scholarly journals Urea minimizes brain complications following rapid correction of chronic hyponatremia compared with vasopressin antagonist or hypertonic saline

2015 ◽  
Vol 87 (2) ◽  
pp. 323-331 ◽  
Author(s):  
Fabrice Gankam Kengne ◽  
Bruno S. Couturier ◽  
Alain Soupart ◽  
Guy Decaux
Keyword(s):  
Hypertonic Saline ◽  
Vasopressin Antagonist ◽  
Brain Complications ◽  
Chronic Hyponatremia ◽  
Rapid Correction

Suspected myelinolysis following rapid correction of hyponatremia in a dog

1999 ◽  
Vol 35 (6) ◽  
pp. 493-497 ◽  
Author(s):  
RK Churcher ◽  
AD Watson ◽  
A Eaton
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neurological Dysfunction ◽  
Laboratory Findings ◽  
Neurological Signs ◽  
Therapeutic Guidelines ◽  
Chronic Hyponatremia ◽  
Iatrogenic Damage ◽  
Gastrointestinal Parasitism ◽  
Rapid Correction

A dog developed signs of neurological dysfunction five days after rapid correction of severe electrolyte derangements, including hyponatremia, caused by gastrointestinal parasitism (i.e., trichuriasis). History, laboratory findings, and onset of neurological signs following correction of hyponatremia led to a diagnosis of myelinolysis. Myelinolysis is a noninflammatory, demyelinating brain disease caused by sudden, upward osmotic shifts in central nervous system plasma, often a result of rapid correction of chronic hyponatremia. The pathogenesis is complex, but recovery is possible. Iatrogenic damage due to myelinolysis can be avoided by adherence to therapeutic guidelines for correction of chronic hyponatremia.

scholarly journals Relowering of Serum Na for Osmotic Demyelinating Syndrome

2012 ◽  
Vol 2012 ◽  
pp. 1-2 ◽  
Author(s):  
Hideomi Yamada ◽  
Koji Takano ◽  
Nobuhiro Ayuzawa ◽  
George Seki ◽  
Toshiro Fujita
Keyword(s):  
Serum Sodium ◽  
Central Pontine Myelinolysis ◽  
Supportive Therapy ◽  
Chronic Hyponatremia ◽  
Pontine Myelinolysis ◽  
Extreme Care ◽  
The Brain ◽  
Osmotic Demyelinating Syndrome ◽  
Central Pontine ◽  
Rapid Correction

We report a case in whom slow correction of hyponatremia (5 mmol/day for 3 days) induced central pontine myelinolysis (CPM). After the diagnosis was confirmed by imaging, we started to relower serum Na that completely recovered the sign and symptoms of CPM. Rapid correction of serum sodium is known to be associated with CPM. However, it may occur even after slow correction of hyponatremia. Currently, there is no standard therapy for CPM other than supportive therapy. Other therapy includes sterioid, plasmaphresis and IVIG, but these therapies have not been shown to be particularly effective. The pathophysiology of CPM is related to a relative dehydration of the brain during the correction of hyponatremia, resulting in cell death and demyelination, therefore gentle rehydration with lowering serum sodium may not be an unreasonable therapy. The present case provides supportive evidence that reinduction of hyponatremia is effective in treating CPM if started immediately after the diagnosis is suggested. The present case tells us that severe chronic hyponatremia must be managed with extreme care especially in patients with chronic debilitating illness and that relowering serum Na is a treatment of choice when CPM is suggested.

Symptomatic hyponatremia in rats: effect of treatment on mortality and brain lesions

1989 ◽  
Vol 257 (1) ◽  
pp. F18-F22 ◽  
Author(s):  
J. C. Ayus ◽  
R. K. Krothapalli ◽  
D. L. Armstrong ◽  
H. J. Norton
Keyword(s):  
Hypertonic Saline ◽  
Serum Sodium ◽  
Brain Lesions ◽  
The Other ◽  
Absolute Change ◽  
Spontaneous Correction ◽  
Survival And Development ◽  
Effect Of Treatment ◽  
The Absolute ◽  
Rapid Correction

Hyponatremia was induced in rats over 3 days with dextrose in water and vasopressin. Eighty-five percent of the rats survived for 5 mo after spontaneous correction of mild hyponatremia. However, spontaneous correction of symptomatic hyponatremia (serum sodium less than 120 meq/l) resulted in 32% survival. Rapid correction of symptomatic hyponatremia by hypertonic saline with an absolute change in serum sodium of greater than 14 and less than 25 meq/l in the first 24 h allowed 100% of the rats to survive for 5 mo without brain lesions. On the other hand, correction of symptomatic hyponatremia with an absolute change in serum sodium of greater than 25 meq/l in the first 24 h resulted in 12% survival and development of brain lesions. We conclude that rapid correction of symptomatic hyponatremia improves survival and is safe if the absolute change in serum sodium is between 14 and 25 meq/l in the first 24 h. Increased mortality and brain lesions are associated with an absolute change in serum sodium of greater than 25 meq/l in the first 24 h.

scholarly journals Thiazide-Associated Hyponatremia, Report of the Hyponatremia Registry: An Observational Multicenter International Study

2017 ◽  
Vol 45 (5) ◽  
pp. 420-430 ◽  
Author(s):  
Volker Burst ◽  
Franziska Grundmann ◽  
Torsten Kubacki ◽  
Arthur Greenberg ◽  
Ingrid Becker ◽  
...  
Keyword(s):  
Hypertonic Saline ◽  
Normal Saline ◽  
Management Practices ◽  
Treatment Success ◽  
Hormone Secretion ◽  
Isotonic Saline ◽  
High Rate ◽  
Adverse Side Effect ◽  
Fluid Restriction ◽  
Rapid Correction

Background: Hyponatremia is a frequent and potentially life-threatening adverse side effect of thiazide diuretics. This sub-analysis of the Hyponatremia Registry database focuses on current management practices of thiazide-associated hyponatremia (TAH) and compares differences between TAH and syndrome of inappropriate antidiuretic hormone secretion (SIADH). Methods: We analyzed 477 patients from 225 US and EU sites with euvolemic hyponatremia ([Na+] ≤130 mEq/L) who were receiving a thiazide diuretic. Of these, 118 met criteria for true thiazide-induced hyponatremia (TIH). Results: Thiazide was withdrawn immediately after hyponatremia was diagnosed only in 57% of TAH; in these patients, the median rate of [Na+] change (Δdaily[Na+]) was significantly higher than those with continued thiazide treatment (3.8 [interquartile range: 4.0] vs. 1.7 [3.8] mEq/L/day). The most frequently employed therapies were isotonic saline (29.6%), fluid restriction (19.9%), the combination of these two (8.2%), and hypertonic saline (5.2%). Hypertonic saline produced the greatest Δdaily[Na+] (8.0[6.4] mEq/L/day) followed by a combination of fluid restriction and normal saline (4.5 [3.8] mEq/L/day) and normal saline alone (3.6 [3.5] mEq/L/day). Fluid restriction was markedly less effective (2.7 [2.7] mEq/L/day). Overly rapid correction of hyponatremia occurred in 3.1% overall, but in up to 21.4% given hypertonic saline. Although there are highly significant differences in the biochemical profiles between TIH and SIADH, no predictive diagnostic test could be derived. Conclusions: Despite its high incidence and potential risks, the management of TAH is often poor. Immediate withdrawal of the thiazide is crucial for treatment success. Hypertonic saline is most effective in correcting hyponatremia but associated with a high rate of overly rapid correction. We could not establish a diagnostic laboratory-based test to differentiate TIH from SIADH.

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