Podcast - Understanding low sodium—causes, symptoms and classification

The video version of this podcast can be found here:

·      https://youtu.be/JxNOCJZP10M

This episode makes reference to guidelines produced by North Bristol NHS Trust, Royal United Hospitals Bath NHS Trust and Royal Cornwall Hospitals NHS Trust. The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by them.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I look at hyponatraemia, its classification, clinical presentation, pathophysiology and causes. I have looked at the guidelines produced by North Bristol NHS Trust, and Royal United Hospitals Bath NHS Trust, as well as other guidance, focusing on what is relevant to Primary Care only. The links to the sources consulted can be found below.

I am not giving medical advice; this video is intended for health care professionals; it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

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The links to the Hyponatraemia guidelines consulted can be found:

North Bristol NHS Trust

·      https://www.nbt.nhs.uk/sites/default/files/Hyponatraemia%20in%20Primary%20Care.pdf

Royal United Hospitals Bath:

·      https://www.ruh.nhs.uk/pathology/documents/clinical_guidelines/PATH-019_hyponatraemia_in_primary_care.pdf

Royal Cornwall Hospitals NHS trust:

·      https://doclibrary-rcht.cornwall.nhs.uk/DocumentsLibrary/RoyalCornwallHospitalsTrust/Clinical/EndocrineAndDiabetes/ManagementOfHyponatraemiaClinicalGuideline.pdf

Greater Glasgow and Clyde:

·      https://handbook.ggcmedicines.org.uk/media/1099/195-hyponatraemia-flowchart-1-final-200717e.pdf

Gloucestershire hospitals NHS Trust

·      https://www.gloshospitals.nhs.uk/media/documents/Hyponatraemia.pdf

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Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I am Fernando, a GP in the UK. Today, we are looking at hyponatraemia, its classification, clinical presentation, pathophysiology and causes. I have looked at the guidelines produced by North Bristol NHS Trust, and Royal United Hospitals Bath NHS Trust, as well as other guidance, focusing on what is relevant to Primary Care only. The links to the sources consulted are in the episode description. The next episode will be on the further assessment and management of hyponatraemia so make sure not to miss it.

Right, without further ado, let’s get started.

Hyponatraemia tends to be more common in the elderly, in patients admitted, in those with a history of alcohol excess and in patients treated with thiazide diuretics. It is associated with complications such as seizures and increased mortality and, the risk increases with the severity of hyponatraemia.  

So, starting with the basics, what is hyponatraemia?

Well, the normal range of sodium is from 135 to 145 mmol/L so hyponatraemia, that is a low sodium, is when the sodium is below 135. However, guidelines in North Bristol and Bath define it as a sodium below 133 mmol/l, so we should always look at our local path lab reference range. 

The severity of hyponatraemia can be classified into mild, moderate and severe. NICE recommends the following thresholds:

·      Mild is when the sodium is between 130-135

·      Moderate is when the sodium is between 125-129 and

·      Severe is when the sodium is less than 125 

However, other guidelines give different thresholds. For example, in Bath severe hyponatraemia is below 120 and in North Bristol is below 115. But, from a primary care perspective, it will be better to err on the side of caution so we will stick to 125. This is a very important for us because we are advised to admit to hospital patients with severe hyponatraemia, as well as those who are symptomatic, irrespective of the sodium levels.  

And what are the symptoms of hyponatraemia? 

The primary symptoms are due to cellular swelling, particularly in the brain, because of the osmotic movement of water into cells in response to low sodium levels. The brain is particularly sensitive to changes in osmolality and, when sodium levels drop, extracellular osmolality also decreases, leading to water moving into brain tissue and leading to a degree of cerebral oedema. This is responsible for most of the clinical manifestations of hyponatremia like cognitive decline, headaches, confusion, anorexia, nausea and vomiting, dizziness, agitation, seizures, and eventually coma and cardiorespiratory arrest. Other potential symptoms are connected to the musculoskeletal system, given that a low sodium also leads to impaired neuromuscular transmission, causing cramps, weakness and fatigue. 

The severity of the symptoms will not only depend on the severity of the hyponatraemia but also on the rate of onset. So, on this basis, hyponatraemia can be classified as: 

·      Chronic when it develops gradually over time and certainly over more than 48 hours. Mild chronic hyponatraemia can be asymptomatic or present with mild non-specific symptoms. On the other hand

·      Acute hyponatraemia is when the sodium level has fallen by more than 10 mmol/L in less than 48 hours and it is a medical emergency given that it is associated with a high mortality and morbidity. Acute hyponatraemia is rare and most often due to marked water intake such as with post-operative fluids, ecstasy use, marathon runners or psychogenic polydipsia.  

Finally, we should also describe two other concepts: 

·      Pseudo hyponatraemia and

·      Hypertonic hyponatraemia. 

In pseudo hyponatraemia, we are talking about a path lab artifact. It is caused by an increased concentration of non-aqueous components in plasma, such as for example high triglycerides or very high proteins like in paraproteinaemia. The sodium concentration is normal but the measured value is falsely low due to the dilution effect in the path lab assay, so it has no clinical significance and the patient will be asymptomatic from that point of view. 

On the other hand, in hypertonic hyponatraemia, there is true hyponatremia which is caused by an osmotic substance, commonly glucose in cases of significant hyperglycaemia, which draws water from the intracellular to the extracellular compartment causing a true dilutional hyponatraemia. There may be symptoms of hyperglycaemia (e.g., polyuria, polydipsia, and dehydration) and although there may be some hyponatremia-related symptoms, it does not cause cerebral oedema because plasma has a high osmolality.  

Let’s now have a look at the causes of hyponatraemia. But perhaps before doing so, let’s have a look at sodium metabolism and homeostasis.  

Most sodium is obtained through dietary intake, mostly from salt and absorption occurs primarily in the small intestine. Sodium can be lost through sweat, and in smaller amounts via faeces, but these mechanisms are less significant compared to renal regulation, which plays a major role in sodium balance by filtering sodium in the glomeruli and reabsorbing it under the influence of certain hormones.

Let’s look at this Hormonal Control: 

·      The Renin-Angiotensin-Aldosterone System is stimulated by hypovolaemia, and low sodium. It increases aldosterone which enhances renal sodium reabsorption.

·      The antidiuretic Hormone or ADH causes water retention and it indirectly influences sodium concentration because it can lead to dilutional hyponatraemia.

·      And finally, the Natriuretic Peptides are released in response to high blood pressure or high blood volume and, as the name indicates, they promote natriuresis by inhibiting renal sodium reabsorption. 

So, the Pathophysiology of Hyponatremia can result from excess water retention or sodium loss. And we can also differentiate the causes according to fluid status: 

·      In Hypovolaemia there is generally a loss of both fluid and sodium, with the loss of sodium being greater relative to water. Examples are Acute Kidney Injury, other renal diseases, Diuretics, Addison’s disease, and significant Vomiting and/or diarrhoea.

·      Hypervolaemia, is often seen in conditions where oedema is a feature. Fluid lost into the interstitial tissues is detected by the body as a loss of intravascular fluid and excess fluid is retained as a compensatory mechanism. Although generally both aldosterone and antidiuretic hormone are stimulated, there is a disproportionate retention of water relative to sodium, giving rise to dilutional hyponatraemia. Examples are Congestive Cardiac Failure, Chronic liver disease, and Nephrotic syndrome.

·      In euvolemic hyponatremia, the issue is typically increased water retention, without significant changes in intravascular volume. Sodium loss is not prominent, and while overall sodium content is normal, excess water causes dilutional hyponatremia. Examples include medications like thiazide diuretics, ACE inhibitors, antidepressants, antiepileptics, or proton pump inhibitors. Other causes include the syndrome of inappropriate ADH secretion, hypothyroidism, and psychogenic polydipsia. Additional causes are very low salt intake (although rare) and reset osmostat syndrome.  

Now, given that we are here, let’s have a look at reset osmostat in a little bit more detail.

Reset osmostat refers to a condition where the body’s regulation of serum sodium is altered such that the "set point" for plasma osmolality and sodium is lower than normal. In this situation, the osmoreceptors in the hypothalamus, which regulate thirst and antidiuretic hormone, function normally but are set at a lower-than-normal threshold. 

A reset osmostat is often seen in conditions associated with chronic illnesses, where long-term adaptation to the lower sodium happens. Examples include: 

·      Chronic malnutrition

·      Chronic heart failure or chronic liver disease like, cirrhosis and

·      Advanced age 

Key Features of a Reset Osmostat are: 

·   Stable, Mild Hyponatremia

·   Appropriate ADH Response

·   No Water Retention Issues and

·   Normal response to Fluid Challenges

A reset osmostat is an important condition to recognize because it represents a benign and adaptive form of hyponatremia. Unlike other causes, which can lead to complications, patients with a reset osmostat often do not require aggressive treatment, and treatment to raise sodium levels could potentially lead to harm. 

So that is it, an introduction to hyponatraemia relevant to primary care. Remember that the next episode will be on the further assessment and management of hyponatraemia so make sure not to miss it. 

We have come to the end of this episode. Remember that this is not medical advice and it is only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.