Internal Medicine Nephrology

Hyperkalemia

Hyperkalemia ECG
Increased T and S wave amplitudes are common ECG abnormalities in hyperkalemia.

Introduction – Hyperkalemia

Hyperkalemia (Serum potassium> 5.6 mmol/l) is often a sign of other underlying disease that requires a specific diagnosis and treatment. In addition, it is common for hyperkalemia to be a side effect of drug therapy, often in combination with other adverse conditions such as decreased extracellular volume (dehydration).

When assessing hyperkalemia, it should be borne in mind that 98% of potassium in the body is intracellular. Treatment is initially nonspecific, but should afterward address the underlying cause. Untreated hyperkalemia can be fatal.


Causes – Hyperkalemia

The most common cause of hyperkalemia is medication. In hospitalized patients, it is not uncommon for a combination of several different factors to be present, where dehydration (reduced extracellular volume) is highly contributing.

  • False hyperkalemia
    – Stasis during routine hematological testing
    – Leukemia with pronounced leukocytosis or thrombocytosis (megakaryocytosis)
  • Redistribution of potassium
    – Acidosis, especially in concomitant insulin and fluid deficiency (diabetic ketoacidosis)
    – Digitalis intoxication
  • Reduced renal excretion of potassium
    Renal
    – Adrenocortical deficiency: Addison disease or isolated aldosterone deficiency
    – Drug: potassium-sparing diuretics, which include aldosterone antagonists (spironolactone, eplerenone), amiloride, ACE inhibitors, NSAIDs, trimethoprim and heparin
    – Interstitial nephritis
  • Increased serum potassium concentration
    – Hemolysis or pronounced muscle necrosis

Symptoms and Clinical Findings – Hyperkalemia

  • Neuromuscular symptoms
    – Muscular weakness
    – Loss of tendon reflexes
    – Paralysis
    – Anxiety and confusion may occur
  • ECG changes and arrhythmia
    Initially, increased amplitude of T and S waves and reduced R wave amplitudes. Later, prolongation of QRS complexes and PR intervals with increased risk of ventricular tachycardia and asystole. In severe hyperkalemia, small ECG changes can rapidly progress to severe arrhythmias.

Diagnostics

The diagnostic investigation aims to find the underlying condition/disease and to rule out false hyperkalemia. In the case of Serum potassium >7 mmol/l and/or the occurrence of ECG abnormalities, urgent treatment should be given during cardiac monitoring while continuing the diagnostic procedures.

  • In clinically unaffected patients without ECG changes, falsely elevated values ​​are excluded by simultaneous measurement of serum and plasma potassium and/or retesting of venous samples without stasis.
  • Clinical Medication Review.
  • Plasma glucose test to exclude diabetic ketoacidosis.
  • Test of renal function (S-creatinine, urea), evaluation of urine production (history and measurement) and determination of S-Na and S-Ca.
  • Check blood gas (pH and bicarbonate/base excess).
  • Other targeted testing depending on clinical status (eg P-glucose, CBC, CK, LD, serum cortisol).
  • Blood pressure and other clinical estimates of the degree of hydration (mucous membranes, skin turgor, etc.).

Treatment suggestion – Hyperkalemia

Acute treatment is given if Serum potassium >7 mmol/l and/or the presence of ECG abnormalities. The treatment is aimed at reducing the cardiac toxic effects of potassium as well as transporting potassium from the extracellular compartment to the intracellular. A longer-term strategy is to reduce the gastrointestinal uptake of potassium and to increase the urinary output of potassium.

In the case of severe renal insufficiency with concomitant oligo- or anuria, the same treatment is appropriate, but acute dialysis should be considered. In insulin infusion and bicarbonate administration in acidosis, serum potassium levels can drop rapidly, especially if the total amount of potassium in the body is normal or decreased, as is often the case with diabetic ketoacidosis. Monitoring of S-potassium should, therefore, be carried out at least 2 times/hour during such treatment.

  • Iv Ca 2+ (10 ml Calcium-Sandoz 9 mg/ml for 3 minutes). Effect on ECG abnormalities and/or arrhythmia should be seen after a few minutes and last for 30-60 minutes.
  • In case of signs/suspicion of hypovolemia ensure infusion of isotonic sodium chloride solution (0.9 mg/ml).
  • Insulin infusion with adequate glucose to prevent hypoglycemia (eg 20 IU fast-acting insulin Actrapid, Humulin Regular or Insuman Rapid in 1000 ml 5% glucose solution with an infusion rate of between 100-200 ml per hour). Insulin shifts potassium intracellularly.
  • Bicarbonate infusion in the presence of acidosis. Sodium bicarbonate 50 mg/ml or 60 mmol/100 ml at a dose estimated by the formula:

    Reduction in standard HCO3  (mmol / L) * 0.3 * weight in kg = deficit in mmol

    Half estimated deficit is given and acid-base status is re-checked.
  • Loop diuretics that increase potassium excretion from the kidneys. Consider simultaneous infusion of isotonic NaCl solution to prevent hypovolemia.
  • Resin administered orally or rectally. The usual oral dose of Resonium is 15g x 3–4 daily which can also be administered in a gastric tube. An equal dose can be given rectally.

Insulin and diuretic therapy may be discontinued when the serum potassium concentration is normal, while resin therapy is recommended to be discontinued when S-potassium reaches 5 mmol/L. The underlying cause should be treated and any drugs contributing to the hyperkalemia should be discontinued.


Further Reading