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      Urea for treatment of acute SIADH in patients with subarachnoid hemorrhage: a single-center experience

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          Abstract

          Background

          Hyponatremia occurring as a result of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) or cerebral salt wasting syndrome is a common complication in patients with subarachnoid hemorrhage (SAH). The efficacy and safety of urea as treatment for SIADH-induced hyponatremia has not been reported in this population.

          Methods

          This is a retrospective analysis of all patients admitted to our department for nontraumatic SAH between January 2003 and December 2008 (n = 368). All patients with SIADH-induced hyponatremia (plasma sodium < 135 mEq/L, urine sodium > 20 mEq/L, and osmolality > 200 mOsm/kg; absence of overt dehydration or hypovolemia; no peripheral edema or renal failure; no history of adrenal or thyroid disease) routinely received urea per os when hyponatremia was associated with clinical deterioration or remained less than 130 mEq/L despite saline solution administration.

          Results

          Forty-two patients developed SIADH and were treated with urea. Urea was started after a median of 7 (IQR, 5–10) days and given orally at doses of 15–30 g tid or qid for a median of 5 (IQR, 3–7) days. The median plasma sodium increase over the first day of treatment was 3 (IQR, 1–6) mEq/L. Hyponatremia was corrected in all patients, with median times to Na + >130 and >135 mEq/L of 1 (IQR, 1–2) and 3 (IQR, 2–4) days, respectively. Urea was well tolerated, and no adverse effects were reported.

          Conclusions

          Oral urea is an effective and well-tolerated treatment for SIADH-induced hyponatremia in SAH patients.

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          Most cited references27

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          Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomographic scanning.

          In 47 cases of verified ruptured saccular aneurysm, we investigated the relationship of the amount and distribution of subarachnoid blood detected by computerized tomography to the later development of cerebral vasospasm. When the subarachnoid blood was not detected or was distributed diffusely, severe vasospasm was almost never encounters (1 of 18 cases). In the presence of subarachnoid blood clots larger than 5 X 3 mm (measured on the reproduced images) or layers of blood 1 mm or more thick in fissures and vertical cisterns, severe spasm followed almost invariably (23 of 24 cases). There was an almost exact correspondence between the site of the major subarachnoid blood clots and the location of severe vasospasm. Every patient with severe vasospasm manifested delayed symptoms and signs. Excellent correlation existed between the particular artery in vasospasm and the delayed clinical syndrome. Severe vasospasm involved the anterior cerebral artery in 20 cases and the middle cerebral artery in only 14. As the grading system used is partly subjective, the findings should be regarded as preliminary. The results, if confirmed, indicate that blood localized in the subarachnoid space in sufficient amount at specific sites is the only important etiological factor in vasospasm. It should be possible to identify patients in jeopardy from vasospasm and institute early preventive measures. (Neurosurgery, 6: 1--9, 1980)
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            Report of World Federation of Neurological Surgeons Committee on a Universal Subarachnoid Hemorrhage Grading Scale.

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              Osmotic demyelination syndrome following correction of hyponatremia.

              The treatment of hyponatremia is controversial: some authorities have cautioned that rapid correction causes central pontine myelinolysis, and others warn that severe hyponatremia has a high mortality rate unless it is corrected rapidly. Eight patients treated over a five-year period at our two institutions had a neurologic syndrome with clinical or pathological findings typical of central pontine myelinolysis, which developed after the patients presented with severe hyponatremia. Each patient's condition worsened after relatively rapid correction of hyponatremia (greater than 12 mmol of sodium per liter per day)--a phenomenon that we have called the osmotic demyelination syndrome. Five of the patients were treated at one hospital, and accounted for all the neurologic complications recorded among 60 patients with serum sodium concentrations below 116 mmol per liter; no patient in whom the sodium level was raised by less than 12 mmol per liter per day had any neurologic sequelae. Reviewing published reports on patients with very severe hyponatremia (serum sodium less than 106 mmol per liter) revealed that neurologic sequelae were associated with correction of hyponatremia by more than 12 mmol per liter per day; when correction proceeded more slowly, patients had uneventful recoveries. We suggest that the osmotic demyelination syndrome is a preventable complication of overly rapid correction of chronic hyponatremia.
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                Author and article information

                Journal
                Ann Intensive Care
                Ann Intensive Care
                Annals of Intensive Care
                Springer
                2110-5820
                2012
                30 May 2012
                : 2
                : 13
                Affiliations
                [1 ]Department of Intensive Care, Erasme Hospital, Université Libre de Bruxelles, Brussels, Belgium
                [2 ]Department of Internal Medicine, Erasme Hospital, Université Libre de Bruxelles, Brussels, Belgium
                [3 ]Department of Intensive Care, Erasme University Hospital, Route de Lennik, 808, Brussels, B-1070, Belgium
                Article
                2110-5820-2-13
                10.1186/2110-5820-2-13
                3488535
                22647340
                69f052ce-3ce2-451f-958b-b084a13c5525
                Copyright ©2012 Pierrakos et al.; licensee Springer.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 30 December 2011
                : 4 April 2012
                Categories
                Research

                Emergency medicine & Trauma
                siadh,subarachnoid hemorrhage,hyponatremia,urea,sodium
                Emergency medicine & Trauma
                siadh, subarachnoid hemorrhage, hyponatremia, urea, sodium

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