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abnormally low level of potassium in the circulating blood leading to weakness and heart abnormalities; associated with adrenal tumors or starvation or taking diuretics

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/06/26 07:14:48」(JST)

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Hypokalemia (American English) or hypokalaemia (British English), also hypopotassemia or hypopotassaemia (ICD-9), refers to the condition in which the concentration of potassium (K⁺) in the blood is low. The prefix hypo- means "under" (contrast with hyper-, meaning "over"); kal- refers to kalium, the Neo-Latin for potassium, and -emia means "condition of the blood."

Normal plasma potassium levels are between 3.5 and 5.0 meq/l;^[1] about 98% of the body's potassium is found inside cells, with the remainder in the extracellular fluid including the blood. Alternately, the NIH denotes 3.7–5.2 meq/l as a normal range.^[2] This concentration gradient is maintained principally by the Na⁺/K⁺ pump.

Opposite condition: Hyperkalemia refers to the condition in which the concentration of the electrolyte potassium (K⁺) in the blood is elevated.

Signs and symptoms

Mild hypokalemia is often without symptoms, although it may cause a small elevation of blood pressure,^[3] and can occasionally provoke the development of an abnormal heart rhythm. Severe hypokalemia, with serum potassium concentrations of 2.5–3 meq/l (Nl: 3.5–5.0 meq/l), may cause muscle weakness, myalgia, tremor, and muscle cramps (owing to disturbed function of skeletal muscle), and constipation (from disturbed function of smooth muscle). With more severe hypokalemia, flaccid paralysis and hyporeflexia may result. Reports exist of rhabdomyolysis occurring with profound hypokalemia with serum potassium levels less than 2 meq/l.^{[citation needed]} Respiratory depression from severe impairment of skeletal muscle function is found in many patients.^{[citation needed]}

Some electrocardiographic (ECG) findings associated with hypokalemia include flattened or inverted T waves, a U wave, ST depression, and a wide PR interval. Due to prolonged repolarization of ventricular Purkinje fibers, a prominent U wave occurs, frequently superimposed upon the T wave and therefore produces the appearance of a prolonged QT interval.^[4]

Causes

Hypokalemia can result from one or more of these medical conditions:

Inadequate potassium intake

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

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 muscle-crush injury, or surgical procedures. Vomiting can also cause hypokalemia, although not much potassium is lost from the vomitus. Rather, heavy urinary losses of K⁺ in the setting of postemetic bicarbonaturia force urinary potassium excretion (see Alkalosis below). Other GI causes include pancreatic fistulae and the presence of adenoma.

Urinary loss

Certain medications can cause excess potassium loss in the urine. Blood pressure medications such as loop diuretics (e.g. furosemide) and thiazide diuretics (e.g. hydrochlorothiazide) commonly cause hypokalemia. Other medications such as the antifungal, amphotericin B, or the cancer drug, cisplatin, can also cause long-term hypokalemia.
A special case of potassium loss occurs with diabetic ketoacidosis. Hypokalemia is observed with low total body potassium and a low intracellular concentration of potassium. In addition to urinary losses from polyuria and volume contraction, also an obligate loss of potassium from kidney tubules occurs as a cationic partner to the negatively charged ketone, β-hydroxybutyrate.
A low level of magnesium in the blood can also cause hypokalemia. Magnesium is required for adequate processing of potassium. This may become evident when hypokalemia persists despite potassium supplementation. Other electrolyte abnormalities may also be present.
An increase in the pH of the blood can cause temporary 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⁺ pump activity.^[5] 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.^[6] 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 nonmalignant) of the adrenal glands, e.g., Conn's syndrome (primary hyperaldosteronism). Cushing's syndrome can also lead to hypokalemia due to excess cortisol binding the Na⁺/K⁺ pump and acting like aldosterone. Hypertension and hypokalemia 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

In addition to alkalosis, other factors can cause transient shifting of potassium into cells, presumably by stimulation of the Na⁺/K⁺ pump.^[5] These hormones and medications include insulin, epinephrine, and other beta agonists (e.g. salbutamol or salmeterol), and xanthines (e.g. theophylline).^[7]
Rare hereditary defects of muscular ion channels and transporters that cause hypokalemic periodic paralysis can precipitate occasional attacks of severe hypokalemia 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

A handful of published reports describe individuals with severe hypokalemia related to chronic extreme consumption (4–10 l/day) of colas.^[8] The hypokalemia is thought to be from the combination of the diuretic effect of caffeine^[9] and copious fluid intake, although it may also be related to diarrhea caused by heavy fructose ingestion.^[10]^[11] A physiological response to hypercapnia, blood potassium (as well as calcium) helps offset acidosis, which is consistent with chronic, extreme consumption of carbonated beverages.

Pseudohypokalemia

Pseudohypokalemia is a decrease in the amount of potassium that occurs due to excessive uptake of potassium by metabolically active cells in a blood sample after it has been drawn. It is a laboratory artifact that may occur when blood samples remain in warm conditions for several hours before processing.^[12]

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. Lower potassium levels in the extracellular space 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 to initiate an action potential.

In the heart, hypokalemia causes hyperpolarization in the myocytes' resting membrane potential. The more negative membrane potentials in the atrium may cause arrhythmias because of more complete recovery from sodium-channel inactivation, making the triggering of an action potential less likely. In addition, the reduced extracellular potassium (paradoxically) inhibits the activity of the I_Kr potassium current^[13] and delays ventricular repolarization. This delayed repolarization may promote reentrant arrhythmias.

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 hypokalemia 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, coconut water, citrus fruits, oranges, or bananas.^[14] Both dietary and pharmaceutical supplements are used for people taking diuretic medications.

Severe hypokalemia (<3.0 meq/l) may require intravenous supplementation. Typically, a saline solution is used, with 20–40 meq/l KCl per liter over 3–4 hours. Giving IV 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. Even in severe hypokalemia, oral supplementation is preferred given its safety profile. Sustained-release formulations should be avoided in acute settings.

Difficult or resistant cases of hypokalemia may be amenable to a potassium-sparing diuretic, such as amiloride, triamterene, spironolactone, or eplerenone. Concomittant hypomagnesemia will inhibit potassium replacement, as magnesium is a cofactor for potassium uptake.^[15]

When replacing potassium intravenously, infusion by a central line is encouraged to avoid the frequent occurrence of a burning sensation at the site of a peripheral infusion, 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 fluid, or mixing 3 ml of 1% lidocaine to each 10 meq of KCl per 50 ml of fluid. The practice of adding lidocaine, however, raises the likelihood of serious medical errors.^[16]

References

^ Kratz, A; Ferraro, M; Sluss, PM; Lewandrowski, KB; Ellender, Stacey M.; Peters, Christine C.; Kratz, Alexander; Ferraro, Maryjane; Sluss, Patrick M.; Lewandrowski, Kent B. (2004). "Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Laboratory reference values". The New England Journal of Medicine 351 (15): 1548–63. doi:10.1056/NEJMcpc049016. PMID 15470219.
^ Dugdale, David. "MedlinePlus: Potassium Test". Retrieved 12 January 2013.
^ Krishna, GG; Miller, E; Kapoor, S (1989). "Increased blood pressure during potassium depletion in normotensive men". The New England Journal of Medicine 320 (18): 1177–82. doi:10.1056/NEJM198905043201804. PMID 2624617.
^ Goldman, M.J. (1973). Principles of Clinical Electrocardiography 8th ed. Los Altos, California: LANGE medical Publications. p. 293.
^ ^a ^b Halperin, ML; Kamel, KS (1998). "Potassium". Lancet 352 (9122): 135–40. doi:10.1016/S0140-6736(98)85044-7. PMID 9672294.
^ Walmsley RN, White GH (August 1984). "Occult causes of hypokalaemia". Clin. Chem. 30 (8): 1406–8. PMID 6744598.
^ 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.
^ 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.
^ 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/CS20020055. PMID 12401118.
^ 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.
^ HealthGuru (2012-03-01). "Health.yahoo.com". Health.yahoo.com. Retrieved 2012-03-10.
^ 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.
^ Sanguinetti, MC; Jurkiewicz, NK (February 1992). "Role of external Ca2+ and K+ in gating of cardiac delayed rectifier K+ currents". Pflugers Archiv : European journal of physiology 420 (2): 180–6. doi:10.1007/BF00374988. PMID 1620577.
^ "Sources of Dietary Protein" (PDF). University of Massachusetts Medical School. Retrieved 2012-03-10.
^ "New Guidelines for Potassium Replacement in Clinical Practice". Retrieved 2011-02-16.
^ "Safety Issues With Adding Lidocaine to IV Potassium Infustions (Excerpt)". Retrieved 2009-05-09.

External links

MayoClinic.com: Low potassium (hypokalemia)
MedicineNet.com: Low Potassium (Hypokalemia)
eMedicineHealth.com: Low Potassium (Hypokalemia)
Content of Selected Foods per Common Measure, sorted by nutrient content (Potassium)
List of foods rich in potassium (U. Mass. Med.)
National Organization for Rare Disorders: Hypokalemia

UpToDate Contents

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1. 成人における低カリウム血症の臨床症状および治療 clinical manifestations and treatment of hypokalemia in adults
2. 成人における低カリウム血症の原因 causes of hypokalemia in adults
3. 低カリウム血症成人患者の評価 evaluation of the adult patient with hypokalemia
4. 小児における低カリウム血症 hypokalemia in children
5. 低カリウム血症を合併した高血圧症へのアプローチ approach to the patient with hypertension and hypokalemia

English Journal

[Simultaneous presentation of Brugada syndrome and primary aldosteronism].

Tomcsányi J, Sármán B.SourceBudai Irgalmasrendi Kórház Kardiológia Budapest Frankel Leó út 54. 1023.
Orvosi hetilap.Orv Hetil.2012 Nov 11;153(45):1797-9. doi: 10.1556/OH.2012.29485.
The authors present a case of a 42-year-old male patient, who was referred for evaluation for tachycardia. Detailed studies revealed Brugada syndrome and hypokalaemia due to primary aldosteronism. With this case report the authors draw attention to the risk of malignant ventricular tachycardia in a
PMID 23123328

A Multicenter Phase II Study of Adjuvant Chemotherapy With Oral Fluoropyrimidine S-1 for Non-Small-Cell Lung Cancer: High Completion and Survival Rates.

Tsuchiya T, Nagayasu T, Yamasaki N, Matsumoto K, Miyazaki T, Tagawa T, Nakamura A, Minami H, Taniguchi H, Akamine S, Hisano H, Taniguchi Y.SourceDivision of Surgical Oncology, Department of Translational Medical Sciences, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki City, Japan.
Clinical lung cancer.Clin Lung Cancer.2012 Nov;13(6):464-9. doi: 10.1016/j.cllc.2012.01.005. Epub 2012 Mar 14.
BACKGROUND: Oral adjuvant chemotherapy without hospitalization might reduce the physiological and psychological burden on patients if effectiveness could be guaranteed. We conducted a multicenter feasibility study using S-1, an oral derivative of 5-fluorouracil, as postoperative adjuvant chemotherap
PMID 22424872

Japanese Journal

慢性腎不全で低カリウム血症をきたし, 大腸絨毛腫瘍からのカリウム喪失が疑われた3例

江口智子,岡田麻衣子,津田安都子,松浦基夫,塚口眞知子,大成功一,金万和志
日本内科学会雑誌 101(1), 154-156, 2012-01-10
NAID 10030391399

A 6-year-old boy with secondary long QT syndrome

Kojo Kanami,Yoshinaga Masao,Kucho Yu,Hazeki Daisuke,Tanaka Yuji,Mizota Michiyo
Journal of Arrhythmia 28(1), 61-64, 2012
… One of the main metabolic causes is hypokalemia. …
NAID 130002129816

Eplerenone Improved Hypokalemia in a Patient with Gitelman's Syndrome

Ito Yukiko,Yoshida Masanori,Nakayama Mikihiro,Tsutaya Shoji,Ogawa Koichiro,Maeda Harumi,Miyata Misaki,Oiso Yutaka
Internal Medicine 51(1), 83-86, 2012
… A 47-year-old woman presented with hypokalemia (2.4 mmol/L). …
NAID 130002062414

Related Pictures

★リンクテーブル★

リンク元	「低カリウム血症」「高カリウム血症」「慢性間質性腎炎」「水様下痢低カリウム血症無胃酸症候群」「5H5T」
拡張検索	「watery diarrhea hypokalemia-achlorhydria syndrome」「watery diarrhea, hypokalemia and achlorhydria症候群」「watery diarrhea-hypokalemia-achlorhydria syndrome」「watery diarrhea-hypokalemia-acidosis syndrome」

「低カリウム血症」

Hypokalemia
	An ECG in a person with a potassium level of 1.1 showing the classical ECG changes of ST segment depression, inverted T waves, large U waves, and a slightly prolonged PR interval
Classification and external resources
ICD-10	E87.6
ICD-9	276.8
DiseasesDB	6445
MedlinePlus	000479
eMedicine	article/242008 emerg/273
Patient UK	Hypokalemia
MeSH	D007008

　　[★]

英: hypokalemia, hypopotassemia
同: 低K血症
関: カリウム。高カリウム血症。電解質異常

定義

血清カリウム　＜3.5mEq/l ⇔　基準範囲：3.4-4.5 mEq/l (臨床検査法提要第32版)

原因

カリウム分布の異常

周期性四肢麻痺発作時、インスリン・グルコースの投与(細胞のNa-K ATPaseを活性化するため)

体内カリウム量の低下

摂取低下

高齢者、神経性食欲不振症

喪失亢進

代謝性アシドーシス、下痢、嘔吐(代謝性アルカローシスを合併)
尿からの喪失

内分泌(アルドステロン症(原発性アルドステロン症、続発性アルドステロン症)、クッシング症候群)
腎(腎盂腎炎、ファンコーニ症候群、腎尿細管性アシドーシス)
医原性(利尿薬の使用)

病因

ぽけめ

細胞間シフト

アルカレミア、インスリン使用、カテコラミン使用、低下リウム性周期性四肢麻痺、急激な造血(VB12で治療中の巨赤芽球性貧血、AMLの急性転化)、低体温

消化管からのK喪失：(Uk<25mEq/日または15mEq/L、またはTTKG<3)

消化管からの喪失+代謝性アシドーシス：下痢、緩下薬乱用、絨毛腺腫
嘔吐とNGTドレナージによるカリウム喪失

腎性K喪失：(Uk>30mEq/日または15mEq/L、またはTTKG>7)

低血圧または正常血圧

アシドーシス：DKA、RTA(近位RTA(2型)と多くの遠位RTA(1型))

アルカローシス

利尿薬、嘔吐、NGTドレナージ(続発性高アルドステロン症)

Bartter症候群(HHenleのループ機能異常：フロセミド様効果)

Gitelmann症候群(遠位曲尿細管の機能異常：サイアザイド様効果)

Mg欠乏：遠位でのK分泌亢進が原因の可能性

高血圧性：ミネラルコルチコイドの過剰

原発性高アルドステロン症：Conn症候群など

続発性高アルドステロン症：腎血管性疾患、レニン分泌性腫瘍

非アルドステロン性ミネラルコルチコイド(Cushing症候群、Liddle症候群、外因性ミネラルコルチコイド、肝臓)

病態生理

検査

鑑別診断のために

検査としては尿検査(Uk,UCl,Uosm),血液検査(Bosm,Mg,K),血ガス

心電図

ECGの変化は心室の再分極が遅延し、心筋細胞内のK+濃度をうまく補正できないことによる。

QT延長：細胞外K濃度が低い→静止膜電位が低下→再分極に時間がかかる？
QRS幅延長
T波の平低化、U波出現
ST低下
期外収縮
(最初に)T平坦,U出現,ST低下,QT延長　→　(重度になれば)PR延長, QRS減高, QRS幅拡大　→　VFリスク↑

症状

<3mEq/Lでなければ症状が出現することはほとんどない。(HIM.282)

神経系：感覚鈍麻、傾眠傾向、無関心
心血管系：心筋壊死、心筋線維症、、末梢血管収縮
消化器：食欲不振、悪心・嘔吐、イレウス
筋骨格：筋力低下、呼吸筋麻痺

impaired muscle metabolism and the blunted hyperemic response to exercise associated with profound K+ depletion increase the risk of rhabdomyolysis.(HIM.282)

泌尿器：多尿、腎濃縮力低下、糸球体濾過量・腎血漿流量低下、尿細管間質性腎炎、慢性腎盂腎炎
内分泌：糖忍容力低下(インスリンと共にカリウムが細胞に入っていかない、インスリン分泌能↓＋インスリン抵抗性↑(HIM.282))、その他の代謝異常(負の窒素バランス、代謝性アルカローシス)