Hypokalemia (Low Potassium Levels) in Animals

Hypokalemia (Low Potassium Levels) in Animals

Hypokalemia is a term that refers to a low blood concentration of potassium. Potassium is an important electrolyte within the body and is vital for the normal function of muscles and nerves. In some situations, the normal control of body potassium concentration is lost, resulting in depletion of potassium and low blood potassium concentrations. 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. Total body potassium depletion leads to muscle weakness and may or may not be associated with low plasma potassium concentration (hypokalemia). More often, hypokalemia is observed on a serum biochemistry profile in animals without potassium depletion (potassium redistribution). The clinical significance of hypokalemia cannot be ascertained without considering the other electrolytes as well as the acid-base status. Moreover, the physical examination and complete history dictate whether intervention is necessary

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.

What are the clinical signs associated with hypokalemia?

Mild to moderate hypokalemia does not usually cause significant clinical signs. However, if severe hypokalemia develops, it can cause profound and life-threatening clinical signs. The main effect of severe hypokalemia is generalized muscle weakness. Affected animals have difficulty in getting up and walking, and may appear almost “drunk” because of their weakness. The inability to raise the head into a normal position, so that the head is held down or the neck is bent, tends to occur much less frequently in animals when compared to cats. Hypokalemia can also cause marked depression and lack of appetite. Some animals with hypokalemia may become constipated. In many cases, the dog will have a poor-quality coat.

Clinical signs

Muscle weakness may be observed when serum potassium concentration falls below 2.5-3.0 mEq/L. Rear limb weakness and, in cats, weakness of neck muscles with ventroflexion of the head are commonly observed. Cardiac arrhythmias may develop because hypokalemia increases automaticity and delays ventricular repolarization. In dogs and cats, the electrocardiographic changes associated with hypokalemia are inconsistent but ventricular arrhythmias may be observed. Polyuria, polydipsia, and defective urinary concentrating ability may be observed in hypokalemia.

Diagnosis

The clinical history often will provide information about the likely source of potassium loss (e.g. vomiting, diuretic administration). Determination of the fractional excretion of potassium (FEK as a percentage = UKPCr/PKUCr X 100) may help differentiate renal and non-renal sources of potassium loss. The FEK should be < 4% for non-renal sources of loss and values > 4% indicate inappropriate renal loss in the face of hypokalemia. The occurrence of hypokalemia with metabolic alkalosis suggests vomiting of stomach contents or diuretic administration as likely causes of potassium loss.

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

Compiled  & Shared by- Team, LITD (Livestock Institute of Training & Development)

Image-Courtesy-Google

Reference-On Request.

Please follow and like us: