- Poster presentation
- Open Access
Incidence of cerebral salt wasting syndrome: comparison in subarachnoid haemorrhagic compared with head trauma
© BioMed Central Ltd. 2010
- Published: 1 March 2010
- Antidiuretic Hormone
- Critical Care
- Head Injury
- Subarachnoid Haemorrhage
- Proximal Tubule
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 difference 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.
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.
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 first 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.
Differential diagnosis of ICU hyponatriemia is important in determining patient outcome. CSWS treatment required an appropriate fluid and salt replacement to normalize hydroelectrolytic balance. CSWS has a different distribution in patients with subarachnoid haemorrhage compared with traumatic head injury. Furthermore, the syndrome starts earlier and lasts longer in SAH compared with HI.