Treatment of euvolemic hyponatremia in the intensive care unit by urea

Introduction: Hyponatremia in the intensive care unit (ICU) is most commonly related to inappropriate secretion of antidiuretic hormone (SIADH). Fluid restriction is difficult to apply in these patients. We wanted to report the treatment of hyponatremia with urea in these patients.Methods: Two groups of patients are reported. The first one is represented by a retrospective study of 50 consecutive patients with mild hyponatremia treated with urea. The second group is presented by a series of 35 consecutive patients with severe hyponatremia acquired outside the hospital (≤ 115 mEq/L) who where treated by isotonic saline and urea (0.5 to 1 g/kg/day), administered usually by gastric tube.Results: In the first group with mild hyponatremia (128 ± 4 mEq/L) the serum sodium (SNa) increased to a mean value of 135 ± 4 mEq/L (P 2 L/day). The mean duration of urea therapy was six days (from 2 to 42 days). Six patients developed hyponatremia again once the urea was stopped, which necessitated its reintroduction. Six patients developed hypernatremia (maximum value 155 mEq/L). In the second group, SNa increased from 111 ± 3 mEq/L to 122 ± 4 mEq/L in one day (P < 0.001). All the patients with neurological symptoms made a rapid recovery. No side effects were observed.Conclusions: These data show that urea is a simple and inexpensive therapy to treat euvolemic hyponatremia in the ICU. © 2010 Decaux et al. licensee BioMed Central Ltd.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Acute Cardiac Tamponade in a 77-year-old Italian Woman with Erdheim-Chester Disease

Erdheim-Chester disease (ECD) is a non-Langerhans’ histiocytosis and a very rare multisystemic disease of unknown aetiology, with skeletal involvement of the long bones and in more than 50% of cases with extraskeletal involvement. The disease was described in 1930 by the anatomopathologist Jakob Erdheim and his student William Chester. More than 500 cases have since been reported. We report the case of a 77-year-old Italian woman with ECD who was admitted to hospital for acute cardiac tamponade. The patient presented with simultaneous cutaneous, retro-orbital, skeletal, cerebral and cardiovascular manifestations and was successfully treated with corticosteroids followed by interferon

Guía de práctica clínica sobre el diagnóstico y tratamiento de la hiponatremia

La hiponatremia se define como una concentración sérica de sodio <135 mmol/L y es el trastorno hidroelectrolítico más frecuente en la práctica clínica. La hiponatremia puede causar un amplio espectro de síntomas clínicos, desde sutiles hasta graves o incluso mortales, y se asocia con aumento de la morbimortalidad y prolongación de la estancia hospitalaria. A pesar de ello, el manejo de los pacientes con hiponatremia sigue siendo problemático. La prevalencia de hiponatremia en enfermedades muy diferentes y su manejo por muy diversos especialistas han fomentado la existencia de protocolos de diagnóstico y tratamiento muy diversos, que varían con la especialidad y la institución. La Sociedad Europea de Medicina Intensiva (ESICM), la Sociedad Europea de Endocrinología (ESE) y la Asociación Renal Europea-Asociación Europea de Diálisis y Trasplante (ERA-EDTA), representada por la European Renal Best Practices (ERBP), han desarrollado la guía de práctica clínica sobre el enfoque diagnóstico y tratamiento de la hiponatremia como una empresa conjunta de las 3 sociedades que representan a los especialistas con un interés natural en la hiponatremia, a fin de ofrecer una visión común y holística del abordaje del problema. Además de ofrecer un enfoque riguroso en la metodología y la evaluación de la evidencia, el documento está centrado en resultados importantes para el paciente y en facilitar una herramienta útil para los médicos en la práctica clínica cotidiana. Presentamos ahora una versión abreviada de las recomendaciones y sugerencias sobre el diagnóstico y el tratamiento de la hiponatremia recogidas en la guía completa

Long-term treatment of patients with inappropriate secretion of antidiuretic hormone by the vasopressin receptor antagonist conivaptan, urea, or furosemide.

SCOPUS: ar.jinfo:eu-repo/semantics/publishe

V2-antagonists for the treatment of hyponatraemia

SCOPUS: no.jinfo:eu-repo/semantics/publishe

Measurement of urinary creatinine in chronic SIADH can be used to estimate solute and fluid intake

SCOPUS: ar.jDecretOANoAutActifinfo:eu-repo/semantics/publishe

Uric acid level in cirrhosis [2]

SCOPUS: le.jinfo:eu-repo/semantics/publishe

Morbidity Associated with Chronic Hyponatremia

This article will discuss the consequences of chronic hyponatremia. In conditions such as cancer, heart failure, liver cirrhosis, or chronic kidney disease, the presence and magnitude of hypotonic hyponatremia are considered to reflect the severity of the underlying disease and are associated with increased morbidity as well as mortality. Hyponatremia can be acute (&lt;48 h) or chronic (&gt;2&ndash;3 days). Chronic hyponatremia is associated with attention deficit, dizziness, tiredness, gait disturbance, falls, sarcopenia, bone fractures, osteoporosis, hypercalciuria (in the syndrome of inappropriate antidiuresis&mdash;SIADH), and kidney stones. In vitro studies have shown that cells grown in a low concentration of extracellular sodium have a greater proliferation rate and motility. Patients with chronic hyponatremia are more likely to develop cancer. We will not review the clinical consequences of respiratory arrest and osmotic demyelination syndrome (ODS) of the too-late or excessive treatment of hyponatremia

Variations in daily urine solute output in patients with NDI, CDI, SIADH, and NSIAD: Clinical implications

Introduction: We aimed to study the effects of daily variation in solute intake on urine volume in patients with syndrome of inappropriate secretion of antidiuretic hormone secretion (SIADH), syndrome of nephrogenic antidiuresis (NSIAD), central diabetes insipidus (CDI), or nephrogenic diabetes insipidus (NDI). Materials and methods: In 6 patients with CDI, 7 patients with NDI, 7 patients with SIADH, and 2 patients with NSIAD we had the opportunity to have 24-hour urine collections during normal diet before any treatment. We had two 24-hour urine collections with a difference of at least 20% in solute output (measured by the formula urine osmolality × urine volume). In 1 patient with NDI taking a high protein diet we analyzed the effect of a normal protein intake on diuresis. With respect to patients with NDI and CDI we included only patients with a urine osmolality lower than 110 mOsm/kgH2O, and for SIADH/NSIAD we included only patients with a urine osmolality between 500 and 700 mOsm/kgH2O. Results: When the data of the patients with CDI/NDI were pooled, a high correlation between urine volume and solute output was observed (R = 0.83; p < 0.001). In 1 patient with X-linked NDI, we decreased urine volume simply by decreasing protein intake. If we pooled the data concerning SIADH/NSIAD, a correlation was observed between urine volume and solute output (R = 0.94; p < 0.001). As expected, increasing solute intake is beneficial in SIADH/NSIAD, while decreasing it decreases diuresis in NDI. Conclusion: Daily variations in solute output affect urine volume in NDI/CDI/SIADH/NSIAD, this could affect serum sodium (SNa) despite no variation in fluid intake. In SIADH, if solute intake is lower than usual for a few days it may significantly influence the SNa level despite no variation in fluid intake.SCOPUS: ar.jDecretOANoAutActifinfo:eu-repo/semantics/publishe

High 6-thioguanine nucleotide levels and low thiopurine methyltransferase activity in patients with lupus erythematosus treated with azathioprine

SCOPUS: ar.jinfo:eu-repo/semantics/publishe