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HypoKaleMia

Date post: 01-Nov-2014
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Epidemiologi hingga tatalaksana hipokalemia
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Hypokalemia • a relatively common finding in both outpatients and inpatients, perhaps the most common electrolyte abnormality encountered in clinical practice. • it is found in up to 20% of hospitalized patients. • Hypokalemia is also a common finding in patients receiving peritoneal dialysis, with 10% to 20% requiring potassium supplementation. • Hypokalemia in itself can increase the in-hospital mortality rate up to 10- fold, likely due to the profound effects on arrhythmogenesis, blood pressure, and cardiovascular morbidity.
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Hypokalemia• a relatively common finding in both outpatients

and inpatients, perhaps the most common electrolyte abnormality encountered in clinical practice.

• it is found in up to 20% of hospitalized patients.• Hypokalemia is also a common finding in patients

receiving peritoneal dialysis, with 10% to 20% requiring potassium supplementation.

• Hypokalemia in itself can increase the in-hospital mortality rate up to 10-fold, likely due to the profound effects on arrhythmogenesis, blood pressure, and cardiovascular morbidity.

Spurious Hypokalemia

• Delayed sample analysis• patients with profound leukocytosis

Redistribution & Hypokalemia

Insulin

• Insulin and K appear to form a feedback loop of sorts, in that eases in plasma K have a marked stimulatory effect on insulin levels.

• Insulin-mediated K+ uptake is thus modulated by the factors that serve to preserve plasma K+ in the setting of K deprivation

Sympathetic Nervous System

• The sympathetic nervous system plays a prominent role in regulating the balance between extracellular and intracellular K.

• The hypokalemic effect of catecholamines appears to be largely independent of changes in circulating insulin and has been reported in nephrectomized animals

• The cellular mechanisms whereby catecholamines induce K + uptake in muscle include an activation of Na ATPase, likely via increases in cyclic adenosine monophosphate (cAMP).

• However, ß-adrenergic receptors in skeletal muscle also activate the inwardly directed Na-K-2Cl cotransporter NKCC1, which may account for as much as one third of the uptake response to catecholamines.

• Whereas ß-agonist-agonists activate K uptake via Na+K+ATPase, one would expect that inhibition of passive K efflux would also lead to hypokalemia; this is accomplished by barium, a potent inhibitor of K+ channels

Renal Potassium Loss

• Drugs• Hyperaldosteronism• Syndromes of Apparent Mineralocorticoid

Excess• Liddle’s Syndrome• Familial Hypokalemic Alkalosis• Bartter’s Syndrome• Gitelman’s Syndrome

• Renal Tubular Acidosis• Magnesium Deficiency

Clinical Approach to Hypokalemia

• The initial priority in the evaluation of hypokalemia is an assessment for signs and/or symptoms (muscle weakness,ECG changes, etc.) suggestive of an impending emergency that requires immediate treatment

• The history should focus on medications (e.g., diuretics,laxatives, antibiotics, herbal medications), diet and dietary supplements (e.g., licorice), and associated symptoms (e.g.,diarrhea)

• the physical examination, particular attention should be paid to blood pressure,volume status,and signs suggestive of specific disorders associated with hypokalemia (hyperthyroidism, Cushing’s syndrome, etc.)

Initial laboratory tests

• plasma electrolyte, urea, and creatinine levels;• plasma osmolality; • plasma Mg and Ca2+ concentrations;• a complete blood count; • and urinary pH, osmolality, creatinine level,

and electrolyte levels

Treatment of Hypokalemia

• The goals of therapy in hypokalemia are to prevent lifethreatening conditions(diaphragmatic weakness, rhabdomyolysis,and cardiac arrhythmias),to replace any K+deficit, and to diagnose and correct the underlying cause.

• Oral• Parenteral : arrhythmias,failure of respiratory

muscles• Dosage : 10-20 meq/hours


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