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Hypokalemia diagnosis, causes and treatment
- 1. Approach to Hypokalemia Dr Garima Aggarwal 22.09.2014
- 2. APPROACH TO HYPOKALEMIA PATHOPHYSIOLOGY CLINICAL APPROACH TREATMENT
- 4. Potassium homeostasis . The ratio of intracellular to extracellular potassium determines the cellular membrane potential. Small changes - profound effects on the function of the cardiovascular and neuromuscular systems.
- 5. Cellular K+ Content Intracellular K+ affects intra to extracellular K+ With K+ depletion , K+ loss from ECF > ICF loss causing increased Ki + / Ke+ K+ depletion : hyperpolarization K+ retention : depolarization
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- 9. Factors modifying transcellular K+ distribution Acid base status Pancreatic hormones : insulin , glucagon Catecholamines Aldosterone Plasma Osmolality Exercise Cellular K+ content
- 10. Acid Base Status Alkalemia promotes K+ uptake by cells Acidemia diminishes K+ uptake by cells H+ K+ K+ H+ ACIDOSI S ALKALOSIS An oversimplification in acidosis
- 12. Exercise Recurrentcontraction increases K+ egress from muscle Modest exercise : high K+ in ECF in local environment produces vasodilatation & thereby increased regional blood flow Severe exercise : increase plasma K+ modestly Physical training increases Na+K+ATPase activity in skeletal muscle which helps skeletal muscle to take up K+ again
- 13. RENAL ADAPTATION Kidneys adapt to both acute and chronic alterations in potassium intake. obligatory renal losses are 10-15 mEq/d. Maintain potassium homeostasis until the glomerular filtration rate drops to less than 15-20 mL/min. In the presence of renal failure, the proportion of potassium excreted through the gut increases. However, as renal function worsens, the kidneys may not be capable of handling an acute potassium load.
- 14. Renal Handling ofK+ Glomerulus: freely filtered PCT, Thick As limb LOH : reabsorbed DCT, CNT, CCD – secreted
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- 19. RENAL ADAPTATION Excretionis increased by (1) aldosterone, (2) high sodium delivery to the collecting duct (eg, diuretics), (3) high urine flow (eg, osmotic diuresis), (4) high serum potassium level
- 20. Invitro studies Aldosterone stimulates Na+K+ATPase and thereby activating Na + influx Aldosterone
- 21. Hypokalemia Definedas plasma concentration of K+ < 3.5 mEq/L Mild Hypokalemia : 3.0 – 3.5 mEq/L : asymptomatic Moderate Hypokalemia < 3.0 mEq/L : symptomatic Severe Hypokalemia <2.5 mEq/L Clinical manifestations of hypokalemia vary greatly between individual patients & their severity depends on degree of hypokalemia
- 22. Hypokalemia Decreased intake Redistribution into cells Increased loss Renal Extra renal
- 23. PSEUDOHYPOKALEMIA -spurious "pseudohypokalemia" occurs in acute myelogenous leukemia large number of leucocytes in the blood specimen (stored at room temperature) sponge-up the extracellular potassium => artefactually low serum potassium reading
- 24. Decrease K intake Dietary – starvation, clay ingestion IV therapy
- 25. Redistribution into cells Alkalosis Insulin Excess Beta-2 agonist Alpha antagonist Hypokalemic periodic paralysis Anabolic state-vit. B 12, folic acid •GM CSF •Total parenteral nutrition •Hypothermia •Barium toxicity •Pseudohypokalemia
- 26. GI LOSS ofK+ Secretory diarrhea GIT fistula or small bowel enterostomy malabsorption syndrome excessive, voluminous vomiting laxative abuse
- 27. Transtubular potassium gradient (TTKG) To account for the potentially confounding effect of urine concentration on the interpretation of the urine potassium the serum-to-tubular fluid ratio of potassium at the level of the cortical collecting tubule, where potassium is secreted. TTKG = (Urine potassium/urine osmolality : serum potassium /serum osmolality) A value less than 3 suggests that the kidney is not wasting excessive potassium, while a value greater than 7 suggests a significant renal loss..
- 28. DISTAL K+ SECRETION(TTKG>4) With normal or low blood pressure 1.With alkalosis – Diuretic therapy, Bartters and gitelmans syndrome 2. With acidosis – RTA type 1& 2, carbonic anhydrase inhibitor therapy 3. With variable pH – post obstructive diuresis, Recovery after ATN,Mg depletion,amphotericine B
- 29. Barrter’s Syndrome Site of lesion – TAL Abnormal NKCC2,ROMK,Cl channel Na wasting,volume contraction RAASNa reabs by CT K&H secretion,met alkalosis,hypokalemia
- 30. Gitelman’s syndrome Autosomal recessive Abnormal NCCT Na wasting RAAS activation K & H secretion metabolic alkalosis,hypokalemia
- 31. DISTAL K+ SECRETION(TTKG>4) With Hypertension 1.Hyperaldosteronism- Primary - Conns syndrome Secondary - Renal ischemia, malignant HTN,hypovolemia, renin secreting tumours 2. Other forms of mineralocorticoids receptor activation - cushing syndrome, apparent min. excess 3. Liddles syndrome
- 32. Hypokalemia,Hypertension & Alkalosis Disease S.aldost erone PRA S.cortisol Response to steroids Primary aldosteronism No GRA Yes AME Yes Liddle’s synd No Adr enz def Yes
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- 34. HYPOKALEMIA-TREATMENT (1) decreasingpotassium losses, (2) replenishing potassium stores, (3) evaluating for potential toxicities, (4) determining the cause in order to prevent future episodes.
- 35. HYPOKALEMIA-TREATMENT Intreating hypokalemia, the first step is to identify and stop ongoing losses of potassium. Discontinue diuretics/laxatives. Use potassium-sparing diuretics if diuretic therapy is required (eg, severe heart failure). Treat diarrhea or vomiting. Use H2 blockers to decrease nasogastric suction losses. Control hyperglycemia if glycosuria is present.
- 36. HYPOKALEMIA-TREATMENT Repletionof potassium losses is the second step. As a first approximation, for every decrease in serum potassium of 1 mEq/L, the potassium deficit is approximately 200-400 mEq.. Oral potassium is absorbed readily. Relatively large doses can be given safely.
- 37. HYPOKALEMIA-TREATMENT ifthe hypokalemia is mild-moderate => po administration potassium chloride should occur more slowly over several days at 80 - 160 meq/day in divided doses .
- 38. HYPOKALEMIA-TREATMENT Intravenouspotassium is less well tolerated because it can be highly irritating to veins and can be given only in relatively small doses, generally 10 mEq/h. Under close cardiac supervision in emergent circumstances, as much as 40 mEq/h can be administered through a central line. Oral and parenteral potassium can be used safely simultaneously. Take ongoing potassium losses into consideration
- 39. HYPOKALEMIA-TREATMENT avoidglucose-containing parenteral fluids to prevent an insulin-induced shift of potassium into the cells. If the patient is acidotic, correct the potassium first to prevent an alkali-induced shift of potassium into the cells. Replete magnesium if low. Digoxin , liver disease –keep at 4.0 meq/l
- 40. Potassium replacement therapy - cardiac monitoring is necessary in patients with profound hypokalemia (< 2.5 meq/L), or if cardiac arrhythmias are present, if IV potassium is planned - rapid IV bolus administration of potassium is usually contra-indicated - the body has a limited ability to rapidly absorb potassium and lethal cardiac arrhythmias may result
- 41. Potassium replacement therapy - IV potassium diluted in saline solution the maximum concentration is 40 meq/L (peripheral lines) or 60 meq/L (central lines) 10 - 20 meq/hour (in the average-sized adult) for hypokalemia - if po potassium replacement therapy cannot be tolerated or if a malabsorption syndrome is suspected
- 42. IV infusion ratefor severe or symptomatic hypokalemia 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
- 43. Thank you foryour attention