Sandbox:Vindhya: Difference between revisions

Jump to navigation Jump to search
VisualWikitext
No edit summary
Line 36: Line 36:
==Classification==
==Classification==


[[SIADH]] may be classified in to several sub-types based on the pattern of AVP secretion across a range of plasma osmolalities:
*Acute setting (<48 hours since onset) where moderate symptoms are noted, treatment options for hyponatremia include the following:
*3% hypertonic saline (513 mEq/L)
*Loop diuretics with saline
*Vasopressin-2 receptor antagonists (aquaretics, such as conivaptan or tolvaptan)
* Water restriction


*Type A : is the commonest form of [[SIADH]] responsible for a much higher proportion of SIADH, at around 60–70%. Characteristically, type A patients exhibit excessive, random secretion of AVP, with loss of the close linear relationship between plasma osmolality and plasma[[ AVP]]. Type A is common in [[lung cancer]]; in[[ vitro studie]]s have demonstrated that some lung tumours synthesize AVP, and that tumour tissue stains positive for AVP[[ mRNA]].Plasma AVP concentrations in type A SIADH are not suppressed [[physiologically]] by drinking , which makes patients vulnerable to the development of severe [[hyponatremia]]. Studies have also demonstrated a lower[[ osmotic]] threshold for [[thirst]] appreciation in this type of SIADH. This type of SIADH is also characteristic of [[nasopharyngeal tumours]], which also stain positive for AVP mRNA.
* In chronic asymptomatic setting, the treatment is as follows:
*Fluid restriction
*Vasopressin-2 receptor antagonists
*Other agents to be considered include loop diuretics with increased salt intake, urea, and demeclocycline


*Raise serum sodium by 0.5-1 mEq/hr, and not more than 10-12 mEq in the first 24 hours,to avoid complications like Osmotic demyelination syndrome.


*Type B: is also common (20–40%). The osmotic[[ threshold ]]for AVP release is lowered – a [[reset osmostat]] – such that secretion of AVP occurs at lower plasma [[osmolalities]] than normal. Because [[AVP]] is suppressed at plasma osmolalities below the lower, reset threshold, further over-hydration leads to suppression of AVP release, which protects against the progression to severe[[ hyponatraemia]]. Although most [[tumours]] manifest type A[[ SIADH]], some also present with type B SIADH, so the[[ pattern]] of [[abnormal]] AVP secretion cannot be utilized to predict the [[causation]] of SIADH.
*In rare medical emergencies more commonly seen in cardiology in the context of hypervolemic severe hyponatremia rather than in SIADH : 
 
* Continuous veno-venous hemofiltration (CVVH)
 
*Slow, low-efficiency daily dialysis (SLEDD  have been used to improve hyponatremia. These methods are invasive so their use is very limited.<ref name="pmid19628685">{{cite journal |vauthors=Salahudeen AK, Kumar V, Madan N, Xiao L, Lahoti A, Samuels J, Nates J, Price K |title=Sustained low efficiency dialysis in the continuous mode (C-SLED): dialysis efficacy, clinical outcomes, and survival predictors in critically ill cancer patients |journal=Clin J Am Soc Nephrol |volume=4 |issue=8 |pages=1338–46 |year=2009 |pmid=19628685 |pmc=2723965 |doi=10.2215/CJN.02130309 |url=}}</ref>
*Type C :is a rare condition characterized by failure to suppress AVP secretion at plasma osmolalities below the osmotic threshold. Plasma AVP concentrations are thus inappropriately high at low plasma osmolalities, but there is a normal relationship between plasma osmolality and plasma AVP at physiological plasma osmolalities. This variant may be due to dysfunction of inhibitory neurons in the hypothalamus, leading to persistent low-grade basal AVP secretion.
 
 
*Type D: is a rare clinical picture of SIADH with low or undetectable AVP levels and no detectable abnormality in circulating AVP response . It is thought that a nephrogenic SIADH (NSIAD) may be responsible for this picture . Gain-of-function mutations in the V2 receptor leading to a clinical picture of SIADH, with undetectable AVP levels, have been described. The identified mutations had different nucleotide substitutions causing different levels of V2 receptor activation. This syndrome appears to be inherited in an X-linked manner,although heterozygous females may have varying degrees of inappropriate antidiuresis. Owing to variable expressivity of the gene involved, NSIAD may be clinically undetectable for years, until other contributing factors in later life lead to clinically significant hyponatraemia . <ref name="pmid20164214">{{cite journal |vauthors=Hannon MJ, Thompson CJ |title=The syndrome of inappropriate antidiuretic hormone: prevalence, causes and consequences |journal=Eur. J. Endocrinol. |volume=162 Suppl 1 |issue= |pages=S5–12 |year=2010 |pmid=20164214 |doi=10.1530/EJE-09-1063 |url=}}</ref>

Revision as of 13:30, 15 August 2017

Medical and Neurologic causes

Neurologic disorders Cerebral neoplasms, cerebral trauma and post concussive syndromes ,Cerebrovascular disease, subarachnoid hemorrhage, Migraine, encephalitis,cerebral syphilis, Multiple sclerosis,Wilsons disease,Huntington disease,Epilepsy
Endocrine disorder Pituitary dysfunction, Thyroid dysfunction, parathyroid dysfunction, Adrenal dysfunction,pheochromocytoma
Systemic conditions Hypoxia, Cardiovascular disease, pulmonary insufficiency, anemia
Inflammatory disorders Lupus erythematosus, rheumatoid arthritis, polyarteritis nodosa, temporal arteritis
Deficiency states Vitamin B12 deficiency, pellagra
Miscellaneous hypoglycemia, carcinoid syndrome, uremia, premenstrual syndrome, porphyria
Substances Caffeine,cannabis,Hallucinogens, theophylline, amphetamines,yohimbine,sympathomimetics, mercury, Arsenic,organophosphates,benzene
Withdrawal alcohol,caffeine, opiods,antihypertensives

siadh classification

Classification

  • Acute setting (<48 hours since onset) where moderate symptoms are noted, treatment options for hyponatremia include the following:
  • 3% hypertonic saline (513 mEq/L)
  • Loop diuretics with saline
  • Vasopressin-2 receptor antagonists (aquaretics, such as conivaptan or tolvaptan)
  • Water restriction
  • In chronic asymptomatic setting, the treatment is as follows:
  • Fluid restriction
  • Vasopressin-2 receptor antagonists
  • Other agents to be considered include loop diuretics with increased salt intake, urea, and demeclocycline
  • Raise serum sodium by 0.5-1 mEq/hr, and not more than 10-12 mEq in the first 24 hours,to avoid complications like Osmotic demyelination syndrome.
  • In rare medical emergencies more commonly seen in cardiology in the context of hypervolemic severe hyponatremia rather than in SIADH :
  • Continuous veno-venous hemofiltration (CVVH)
  • Slow, low-efficiency daily dialysis (SLEDD have been used to improve hyponatremia. These methods are invasive so their use is very limited.[1]
  1. ↑ Salahudeen AK, Kumar V, Madan N, Xiao L, Lahoti A, Samuels J, Nates J, Price K (2009). "Sustained low efficiency dialysis in the continuous mode (C-SLED): dialysis efficacy, clinical outcomes, and survival predictors in critically ill cancer patients". Clin J Am Soc Nephrol. 4 (8): 1338–46. doi:10.2215/CJN.02130309. PMC 2723965. PMID 19628685.
Retrieved from "https://www.wikidoc.org/index.php?title=Sandbox:Vindhya&oldid=1341506"