Hyponatremia is defined as a plasma sodium concentration below 135 mmol / L. This is a common occurrence (20-50%) during subarachnoid hemorrhage (SAH). Its appearance is often associated with vasospasm. It is associated with an increase in morbidity and mortality linked to induced neurological disorders. Hyponatremia is caused by two etiologies: the syndrome of inappropriate secretion of anti-diuretic hormone (SIADH), and the cerebral salt wasting syndrome, CSWS. Theoretically, these two entities are differentiated by the patient's volemia; in practice, this parameter is difficult to measure. In addition, the correction of hyponatremia is diametrically opposed according to its mechanism: water restriction in the case of SIADH, sodium intake in the event of CSWS. Urea is offered as a second-line treatment in the event of treatment failure to correct hyponatremia. However, the efficacy of this treatment is based on small, observational, retrospective studies. Moreover, the mechanism of action of urea remains poorly understood: it could be a hyperosmolar effect or passive renal reabsorption of sodium.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
TREATMENT
Masking
DOUBLE
Enrollment
52
the experimental group will be treated during 5 days by urea dose per administration : 1g / kg / 24 hours in 2 or 3 doses morning, noon and evening (dose adjustment of urea according to weight) If hyponatremia persists beyond D8 after initiation of the study treatment (urea or placebo), that is to say after the date of the collection of the primary endpoint, it will be possible to introduce corticosteroids (fludrocortisone or others). These treatments will be collated. If during patient monitoring the serum sodium exceeds 145 mmol / L, treatment should no longer be administered.
the control group will be treated during 5 days by ergytonyl dose per administration : 5mL
University Hospital Grenoble
Grenoble, France
To demonstrate the effectiveness of urea therapy in correcting persistent hyponatremia despite adequate management during subarachnoid hemorrhage
Change in blood serum in mmol / L measured before initiation of treatment and on the day of discontinuation of treatment
Time frame: 5 days
To compare the sodium intake required to correct the natremia.
Measurement of daily sodium intake in each group
Time frame: 8 days
To study the mechanism of action of urea
Daily plasma co-peptin levels in each group during treatment and 48 hours after cessation of treatment.
Time frame: 48 hours after the end of treatment
To assess the impact of treatment on length of stay
Length of stay in intensive care and/or continuing care unit
Time frame: 3 months
To assess the impact of treatment on neurological outcome at 3 months from inclusion
Measurement of modified Rankin score
Time frame: 3 months
To assess the adverse effects of treatment
Prevalence of adverse effects of urea (headaches, digestive disorders, etc.)
Time frame: 3 months
Persistence of correction of natraemia 48H after cessation of treatment
Variation in natraemia mmol/L measured before introduction of treatment and 48 hours after cessation of treatment
Time frame: 48 hours after the end of treatment
To compare the speed of correction of natraemia
Average time taken for natraemia to correct to Na \> 135 mmol/L after initiation of treatment.
Time frame: 5 days
This platform is for informational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional.