Hyponatremia

Hyponatremia is a decrease in the serum sodium concentration to values ??<136 mEq / l, which is caused by an excess of water in relation to solutes. Common causes include diuretic therapy, diarrhea, heart failure, liver disease, kidney failure and the syndrome of inadequaten antidiuretic hormone secretion (SIADH). The manifestation of hyponatremia caused by an osmotic movement of water into the brain cells, thereby edema arises, particularly in the acute hyponatremia. The symptoms include headache, confusion, stupor, seizures, and at worst a coma. The diagnosis results from the determination of serum sodium. The determination of serum and urinary electrolytes and osmolality as well as the assessment of volume status contribute to the cause. The treatment consists in a restriction of the water supply and conveyance of the water loss. The sodium deficit is replaced and addresses the underlying Krnakheit.

(See also water and sodium balance.)

Hyponatremia is a decrease in the serum sodium concentration to values ??<136 mEq / l, which is caused by an excess of water in relation to solutes. Common causes include diuretic therapy, diarrhea, heart failure, liver disease, kidney failure and the syndrome of inadequaten antidiuretic hormone secretion (SIADH). The manifestation of hyponatremia caused by an osmotic movement of water into the brain cells, thereby edema arises, particularly in the acute hyponatremia. The symptoms include headache, confusion, stupor, seizures, and at worst a coma. The diagnosis results from the determination of serum sodium. The determination of serum and urinary electrolytes and osmolality as well as the assessment of volume status contribute to the cause. The treatment consists in a restriction of the water supply and conveyance of the water loss. The sodium deficit is replaced and addresses the underlying Krnakheit. (See also water and sodium balance.) Etiology Hyponatremia is caused by an excess of total body water (TBW) in relation to the total body amount of sodium. Since the total body volume is determined on sodium by the volume status of the ECF, a hyponatremia must be considered together with the status of the ECF volume: A distinction hypovolemia, a normovolaemia and Hypervolaemia (see Table: Major causes of hyponatremia). Note that the ECF volume, and the effective plasma volume are not identical. A reduction of the effective plasma volume can occur, for example together with reduced ECF Volume (such as in the use of diuretics or hemorrhagic shock), but can also at elevated ECF Volume (z. B. in heart failure, in hypoalbuminemia or in capillary leak syndrome) occur. Sometimes a low serum sodium is measured rather by an excess of certain substances (for example, glucose, lipid) in blood (translocational hyponatremia, pseudohyponatremia) caused as by a water-sodium imbalance. Important causes of hyponatremia mechanism Category examples Hypovolaemic hyponatremia Reduced TBW and sodium with relatively greater loss of sodium Gastrointestinal losses * diarrhea vomiting losses in the "third space" * burns pancreatitis peritonitis rhabdomyolysis small bowel obstruction Renal losses diuretics osmotic diuresis Mineralokortikoidmangel (glucose, urea, mannitol) salt-wasting nephropathy (eg. As interstitial nephritis, medullary cystic disease, partial urinary tract obstruction, polycystic kidney disease) normovolemic hyponatremia Increased TBW with near-normal total body amount of sodium drug thiazide diuretics, barbiturates, carbamazepine, chlorpropamide, clofibrate, opioids, tolbutamide, vincristine 3,4-methylenedioxymethamphetamine (MDMA [Ecstasy ]) may cyclophosphamide, NSAIDS, oxytocin, SSRIs disease adrenal insufficiency as in Addison's disease hypothyroidism syndrome of inappropriate antidiuretic hormone release increase Increased intake of liquids Primary polydipsia states that do not osmotic release of vasopressin (ADH) Emotional stress nausea pain states Increased after surgery hypervolaemic hyponatremia total body sodium with relatively greater increase in TBW Extrarenal disorders cirrhosis heart failure Kidney disease Acute kidney injury Chronic kidney disease nephrotic syndrome * Gastrointestinal losses and losses in the "third space" cause hyponatremia if the fluid replacement compared with the losses is hypotonic. TBW = total body water (total body water). Hypovolemic hyponatremia (see also volume depletion.) A reduction of both the TBW and the total amount of sodium body occurs, but the lack of sodium is greater than the water. The sodium deficiency causes hypovolemia. In hypovolemic hyponatremia both the serum osmolality and blood volume decreases. Vasopressin (antidiuretic hormone - ADH secretion increases despite reduced osmolality to obtain the blood volume upright The resulting fluid retention increases the plasma dilution and hyponatremia Extrarenal fluid losses, such as those for loss of sodium-liquids by protracted vomiting, severe diarrhea or.. loss of fluid in the third space may occur (see Table: composition of body fluids), may typically cause hyponatremia, if the losses by supplying pure water or a low sodium liquids (see Table: sodium content of beverages (estimated)), or hypotonic infusion solutions to be replaced. significant losses of extracellular fluid cause vasopressin release. This leads to renal water retention, which may maintain or worsen hyponatremia In extrarenal causes of hypovolemia beträ. gt urine sodium concentration as the usual reaction volume on the kidney losses is usually <10 mEq / l of a sodium preservatives. Composition of body fluids source of liquid sodium * * potassium chloride * stomach pancreas 20-80 5-20 100-150 120-140 90-120 5-15 100-140 5-15 small intestine 90-130 bile 120-140 5-15 80-120 3-15 20-115 45-135 ileostomy diarrhea 10-90 10-80 10-110 3-10 10-35 10-30 sweat Burns 140 5110 * unit is mEq / l. Sodium content beverages (estimated) Drink sodium (mmol / l) Apple juice 1.3 2.2 beer Coffee Cola 5-6.5 1 Diet Cola 4.5-6.5 Light beer 1.3 3.7 Orange sports drink 8-33 water (including tap water) <1 Renal fluid losses that lead to hypovolemic hyponatremia, occur in Mineralokortikoidmangel, Thiaziddiuretikatherapie, osmotic diuresis or a salt-losing nephropathy. The salt-wasting nephropathy comprises a vaguely defined group of renal diseases with primary renal Tubulusdysfunktion. This group includes the interstitial nephritis, medullary cystic disease, partial urinary tract obstruction and occasionally polycystic kidney disease. Renal causes of hypovolemic hyponatremia can usually be distinguished by means of the history of extrarenal causes. Patients with continuous fluid losses via the kidneys can be distinguished from patients with extrarenal liquid losses, since the urine sodium concentration is unduly high (> 20 mEq / l). The urinary sodium concentration can not be used to distinguish if a metabolic alkalosis, as occurs in protracted vomiting is present, and if large amounts of bicarbonate are released into the urine, making for maintaining electrical neutrality a corresponding sodium excretion necessary. When metabolic alkalosis can be distinguished by the urine chloride concentrations between renal and extrarenal causes of volume depletion. cause diuretics Can a hypovolemic hyponatremia. Especially thiazide diuretics reduce the dilution capacity of the kidneys and increase sodium excretion. then enters volume depletion on the release of vasopressin worsens the hyponatremia by the following water retention. An additional hypokalemia leads to the transport of sodium into the cells and enhances the vasopressin release, making the hyponatremia can be further deteriorated. This Thiazideffekt can last up to 2 weeks after discontinuation of therapy. While the drug effect gradually wears off, hyponatremia usually responds to a potassium replacement and replacement of fluid deficit. Elderly patients may have an increased Natriumdiurese and are particularly vulnerable to a thiazide hyponatremia, especially if there are already restrictions on the renal capacity to excrete free water. Rarely, such patients develop severe, life-threatening hyponatremia within weeks of taking the start of a thiazide diuretic. Loop diuretics cause much rarer one Hyponaträmie.Normovolämische hyponatremia When normovolaemic (dilution) hyponatremia total body amount of sodium and thus the volume of the ECF are normal or nearly normal. TBW is increased. Primarily a polydipsia can cause such hyponatremia, when the water absorption exceeds the ability of the kidneys to water excretion. Since healthy kidney can excrete urine / day to 25 l, hyponatremia occurs due to a polydipsia only when very large amounts of liquid are added or when defects in the renal capacity exist for excretion of free water. Affected patients usually have a psychosis or only a moderate polydipsia with renal insufficiency. A normovolemic hyponatremia can also consist of excessive water absorption under a Addison’s disease, hypothyroidism or a non-osmotic vasopressin release (z. B. stress, in the postoperative period, by taking medications such as chlorpropamide, tolbutamide, opioids, barbiturates, vincristine , clofibrate or carbamazepine) result. Postoperative hyponatremia usually occurs due to a combination of a inappropriaten vasopressin release and an excessive supply of hypotonic fluid according to an operation. Certain medications (eg., Cyclophosphamide, NSAIDS, chlorpropamide) reinforce the renal effects of endogenous vasopressin, while others (eg. As oxytocin) have a direct vasopressin-like effect on the kidneys. Intoxication with 3,4-Methylenedioxymethamphetamine (MDMA [Ecstasy]) gives hyponatremia by inducing excessive water drinking and improvement of vasopressin secretion. A lack of water excretion is common to all faults. Diuretics can cause normovolemic hyponatremia or contribute to its development when it comes to water retention or excessive water intake due to another circumstance. The syndrome of inappropriate antidiuretic hormone secretion (SIADH, syndrome of inappropriate antidiuretic hormone) is another cause of normovolemic hyponatremia. Syndrome of inappropriate antidiuretic hormone secretion syndrome of inappropriate antidiuretic hormone (vasopressin) secretion (SIADH) due to excessive vasopressin) release. It is defined as a non-maximum of dilute urine at a Plasmahypoosmolalität (hyponatremia) without volume depletion or overload triggered by emotional stress, pain, diuretic therapy or taking other medications as chlorpropamide, carbamazepine, vincristine (z., Clofibrate, antipsychotics, aspirin, ibuprofen , vasopressin) that stimulate vasopressin release in patients with normal functioning of the heart, kidneys, liver, adrenal and thyroid glands. The SIADH is associated with a variety of disorders (see Table: diseases that are associated with the syndrome of inappropriate antidiuretic hormone secretion). Diseases that are associated with the syndrome of inappropriate antidiuretic hormone secretion disease Examples malignancy CNS duodenal Lung (especially small cell carcinoma) lymphoma pancreatic Neurological Disorders Acute intermittent porphyria Acute psychosis brain abscess encephalitis Guillain-Barre Syndrome traumatic brain injury Meningitis Stroke Subdural or subarachnoid Pulmonary circulation diseases and treatments Aspergillosis lung abscess pneumonia Positive pressure respiratory tuberculosis Other protein-energy malnutrition hypervolaemic hyponatremia The hypervolaemic hyponatremia is characterized by an increase of both the total body atrium (and so also of the extracellular volume) and the TBW. The increase in TBW is relatively larger. Various associated with edema formation disturbances such. As heart failure or cirrhosis cause hypervolaemic hyponatremia. Very rarely, in the context of nephrotic syndrome of hyponatremia. However, a Pseudohyponaträmie can be caused by an impairment of the sodium measurement by increased lipid levels. In each of these disorders, the decrease of the effective circulating volume leads to a release of vasopressin and angiotensin II The following factors contribute to hyponatremia in. Antidiuretic effects of vasopressin on the kidney restriction of renal water excretion by angiotensin II Reduced GFR generating a thirst feeling by angiotensin II the urinary sodium excretion is normally <10 mEq / l, and urine osmolality is in comparison to the serum osmolality hoch.Hyponaträmie in AIDS A hyponatremia is at> 50% of the observed inpatients with AIDS. Some of the many causative factors are supply of hypotonic fluids Renal impairment Not osmotic vasopressin release therapy with drugs that lead to a restriction of water excretion addition as a result of intravascular volume depletion that adrenal insufficiency in patients with AIDS is increasingly common. The reasons for this may be a Adrenalitis as part of a cytomegalovirus infection, mycobacterial infection, or an interaction between the adrenal glucocorticoid and Mineralokortikoidsynthese and ketoconazole. SIADH can occur at the same time existing pulmonary or cerebral infection. Symptoms and complaints The hyponatremia manifested with disorders of the central nervous system function. Signs of ECF volume depletion or volume overload occur in addition to hyponatremia when changes in total body atrium exist. In general, older, chronically ill patients more likely to develop symptoms than younger, otherwise healthy patients with hyponatremia. The symptoms are more severe in a rapidly developing hyponatremia. Symptoms usually occur when the plasma osmolality drops below <240 mOsm / kg. The symptoms can be very discreet and consist mainly of changes in mental status such. B. personality changes, lethargy and confusion. If the serum sodium concentration falls to <115 mEq / L, stupor, neuromuscular excitability, hyperreflexia, seizures, coma and even death can occur. Premenopausal women, at an acute hyponatremia occasionally severe cerebral edema, probably because estrogen and progesterone cerebral Na +, K + -ATPase inhibiting and thus interfere with the transport of dissolved particles from the brain cells. The consequences are both hypothalamic infarction and infarction of the posterior pituitary and in some cases an osmotic Demyelinisierungssyndrom or herniation of the brainstem. Diagnostic serum and urine electrolytes and osmolality Clinical assessment of volume status suspected hyponatremia is uncommon in patients with neurological abnormalities and increased risk. However, since the findings are nonspecific, hyponatremia is often detected only after determination of serum electrolytes. Exclusion of displaced hyponatremia and Pseudohyponatremiie serum sodium may be low, when a severe hyperglycemia (or exogenously administered mannitol or glycerol), the osmolality increased and water migrates out of the cells into the extracellular volume. The serum sodium concentration falls to 1,6 mEq / l per increase in serum glucose concentration to 100 mg / dl (5.55 mmol / l) than the standard values. This condition is often called Verschiebungshyponaträmie because it is caused by a shift of water through the cell walls. A Pseudohyponaträmie with normal serum osmolality may occur with hyperlipidemia or extreme hyperproteinaemia because the lipids or proteins take up space in the used for the analysis of serum volume. The sodium concentration in the serum itself is not affected. With newer methods for the measurement of serum electrolytes, which work with ion-selective electrodes, this problem no longer occurs. Clinical calculator: sodium correction of hyperglycemia clinical calculator: sodium change in clinical hypertriglyceridemia computer: Change of sodium at hyperproteinemia identify the cause The cause of hyponatremia can be complex. Sometimes results from the history of a notice for. B. substantial fluid losses from vomiting or diarrhea, kidney disease, compulsive fluid intake, taking medications that promote vasopressin secretion or enhance the vasopressin effect. The volume status, in particular the appearance of a volume deficiency or volume overload, makes various causes likely (see Table: Common causes of volume depletion). Obviously hypovolemic patients usually have an easy-to-find cause of their fluid losses and were usually treated with hypotonic fluid replacement. also obvious hypervolaemic patients often show a slightly auszumachende cause such. As heart failure, kidney or liver disease. Normovolemic patients or patients with an unclear volume status require more thorough laboratory tests to determine the cause. Laboratory tests should include serum and urine osmolality and electrolytes. Normovolemic patients should also be checked with regard to the function of the thyroid and adrenal glands. Hypoosmolalität at a normovolemic patients should lead dilute to precipitate a large amount of urine (z. B. having an osmolality <100 mOsm / kg and a specific gravity <1.003). Low serum sodium concentration and low serum osmolality, and urine osmolality that is unduly high compared to low serum osmolality (120-150 mmol / l), gives an indication of a volume overload, volume deficiency or SIADH. Volume overload and volume depletion are clinically distinguished. If neither volume overload volume collection still seems likely to draw is SIADH into consideration. Patients with SIADH are usually normovolemic or hypervolemic slightly. Blood urea nitrogen and creatinine levels are normal, and serum uric acid values ??are rather low. The urine sodium concentration is> 30 mmol / l and fractional sodium excretion is> 1% (calculation examination of renal patients: Other urine tests). In a patient with hypovolemia and normal renal function, sodium re leads to urinary sodium <20 mmol / l. A urine atrium> 20 mmol / l at a hypovolemic patient indicates a Mineralokortikoidmangel or a Salzverlustnephropathie. Hyperkalemia directs the suspected adrenal insufficiency. Treatment If hypovolemic, 0.9% saline When hypervolemic, hydration, sometimes diuretic, occasionally a vasopressin antagonist If normovolemic, treating cause If severe, fast onset or highly symptomatic hyponatremia, partly quick correction with hypertonic (3%) saline hyponatremia can be life-threatening and requires immediate recognition and appropriate treatment. Too rapid correction of hyponatremia involves the risk of neurological complications such. As the osmotic Demyelinisierungssyndroms. Even with severe hyponatremia, serum sodium concentration should not be increased to be in the first 24 hours more than 8 mEq / l. And sodium should not be corrected except perhaps in the first few hours after the treatment of severe hyponatremia, faster than 0.5 mEq / L / hour. The degree of hyponatremia, the duration and the speed of onset and the patient’s symptoms are used to determine which treatment is most appropriate. Clinical calculator: rate of infusate for the correction of hyponatremia in patients with hypovolemia and normal function of the adrenal usually corrects the infusion of 0.9% saline both hyponatremia and the hypovolemia. If the serum sodium has dropped below <120 mEq / l, it may be that a replacement of the intravascular volume not completely sufficient for the correction of hyponatremia. In this case, a limitation of the uptake of free water to 500-1000 ml / 24 hrs is required. In volume overload patients in whom the hyponatremia due to renal sodium retention (for. Example, in the context of a heart failure, cirrhosis, a nephrotic syndrome), and a dilution is made, the restriction of water uptake in combination with the treatment of the underlying disease is required. In patients with heart failure an ACE inhibitor in combination with a diuretic can correct refractory hyponatremia. In other patients, in which a fluid restriction is ineffective, a loop diuretic, may be given along with an infusion of saline, in an ascending dosage can. Potassium and other electrolytes that are excreted in the urine must be replaced. If the hyponatremia is more severe and does not respond to therapy with diuretics, an intermittent or continuous hemofiltration may be necessary to maintain the extracellular volume in control while the hyponatremia is compensated by physiological saline. A severe or resistant hyponatremia generally occurs only when a heart or liver problem is almost at the final stage. In normovolemia the therapy depends on the cause (z. B. hypothyroidism, adrenal insufficiency, diuretic therapy). If a SIADH is present, strict drinking flow limitation (z. B. 250-500 ml / 24 hours) is generally necessary. In addition, a loop diuretic with the infusion of 0.9% saline may be combined as in the treatment of hypervolemic hyponatremia. A permanent correction can only be achieved after successful treatment of the underlying disease. If the underlying disorder is not treatable, like a metastatic malignancy, and patients feel a significant water restriction as unacceptable, demeclocycline may 300-600 mg po every 12 hours be helpful to induce a concentration defect in the kidneys. However, demeclocycline is not widely used because of the possibility of drug-induced acute kidney injury. Intravenous conivaptan, a vasopressin receptor antagonist, effectively resulting in a water diuresis without this leading to significant loss of electrolytes in the urine, and can be used in hospitalized patients for the treatment of drug-resistant hyponatremia. Orales Tolvaptan ist ein weiterer Vasopressin- Rezeptor-Antagonist mit ähnlicher Wirkung bei Conivaptan. Die Verwendung von Tolvaptan ist aufgrund einer möglichen Lebertoxizität auf weniger als 30 Tage beschränkt und sollte nicht bei Patienten mit Leber- oder Nierenerkrankung eingesetzt werden. Leichte bis mäßig schwere Hyponatriämie Geringgradige, asymptomatische Hyponatriämie (d. h. Serumnatrium > 121 und < 135 mEq/l) erfordert Zurückhaltung, weil kleine Anpassungen in der Regel ausreichen. Bei einer diuretikainduzierten Hyponaträmie kann das Absetzen der Therapie bereits ausreichen. Einige Patienten brauchen dennoch eine Natrium- oder Kaliumsupplementierung. Eine geringgradige Hyponaträmie, die durch eine unangemessene hypotone parenterale Flüssigkeitstherapie bei Patienten mit beeinträchtigter Fähigkeit zur Wasserausscheidung verursacht wurde, ist meist schon durch das Verändern der Flüssigkeitsgabe ausreichend therapiert.Schwere Hyponaträmie Bei asymptomatischen Patienten kann eine schwere Hyponaträmie (Serumnatrium < 121 mEq/l; effektive Osmolalität < 240 mOsm/kg) mit einer strengen Einschränkung der täglichen Wasseraufnahme sicher behandelt werden. Bei Patienten mit neurologischen Symptomen (z. B. Verwirrung, Lethargie, Krampfanfälle, Koma) ist eine Therapie umstrittener. Die Diskussio

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