMARK OF AKA IS KETOACIDOSIS WITHOUT MARKED HYPERGLYCEMIA * FREE FATTY ACIDS - MARKEDLY INCREASED * SERUM INSULIN LEVELS - LOW * GLUCAGON LEVELS - HIGH * SERUM CORTISOL LEVELS & CATECHOLAMINE LEVELS - MARKEDLY ELEVATED * HYPONATREMIA & HYPOKALEMIA DUE TO VOMITINGS
TYPENOTES
Medical Care Treatment of AKA is directed toward reversing the 3 major pathophysiologic causes of the syndrome, which are (1) extracellular fluid volume depletion, (2) glycogen depletion, and (3) an elevated ratio of the reduced form of nicotinamide adenine dinucleotide to nicotinamide adenine dinucleotide. Extracellular volume repletion with normal saline inhibits the release of counterregulatory hormones and facilitates urinary ketone excretion. The degree of weight loss is a good indicator of the extent of dehydration and the quantity of fluid required. Normal saline at about 20 ml/kg over 30-60 minutes is required in patients with severe hypotension or hypovolemic shock. After restoration of blood pressure and renal perfusion (urine flow is 50-100 mL/h) the fluid choice and rate depends on the state of hydration, serum electrolytes, and urine output. The rate is decreased to 5-10 mL/kg/h until resolution of ketoacidosis (usually within 24 h). The acid-base parameters that define resolution of ketoacidosis are serum bicarbonate levels greater than 18 mmol/L, pH greater than 7.30, and anion gap les than 14 mmol/L. Normal saline alone does not correct the acidosis of AKA as rapidly as dextrose and saline. Glucose administration interrupts ketogenesis by stimulationof insulin secretion and repletion of glycogen stores. Patients presenting with moderate-to-severe hypoglycemia (glucose levels <50 mg/dL) may require intravenous administration of 25-50 g of 50% dextrose followed by continuous 10% dextrose infusion until glucose level is greater than 120 mg/dL. Glucagon injections alone might not correct hypoglycemia due to the depletion of hepatic glycogen stores. Hypoglycemia can be a potentially lethal complication of AKA. Generally, insulin is not indicated in the treatment of AKA but should be used judiciously in very low doses in patients with blood glucose concentrations greater than 250 mg/dL. Consider diabetic ketoacidosis in these patients. Potassium repletion is indicated in hypokalemic and normokalemic patients with acidemia. These patients should initially receive at 10-30 mEq of potassium chloride per hour intravenously. The subsequent rate and total dose of potassium are determined by subsequent potassium measurements. In the absence of renal insufficiency, magnesium repletion is indicated in all patients to help restore calcium and potassium homeostasis and to forestall alcohol withdrawal. Magnesium sulfate can be given safely at a rate of up to 1 g/h intravenously. Calcium repletion is rarely needed. Magnesium repletion usually allows spontaneous correction of hypocalcemia. Routine use of phosphorus is not encouraged, but when severe hypophosphatemia is present, intravenous phosphate repletion at rate of 0.08-0.16 mmol/kg over 6 hours is recommended. Bicarbonate therapy is rarely needed. In AKA, regeneration of bicarbonate from the metabolism of lactate, ketoacids, and acetate occurs with conservative treatment. Thiamine repletion (100 mg/d) is routinely indicated to increase pyruvate dehydrogenase activity and to provide prophylaxis against the development of Wernicke encephalopathy. DRUG THERAPY : Potassium repletion is indicated in hypokalemic patients and normokalemic patients with acidemia. Magnesium repletion is indicated in all patients to help restore calcium and potassium homeostasis and to prevent alcohol withdrawal. Phosphate repletion is recommended only if severe hypophosphatemia is present. Thiamine repletion is indicated routinely to provide prophylaxis against the development of Wernicke encephalopathy. 1. POTASSIUM CHLORIDE 2. MAGNESIUM SULPHATE 3. PHOSPHATE SALTS 4. THIAMINE ( VIT B1 )
RELATED DISEASE
Not Available Disease
DISEASE
INVESTIGATION
SERUM SODIUM, SERUM POTASSIUM, SERUM CORTISOL ( 8.00 A.M. ), SERUM CORTISOL ( 4.00 P.M. ), COMPLETE BLOOD COUNT, SERUM INSULIN ( FREE ), BLOOD SUGAR ( RANDOM ), BLOOD GASES, SERUM BICARBONATE