Hypokalemia. Back. Practice Essentials. ![]() Hypokalemia is generally defined as a serum potassium level of less than 3. Eq/L (3. 5 mmol/L). Severe hypokalemia is a level of less than 2. Eq/L. Hypokalemia is a potentially life- threatening imbalance that may be iatrogenically induced. Gitelman syndrome is an autosomal recessive disorder characterized by hypokalemic metabolic alkalosis and low blood pressure. Management of Potassium Disorders Adesola Odunayo, DVM, MS. Hyperkalemia and hypokalemia are common electrolyte. Hypokalemia and Hyperkalemia in Infants and Children: Pathophysiology and Treatment. A physiologic-based approach to the evaluation of a patient with hypokalemia. Learn about hyperkalemia, a condition caused by abnormally high levels of potassium in the blood. Lose weight without dieting! See the image below. Signs and symptoms. Patients are often asymptomatic, particularly those with mild hypokalemia. Hypokalemia; Synonyms: hypopotassaemia, hypopotassemia. Symptoms that are present are often from the underlying cause of the hypokalemia rather than the hypokalemia itself. The symptoms of hypokalemia are nonspecific and predominantly are related to muscular or cardiac function. Complaints may include the following: Weakness and fatigue (most common)Muscle cramps and pain (severe cases)Worsening diabetes control or polyuria. ![]() Palpitations. Psychological symptoms (eg, psychosis, delirium, hallucinations, depression)Physical findings are often within the reference range. Abnormal findings may reflect the underlying disorder. Severe hypokalemia may manifest as bradycardia with cardiovascular collapse. Cardiac arrhythmias and acute respiratory failure from muscle paralysis are life- threatening complications that require immediate diagnosis. See Presentation for more detail. Diagnosis. In most cases, the cause of hypokalemia is apparent from the history and physical examination. First- line studies include measurement of urine potassium, a serum magnesium assay, and an electrocardiogram (ECG). If the urine potassium level is less than 2. Eq/L, consider the following: Diarrhea and use of laxatives. Diet or total parenteral nutrition (TPN) contents. The use of insulin, excessive bicarbonate supplements, and episodic weakness. If the urine potassium level is higher than 4. Eq/L, consider diuretics. If diuretic use has been excluded, measure arterial blood gases (ABG) and determine the acid- base balance. Alkalosis suggests one of the following: Vomiting. Bartter syndrome. Gitelman syndrome. Mineralocorticoid excess. Depending on history, physical examination findings, clinical impressions, and urine potassium results, the following tests may be appropriate, but they should not be first- line tests unless the clinical index of suspicion for the disorder is high: Drug screen in urine and/or serum for diuretics, amphetamines, and other sympathomimetic stimulants. Serum renin, aldosterone, and cortisol. Pituitary imaging to evaluate for Cushing syndrome. Adrenal imaging to evaluate for adenoma. Evaluation for renal artery stenosis. Enzyme assays for 1. Thyroid function studies in patients with tachycardia, especially Asians. Moderate hypokalemia is a serum level of 2. Eq/L, and severe hypokalemia is a level of less than 2. Eq/L. Hypokalemia is a potentially life- threatening imbalance that may be iatrogenically induced. Potassium, the most abundant intracellular cation, is essential for the life of an organism. Potassium homeostasis is integral to normal cellular function, particularly of nerve and muscle cells, and is tightly regulated by specific ion- exchange pumps, primarily by cellular, membrane- bound, sodium- potassium adenosine triphosphatase (ATPase) pumps. Potassium homeostasis is maintained predominantly through the regulation of renal excretion; the adrenal gland and pancreas also play significant roles (see Pathophysiology). Hypokalemia may result from inadequate potassium intake, increased potassium excretion, or a shift of potassium from the extracellular to the intracellular space. Increased excretion is the most common mechanism. Poor intake or an intracellular shift by itself is a distinctly uncommon cause, but several causes often are present simultaneously. Weakness and fatigue are the most common complaints. An electrocardiogram (ECG) may show atrial or ventricular tachyarrhythmias. In most cases, the cause of hypokalemia is apparent from the history and physical examination (see Presentation). Measurement of urine potassium is of vital importance because it establishes the pathophysiologic mechanism and, thus, is used in formulating the differential diagnosis. This, in turn, will guide the choice of further tests (see Workup). The treatment of hypokalemia has four facets, as follows (see Treatment): Reduction of potassium losses. Replenishment of potassium stores. Evaluation for potential toxicities. Determination of the cause to prevent future episodes, if possible. Prognosis. The prognosis for patients with hypokalemia depends entirely on the condition’s underlying cause. For example, a patient with an acute episode of hypokalemia resulting from diarrhea has an excellent prognosis. Hypokalemia due to a congenital disorder such as Bartter syndrome has a poor to nonexistent potential for resolution. Pathophysiology. Gastrointestinal absorption of potassium is complete, resulting in daily excess intake of approximately 1 m. Eq/kg/day (6. 0- 1. Eq). Ninety percent of this excess is excreted through the kidneys, and 1. Potassium homeostasis is maintained predominantly through the regulation of renal excretion. The most important site of regulation is the collecting duct, where aldosterone receptors are present. Potassium excretion is increased by the following factors: Aldosterone. High sodium delivery to the collecting duct (eg, diuretics)High urine flow (eg, osmotic diuresis)High serum potassium levels. Delivery of negatively charged ions to the collecting duct (eg, bicarbonate)Potassium excretion is decreased by the following factors: Absolute aldosterone deficiency or resistance to aldosterone effects. Low sodium delivery to the collecting duct. Low urine flow. Low serum potassium levels. Renal failure. An acute increase in osmolality causes potassium to exit from cells. An acute cell/tissue breakdown releases potassium into extracellular space. Renal factors in potassium homeostasis. Kidneys adapt to acute and chronic alterations in potassium intake. When potassium intake is chronically high, potassium excretion likewise is increased. In the absence of potassium intake, however, obligatory renal losses are 1. Eq/day. Thus, chronic losses occur in the absence of any ingested potassium. The kidney maintains a central role in the maintenance of potassium homeostasis, even in the setting of chronic renal failure. Renal adaptive mechanisms allow the kidneys to maintain potassium homeostasis until the glomerular filtration rate drops to less than 1. L/min. Additionally, in the presence of renal failure, the proportion of potassium excreted through the gut increases. The colon is the major site of gut regulation of potassium excretion. Therefore, potassium levels can remain relatively normal under stable conditions, even with advanced renal insufficiency. However, as renal function worsens, the kidneys may not be capable of handling an acute potassium load. Potassium distribution. Potassium is predominantly an intracellular cation; therefore, serum potassium levels can be a very poor indicator of total body stores. Because potassium moves easily across cell membranes, serum potassium levels reflect movement of potassium between intracellular and extracellular fluid compartments, as well as total body potassium homeostasis. Several factors regulate the distribution of potassium between the intracellular and extracellular space, as follows: Glycoregulatory hormones: (1) Insulin enhances potassium entry into cells, and (2) glucagon impairs potassium entry into cells. Adrenergic stimuli: (1) Beta- adrenergic stimuli enhance potassium entry into cells, and (2) alpha- adrenergic stimuli impair potassium entry into cellsp. H: (1) Alkalosis enhances potassium entry into cells, and (2) acidosis impairs potassium entry into cells. Physiologic mechanisms for sensing extracellular potassium concentration are not well understood. Adrenal glomerulosa cells and pancreatic beta cells may play a role in potassium sensing, resulting in alterations in aldosterone and insulin secretion. Potassium ingestion stimulates the secretion of insulin, which increases the activity of the sodium pump in muscle cells, resulting in an increased uptake of potassium. Studies in a model of potassium deprivation demonstrate that acutely, skeletal muscle develops resistance to insulin- stimulated potassium uptake even in the absence of changes in muscle cell sodium pump expression. However, prolonged potassium deprivation leads to a decrease in muscle cell sodium- pump expression, resulting in decreased muscle uptake of potassium. High potassium states stimulate cellular uptake via insulin- mediated stimulation of sodium- pump activity in muscle and stimulate potassium secretion by the kidney via aldosterone- mediated enhancement of distal renal expression of secretory potassium channels (ROMK). Low potassium states result in insulin resistance, impairing potassium uptake into muscle cells, and cause decreased aldosterone release, lessening renal potassium excretion. This system results in rapid adjustments in immediate potassium disposal and helps to provide long- term potassium homeostasis. Pathogenic mechanisms. Hypokalemia can occur via the following pathogenetic mechanisms: Deficient intake. Increased excretion. A shift from the extracellular to the intracellular space. Although poor intake or an intracellular shift by itself is a distinctly uncommon cause, several causes often are present simultaneously. Increased excretion. The most common mechanisms leading to increased renal potassium losses include the following: Enhanced sodium delivery to the collecting duct, as with diuretics. Mineralocorticoid excess, as with primary or secondary hyperaldosteronism. Increased urine flow, as with an osmotic diuresis. Gastrointestinal losses, from diarrhea, vomiting, or nasogastric suctioning, also are common causes of hypokalemia. Vomiting leads to hypokalemia via a complex pathogenesis. Gastric fluid itself contains little potassium, approximately 1.
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