BACKGROUND: Patients with severe hyponatremia have a high risk for centropontine myelinolysis (CPM) during treatment, but the incidence rate and risk factors have not been well-assessed. METHODS: This study was conducted in a medical intensive care unit (ICU) of a university teaching hospital. All patients with a serum sodium concentration < 120 mmol/l and a serum osmolality level < 250 mosmol/kg upon ICU admission were enrolled in this prospective study and were included if they underwent a baseline brain computerized tomography scan (CT scan) and a follow-up brain magnetic resonance imaging 1 month after admission. The diagnosis of CPM was based on cerebral magnetic resonance imaging findings, i.e. T1-weighted images with T2-weighted images showing hyperintense signal in the corresponding areas which were not apparent on the initial cerebral CT scan. RESULTS. Of the 22 patients included, 12 were considered as having acute hyponatremia and 8 were chronic alcoholics. In 12 patients, the increase in serum sodium level was < 12 mmol/I in any 24-hour period. CPM was diagnosed in 7/22 patients (31.8%) and was asymptomatic in 4 of them. CPM was present in 4 patients with acute hyponatremia and in 4 chronic alcoholics. It was associated with a lower baseline potassium level (p = 0.05) and NaCl administration during the first 24 hours (p = 0.005). However, non-acute hyponatremia, chronic alcoholism and rapid correction of serum sodium did not appear as risk factors. CONCLUSION: The incidence rate of CPM following severe hyponatremia is high and can develop even when there is a slow correction of serum sodium level. Hypokalemia is a predisposing factor.
BACKGROUND:Patients with severe hyponatremia have a high risk for centropontine myelinolysis (CPM) during treatment, but the incidence rate and risk factors have not been well-assessed. METHODS: This study was conducted in a medical intensive care unit (ICU) of a university teaching hospital. All patients with a serum sodium concentration < 120 mmol/l and a serum osmolality level < 250 mosmol/kg upon ICU admission were enrolled in this prospective study and were included if they underwent a baseline brain computerized tomography scan (CT scan) and a follow-up brain magnetic resonance imaging 1 month after admission. The diagnosis of CPM was based on cerebral magnetic resonance imaging findings, i.e. T1-weighted images with T2-weighted images showing hyperintense signal in the corresponding areas which were not apparent on the initial cerebral CT scan. RESULTS. Of the 22 patients included, 12 were considered as having acute hyponatremia and 8 were chronic alcoholics. In 12 patients, the increase in serum sodium level was < 12 mmol/I in any 24-hour period. CPM was diagnosed in 7/22 patients (31.8%) and was asymptomatic in 4 of them. CPM was present in 4 patients with acute hyponatremia and in 4 chronic alcoholics. It was associated with a lower baseline potassium level (p = 0.05) and NaCl administration during the first 24 hours (p = 0.005). However, non-acute hyponatremia, chronic alcoholism and rapid correction of serum sodium did not appear as risk factors. CONCLUSION: The incidence rate of CPM following severe hyponatremia is high and can develop even when there is a slow correction of serum sodium level. Hypokalemia is a predisposing factor.
Authors: Kamel A Gharaibeh; Matthew J Craig; Christian A Koch; Anna A Lerant; Tibor Fülöp; Eva Csongrádi Journal: World J Clin Cases Date: 2013-08-16 Impact factor: 1.337
Authors: Pervaiz M Zunga; Omar Farooq; Mohd I Dar; Ishrat H Dar; Samia Rashid; Abdul Q Rather; Javid A Basu; Mohammed Ashraf; Jahangeer A Bhat Journal: Ann Neurosci Date: 2015-01
Authors: Parvaiz A Koul; Umar Hafiz Khan; Rafi A Jan; Sanaullah Shah; Abdul Baseer Qadri; Burhan Wani; Mohammed Ashraf; Feroze Ahmad; Sajjad R Bazaz Journal: Indian J Crit Care Med Date: 2013-07