DDAVP Is Effective in Preventing and Reversing Inadvertent Overcorrection of Hyponatremia

Perianayagam, Anjana; Sterns, Richard H.; Silver, Solomon; Grieff, Marvin; Mayo, Robert; Hix, John K.; Kouides, Ruth

doi:10.2215/cjn.03190807

Cited by 153 publications

(93 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…38 Rapid recognition of ODS could aid in treatment because prompt reduction in serum sodium levels can benefit patients in the early stages of the disease. 39,40 Therefore, we investigated whether the early neurologic manifestations and fatal outcome in ODS could be predicted on the basis of serum S100B levels. Compared with asymptomatic rats, we showed that 24 hours after serum sodium correction, S100B was significantly higher in rats undergoing early neurologic manifestations (within 2 days postcorrection).…”

Section: Serum Levels Of the Astrocytic Protein S100b Predict Inadvermentioning

confidence: 99%

Astrocytes Are an Early Target in Osmotic Demyelination Syndrome

Kengne

Nicaise²,

Soupart³

et al. 2011

Journal of the American Society of Nephrology

View full text Add to dashboard Cite

Abrupt osmotic changes during rapid correction of chronic hyponatremia result in demyelinative brain lesions, but the sequence of events linking rapid osmotic changes to myelin loss is not yet understood. Here, in a rat model of osmotic demyelination syndrome, we found that massive astrocyte death occurred after rapid correction of hyponatremia, delineating the regions of future myelin loss. Astrocyte death caused a disruption of the astrocyte-oligodendrocyte network, rapidly upregulated inflammatory cytokines genes, and increased serum S100B, which predicted clinical manifestations and outcome of osmotic demyelination. These results support a model for the pathophysiology of osmotic brain injury in which rapid correction of hyponatremia triggers apoptosis in astrocytes followed by a loss of trophic communication between astrocytes and oligodendrocytes, secondary inflammation, microglial activation, and finally demyelination.

show abstract

Section: Serum Levels Of the Astrocytic Protein S100b Predict Inadvermentioning

confidence: 99%

Astrocytes Are an Early Target in Osmotic Demyelination Syndrome

Kengne

Nicaise²,

Soupart³

et al. 2011

Journal of the American Society of Nephrology

View full text Add to dashboard Cite

show abstract

“…When this formula predicts a rather inappropriate increase of serum sodium levels proper modifications of the infused solutions should be performed (f.e. administration of hypotonic sodium solutions or even 5% dextrose in water, or simultaneous administration of desmopressin (a synthetic vasopressin) to prevent and reverse inadvertent overcorrection of hyponatremia [20,21] .…”

mentioning

confidence: 99%

Treatment of Hyponatremia: What the Clinician Needs to Know

Elisaf

Liamis

2015

Journal of Nephrology Research

View full text Add to dashboard Cite

have been recently reported [3,4] , several aspects of the proper management of these patients are not clear [5,6] . In this editorial some basic principles for the appropriate management of patients with decreased serum sodium levels are briefly summarized.1) It should be stressed that non hypotonic hyponatremia (with normal or increased Posm) should be carefully excluded by a meticulous medical history and the appropriate laboratory investigation. Consequently, the initial approach to the hyponatremic patient includes the determination of Posm (by an osmometer if it is available) as well as the exclusion of pseudohyponatremia (due to severe hypercholesterolemia, hypertriglyceridemia, and hyperproteinemia) or hypertonic hyponatremia [due to the presence of osmotic active agents, such as glucose (hyperglycemia) or the administration of mannitol or glycine] [2,7,8] . It is worth mentioning that in hyperglycemic individuals the corrected serum sodium levels should be calculated by increasing the measured serum sodium levels by 2.4 mEq/L for each 100mg/dl of glucose above normal [4,8] .2) A growing list of drugs, including thiazides, ecstacy and SSRIs, can cause hyponatremia, while endocrine causes of hyponatremia (mainly adrenal insufficiency) should be carefully and appropriately assessed [9,10] .3) Urine sodium in a random urine specimen is commonly used to differentiate between hypovolemia-induced hyponatremia (urine sodium <20 mEq/L) and the syndrome of inappropriate antidiuresis (SIADH, urine sodium >30 mEq/L). However, increased urine sodium levels (>30 mEq/L) can also be encountered in patients with extracellular volume contraction with renal or adrenal insufficiency, severe metabolic alkalosis, osmotic diuresis, as well as in those on thiazides [2,8] .4) In cases of hypovolemia-associated hyponatremia, 0.9% sodium chloride solution should be administered (with potassium chloride 10% if hypokalemia is also present). In this setting potassium anions should be taken into account in the calculation of the tonicity of the infused solutions. Interestingly, the infusate formula proposed by the Adrogue-Madias and verified by Liamis et al can reliably project the effect of gaining 1L of any infusate on the patient's serum sodium (ΔΝα + s) and thus can be used to calculate the rate of the administered 0.9% NaCl solution [2,11,12] . ABSTRACTHyponatremia due to different pathogenetic mechanisms is the most common electrolyte abnormality and is associated with increased morbidity and mortality. However, several aspects of the proper management of these patients are not clear. In this editorial a brief overview of the basic principles for the appropriate treatment of hyponatremia are summarized. EDITORIALHyponatremia (serum sodium <135mEq/L) is the most common electrolyte abnormality, is due to different pathophysiologic mechanisms, is associated with increased morbidity and mortality and its appropriate treatment is still a therapeutic challenge [1,2] . Even though clinical practice guidelines on the treatment of hyp...

show abstract

“…Thus far, re-lowering serum sodium is the most beneficial treatment when the initial osmotic injury has already occurred. 6,[33][34][35] Our results suggest that, in clinical practice, early administration of minocycline might have a role in preventing neurologic damage in hyponatremic patients who underwent rapid correction of their sodium deficit. Nevertheless, re-lowering of serum sodium should remain the treatment of choice when a toxic gradient is achieved until further work is done to fully explore the possibilities of minocycline in management of rapid correction of chronic hyponatremia in terms of the minimal effective dose and possible combination with re-lowering of serum sodium.…”

Section: Discussionmentioning

confidence: 69%

Minocycline Protects against Neurologic Complications of Rapid Correction of Hyponatremia

Gankam-Kengne

Soupart

Pochet

et al. 2010

Journal of the American Society of Nephrology

View full text Add to dashboard Cite

Osmotic demyelination syndrome is a devastating neurologic condition that occurs after rapid correction of serum sodium in patients with hyponatremia. Pathologic features of this injury include a well-demarcated region of myelin loss, a breakdown of the blood-brain barrier, and infiltration of microglia. The semisynthetic tetracycline minocycline is protective in some animal models of central nervous system injury, including demyelination, suggesting that it may also protect against demyelination resulting from rapid correction of chronic hyponatremia. Using a rat model of osmotic demyelination syndrome, we found that treatment with minocycline significantly decreases brain demyelination, alleviates neurologic manifestations, and reduces mortality associated with rapid correction of hyponatremia. Mechanistically, minocycline decreased the permeability of the bloodbrain barrier, inhibited microglial activation, decreased both the expression of IL1␣ and protein nitrosylation, and reduced the loss of GFAP immunoreactivity. In conclusion, minocycline modifies the course of osmotic demyelination in rats, suggesting its possible therapeutic use in the setting of inadvertent rapid correction of chronic hyponatremia in humans. Osmotic demyelination syndrome (ODS) is a severe neurologic condition that is characterized by severe demyelination in the central nervous system (CNS) secondary to osmotic imbalance. In a clinical setting, this syndrome often occurs after too rapid correction of chronic hyponatremia. [1][2][3][4][5] In ODS, demyelination is widespread in the brain, with predominance in hippocampus, basal ganglia, and subcortical regions. The physiopathology of this disorder is not yet fully understood, and an experimental murine model has been developed to better understand the mechanisms leading to myelin damage after an osmotic injury. 2,5,6 Previous experiments have suggested that ODS might share key characteristics with other models of central nervous system demyelination in which both opening of the blood-brain barrier (BBB) and microglia-macrophage activation are involved in the genesis of demyelinative changes. [7][8][9][10][11] Minocycline is a second-generation tetracycline that has been well studied in various models of brain pathology including autoimmune or ischemic myelin damage, and others have reported that administration of minocycline in CNS injury was associated with a striking reduction in BBB permeability, inhibition of microglia-macrophage activation, and inflammatory

show abstract

DDAVP Is Effective in Preventing and Reversing Inadvertent Overcorrection of Hyponatremia

Cited by 153 publications

References 15 publications

Astrocytes Are an Early Target in Osmotic Demyelination Syndrome

Astrocytes Are an Early Target in Osmotic Demyelination Syndrome

Treatment of Hyponatremia: What the Clinician Needs to Know

Minocycline Protects against Neurologic Complications of Rapid Correction of Hyponatremia

Contact Info

Product

Resources

About