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Hyperkalemia

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Hyperkalemia

  1. 1. approach to Hyperkalemia Dr Vilas Naik DM (nephrology) Fellowship in Nephrology (Toronto, Canada)
  2. 2. Hyperkalemia: Life threatening Emergency Common Treatable
  3. 3. K physiology • Total body K stores are approximately 3000 meq • K: primarily intracellular cation {98 % of body K} • Ratio of the K concentrations in the cells and outside: major determinant of the resting membrane potential across the cell membrane • Generation of the action potential: essential for normal neural and muscle function • K abnormalities: Muscle weakness and arrythmia
  4. 4. Regulation of urinary potassium excretion Connecting segment & Cortical duct Na comes here Lumen Negative ROMK Electrical gradient For K secretion Na-K ATPase Electrical and chemical gradient for Na reasbsorption
  5. 5. Regulation of urinary potassium excretion Stimulation of K secretion by principal cells • An increase in plasma potassium concentration and/or potassium intake • An increase in aldosterone secretion • Enhanced delivery of sodium and water to the distal potassium secretory site
  6. 6. An increase in plasma potassium concentration and/or potassium intake
  7. 7. An increase in aldosterone secretion Hyperkalemia Renin angiotensin Aldosterone system (RAAS) Na channel Aldosterone deficiency, blockade
  8. 8. Enhanced delivery of sodium and water to the distal potassium secretory site We need Na and Water here. No distal Na (decresed GFR), No K secretion e.g Renal failure Increased distal flow, Increased Na delivary, Increased K secretion Eg diuretics
  9. 9. Distribution of potassium between the cells and the extracellular fluid 98 % K intracellular Maintained by this pump Pump block eg digitalis toxicity Beta blockers Pump stimulation Insulin, beta2 stimulation
  10. 10. Distribution of potassium between the cells and the extracellular fluid
  11. 11. Distribution of potassium between the cells and the extracellular fluid
  12. 12. Hyperkalemia • Increased intake: K adaptation, rapid • Shift: intracellular to extracellular, alone again not enough to sustain hyper K. • Decrease excretion: almost always present – Aldosterone – Decreased distal delivery of Na/ water – Renal dysfunction
  13. 13. Case 1 • 52/ male, DM and HT- 15 yrs • Uncontrolled HT, Edema 3+ • Recent change in medications • Adm: rapid onset quadriparesis over last 24 hours
  14. 14. Case1: examination • ECG: HR of 30, broad QRS, CHB like pattern • Rest vitals stable • Higher functions normal • Quadriparesis (grade 2 power, absent reflexes)
  15. 15. Case 1: Labs • Na 129 • K 8.7 • Cl 96 • HCO3 16 • AG 17 • Creat 4.4 • Glucose 600 • CBC leucocytosis • Urine • Sugar- 4+ • Ketones- nil • Plenty pus cells
  16. 16. Hyperkalemia appraoch • Intake • Shift • Impaired excretion
  17. 17. Case: analysis • Intake: propably reduced (UTI, blood sugars) • Shift: – Severe hyperglycemia – Insulin deficiency – Acidosis
  18. 18. Case analysis • Decreased renal excretion (almost always) • Was started on ramipril (ACEI) for HT – RAAS blockade (decreased aldosterone) Decreased GFR so decreased distal delivery of Na and water, no Na reabsorption, no electronegative potential in lumen No secretion of K
  19. 19. Na+ -- -- -- -- -- K+
  20. 20. Case analysis • The patient was also started on spironolactone which blocked aldosterone action • NSAIDS for fever – Deceased GFR – Renal failure
  21. 21. More mechanisms • K loading increases ROMK expression and insertion into CCD luminal membrane • ? May be gut signal to kidney to change ROMK • Another K channel in CCD – High capacity K channels (big K or Maxi K) – Activated of high flow (water and Na delivery) – Activated by K depletion – Aldosterone independent action
  22. 22. Another K channel: intercalated cells • H-K exchanger in IC cells of CCD • Activated in K depletion • Absorbs K+ and secretion of H+
  23. 23. Evaluation of hyperkalemia • Exclude Pseudohyperkalemia – potassium movement out of the cells during or after the blood collection – Torniquet – Thrombocytosis, high WBC counts (leukemias)
  24. 24. Assessing K excretion • Kidneys can vary K excretion from < 5 Meq/L to 400 Meq/L, with decreased or increased intake • Urine K/ Creatinine ratio – < 15 mmol/gm in K depletion – >200 mmol/gm in hyperkalemia –
  25. 25. Case 1 • Urine Na- 120 Meq/L • Urine K- 15 Meq/L • SO distal delivery of Na is adequate • Severely impaired K excretion • Aldosterone deficiency: hyporeninemic hypoaldosteronism in DM • Drugs blocking aldosterone production and action • Decreased GFR
  26. 26. Case 1 • NSAIDS: worsening of RFT (GFR) • PG synthesis inhibited – PG inhibit renin –reduce aldosterone • So in this patients, almost all things to increase his K has been done – ACEI, aldosterone blockade – NSAIDS
  27. 27. Treatment of severe hyperkalemia • Calcium: if hypocalcemia or ECG changes • Shift inside the cells: – Insulin alone (hyperglycemia) or with 25 % Dextrose – B2 agonist – Bicarbonate if acidosis
  28. 28. Treatment • Excretion – Saline, especially if depleted – Thiazide and loop diuretic – K binding resins, small effect, increasing GI excretion, given with lactulose • Dialysis- the most rapid and effective means in the presence of renal dysfuction and fluid overload
  29. 29. Case 1 • We started the patient on dialysis, normal sinus rhythem in 45 minutes • Stopped implicated drugs, treated UTI • Baseline creatinine of 2 mg % on follow up. • K normal
  30. 30. Thanks for your patience

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