Hyperkalemia
From Felipedia
Potassium is the major intracellular cation in feline cells and is largely responsible for maintenance of intracellular volume. Serum potassium concentrations slightly exceed plasma concentrations because potassium is released from platelets during the clotting process. Potassium is responsible for maintaining resting cell membrane potential. Therefore, disorders of potassium concentration affect excitable membranes. Clinical signs are related to disturbances in skeletal (weakness) and cardiac (arrhythmia) muscles.
Chronic hyperkalemia almost always is associated with impairment in urinary potassium excretion. Clinical manifestations of hyperkalemia reflect changes in cell membrane excitability with muscle weakness and cardiac electrical conduction abnormalities. ECG changes in mild hyperkalemia include increased amplitude and narrowing of the T wave and shortening of the QT interval. Moderate hyperkalemia causes prolongation of the PR interval and widening of the QRS. As hyperkalemia progresses, P waves decrease in amplitude, become wide and eventually disappear. Bradycardia due to a sinoventricular rhythm may be observed, although is less pronounced in cats. The QRS may merge with the T wave creating a sine wave appearance. Clinical and ECG signs do not necessarily correlate with potassium concentration, but ECG and muscle strength reflect the functional consequences of hyperkalemia. Increased intake of potassium only causes sustained hyperkalemia if renal excretion of potassium is abnormal. Exceptions include iatrogenic hyperkalemia resulting from calculation errors during IV infusion of potassium and administration of drugs known to predispose to hyperkalemia (e.g. betablockers or ACE inhibitors) with concurrent potassium supplementation[1].
Translocation of potassium from ICF to ECF can occur in diabetic patients. Insulin deficiency and hyperosmolality contribute to the development of hyperkalemia in diabetic patients. Massive tissue breakdown may lead to transient hyperkalemia until released potassium is excreted by the kidneys. This may occur after reperfusion of aortic thromboembolism. Nonspecific beta-blockers (e.g. propranolol) decrease cellular uptake of potassium, and may cause hyperkalemia in the presence of a potassium load or decreased renal function.
Decreased urinary excretion of potassium is the most important cause of hyperkalemia in feline practice. It usually results from urethral obstruction, ruptured bladder, and anuric or oliguric renal failure. Oliguria or anuria with hyperkalemia are more likely to occur in acute renal failure, but they may be observed terminally in chronic renal failure. Patients with chronic renal disease have reduced ability to tolerate an acute potassium load and may require 1-3 days to reestablish external potassium balance when intake of potassium is abruptly increased (e.g., fluid therapy). Several drugs may reduce renal excretion of potassium. ACE inhibitors interfere with angiotensin II-mediated aldosterone secretion, whereas spironolactone competitively blocks aldosterone. Treatment of hyperkalemia will depend on the magnitude and rapidity of onset of the hyperkalemia. Patients with symptomatic hyperkalemia or ECG abnormalities should be treated. Mild chronic hyperkalemia (K < 6,5 mEq/L) may not require immediate therapy. Asymptomatic, non-oliguric patient: The underlying disease process should be treated and any source of potassium intake or drugs that cause potassium retention should be discontinued, if possible. Fluid therapy with potassium-free solutions ameliorates mild hyperkalemia by improving renal perfusion, enhancing urinary excretion of potassium, and by diluting the potassium in ECF.
Mild Hyperkalemia
Commonly seen associated with urolithiasis in cats with Feline lower urinary tract disease (FLUTD), who often have concurrent metabolic acidosis.
- Insulin/glucose
Administration of glucose or NaHCO3 can be attempted in patients with mild hyperkalemia that did not respond to potassium discontinuation and fluid therapy. Administration of glucose (1-2 ml/kg of the 50% solution) will cause release of insulin and move potassium into the cells. The effects begin within an hour and last a few hours. Concurrent administration of insulin may improve the response but it increases the risk of hypoglycemia. Sodium bicarbonate (1-2 mEq/Kg, repeated if necessary) also will move potassium inside cells within an hour. All potassium driven inside the cells will come back out after a few hours. Therefore, drugs that translocate potassium have a short duration of action[2].
- 10% calcium gluconate
Give 1 ml/kg of 10% calcium gluconate by slow IV infusion over 2-3 mins. Monitoring by ECG if available. This treatment antagonises the effects of hyperkalaemia on cell membranes and works immediately and lasts for approx. 20-30 mins. It does not affect serum K+ and corrects any hypocalcaemia.
Moderate to severe hyperkalemia
Cases of moderate to severe hyperkalemia are emergencies. Administration of calcium gluconate (2-10 ml of a 10% solution given slowly with ECG monitoring) may antagonize the adverse electrophysiologic effects of hyperkalemia. Potassium concentration, however, will remain increased and the beneficial effects of calcium are short-lived (less than one hour). Administration of glucose or NaHCO3 is recommended to lower potassium concentration.
- Adjunctive therapy: in selected cases of hyperkalemia, loop diuretics may be used to enhance the flow rate in the distal nephron and increase potassium excretion. Patients with renal failure are unlike to benefit from this maneuver.
- When Everything Failed: Atropine may be attempted in patients that are bradycardic. During the hyperkalemia-induced bradycardia, the SA-node still works (the so-called sinoventricular rhythm) and is under vagal influence. Atropine injection may cause a mild increase of heart rate and temporarily reestablish cardiac output and blood pressure. Refractory cases may require hemodialysis or continuous renal replacement therapy.
