POTTASIUM METABOLISM & APPROACH TO HYPERKALEMIA BY DR.RAVI KUMAR S 1 ST YEAR PEDIATRIC PG MGMCRI
TABLE OF CONTENTS INTRODUCTION PHYSIOLOGY OF K ⁺ EXCRETION OF K⁺ DEFINITION OF HYPERKALEMIA CLINICAL FEATURES ETIOLOGY TREATMENT
Introduction Potassium an essential cation for cellular functions, is widely distributed in body. One of the most commonly affected ions in sick children. Normal Sr.K ⁺ ranges between 3.5 to 5 mEq /L Common K⁺ rich foods are Meats, Beans, Fruits & Potatoes.
Physiology Nearly 98% of potassium is distributed in the ICS with a conc. Of 140-150 mEq /L. About 3/4 th of Intracellular K⁺ is in muscles, 2% K⁺ is in ECS, mostly in bones. The intercellular to extracellular potassium gradient is maintained by sodium potassium triphosphatase and selective K⁺ channel. Na-K-ATPase allows active transport of Potassium into cells whereas selective channels allow passive diffusion of K⁺ out of cells. Potassium homeostasis depends on a number of renal and extra renal factors like intake,GI and Urinary losses and transcellular shift. Daily requirement of K is about 1-2 mEq /kg.
Excretion of K⁺ Kidney is the primary organ for excretion of K⁺ upto 90% Nearly 85-90% of K⁺ is reabsorbed up to distal tubules and only 10-15% reaches cortical and outer medullary collecting ducts, which is the principle site of regulation of potassium excretion. Potassium secretion in cortical collecting duct (CCD) is regulated by aldosterone secreted from adrenal cortex. The net K⁺ secretion of CCD level evaluated by Transtubular K⁺ conc gradient (TTKG) TTKG = Urine K⁺ x Sr osmolality / Sr potassium x Urine Osmolality) In Hypokalemic children TTKG >4 indicates renal loss of K⁺ In Hyperkalemic children TTKG <8 indicates impaired renal secretion of K⁺
Hyperkalemia DEFINITION Sr.K ⁺ >5.5 mEq /L Based on the Sr. K⁺ concentration, Hyperkalemia can be categorized as Mild (5.5 to 6.5 mEq /L) Moderate (6.6 to 8 mEq /L) Severe (>8 mEq /L)
Etiology Spurious raised levels : Release of K⁺ from Hemolysed RBC at the time of blood sampling. True Hyperkalemia : Increased load Impaired renal excretion Transcellular shift of K⁺
Etiology Increased Load A) Exogenous Source : Salt Supplements, Transfusion. B) Endogenous Source : Intravascular hemolysis , resolving hematoma, rhabdomyolysis & tumor lysis. Impaired Renal E xcretion A) ↓ ed Na & H20 delivery to distal cortical tubules : AKD or Volume Depletion B) Functional Aldosterone : Hypoaldosteronism with ed Renin levels – Primary Adrenal Disease(Addison, CAH ) , Aldosterone synthase deficiency, use of drugs (ACE inhibitors, Angiotensin receptor blocker) Renal Tubular Diseases : Bartter syndrome –type II, Urinary Tract obstruction, Kidney transplant Potassium sparing diuretics & NSAIDS
TREATMENT If plasma K⁺ >6.5 mEq /L or ECG abnormalities are detected, emergency treatment should be initiated. Priority of Rx Withdrawl of Source if any; in case blood transfusion is urgently needed use of fresh & washed RBC’s are recommended, Stabilization of myocardial cells. Rapid reduction of plasma K levels with transcellular shift. Enhance K elimination from body Treatement of underlying cause.
TREATMENT 10 % calcium gluconate 0.5-1 ml/kg (max 10 ml) 1:1 diluted with saline over 10 min under cardiac monitoring. Glucose insulin infusion : Infants & Young children : 2ml/kg of 25% D with 0.1 Units/kg of regular insulin over 30 mins . Older children : 50 ml in 50% D with 10 Units of regular insulin to be infused over 30 min.Should be monitored for hypoglycemia . Short acting beta agonist : Salbutamol Neb 2.5 -5 ml in 3ml NS over 20 mins If there is Non anion gap acidosis, 1-2mEq/kg of Sodium bicarbonate iv over 30 mins . Ion exchange Resin : sodium polysterene sulfonate ( Kayexalate ) 1-2g/kg PO or PR IV Furosemide 1-2 mg/kg if Kidney function is normal Hemodialysis / Peritoneal Dialysis with K free fluid.