Syndrome of inappropriate antidiuretic hormone secretion

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Syndrome of inappropriate antidiuretic hormone secretion
Classification and external resources
ICD-10E22.2
ICD-9253.6
DiseasesDB12050
MedlinePlus003702
eMedicineemerg/784 med/3541 ped/2190
MeSHD007177
 
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Syndrome of inappropriate antidiuretic hormone secretion
Classification and external resources
ICD-10E22.2
ICD-9253.6
DiseasesDB12050
MedlinePlus003702
eMedicineemerg/784 med/3541 ped/2190
MeSHD007177

The syndrome of inappropriate antidiuretic hormone secretion or SIADH (other names: Schwartz-Bartter syndrome, SIAD -- syndrome of inadequate antidiuresis) is characterized by excessive release of antidiuretic hormone from the posterior pituitary gland or another source. The result is hyponatremia and sometimes fluid overload. It is usually found in patients diagnosed with pneumonia, brain tumors, head trauma, strokes, meningitis, encephalitis, or small-cell carcinoma of the lung.

Contents

Pathophysiology

The normal function of ADH on the kidneys is to control the amount of water reabsorbed by kidney nephrons. ADH acts in the distal portion of the renal tubule (Distal Convoluted Tubule) as well as on the collecting duct and causes the retention of water, but not solute. Hence, ADH activity effectively dilutes the blood (decreasing the concentrations of solutes such as sodium).

ADH is secreted to prevent water loss in the kidneys. When water is ingested, it is taken up into the circulation and results in a dilution of the plasma. This dilution, otherwise described as a reduction in plasma osmolality, is detected by osmoreceptors in the hypothalamus of the brain and these then switch off the release of ADH. The decreasing concentration of ADH effectively inhibits the aquaporins in the collecting ducts and distal convoluted tubules in the nephrons of the kidney. Hence, less water is reabsorbed, thereby increasing urine output, decreasing urine osmolality, and normalizing blood osmolality. In SIADH the release of ADH is not inhibited by a reduction in plasma osmolality when the individual ingests water and the osmolality of the plasma drops. As the main solute of plasma is sodium, this hypoosmolar state is usually detected as a low sodium level on laboratory testing. SIADH is therefore primarily a condition that results in the abnormal handling of water loading and not a problem with excessive solute loss. This is why it is usually treated with fluid (in particular water) restriction. Diuretics may also be given to decrease reabsorption of water, but care must be taken not to correct water imbalances too rapidly.

This causes dilutional hyponatremia and all the consequences associated with that condition: headache, nausea, vomiting, and confusion may ensue. Severe hyponatremia may cause convulsions or coma.

The abnormalities underlying type D syndrome of inappropriate antidiuretic hormone hypersecretion concern individuals where vasopressin release and response are normal but where abnormal renal expression and translocation of aquaporin 2, or both are found.[1] It has been suggested that this is due to abnormalities in the secretion of secretin in the brain and that "Secretin as a neurosecretory hormone from the posterior pituitary, therefore, could be the long-sought vasopressin independent mechanism to solve the riddle that has puzzled clinicians and physiologists for decades."[1]

Clinical Findings

In general, increased ADH causes water retention and extracellular fluid volume expansion without edema or hypertension, owing to natriuresis (the excretion of sodium by the kidneys). The water retention and sodium loss both cause hyponatremia, which is a key feature in SIADH. Hyponatremia and concentrated urine (UOsm >300 mOsm) (reference required - usual criteria cited are Ur Osmo > 100 mOsm/kg and Ur [Na] > 40 mEq/L ) are seen, as well as no signs of edema or dehydration. When hyponatremia is severe (sodium <120 mOsm), or acute in onset, symptoms of cerebral edema become prominent (irritability, confusion, seizures, and coma).

Diagnosis

Laboratory findings in diagnosis of SIADH include:

Other findings include:

Causes

Some common causes of SIADH include: [2]

Management

Management of SIADH includes:

No head to head study is currently available to quantify and compare the relative efficacies of V2 vasopressin receptor antagonists with demeclocycline or other treatment options.

Care must be taken when correcting hyponatremia. A rapid rise in the sodium level may cause central pontine myelinolysis.[7] Avoid correction by more than 12 mEq/L/day. Initial treatment with hypertonic saline may abruptly lead to a rapid dilute diuresis and fall in ADH. Rapid diuresis may lead to over-rapid rise in serum sodium, and should be managed with extreme care.

Differential diagnosis

Cerebral salt wasting syndrome also presents with hyponatremia, there are signs of dehydration. In SIADH, the patient is clinically overloaded or may be euvolaemic.

History

The condition was first described by researchers from Boston, Massachusetts and Bethesda, Maryland (including Dr Frederic Bartter) in two patients with lung cancer.[8] Criteria were developed by Schwartz and Bartter in 1967[9] and have remained essentially unchanged since then.[10] The condition is occasionally referred to by the names of the authors of the first report - Schwartz-Bartter syndrome.[11]

References

  1. ^ a b Chu JY, Lee LT, Lai CH, Vaudry H, Chan YS, Yung WH, Chow BK.(2009). Secretin as a neurohypophysial factor regulating body water homeostasis. Proceedings of the National Academy of Sciences USA, 106:15961–15966. doi:10.1073/pnas.0903695106
  2. ^ also, www.ccmtutorials.com/problems/explore/name/siadh.htm
  3. ^ Schürer, L.; Wolf, S.; Lumenta, C. B. (2010). Water and Electrolyte Regulation. pp. 611. doi:10.1007/978-3-540-79565-0_40.  edit
  4. ^ a b c Zietse, Robert; van der Lubbe N, Hoorn E (2009). "Current and Future Treatment Options in SIADH". Nephrology Dialysis Transplantation 2 [Suppl 3] (Suppl_3): iii12–iii19. doi:10.1093/ndtplus/sfp154. PMC 2762827. PMID 19881932. //www.ncbi.nlm.nih.gov/pmc/articles/PMC2762827/. 
  5. ^ "Vaprisol (conivaptan hydrochloride) Liquid [Astellas Pharma US, Inc."]. http://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?id=3621#nlm34067-9. Retrieved 2007-06-08. 
  6. ^ Schrier RW, Gross P, Gheorghiade M, et al. (2006). "Tolvaptan, a selective oral vasopressin V2-receptor antagonist, for hyponatremia". N. Engl. J. Med. 355 (20): 2099–112. doi:10.1056/NEJMoa065181. PMID 17105757. 
  7. ^ Ashrafian H, Davey P (2001). "A review of the causes of central pontine myelinosis: yet another apoptotic illness?". Eur. J. Neurol. 8 (2): 103–9. doi:10.1046/j.1468-1331.2001.00176.x. PMID 11430268. 
  8. ^ Schwarts WB, Bennett W, Curelop S, Bartter FC (1957). "A syndrome of renal sodium loss and hyponatremia probably resulting from inappropriate secretion of antidiuretic hormone". Am. J. Med. 23 (4): 529–42. doi:10.1016/0002-9343(57)90224-3. PMID 13469824.  reproduced in Schwartz WB, Bennett W, Curelop S, Bartter FC (1 December 2001). "A syndrome of renal sodium loss and hyponatremia probably resulting from inappropriate secretion of antidiuretic hormone. 1957". J. Am. Soc. Nephrol. 12 (12): 2860–70. PMID 11729259. http://jasn.asnjournals.org/cgi/content/full/12/12/2860. 
  9. ^ Bartter FC, Schwartz WB (1967). "The syndrome of inappropriate secretion of antidiuretic hormone". Am. J. Med. 42 (5): 790–806. doi:10.1016/0002-9343(67)90096-4. PMID 5337379. 
  10. ^ Verbalis JG, Goldsmith SR, Greenberg A, Schrier RW, Sterns RH (2007). "Hyponatremia treatment guidelines 2007: expert panel recommendations". Am. J. Med. 120 (11 Suppl 1): S1–21. doi:10.1016/j.amjmed.2007.09.001. PMID 17981159. 
  11. ^ Schwartz-Bartter syndrome at Who Named It?