Hyponatremia
Classification according to ICD-10 | |
---|---|
E87.1 | Hypoosmolality and Hyponatremia Sodium Deficiency |
ICD-10 online (WHO version 2019) |
The electrolyte disorder hyponatremia is a low sodium concentration in the blood serum . Sodium, by far the most common positively charged electrolyte, determines the osmolarity of the extracellular fluid ; If one disregards the cases of hypertonic hyponatremia (compensatory hyponatremia in the case of an excess of non-ionic osmolytes such as glucose), it is therefore a hypoosmolar disorder caused by a relative excess of water. Often an absolute excess of water is the cause, the low concentration being caused by dilution with normal or increased sodium levels. Since osmoregulation (compensatory water loss in the event of sodium loss) has priority over volume regulation in the physiological framework , sodium loss only manifests itself in an advanced stage as hyponatremia, which is then also referred to as hypotonic hypohydration .
Since sodium is measured very often, a reduced concentration is quickly noticeable in inpatients or in people who regularly visit a doctor for check-ups. Severe hyponatremia cases with a sodium concentration below 120 mmol / l are rare; they are to be classified as threatening and usually require immediate inpatient treatment.
classification
Real sodium deficiency
-
Hyponatremia with absolute or relative excess water (too low level of total body sodium)
- in heart failure , liver cirrhosis and nephrotic syndrome due to disruption of the hypothalamic osmoregulation.
- in advanced renal insufficiency due to increased sodium excretion.
-
Hyponatremia with extracellular volume depletion (lack of total body sodium)
- extrarenal (outside the kidneys) sodium and fluid loss (urine Na <10 mmol / l): for example vomiting, diarrhea, infection, burns
- Renal (in the kidneys) sodium and fluid loss (urine Na> 20 mmol / l): as with diuretics , aldosterone deficiency and with cortisol deficiency
-
Hyponatremia in isovolaemia (normal total body sodium)
- drug-related
- through increased ADH release, for example through chlorpropamide (for the treatment of diabetes mellitus ), amitriptyline , isoproterenol , nicotine or morphine
- through increased ADH effects, for example through chlorpropamide, cyclophosphamide (relatively common) or indomethacin (also other NSAIDs )
- Syndrome of inadequate ADH secretion ( SIADH ), for example in tumors
- drug-related
Dilution hyponatremia
If the human body is given more water that contains little salt, dilution hyponatremia can occur. The amount of sodium in the blood is actually normal, but the amount of fluid is too high. Dilution hyponatremia is found, for example, when there is a pathological increase in water intake ( polydipsia ) or often occurs in marathon runners who consume too much water.
Pseudohyponatremia
The proportion of sodium in the total plasma decreases as a result of greatly increased plasma lipids or plasma proteins . If you only look at the plasma water, the values are normal. It is not true hyponatremia.
causes
- Hyponatremia through dilution ("water poisoning")
- Gastric lavage with large amounts of tap water (water overload)
- drinking too much water (hypotonic fluid)
- psychogenic polydipsia
- Excessive drinking when hungry , anorexic , after dialysis
- Hyponatremia due to sodium loss
- severe diarrhea
- renal salt loss syndrome
- Hyponatremia due to hypovolaemia (release of ADH in hypotension)
- Desiccosis in derailed diabetes mellitus
- severe heart failure, cirrhosis of the liver
- Infusion of hyperosmolar solution, mannitol or glucose
- Hyponatremia as a side effect of medication
- Diuretics (thiazides, spironolactone)
- ACE inhibitors
- Carbamazepine / oxcarbazepine
- Antidepressants ( SSRI , SNRI )
- Hyponatremia as a side effect of using MDMA (" Ecstasy- Induced Hyponatremia"), mostly in women
- Hyponatremia in endocrine diseases
- Adrenal insufficiency
- Pituitary insufficiency , e.g. B. by pituitary tumor
- Inadequate ADH secretion syndrome ( SIADH )
- central salt loss syndrome (CSWS)
- Hypothyroidism
- Pseudohyponatremia in plasmacytoma with hyperproteinemia
- Pseudohyponatremia in lipemic serum
Laboratory values
- Normal sodium level 135–150 mmol / l (adults)
- Normal sodium level 132–145 mmol / l (children)
- Normal sodium level 130–150 mmol / l ( newborns )
- mild hyponatremia 130–135 mmol / l
- moderate hyponatremia 125–130 mmol / l
- severe hyponatremia <125 mmol / l
The plasma sodium concentration does not say anything about how much sodium is present in the body. Hyponatremia occurs either as a result of sodium loss or as a result of the dilution effect due to reduced water excretion or increased water intake. It is therefore essential that other parameters are measured in order to be able to fully diagnose hyponatremia. This includes the osmolarity in the serum and in the urine .
Symptoms
Rapid development of hyponatremia leads to cerebral edema with headache, nausea, tremor and epileptic seizures . With slow development over more than two days, fatigue, confusion, inappetence and changes in personality are in the foreground.
In chronic hyponatremia, impaired gait and alertness lead to more frequent falls. In addition, hyponatremia leads to reduced mineralization of the bone and increased activity of osteoclasts , cells that break down bone substance. The consequence is a tendency to osteoporosis and, in connection with more frequent falls, an increased incidence of bone fractures .
therapy
Depending on the development of the hyponatremia, either fluid restriction (limitation of water intake; with SIADH ) or the administration of isotonic infusion solutions is indicated if the cause of the hyponatremia is a lack of volume (body water). The administration of highly concentrated saline as an infusion is only indicated in an emergency in severe hyponatremia with neurological symptoms. Table salt tablets are only useful in exceptional cases.
Central pontine myelinolysis is the most dreaded complication of a too rapid rise in the sodium level . Therefore, the sodium values should be balanced slowly (maximum 12 mmol / l in 24 h) and with frequent laboratory checks.
The tetracycline demeclocycline, which is no longer used , and drugs from the class of vaptans inhibit the effect of antidiuretic hormone (ADH) on the receptor in the kidney. Tolvaptan increases serum sodium in patients with hyponatremia and normal or increased extracellular volume. Conivaptan , another representative of the Vaptans, is now approved in the USA for the treatment of hyponatremia in hospital patients with normal or increased extracellular volume. Lixivaptan and satavaptan are in clinical trials .
literature
- HJ Milionis, GL Liamis, MS Elisaf: The hyponatremic patient: a systematic approach to laboratory diagnosis. In: Canadian Medical Association Journal. Volume 166, Number 8, April 2002, pp. 1056-1062, PMID 12002984 . PMC 100882 (free full text). (Review).
- Michael Obladen, Rolf F. Maier (Ed.): Neonatal Intensive Care Medicine. 7., completely revised. u. act. Edition. Springer, 2006, ISBN 3-540-33737-7 .
Individual evidence
- ↑ Spasovski, G., Vanholder, R., Allolio, B., Annane, D., Ball, S., Bichet, D., Decaux, G., Fenske, W., Hoorn, E., Ichai, C. , Joannidis, M., Soupart, A., Zietse, R., Haller, M., van der Veer, S., Van Biesen, W., & Nagler, E. (2014). Clinical practice guideline on diagnosis and treatment of hyponatraemia, European Journal of Endocrinology, 170 (3), G1-G47
- ↑ HJ Milionis, GL Liamis, MS elisaf: The hyponatremic patient: a systematic approach to laboratory diagnosis. In: Canadian Medical Association Journal. Volume 166, Number 8, April 2002, pp. 1056-1062, PMID 12002984 . PMC 100882 (free full text). (Review).
- ↑ JC Ayus, ML Moritz: Bone disease as a new complication of hyponatremia: moving beyond brain injury. In: Clinical Journal of the American Society of Nephrology . Volume 5, Number 2, February 2010, pp. 167-168. doi: 10.2215 / CJN.09281209 . PMID 20089487 .
- ^ S. Kinsella, S. Moran, MO Sullivan, MG Molloy, JA Eustace: Hyponatremia independent of osteoporosis is associated with fracture occurrence. In: Clinical Journal of the American Society of Nephrology. Volume 5, Number 2, February 2010, pp. 275-280. doi: 10.2215 / CJN.06120809 . PMID 20056759 . PMC 2827601 (free full text).
- ↑ Goce Spasovski, Raymond Vanholder, Bruno Allolio, Djillali Annane, Steve Ball, Daniel Bichet, Guy Decaux, Wiebke Fenske, Ewout J Hoorn, Carole Ichai, Michael Joannidis, Alain Soupart, Robert Zietse, Maria Haller, Sabine van der Veer, Wim Van Biesen and Evi Nagler: Clinical practice guideline on diagnosis and treatment of hyponatraemia. (pdf) European Journal of Endocrinology, 2014, p. 47 , accessed on July 22, 2018 (English).
- ↑ RW Schrier, P. Gross, M. Gheorghiade, T. Berl, JG Verbalis, FS Czerwiec, C. Orlandi: Tolvaptan, a selective oral vasopressin V2-receptor antagonist, for hyponatremia. In: The New England journal of medicine . Volume 355, Number 20, November 2006, pp. 2099-2112. doi: 10.1056 / NEJMoa065181 . PMID 17105757 .
- ↑ Vaprisol (conivaptan) Center Watch Newly Approved Drug Therapies listing .