scholarly journals Osmotic Demyelination Syndrome: A Case Report

1970 ◽  
Vol 21 (2) ◽  
pp. 170-173
Author(s):  
M Azizul Hoque ◽  
M Zahirul Haque ◽  
ABM Saiful Alam ◽  
AHM Tohurul Islam ◽  
DA Rashid ◽  
...  

We report a case of a middle aged lady who presented with alteration of consciousness and dysphasia. She was found to have hyponatremia which was corrected rapidly. After initial improvement, she subsequently developed marked deterioration of conscious level with upper motor sign signs in all four limbs. Osmotic demyelination syndrome was diagnosed by MRI. Severe hyponatremia carries a risk of cerebral edema with a significant mortality, but correcting it too rapidly can result in even more disastrous condition- osmotic demyelination syndrome. doi: 10.3329/taj.v21i2.3800   TAJ 2008; 21(2): 170-173

Author(s):  
Miguel García-Grimshaw ◽  
Amado Jiménez-Ruiz ◽  
José Luis Ruiz-Sandoval ◽  
Carlos Cantú-Brito ◽  
Erwin Chiquete

Author(s):  
Tiziana Carandini ◽  
Mattia Pozzato ◽  
Elisa Scola ◽  
Sabrina Avignone ◽  
Anna M Pietroboni

Author(s):  
Tzy Harn Chua ◽  
Wann Jia Loh

Summary Severe hyponatremia and osmotic demyelination syndrome (ODS) are opposite ends of a spectrum of emergency disorders related to sodium concentrations. Management of severe hyponatremia is challenging because of the difficulty in balancing the risk of overcorrection leading to ODS as well as under-correction causing cerebral oedema, particularly in a patient with chronic hypocortisolism and hypothyroidism. We report a case of a patient with Noonan syndrome and untreated anterior hypopituitarism who presented with symptomatic hyponatremia and developed transient ODS. Learning points: Patients with severe anterior hypopituitarism with severe hyponatremia are susceptible to the rapid rise of sodium level with a small amount of fluid and hydrocortisone. These patients with chronic anterior hypopituitarism are at high risk of developing ODS and therefore, care should be taken to avoid a rise of more than 4–6 mmol/L per day. Early recognition and rescue desmopressin and i.v. dextrose 5% fluids to reduce serum sodium concentration may be helpful in treating acute ODS.


2021 ◽  
Vol 9 (37) ◽  
pp. 45-53
Author(s):  
Dominique Gagnon

Central pontine myelinolysis (CPM), first described in 1959, is a symmetrical non-inflammatory demyelinating disease with loss of oligodendrocytes that occurs most often following a rapid correction of severe hyponatremia (i.e., <120 mmol/L). It presents as a biphasic disease with initial seizure or encephalopathy, followed by clinical improvement and subsequent rapid deterioration with bulbar dysfunction, oculomotor dysfunction, various degree of paresis, and even locked in syndrome. Its occurrence is rare (≈0.6% of severe hyponatremia), it is diagnosed clinically and confirmed with brain imaging, ideally with magnetic resonance image, and it is reversible in approximately half the patients. Lesions are classically identified in the pons but extra pontine lesions (in basal ganglia, cerebellar white matter, thalamus, and hippocampus) have also been identified. The most commonly accepted molecular mechanism involves brain cell volume regulation with a rapid shift of osmole following brain edema which establishes during the chronic hyponatremic phase. For these reasons, osmotic demyelination syndrome (ODS) is a better term. The most identified risk factor is severe hyponatremia, but other electrolyte abnormalities can contribute, in particular, if the patient is an alcoholic or malnourished. This diagnosis should also be suspected in post-op patients with nausea and headache non-responsive to antiemetic and analgesic drugs. An essential step is an appropriate medical history, a list of medications, physical examination, and basic initial lab tests with the goal of identifying possible easily reversible causes of hyponatremia. Correction of severe hyponatremia with neurological symptoms should be done using rapid boluses of hypertonic saline solution in rapid succession with goals of increasing serum sodium by 5-6 mEq/L in the first two hours, which should be stopped if the level has risen by 10 mEq/L in the first five hours, and with the overall correction goal not to exceed 15-20 mEq/L in 48 hrs. This method has been shown safe in all hospital settings studied. Serial measurements of electrolyte levels and neurological examinations are recommended, as are correction of all electrolyte abnormalities, in particular magnesium and potassium. Thiamine should be given to all patients with chronic alcohol use who present with hyponatremia and encephalopathy.


2015 ◽  
Vol 27 (4) ◽  
pp. 157 ◽  
Author(s):  
WaseemR Dar ◽  
NajeebU Sofi ◽  
Muzamil Latief ◽  
ImtiyazA Dar ◽  
Moomin Hussain

2019 ◽  
Vol 2019 ◽  
pp. 1-4 ◽  
Author(s):  
Ruhin Yuridullah ◽  
Vinod Kumar ◽  
Sushant Nanavati ◽  
Monisha Singhal ◽  
Chandra Chandran

Osmotic Demyelination Syndrome (ODS) occurs after rapid overcorrection of severe chronic hyponatremia usually in those with a predisposition such as chronic alcoholism, malnutrition, or liver disease. Rarely, do patients make a full recovery. We report a case of ODS secondary to overcorrection of severe hyponatremia with pathognomonic clinical and radiologic signs making a complete neurological recovery. A detailed course of events, review of literature, and optimal and aggressive management strategies are discussed. There is some controversy in the literature regarding the prognosis of these patients. Our aim here is to show that, with aggressive therapy and long-term care, recovery is possible in these patients.


Sign in / Sign up

Export Citation Format

Share Document