Hyperkalemia

hyperkalemia and its management

1. HYPERKALEMIA UNDER THE GUIDANCE OF : Dr. Mukesh Rana Sir Dr. Brijesh Sir Dr. Asif Akhtar Sir Dr. Javed Sir Dr. Rajesh Sir Presented By : Abhishek Kumar Yadav Roll No. - 04 PARA 15

2. Hyperkalemia is defined as a plasma potassium level of 5.5 m M ; and severe hyperkalemia as a plasma potassium level of > 6.0 m M .

3. Causes of Hyperkalemia : I . Pseudohyperkalemia II . Intra- to extracellular shift III . Inadequate excretion

4. I. Pseudohyperkalemia Factitious hyperkalemia Artifactual increase in serum K + due to the release of K + during or after venipuncture . Causes : Cellular efflux; thrombocytosis , erythrocytosis , leukocytosis , in-vitro hemolysis Hereditary defects in red cell membrane transport

5. II. Intra- to extracellular shift Acidosis Hyperosmolality ; radiocontrast , hypertonic dextrose , mannitol Lysine, arginine , epsilonaminocaproic acid (structurally similar, positively charged) Digoxin and related glycosides (yellow oleander) Succinylcholine ; thermal trauma, neuromuscular injury, disuse atrophy, mucositis , or prolonged immobilization Rapid tumor lysis β 2 -Adrenergic antagonists ( noncardioselective agents) Hyperkalemic periodic paralysis ( HYPP )

6. III. Inadequate excretion A. Inhibition of RAAS ; ↑ risk of hyperkalemia when used in combination :  ACE inhibitors, ARBs , Mineralocorticoid receptor blockers, Blockade of the ENaC B. Decreased distal delivery eg ., CHF C. Hyporeninemic hypoaldosteronism 1. Tubulointerstitial diseases: SLE , sickle cell anemia 2. Diabetes, diabetic nephropathy 3. Drugs: NSAIDs , β-blockers, cyclosporine 4. Chronic kidney disease, advanced age

7. D. Advanced renal insufficiency eg ., CKD, ESRD E. Primary adrenal insufficiency 1. Autoimmune: Addison’s disease 2. Infectious: HIV, CMV , TB 3. Infiltrative: amyloidosis , malignancy 4. Drug-associated: heparin, LMWH 5. Hereditary: adrenal hypoplasia congenita

8. (A) ACIDOSIS : Acidemia → cellular uptake of H+ → efflux of K+ - via K + -H + exchange - this effect is limited to non–anion gap metabolic acidosis and, to a lesser extent, respiratory causes of acidosis; -does not occur in the anion gap acidoses - lactic acidosis and ketoacidosis .

9. (B) HYPEROSMOLALITY - Due to osmotic gradient ("solvent drag" effect) : - Hyperkalemia due to hypertonic mannitol , hypertonic saline, and intravenous immune globulin is due to osmotic gradient. - Diabetics are also prone to osmotic hyperkalemia in response to intravenous hypertonic glucose, when given without adequate insulin.

10. (C) Cationic amino acids , as lysine, arginine , and the structurally related drug epsilonaminocaproic acid, cause efflux of K+ and hyperkalemia via effective cation -K + exchange.

11. (D) Digoxin → inhibits Na + /K +- ATPase → impairs uptake of K + by skeletal muscle, so, digoxin overdose → hyperkalemia . Structurally related glycosides found in yellow oleander, foxglove and in the cane toad, Bufo marinus ( bufadienolide ) act via same pathway and cause hyperkalemia .

12. (E) Succinylcholine ( SCh ) → depolarizes muscle cells→ efflux of K+ through acetylcholine receptors ( AChRs ). Contraindicated in patients who have sustained thermal trauma, neuromuscular injury, disuse atrophy, mucositis , or prolonged immobilization becasue it leads to an exaggerated efflux of K +  acute hyperkalemia .

13. (F) Excess Intake or Tissue Necrosis Following conditions provoke severe hyperkalemia in susceptible patients : Foods rich in potassium include tomatoes, bananas, and citrus fruits ; Simple overreplacement with K + - Cl – or the administration of a K + -containing medication (e.g., K + -penicillin ) Red cell transfusion, typically massive transfusions . Finally , severe tissue necrosis, as in acute tumor lysis syndrome and rhabdomyolysis .

14. Clinical Features Medical emergency due to its effects on heart, i.e., cardiac arrhythmias .  Other modes of presentation : Ascending paralysis, denoted secondary hyperkalemic paralysis : includes diaphragmatic paralysis and respiratory failure. Patients with familial HYPP develop myopathic weakness during hyperkalemia induced by increased K + intake or rest after heavy exercise.

15. ECG Electrocardiographic manifestations in hyperkalemia : (At increasing K + levels)

16. Diagnostic Approach First priority is to assess the need for emergency treatment, followed by a comprehensive workup to determine the cause. Laboratory tests - Electrolytes, BUN, creatinine , serum osmolality , Mg 2 + and Ca 2 +, CBC - Urinary pH, osmolality , creatinine , and electrolytes.

17. Trans-tubular potassium gradient ( TTKG ) : index reflecting the conservation of potassium in the cortical collecting ducts ( CCD ) of the kidneys.   < 3 in the presence of hypokalemia > 7–8 in the presence of hyperkalemia

18. Treatment : The treatment of hyperkalemia is divided into three stages : 1 . Immediate antagonism of the cardiac effects of hyperkalemia - Intravenous calcium 2. Rapid reduction in plasma K + concentration by redistribution into cells Insulin β 2 -agonists (most commonly albuterol ) 3 . Removal of potassium - using cation exchange resins, diuretics, and/or dialysis. - Hemodialysis is the most effective and reliable method to reduce plasma K+ concentration.

19. Drugs Dosage Onset Length of effect MOA Cautions Ca 2+ gluconate 10-20 mL of 10% solution IV over 2-3 minutes Immediate 30 minutes Protects myocardium from toxic effects of Ca 2 + Can worsen digoxin toxicity Insulin Regular insulin 10 units IV with 50 mL of 50% glucose 15-30 minutes 2-6 hrs. Shifts K + out of the vascular space and into the cells Consider 5% Dextrose solution infusion at 100 mL /hr to prevent hypoglycemia with repeated doses. Glucose unnecessary if blood sugar elevated above 250mg / dL Albuterol ( Ventolin ) 10-20 mg by nebulizer over 10 minutes (use conc. form, 5mg/mL) 15-30 minutes 2-3 hrs. Shifts K + into the cells, additive to the effect of insulin May cause a brief initial rise in serum potassium

20. Furosemide ( Lasix ) 20-40 mg IV, give with saline if volume depletion is a concern 15 min. - 1 hr. 4 hrs. Increases renal excretion of potassium Only effective if adequate renal response to loop diuretic Sodium polystyrene sulfonate (Kayexalate) Oral : 50 g in 30 mL of sorbitol solution Rectal : 50 g in a retention enema 1-2 hrs. (Rectal route is faster) 4-6 hrs. Removes potassium from the gut in exchange for sodium Sorbitol may be associated with Bowel necrosis. Drugs Dosage Onset Length of effect MOA Cautions

21. THANK YOU