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| {{Infobox_Disease |
| | __NOTOC__ |
| Name = Hypokalemia |
| | {| class="infobox" style="float:right;" |
| Image = K-TableImage.png |
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| Caption = [[Potassium]] |
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| DiseasesDB = 6445 |
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| ICD10 = {{ICD10|E|87|6|e|70}} |
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| ICD9 = {{ICD9|276.8}} |
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| ICDO = |
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| OMIM = |
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| MedlinePlus = 000479 |
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| MeshID = D007008 |
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| }}
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| {{Hypokalemia}}
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| {{CMG}}'''; Associate Editor-In-Chief:''' {{CZ}}; '''Assistant Editor(s)-In-Chief:''' [[User:Jack Khouri|Jack Khouri]]
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| ==Overview==
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| '''Hypokalemia''' is a potentially fatal condition in which the body fails to retain sufficient [[potassium]] to maintain health. It is defined as a serum potassium level below 3.5 mEq/L. The condition is also known as '''potassium deficiency'''. The prefix ''hypo-'' means low (contrast with ''hyper-'', meaning high). The middle ''kal'' refers to ''kalium'', which is Neo-Latin for potassium. The end portion of the word, ''-emia'', means "in the blood" (note, however, that hypokalemia is usually indicative of a ''systemic'' potassium deficit).
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| ==Pathophysiology==
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| Potassium is the most abundant intracellular cation. Any derangement of potassium serum levels can disturb the transmembrane potential and renders excitable cells (nerve and muscle) hyperpolarized and less excitable. However, cardiac cells don't obey this rule and become hyperexcitable.
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| ==Causes==
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| Hypokalemia can be the consequence of decreased ingestion, increased losses (renal, GI or excessive sweating) or transcellular shift from the extracellular to the intracellular compartment. The most common causes are diarrhea, vomiting and diuretic use (mostly loop and thiazide diuretics).
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| ==Diagnosis==
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| Diagnosis relies on a constellation of findings including:
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| ===Symptoms===
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| Mostly constitutive with predominance of muscle weakness and cramping. The heart can be affected; ECG can reveal arrhythmias and other major changes. The kidney can be involved: nephrogenic diabetes insipidus and hyponatremia can occur.
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| ===History===
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| It should include the past medical history to point out some relevant diseases and conditions that can result in hypokalemia (eg hyperthyroidism, hyperaldosteronism, Cushing's disease,etc). The medication history should be detailed given the long list of medications that can be culprit.
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| ===Laboratory findings===
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| Many labs can be helpful. The transtubular potasium gradient (TTKG), urine potassium and urine chloride levels can help define the etiology of hypokalemia.
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| ==Treatment==
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| The oral route is the safest. There are many oral potassium salts that can be prescribed including potassium chloride KCl (the most popular) and the organic alkalinizing salts that are metabolized to potassium bicarbonate KHCO3 in the body. Severe hypokalemia ca be treated via IV KCl infusion with doses that shouldn't exceed 60 mEq/L unless ECG monitoring is provided. A central line can be used for administration of greater concentrations of KCl.
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| == Potassium Homeostasis ==
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| === The role of the kidney ===
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| Normally, total potassium excretion in stool is low and most ingested potassium is absorbed. The kidney is the main regulator of Potassium balance through excretion (the kidney excretes 90-95% of dietary potassium). At the glomerulus, potassium is freely filtered and then largely reabsorbed in the proximal tubule and thick ascending loop of Henle (>60 % of filtered potassium). The cortical collecting duct receives 10–15%of filtered potassium and constitutes the kidney’s major site of potassium excretion. Potassium excretion at the cortical collecting duct depends on the amount of Sodium delivered there and the activity of aldosterone. The absorption of sodium by the principal cells of the cortical collecting ducts is mediated by the apical epithelial sodium channels (ENaC); when the amount of sodium delivered to the cortical collecting duct is very high, the absorption of sodium increases without concomitant absorption of the accompanying anions (eg, bicarbonates and chloride ions) which are not easy to absorb. This physiologic process causes the formation of a negative charge within the cortical collecting duct lumen causing potassium and proton secretion. Aldosterone increases sodium absorption at the cortical collecting duct by means of enhancing the activity of Na-K-ATPase pumps, and augmenting the number of the ENaC channels.
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| === Factors increasing kidney potassium excretion ===
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| *Aldosterone
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| *High urine flow rate
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| *High distal sodium delivery
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| *Metabolic alkalosis
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| === Some factors affecting potassium distribution between the cells and the extracellular fluid ===
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| *Na/K ATPase
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| *Insulin
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| *Catecholamines
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| *plasma potassium concentration
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| *Extracellular pH
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| *Hyperosmolarity
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| ==Pathophysiology==
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| === The physiologic role of potassium ===
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| Potassium is essential for many body functions, especially excitable cells such as [[muscle]] and [[nerve]] cells. Diet, mostly meats and fruits, is the major source of potassium for the body. Potassium is the principal [[intracellular]] [[cation]], with a concentration of about 145 mEq/L, as compared with a normal value of 3.5 - 5.0 mEq/L in [[extracellular]] fluid, including blood. More than 98% of the body's potassium is intracellular; measuring it from a blood sample is relatively insensitive, with small fluctuations in the blood corresponding to very large changes in the total bodily reservoir of potassium.
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| === The cellular effect of Hypokalemia ===
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| The electrochemical gradient of potassium between 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 ie, it becomes more negative. This [[hyperpolarization (biology)|hyperpolarization]] is caused by the effect of the altered potassium gradient on [[resting membrane potential]] as defined by the [[Goldman equation]]. As a result, the cell becomes less sensitive to excitation and a greater than normal stimulus is required for depolarization of the membrane in order to initiate an action potential. Clinically, this membrane hyperpolarization results in muscle flaccid paralysis, rhabdomyolysis (in severe hypokalemia) and paralytic ileus. At the Renal level, hypokalemia can cause metabolic alkalosis due to potassium/proton exchange across the cells and nephrogenic diabetes insipidus.
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| === Pathophysiology of Hypokalemic Heart Arrhythmias ===
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| Potassium is essential to the normal muscular function, in both voluntary (i.e skeletal muscle, e.g. the arms and hands) and involuntary muscle (i.e. smooth muscle in the intestines or cardiac muscle in the heart). Severe abnormalities in potassium levels can seriously disrupt [[heart|cardiac function]], even to the point of causing [[cardiac arrest]] and [[death]]. As explained above, hypokalemia makes the resting potential of potassium [E(K)] more negative. In certain conditions, this will make cells less excitable. '''However, in the heart, it causes myocytes to become hyperexcitable'''. This is due to two independent effects that may lead to aberrant cardiac conduction and subsequent arrhythmia:
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| #There are more inactivated sodium (Na) channels available to fire, and
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| #The overall potassium permeability of the ventricle is reduced (perhaps by the loss of a direct effect of extracellular potassium on some of the potassium channels), which can delay ventricular repolarization.
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| ==Causes==
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| Hypokalemia can be the consequence of decreased ingestion, increased losses or transcellular shift from the extracellular to the intracellular compartment.
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| * Perhaps the most obvious cause is insufficient [[eating|consumption]] of potassium (that is, a low-potassium diet). However, without excessive potassium loss from the body, this is a rare cause of hypokalemia. Alcoholism, anorexia nervosa, dental problems and dysphagia can all impair food intake and cause hypokalemia. In the hospital setting, hypokalemia can present in patients on total parenteral nutrition or potassium-free IV fluids.
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| * Excessive loss of potassium, often associated with excess [[water]] loss, which "flushes" potassium out of the body. Typically, this is a consequence of GI losses ([[vomiting]] and [[diarrhea]]), or excessive [[perspiration]].
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| *Increased urinary losses:
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| ** Certain [[medication]]s can accelerate the removal of potassium from the body; including [[thiazide diuretic]]s, such as [[hydrochlorothiazide]]; [[loop diuretic]]s, such as [[furosemide]]; as well as various [[laxative]]s. The antifungal [[amphotericin B]] has also been associated with hypokalemia.
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| ** A special case of potassium loss occurs with [[DKA|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.
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| ** [[Hypomagnesemia]] can 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.
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| ** 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 hypokalemia can also be seen with a deficiency of the 11β-hydroxylase enzyme which allows cortisol to stimulate aldosterone receptors. This deficiency 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.
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| **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.
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| * Transcellular potassium shift to the intracellular space:
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| ** Increased extracellular pH (each 0.11 unit increase in pH corresponds to a 0.4 meq/l decrease in potassium level)
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| ** Elevated insulin
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| ** Elevated beta-adrenergic activity (stress, beta-agonist intake, etc)
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| ** 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 [[catechols]] and/or [[insulin]] and/or [[thyroid hormone]] that lead to sudden influx of potassium from the extracellular fluid into the muscle cells.
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| ** Hypothermia
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| ** Thyrotoxicosis
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| ** Theophylline
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| ** Rapid expansion of cell mass (eg, during refeeding after prolonged starvation, when patients with pernicious anemia are treated with vitamin B12 and with tumors having rapid cell turnover)
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| == Differential Diagnosis ==
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| {|style="width:75%; height:100px" border="1" | |
| |style="height:100px"; style="width:25%" border="1" bgcolor="LightSteelBlue" | '''Cardiovascular'''
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| |style="height:100px"; style="width:75%" border="1" bgcolor="Beige" | [[Congestive Heart Failure]]
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Chemical / poisoning'''
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| |bgcolor="Beige"| Barium or toluene ingestion, Chloroquine overdose
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Drug Side Effect'''
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| |bgcolor="Beige"| Licorice, digitalis, chronic laxative abuse, beta agonists, Amphotericin B, diuretics, corticosteroids
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Endocrine'''
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| |bgcolor="Beige"| 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
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Gastroenterologic'''
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| |bgcolor="Beige"| 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
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Genetic'''
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| |bgcolor="Beige"| hypokalemic periodic paralysis
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Iatrogenic'''
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| |bgcolor="Beige"| total parenteral nutrition, ureterosigmoidostomy, nasogastric suction
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Nutritional / Metabolic'''
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| |bgcolor="Beige"| malnutrition
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Oncologic'''
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| |bgcolor="Beige"| tumors with rapid cell turnover (leukemias)
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Psychiatric'''
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| |bgcolor="Beige"| Clay ingestion, acute hyperventilation, anorexia Nervosa, bulimia
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Renal / Electrolyte'''
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| |bgcolor="Beige"| 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
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| |- | | |- |
| | | <figure-inline><figure-inline>[[File:Siren.gif|link=Hypokalemia resident survival guide|41x41px]]</figure-inline></figure-inline>|| <br> || <br> |
| | | [[Hypokalemia resident survival guide|'''Resident'''<br>'''Survival'''<br>'''Guide''']] |
| |} | | |} |
| | {{Hypokalemia}} |
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| ==Diagnosis==
| | '''For patient information on this page, click [[Hypokalemia (patient information)|here]]''' |
| === Symptoms ===
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| The severity of symptoms depends on the degree of hypokalemia, but keep in mind that there is marked individual variability.
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| ==== Constitutional ====
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| * [[Ddx:Fatigue|Fatigue]]
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| * Weakness
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| * [[Ddx:Nausea and Vomiting|Vomiting]]
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| * [[Ddx:Constipation|Constipation]]
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| * Muscle cramps and paralysis (the lower extremity muscles are most commonly involved) which may involve the intestine and cause ileus
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| * Respiratory muscle weakness leading to respiratory failure
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| ==== Cardiac ====
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| * Hypertension
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| * Arrhythmias including premature atrial and ventricular complexes, paroxysmal atrial or junctional tachycardia and even ventricular tachycardia or fibrillation
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| * Heart block
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| * Digoxin therapy, CAD and left ventricular hypertrophy potentiate hypokalemia effects on the heart
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| ==== Renal ====
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| *Nephrogenic diabetes insipidus due to decreased concentrating ability. As a consequence, the patient presents with polyuria and polydipsia
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| *Increased bicarbonate reabsorption
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| *Increased ammonia formation which may precipitate hepatic encephalopathy in cirrhotic patients
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| *Decreased sodium reabsorption resulting in hyponatremia
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| ==== Other ====
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| * Rhabdomyolysis
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| * [[Ddx:Hyperglycemia|Hyperglycemia]]
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| === History ===
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| A detailed history can help depict the cause of hypokalemia.
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| ==== Dietary history ====
| | {{CMG}}'''; Associate Editor-In-Chief:''' {{CZ}}; {{AIDA}} [[User:Aditya Govindavarjhulla|Aditya Govindavarjhulla, M.B.B.S.]] [mailto:agovi@wikidoc.org] ; '''Assistant Editor(s)-In-Chief:''' [[User:Jack Khouri|Jack Khouri]] |
| Malnutrition: lack of meat and fruit intake
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| ==== Medication history ====
| | {{SK}} Hypokalaemia; potassium levels low (plasma or serum); potassium - low; low blood potassium; potassium depletion |
| *Diuretics (loop and thiazides)
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| *Beta agonists
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| *Chloroquine
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| *Theophylline
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| *Insulin
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| *Corticosteroids
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| *Licorice
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| *Nephrotoxic drugs (platinum-based chemotherapy, aminoglycosides)
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| *Laxatives
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| ==== Past medical history ==== | | ==[[Hypokalemia overview|Overview]]== |
| *Uncontrolled diabetes
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| *Hyperthyroidism
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| *Pernicious anemia
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| *COPD (treated with Beta agonists and theophylline)
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| *Cushing’s disease
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| *Periodic paralysis
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| *Ileostomy/short bowel
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| *Primary hyperaldosteronism
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| *Liddle syndrome
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| *Bartter and Gitelman syndrome
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| *Prolonged starvation
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| *Cancer
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| *Renal tubular acidosis type I and type II
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| == Laboratory Findings == | | ==[[Hypokalemia historical perspective|Historical Perspective]]== |
| * Complete blood count (CBC)
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| * Blood urea nitrogen (BUN)/creatinine
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| * Calcium
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| * Magnesium
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| * Glucose
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| * Arterial blood gases
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| * Aldosterone level
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| * Renin levels
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| * Urinary sodium
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| * Urine potassium
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| ** 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
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| ** Higher potassium excretion suggest renal losses.
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| * Transtubular potassium gradient (TTKG)
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| ** TTKG= (Urine K x Plasma osmolarity)/(Plasma K x Urine osmolarity)
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| ** A TTKG less than 2-3 indicates renal potassium conservation in a hypokalemic patient
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| ** A urine osmolality less than plasma osmolality or urine sodium <20 mEq/L, the formula is not applicable
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| * Urine chloride
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| ** <25 meq/L: vomiting or remote diuretic use
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| ** >40 meq/L: diuretics, Bartter's, Gitelman's and mineralocorticoid excess
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| == Electrocardiography == | | ==[[Hypokalemia pathophysiology|Pathophysiology]]== |
| ==== Overview ====
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| *Caused mainly by delayed ventricular repolarization
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| *Seen at potassium levels <3 meq/L (90% of patients with potassium levels <2.7 meq/L have abnormal ECG findings)
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| *Rapidly reversible with potassium repletion
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| ==== ECG changes ==== | | ==[[Hypokalemia causes|Causes]]== |
| # ST segment depression, decreased T wave amplitude, prominent U waves
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| #* seen in 78% of patients with a K < 2.7 meq
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| #* seen in 35% of patients with a K > 2.7 and < 3.0
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| #* seen in 10% of patients with a K > 3.0 and < 3.5
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| #* U waves are also prominent in bradycardia and LVH
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| # Prolongation of the QRS duration
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| #* uncommon except in severe hyperkalemia
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| # Increase in the amplitude and duration of the P-wave
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| # Cardiac arrhythmias and AV block
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| # 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.
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| <div align="center">
| | ==[[Hypokalemia differential diagnosis|Differentiating Hypokalemia from other Diseases]]== |
| <gallery heights="175" widths="175">
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| Image:Hypokalemia.jpg|Long QT interval, ST segment depression, low T waves amplitude and TU wave fusion in a hypokalemic patient.
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| Image:KJcasu18-3.jpg|Consecutive ECGs of a patient with hypokalemia. ECG1
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| </gallery>
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| </div>
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| | ==[[Hypokalemia epidemiology and demographics|Epidemiology and Demographics]]== |
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| <div align="center">
| | ==[[Hypokalemia risk factors|Risk Factors]]== |
| <gallery heights="117" widths="117">
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| Image:KJcasu18-2.jpg|Consecutive ECGs of a patient with hypokalemia. ECG2
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| Image:KJcasu18-1.jpg|Consecutive ECGs of a patient with hypokalemia. After correction of potassium levels.
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| Image:V10.ht14.jpg|Hypokalemia with LVH. Image courtesy of Dr Jose Ganseman
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| </gallery>
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| </div>
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| ==Treatment== | | ==[[Hypokalemia natural history|Natural History, Complications and Prognosis]]== |
| The most important step in severe hypokalemia is removing the cause, such as treating [[diarrhea]] or stopping offending medication.
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| * 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).
| | ==[[Hypokalemia Diagnosis|Diagnosis]]== |
| * The combination of thiazide and loop diuretics should be avoided.
| | [[Hypokalemia laboratory findings#Diagnostic Algorithm|Diagnostic Algorithm]] | [[Hypokalemia history and symptoms | History and Symptoms]] | [[Hypokalemia physical examination|Physical Examination]] | [[Hypokalemia laboratory findings | Laboratory Findings]] | [[Hypokalemia electrocardiogram | Electrocardiogram]] | [[Hypokalemia other diagnostic studies|Other Diagnostic Studies]] |
| * Oral potassium administration is safer than the IV route.
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| * An oral dose should '''not''' exceed 20-40 mEq.
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| * IV potassium infusion should be reserved for symptomatic patients with severe hyperkalemia and patients who can't take oral supplements.
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| === Mild hypokalemia === | | ==[[Hypokalemia treatment|Treatment]]== |
| * Potassium levels in the range 3.0-3.5 mEq/L.
| | [[Hypokalemia medical therapy| Medical Therapy]] | [[Hypokalemia primary prevention|Primary Prevention]] | [[Hypokalemia secondary prevention|Secondary Prevention]] | [[Hypokalemia cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Hypokalemia future or investigational therapies|Future or Investigational Therapies]] |
| * Represent potassium deficit of 200-400 mEq.
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| * 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).
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| * Potassium-containing foods may be recommended, such as tomatoes, oranges or bananas, but they are less effective than oral supplements.
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| * Both dietary and pharmaceutical supplements are used for people taking diuretic medications (see '''Causes''', above).
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| * KCl is the most effective replacement for metabolic alkalosis-associated hypokalemia.
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| * 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).
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| === Severe hypokalemia === | | ==Case Studies== |
| * Potassium levels below 3.0 mEq/L
| | [[Hypokalemia case study one|Case #1]] |
| * Potassium levels between 2.0 and 3.0 correspond to 400-800 mEq deficit.
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| * It may require [[intravenous]] supplementation. Typically, [[saline (medicine)|saline]] is used, with 20-40 mEq KCl per liter over 3-4 hours (ie, at an infusion rate of 10 mEq/L/h)
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| * '''Giving IV potassium at faster rates may predispose to [[ventricular tachycardia]]s and requires intensive ECG monitoring.'''
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| * '''Giving IV KCl at doses >60 mEq/L are painful and can cause venous necrosis.'''
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| * Difficult or resistant cases of hypokalemia may be amenable to [[amiloride]], a potassium-sparing diuretic, or [[spironolactone]].
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| * 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 [http://www.ismp.org/newsletters/acutecare/articles/20040212_2.asp].
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| * 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.'''
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| * Saline solutions are preferred to prevent potassium transcellular shifting that is triggered by dextrose-induced insulin release!
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| ==See also== | | ==Related Chapters== |
| * [[Hypomagnesemia]] | | * [[Hypomagnesemia]] |
| * [[Hyperkalemia]] | | * [[Hyperkalemia]] |
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| ==References==
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| {{Reflist|2}}
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| [[Category:Electrophysiology]] | | [[Category:Electrophysiology]] |
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| [[Category:Intensive care medicine]] | | [[Category:Intensive care medicine]] |
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| [[fr:Hypokaliémie]]
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| [[pl:Hipokaliemia]]
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| [[pt:Hipocaliémia]]
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| [[ru:Гипокалиемия]]
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| [[vi:Hạ kali máu]]
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| [[Category:Inborn errors of metabolism]]
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| {{WikiDoc Help Menu}} | | {{WikiDoc Help Menu}} |
| {{WikiDoc Sources}} | | {{WikiDoc Sources}} |
</figure-inline></figure-inline>