Como Tratar Hipo K

Hypokalemia refers to a serum potassium concentration of <3.5 mEq/L (normal 3.5–5.5 mEq/L). Hypokalemia can result from dilution, decreased intake, poor transmembrane distribution or excessive loss through the GI or urine.

Signs of hypokalemia are related to the alteration of the membrane potential and include muscle weakness, lethargy, paralytic ileum and eventually cardiac conductivity abnormalities, although they are never as severe as in the cases of hyperkalemia.

ECG changes appear when hypokalemia is <2.5 mEq/L but are not as clear as those seen in hyperkalemia.

Hypokalemia can prolong hypochloremic metabolic alkalosis as a result of HCO₃^- reabsorption mechanisms in the proximal tubule. Hypochloremia associated with volume depletion contributes to the perpetuation of hypokalemia secondary to aldosterone secretion.

However, some studies had demonstrated that dogs that sustained potassium depletion over a 2–4-week period, without concomitant depletion of chlorine developed metabolic acidosis and not alkalosis. The reduction in net acid excretion was apparently related to reduced aldosterone secretion and impairment of urinary acidification in the distal tubule. Metabolic acidosis was corrected after 5 days of oral supplementation of potassium. Chronic potassium depletion also induced metabolic acidosis in animals fed restricted diets, which reversed with supplementation of this element in cats.

Treatment

2,0 ml/kg/h, se suplementa K⁺ de acuerdo a la concentración sérica del paciente (Tabla 1).">The treatment of acute or severe hypokalemia requires intravenous potassium chloride. If urine output is >2.0 ml/kg/h, K⁺ is supplemented according to patient serum and the information provided in Table 1.

As long as the rate of administration does not exceed 0.5 mEq/kg/h, fluids with 20–40 mEq/l of K⁺ can be administered in patients with normal renal function. In severe situations the infusion rate may be increased to 1.5 mEq/L/hour under strict ECG monitoring.

Although the table suggests a maximum of 10 mEq/kg within 24 hours, these values must be adjusted to the patient's needs; patients with diabetic ketoacidosis may require up to three times those values in the first 24 hours.

Since insulin promotes the intracellular translocation of potassium ion reducing serum potassium, in diabetic patients insulin administration should be started only when serum potassium is in the high-normal range.

If hypokalemic signs persist despite aggressive supplementation of K⁺, hypomagnesaemia must be corrected by supplementing magnesium 0.75–1.0 mEq/ kg/day CRI in 5% dextrose sulfate. The dose is gradually reduced to 50% in 3–5 days.

Total body potassium depletion is generally so severe that serum potassium corrections usually occur gradually over several days and concomitant deficits of magnesium and chlorine that perpetuate renal potassium loss should be corrected.

Table 1. Guide for potassium supplementation

References

1.  Stephen DiBartola. Fluidoterapia, Electrolitos y Desequilibrios Ácido-Base en Pequeños Animales. 3a Edición. Multimédica Ediciones Veterinarias; 2008.

2.  Marcia Mery Kogica, Helio Autran de Morais. Hypokalemia: a quick reference. Advances in fluid, electrolyte and acid-base disorders. Veterinary Clinics of North America: Small Animal Practice. 2008;38(3):481–484.

3.  Michael Schaer. Therapeutic approach to electrolyte emergencies. Advances in fluid, electrolyte and acid-base disorders. Veterinary Clinics of North America: Small Animal Practice. 2008;38(3):513–534.

4.  Michael Willard. Therapeutic approach to chronic electrolyte disorders. Advances in fluid, electrolyte and acid-base disorders. Veterinary Clinics of North America: Small Animal Practice. 2008;38(3):535–542.