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K balance
- 1. Potassium balance and clinicaldisorders Mahmood Reza Khazaei Pediatric nephrologist Islamic Azad Mashhad Medical Sciences University
- 2. Objectives • Vital functionsof Potassium ion • Potassium balance • Factors influencing internal and external potassium balance • Hypokalemia: ▫ Etiology ▫ Clinical features and diagnostic approach ▫ Therapy • Hyperkalemia: ▫ Etiology ▫ Clinical features and diagnostic approach ▫ Therapy; urgent and non-urgent
- 3. Potassium ion vitalfunctions •Normal p.K+ : 3.5-5.5 mEq/L •Vital functions: ▫ Maintains cell electro-neutrality ▫ Assists in conduction of nerve impulse ▫ Directly affects cardiac and skeletal muscle contraction; repolarization phase of action potential ▫ Plays a major role in acid-base balance
- 4. Distribution of potassium ECFpotassium is 24 mEq in 30 kg boy, compared to total body potassium of 1950 mEq Total Body water = 60%Wt ECF (33%) ICF (66%) ECF (20%wt) ICF (40%wt) 4 160
- 5. Distribution of potassium •Clinical estimation of serum K represents only that portion of K in the body ( 2 %), not total body K • Occurrence of hyperkalemia or hypokalemia dose not mean increase or decrease of total body potassium; potassium depletion can occur despite hyperkalemia ( DKA)
- 6. Routes of Kexcretion •Fixed routes; ▫Sweat ( 2 % ); there is 200 ml of sweat per day total K+ losses about 2 mEq/ day ▫Stool ( 10 % ); ～ 10 mEq/ day, ▫Increased in: ▫ diarrhea episodes, increase significantly, ▫ vomiting ▫ CRF; up to 50% of potassium intake
- 7. Routes of Kexcretion •Variable route; ▫Renal K excretion; major route account for 78% of potassium excretion per day in normal individuals, 60-80 mEq/ day ▫GFR of 150 L per day, 600 mEq of potassium are filtered, only 60-80 mEq on average excreted in urine, so 85% of filtered potassium is reabsorbed
- 8. Potassium renal excretion •Thekidney is Major potassium regulator •Healthy kidney can Excrete potassium as low as 10 to up to 400 mEq/ day depending upon potassium intake.
- 9. Potassium renal excretion •Potassium secretion is dependent on the delivery of sodium and water to the CCT and on the action of the hormone aldosterone. • Aldosterone increases sodium reabsorption from the lumen and promotes potassium secretion into the lumen, restoring electrical neutrality.
- 10. 600-700 mEq 70-80% 15-20% 60-90mEq 10% of filtered load (FEk～10%) MAJOR SITE OF K+ SECRETION Mediated by effect of aldosterone on principal cells of late DCT & CCD A: Bulk Reabsorption B: Fine Tuning Concentration Control
- 11. Factors influenced renalK excretion • Increased • Aldosterone • Increased sodium delivery to distal nephron; • Diuretics • Osmotic diuresis • Saline infusion • Presence of poorly reabsorbed anion (HCO3,Cl) • Insulin • B2 adrenergic agonist • Increase intracellular K • Decreased • Non-anion gap academia • Decrease intracellular K • Alpha adrenergic agonist
- 12. Renal potassium lossestimation interpretation Normal range Indicator <15 Extra-renal loss or inadequate intake 20-40 mEq/Lit Urine Potassium Less than 20 mEq/day 24 hr. urine potassium <1 renal K+. wasting >1 Na+/K+ ratio >30% renal K+. Wasting <10% FEk+ See next TTKG
- 13. Transtubular K gradient( TTKG) • TTKG used to assess renal handling of potassium (aldosterone activity/ effect on late DCT & CCD). • TTKG calculation will done if: • Urine potassium level is >20 mEq/L but <40 mEq/L, • Urine Na+ level should be greater than 10 mEq/L Urine • Urine osmolality should be greater than or equal to serum osmolality. Urine K+ × serum osmolality/serum K+ × urine osmolality
- 14. Transtubular K gradient( TTKG) Condition TTKG Result Hypokalemia <3 No renal loss (normal kidney function) Hypokalemia >7 (>4) mineralocorticoid excess Hyperkalemia >10 normal aldosterone activity Hyperkalemia <5 aldosterone deficiency/resistance ………………………………………………………………………………………………………………………………… Hypokalemia + high TTKG; Hyperaldosteronism pseudohyperaldosteronism (e.g. Cushing's syndrome, Liddle's syndrome) Hyperkalemia + low TTKG: RTA-IV, CAH, potassium sparing diuretics; triamterene , Amiloride, spironolactone
- 15. HYPOKALEMIA Hypokalemia is definedas a plasma potassium level less than 3.5 mEq/L. Serum potassium (mEq/L) Severity 3.0 - 3.4 Mild 2.5 - 3.0 Moderate 2.0 - 2.4 Severe <2.0 Critical
- 16. Decreased intake Increased losses Transcellular shifts MedicinesSpurious Illness Fasting Prolonged IV fluids not containing potassium Eating disorder Gastrointestinal • Vomiting • Diarrhoea • Fistula Renal • Diuretics • Osmotic diuresis • Aldosterone excess • Mineralocorticoid excess • Congenital disorders • Renal artery stenosis Alkalosis Hypomagnesaemia Hypernatraemia Glucose/insulin infusion Diabetic ketoacidosis Refeeding syndrome Loop diuretics (eg frusemide) Thiazide diuretics Amphotericin Cisplatin Insulin Salbutamol Adrenaline Sampling error • Recent line flush • IV fluids near sampling site Hypokalemia; etiology
- 17. Hypokalemia; diagnosis •History; renalor extra-renal losses, diabetes mellitus, thyroid disease, family history, drug history. •O/E; Growth pattern, body weight, pulse, HTN, respiratory pattern •Investigations; WBC, ABG, anion gap, urine potassium excretion per 24 hours, TTKG, Ser. Mg
- 18. Hypokalemia; Clinical consequences •muscle weakness, cramps, paralysis • hyporeflexia • constipation, ileus • lethargy, confusion • rhabdomyolysis (rare) • Nephrogenic diabetes insipidus • ECG changes in hypokalemia • Flattened T waves and prominent U waves (apparent QT prolongation) • Prominent U waves combined with depressed ST segments and flattened T waves • widening of QRS complex • fibrillation
- 19. Pull and pusheffect” of potassium on T wave of ECG
- 20. Urine K+ excretion DKA RTA-I RTA-II Amphotricin >15 mEq/L Assess acid –base status Hypertension? TTKG<3 Assess K + secretion TTKG>4 Met. Alkalosis < 15 mEq/L Met. Acidosis Lower GI K+ loss Diuretic vomiting Sweet K + loss Assess acid –base status Met. Alkalosis Met. Acidosis Vomiting Barter/Gitelman Hypomagnesemia Diuretic abuse Renal vascular stenosis Hyperaldostronism Liddle’s synd. Na+ wasting nephropathy Osmotic diuresis Diuretics (+) (-) Lab. data 1- RFT 2- ABG, FBS, s.Mg+2 3- Urine K & Cl 4- PRA & Aldosterone 5- TTKG
- 21. Hypokalemia; management •Is thereacid base imbalance? •Consider the degree and source of potassium losses. •Check the serum magnesium level in complicated, severe and chronic hypokalaemia.
- 22. Choice of dosingroute • Oral is the preferred route of administration • Oral potassium is well absorbed from the GI tract. • Taken with or soon after food to reduce GI irritation. • Consider intravenous replacement if: • child is unable to tolerate oral medication, • serum potassium <2.5 mEq/L, or • ECG changes present
- 23. Oral/enteral dosing • Acutereplacement dose • 1 - 2 mEq/kg/dose orally (maximum 20 mEq per dose) • Dose may be repeated, after checking serum potassium level, to a maximum of 5 mEq/kg/DAY (maximum daily dose 50 mEq) • Maintenance dose(if required) • 2 - 5 mEq/kg/DAY orally in divided doses (maximum 20 mEq per dose) • Hypokalemia + high urine Cl: Oral Potassium Chloride • Hypokalemia + Met. Acidosis: K. citrate salt • Magnesium deficiency should be corrected if refractory hypokalemia
- 24. Medication Forms: • VialKCl 15% 2mEq/ml • Vial KCl 10% 1.33 mEq/ml • Tab. Eff K. 1gr 14 mEq/Tab • EC Tab 600 mg 8 mEq/tab • Tab potassium Citrate 5 & 10 mEq/tab
- 25. Potassium replacement therapy IVpotassium indicated in: severe hypokalemia symptomatic hypokalemia (cardiac/respiratory) Oral potassium cannot be tolerated Malabsorption syndrome is suspected - IV potassium preparation: should normally be diluted in saline solution maximum concentration: peripheral lines up to 40 mEq/L central lines more than 40 mEq/L 1 meq/kg of K+ → ser K+ 1mEq ↑
- 26. Potassium replacement therapy -cardiac monitoring is necessary in patients with profound hypokalemia (< 2.5 mEq/L) if cardiac arrhythmias are present, if IV potassium is going to be rapidly administered - rapid IV bolus administration of potassium is usually contra-indicated - rapid IV administration of potassium (5 - 10 mEq over 10 minutes) in: respiratory muscle paralysis hypokalemia-induced malignant arrhythmias Consideration: 1. IV administration via a central line 2. physician-supervised, 3. Cardiac monitoring 4. repeat serum K+ level q 30 minutes
- 27. K+ supplementation therapyfor hypokalemia 5 - 10 meq/hour If heart block or renal insufficiency exists 10 - 20 meq/hour Standard IV replacement rate 20 - 40 meq/hour Serum potassium < 2.5 mEq/L or moderate-severe symptoms > 40 meq/hour Serum potassium < 2.0 mEq/L or life-threatening symptoms Ser K+: 3-3.5 Oral→1-2 mEq/kg/day (max 40-120 mEq/day) 2.5-3 Oral-iv → 40-60 mEq/lit 2 – 2.5 iv → 0.5-1 mEq/kg/hr (max 10 mEq/hr) < 2 iv →2-3 mEq/kg/hr IV infusion rate for severe or symptomatic hypokalemia • Maximum potassium concentration for peripheral IV access is 40 mEq/Lit • Maximum potassium replacement should not exceed 100 mEq/ day, or even lower if there is oliguria, or renal dysfunction exist. • Maximum potassium concentration for peripheral IV access is 40 mEq/Lit • Maximum potassium replacement should not exceed 100 mEq/ day, or even lower if there is oliguria, or renal dysfunction exist.
- 28. HYPERKALEMIA Hyperkalemia is definedas a plasma potassium level less than 5.5 mEq/L. Serum potassium (mEq/L) Severity 5.5 - 6.0 Mild 6.0 - 6.5 Moderate > 6.5 Severe
- 29. Hyperkalemia • Spurious (pseudohyperkalemia) •Marked leuckocytosis ( >100000/ mm), • Sever thrombocytosis, • Hemolysis, • Tumor lysis syndrome, • Rhabdomyolysis • Redistribution ( potassium shift out cells) • Acidemia • Hyperkalemic periodic paralysis • B2 adrenergic blockers • miscellaneous • Renal failure • Aldosterone deficiency • Drugs: • ACEI, ARBS, cyclosporine, Spironolactone, NSAID, Digoxin, B2 agonists, Most common: Renal Failure, Drugs and potassium shift
- 30. Hyperkalemia; Clinical consequences •Usually occur when potassium conc. > 6.5 mEq/ L, • Neuromuscular; weakness, ascending paralysis, and respiratory failure • progressive ECG changes; peaked T Wave, fattened P wave, prologned PR interval, idioventricular rhythm, and widened QRS complex, and deep S wave, followed by ventricular fibrittation. • These cardiac changes may occur suddenly without warning
- 33. Therapy of hyperkalemia •Medication Overview: Mechanism of action • Emergency treatment: Antagonism of membrane actions of potassium • Calcium chloride • Calcium gluconate 10% • Temporizing treatment: Shift potassium intracellularly • Glucose / insulin • Alkalinize ( Sodium bicarbonate IV) • Inhaled 2 adrenergic agonist (albuterol) • Chelating therapy: Removal of potassium from the body • Loop / thiazide diuretics • Cation exchange resin: sodium polstyrene sulfonate (Kayexelate®) • Dialysis
- 34. Control of underlinedisease Stop Potassium retaining drugs Diet modification Monitor potassium level Control of underline disease Stop Potassium retaining drugs Diet modification Monitor potassium level Mild (K+=5.4-5.9) Moderate (K+=6.0-6.4) severe(K+>6.5) ECG; Are ECG changes presents? ECG; Are ECG changes presents? Emergency treatment Calcium Gluconate Repeat after 5 min if persisted ECG findings Emergency treatment Calcium Gluconate Repeat after 5 min if persisted ECG findings Temporizing treatment albuterol Glucose/Insulin Bicarbonate Temporizing treatment albuterol Glucose/Insulin Bicarbonate Chelating therapy Loop / thiazide diuretics Cation exchange resin (Kayexelate®) Dialysis Chelating therapy Loop / thiazide diuretics Cation exchange resin (Kayexelate®) Dialysis yes No
- 36. Calcium: 2 solutions : •Calciumgluconate 10%: 0.5 mL/kg slow IV injection • 2-5 minutes if unstable, over 15-20 min if stable (Max: 20 mL) • Preferable if only peripheral line available OR •Calcium Chloride 10% : 0.1-0.2 mL/kg slow IV injection (as above) (Max: 10 mL) Note: Give under cardiac monitoring, discontinue if HR dropping significantly Avoid extravasations NOT to be given simultaneously with bicarbonate NOT to be given if digoxin toxicity Onset of Action: <3 minutes, should see normalization of ECG. If not: repeat dose (twice) Duration: ~30 minutes
- 37. Salbutamol (Albuterol): o Salbutamol:nebulization ▪ Less than 25 kg : 2.5 mg neb 1-2 hourly ▪ More than 25 kg : 5 mg neb (Adu max 10-20 mg) 1-2 hourly o Salbutamol : IV *Only if severe hyperkalemia under supervision by physician on tertiary center with monitoring for tachycardia Onset of Action: 30 minutes Duration: 2-3 hours
- 38. Insulin/glucose, to begiven at the same time If severe hyperkalemia: o Dextrose 10% : 5 mL/kg IV bolus (if no hyponatremia) o Insulin short action: 0.1 U/kg IV bolus (max 10 units) Then followed by infusion insulin/glucose (see below) If moderate hyperklemia: o Dextrose 10% IV at maintenance with 0.9% sodium chloride (normal saline) o Insulin short action infusion : 0.1 U/kg/h IV Note: Close monitoring of glucose every 30-60 minutes Onset of Action: 15 minutes Duration: peak 60 minutes, 2-3 hours
- 39. Bicarbonate In metabolic acidosisonly Severe hyperkalemia and metabolic acidosis o Sodium Bicarbonate 8.4% 1 mEq/mL : 1-3ml/kg IV over 5 minutes Mild to moderate hyperkalemia and metabolic acidosis: o Sodium Bicarbonate 8.4% 1 mEq/mL : 1 mL/kg slow IV infusion over 30 minutes Note: Do NOT give simultaneously with Calcium Onset of Action: 30-60 minutes Duration: 2-3 hours
- 40. Polystyrene sulfonate (Kayexalate) Mildeffect, multiple doses necessary, may be used as long term agent Dose: 0.3-1 g/kg 6 hourly (max 15-30 g) PR or oral (with lactulose) Note: NOT to be used if ileus, recent abdominal surgery, perforation, hypernatremia Onset of Action: 1 hour PR, 4-6 hours oral Duration: variable
- 42. Hyperkalemia;non-urgent manangement • Anyunderlying causes should be diagnosed and treated: • Offending drugs discontinued • Low potassium diet considered (CKD) • Metabolic acidosis • Fludrocortisone may be useful in the setting of hypoaldosteronism.
- 43. Hyperkalemia;non-urgent manangement • Increasedrenal potassium elimination may be achieved by • volume expansion with normal saline • Judicious use of loop diuretics to improve the distal delivery of sodium and water.