Introduction Cerebral salt wasting syndrome (CSWS) is characterized by severe hyponatriemia, caused by the reduction of sodium reabsorption at the level of proximal tubule, with associated polyuria and hypovolemia. For decades, this syndrome was confused with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), but in CSWS the antidiuretic hormone is physiologically secreted. The only way to make a diff erence in the diagnosis is the assessment of the extracellular volume, not easily measurable in critical care patients. We designed this study to assess the frequency, the onset and the duration of the symptoms of CSWS in patients hospitalized in post-neurosurgery critical care. Methods In the 2-year period 2008 to 2009 in the post-neurosurgery ICU, 131 patients were studied retrospectively; 63 patients had subarachnoid haemorrhage (SAH) caused by the rupture of a cerebral aneurysm and 68 patients had severe head trauma (HI). CSWS diagnosis was done evaluating sodiemia, serum osmolality, sodiuria 24 hours and central venous pressure. The time from the onset of hyponatriemia during ICU stay and duration of symptoms was also evaluated. Results Patients developed CSWS in 12.7%, of whom 7.9% within 1 week from admission and 4.8% after. Among the patients with HI, 5.8% developed CSWS, of whom 2.9% within the fi rst week while the other 2.9% after. CSWS symptoms lasted for more than 1 week in 11.1% of patients with SAH, and less only in 1.6%, while in HI the symptoms lasted less than 1 week in 2.9% and more than 1 week in 2.9% of patients. Conclusions Diff erential diagnosis of ICU hyponatriemia is important in determining patient outcome. CSWS treatment required an appropriate fl uid and salt replacement to normalize hydroelectrolytic balance. CSWS has a diff erent distribution in patients with subarachnoid haemorrhage compared with traumatic head injury. Furthermore, the syndrome starts earlier and lasts longer in SAH compared with HI.

Incidence of cerebral salt wasting syndrome: comparison in haemorrhagic subarachnoid compared to head trauma

C Conversano;
2010-01-01

Abstract

Introduction Cerebral salt wasting syndrome (CSWS) is characterized by severe hyponatriemia, caused by the reduction of sodium reabsorption at the level of proximal tubule, with associated polyuria and hypovolemia. For decades, this syndrome was confused with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), but in CSWS the antidiuretic hormone is physiologically secreted. The only way to make a diff erence in the diagnosis is the assessment of the extracellular volume, not easily measurable in critical care patients. We designed this study to assess the frequency, the onset and the duration of the symptoms of CSWS in patients hospitalized in post-neurosurgery critical care. Methods In the 2-year period 2008 to 2009 in the post-neurosurgery ICU, 131 patients were studied retrospectively; 63 patients had subarachnoid haemorrhage (SAH) caused by the rupture of a cerebral aneurysm and 68 patients had severe head trauma (HI). CSWS diagnosis was done evaluating sodiemia, serum osmolality, sodiuria 24 hours and central venous pressure. The time from the onset of hyponatriemia during ICU stay and duration of symptoms was also evaluated. Results Patients developed CSWS in 12.7%, of whom 7.9% within 1 week from admission and 4.8% after. Among the patients with HI, 5.8% developed CSWS, of whom 2.9% within the fi rst week while the other 2.9% after. CSWS symptoms lasted for more than 1 week in 11.1% of patients with SAH, and less only in 1.6%, while in HI the symptoms lasted less than 1 week in 2.9% and more than 1 week in 2.9% of patients. Conclusions Diff erential diagnosis of ICU hyponatriemia is important in determining patient outcome. CSWS treatment required an appropriate fl uid and salt replacement to normalize hydroelectrolytic balance. CSWS has a diff erent distribution in patients with subarachnoid haemorrhage compared with traumatic head injury. Furthermore, the syndrome starts earlier and lasts longer in SAH compared with HI.
2010
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11568/995860
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