In column 2 of Table 7 on page G16, the last disorder under Pulmonary disorders should be Respiratory failure associated with positive-pressure breathing and not as published. Correction 2 On page G20, only SI units should be used in the equation for estimates of the serum sodium concentration corrected for the presence of hyperglycaemia and not as published. The correct equation is as follows: Corrected serum ðNa C Þ Z measured ðNa C Þ C 2:4 ! ðglucose ðmmol=lÞK100 ðmmol=lÞ 100 mmol=l Corrected ðNa C Þ Z measured ðNa C Þ C 2:4 ! ðglucose ðmmol=lÞK5:5 ðmmol=lÞ 5:5 mmol=l

Hyponatraemia, defined as a serum sodium concentration !135 mmol/l, is the most common disorder of body fluid and electrolyte balance encountered in clinical practice. It can lead to a wide spectrum of clinical symptoms, from subtle to severe or even life threatening, and is associated with increased mortality, morbidity and length of hospital stay in patients presenting with a range of conditions. Despite this, the management of patients remains problematic. The prevalence of hyponatraemia in widely different conditions and the fact that hyponatraemia is managed by clinicians with a broad variety of backgrounds have fostered diverse institution-and speciality-based approaches to diagnosis and treatment. To obtain a common and holistic view, the European Society of Intensive Care Medicine (ESICM), the European Society of Endocrinology (ESE) and the European Renal Association -European Dialysis and Transplant Association (ERA-EDTA), represented by European Renal Best Practice (ERBP), have developed the Clinical Practice Guideline on the diagnostic approach and treatment of hyponatraemia as a joint venture of three societies representing specialists with a natural interest in hyponatraemia. In addition to a rigorous approach to methodology and evaluation, we were keen to ensure that the document focused on patient-important outcomes and included utility for clinicians involved in everyday practice.

Hyponatraemia, defined as a serum sodium concentration <135 mmol/l, is the most common disorder of body fluid and electrolyte balance encountered in clinical practice. It can lead to a wide spectrum of clinical symptoms, from subtle to severe or even life threatening, and is associated with increased mortality, morbidity and length of hospital stay in patients presenting with a range of conditions. Despite this, the management of patients remains problematic. The prevalence of hyponatraemia in widely different conditions and the fact that hyponatraemia is managed by clinicians with a broad variety of backgrounds have fostered diverse institution- and speciality-based approaches to diagnosis and treatment. To obtain a common and holistic view, the European Society of Intensive Care Medicine (ESICM), the European Society of Endocrinology (ESE) and the European Renal Association - European Dialysis and Transplant Association (ERA-EDTA), represented by European Renal Best Practice (ERBP), have developed the Clinical Practice Guideline on the diagnostic approach and treatment of hyponatraemia as a joint venture of three societies representing specialists with a natural interest in hyponatraemia. In addition to a rigorous approach to methodology and evaluation, we were keen to ensure that the document focused on patient-important outcomes and included utility for clinicians involved in everyday practice.

No abstract

Hyponatraemia, defined as a serum sodium concentration <135 mmol/L, is the most common disorder of body fluid and electrolyte balance encountered in clinical practice. Hyponatraemia is present in 15-20% of emergency admissions to hospital and occurs in up to 20% of critically ill patients. Symptomatology may vary from subtle to severe or even life threatening. Despite this, the management of patients remains problematic. Against this background, the European Society of Intensive Care Medicine, the European Society of Endocrinology and the European Renal Association-European Dialysis and Transplant Association, represented by European Renal Best Practice have developed a Clinical Practice Guideline on the diagnostic approach and treatment of hyponatraemia as a joint venture of three societies representing specialists with a natural interest in hyponatraemia.

No abstract

The effects of satavaptan (SR121463B), a novel long-acting orally active vasopressin V 2 -receptor antagonist, were investigated in patients with the syndrome of inappropriate antidiuretic hormone secretion (SIADH). In the first part of this randomized, double-blind study, 34 patients first were treated with satavaptan ( V asopressin is involved in most cases of sustained hyponatremia (1). Therefore, the use of specific blockers of vasopressin receptors is a logical approach in the treatment of patients with syndrome of inappropriate antidiuretic hormone secretion (SIADH) and may present advantages over current available therapies (2). Selective nonpeptide V 2 -receptor antagonists (V 2 RA) have been in development since 1992 (3-6). Oral compounds have been synthesized more recently, and, to our knowledge, publications have focused mainly on patients with SIADH that is treated with an oral V 2 RA for a short period of time (Ͻ1 wk) (7-10).In this study, we investigated the efficacy and the safety of a new oral nonpeptide V 2 RA, satavaptan (SR121463B) (11), in correcting hyponatremia in patients with SIADH of various origins. After the initial phase of the study (short-term, 1 mo), we evaluated for the first time the efficacy and the tolerance of a V 2 RA over a long-term period (12 mo). Materials and Methods PatientsFrom June 2001 to June 2003, a total of 35 patients from four countries (Belgium, Germany, Hungary, and France) were included in a randomized, double-blind, placebo-controlled study to assess the efficacy and the safety of different dosages of satavaptan in SIADH. The diagnosis of SIADH was based on several criteria: True serum hypo-osmolality; inappropriate urinary osmolality; clinical euvolemia; elevated urinary sodium excretion while on a normal salt and water intake; and normal renal, adrenal, and thyroid functions. Patients with low sodium excretion (Յ20 mmol/L) as a result of low solute intake (anorexia) were included. Drug-induced SIADH was limited to carbamazepine and antidepressants. The search for the cause of SIADH (especially neoplasia and iatrogenic) was performed carefully by each investigator before considering the origin as idiopathic.Inclusion criteria were age 18 yr or older, stable hyponatremia (serum sodium [SNa] increase Յ4 mmol/L between two measurements of 24 h apart) between 115 and 132 mmol/L during the screening period,

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.