scholarly journals Osmotic demyelination syndrome in a patient with Noonan syndrome and anterior hypopituitarism

2020 ◽  
Vol 2020 ◽  
Author(s):  
Tzy Harn Chua ◽  
Wann Jia Loh
Keyword(s):  
Noonan Syndrome ◽  
Cerebral Oedema ◽  
Early Recognition ◽  
Sodium Concentration ◽  
List Type ◽  
Rapid Rise ◽  
Osmotic Demyelination Syndrome ◽  
Severe Hyponatremia ◽  
Osmotic Demyelination ◽  
Learning Points

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.

scholarly journals Carbimazole induced rhabdomyolysis

2021 ◽  
Vol 2021 ◽  
Author(s):  
Niamh O’Donnell ◽  
Aisling McCarthy ◽  
Ken Thong
Keyword(s):  
Adverse Effect ◽  
Creatine Kinase ◽  
Side Effects ◽  
Temporal Relationship ◽  
Early Recognition ◽  
Antithyroid Drug ◽  
Graves Disease ◽  
List Type ◽  
Musculoskeletal Complaints ◽  
Learning Points

Summary Carbimazole is a commonly used antithyroid drug (ATD), which is associated with several well-established side effects. However, Carbimazole-induced rhabdomyolysis is rarely reported in the literature. We report a 27-year-old male who presented with upper limb myalgia and significantly raised creatine kinase elevation, 1-month post commencement of Carbimazole for Graves’ disease. Carbimazole was ceased with subsequent clinical and biochemical improvement. Though the pathophysiology remains unclear, we hope to raise awareness regarding this rare adverse effect with a view to promote early recognition and prompt discontinuation of the offending medication caused by a commonly used medication in endocrinology. Learning points Musculoskeletal complaints can relate to unidentified and untreated hyperthyroidism. However one must be mindful that the treatment for these disorders can too induce myopathies. ATD-induced myopathy should be considered when there is a temporal relationship between introduction of ATDs and the onset of symptoms. If ATD-induced myopathy is being considered, other causes of myopathy should still be outruled. Prompt discontinuation of potentially offending medications may provide resolution of symptoms and avoid significant consequences.

scholarly journals Hyponatremia, osmotic demyelination syndrome, and the importance of the patient’s history

2021 ◽  
Vol 9 (37) ◽  
pp. 45-53
Author(s):  
Dominique Gagnon
Keyword(s):  
Demyelinating Disease ◽  
Central Pontine Myelinolysis ◽  
Cell Volume Regulation ◽  
Brain Cell ◽  
Osmotic Demyelination Syndrome ◽  
Severe Hyponatremia ◽  
Hypertonic Saline Solution ◽  
Osmotic Demyelination ◽  
Pontine Myelinolysis ◽  
Electrolyte Abnormalities

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.

scholarly journals Isolated Extrapontine Myelinolysis of Osmotic Demyelination Syndrome

2013 ◽  
Vol 114 (1) ◽  
pp. 35-38
Author(s):  
Ömer Yılmaz ◽  
H. H. Armağn ◽  
A. Turan ◽  
M. Duymuş
Keyword(s):  
Serum Sodium ◽  
Rare Case ◽  
Sodium Concentration ◽  
Osmotic Demyelination Syndrome ◽  
Osmotic Demyelination ◽  
Extracellular Compartment ◽  
Rapid Changes ◽  
The Brain ◽  
Current Report ◽  
Rapid Correction

The osmotic demyelination syndrome (ODS) has been identified as a complication of the rapid correction of hyponatremia for decades (King and Rosner, 2010). However, in recent years, a variety of other medical conditions have been associated with the development of ODS, independent of changes in serum sodium which cause a rapid changes in osmolality of the interstitial (extracellular) compartment of the brain leading to dehydration of energy-depleted cells with subsequent axonal damage that occurs in characteristic areas (King and Rosner, 2010). Slow correction of the serum sodium concentration and additional administration of corticosteroids seems to be a major prevention step in ODS patients. In the current report we aimed to share a rare case which we observed in our clinic.

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 ◽  
...  
Keyword(s):  
Case Report ◽  
Cerebral Edema ◽  
Osmotic Demyelination Syndrome ◽  
Middle Aged ◽  
Severe Hyponatremia ◽  
Osmotic Demyelination ◽  
Conscious Level ◽  
Initial Improvement ◽  
Alteration Of Consciousness ◽  
Significant Mortality

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

scholarly journals Clinical Resolution of Osmotic Demyelination Syndrome following Overcorrection of Severe Hyponatremia

2019 ◽  
Vol 2019 ◽  
pp. 1-4 ◽  
Author(s):  
Ruhin Yuridullah ◽  
Vinod Kumar ◽  
Sushant Nanavati ◽  
Monisha Singhal ◽  
Chandra Chandran
Keyword(s):  
Management Strategies ◽  
Chronic Alcoholism ◽  
Review Of Literature ◽  
Osmotic Demyelination Syndrome ◽  
Severe Hyponatremia ◽  
Term Care ◽  
Aggressive Management ◽  
Osmotic Demyelination ◽  
Chronic Hyponatremia

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.

scholarly journals Osmotic Demyelination Syndrome in a Patient with Hypokalemia but No Hyponatremia

2020 ◽  
Vol 2020 ◽  
pp. 1-4
Author(s):  
Carolina Ormonde ◽  
Raquel Cabral ◽  
Sara Serpa
Keyword(s):  
Risk Factors ◽  
Central Nervous System ◽  
Nervous System ◽  
Rare Case ◽  
Rapid Rise ◽  
Osmotic Demyelination Syndrome ◽  
Multiple Risk Factors ◽  
Osmotic Demyelination ◽  
The Central Nervous System ◽  
Rapid Correction

Osmotic demyelination syndrome (ODS) is characterized by loss of myelin in various parts of the central nervous system. It is mainly caused by a rapid correction of hyponatremia, although other factors that may cause rapid rise in serum osmolality can also be associated with its development. Its prognosis is poor and the recovery rate is unknown. The authors report a rare case of a patient with multiple risk factors for ODS, without hyponatremia, who developed ODS and surprisingly recovered. This case report highlights the importance of recognizing risk factors for the development of ODS, even if the main one is not present.

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