Osmotic Demyelination Syndrome / Central Pontine Myelinolysis – final thoughts

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

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.

The Syndrome of Antidiuresis (SIADH)

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.

Hyponatremia 2: Working the Problem

This is the second tutorial in the series on Hyponatremia. I initially discuss why it is important to evaluate volume status in the setting of a low plasma sodium – patients may be isovolemic, hypovolemic or hypovolemic. The overall treatment is different in each case. Regardless, if a patient presents with symptomatic hyponatremia, then the treatment is 3% hypertonic saline solution – targeted at raising the plasma sodium or osmolality level or both and relieving symptoms. During the remainder of the tutorial I explore several clinical scenarios where patients present with acute symptomatic hyponatremia and work the problem of each seeking the definitive diagnosis.

Hyponatremia – 1. Understanding and Working the Problem

This is the first tutorial in a short series on hyponatremia. About 15% of our critical care patients has a problem with dysnatremia — high or low sodium levels in plasma. Hyponatremia, with symptoms, is a medical emergency as it can result in cerebral edema and irreversible brain injury.

In this tutorial I first present two case of hyponatremia – one that needs to be treated emergently and one that does not, despite both having the same plasma sodium levels. I then proceed to discuss the physiology of sodium and why it is a key component of body osmolality. The main part of the tutorial is developing a decision tree for working the hyponatremic problem. The key question is whether this is hypotonic or non hypotonic hyponatremia. If it is non hypotonic you need to look for other sources of unmeasured osmoles (usually alcohols). Hypotonic hyponatremia may be associated with myriad problems – but your main concern is whether or not this is being caused by kidney injury or blockade or normal renal pathways (e.g. diuretics). Ultimately I provide an algorithm for how to make a firm diagnosis of the cause of hyponatremia.  @ccmtutorials