hipokalemia
TRANSCRIPT
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A C TA M E D I N D O N E S - I N D O N E S J I N T E R N M E D
APPROACH TO HYPOKALEMIA
Jurnal Reading
dr. Agung Wistara Widya
S A L I M L I M
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INTRODUCTION
• Potassium is the major intracellular cation.• Approximately 98% of the total K+ is located
intracellular, primarily in skeletal muscle and to a lesser extent in liver, and the remaining 1 to 2% is located extracellular.
• The ratio of intracellular to extracellular potassium regulated primarily by the Na+/K+ ATPase pump located on the plasma membrane of most cells.
• The normal serum K+ concentration is 3.5 to 5.0 mmol/l; whereas that inside cell is about 150 mmol/l.
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CLINICAL MANIFESTATIONS OF HYPOKALEMIA
• Hypokalemia appears to increase the risks of cardiac arrhythmias in patients with ischemic heart disease or patients taking digoxin.• Patients with more severe hypokalemia (serum
K+ less than 3 mmol/l) usually present with generalized weakness, fatigue and constipation• Moderate and severe hypokalemia can induce
electrocardiographic changes, including a prominent U wave, a attened T wave, and a widened QRS complex.
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APPROACH TO HYPOKALEMIA
• The kidney can conserve K+, such that hypokalemia due to inadequate K+ intake is a rare event requiring prolonged starvation over several months.
• The most common causes of hypokalemia are due to drugs including diuretics and gastrointestinal loss secondary to diarrhea or vomiting.
• Less frequently, hypokalemia occurs because of an abrupt transcellular shift of K+ from the extracellular to intracellular compartment, that can induce by several drugs and conditions.
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APPROACH TO HYPOKALEMIA
• The mechanism of these conditions to induce hypokalemia are variable, • Patients with psedohypokalemia do not have
clinical manifestations of hypokalemia, as their in vivo serum K+ values are normal.• Differentiating between pseudohypokalemia and
true hypokalemia requires rapid separation of the plasma from the cells or storing the blood sample on ice.
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APPROACH TO HYPOKALEMIA
• Patients with moderate to severe hypokalemia are at increased risk of life-threatening cardiac arrhythmias and respiratory muscles weakness, especially if there is a need for increased ventilation.
• This possible threat is best evaluated by examining the electrocardiogram (ECG) and arterial PCO2.
• The first step to evaluate the etiology of hypokalemia is to exclude pseudohypokalemia and conditions or drugs causing transcellular K+ shift.
• The next step is to assess renal K+ excretion, which will allow us to determine whether hypokalemia is due to renal or extrarenal causes.
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APPROACH TO HYPOKALEMIA
• A 24-hr urine collection for K+ can be used to assess renal K+ handling with value of less than 20 mmol/24-hr urine specimen suggests appropriate renal conservation of K+.
• 24-hr urine collection is inconvenient and time consuming.• Study has shown that the kidney can excrete approximately
half of the administered K+ in the rst 6 hours, some of the administered K+ will be excreted by the kidney causing urinary K+ excretion to be deceptively high.
• A random UK/Ucr ratio (mmol/g) > 15 suggests a renal cause, whereas a ratio < 15 suggests an extrarenal cause of hypokalemia, can be due to transcellular K+ shift into cells, extrarenal K+ loss, low K+ intake or former renal K+ loss
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HYPOKALEMIA DUE TO EXTRARENAL LOSS
• If hypokalemia with low rate of K excretionv(UK/UCr ratio < 15 mmol/g) is not accompanied by acute paralysis, the hypokalemia is most likely due to extrarenal K+ loss, low K+ intake or former renal K+ loss.
• Hypokalemia due to villous adenoma or laxative abuse may be associated with metabolic acidosis, alkalosis, or no acid-base disturbance.
• Inadequate K+ intake is a rare cause of hypokalemia because it requires prolonged starvation over several months (tea and toast diet)
• Signicant loss of K+ in sweat sufcient to cause hypokalemia is uncommon since the volume of sweat is low and the K+ concentration is only 5 mmol/l
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HYPOKALEMIA DUE TO RENAL LOSS
• Once high rate of K+ excretion has been conrmed (UK/UCr ratio > 15), the next step of investigation is evaluation of acid base status.
• Patients with hyperchloremic metabolic acidosis are divided in two groups based on the rate of ammonium (NH4+) excretion.
• Those with a low rate of NH4 + excretion have a renal acidication defect, whereas those with a high rate of NH4 + excretion has a normal renal acidication
• There are two ways to assess NH4 + excretion rate: urine anion gap (UAG) and urine osmolal gap (UOG)
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HYPOKALEMIA DUE TO RENAL LOSS WITHMETABOLIC ALKALOSIS
• Patients with hypokalemia due to renal loss with metabolic alkalosis can be separated into two groups based on their urinary chloride excretion.• The probable causes of low urinary chloride
excretion (< 10 mmol/l) are vomiting, nasogastric suction, posthypercapnia and congenital chloride diarrhea.• Patients with high urinary chloride excretion (>
20 mmol/l) can be divided into two groups based on their blood pressure.• Those with normal blood pressure are caused by
diuretics, Bartter’s syndrome and Gitelman’s syndrome
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HYPOKALEMIA DUE TO RENAL LOSS WITHMETABOLIC ALKALOSIS AND HYPERTENSION
• The underlying mechanism of this condition is increased reabsorption of Na+ via amiloride-sensitive sodium channel.• The cause includes gain-of-function mutation in
the ENAC, higher aldosterone levels, increases in a non-aldosterone mineralocorticoid levels or increased mineralocorticoid like effect• Measurement of serum aldosterone levels, renin
activity and serum cortisol levels can help subdivide these patients.
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TREATMENT OF HYPOKALEMIA
• The rst step to treat hypokalemia is to identify the cause of hypokalemia and to stop the ongoing losses of K+ such as treating diarrhea, vomiting, hyperglycemia or discontinuing diuretics.
• The next step is to replete potassium and magnesium decit.
• There are four types of potassium preparations: potassium chloride, potassium phosphate, potassium bicarbonate and potassium citrate
• Unless life-threatening cardiac arrhythmias or respiratory muscles weakness is present, potassium repletion is rarely an urgent undertaking
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CONCLUSION
• When given intravenously, the rate of K+ administration should not exceed 20 mmol/hour. When potassium is administered intravenously through a peripheral vein, the concentrations should not exceed 50 mmol/l.• Potassium should be diluted in saline rather than
dextrose solution since the administration of dextrose can further lower potassiu concentrations and in susceptible individuals can lead to life-threatening cardiac arrhtymia
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THANK YOU...