Hyponatremia in aneurysmal subarachnoid hemorrhage is due to the syndrome of inappropriate antidiuresis and acute glucocorticoid deficiency

Hdl Handle:
http://hdl.handle.net/10147/244215
Title:
Hyponatremia in aneurysmal subarachnoid hemorrhage is due to the syndrome of inappropriate antidiuresis and acute glucocorticoid deficiency
Authors:
Hannon, M J; Behan, L A; Rogers, B; Sherlock, M; Smith, D M; Agha, A; Thompson, C J
Citation:
Endocrine Reviews (2011) 32:3 Meeting Abstracts. : June 2011
Journal:
Endocrine Reviews
Issue Date:
Jun-2011
URI:
http://hdl.handle.net/10147/244215
Abstract:
Hyponatraemia is the most common electrolyte abnormality following subarachnoid haemorrhage (SAH) and contributes to increased morbidity and mortality. Retrospective data suggests that the syndrome of inappropriate diuresis (SIAD) is the most common cause of hyponatraemia in SAH, though cerebral salt wasting has been postulated by some workers to be the predominant abnormality. Data which has shown acute glucocorticoid deficiency following SAH has suggested that some cases of euvolaemic hyponatraemia may also be caused by this mechanism.We prospectively studied the hormonal and haemodynamic influences involved in the development of hyponatraemia in 100 patients (61% female, median age 53 (range 16-82)) with non-traumatic aneurysmal SAH. Each patient had plasma sodium (pNa), urea, osmolality, glucose and 0900h cortisol (PC), and urinary sodium and osmolality measured on days 1, 2, 3, 4, 6, 8, 10 and 12 following SAH. Fluid balance and haemodynamic parameters were recorded daily. Results were compared with 15 patients admitted to ITU following vascular surgery. A PC<300nmol/L in a patient in ITU was regarded clinically as inappropriately low.49% of patients developed hyponatraemia (pNa<135 mmol/L), including 14% who developed clinically significantly hyponatraemia (pNa<130 mmol/L). 36/49 (73.4%) developed hyponatraemia between days 1 and 3 post SAH. The median duration of hyponatraemia was 3 days (range 1–10 days).In 35/49 (71.4%), hyponatraemia was due to SIAD as defined by standard diagnostic criteria. 14% of SAH patients had at least one PC<300nmol/L; 5 of these (35.7%) developed hyponatraemia. In 4 patients hyponatraemia was preceded by acute cortisol deficiency and responded to hydrocortisone treatment. In contrast, all controls had PC>500 nmol/L on day 1, and >300 nmol on days 3–12. There were no cases of cerebral salt wasting. There was no relationship between the incidence of hyponatraemia and the defined anatomical territory or severity of SAH. There was no difference in the incidence of hyponatraemia between those patients who had an intervention and those who did not (p=0.11), or in the incidence of hyponatraemia between those patients who had clipping and those who had coiling.In the first prospective study of its kind, hyponatraemia occurs in over half of aneurysmal SAH cases, predominantly due to SIAD. Acute glucocorticoid deficiency is a treatable cause of a minority of cases of hyponatraemia. We found no evidence of cerebral salt wasting.
Item Type:
Conference Poster
Language:
en

Full metadata record

DC FieldValue Language
dc.contributor.authorHannon, M Jen_GB
dc.contributor.authorBehan, L Aen_GB
dc.contributor.authorRogers, Ben_GB
dc.contributor.authorSherlock, Men_GB
dc.contributor.authorSmith, D Men_GB
dc.contributor.authorAgha, Aen_GB
dc.contributor.authorThompson, C Jen_GB
dc.date.accessioned2012-09-17T08:43:24Z-
dc.date.available2012-09-17T08:43:24Z-
dc.date.issued2011-06-
dc.identifier.citationEndocrine Reviews (2011) 32:3 Meeting Abstracts. : June 2011en_GB
dc.identifier.urihttp://hdl.handle.net/10147/244215-
dc.description.abstractHyponatraemia is the most common electrolyte abnormality following subarachnoid haemorrhage (SAH) and contributes to increased morbidity and mortality. Retrospective data suggests that the syndrome of inappropriate diuresis (SIAD) is the most common cause of hyponatraemia in SAH, though cerebral salt wasting has been postulated by some workers to be the predominant abnormality. Data which has shown acute glucocorticoid deficiency following SAH has suggested that some cases of euvolaemic hyponatraemia may also be caused by this mechanism.We prospectively studied the hormonal and haemodynamic influences involved in the development of hyponatraemia in 100 patients (61% female, median age 53 (range 16-82)) with non-traumatic aneurysmal SAH. Each patient had plasma sodium (pNa), urea, osmolality, glucose and 0900h cortisol (PC), and urinary sodium and osmolality measured on days 1, 2, 3, 4, 6, 8, 10 and 12 following SAH. Fluid balance and haemodynamic parameters were recorded daily. Results were compared with 15 patients admitted to ITU following vascular surgery. A PC<300nmol/L in a patient in ITU was regarded clinically as inappropriately low.49% of patients developed hyponatraemia (pNa<135 mmol/L), including 14% who developed clinically significantly hyponatraemia (pNa<130 mmol/L). 36/49 (73.4%) developed hyponatraemia between days 1 and 3 post SAH. The median duration of hyponatraemia was 3 days (range 1–10 days).In 35/49 (71.4%), hyponatraemia was due to SIAD as defined by standard diagnostic criteria. 14% of SAH patients had at least one PC<300nmol/L; 5 of these (35.7%) developed hyponatraemia. In 4 patients hyponatraemia was preceded by acute cortisol deficiency and responded to hydrocortisone treatment. In contrast, all controls had PC>500 nmol/L on day 1, and >300 nmol on days 3–12. There were no cases of cerebral salt wasting. There was no relationship between the incidence of hyponatraemia and the defined anatomical territory or severity of SAH. There was no difference in the incidence of hyponatraemia between those patients who had an intervention and those who did not (p=0.11), or in the incidence of hyponatraemia between those patients who had clipping and those who had coiling.In the first prospective study of its kind, hyponatraemia occurs in over half of aneurysmal SAH cases, predominantly due to SIAD. Acute glucocorticoid deficiency is a treatable cause of a minority of cases of hyponatraemia. We found no evidence of cerebral salt wasting.en_GB
dc.language.isoenen
dc.titleHyponatremia in aneurysmal subarachnoid hemorrhage is due to the syndrome of inappropriate antidiuresis and acute glucocorticoid deficiencyen_GB
dc.typeConference Posteren
dc.identifier.journalEndocrine Reviewsen_GB
dc.description.provinceLeinsteren
All Items in Lenus, The Irish Health Repository are protected by copyright, with all rights reserved, unless otherwise indicated.