BACKGROUND: Hyponatremia occurs commonly after acute brain injury and is often due to the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Urea administration is 1 therapeutic option. METHODS: In our Department, enteral urea is routinely administered to patients with acute brain injury who develop hyponatremia consistent with SIADH and do not respond to an initial sodium load. We reviewed the records of all patients over a 2-year period, who had acute brain injury, received enteral urea because of hyponatremia, and had intracranial pressure (ICP) monitoring using an intraventricular catheter. We recorded demographic, biological, and clinical data; mean ICP values during the 6 hours before and after the first dose of urea were also recorded. RESULTS: We included 40 patients (23 subarachnoid hemorrhage, 8 traumatic brain injury, 6 intracranial hemorrhage, 2 postbrain tumor surgery, and 1 ischemic stroke); median age was 54 years (IQRs, 44 to 63 y) and median admission APACHE II score was 19 (13 to 19); 6-month survival was 63%. Median baseline sodium was 133 mEq/L (131 to 135 mEq/L). No patients received additional therapy to decrease ICP during the 6 hours following urea initiation. After the first urea dose (15 g), ICP decreased from 14 (13 to 18 mm Hg) to 11 mm Hg (8 to 13 mm Hg) (P<0.001). Changes in ICP were not correlated to changes in sodium (r=0.02). The reduction in ICP was larger in patients with ICP≥15 mm Hg (n=22) than in the others (-8 mm Hg [-14 to -3 mm Hg] vs. -2 mm Hg [-3 to 0 mm Hg], P=0.001). CONCLUSIONS: Enteral urea administration in patients with acute brain injury and hyponatremia is associated with a significant reduction in ICP independent of changes in sodium levels.
BACKGROUND:Hyponatremia occurs commonly after acute brain injury and is often due to the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Urea administration is 1 therapeutic option. METHODS: In our Department, enteral urea is routinely administered to patients with acute brain injury who develop hyponatremia consistent with SIADH and do not respond to an initial sodium load. We reviewed the records of all patients over a 2-year period, who had acute brain injury, received enteral urea because of hyponatremia, and had intracranial pressure (ICP) monitoring using an intraventricular catheter. We recorded demographic, biological, and clinical data; mean ICP values during the 6 hours before and after the first dose of urea were also recorded. RESULTS: We included 40 patients (23 subarachnoid hemorrhage, 8 traumatic brain injury, 6 intracranial hemorrhage, 2 postbrain tumor surgery, and 1 ischemic stroke); median age was 54 years (IQRs, 44 to 63 y) and median admission APACHE II score was 19 (13 to 19); 6-month survival was 63%. Median baseline sodium was 133 mEq/L (131 to 135 mEq/L). No patients received additional therapy to decrease ICP during the 6 hours following urea initiation. After the first urea dose (15 g), ICP decreased from 14 (13 to 18 mm Hg) to 11 mm Hg (8 to 13 mm Hg) (P<0.001). Changes in ICP were not correlated to changes in sodium (r=0.02). The reduction in ICP was larger in patients with ICP≥15 mm Hg (n=22) than in the others (-8 mm Hg [-14 to -3 mm Hg] vs. -2 mm Hg [-3 to 0 mm Hg], P=0.001). CONCLUSIONS: Enteral urea administration in patients with acute brain injury and hyponatremia is associated with a significant reduction in ICP independent of changes in sodium levels.
Authors: Tibor Fülöp; Lajos Zsom; Rafael D Rodríguez; Jorge O Chabrier-Rosello; Mehrdad Hamrahian; Christian A Koch Journal: Rev Endocr Metab Disord Date: 2019-03 Impact factor: 6.514
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Authors: Maciej J Frączek; Miłosz J Błoński; Kornelia M Kliś; Roger M Krzyżewski; Jarosław Polak; Krzysztof Stachura; Borys M Kwinta Journal: Acta Neurol Belg Date: 2022-06-27 Impact factor: 2.396