Postoperative Hyponatremic Encephalopathy in Menstruant Women

Ayus, Juan Carlos; Wheeler, James M.; Arieff, Allen I.

doi:10.7326/0003-4819-117-11-891

Cited by 398 publications

(224 citation statements)

References 23 publications

Supporting

Mentioning

208

Contrasting

Unclassified

Order By: Relevance

“…Postoperative hyponatraemia is a frequent and potentially dangerous complication in adults (Ayus et al, 1992), and is usually secondary to inappropriate hypotonic¯uid replacement, though plasma vasopressin concentration may also be increased in the postoperative period (Chung et al, 1986). Irrigation of the bladder with hypotonic glycine solutions during transurethral resection of the prostate can lead to direct absorption of water from the bladder into the venous circulation, producing dilutional hyponatraemia (Osborne et al, 1980).…”

Section: Euvolaemic Hyponatraemiamentioning

confidence: 99%

Hyponatraemia

Smith

McKenna

Thompson

2000

Clinical Endocrinology

121

102

View full text Add to dashboard Cite

Section: Euvolaemic Hyponatraemiamentioning

confidence: 99%

Hyponatraemia

Smith

McKenna

Thompson

2000

Clinical Endocrinology

121

102

View full text Add to dashboard Cite

“…Among patients with hyponatremia, 1% develop encephalopathy, and of these, -20% die or suffer permanent brain damage (3,7). Death in such patients is largely the result of brain edema, which, if the brain is unable to adapt, often leads to cerebral herniation (3,7).…”

Section: Introductionmentioning

confidence: 99%

Hypoxic and ischemic hypoxia exacerbate brain injury associated with metabolic encephalopathy in laboratory animals.

Vexler

Ayus²,

Roberts³

et al. 1994

J. Clin. Invest.

View full text Add to dashboard Cite

Hypoxemia is a major comorbid factor for permanent brain damage in several metabolic encephalopathies. To determine whether hypoxia impairs brain adaptation to hyponatremia, worsening brain edema, we performed in vitro and in vivo studies in cats and rats with hyponatremia plus either ischemic or hypoxic hypoxia. Mortality with hypoxic hypoxia was 0%; with hyponatremia, 22%; and with hyponatremia + hypoxia, 100%. Hyponatremia in cats produced brain edema, with a compensatory decrease of brain sodium. Ischemic hypoxia also resulted in brain edema, but with elevation of brain sodium. However, when ischemic hypoxia was superimposed upon hyponatremia, there was elevation of brain sodium with further elevation of water. Outward sodium transport in cat cerebral cortex synaptosomes was measured via three major pathways through which brain osmolality can be decreased. After hyponatremia, sodium transport was significantly altered such that brain cell osmolality would decrease: 44% increase in Na+-K+-ATPase transport activity (ouabain inhibitable); 26% decrease in amiloride-sensitive sodium uptake. The change in veratridine-stimulated sodium uptake was not significant (P > 0.05). When ischemic hypoxia was superimposed upon hyponatremia, all of the cerebral adaptive changes induced by hyponatremia alone were eliminated. Thus, hypoxia combined with hyponatremia produces a major increase in brain edema and mortality, probably by eliminating the compensatory mechanisms of sodium transport initiated by hyponatremia that tend to minimize brain swelling. (J. Clin. Invest. 1994.93:256-264.)

show abstract

“…[31][32][33] Observational studies report variable occurrences of early postoperative hyponatremia, largely due to different surgical populations and serum [Na ? ] thresholds for defining hyponatremia.…”

Section: Iso-osmolar Hyponatremiamentioning

confidence: 99%

“…The implications are that women may have a greater tendency to retain free water in response to surgical stress. In a casecontrol study, Ayus et al 33 found that women and men are equally likely to develop hyponatremia and hyponatremic encephalopathy after surgery; however, menstruant women were 28 times more likely than men or postmenopausal women to die or to suffer permanent neurologic injury. There is speculation that estrogen and/or progesterone may facilitate brain cell adaptation to plasma hypotonicity and that decreased levels may interfere with the normal compensatory decreases in brain cell osmolality that occur in response to changes in extracellular tonicity.…”

Section: Iso-osmolar Hyponatremiamentioning

confidence: 99%

“…There is speculation that estrogen and/or progesterone may facilitate brain cell adaptation to plasma hypotonicity and that decreased levels may interfere with the normal compensatory decreases in brain cell osmolality that occur in response to changes in extracellular tonicity. 33,41 The concept of ''sick cell syndrome'' may be an underrecognized mechanism of hyponatremia in critically ill and postoperative patients. [42][43][44][45] Sick cell syndrome is believed to be caused by dysfunctional cell membrane integrity and increased permeability associated with cellular Na ?…”

Section: Iso-osmolar Hyponatremiamentioning

confidence: 99%

See 1 more Smart Citation

Les troubles de l’équilibre hydrosodé chez les patients hospitalisés

Bagshaw

Townsend

McDermid

2008

Can J Anesth/J Can Anesth

View full text Add to dashboard Cite

Purpose To review and discuss the epidemiology, contributing factors, and approach to clinical management of disorders of sodium and water balance in hospitalized patients. Source An electronic search of the MEDLINE, Embase, and Cochrane Central Register of Controlled Trials databases and a search of the bibliographies of all relevant studies and review articles for recent reports on hyponatremia and hypernatremia with a focus on critically ill patients. Principal findings Disorders of sodium and water balance are exceedingly common in hospitalized patients, particularly those with critical illness and are often iatrogenic. These disorders are broadly categorized as hypo-osmolar or hyper-osmolar, depending on the balance (i.e., excess or deficit) of total body water relative to total body sodium content and are classically recognized as either hyponatremia or hypernatremia. These disorders may represent a surrogate for increased neurohormonal activation, organ dysfunction, worsening severity of illness, or progression of underlying chronic disease. Hyponatremic disorders may be caused by appropriately elevated (volume depletion) or inappropriately elevated (SIADH) arginine vasopressin levels, appropriately suppressed arginine vasopressin levels (kidney dysfunction), or alterations in plasma osmolality (drugs or body cavity irrigation with hypotonic solutions). Hypernatremia is most commonly due to unreplaced hypotonic water depletion (impaired mental status and/or access to free water), but it may also be caused by transient water shift into cells (from convulsive seizures) and iatrogenic sodium loading (from salt intake or administration of hypertonic solutions). Conclusion In hospitalized patients, hyponatremia and hypernatremia are often iatrogenic and may contribute to serious morbidity and increased risk of death. These disorders require timely recognition and can often be reversed with appropriate intervention and treatment of underlying predisposing factors.

show abstract

Postoperative Hyponatremic Encephalopathy in Menstruant Women

Cited by 398 publications

References 23 publications

Hyponatraemia

Hyponatraemia

Hypoxic and ischemic hypoxia exacerbate brain injury associated with metabolic encephalopathy in laboratory animals.

Les troubles de l’équilibre hydrosodé chez les patients hospitalisés

Contact Info

Product

Resources

About