Monthly Archives: January 2024

Osmotic Demyelination Syndrome / Central Pontine Myelinolysis – final thoughts

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I often wonder if the obsession amongst physicians regarding the prevention of Osmotic Demyelination Syndrome (ODS or Central Pontine Myelinolysis – CPM) results in adverse patient outcomes – for example a greater incidence of iatrogenic complications, prolonged length of stay etc.

In this discussion, I look at the history of ODS/CPM, how it became identified with rapid correction of hyponatremia and what patients are at particular risk of this disorder. In the second part of the discussion I address the re-ignited controversy about Sodium/Osmolality correction subsequent to the publication of a major study in NEJM Evidence in 2023.

Ultimately each clinician must make up their own minds on the evidence that is available. It appears to me that there is little or no risk of ODS/CPM in patients with acute hyponatremia, symptomatic or not, and those with a plasma sodium of greater than 120mmol/L. Patients with Sodium levels below 105mmol/L, alcoholics or cirrhotics and malnourished patient appear to be at very high risk. Finally attention should be paid not only to the speed of correction, but where the plasma sodium levels ends up. In many studies – ODS/CMP is a late diagnosis and patients, at the time of diagnosis are hypernatremic (greater than 145mmol/l) – although the rise in Sodium/Osmolality may appear slow over days or weeks.

Urinary Osmolality, Elderly Patients, Alcoholics and Hyponatremia

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This discussion came about following a discussion with my colleague, Dr Bairbre McNicholas. It focuses principally on the problem of hyponatremia in elderly patients and undernourished alcoholics. I explain why the lack of dietary salt and protein intake massively inhibits water excretion resulting in hypotonic hyponatremia, often with fluid overload. The traditional approach to managing hyponatremia – fluid restriction – frequently fails because it is a problem of solute “underload” rather than water overload. Commencing iv fluids may precipitate a rapid and potentially dangerous diuresis – hence the most effective therapy for these patients is the FEED them.

I guarantee you’ll learn something.

Careful Sodium Correction and Osmotic Demylination Syndrome

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Patients who present with symptomatic hyponatremia (usually the Na+ is lower than 120mmol/L) should be treated with hypertonic saline (HTS) and then fluid restricted. The goal of HTS therapy is to reverse the symptoms and raise the plasma Na+ by 5mmol per liter. What then? It depends on the circumstance – acute or chronic, high risk or low risk. This tutorial addresses the issue of rate of correction of plasma sodium, explains why you need to modify that rate in high risk patients (very low sodium, alcoholics, the malnourished, those with liver disease and profound hypokalemia). The reason why you need to be careful is because of concerns regarding the development of Central Pontine Myelinolysis – usually known now as Osmotic Demyelination Syndrome.

I wish to acknowledge the help of my colleagues Dr Bairbre McNicholas, Dr Peter Moran, Prof. John Bates, Dr Leo Kevin and Ms Aoife Boyle for clarifying my thoughts on this topic.

Click on this link for the 2014 European Guidelines (and a good review of the topic).

The Syndrome of Antidiuresis (SIADH)

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This tutorial is about the Syndrome of Inappropriate Diuresis. SIAD also known as SIADH is a form of hypotonic hyponatremia associated with iso- or hypervolemia, high urinary osmolality and high urinary sodium. Traditionally this is associated with high levels of circulating vasopressin (antidiuretic hormone – ADH), that may be associated with sepsis, acute critical illness, pneumonia or mechanical ventilation. However, SIAD is also associated with a variety of brain injuries, drugs (SSRIs and anticonvulsants) and a variety of cancers.

Treatment of symptomatic SIAD is with hypertonic saline (150ml of 3% over 20 minutes). Chronic or asymptomatic SIAD is treated with fluid restriction (determined by the Furst equation uNa + uK/pNa – if the result is less than1 the patient is suitable for fluid restriction).

Alternative inexpensive therapies include Urea (30 to 60mg per day), salt tablets plus frusemide or demeclocycline.

Vaptan agents, the block the V2 receptors, appear to be effective for long term therapy. Tolvaptan is available commercially but quite expensive for the majority of patients.

Cerebral salt wasting is associated with subarachnoid hemorrhage. It shares the same blood and urinary profile as SIAD(H) but is associated with hypovolemia. The disorder is self limiting and is treated with isotonic fluids.