Hypokalemia: Wikis

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Hypokalaemia
Classification and external resources

Potassium
ICD-10 E87.6
ICD-9 276.8
DiseasesDB 6445
MedlinePlus 000479
eMedicine emerg/273
MeSH D007008

Hypokalemia (American English), or hypokalaemia (British English), refers to the condition in which the concentration of potassium (K+) in the blood is low. The prefix hypo- means low (contrast with hyper-, meaning high). Kal refers to kalium, the Neo-Latin for potassium, and -emia means "in the blood."

Normal serum potassium levels are between 3.5 to 5.0 mEq/L[1]; at least 95% of the body's potassium is found inside cells, with the remainder in the blood. This concentration gradient is maintained principally by the Na+/K+ pump.

Contents

Signs and symptoms

Mild hypokalaemia is often without symptoms, although it may cause a small elevation of blood pressure,[2] and can occasionally provoke cardiac arrhythmias. Moderate hypokalaemia, with serum potassium concentrations of 2.5-3 mEq/L, may cause muscular weakness, myalgia, and muscle cramps (owing to disturbed function of the skeletal muscles), and constipation (from disturbed function of smooth muscles). With more severe hypokalemia, flaccid paralysis, hyporeflexia, and tetany may result. There are reports of rhabdomyolysis occurring with profound hypokalaemia with serum potassium levels less than 2 mEq/L. Respiratory depression from severe impairment of skeletal muscle function is found in many patients.

Some electrocardiographic (ECG) findings associated with hypokalaemia are flattened or inverted T waves, a U wave, and prolongation of the QT interval. The prolonged QT interval may lead to arrhythmias.

Causes

Hypokalaemia can result from one or more of the following medical conditions:

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Inadequate potassium intake

  • Perhaps the most obvious cause is insufficient consumption of potassium (that is, a low-potassium diet). However, without excessive potassium loss from the body, this is a rare cause of hypokalaemia.

Gastrointestinal/integument loss

  • A more common cause is excessive loss of potassium, often associated with heavy fluid losses that "flush" potassium out of the body. Typically, this is a consequence of diarrhea, excessive perspiration, or losses associated with surgical procedures. Vomiting can also cause hypokalaemia, although not much potassium is lost from the vomitus. Rather, there are heavy urinary losses of K+ in the setting of post-emetic bicarbonaturia that force urinary potassium excretion (see Alkalosis below).

Urinary loss

  • Certain medications can cause excess potassium loss in the urine. Diuretics, including thiazide diuretics (e.g. hydrochlorothiazide) and loop diuretics (e.g. furosemide) are a common cause of hypokalemia. Other medications such as the antifungal, amphotericin B, or the cancer drug, cisplatin, can also cause long-term hypokalaemia.
  • A special case of potassium loss occurs with diabetic ketoacidosis. In addition to urinary losses from polyuria and volume contraction, there is also obligate loss of potassium from kidney tubules as a cationic partner to the negatively charged ketone, β-hydroxybutyrate.
  • Hypomagnesemia can cause hypokalemia. Magnesium is required for adequate processing of potassium. This may become evident when hypokalaemia persists despite potassium supplementation. Other electrolyte abnormalities may also be present.
  • Alkalosis can cause transient hypokalemia by two mechanisms. First, the alkalosis causes a shift of potassium from the plasma and interstitial fluids into cells; perhaps mediated by stimulation of Na+-H+ exchange and a subsequent activation of Na+/K+-ATPase activity.[3] Second, an acute rise of plasma HCO3- concentration (caused by vomiting, for example) will exceed the capacity of the renal proximal tubule to reabsorb this anion, and potassium will be excreted as an obligate cation partner to the bicarbonate.[4] It should be noted that metabolic alkalosis is often present in states of volume depletion, so potassium is also lost via aldosterone-mediated mechanisms.
  • Disease states that lead to abnormally high aldosterone levels can cause hypertension and excessive urinary losses of potassium. These include renal artery stenosis and tumors (generally non-malignant) of the adrenal glands. Hypertension and hypokalaemia can also be seen with a deficiency of the 11-beta-hydroxysteroid dehydrogenase type 2 enzyme which allows cortisols to stimulate aldosterone receptors. This deficiency -- known as apparent mineralocorticoid excess syndrome -- can either be congenital or caused by consumption of glycyrrhizin, which is contained in extract of licorice, sometimes found in herbal supplements, candies and chewing tobacco.
  • Rare hereditary defects of renal salt transporters, such as Bartter syndrome or Gitelman syndrome, can cause hypokalemia, in a manner similar to that of diuretics. As opposed to disease states of primary excesses of aldosterone, blood pressure is either normal or low in Bartter's or Gitelman's.

Distribution away from ECF

  • Rare hereditary defects of muscular ion channels and transporters that cause hypokalaemic periodic paralysis can precipitate occasional attacks of severe hypokalaemia and muscle weakness. These defects cause a heightened sensitivity to the normal changes in potassium produced by catechols and/or insulin and/or thyroid hormone, which lead to movement of potassium from the extracellular fluid into the muscle cells.

Other/ungrouped

  • There have been a handful of published reports describing individuals with severe hypokalemia related to chronic extreme consumption (4-10 L/day) of colas[6]. The hypokalaemia is thought to be from the combination of the diuretic effect of caffeine[7] and copious fluid intake, although it may also be related to diarrhea caused by heavy fructose ingestion.[8][9]

Pseudohypokalemia

  • Pseudohypokalemia is a decrease in the amount of potassium that occurs due to excessive uptake of potassium by metabolically active cells after blood has been drawn. It is a laboratory artifact that may occur when blood samples remain in warm conditions for several hours before processing.[10]

Pathophysiology

Potassium is essential for many body functions, including muscle and nerve activity. The electrochemical gradient of potassium between the intracellular and extracellular space is essential for nerve function; in particular, potassium is needed to repolarize the cell membrane to a resting state after an action potential has passed. Decreased potassium levels in the extracellular space will cause hyperpolarization of the resting membrane potential. This hyperpolarization is caused by the effect of the altered potassium gradient on resting membrane potential as defined by the Goldman equation. As a result, a greater than normal stimulus is required for depolarization of the membrane in order to initiate an action potential.

In certain conditions, this will make cells less excitable. However, in the heart, it causes myocytes to become hyperexcitable. Lower membrane potentials in the atrium may cause arrhythmias because of more complete recovery from sodium-channel inactivation, making the triggering of an action potential more likely. In addition, the reduced extracellular potassium (paradoxically) inhibits the activity of the IKr potassium current[11] and delays ventricular repolarization. This delayed repolarization may promote reentrant arrythmias.

Treatment

The most important treatment in severe hypokalemia is addressing the cause, such as improving the diet, treating diarrhea or stopping an offending medication. Patients without a significant source of potassium loss and who show no symptoms of hypokalaemia may not require treatment.

Mild hypokalemia (>3.0 mEq/L) may be treated with oral potassium chloride supplements (Klor-Con, Sando-K, Slow-K). As this is often part of a poor nutritional intake, potassium-containing foods may be recommended, such as leafy green vegetables, tomatoes, citrus fruits, oranges or bananas.[12] Both dietary and pharmaceutical supplements are used for people taking diuretic medications (see Causes, above).

Severe hypokalaemia (<3.0 mEq/L) may require intravenous supplementation. Typically, saline is used, with 20-40 mEq KCl per liter over 3-4 hours. Giving intravenous potassium at faster rates (20-25 mEq/hr) may predispose to ventricular tachycardias and requires intensive monitoring. A generally safe rate is 10 mEq/hr.

Difficult or resistant cases of hypokalemia may be amenable to a potassium-sparing diuretic such as amiloride, triamterene, or spironolactone. In contrast to the more commonly used diuretics like hydrochlorothiazide and furosemide, these potassium-sparing diuretics actually reduce the kidney's excretion of potassium.

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, or the rare occurrence of damage to the vein. 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.[13]

Hypokalaemia in pets

Cats can develop hypokalemia, which may be manifested by abnormal gait and an inability to keep head elevated. Cats respond well to dietary supplementation of potassium chloride.[14] A feline form of hypokalaemic periodic paralysis has been described in Burmese kittens, which appears to be related to an autosomal recessive mutation. Although these kittens are not hypokalaemic between episodes, regular supplementation of [KCl] seems effective.[15]

See also

External links

USDA National Nutrient Database for Standard Reference, Release 20

References

  1. ^ Kratz A et al. (2004) Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Laboratory reference values. N Engl J Med., 351(15):1548-63; PMID 15470219.
  2. ^ Krishna GG et al. (1989) Increased blood pressure during potassium depletion in normotensive men. N Engl J Med., 320(18):1177-82; PMID 2624617.
  3. ^ Halperin ML and Kamel KS (1998) Potassium. Lancet, 352:155-40; PMID 9672294.
  4. ^ Walmsley RN, White GH (August 1984). "Occult causes of hypokalaemia". Clin. Chem. 30 (8): 1406–8. PMID 6744598. 
  5. ^ Whyte KF, Addis GJ, Whitesmith R, Reid JL (April 1987). "Failure of chronic theophylline therapy to alter circulating catecholamines". Eur J Respir Dis 70 (4): 221–8. PMID 3582518. 
  6. ^ Tsimihodimos V, Kakaidi V, & Elisaf M. (June 2009). "Cola-induced hypokalaemia: pathophysiological mechanisms and clinical implications". International Journal of Clinical Practice 63 (6): 900–2. doi:10.1111/j.1742-1241.2009.02051.x. PMID 19490200. http://www3.interscience.wiley.com/journal/122384349/abstract. free full text
  7. ^ Shirley DG, Walter SJ, Noormohamed FH (November 2002). "Natriuretic effect of caffeine: assessment of segmental sodium reabsorption in humans". Clin. Sci. 103 (5): 461–6. doi:10.1042/ (inactive 2009-11-25). PMID 12401118. 
  8. ^ Packer, C.D. (June 2009). "Cola-induced hypokalaemia: a super-sized problem". International Journal of Clinical Practice 63 (6): 833–5. doi:10.1111/j.1742-1241.2009.02066.x. PMID 19490191. http://www3.interscience.wiley.com/journal/122384352/abstract. 
  9. ^ Health.yahoo.com
  10. ^ Sodi R, Davison AS, Holmes E, Hine TJ, Roberts NB (June 2009). "The phenomenon of seasonal pseudohypokalemia: effects of ambient temperature, plasma glucose and role for sodium-potassium-exchanging-ATPase". Clin. Biochem. 42 (9): 813–8. doi:10.1016/j.clinbiochem.2009.01.024. PMID 19232334. 
  11. ^ Sanguinetti MC and Jurkiewicz NK. (1992) Role of external Ca2+ and K+ in gating of cardiac delayed rectifier K+ currents. Pflugers Arch., 420(2):180-6; PMID 1620577.
  12. ^ Umassmed.edu
  13. ^ "Safety Issues With Adding Lidocaine to IV Potassium Infustions (Excerpt)". http://www.ismp.org/newsletters/acutecare/articles/20040212_2.asp. Retrieved 2009-05-09. 
  14. ^ Feline Hypokalaemic Polymyopathy. in The Merck Veterinary Manual, 9th edition By Merck & Co. 2006. ISBN 0-911910-50-6
  15. ^ Gaschen F, Jaggy A, Jones B (December 2004). "Congenital diseases of feline muscle and neuromuscular junction". J. Feline Med. Surg. 6 (6): 355–66. doi:10.1016/j.jfms.2004.02.003. PMID 15546767. 

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