Hypokalemia. Etiology of hypokalemia

Transcription

1 Hypokalemia The total body K+ storage: 50~55 meq/kg ( approximately 3000~4000 meq) 98% of the body K+ is located in the cells The net effect is that [K+c] is about 140 meq/l and [K+e] is only 4~5 meq/l Daily potassium intake: 40~120 meq/day Normal daily fecal K+ loss: 5~10 meq/day # Table. Etiology of hypokalemia Decreased net intake Etiology of hypokalemia A. Low dietary intake or K-free intravenous fluids B. Clay ingestion Increased entry into cells, leading to transient hypokalemia A. Elevation in extracellular ph B. Increased availability of insulin C. Elevated B-adrenergic activity: stress, coronary ischemia, delirium tremens, administration of B-adrenergic agonists for asthma or heart failure D. Peroid paralysis hypokalemic form E. Treatment of megaloblastic anemias with vita B12 or folic acid, or of neutropenia with GM-CSF F. Pseudohypokalemia G. Hypothermia H. Chloroquine intoxication Increased gastrointestinal losses Increased urinary losses A. loop and thiazide-type diuretics B. Mineralocorticoid excess ( 見下頁 table2) C. Liddle s syndrome D. Bartter s or Gitelman s syndrome E. Increased flow to the distal nephron 1. Loop and thiazide-type diuretics 2. Salt-wasting nephropaties

2 F. Sodium reabsorption iwht a nonreabsorbable anion 1. Vomiting or NG suction 2. Metabolic acidosis 3. Penicillin derivativies G. AmphotericinB H. Hypomagnesemia I. Polyuria J. L-dopa Increase sweat losses Dialysis Potassium depletion without hypokalemia Symptoms of hypokalemia -Muscle weakness or paralysis (including intestinal ileus) -Cardiac arrhythmias, especially with digitalis, coronary ischemia, or perhaps left ventricular hypertrophy) -Rhabdomyolysis -Renal dysfunction A. Impaired concentrating ability, leading to polyuria and polydipasia B. Increased ammonia production (can induce hepatic coma in cirrhosis) C. Impaired urinary acidification D. Incrased bicarbonate reabsorption E. Renal insufficiency F. Abnormal NaCl reabsorption -Hyperglycemia

3 Clinical approach to hypokalemia 1. Please collect urine data before supplement 2. Check serum Na, K, Cl, Ca, P, Mg, BUN, Cr, Osmo, Hb/Ht ( 抽完請檢驗室先離心處理檢體, 否則 cell lysis 會影響數據 ) 3. Check urine Na, K, Cl, Cr, Osmo ( Ca, P, Mg, uric acid, urea ) 4. Check blood gas ( vein is also OK ) 5. TTKG = [K]u OSM P [K]p OSM U 6. Urine anion gap (UAG) 代表 NH 4 + excretion UAG = ([Na + ]+[K + ])-[Cl - ] 7. Urine osmolal gap (UOG) UOG = urine osmolality 2x ([Na + ]+[K + ])-[glucose]/18 BUN/2.8 1 TTKG < 3 or UK + /UCr < 0.2 Hypokalemia 2 TTKG > 3 or UK + /UCr > 0.2 Shift Non-renal K + loss Former renal K + loss High K + excretion K + : meq/l, Cr: mg/dl 1. TTKG < 3 or UK + /UCr < 0.2 Metabolic acidosis Metabolic alkalosis Normal acid-base Lower gastrointestinal K + loss Remote vomiting Remote diuretic Thyrotoxic periodic paralysis Familial periodic paralysis Sporadic periodic paralysis

4 TTKG > 3 or UK + /UCr > 0.2 Metabolic acidosis Metabolic alkalosis NH4 + excretion ( UAG, UOG) High BP Normal BP High Low Mineralocorticoid excess UCl - UCl - Toluene abuse Profound diarrhea Ureteral diversion Renal tubular Acidosis( 詳見 RTA 章節 Recent diuretic use Bartter s syndrome Recent vomiting Gitelman s syndrome ( 詳見 Bartter s syndrome & gitelman s syndrome 章節 ) Mineralocorticoid excess Renin Aldosterone Renin Aldosterone Renin Aldosterone Malignant HTN Renovascular HTN Cortisol Renin-secreting tumor Cushing syndrome Ectopic ACTH Cortisol Cortisol normal 11βor 17α -hydroxylase deficiency Primary hyperaldosteronism ( 詳見下面 hypokalemia & primary hyperaldosteronism) Aldosterone analogue Apparent mineralocorticoid excess Licorice ingestion Liddle s syndrome

5 Treatment Monitoring of the ECG and muscle strength, which reflect the functionalc onsequences of K+ depletion Potassium deficit [K+] from 4.0 to 3.0 meq/l requires the loss of 200~400 meq of K+ Acidemia (in renal failure or renal tubular acidosis) or hyperosmolality (in DKA) frequently raises the plasma [K+] and masks the severity of the K+ depletion Use of Potassium Chloride Oral The traditional therapy with K+-rich foods such as orange juice or bananas is less desirable. - phosphate and citrate content rather than chloride - less to correct the hypokalemia and meta. Alkalosis Intravenous K+ supplementation should be given in a non-dextrose- containing solution, usually in a concentration of 40 meq/l. More than 60 meq/l should be given through a central vein. Medication at MMH: Potassium chloride oral 600 mg/tab (8 meq/tab) inj. 20 meq/10 ml/amp (2 meq/ml) Potassium phosphate inj. 88 meq/20 ml/amp (4.4 meq/ml) How to supply Potassium Decrease 1 meq/l means deficient 200~400 meq K Check the Osmolarity and Acid-base status, especially DKA and acidosis will mask the K deficient condition Don't use sugar content IVF Cl Every bottle (500 cc) < 20 meq KCl, except femoral line is available

6 Rate of Potassium repletion In mild~moderate hypokalemia ([k+]: 3.0~3.5 meq/l) - Treatment is not urgent. - Treated with oral KCl at an initial dose of 60~80 meq/day. Severe symptoms or marked hypokalemia - K+ must be given more rapidly - More easily done orally [K+] will rise 1.0~1.5 meq/l after 40~60 meq & 2.5~3.5 meq/l after 135~160 meq. - The maximum effects are transient Large doses of K+ are much more difficult to given intravenously (limited to concentration and volume of fluid) IV K+ administration: Maximum rate of 10~20 meq/h At paralysis or life-threatening arrhythmias Rate of 40~100 meq/h ( [K+] 200 meq/l ) - Rapid administration of K+ is potentially dangerous even in severely K+-depleted patients and should be used only in life-threatening situations. - Continuous monitoring of the ECG is essential! Hypokalemia & Primary mineralocorticoid excess Table2. Causes of primary mineralocorticoid excess Primary hyperaldosteronism A. Adenoma B. Hyperplasia C. Carcinoma Cushing s disease (some cases) Chronic ingestion of exogenous mineralocorticoid A. fludrocortisone Hyperreninism A. Renal artery stenosis B. Renin-secreting tumor Glucocorticoid-remediable hyperaldosteronism Hypersecretion of deoxycorticosterone or other mineralocorticoid A. CYP17 (17a-hydroxylase) deficiency B. CYP11B1 (11B-hydroxylase) deficiency C. Normal levels of cortisol with chronic licorice ingestion or the syndrome of apparent minerlocorticoid excess

7 # Diagnosis of primary mineralocorticoid excess HTN + unexplained hypokalemia or normokalemia (50%) primary mineralocorticoid excess should be suspected # The way of approach of primary mineralocorticoid excess 24-h urine collection 先 DC diuretics correct volume depletion high-na+ diet Plasma renin activity High: renovascular or malignant HTN, diuretic usage, renin-secreting tumor Low: some form of mineralocorticoid excess, Liddle s syndrome Aldosterone secretion Low Overproduction of a nonaldosterone mineralocorticoid (Cushing s syndrome, DOC-producing tumor, licorice ingestion, syndrome of appropriate mineralocorticoid excess, Liddle s syndrome etc.) High 指 : [aldo] >30 ng/dl or 24-h aldo > 15 ug/day 此時加做 Suppression test & Prolonged suppression test Plasma aldosterone (PA) to renin (PRA) ratio ** Before the test ** 1. Correct hypokalemia with KCL 2. DC diuretics, CCB, high-dose beta-blockers 判別方式 : PA/PRA ratio 4~5 Normal, essential HTN PA/PRA ratio >30~50 Primary hyperaldosteronism

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