Myelinolysis after Correction of Hyponatremia

Laureno, Robert; Karp, Barbara I.

doi:10.7326/0003-4819-126-1-199701010-00008

Cited by 369 publications

(229 citation statements)

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“…Some authorities have suggested that hypertonic saline should be used only in critical care units (12) or that it be limited to patients with repeated convulsions, agitated confusion, or coma (13). At our institution, hypertonic saline is permitted outside the critical care units, but oversight by nephrologists is strongly encouraged and is required for administration of Ͼ200 ml.…”

Section: Discussionmentioning

confidence: 99%

Hypertonic Saline for Hyponatremia

Mohmand

Issa

Ahmad

et al. 2007

Clinical Journal of the American Society of Nephrology

159

112

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Background and objectives: Data regarding dosage-response relationships for using hypertonic saline in treatment of hyponatremia are extremely limited. Objectives of this study were to assess adherence to previously published guidelines (limiting correction to <12 mEq/L per d and <18 mEq/L per 48 h) in treating hyponatremia with hypertonic saline and to determine the predictive accuracy of the Adrogué-Madias formula.Design, setting, participants & measurements: A retrospective review was conducted of all 62 adult, hyponatremic patients who were treated with hypertonic saline during 5 yr at a 528-bed, acute care, teaching hospital.Results: Median infusion rate was 0.38 ml/kg per h, increasing serum sodium concentration by 0.47 ؎ 0.05 mEq/L per h, 7.1 ؎ 0.6 mEq/L per 24 h, and 11.3 ؎ 0.7 mEq/L per 48 h. In 11.3% of cases, the increase was >12 mEq/L per 24 h and in 9.7% was >18 mEq/L per 48 h. No patient's rate was corrected by >25 mEq/L per 48 h. Among patients with serum sodium <120 mEq/L, the observed increase in sodium exceeded the rise predicted by the Adrogué-Madias formula in 74.2%; the average correction in overcorrectors was 2.4 times the predicted. Inadvertent overcorrection was due to documented water diuresis in 40% of cases.Conclusions: The Adrogué-Madias formula underestimates increase in sodium concentration after hypertonic saline therapy. Unrecognized hypovolemia and other reversible causes of water retention pose a risk for inadvertent overcorrection. Hypertonic saline should be infused at rates lower than those predicted by formulas with close monitoring of serum sodium and urine output.

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Section: Discussionmentioning

confidence: 99%

Hypertonic Saline for Hyponatremia

Mohmand

Issa

Ahmad

et al. 2007

Clinical Journal of the American Society of Nephrology

159

112

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“…The correction of hyponatremia should be slow enough (less than 10 mmol/L in a 24-hour period) to avoid any risk for central pontine myelinolysis, which occurs more often in chronic than in acute hyponatremia. 21 Studies of combination therapy are necessary to establish whether VPA could prevent the diuretic-induced hyponatremia occurring in approximately 25% of patients and increase the efficacy of treatment. Studies in rats simultaneously treated with high doses of furosemide did not show any decrease in aquaretic effect of VPA, nor interaction of VPA with the natriuretic effect of furosemide, which suggests that combination of these treatments could be efficient.…”

Section: Discussionmentioning

confidence: 99%

Pharmacodynamic effects of a nonpeptide antidiuretic hormone V2 antagonist in cirrhotic patients with ascites

Guyader

Patat²,

Ellis-Grosse³

et al. 2002

Hepatology

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Water retention and dilutional hyponatremia, mainly attributable to an impairment of free water excretion and increased vasopressin activity, are well-documented complications in cirrhotic patients with ascites. VPA-985 is a selective, nonpeptide, orally active, vasopressin-2-receptor antagonist. The aim of this study was to determine the pharmacodynamics, safety, and pharmacokinetics of ascending single doses (25, 50, 100, 200, and 300 mg) in cirrhotic patients with ascites in a randomized, double-blind, placebo-controlled trial. Each dose level was studied in 5 patients (4 active and 1 placebo). After an overnight fast and fluid restriction (continued for 4 hours after dose administration), all patients were given placebo on baseline day and an oral suspension of VPA or placebo on the following day. VPA produced a significant dose-related increase in daily urine output (1,454 ؎ 858 mL to 4,568 ؎ 4,385 mL with VPA 300 mg) and a dose-related decrease in urine osmolality. The free water clearance reached greater than 3 mL/min for doses 100 mg or greater. Simultaneously, significant increases in serum osmolality, sodium, and vasopressin levels were found. There was a significant increase in sodium urine excretion. VPA was rapidly absorbed and maximum serum concentrations were achieved within 1 hour after administration. I n normal individuals, the administration of a water load (20 mL/kg body weight of 5% glucose intravenously or water orally over 45 min) is followed by an increase in the excretion of a hypotonic (Ͻ100 mOsm/ kg) urine flow responsible for an increase in free water clearance (FWC) reaching 6 to 12 mL/min. Cirrhotic patients without ascites have normal water handling. 1 Up to 75% of cirrhotic patients with ascites, however, have moderate reduction (1-6 mL/min) of FWC after a water load. In approximately 30% of cases, the impairment is severe (Ͻ1 mL/min after water load) leading to spontaneous hyponatremia because those patients are unable to excrete regular water intake. 2 Hyponatremia can also be triggered or aggravated by the use of diuretics in about 25% of cases. Pathophysiologic mechanisms leading to water overload are not fully understood, but several factors may be involved, among them: (1) reduced delivery of filtrate to the ascending limb of the loop of Henle, secondary to enhancement of proximal sodium reabsorption and decrease of glomerular filtration rate; (2) reduced renal synthesis of prostaglandins; and (3) increased secretion of antidiuretic hormone. 3 There is some evidence to indicate that increased plasma arginine vasopressin (AVP) concentration plays a major role: a correlation between plasma AVP levels and the magnitude of FWC impairment 4 ; the temporal relationship between impairment of water excretion and vasopressin hypersecretion in rats with experimental cirrhosis; 5 the aquaretic effect of -opioid agonists, which act through inhibition of AVP release

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“…The severity of symptoms depends on the degree and rate of development of hyponatremia. A rapid decrease in sodium levels may lead to coma and seizures, but if hyponatremia develops slowly, patients are much less symptomatic 4 . The risk factors for development of ODS after correction of chronic hyponatremia include hypokalemia, malnutrition, chronic alcoholism 5 , hypoxia 6 , burn injury, surgical removal of pituitary tumor and those who have undergone orthotopic liver transplant 7 .…”

Section: Discussionmentioning

confidence: 99%

Pontine and extrapontine osmotic myelinolysis after the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with fluoxetine: case report

Twardowschy

Bertolucci

Gracia

2007

Arq. Neuro-Psiquiatr.

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-Osmotic demyelination syndrome (ODS) may be precipitated by aggressive correction of a hypo or hyper-osmolar states. We describe the case of a 53-year-old woman that was started on fluoxetine 20 mg/day for depression and nine days later was found to have fluoxetine-induced syndrome of inappropriate secretion of antidiuretic hormone. After hyponatremia correction the mental status of the patient gradually improved, but subsequently she had intermittent difficulty in speaking, naming objects, memory deficits and psychomotor slowness. Magnetic resonance revealed bilateral symmetric hyperintense lesions in the basal ganglia, temporal lobe and hippocampal formation compatible with ODS. These symptoms gradually resolved and she was discharged home without any deficits. Two months later, a new image showed lesion in pons and the other lesions had disappeared. Fluoxetine therapy had never been related with a complication like that.KEY WORDS: central pontine and extrapontine myelinolysis, osmotic demyelination syndrome, hyponatremia, fluoxetine.Mielinólise osmótica pontina e extrapontina após a síndrome da secreção inapropriada de hormônio antidiurético associada com fluoxetina: relato de caso RESUMO -A síndrome de desmielinização osmótica (SDO) pode ser precipitada pela correção agressiva de um estado hiper ou hipoosmolar. Nós descrevemos o caso de mulher de 53 anos que havia iniciado o uso de fluoxetina 20 mg/dia para depressão e que nove dias depois foi diagnosticada como tendo síndrome da secreção inapropriada de hormônio antidiurético induzida por fluoxetina. Depois da correção da hiponatremia o estado mental da paciente gradualmente melhorou, mas subsequentemente ela apresentou dificuldade intermitente para fala e para nomear objetos, déficits de memória recente e lentidão psicomotora. Ressonância magnética revelou lesões hiperintensas bilaterais e simétricas na região dos gânglios da base, lobo temporal e hipocampo compatíveis com SDO. Estes sintomas gradualmente se resolveram e a paciente foi de alta sem qualquer déficit. Dois meses mais tarde uma nova imagem cerebral mostrou lesão na ponte e ausência das lesões antigas. Até onde sabemos a terapia com fluoxetina nunca foi relacionada a uma complicação tardia como esta. PALAVRAS-CHAVE: mielinólise central pontina e extrapontina, síndrome de desmielinização osmótica, hiponatremia, fluoxetina.

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Myelinolysis after Correction of Hyponatremia

Cited by 369 publications

References 0 publications

Hypertonic Saline for Hyponatremia

Hypertonic Saline for Hyponatremia

Pharmacodynamic effects of a nonpeptide antidiuretic hormone V2 antagonist in cirrhotic patients with ascites

Pontine and extrapontine osmotic myelinolysis after the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with fluoxetine: case report

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