This document discusses potassium metabolism and the approach to hyperkalemia. It begins with an introduction to potassium physiology and homeostasis. The kidney plays a key role in potassium excretion, reabsorbing 85-90% in the distal tubules where regulation occurs. Hyperkalemia is defined as a serum potassium over 5.5 mEq/L and can be caused by increased potassium load, impaired excretion, or transcellular shifting. Treatment focuses on stabilizing cardiac cells, rapidly lowering potassium levels, and enhancing elimination while addressing the underlying cause. Emergency therapies include calcium gluconate, insulin therapy, beta agonists, and sodium polystyrene sulfonate.

1. POTTASIUM METABOLISM
& APPROACH TO
HYPERKALEMIA
BY DR.RAVI KUMAR S
1ST YEAR PEDIATRIC PG
MGMCRI

2. TABLE OF CONTENTS
INTRODUCTION
PHYSIOLOGY OF K⁺
EXCRETION OF K⁺
DEFINITION OF HYPERKALEMIA
CLINICAL FEATURES
ETIOLOGY
TREATMENT

3. 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.

4. Physiology
Nearly 98% of potassium is distributed in the ICS with a conc. Of 140-150 mEq/L.
About 3/4th 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.

6. 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⁺

8. 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)

9. 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⁺

10. Etiology
Increased Load
A) Exogenous Source : Salt Supplements, Transfusion.
B) Endogenous Source : Intravascular hemolysis, resolving hematoma, rhabdomyolysis & tumor lysis.
Impaired Renal Excretion
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

11. Etiology
Transcellular shift
Acidosis
Hypertonicity
Exercise
Diabetes
Myolysis
Drugs like Digoxin, Beta blockers & Succinylcholine
Extensive Muscle/ Cellular Injury
Malignant hyperthermia

12. Clinical Features

13. TREATMENT
If plasma K⁺ >6.5 mEq/L or ECG abnormalities are detected, emergency treatment should be
initiated.
Priority of Rx
1. Withdrawl of Source if any; in case blood transfusion is urgently needed use of fresh &
washed RBC’s are recommended,
2. Stabilization of myocardial cells.
3. Rapid reduction of plasma K levels with transcellular shift.
4. Enhance K elimination from body
5. Treatement of underlying cause.

14. 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.