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HYPERKALEMIA THÁI BÌNH DƯƠNG – hump Updated on 20/9/18 BASIC Total body K+: 50mEq/Kg: - K+ in Intracellular fluid: 98% - K+ in Extracellular fluid: 2% Plasma accounts for 20% of extracellular fluid K+ in plasma = 0,4% total body K+ Ex: a 50 kg person: 2500mEq total body K+ K+ plasma: 10mEq This emphasizes the limited size of the K+ pool that is available for evaluating total body potassium BASIC K+ is lost in stool (5-10 mEq/d), swear(0-10 mEq/d), and the major lost is in urine (40-120 mEq/d), depending on K+ intake K+ is: - Filtered at the glomerulus - Passively absorbed in the proximal tubules - Secreted in the distal tubules and collecting ducts - Potassium excretion in urine is controlled by plasma K+ and aldosteron HYPERKALEMIA > 5,5 mEq/l Life-threating condition!!! Pseudohyperkalemia: - Potassium release from traumatic hemolysis during venipuncture (20%) - K+ release from muscle during fist clenching - Severe leukocytosis (>50000/mm3) - Severe thrombocytosis (>1million/mm3) ETIOLOGY Excessive intake K+: foods, drinks, IV fluid Transcellular shift Impaired renal excretion ETIOLOGY Transcellular shift Acidosis: BUT - Organic acidosis ( lactic acidosis and ketoacidosis) is not associated with hyperkalemia (MARINO THE ICU BOOK 4th) - Respiratory acidosis has an inconsistent relationship with hyperkalemia Drugs: digitalis( only when acute toxicity, not chronic), beta blockers,……… Blood transfusions (massive transfusion, at least units of RBC!!!) Rhabdomyolysis Tumor lysis syndrome: within days after the initial chemical therapy Rhabdomyolysis (tiêu vân) ETIOLOGY Impaired renal excretion Decreased GFR: - Oliguric or anuric AKI - End-stage CKD Normal GFR but decreased renal excretion of K+ - Cirrhosis, CHF: Decreased EABV - NSAIDS, HIV, diabetic nephropathy: Decreased renin - ACEI, ARB, heparin, primary adrenal insufficient: Decreased aldosterol - K+-sparing diuretic, bactrim, SLE, diabetes: Decreased response to aldosterol EABV: effective arterial blood volume Clinical manifestations Twitch: co giật Paresthesia: ngủ Irritability: kích thích, kích động ECG abnormalities (from mild to severe) Peaked T-waves AMI Hyperkalemia Acute pericarditis LVH BER Bundle branch block Pre-excitation syndromes Normal variant TREATMENTS For simple: K+ > 6,5 mEq/l Or ECG changes SEVERE HYPERKALEMIA GOALS Antagonism of the cardiac effects of hyperkalemia Transcellular shift of K+ into cells Removal of excess K+ from the body MEMBRANE ANTAGONISM - Mechanism: Calcium increases the electrical charge difference across myocardial cell membranes, oppose the depolarization produced by hyperkalemia Stabilizes cell membrane Calcium gluconate 10% 10ml = ampule contains 1g elemental calcium Calcium chloride contains three times the concentration of elemental calcium compared with calcium gluconate (13.6 versus 4.6 meq in 10 mL of a 10 percent solution) However, calcium gluconate is generally preferred because calcium chloride may cause local irritation at the injection site Use: ampule IV over min, repeat after if necessary MEMBRANE ANTAGONISM Caution With the patients on digitalis, hypercalcemia can aggravates digitalis toxicity Calcium gluconate can be added in 100 ml of NaCl 0,9% IV over 20-30 If hyperkalemia is a manifestation of digitalis toxicity, calcium is contraindicated Hyperkalemia + shock, cardiac arrest: CaCl2 is preferred BRINGS TO HOME: Should be the initial treatment, especially if ECG abnormalities because it helps prevent cardiac complications, early onset in < it should be combined with other therapies Transcellular shift Insulin + dextrose Regular insulin: 10 UI IV bolus 50% dextrose: 50 ml IV bolus 10% dextrose at 50 – 75 ml/h Monitoring blood glucose every 4-6h Regular insulin: 10 – 20 UI 10% dextrose: 500 ml IV in 60 If the patient has been already hyperglycemic ( the serum glucose is ≥250 mg/dL = 13.9 mmol/L) , only insulin and no dextrose Transcellular shift SALBUTAMOL Use: Salbutamol 0,5 mg IV ( ampule salbutamol 0,5mg/1 ml) OR 10 – 20 mg ( ampule ventolin 2,5 mg in ml saline) nebulized over 10 Caution: Salbutamol dose is needed to significantly drop K+ is at – times the bronchodilation dose unwanted side effects not advised Side effects: Mild Tachycardia, angina should probably be avoided in patients with active coronary disease Transcellular shift Bicarbonate There have been no studies that actually demonstrate an immediate or significant benefit (acute change in the serum potassium level) with bicarbonate Short-term have no effect on serum K+ Bicarbonate can form complexes with calcium It should be avoided unless there is acidemia In that case, we recommended isotonic bicarbonate 1,4% BRINGS TO HOME: Administer bicarbonate to the patient with severe hyperkalemia who is not responding to traditional therapies, such as insulin and glucose and beta-2 agonists https://docs.google.com/document/d/1VJaWkMFTt2JIIPVABqeV0y8R625vwCKledcQ9p-ASpE/edit Potassium removal Via the bowel: cation-exchange resin (Kayexalate) Via the blood stream: hemodialysis is the most effect method) Via the urinary tract: Furosemide ( in patients without severe renal impairment) 40 mg every 12 hours Kayexalate??? Sodium polystyrene (Kayexalate) is a cation exchange resin administered orally or rectally that exchanges sodium for K+ and eliminates K+ via the gastrointestinal tract The evidence advocating the use of Kayexalate to treat hyperkalemia originates from a single study published in the 1960s that demonstrated a reduction in serum K+ in patients with acute and chronic renal failure Recent literature, however, recommends against routine administration of Kayexalate in the hyperkalemic patient due to an unpredictable reduction of serum K+ and an increased risk of colonic necrosis http://rebelem.com/kayexalate-useful-treatment-hyperkalemia-emergency-department/ So in almost cases, you just remember… Calcium gluconate 10% 10ml : ampule IV over min, repeat after if necessary (first treatment!!) 10 – 20 UI regular insulin AND 10% dextrose 500 ml: IV in 60 minutes, check blood glucose – h Furosemide ( in patients without severe renal impairment) 40 mg every 12 hours Some conclusions Serum Potassium is just only the tip of the iceberg And the iceberg here is total body potassium !!! Remember a number 0,4% Hypokalemia is often well tolerated BUT hyperkalemia is life-threatening condition Remember to rule out pseudohyperkalemia before management of hyperkalemia ECG is not sensitive Don’t depends totally on ECG to diagnose Before administering calcium, you must check if the patient is using digitalis or not, check for the manifestations of digitalis toxicity You need to make sure that goals is done concomitantly: Calcium gluconate , insulin + dextrose and Furosemide Some questions for you!! How much does the serum potassium accounts for of total body potassium? List some causes that induce hyperkalemia? What is goals in management of severe hyperkalemia? Can you list some ECG abnormalities in hyperkalemia (from mild to severe)? Give me some manifestations of hyperkalemia? How we use calcium in management of hyperkalemia? How we use calcium in the Patients who are using digitalis (but not digoxin toxicity)? How can we push K+ into cells to decrease serum K+? How we use insulin in management of hyperkalemia? In case of patients with hyperglycemia? How we use loop diuretics in management of hyperkalemia? SOME MORE INFORMATION FOR YOU A 3-PRONGED APPROACH TO THE TREATMENT OF HYPERKALEMIA https://docs.google.com/document/d/1bXICT0WxH6yJiqN-ASdWOr1cAU2-MfwP1bAUZQoXEmI/edit ... induce hyperkalemia? What is goals in management of severe hyperkalemia? Can you list some ECG abnormalities in hyperkalemia (from mild to severe)? Give me some manifestations of hyperkalemia? ... Hypokalemia is often well tolerated BUT hyperkalemia is life-threatening condition Remember to rule out pseudohyperkalemia before management of hyperkalemia ECG is not sensitive Don’t depends... of hyperkalemia? In case of patients with hyperglycemia? How we use loop diuretics in management of hyperkalemia? SOME MORE INFORMATION FOR YOU A 3-PRONGED APPROACH TO THE TREATMENT OF HYPERKALEMIA
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