Hypokalemia

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Hypokalemia
Potassium
ICD-10 E87.6
ICD-9 276.8
DiseasesDB 6445
MedlinePlus 000479
MeSH D007008

Hypokalemia Microchapters

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Assistant Editor(s)-In-Chief: Jack Khouri

Overview

Pathophysiology

Causes

Differential Diagnosis

Cardiovascular Congestive Heart Failure
Chemical / poisoning Barium or toluene ingestion, Chloroquine overdose
Drug Side Effect Licorice, digitalis, chronic laxative abuse, beta agonists, Amphotericin B, diuretics, corticosteroids
Endocrine Adrenogenital Syndrome, Bilateral Adrenal Hyperplasia, Chewing tobacco, Cushing's Syndrome, Diabetes Insipidus, Diabetes with glucosuria, Diabetic Ketoacidosis, Hereditary pseudohyperaldosteronism, Hyperaldosteronism, Renin-secreting tumor, Steroid therapy, Stress
Gastroenterologic Vomiting, diarrhea, villous adenoma of the rectum, acute pancreatitis, alcoholism with reduced intestinal absorption of potassium, chronic inflammatory bowel disease, GI fistula, "Fad" diets, pyloric stenosis, starvation, ileus
Genetic hypokalemic periodic paralysis
Iatrogenic total parenteral nutrition, ureterosigmoidostomy, nasogastric suction
Nutritional / Metabolic malnutrition
Oncologic tumors with rapid cell turnover (leukemias)
Psychiatric Clay ingestion, acute hyperventilation, anorexia Nervosa, bulimia
Renal / Electrolyte Alkalosis, Bartter's Syndrome, chronic glomerulonephritis, hypomagnesemia, hypovolemia, Liddle's Syndrome, malignant hypertension, metabolic acidosis, polyuric phase after acute renal failure, pseudohypokalemia, Renal Artery Stenosis, Renal Tubular Acidosis

Diagnosis

Symptoms

The severity of symptoms depends on the degree of hypokalemia, but keep in mind that there is marked individual variability.

Constitutional

  • Fatigue
  • Weakness
  • Vomiting
  • Constipation
  • Muscle cramps and paralysis (the lower extremity muscles are most commonly involved) which may involve the intestine and cause ileus
  • Respiratory muscle weakness leading to respiratory failure

Cardiac

  • Hypertension
  • Arrhythmias including premature atrial and ventricular complexes, paroxysmal atrial or junctional tachycardia and even ventricular tachycardia or fibrillation
  • Heart block
  • Digoxin therapy, CAD and left ventricular hypertrophy potentiate hypokalemia effects on the heart

Renal

  • Nephrogenic diabetes insipidus due to decreased concentrating ability. As a consequence, the patient presents with polyuria and polydipsia
  • Increased bicarbonate reabsorption
  • Increased ammonia formation which may precipitate hepatic encephalopathy in cirrhotic patients
  • Decreased sodium reabsorption resulting in hyponatremia

Other

History

A detailed history can help depict the cause of hypokalemia.

Dietary history

Malnutrition: lack of meat and fruit intake

Medication history

  • Diuretics (loop and thiazides)
  • Beta agonists
  • Chloroquine
  • Theophylline
  • Insulin
  • Corticosteroids
  • Licorice
  • Nephrotoxic drugs (platinum-based chemotherapy, aminoglycosides)
  • Laxatives

Past medical history

  • Uncontrolled diabetes
  • Hyperthyroidism
  • Pernicious anemia
  • COPD (treated with Beta agonists and theophylline)
  • Cushing’s disease
  • Periodic paralysis
  • Ileostomy/short bowel
  • Primary hyperaldosteronism
  • Liddle syndrome
  • Bartter and Gitelman syndrome
  • Prolonged starvation
  • Cancer
  • Renal tubular acidosis type I and type II

Laboratory Findings

  • Complete blood count (CBC)
  • Blood urea nitrogen (BUN)/creatinine
  • Calcium
  • Magnesium
  • Glucose
  • Arterial blood gases
  • Aldosterone level
  • Renin levels
  • Urinary sodium
  • Urine potassium
    • Levels <25 meq/day (or <15 meq/L on urine spot) rule out a renal cause of hypokalemia and suggest extrarenal potassium loss or transcellular shift
    • Higher potassium excretion suggest renal losses.
  • Transtubular potassium gradient (TTKG)
    • TTKG= (Urine K x Plasma osmolarity)/(Plasma K x Urine osmolarity)
    • A TTKG less than 2-3 indicates renal potassium conservation in a hypokalemic patient
    • A urine osmolality less than plasma osmolality or urine sodium <20 mEq/L, the formula is not applicable
  • Urine chloride
    • <25 meq/L: vomiting or remote diuretic use
    • >40 meq/L: diuretics, Bartter's, Gitelman's and mineralocorticoid excess

Electrocardiography

Overview

  • Caused mainly by delayed ventricular repolarization
  • Seen at potassium levels <3 meq/L (90% of patients with potassium levels <2.7 meq/L have abnormal ECG findings)
  • Rapidly reversible with potassium repletion

ECG changes

  1. ST segment depression, decreased T wave amplitude, prominent U waves
    • seen in 78% of patients with a K < 2.7 meq
    • seen in 35% of patients with a K > 2.7 and < 3.0
    • seen in 10% of patients with a K > 3.0 and < 3.5
    • U waves are also prominent in bradycardia and LVH
  2. Prolongation of the QRS duration
    • uncommon except in severe hyperkalemia
  3. Increase in the amplitude and duration of the P-wave
  4. Cardiac arrhythmias and AV block
  5. Contrary to popular belief there is not prolongation of the QTc, this is artifactually prolonged due to the U wave. In some cases there is fusion of the T and the U wave making interpretation impossible.


Treatment

The most important step in severe hypokalemia is removing the cause, such as treating diarrhea or stopping offending medication.

  • Patients treated with loop or thiazide diuretics can be offered medications that counteract their kaliuretic effect such as aldosterone antagonists (spironolactone and eplerenone) or distal sodium channel blockers (eg, amiloride).
  • The combination of thiazide and loop diuretics should be avoided.
  • Oral potassium administration is safer than the IV route.
  • An oral dose should not exceed 20-40 mEq.
  • IV potassium infusion should be reserved for symptomatic patients with severe hyperkalemia and patients who can't take oral supplements.

Mild hypokalemia

  • Potassium levels in the range 3.0-3.5 mEq/L.
  • Represent potassium deficit of 200-400 mEq.
  • May be treated with oral potassium salt supplements: potassium chloride KCl (Sando-K®, Slow-K®) or potassium bicarbonate KHCO3 (which can be generated from the metabolism of many organic salts eg, potassium citrate, potassium gluconate, etc).
  • Potassium-containing foods may be recommended, such as tomatoes, oranges or bananas, but they are less effective than oral supplements.
  • Both dietary and pharmaceutical supplements are used for people taking diuretic medications (see Causes, above).
  • KCl is the most effective replacement for metabolic alkalosis-associated hypokalemia.
  • KHCO3 and the organic "alkalinizing" salts K-citrate and K-gluconate are recommended for hypokalemia associated with metabolic acidosis (chronic diarrhea, renal tubular acidosis,etc).

Severe hypokalemia

  • Potassium levels below 3.0 mEq/L
  • Potassium levels between 2.0 and 3.0 correspond to 400-800 mEq deficit.
  • It may require intravenous supplementation. Typically, saline is used, with 20-40 mEq KCl per liter over 3-4 hours (ie, at an infusion rate of 10 mEq/L/h)
  • Giving IV potassium at faster rates may predispose to ventricular tachycardias and requires intensive ECG monitoring.
  • Giving IV KCl at doses >60 mEq/L are painful and can cause venous necrosis.
  • Difficult or resistant cases of hypokalemia may be amenable to amiloride, a potassium-sparing diuretic, or spironolactone.
  • When replacing potassium intravenously, infusion via central line is encouraged to avoid the frequent occurrence of a burning sensation at the site of a peripheral IV and the aforementioned venous necrosis. When peripheral infusions are necessary, the burning can be reduced by diluting the potassium in larger amounts of IV fluid, or mixing 3 ml of 1% lidocaine to each 10 meq of kcl per 50 ml of IV fluid. The practice of adding lidocaine, however, raises the likelihood of serious medical errors [3].
  • Potassium infusions via a central line can reach 200 mEq/L (20 mEq in 100 mL of isotonic saline (see below)) but the administration rate should not be greater than 10–20 mEq per hour.
  • Saline solutions are preferred to prevent potassium transcellular shifting that is triggered by dextrose-induced insulin release!

See also

References


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