Thursday, 18 April 2013

Evaluation of hypokalemia

Urgent Considerations

Any of the conditions that cause hypokalemia may result in varying degrees of clinical severity depending on duration of the cause and presence of other comorbid conditions. However, certain conditions are more likely to result in severe hypokalemia, such as unreplaced GI or urinary losses. Potassium replacement is required urgently in patients with severe hypokalemia (serum potassium 2.5 mEq/L) or in patients who are symptomatic. Additional caution is required when replacing potassium in patients with a concurrent disorder or therapy (such as during diuretic therapy for heart failure or insulin therapy for diabetic ketoacidosis or nonketotic hyperglycemia).

Urgent potassium replacement

Potassium replacement is required urgently in patients with severe hypokalemia (serum potassium 2.5 mEq/L) or in patients who are symptomatic. Serum potassium concentration is monitored frequently during repletion, to avoid hyperkalemia. The method of replacement depends on the clinical situation:
  • Patients able to tolerate oral intake: if the patient does not have diabetic ketoacidosis or nonketotic hyperglycemia, potassium repletion is most easily done orally, even in people with severe hypokalemia. The serum potassium concentration can rise acutely by as much as 1 to 1.5 mEq/L after an oral dose of 40 to 60 mEq of potassium. IV potassium chloride may be used as an adjunct to oral replacement if large doses are required, as these can cause gastric irritation.

  • Patients unable to tolerate oral intake: IV potassium replacement is required. However, even low rates of administration can sometimes result in hyperkalemia, so caution is required. There is also a potential risk of fluid overload in susceptible patients. The maximum recommended rate of IV potassium administration is 10 to 20 mEq/hour (daily maximum 400 mEq/day). [11] Faster rates may be considered if there are serious manifestations such as ECG manifestations, muscle weakness, or paralysis. Potassium solutions with concentrations more than 60 mEq/L are often painful, and should be infused into a large vein, preferably a central vein.
  • Patients with diabetic ketoacidosis or nonketotic hyperglycemia: IV potassium replacement is needed if hypokalemia occurs, as there are usually marked potassium losses. The maximum recommended rate of IV potassium administration is 10 to 20 mEq/hour (daily maximum 400 mEq/day); higher rates of administration carry a risk hyperkalemia. [11]
Throughout repletion, careful monitoring of the physiologic effects of severe hypokalemia (ECG abnormalities with continuous cardiac monitoring, muscle weakness, or paralysis) is essential. If a rate of repletion greater than 20 mEq/hour is used, the rate should be slowed to 10 to 20 mEq/hour as soon possible.
Any potassium supplement in patients who are taking a potassium-sparing diuretic requires particularly careful monitoring to prevent the possible development of hyperkalemia. This can be a problem in patients with moderate to severe heart failure. These patients have decreased renal perfusion, due to the fall in cardiac output, and are often treated with an ACE inhibitor and/or angiotensin II receptor blocker, plus an aldosterone antagonist (spironolactone or eplerenone). This combination of factors results in a marked reduction in urinary potassium excretion and an increased risk of hyperkalemia.

Concurrent hypomagnesemia

IV magnesium replacement therapy is indicated if serum magnesium is less than 1 mEq/L. A loading dose of magnesium can be given IV (adults: 1-2 g over 15 minutes; children: 25-50 mg/kg over 15 minutes), followed by a continuous IV infusion (maximum 4 g/24 hours, including loading dose), as required. Alternative dosing routes include intramuscular (adults: 1 g every 6 hours, maximum 4 g/24 hours) and intraosseous (children: 25-50 mg/kg, maximum 2 g/24 hours).Oral replacement is given in the asymptomatic patient. Patients suspected of having hypomagnesemic-hypokalemic ventricular arrhythmias receive IV magnesium slowly over 8 to 24 hours.

Severe muscle weakness or paralysis

Severe muscle weakness is a complication of hypokalemia. Provided the hypokalemia develops slowly, it does not usually occur at potassium concentrations more than 2.5 mEq/L. [11] Weakness usually begins with the lower extremities, progresses to the torso and upper extremities, and can worsen to the point of paralysis. Respiratory muscle weakness can sometimes be severe enough to result in respiratory failure and death. Involvement of the GI muscles can result in ileus and its associated symptoms of distension, anorexia, nausea, and vomiting. Cramps, paresthesias, tetany, muscle tenderness, and atrophy can also occur. Urgent potassium replacement is required.

Cardiac arrhythmias

A variety of arrhythmias may be associated with hypokalemia. There is considerable variability in potassium concentrations associated with the progression of ECG changes. Arrhythmias include sinus bradycardia, premature atrial and ventricular beats, paroxysmal atrial or junctional tachycardia, atrioventricular block, and ventricular tachycardia or fibrillation. [11] Typically, there is depression of the ST segment, decrease in the amplitude of the T wave, and an increase in the amplitude of U waves (often seen in the lateral precordial leads V4 to V6). image
The presence of concomitant factors, such as coronary ischemia, digitalis use, increased beta-adrenergic activity, and magnesium depletion, can promote arrhythmias due to hypokalemia. In addition, diuretic-induced magnesium depletion promotes arrhythmias, particularly in patients also treated with drugs that prolong the QT interval, which can predispose to torsades de pointes. [33] Urgent potassium replacement is required.

Renal abnormalities

Chronic hypokalemia may result in renal dysfunction. It can induce impaired urinary concentrating ability (which may be symptomatic with nocturia, polyuria, and polydipsia), increase renal ammonia production due to intracellular acidosis, increase renal bicarbonate reabsorption, and lead to hypokalemic nephropathy. [34]

Hypokalemic periodic paralysis

This is a rare disorder characterized by potentially fatal episodes of muscle weakness or paralysis that can affect the respiratory muscles. Hypokalemic periodic paralysis is often precipitated by exercise, stress, an excessively large carbohydrate meal, or conditions associated with increased release of epinephrine, cortisol, aldosterone, or insulin. [8] Acute attacks can lower the plasma potassium concentration 1.5 to 2.5 mEq/L and are often accompanied by hypophosphatemia and hypomagnesemia. [9] Urgent potassium replacement is required.

Diabetic ketoacidosis and nonketotic hyperglycemia

Renal potassium excretion increases primarily related to glucose osmotic diuresis and to hypovolemia-induced hyperaldosteronism. However, in diabetic ketoacidosis, because of a shift of potassium out of the cells, serum potassium is often elevated at presentation. With the administration of insulin, the serum potassium concentration often falls dramatically.
Serum potassium is maintained between 4.0 and 5.0 mEq/L to prevent hypokalemia. Potassium chloride at a rate of 20 to 30 mEq/L is generally added to the IV replacement fluids once the serum potassium concentration falls below 5.3 mEq/L, assuming a urine output above 50 mL/hour. Insulin therapy is delayed until the serum potassium is more than 3.3 mEq/L to avoid possible arrhythmias, cardiac arrest, and respiratory muscle weakness.
Potassium repletion is more urgent in patients with massive potassium deficits who are hypokalemic before therapy. If the initial serum potassium level is less than 3.3 mEq/L, aggressive potassium replacement with 20 to 30 mEq/hour is given; this usually requires 40 to 60 mEq/L with fluid replacement.

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