♣Que ,Francesca ♣ Lin, Yun Hsing ♣Reyes, Elaine HYPERKALEMIA WORSHOP ♣Que ,Francesca ♣ Lin, Yun Hsing ♣Reyes, Elaine

POTASSIUM IN THE BODY Potassium: major ion of the body. Nearly 98% intracellular ( Na+/K+–ATPase pump) The ratio of intracellular to extracellular potassium is important in determining the cellular membrane potential. A balance of GI intake and renal potassium excretion achieves long-term potassium balance. Normal potassium level: 3.5-5.0 mEq/L, Total body potassium stores are approximately 50 mEq/kg (3500 mEq in a 70-kg person).

HYPERKALEMIA defined as a potassium level greater than 5.5 mEq/L Ranges are as follows: 5.5-6.0 mEq/L - Mild condition 6.1-7.0 mEq/L - Moderate condition 7.0 mEq/L and greater - Severe condition

CAUSES OF HYPERKALEMIA

A. Decreased or impaired potassium excretion Decreased GFR (eg, acute /chronic renal failure) - most common Decreased mineral corticoid activity (Addison’s dse) Defect in tubular secretion (eg, renal tubular acidosis II and IV) Drugs (eg, NSAIDs, cyclosporine, potassium-sparing diuretics) B. Excessive endogenous potassium load Internal hemorrhage/ Hemolysis Rhabdomyolysis C.Exogenous potassium load Parenteral administration Excess in diet Potassium supplements/Salt substitutes D.Transmembrane shifts / Redistribution Metabolic Acidosis (uncontrolled DM) Insulin deficiency Drugs (e.g.beta-blockers,digoxin,succinylcholine) E.Factitious or pseudohyperkalemia Hemolysis (in lab tubes) / Venipuncture - most common Thrombocytosis , Leukocytosi

HISTORY TAKING Generalized fatigue Weakness Paresthesias Paralysis Hyperkalemia can be difficult to diagnose clinically because complaints may be vague. Frequently is discovered as an incidental laboratory finding. Patients may be asymptomatic or report the following: Generalized fatigue Weakness Paresthesias Paralysis Palpitations Hyperkalemia is suggested in any patient with a predisposition toward elevated potassium level.

PHYSICAL EXAMINATION Evaluation of vital signs (to determine hemodynamic stability & presence of arrhythmias) Cardiac examination may reveal extrasystoles, pauses, or bradycardia. Neurologic examination may reveal diminished deep tendon reflexes or decreased motor strength. In rare cases, muscular paralysis and hypoventilation may be observed. Search for the stigmata of renal failure, such as edema, skin changes, and dialysis sites. Look for signs of trauma that could put the patient at risk for rhabdomyolysis

CASE SCENARIO A 62 year old male diabetic with chronic kidney disease and a creatinine level of 3.5 mg.dl with an estimated GFR of of 15ml/min. He has been eating fruits with each meal for the past two weeks . he consulted because of inability to lift himself from a chair. On PE, he was conscious with BP 110/ 70. PR 90/min, RR 28/min. He had pale, palpebral conjunctivae, poor skin turgor, and marked proximal weakness. The rest of the findings were normal. 12L ECG showed peak T-waves and some widening of the P wave and QRS complex. Lab exams showed Na 130 meq/L, K 8.5 meq/L, Cl 98 meq/L, HCO 7meq/L , SCr 3.5 mg/dl . Arterial pH 7.30, CBG 400 mmol/L , serum acetone (+).

SALIENT FEATURES 62 year old diabetic chronic kidney disease poor skin turgor marked proximal weakness 12L ECG : peak T-waves widening of the P wave and QRS complex CHIEF COMPLAINT : inability to lift himself from a chair .

Lab Results 130 meq/L HYPONATREMIA 8.5 meq/L HYPERKALEMIA 98 MEQ/L Cl (98-106 meq/L) 98 MEQ/L NORMAL HCO3 (21-30 meq/L) 7meq/L METABOLIC ACIDOSIS pH (7.35-7.45) 7.30 Crea (<1.5 mg/dL) 3.5 mg/dL

What are the most likely factors responsible for the elevation of the plasma K+ concentration? Diabetes Insulin deficiency and hypertonicity (e.g. hyperglycemia) promote K+ shift from ICF to ECF Chronic kidney disease ↓ renal K+ excretion: impaired secretion or diminished distal solute delivery ↓ K+ secretion by principal cells: impaired Na+ reabsorption or ↑ Cl- reabsorption in acute oliguric renal failure: ↑ K+ release from cells (acidosis, catabolism) and ↓ excretion in chronic renal insufficiency: ↑ distal flow rate and K+ secretion per nephron compensate for decreased renal mass --- adaptive mechanisms eventually fail to maintain K+ balance when GFR falls below 10-15 ml/min or oliguria ensues Eating fruits with each meal for the past 2 weeks ↑ K+ intake rarely the sole cause of hyperkalemia since the phenomenon of potassium adaptation ensures rapid K+ excretion in response to increases in dietary consumption

2. How do you know that this is not pseudohyperkalemia? artificially elevated plasma K+ concentration due to K+ movement out of cells immediately prior to or following venipuncture Contributing factors prolonged use of a tourniquet with or without repeated fist clenching hemolysis and marked leukocytosis or thrombocytosis: elevated serum K+ concentration due to release of intracellular K+ following clot formation should be suspected in an otherwise asymptomatic patient with no obvious underlying cause. If proper venipuncture technique is used and a plasma (not serum) K+ concentration is measured, it should be normal.

Signs & Symptoms

3. What are the signs and symptoms of hyperkalemia in this patient? Explain the pathophysiology. A. Marked proximal weakness Increase in membrane excitability RMP closer to threshold potential  depolarization Na channel become inactivated Decrease in excitability

Inhibits ammoniagenesis B . Metabolic Acidosis Hyperkalemia Inhibits ammoniagenesis Reabsorption of NH4 Impaired net acid secretion K moves out of the cell

Peaked T waves – ventricular repolarization C. ECG changes Peaked T waves – ventricular repolarization Widening of the P wave – atrial depolarization & QRS complex – ventricular depolarization decrease membrane potential Decreases upstroke velocity Slows intraventricular conduction Depression of conduction in myocardium

Peaked t-waves in hyperkalemia

Widened QRS interval in hyperkalemia

Treatment

2. Emergency treatment – reversal of membrane abnormalities by giving: 1. Immediate discontinuation of all sources of potassium intake and agents that affect potassium homeostasis 2. Emergency treatment – reversal of membrane abnormalities by giving: Calcium gluconate (Decrease membrane excitability) 10mL of 10% solution infused in 2-3min repeat if no change in electrocardiogram after 5-10min Hypertonic sodium chloride (for hyponatremic patients)

3. Redistribution of potassium from extracellular space to intracellular space using: Intravenous sodium bicarbonate Insulin and glucose Stimulation of β2 adrenergic receptors Salbutamol + nebulization

4. External removal of potassium through: Stools Sodium polystrene sulfonate is a cation exchange resin that promotes the exchange of sodium for potassium in the GIT Urine Loop + thiazide diuretics enhances renal excretion if renal function is adequate. Dialysis Hemodialysis Most rapid & effective Peritoneal dialysis 15 – 20% as effective as hemodialysis

5. Treatment of underlying cause: Dietary modification Correction of metabolic acidosis Volume expansion Administration of exogenous mineralocorticoid