Primary Care Guidelines

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:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

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

·   The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

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

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

Music provided by Audio Library Plus 

Watch: https://youtu.be/aBGk6aJM3IU 

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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.

The video version of this podcast can be found here:

·      https://youtu.be/SA7pJQLlmvg

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". 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 NICE.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through new and updated recommendations published in August 2024 by the National Institute for Health and Care Excellence (NICE), focusing on those that are relevant to Primary Care only.

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:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

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

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The Full NICE News bulletin for August 2024 can be found here:

·      https://www.nice.org.uk/guidance/published?from=2024-08-01&to=2024-08-31&ndt=Guidance&ndt=Quality+standard

The links to the current guidance can be found here:

Diabetic retinopathy: Management and monitoring:

·      https://www.nice.org.uk/guidance/ng242

Abaloparatide for treating osteoporosis after menopause:

·      https://www.nice.org.uk/guidance/ta991

National Osteoporosis Guideline Group (NOGG) clinical guideline for the prevention and treatment of osteoporosis:

·      https://www.nogg.org.uk/full-guideline

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

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 the NICE updates published in August 2024, focusing on what is relevant to Primary Care only.

We are going to cover just two areas, the treatment of osteoporosis and the management of diabetic retinopathy, so it is a brief episode.

Let’s jump into it.

The first area is a technology appraisal on Abaloparatide for treating osteoporosis after the menopause.

And you may be thinking, Abaloparatide, is this really something that we need to know about in Primary Care?

And the answer is yes. And let’s see why.

And we will start by saying that treatments of osteoporosis can be broadly divided into 2 types:

·    antiresorptive treatments (which slow the rate of bone breakdown), such as our usual bisphosphonates and

·    anabolic (or bone-forming) treatments.

Treatment with anabolic skeletal agents result in rapid and greater fracture risk reductions than bisphosphonates. So, if we are used to prescribing bisphosphonates for the majority of our patients, who should be getting anabolic agents instead?

And the guidelines stipulate that people with a very high fracture risk should be referred for the consideration of these agents. According to the National Osteoporosis Guideline Group, 'very high risk' is defined as a FRAX-based fracture probability that exceeds the intervention threshold by 60%.

So, looking at this diagram based on FRAX, we can see how patients can fall into the different risk categories depending on their scores.

Apart from the patients already in the very high risk of fractures, we should also consider additional clinical risk factors for patients in the high-risk category, (e.g., frequent falls, or a very low spine Bone Mass Density) in case that they may move them from high to very high risk of fracture.

So, in summary, we need to be aware that these anabolic drugs exist and that they are recommended for people with a very high risk of fractures so that when we see such patients, we refer them appropriately to get these drugs.

Existing anabolic treatments are Romosozumab and Teriparatide and, following this technology appraisal, NICE recommends Abaloparatide too.

These anabolic agents can only be taken for a limited time between 12 and 24 months depending on the drug, and afterwards patients will continue to receive an antiresorptive treatment (such as an oral bisphosphonate).

Although abaloparatide is licensed for 'treatment of osteoporosis in postmenopausal women', we must also include trans men and non-binary people registered female at birth.

The next area is a brand-new NICE guideline on Diabetic retinopathy, its management and monitoring. It is mostly aimed at the diabetic retinal screening service and ophthalmologists but it also covers some areas of diabetic care that affects us in primary care. Let’s have a look at it.

1.   Firstly, we should always discuss with patients that good long-term diabetic control can have long-term benefits for their vision.

2.   Then the second recommendation refers to the effects on retinopathy of a rapid reduction in HbA1c.This is because there is some, although limited, evidence about the potential risk of worsening retinopathy from treatments that result in a rapid, substantial drop in HbA1c. Early worsening of diabetic retinopathy does not necessarily mean that the treatment is harmful in the long term but, instead, it highlights the need for close monitoring. NICE therefore recommended that an ophthalmologist should assess the patient before intensive glycaemic treatment is started, and then closely monitors for changes afterwards.

3.   We know that both HbA1c and blood pressure levels can be used to predict the likelihood of retinopathy progression. So, the third recommendation is that ophthalmologists should have access to a person's HbA1c and blood pressure records.

4.   Additionally, NICE has highlighted that the presence of renal disease can also influence retinopathy progression. The evidence for this is of low quality, but is supported by clinical experience.

5.   Also, we know that managing blood pressure in hypertensive patients can reduce retinopathy progression, so achieving good blood pressure control is important. However, we must also be aware that reducing blood pressure with antihypertensives in people who do not have hypertension has no such positive effect.

6.   There is some evidence that fenofibrate is beneficial for people with type 2 diabetes in respect of retinopathy progression. However, there is no evidence on other outcomes such as visual acuity or quality of life. NICE therefore recommends that it should be ophthalmologists who initiate fenofibrate for this indication. There is no evidence for people with type 1 diabetes, so they are not included in the recommendation.

7.   NICE has recommended further research about statins preventing retinopathy progression, because there is no strong evidence to this effect.

8.   The rest of the recommendations are entirely for secondary care and cover areas such as cataract surgery as well as recommendations of the treatment and frequency of monitoring for both proliferative and non-proliferative diabetic retinopathy and diabetic macular oedema.

So that is it, a review of the NICE updates relevant to primary care.

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.

The video version of this podcast can be found here:

·      https://youtu.be/pxOeszuHRsI

This episode makes reference to guidelines produced for NHS Greater Glasgow and Clyde and Liverpool University Hospitals NHS Trust. Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that 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 go through the management of hypocalcaemia, in particular, we will look at the guidance on the management of hypocalcaemia in NHS Greater Glasgow and Clyde and in Liverpool University Hospitals NHS Trust, always focusing on what is relevant in Primary Care only.  

I am not giving medical advice; this episode 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:

●      Apple podcast: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

●      Spotify: https://open.spotify.com/show/2kmGZkt1ssZ9Ei8n8mMaE0?si=9d30d1993449494e

●      Amazon Music: https://music.amazon.co.uk/podcasts/0edb5fd8-affb-4c5a-9a6d-6962c1b7f0a1/primary-care-guidelines?ref=dm_sh_NnjF2h4UuQxyX0X3Lb3WQtR5P

●      Google Podcast: https://www.google.com/podcasts?feed=aHR0cHM6Ly9mZWVkcy5yZWRjaXJjbGUuY29tLzI1ODdhZDc4LTc3MzAtNDhmNi04OTRlLWYxZjQxNzhlMzdjMw%3D%3D

●      Redcircle: https://redcircle.com/shows/2587ad78-7730-48f6-894e-f1f4178e37c3

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

●       The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk 

The resources consulted can be found here:

The guidance on the management of hypocalcaemia by Liverpool University Hospitals NHS Trust can be found here:

·      https://pathlabs.rlbuht.nhs.uk/Guideline%20for%20Treating%20and%20Monitoring%20Hypocalcaemia%20for%20non-critical%20areas%20of%20Trust.pdf

The guidance on the management of hypocalcaemia by the Adult Therapeutics Handbook for the NHS Greater Glasgow and Clyde can be found here:

·      https://handbook.ggcmedicines.org.uk/guidelines/electrolyte-disturbances/management-of-hypocalcaemia/

Calcium – The Lancet - Bushinksy DA, Monk RD. Calcium. Lancet 1998; 352 (9124): 306-311:

·      https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(97)12331-5/abstract 

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

●       Music provided by Audio Library Plus 

●       Watch: https://youtu.be/aBGk6aJM3IU 

●       Free Download / Stream: https://alplus.io/halfway-through 

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’m Fernando, a GP in the UK. Today we are going to go through the management of hypocalcaemia, in particular, we will look at the guidance on the management of hypocalcaemia in NHS Greater Glasgow and Clyde, and in Liverpool University Hospitals NHS Trust, always focusing on what is relevant in Primary Care only. The links to their guidelines and the other sources consulted are in the episode description. 

Right, without further ado, let’s jump into it. 

As a quick overview of calcium metabolism, I will simply say that it is tightly regulated by vitamin D and the parathyroid hormone or PTH. Active vitamin D or calcitriol enhances intestinal calcium absorption and PTH both enhances calcium reabsorption in the kidneys, and releases calcium from the bones by increasing osteoclast activity and bone resorption. 

Both phosphate and magnesium can also affect calcium levels. For example, a low magnesium can impair PTH secretion and action, resulting in hypocalcaemia.  

On the other hand, a high phosphate, like seen in CKD, can lead to the precipitation of calcium with phosphate and the consequent reduction in serum calcium and hypocalcaemia.

Right, now that we have done this review, let’s now look at hypocalcaemia itself.

The reference range for adjusted serum calcium is 2.2 - 2.6mmol/L.

Symptoms of hypocalcaemia, typically develop when serum adjusted calcium falls below 1.9mmol/L. However, this threshold varies and symptoms also depend on the rate of fall. 

So, we will talk of hypocalcaemia when we have an adjusted serum calcium less than 2.2 mmol/L, although you should always take into account your local path lab reference range.  

The cause of hypocalcaemia may be varied depending on whether we are talking about acute or chronic hypocalcaemia. And we must remember that hypocalcaemia is far less common than hypercalcaemia because of the role of the bones as a calcium reserve to maintain homeostasis. 

So, let’s look at causes of acute hypocalcaemia first. The most common cause is hyperventilation which induces transient hypocalcaemia with normal serum total calcium levels normal. Let’s quickly see why this is the case. 

• When a person hyperventilates, they breathe out excessive CO₂ which leads to a decrease of carbonic acid, and respiratory alkalosis.
• Alkalosis causes more calcium to bind to albumin, reducing the concentration of free (ionized) calcium. Given that the ionized form is the physiologically active form, this decrease leads to symptoms of hypocalcaemia.
• However, despite the decrease in ionized calcium, the total serum calcium remains normal because this value includes the calcium bound to albumin. 

Other less common causes are:

·      Other forms of alkalosis.

·      Medications, for example post IV bisphosphonate or denusomab treatment

·      A high phosphate. We have to remember that phosphate and calcium often behave like two parts of a seesaw, where changes in one can inversely affect the other. Therefore, hypocalcaemia can be seen in clinical situations where phosphate is high, like in:

• rapid tumour lysis – like e.g. during cytotoxic treatment of leukaemia or
• in excessive phosphate intake – like for example excessive phosphate containing enemas.
• And finally, another less common cause of hypocalcaemia is acute pancreatitis. 

Let’s now look at the causes of chronic hypocalcaemia. And the most common cause is a decrease in levels of active vitamin D. This could be because there is:

• An overall vitamin D deficiency, like in dietary causes, malabsorption, and lack of sunlight or
• A reduction in the active form of vitamin D or calcitriol, due to poor renal conversion as seen in CKD

Less common causes are:

• hypoparathyroidism which can be post-surgical, autoimmune, genetic, idiopathic etc.
• hypomagnesaemia, because low magnesium impair the secretion and function of PTH, giving rise to a functional hypoparathyroidism.
• Pseudohypoparathyroidism, which is a rare, genetic disorder characterized by the body’s resistance to PTH despite normal or elevated PTH levels and finally
• low plasma albumin caused by, for example, malnutrition, or liver disease. However, it is worth mentioning that a low plasma albumin can lead to low total calcium levels but it does not cause true hypocalcaemia (understood as a low ionized or free calcium). Instead, it leads to pseudohypocalcaemia, where only the bound calcium is reduced, so patients typically do not experience symptoms of low calcium unless their ionized calcium is also low.

It is also worth mentioning that dietary lack of calcium intake is a very rare cause of hypocalcaemia. 

What are the symptoms and signs of hypocalcaemia?

Well, the clinical features of hypocalcaemia are connected to its effects on the nerves and muscles. Typical features include: 

·      Effects on the nervous system like:

• Paraesthesia
• convulsions which may occur because hypocalcaemia lowers the seizure threshold, and
• psychiatric effects, from general malaise to overt psychosis in chronic hypocalcaemia
• Effects on the muscles like:
• painful cramps
• tetany, which may result in spontaneous muscular spasms largely precipitated by exercise
• laryngeal spasm causing stridor, and obstructive respiratory symptoms and
• latent tetany, which may be demonstrated by Trousseau's and Chvostek's signs. Let’s quickly have a look at them:

For Trousseau’s sign, a blood pressure cuff is inflated usually about 20 mm Hg above the systolic BP, and it is left inflated for about 3 minutes. A positive sign is indicated by involuntary contraction of the muscles in the hand and fingers, known as carpal spasm or "Trousseau’s phenomenon." 

On the other hand, Chvostek's sign is performed by tapping on the facial nerve just in front of the ear, at the angle of the jaw, which is the area where the facial nerve crosses the masseter muscle. A positive sign is indicated by twitching of the facial muscles on that same side.  

Both Trousseau's and Chvostek's signs are indicative of increased neuromuscular excitability, which is often associated with hypocalcemia, although not exclusively. 

Other features of chronic hypocalcaemia depend on the underlying cause. They can be very varied so I will mention only a few like:

• candidiasis
• nail dystrophy
• alopecia, and
• rickets or osteomalacia - from chronic vitamin D deficiency

What investigations should be carried out in primary care if we find hypocalcaemia? And we are obviously talking about mild asymptomatic hypocalcaemia because patients with severe or symptomatic hypocalcaemia should be referred to hospital. 

Initial investigations should include as a minimum: 

• A repeat serum adjusted calcium and phosphate
• Parathyroid hormone (PTH)
• Urea and electrolytes
• Magnesium
• Vitamin D and
• A 12-lead ECG as there is a significant likelihood of QT prolongation, in which case cardiac monitoring may be required.

We should monitor calcium concentrations regularly to judge response and review treatment. Serum bone profile should be checked regularly according to clinical judgement, perhaps weekly or fortnightly depending on the case until concentrations are stable. 

Let’s now have a look at the treatment of hypocalcaemia. 

The treatment depends on the severity of symptoms and underlying condition: 

• treatment generally invovles administration of calcium. How calcium is administered and the need for additional agents such as vitamin D depends on the acuity and severity of the hypocalcaemia as well as the underlying cause.
• Severe Hypocalcaemia, that it, a serum adjusted calcium <1.9mmol/L and/or symptomatic hypocalcaemia should be treated as a medical emergency because it can be life-threatening. So, these patients should be referred to hospital for the administration of IV calcium.
• Chronic, Asymptomatic Mild Hypocalcaemia, that is, serum adjusted calcium between 1.9 - 2.2mmol/L is treated with oral calcium and often vitamin D supplements.
• Because calcium binds with dietary phosphate and oxalate we should advise patients that calcium is better absorbed when taken between meals.
• oral calcium is given to increase its availability and, often, vitamin D to enhance absorption.
• calcium carbonate is widely available in tablet form and we should aim for a daily dose of 1-2.6 g and then adjust according to response.
• Examples of calcium carbonate supplements are adcal and calcichew.
• NHS Greater Glasgow and Clyde recommend starting Calcichew Forte Chewable, 2 tablets twice a day, which is an unlicensed dose, and adjust the dose according to the patient’s requirements. As soon as it is appropriate, we should prescribe the licensed dose of 1 tablet daily.
• Alternatively, Liverpool Hospitals recommend starting oral calcium and vitamin D supplements such as Adcal D3 (2 to 4 tab daily) with monitoring and adjustment.
• calcium citrate and calcium phosphate should be avoided because they may cause problems, especially in patients with renal failure.
• If the patient is vitamin D deficient, we will start oral vitamin D supplementation with loading doses of colecalciferol as per the NICE guideline on vitamin D deficiency.
• vitamin D2 or ergocalciferol and vitamin D3 or colecalciferol at doses of 400 units a day are adequate to avoid nutritional deficiency, although higher doses may be needed in malabsorption.
• However, they require conversion to the active form calcitriol and therefore they are not suitable if the alpha-hydroxylation process is impaired, like for example in renal failure. In these cases, we should be guided by the renal team.
• Other general principles that apply to the management of hypocalcaemia are:
• magnesium levels should be checked and corrected if low. If patient has hypomagnesaemia, we should stop any precipitating drug and admit the patient to hospital for the administration of IV magnesium.
• patients on digoxin should be monitored carefully because administration of calcium may lead to digoxin toxicity and death
• Patients with hypoparathyroidism have decreased renal calcium reabsorption and oral calcium supplementation, may lead to hypercalciuria with possible nephrocalcinosis or kidney stones. Therefore, in hypoparathyroidism, the treatment should be guided by endocrinology.
• If hypocalcaemia is secondary to post-thyroidectomy, we will also seek specialist advice.
• When calcium is given to patients with hyperphosphataemia, there is a risk of soft-tissue calcium phosphate precipitation, so we should get specialist advice on the use of phosphate binders. Calcium supplements may have to be delayed until phosphate levels come down.

Right, so that is 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.

The video version of this podcast can be found here:

·      https://youtu.be/2scjC_NoKfc

This episode makes reference to guidelines produced for the Maidstone and Tunbridge Wells NHS Trust, and NHS Greater Glasgow and Clyde. Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that 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 go through the guidance on hypercalcaemia produced by the Maidstone and Tunbridge Wells NHS Trust, and the guidance in NHS Greater Glasgow and Clyde, always focusing on what is relevant in Primary Care only.

I am not giving medical advice; this episode 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:

●      Apple podcast: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

●      Spotify: https://open.spotify.com/show/2kmGZkt1ssZ9Ei8n8mMaE0?si=9d30d1993449494e

●      Amazon Music: https://music.amazon.co.uk/podcasts/0edb5fd8-affb-4c5a-9a6d-6962c1b7f0a1/primary-care-guidelines?ref=dm_sh_NnjF2h4UuQxyX0X3Lb3WQtR5P

●      Google Podcast: https://www.google.com/podcasts?feed=aHR0cHM6Ly9mZWVkcy5yZWRjaXJjbGUuY29tLzI1ODdhZDc4LTc3MzAtNDhmNi04OTRlLWYxZjQxNzhlMzdjMw%3D%3D

●      Redcircle: https://redcircle.com/shows/2587ad78-7730-48f6-894e-f1f4178e37c3

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

●       The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The resources consulted can be found here:

The guidance on the treatment of hypercalcaemia in adults by the Maidstone and Tunbridge Wells NHS Trust can be found here:

·      https://www.formularywkccgmtw.co.uk/media/1629/treatment-of-acute-hypercalcaemia-in-adults.pdf

The guidance on the management of hypercalcaemia by the Adult Therapeutics Handbook for the NHS Greater Glasgow and Clyde can be found here:

·      https://handbook.ggcmedicines.org.uk/guidelines/electrolyte-disturbances/management-of-hypercalcaemia/

Other guidance can be found here:

Joshi D, Center JR, Eisman JA. Investigation of incidental hypercalcaemia. BMJ. 2009;339:b4613

·       http://www.ncbi.nlm.nih.gov/pubmed/19933303

Carroll MF, Schade DS. A practical approach to hypercalcemia. Am Fam Physician. 2003;67(9):1959-66

·      http://www.ncbi.nlm.nih.gov/pubmed/12751658

Smellie WS et al. Best practice in primary care pathology: review 11. J Clin Pathol. 2008;61(4):410-8

·      http://www.ncbi.nlm.nih.gov/pubmed/17965216

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

●       Music provided by Audio Library Plus 

●       Watch: https://youtu.be/aBGk6aJM3IU 

●       Free Download / Stream: https://alplus.io/halfway-through 

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’m Fernando, a GP in the UK. Today we are going to go through the guidance on hypercalcaemia produced by the Maidstone and Tunbridge Wells NHS Trust, as well as other general guidance on the subject, always focusing on what is relevant in Primary Care only. The links to the information consulted can be found in the episode description.

Right, let’s not waste any more time so let’s jump into it.

Before we start, let’s quickly have an overview of calcium metabolism.

Calcium is one of the most abundant electrolytes in the body, and levels are tightly controlled by parathyroid hormone and vitamin D. Serum calcium is bound to albumin, and measurements should be adjusted for it, so we should be primarily concerned about corrected calcium levels.

Calcium is mostly absorbed in the small intestine and active vitamin D (or calcitriol) enhances calcium absorption.

Parathyroid Hormone (or PTH) is also important. When blood calcium levels drop, PTH is secreted, which enhances calcium reabsorption in the kidneys, and also stimulates osteoclasts in the bones, breaking down bone tissue and releasing calcium into the blood stream. This is precisely the opposite effect of calcitonin, which inhibits osteoclast and reduces bone resorption and calcium levels.

So, from a pathophysiological perspective, a high calcium or hypercalcemia can be seen in, for example, hyperparathyroidism, malignancy, or excessive vitamin D intake.

There are also pathophysiological interactions between calcium and levels of phosphate and magnesium.

For example, a high calcium can suppress magnesium renal absorption, leading to hypomagnesaemia. Equally, a high calcium also often leads to a low phosphate due to its effect on PTH.

Right, having had this overview, let’s now have a look at hypercalcaemia itself. It is generally defined as a corrected calcium level greater than 2.6 on two occasions, although we will need to take into account our local path lab reference range.

About 90% of cases are due to either primary hyperparathyroidism or malignancy.

Other rarer causes of hypercalcaemia include:

·      Chronic granulomatous diseases like sarcoidosis or pulmonary Tb

·      Paget's disease with bed rest

·      Immobilisation

·      Vitamin A and/or vitamin D toxicity

·      Drugs like thiazide diuretics and lithium

·      Familial hypocalciuric hypercalcaemia

·      Non-parathyroid endocrine diseases (e.g. thyrotoxicosis, Addison's disease, and phaeochromocytoma) 

·      Milk-alkali syndrome 

·      Chronic kidney disease and

·      Tertiary hyperparathyroidism. By the way, if you want to know more about tertiary hyperparathyroidism, stay until the end because I will give you a brief pathophysiological explanation of it. 

The possible sign and symptoms of hypercalcaemia are often summarised by "stones, bones, thrones, abdominal groans and psychiatric overtones". Let’s see where these come from:

·      "Stones" refer to kidney stones.

·      "Bones" refer to skeletal symptoms such as bone pain, osteoporosis, and fractures associated with underlying bone disorders like in hyperparathyroidism or pathological fractures in malignancy. 

·      "Thrones" refers to polyuria and constipation

·      "Abdominal groans" refer to gastrointestinal symptoms such as nausea, vomiting, anorexia, weight loss, abdominal pain, pancreatitis and peptic ulcer. By the way, peptic ulcers can be an effect of increased gastric acid secretion caused by hypercalcemia.

·      "Psychiatric overtones" refer to effects on the central nervous system such as lethargy, fatigue, depression, confusion, irritability, memory loss, psychosis, ataxia, delirium, and coma.

·      Other: obviously this list of symptoms is not exhaustive. There are others not included, such as flushing, itching and cardiovascular complications, like hypertension, cardiac conduction abnormalities and arrhythmias. 

In general, hypercalcaemia can be classified as:

mild – if corrected calcium levels are between 2.6 – 3.00 mmol/l. It is often asymptomatic and does not usually require urgent correction.

moderate – if between 3.00 – 3.40 mmol/l and it may be well tolerated if it has risen slowly, but it may also be symptomatic and require prompt treatment and

severe – if it is more than 3.40 mmol/l, which requires urgent correction due to the risk of dysrhythmia and coma. The most common cause of severe hypercalcaemia is malignancy.

What initial investigations should we consider in Primary Care for a patient with a high corrected calcium? I am obviously referring to mild hypercalcaemia, given that the more severe cases we will be referring to secondary care for immediate management.

So, as investigations, we should organise Blood Tests in order to check:

·      An FBC

·      Renal function tests, as hypercalcemia can cause renal impairment.

·      Sodium and potassium to assess for electrolyte imbalances that may coexist.

·      To check a repeat corrected calcium to ensure it is not a lab error.

·      Also to check phosphate levels. and

·      Alkaline phosphatase which may suggest bone involvement, such as in malignancy or Paget’s disease.

·      Also to test for Vitamin D levels to assess for vitamin D intoxication or deficiency.

·      To check magnesium levels: As magnesium abnormalities, usually hypomagnesaemia can also be associated to hypercalcaemia.

·      To measure PTH to determine whether the hypercalcaemia is PTH-dependent or PTH-independent. For example,

o  A low PTH in the context of hypercalcaemia suggests a non-PTH-mediated cause, such as malignancy, excess vitamin D, granulomatous disease, or drug-induced causes. On the other hand,

o  A high or normal PTH in the context of hypercalcaemia suggests primary or tertiary hyperparathyroidism or familial hypocalciuric hypercalcemia (FHH). Please note that Familial hypocalciuric hypercalcemia has an inappropriately normal or elevated PTH because the calcium-sensing receptors in the parathyroids glands are less sensitive due to genetic reasons and this tricks the body into believing that the calcium levels are lower than they are.

·      The blood test is also to check thyroid function tests given that hyperthyroidism can also cause hypercalcaemia and we should also

·      Check serum protein electrophoresis if multiple myeloma is suspected.

We should consider additional tests depending on the clinical context such as:

·      A Chest X-ray to screen for granulomatous disease, TB or malignancy

·      An ECG to look for shortened QT intervals or other conduction abnormalities

·      A 24-hour urinary calcium excretion if we need to differentiate between primary hyperparathyroidism and familial hypocalciuric hypercalcemia, which has a low urinary calcium and a

·      Serum cortisol if Addison’s disease is suspected

In terms of treatment, we should get specialist advice and treat the underlying cause.

We should consider:

·      Immediate referral or same day hospital admission in cases of severe hypercalcaemia, that is, with a corrected calcium >3.4 mmol/L. We should also do so, regardless of the level of hypercalcaemia, for symptomatic patients, if there is a suspicion of a serious underlying condition, such as malignancy or a parathyroid crisis, or if there is worsening renal function.

·      Non-urgent outpatient referral would be reserved for patients with mild hypercalcaemia, that is, a corrected calcium less than 3, as long as they are asymptomatic and otherwise stable. We should carefully monitor calcium, renal function, and other relevant tests while awaiting secondary care input. And finally, what do we do with patients with moderate hypercalcaemia? Well,

·      From a primary care perspective, the management of patients with moderate hypercalcaemia, that is, levels between 3.00 and 3.40 mmol/L, is controversial but, in general, it may also be safer to err on the side of caution, and many guidelines recommend immediate hospital referral in these cases too.

Other obvious measures that we should instigate in Primary Care would be to stop drugs associated with hypercalcaemia, such as thiazide diuretics, encourage hydration and, if possible, avoid immobilisation.

I will not indulge in secondary care treatment as this is outside our hands, but one of the limitations is that there are no national guidelines for the management of hyerpcalcaemia, and practice varies widely across UK Hospitals. The acute management in secondary care generally involves:

·      Rehydration:

·      And then assess if IV bisphosphonates such as pamidronate or zolendronic acid are required, followed by the definitive treatment of the underlying cause, like, for example, parathyroidectomy in primary hyperparathyroidism.

Now, as promised, I am going to tell you more about tertiary hyperparathyroidism.

And before I can explain tertiary hyperparathyroidism, we probably need to go through the definitions of primary and secondary hyperparathyroidism first.

Primary hyperparathyroidism is when the parathyroid glands produce excessive amounts of parathyroid hormone (or PTH) without any external trigger, that is, it is an intrinsic problem within the parathyroid glands and the most common cause is a benign tumour or adenoma.

In Secondary hyperparathyroidism, the parathyroid glands overproduce PTH as a compensatory response to low calcium levels in the blood and it is the body's attempt to normalise calcium levels.  Possible causes of secondary hyperparathyroidism are chronic kidney disease and vitamin D deficiency.

And, finally, tertiary hyperparathyroidism involves the autonomous overproduction of PTH due to hyperplastic parathyroid glands that no longer respond to normal regulatory feedback, generally seen after prolonged secondary hyperparathyroidism in patients with CKD.

Let’s quickly examine the pathophysiology of tertiary hyperparathyroidism:

In CKD, the kidneys lose their ability to excrete phosphate, leading to hyperphosphatemia.

In CKD, the kidneys also produce less active vitamin D, resulting in decreased calcium absorption and hypocalcemia.

Both hypocalcemia and hyperphosphatemia stimulate the parathyroid glands to produce more PTH to maintain calcium levels. This is the secondary hyperparathyroidism stage.

However, over time, the continuous stimulation of the parathyroid glands leads to glandular hyperplasia and, as hyperplasia progresses, the parathyroid glands become less responsive to normal feedback mechanisms.

So, in some patients, particularly in those after prolonged and severe secondary hyperparathyroidism, the parathyroid glands can become autonomous, meaning they secrete PTH independently of blood calcium levels. At this stage, even when the initial cause of secondary hyperparathyroidism is corrected (e.g., after a kidney transplant), the overactive parathyroid glands continue to produce excessive PTH which will lead to hypercalcemia. This is when we talk about tertiary hyperparathyroidism.

So that is it, a quick review of the different types of hyperparathyroidism.

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.

The video version of this podcast can be found here:

·      https://youtu.be/1Cwvoflk3LQ

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that I am in no way affiliated with, employed by or funded/sponsored by NICE.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode, I go through the NICE guideline on Thyroid disease: assessment and management [NG145], always focusing on what is relevant in Primary Care only.

I am not giving medical advice; this episode 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:

●      Apple podcast: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

●      Spotify: https://open.spotify.com/show/2kmGZkt1ssZ9Ei8n8mMaE0?si=9d30d1993449494e

●      Amazon Music: https://music.amazon.co.uk/podcasts/0edb5fd8-affb-4c5a-9a6d-6962c1b7f0a1/primary-care-guidelines?ref=dm_sh_NnjF2h4UuQxyX0X3Lb3WQtR5P

●      Google Podcast: https://www.google.com/podcasts?feed=aHR0cHM6Ly9mZWVkcy5yZWRjaXJjbGUuY29tLzI1ODdhZDc4LTc3MzAtNDhmNi04OTRlLWYxZjQxNzhlMzdjMw%3D%3D

●      Redcircle: https://redcircle.com/shows/2587ad78-7730-48f6-894e-f1f4178e37c3

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

●       The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The resources consulted can be found here:

Thyroid disease: assessment and management -NICE guideline [NG145] can be found here:

●      https://www.nice.org.uk/guidance/NG145

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

●       Music provided by Audio Library Plus 

●       Watch: https://youtu.be/aBGk6aJM3IU 

●       Free Download / Stream: https://alplus.io/halfway-through 

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’m Fernando, a GP in the UK. Today we are going to go through the NICE guideline on Thyroid disease, always focusing on what is relevant in Primary Care only.

Right, we are not going to waste any time so let’s jump into it.

We will check TFTs if there is:

●     a clinical suspicion of thyroid disease, bearing in mind that 1 symptom alone may not be indicative of thyroid disease

●     type 1 diabetes or other autoimmune diseases, (but we will not offer testing only because of type 2 diabetes).

●     new-onset AF

●     depression or unexplained anxiety

●     abnormal growth in children and young people, or with an unexplained change in behaviour or school performance.

●     And we will be aware that in menopausal women symptoms of thyroid dysfunction may be mistaken for menopause

We will not test for TFTs during an acute illness unless we suspect the acute illness is due to thyroid dysfunction, because it may affect the test results.

So, what tests do we do as initial screening when thyroid dysfunction is suspected?

This will depend on whether we suspect a primary cause, that is, a cause arising from the thyroid gland, or a secondary cause, that is, a cause arising from the pituitary gland. Although the path lab will have processes to decide what tests are included when we request TFTs, it is important for us to understand what tests results we should expect according to the clinical presentation.

So, we will always measure TSH. Then, if a primary cause is suspected in an adult:

●     if the TSH is high, that is, suggestive of hypothyroidism, we will need the free thyroxine (FT4) level

●     if the TSH is low, that is, suggestive of hyperthyroidism, we will need FT4 and free tri-iodothyronine (FT3)

However, if we suspect a secondary cause, that is, pituitary disease, or if we are testing a child or young person, we will need results for both TSH and FT4 and:

●     If the TSH is low, that is, suggestive of hyperthyroidism, we will need FT3

So, in summary, we test TSH and T4 in hypothyroidism but in hyperthyroidism we need to add FT3 too.

We can repeat these tests if symptoms worsen or new symptoms develop (but no sooner than 6 weeks from the most recent test).

We will also ask patients about their biotin intake because a high consumption of biotin from dietary supplements may lead to falsely high or low test results.

Looking at the management, and monitoring different rules may apply to children and young people and given that we are likely to be getting advice from the paediatricians , I will not cover them here. If a recommendation applies to children, I will mention it, but otherwise this episode will focus on adults unless otherwise specifically stated.

So, we are going to cover:

●     Primary hypothyroidism: which is caused by an insufficient hormone production by the thyroid gland. In this situation the TSH is high, and FT4 is low.

●     Subclinical Primary hypothyroidism: This can sometimes happen as a precursor of clinical hypothyroidism and it is when the TSH is high, but FT4 is normal.

●     Thyrotoxicosis or Primary hyperthyroidism: Thyrotoxicosis is when there is excess thyroid hormone leading to a low TSH and a high FT4 and / or FT3. This can be caused by:

○     Increased production and secretion, as in primary hyperthyroidism or by

○     The release of stored thyroid hormones, as it happens in thyroiditis.

●     Subclinical Primary hyperthyroidism: This can also sometimes happen as a precursor of hyperthyroidism and it is when TSH levels are low, but FT3 and FT4 are normal.

●     And we will also cover Thyroid enlargement with normal thyroid function, which is self explanatory

So let’s start with the management of primary hypothyroidism

So, for all people with confirmed primary hypothyroidism, that is, when we encounter a high TSH and a low FT4, we will:

Check thyroid peroxidase antibodies (TPOAbs)

But in adults, we will not repeat TPOAbs testing. If the antibody test is positive, it maybe worthwhile mentioning that NICE also recommends testing for coeliac disease in people with a diagnosis of autoimmune thyroid disease.

For the actual management, for both adults and children, we will:

Offer levothyroxine as first-line treatment and we will not routinely offer liothyronine or natural thyroid extract for primary hypothyroidism, either alone or in combination with levothyroxine, because there is not enough evidence that it offers benefits over levothyroxine monotherapy, and the long-term adverse effects are uncertain.

We will start levothyroxine at a dosage of 1.6 micrograms per kilogram of body weight per day (rounded to the nearest 25 micrograms) for adults under 65 with primary hypothyroidism and no history of cardiovascular disease.

However, if they are over 65 or with a history of cardiovascular disease, we will start levothyroxine at a dosage of 25 to 50 micrograms per day with titration

How should we follow-up and monitor primary hypothyroidism?

We will aim to maintain TSH levels within the reference range when treating with levothyroxine. If symptoms persist, we will adjust the dose to achieve optimal wellbeing, but we will avoid using doses that cause TSH suppression or thyrotoxicosis.

We also need to be aware that the TSH level can take up to 6 months to return to normal for people who had a very high TSH or a prolonged period of untreated hypothyroidism.

In terms of monitoring, we will need to measure TSH every 3 months until the level has stabilised (that is, until we have had 2 similar measurements within the reference range 3 months apart), and then once a year. But we will also check FT4 as well as TSH if they continue to have symptoms on levothyroxine.

Let’s now look at subclinical hypothyroidism

Once we have confirmed subclinical hypothyroidism, with a high TSH and normal FT4, we will also check TPOAbs.

In terms of the management, we will:

take into account features that might suggest underlying thyroid disease, such as, for example, symptoms of hypothyroidism, or raised levels of thyroid autoantibodies.

Consider levothyroxine if the TSH is 10 mlU/litre or higher on 2 separate occasions 3 months apart, monitoring as per in hypothyroidism

We will also consider a 6-month trial of levothyroxine for adults under 65 with subclinical hypothyroidism who have:

●     a high TSH but lower than 10 mlU/litre on 2 separate occasions 3 months apart, and

●     symptoms of hypothyroidism.

If symptoms do not improve after starting levothyroxine, we will recheck the TSH and if the level remains raised, we will adjust the dose. If symptoms persist when TSH is within the reference range, we will stop levothyroxine and continue monitoring.

So, how do we monitor untreated subclinical hypothyroidism and after stopping treatment?

For them, we will check TSH and FT4:

●     once a year if they have features suggesting underlying thyroid disease, such as previous thyroid surgery or raised levels of thyroid autoantibodies, or

●     once every 2 to 3 years if they have no features suggesting underlying thyroid disease.

Let’s now have a look at thyrotoxicosis

First, we will have confirmed the diagnosis with a low TSH and raised FT4 and / or FT3.

Then we will need to differentiate between thyrotoxicosis with hyperthyroidism (for example, Graves' disease or toxic nodular disease) and thyrotoxicosis without hyperthyroidism (for example, transient thyroiditis). We will do so by:

●     measuring TSH receptor antibodies (TRAbs) to confirm Graves' disease. and

●     considering technetium scanning of the thyroid gland if TRAbs are negative.

We will only consider ultrasound for thyrotoxicosis if they have a palpable thyroid nodule. In terms of treatment, we need to be aware that transient thyrotoxicosis without hyperthyroidism like in thyroiditis usually only needs supportive treatment (for example, beta-blockers).

Otherwise we can consider antithyroid drugs along with supportive treatment for adults with hyperthyroidism who are waiting for specialist assessment and further treatment, bearing in mind that the use of carbimazole is subject to MHRA advice on contraception (Drug Safety Update, February 2019) and risk of acute pancreatitis (Drug Safety Update, February 2019).

Before starting antithyroid drugs,we will check a full blood count and liver function tests.

Antithyroid drugs for hyperthyroidism secondary to a single or multiple toxic nodules, will normally be with a titration regimen of carbimazole.

However, we will consider propylthiouracil for adults:

●     who experience adverse reactions to carbimazole

●     who are pregnant or trying to become pregnant within the following 6 months or

●     with a history of pancreatitis.

We will stop and do not restart any antithyroid drugs if a person develops agranulocytosis and we will refer to a specialist for further management options.

For the monitoring of antithyroid drugs, we will check:

●     TSH, FT4 and FT3 every 6 weeks until their TSH is within the reference range, then

●     TSH every 3 months until antithyroid drugs are stopped, rechecking FT4 and FT3 if the TSH becomes suppressed at any stage.

We will not monitor full blood count and liver function while taking antithyroid drugs unless there is a clinical suspicion of agranulocytosis or liver dysfunction.

After stopping antithyroid drugs in adults, we will check:

●     TSH within 8 weeks of stopping the drug, then

●     TSH every 3 months for a year, then

●     TSH once a year.

●     Always rechecking FT4 and FT3 if the TSH becomes suppressed at any stage.

I will not cover the follow-up and monitoring of hyperthyroidism after radioactive iodine treatment or surgery, as this will be guided by secondary care

In terms of the management and monitoring of subclinical hyperthyroidism, that is, when TSH is low and FT4 and FT3 are normal, We will seek specialist advice if they have:

●     2 TSH readings lower than 0.1 Miu/litre at least 3 months apart and

●     evidence of thyroid disease (for example, a goitre or positive thyroid antibodies) or symptoms of thyrotoxicosis.

Otherwise, in untreated subclinical hyperthyroidism, we will check TSH every 6 months and if the TSH level is outside the normal range, we will also check FT4 and FT3.

We will consider stopping TSH measurement if the TSH level stabilises (that is, we have 2 similar measurements within the normal range 3 to 6 months apart

Let’s now have a look at thyroid enlargement with normal thyroid function

We will:

Offer an ultrasound if there is palpable thyroid enlargement or focal nodularity if malignancy is suspected.

When making decisions about whether to refer for fine needle aspiration cytology, we will take into account the ultrasound comments on echogenicity, microcalcifications, vascularity and lymphadenopathy amongst other factors.

How should these patients be managed?

Well, we will not offer any treatment in non-malignant thyroid enlargement, normal thyroid function and mild or no symptoms unless:

●     they have breathing difficulty or

●     there is clinical concern, for example, because compression is suspected.

But we will repeat the thyroid ultrasound scan and TSH, if:

●     malignancy is subsequently suspected, or

●     compression is suspected or

●     the person's symptoms worsen or

●     they develop symptoms, such as hoarseness, or shortness of breath.

Obviously, if the thyroid enlargement is causing compressive symptoms, we will refer them for further management.

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.

The video version of this podcast can be found here:

·      https://youtu.be/kYcJ3Ym3C0A

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". 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 NICE.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through new and updated recommendations published in July 2024 by the National Institute for Health and Care Excellence (NICE), focusing on those that are relevant to Primary Care only.

There were no updated guidelines or quality standards but, apart from some radiotherapy treatments, there were five technology appraisals, none of which were really relevant to Primary care. However, I give them a very quick overview

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:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

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

The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The Full NICE News bulletin for July 2024 can be found here:

·      https://www.nice.org.uk/guidance/published?from=2024-07-01&to=2024-07-31&ndt=Guidance&ndt=Quality+standard

The links to the current consultations can be found here:

Lebrikizumab for treating moderate to severe atopic dermatitis in people 12 years and over:

·      https://www.nice.org.uk/guidance/ta986/chapter/1-Recommendations

Tenecteplase for treating acute ischaemic stroke:

·      https://www.nice.org.uk/guidance/ta990/chapter/1-Recommendations

Ivacaftor–tezacaftor–elexacaftor, tezacaftor–ivacaftor and lumacaftor–ivacaftor for treating cystic fibrosis:

·      https://www.nice.org.uk/guidance/ta988/chapter/1-Recommendations

Etranacogene dezaparvovec for treating moderately severe or severe haemophilia B:

·      https://www.nice.org.uk/guidance/ta989/chapter/1-Recommendation

Trastuzumab deruxtecan for treating HER2-low metastatic or unresectable breast cancer after chemotherapy:

·      https://www.nice.org.uk/guidance/ta992/chapter/1-Recommendations

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

Music provided by Audio Library Plus 

Watch: https://youtu.be/aBGk6aJM3IU 

Free Download / Stream: https://alplus.io/halfway-through 

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 the NICE updates published in July 2024. This month we have not had any new guidelines or quality standards but we have had a few new technology appraisals, that is, when NICE reviews new treatments to decide whether they should be recommended on the NHS. Apart from some radiotherapy recommendations, there were 5 other new treatments. Although none of them were really relevant to Primary care, I will give you a very quick overview so that we understand where new therapies are coming from and so that we have some knowledge if we come across them.

But do not worry, it is a real summary, and today will be a very brief episode. 

So, let’s jump into it.

The first area refers to the treatment of moderate to severe atopic dermatitis or eczema.

We know that standard treatment includes the topical use of emollients and steroids. If these treatments are not effective, systemic immunosuppressant treatments such as ciclosporin and methotrexate can be added. If there is an inadequate response or they are unsuitable, other agents such as a Janus kinase (JAK) inhibitor or a biological medicine (such as dupilumab or tralokinumab) can be used.

NICE has evaluated a new biological medicine alternative, lebrikizumab and indirect comparisons with Janus Kinase inhibitors and other biological treatments suggest that it is equally effective at an acceptable cost.

The biological treatments lebrikizumab, dupilumab, and tralokinumab are monoclonal antibodies that inhibit interleukin processes, thus reducing inflammation and modulating the immune response in conditions such as eczema and asthma. They are administered via subcutaneous injection and they can now all be used as  treatment options.

The next area covers the treatment of acute ischaemic stroke.

We know that once an intracranial haemorrhage has been ruled out, thrombolytic treatment can be started within 4.5 hours of the onset of stroke symptoms. The current standard thrombolytic treatment for this is alteplase.

Tenecteplase is an alternative to alteplase.  Tenecteplase, just like alteplase, turns plasminogen into plasmin, an enzyme that digests fibrin and acts like a pair of scissors to cut up the fibrin mesh in the clot, leading to clot dissolution and restoration of blood flow.

The evidence shows that tenecteplase is at least as effective as alteplase and a cost comparison suggests that it is less expensive, so it is also recommended.

The next area covers the treatment of cystic fibrosis, which we know affects the lungs, digestive system, and liver, and which reduces life expectancy and quality of life. Usual treatment is very physically demanding and time consuming for patients and their carers.

There are a number of tongue-twisting treatments namely ivacaftor, tezacaftor, elexacaftor, and lumacaftor, which work by improving the transport of chloride across cell membranes which in turn helps to hydrate and thin the mucus, particularly the lungs. They have been shown to improve lung function, growth and weight gain and reduce the number of lung infections.

They come as tablets or sachets and although expensive, NICE considers them to be cost effective, so, they are recommended.

The next area covers a gene therapy for Haemophilia B, etranacogene dezaparvovec, which reduces the number of bleeding episodes a person has each year. However, there is not enough evidence on how well it works in the long term so it is unclear as to whether it is cost effective. It is therefore not recommended for routine use in the NHS, but it can be used with managed access in order to try and collect more data.

The final area refers to the treatment of certain breast cancers with a combination drug, trastuzumab deruxtecan, which works by combining a monoclonal antibody targeting HER2-positive cancer cells with a potent chemotherapy drug, delivering the chemotherapy directly to the cancer cells. However, the cost-effectiveness estimates are unacceptably high, so, it is not recommended.

So that is it, very brief review of the new treatment updates.

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.

The video version of this podcast can be found here:

https://youtu.be/so97zARpmME

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that I am in no way affiliated with, employed by or funded/sponsored by NICE.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode, I go through the NICE guideline on recent onset cardiac chest pain [CG95], always focusing on what is relevant in Primary Care only.

I am not giving medical advice; this episode 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:

·      Apple podcast: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

·      Spotify: https://open.spotify.com/show/2kmGZkt1ssZ9Ei8n8mMaE0?si=9d30d1993449494e

·      Amazon Music: https://music.amazon.co.uk/podcasts/0edb5fd8-affb-4c5a-9a6d-6962c1b7f0a1/primary-care-guidelines?ref=dm_sh_NnjF2h4UuQxyX0X3Lb3WQtR5P

·      Google Podcast: https://www.google.com/podcasts?feed=aHR0cHM6Ly9mZWVkcy5yZWRjaXJjbGUuY29tLzI1ODdhZDc4LTc3MzAtNDhmNi04OTRlLWYxZjQxNzhlMzdjMw%3D%3D

·      Redcircle: https://redcircle.com/shows/2587ad78-7730-48f6-894e-f1f4178e37c3

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

●       The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The resources consulted can be found here:

Recent-onset chest pain of suspected cardiac origin: assessment and diagnosis guideline [CG95] can be found here:

●      https://www.nice.org.uk/guidance/cg95/chapter/recommendations

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

●       Music provided by Audio Library Plus 

●       Watch: https://youtu.be/aBGk6aJM3IU 

●       Free Download / Stream: https://alplus.io/halfway-through 

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’m Fernando, a GP in the UK. Today we are going to go through the NICE guideline on recent onset cardiac chest pain [CG95], always focusing on what is relevant in Primary Care only.

Right, without any further ado, let’s jump into it.

We are going to start by looking at the assessment and diagnosis of recent acute chest pain, suspected to be an acute coronary syndrome. The term ACS covers a range of conditions including unstable angina, ST‑segment-elevation myocardial infarction (or STEMI) and non‑ST‑segment-elevation myocardial infarction (or NSTEMI).

We will not cover the management of these conditions, given that this would be done in the hospital setting.

The first obvious thing is to check whether the patient has chest pain at the time of the consultation.

If the patient is pain free, we will check when their last episode was, particularly if they have had pain in the last 12 hours. We will see the importance of this and the impact on the possible management later.

In order to decide whether the chest pain is cardiac we will consider:

·      the history

·      the presence of cardiovascular risk factors

·      a history of ischaemic heart disease and

·      any previous treatment and investigations for chest pain. 

Symptoms suggestive of an ACS are:

·      pain in the chest and/or, for example, arms, back or jaw, lasting longer than 15 minutes

·      chest pain associated with nausea and vomiting, marked sweating, breathlessness, or particularly a combination of these

·      chest pain associated with haemodynamic instability and

·      new onset chest pain, or abrupt deterioration in previously stable angina, with frequent and recurrent chest pain on little or no exertion, and with episodes often lasting longer than 15 minutes. 

·      But we will bear in mind that not all people with an ACS present with central chest pain as the predominant feature and that

·      we should not use response to glyceryl trinitrate (GTN) to make a diagnosis of ACS. 

If we suspect an ACS, we will refer them to hospital. But NICE makes different recommendations as to who we should send to the emergency department and who we should send for urgent same-day hospital assessment.

So, if we suspect an ACS, we will send the patient as an emergency to the emergency department if:

·      they currently have chest pain or

·      they are currently pain free, but had chest pain in the last 12 hours, and a resting 12‑lead ECG is abnormal or not available 

Otherwise, in the absence of clinical concerns, we will refer for urgent same-day assessment if:

·      they had chest pain in the last 12 hours, but are now pain free with a normal ECG or

·      the last episode of pain was 12 to 72 hours ago 

We will also refer people for a hospital assessment if:

·      the pain has resolved and

·      there are signs of complications such as pulmonary oedema.

But for this group of patients we will use clinical judgement to decide whether referral should be as an emergency or for urgent same-day assessment. 

Right, so that is fairly clear, we will be referring straightaway patients who have had cardiac chest pains in the last 72 hours, regardless of ECG, or whether they have complications, using our clinical judgement as to whether they are for the emergency department or for urgent same day assessment. 

But what do we do if we see someone who had cardiac chest pains more than 72 hours ago and who have no complications such as pulmonary oedema?

NICE says that we should:

·      carry out a clinical assessment

·      confirm the diagnosis with an ECG and blood troponin level and

·      take into account the length of time since the suspected event when interpreting the troponin level, using clinical judgement to decide whether referral is necessary and how urgent this should be. 

And this is where it can get a little controversial.

Should we be doing troponin levels in primary care, bearing in mind that the results may not be available the same day?

If we are worried enough about an ACS to be doing troponin levels, should we be asking our hospital colleagues to assess the patient anyway?

What would be the medicolegal implications in Primary Care if the patient had a serious cardiovascular event in the intervening period?

And all this not to speak that many primary care organisations do not allow or recommend troponin testing in the primary care setting anyway.

As NICE says, it always comes back to us. They say, that we should use our clinical judgement to decide whether referral is necessary and how urgent this should be. So, it will depend on the presentation and our assessment of the risk. And it may very well be that you take the view that most, if not all, of your patients should have their troponin levels checked in hospital.

Is there anything else that we should do before referring them to hospital? Well, we should take an ECG as soon as possible, as long as this does not delay transfer to hospital and we will offer immediate treatment.

Let’s look at the ECG considerations first.

ECG changes that make the diagnosis of an ACS more likely are:

·      ST‑segment changes

·      Deep T wave inversion or

·      A presumed new left bundle branch block consistent with an acute STEMI

·      Also, even in the absence of ST‑segment changes, we will have an increased suspicion of an ACS if there are other changes such as Q waves and T wave changes but

·      Always bearing in mind that we should not exclude an ACS just because of a normal ECG. 

And now, let’s look at the immediate treatment that we should give in a way that is appropriate to the circumstances. So, as soon as we suspect an ACS, we should:

·      Offer pain relief, which may be achieved with either sublingual or buccal GTN, but we will offer intravenous opioids such as morphine, particularly if an acute MI is suspected. 

·      Offer a single loading dose of 300 mg of aspirin as soon as possible unless there is clear evidence that they are allergic to it, ensuring that we also send to hospital with the patient a written record that it has been given.

·      We will not routinely administer oxygen, but we will monitor oxygen saturation, and we will only offer oxygen if:

o  oxygen saturation (SpO2) is less than 94% if the patient is not at risk of hypercapnic respiratory failure, aiming for SpO2 between 94% and 98%

o  if the patient has COPD and is at risk of hypercapnic respiratory failure, we will aim for a target SpO2 between 88% to 92%, until blood gas analysis is available but

o  We also need to be aware that some pulse oximeters can underestimate or overestimate oxygen saturation levels, especially if it is borderline and that overestimation has been reported in people with dark skin.

If an ACS is not suspected, we will consider other causes of the chest pain, some of which may be life-threatening such as a PE, aortic dissection or pneumonia.

In these cases, and until a firm diagnosis is made, we will monitor patients with chest pain including:

·      review of symptoms and effect of pain relief

·      pulse and blood pressure

·      heart rhythm

·      oxygen saturation and

·      repeated ECGs 

OK, we have covered so far patients presenting with new onset chest pain. But what should we do for people with suspected stable angina who present with intermittent stable chest pain?

Let’s have a look at this scenario.

We will start the history and examination documenting:

·      the age and sex

·      the characteristics of the pain, including its location, radiation, severity, duration and frequency, and factors that provoke and relieve the pain

·      any associated symptoms, such as breathlessness

·      any history of angina, MI, or other cardiovascular disease 

·      any cardiovascular risk factors and

·      we will exclude other causes of chest pain and examine for non-coronary causes of angina (for example, severe aortic stenosis or cardiomyopathy) 

The diagnosis of stable angina based on our clinical assessment will depend on how typical of angina the chest pain is.

And anginal pain has these main three features:

·      it is constricting in the chest, or in the neck, shoulders, jaw or arms

·      it is precipitated by physical exertion and

·      it is relieved by rest or GTN within about 5 minutes. 

We will call it typical angina if all three features are present.

We will call it atypical angina if there are only two of the three features present.

And we will call it non-anginal chest pain if only one or none of the features are present.

The factors that make a diagnosis of stable angina more likely are:

·      increased age

·      being male

·      other cardiovascular disease or CAD like, for example, a previous MI and

·      cardiovascular risk factors such as:

o  smoking

o  diabetes

o  hypertension

o  dyslipidaemia or a

o  family history of premature coronary artery disease

On the other hand, features which make a diagnosis of stable angina unlikely are when the chest pain is:

·      continuous or very prolonged 

·      unrelated to activity 

·      brought on by breathing in and / or

·      associated with symptoms such as dizziness, palpitations, tingling or difficulty swallowing

In these cases, we will consider other causes of chest pain such as gastrointestinal or musculoskeletal pain. But if there are cardiovascular risk factors, we will still manage them appropriately.

If we suspect stable angina:

·      we will arrange blood tests to identify conditions which exacerbate angina, such as anaemia,

·      we will only consider chest X‑ray if other diagnoses, such as a lung tumour, are suspected and

·      we will arrange an ECG as soon as possible, even though we will not rule out angina just because the ECG is normal. 

There are a number of ECG changes which may indicate ischaemia or previous infarction. These include:

·      pathological Q waves

·      LBBB and

·      ST‑segment and T wave abnormalities (for example, flattening or inversion). 

If we suspect stable angina:

·      We will consider aspirin until a firm diagnosis is made but we will not offer additional aspirin if they are already taking it regularly or are allergic to it. 

·      We will follow the NICE guideline on stable angina while waiting for the results of investigations and you can check the corresponding episode on stable angina on this channel and 

·      We will refer to cardiology so that they can be offered the necessary diagnostic testing, such as CT coronary angiography or non-invasive functional testing such as myocardial perfusion scintigraphy or stress echocardiography

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.

The video version of this podcast can be found here:

https://youtu.be/z9JZKy592xE

The link to the video on COPD diagnosis can be found here:

https://youtu.be/o_q8TTra3Ys

The link to the video on stable COPD management can be found here:

https://youtu.be/VZMKD0bY1G8

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that I am in no way affiliated with, employed by or funded/sponsored by NICE.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode, I go through the section on exacerbations in the NICE guideline [NG115] on COPD in adults, and also the NICE guideline [NG114] on antimicrobial prescribing on COPD acute exacerbations, always focusing on what is relevant in Primary Care only.

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:

·      Apple podcast: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

·      Spotify: https://open.spotify.com/show/2kmGZkt1ssZ9Ei8n8mMaE0?si=9d30d1993449494e

·      Amazon Music: https://music.amazon.co.uk/podcasts/0edb5fd8-affb-4c5a-9a6d-6962c1b7f0a1/primary-care-guidelines?ref=dm_sh_NnjF2h4UuQxyX0X3Lb3WQtR5P

·      Google Podcast: https://www.google.com/podcasts?feed=aHR0cHM6Ly9mZWVkcy5yZWRjaXJjbGUuY29tLzI1ODdhZDc4LTc3MzAtNDhmNi04OTRlLWYxZjQxNzhlMzdjMw%3D%3D

·      Redcircle: https://redcircle.com/shows/2587ad78-7730-48f6-894e-f1f4178e37c3

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

●       The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The resources consulted can be found here:

Chronic obstructive pulmonary disease in over 16s: diagnosis and management- NICE guideline [NG115] can be found here:

●      https://www.nice.org.uk/guidance/NG115

The visual summary for the treatment of COPD can be found here:

●      https://www.nice.org.uk/guidance/ng115/resources/visual-summary-treatment-algorithm-pdf-6604261741

Chronic obstructive pulmonary disease (acute exacerbation): antimicrobial prescribing - NICE guideline [NG114] can be found here:

●      https://www.nice.org.uk/guidance/ng114

The Medicines and Healthcare products Regulatory Agency advice for restrictions and precautions for using fluoroquinolone antibiotics can be found here:

●      https://www.gov.uk/drug-safety-update/fluoroquinolone-antibiotics-new-restrictions-and-precautions-for-use-due-to-very-rare-reports-of-disabling-and-potentially-long-lasting-or-irreversible-side-effects

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

●       Music provided by Audio Library Plus 

●       Watch: https://youtu.be/aBGk6aJM3IU 

●       Free Download / Stream: https://alplus.io/halfway-through 

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’m Fernando, a GP in the UK. Today we are going to do an up-to-date review of the section on exacerbations in the NICE guideline on COPD in adults, and also the NICE guideline on antimicrobial prescribing for acute exacerbations of COPD, always focusing on what is relevant in Primary Care only. If you wish to know about COPD diagnosis and stable COPD management, please see the corresponding episodes on this channel. The links are in the episode description.

Right, so let’s jump into it.

The first thing to do in General Practice is to determine whether there is a need for hospital treatment or whether the patient can be treated at home. NICE has produced a table including the factors to consider when deciding whether to treat the patient in hospital or in the community. The majority of these factors are straightforward and logical, basically sending to hospital those patients who are more symptomatic, unable to cope at home, frail etc, so I will not labour those points because you can use your clinical judgement when assessing the patient’s symptoms.

Full list for PowerPoint slide:

·      Able to cope at home

·      Breathlessness

·      General condition

·      Level of activity

·      Level of consciousness or confusion

·      On long-term oxygen therapy

·      Social circumstances

·      Rate of onset

·      Significant comorbidity (particularly cardiac disease and insulin-dependent diabetes)

·      CXR abnormality

In terms of examination findings, we will also use our clinical judgement and we will consider sending patients to hospital if they have:

·      Cyanosis

·      Worsening peripheral oedema or an

·      SaO2 < 90%

The diagnosis of an exacerbation is made clinically and does not depend on the results of investigations. However, investigations may sometimes be useful in ensuring appropriate treatment is given. More investigations are recommended for people treated in hospital (who tend to have more severe exacerbations) than for people in the community

For people who have their exacerbation managed in primary care:

·      sputum culture is not routinely recommended but

·      pulse oximetry is of value if there are clinical features of a severe exacerbation.

Increased breathlessness is a common feature of exacerbations, which is usually managed by taking increased doses of short-acting bronchodilators.

Both nebulisers and hand-held inhalers can be used during exacerbations depending on clinical factors. For those admitted to hospital switching them to hand-held inhalers as soon as their condition has stabilised is recommended, because this may allow them to be discharged from hospital earlier. 

In the absence of significant contraindications, we will consider oral steroids in the community for exacerbations with a significant increase in breathlessness. We will offer 30 mg oral prednisolone daily for 5 days, referring to the BNF for guidance as to how to stop it. We will think about osteoporosis prophylaxis for people who need frequent courses of oral corticosteroids. 

For guidance on using antibiotics to treat COPD exacerbations, we will look at its own separate guideline, that is, the NICE guideline on antimicrobial prescribing for acute exacerbations of COPD or NG114.

We will start by saying that a range of factors (including viral infections and smoking) can trigger an exacerbation and that many exacerbations are not caused by bacterial infections so they will not respond to antibiotics

However, some people at risk of exacerbations may have antibiotics to keep at home as part of their exacerbation action plan

Before giving antibiotics, we will take into account:

·      the severity of symptoms and whether they may need to go into hospital

·      previous exacerbation and hospital admission history, and the risk of developing complications

·      previous sputum culture results and

·      the risk of resistance with repeated courses of antibiotics.

If an antibiotic is given, we will advise that symptoms may not be fully resolved when the antibiotic course has been completed

Regardless of whether we give antibiotics or not, we will advise patients to seek further medical advice if symptoms worsen, do not start to improve within an agreed period of time or the patient becomes unwell. In these cases, we will consider:

·      other possible diagnoses, such as pneumonia, cardiorespiratory failure or sepsis and we will also consider

·      antibiotic resistance, and we will send a sputum culture if symptoms have not improved following a course of antibiotics.

We will refer for specialist advice and consideration of intravenous antibiotics if:

·      symptoms are not improving with repeated courses of oral antibiotics or

·      there are bacteria that are resistant to oral antibiotics or

·      the patient cannot take oral medicines

When prescribing an antibiotic for an acute exacerbation of COPD, we will follow the following recommendations:

The first-line oral antibiotics are:

·      Amoxicillin: 500 mg three times a day for 5 days (or an increased dose in severe infections)

·      Doxycycline: 200 mg on first day, then 100 mg once a day for 5‑day course in total (or an increased dose of 200mg daily in severe infections) or

·      Clarithromycin: 500 mg twice a day for 5 days

We will consider Second-line oral antibiotics if there is no improvement in symptoms on first choice taken for at least 2 to 3 days; guided by susceptibilities when available. In that case we will:

·      Use and alternative first line antibiotic

An alternative choice oral antibiotics for patients at higher risk of treatment failure would be:

·      Co‑amoxiclav: 500/125 mg three times a day for 5 days

·      Co‑trimoxazole: 960 mg twice a day for 5 days

·      Levofloxacin: 500 mg once a day for 5 days (but we will offer this with specialist advice if co‑amoxiclav or co‑trimoxazole cannot be used and after considering safety issues

Further general treatment considerations are as follows:

We will check the BNF for appropriate use and dosing in specific populations, for example, in hepatic impairment, and renal impairment.

If a person is having antibiotic prophylaxis, acute treatment should be with an antibiotic from a different class.

People who may be at a higher risk of treatment failure include people who have had repeated courses of antibiotics, a previous or current sputum culture showing resistant bacteria, or people at higher risk of developing complications.

Co‑trimoxazole should only be considered for use in acute exacerbations of COPD when there is bacteriological evidence of sensitivity

We will also follow the MHRA advice for restrictions and precautions for using fluoroquinolone antibiotics due to very rare reports of disabling and potentially long-lasting or irreversible side effects affecting musculoskeletal and nervous systems. Warnings include: stopping treatment at first signs of a serious adverse reaction (such as tendonitis), prescribing with special caution in people over 60 years and avoiding coadministration with a corticosteroid.

And finally, we will consider physiotherapy using positive expiratory pressure devices for selected people with exacerbations of COPD, to help with clearing sputum. 

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.

The video version of this podcast can be found here:

https://youtu.be/VZMKD0bY1G8

The link to the video on COPD diagnosis can be found here:

https://youtu.be/o_q8TTra3Ys

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that I am in no way affiliated with, employed by or funded/sponsored by NICE.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode, I go through the management section of the NICE guideline [NG115] on COPD in adults, always focusing on what is relevant in Primary Care only.

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:

·      Apple podcast: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

·      Spotify: https://open.spotify.com/show/2kmGZkt1ssZ9Ei8n8mMaE0?si=9d30d1993449494e

·      Amazon Music: https://music.amazon.co.uk/podcasts/0edb5fd8-affb-4c5a-9a6d-6962c1b7f0a1/primary-care-guidelines?ref=dm_sh_NnjF2h4UuQxyX0X3Lb3WQtR5P

·      Google Podcast: https://www.google.com/podcasts?feed=aHR0cHM6Ly9mZWVkcy5yZWRjaXJjbGUuY29tLzI1ODdhZDc4LTc3MzAtNDhmNi04OTRlLWYxZjQxNzhlMzdjMw%3D%3D

·      Redcircle: https://redcircle.com/shows/2587ad78-7730-48f6-894e-f1f4178e37c3

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

●       The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The resources consulted can be found here:

Chronic obstructive pulmonary disease in over 16s: diagnosis and management- NICE guideline [NG115]:

●      https://www.nice.org.uk/guidance/NG115

The visual summary for the treatment of COPD can be found here:

●      https://www.nice.org.uk/guidance/ng115/resources/visual-summary-treatment-algorithm-pdf-6604261741

The NICE technology appraisals on oseltamivir, amantadine and zanamivir to prevent and treat flu can be found here:

●      https://www.nice.org.uk/guidance/ta158

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

●       Music provided by Audio Library Plus 

●       Watch: https://youtu.be/aBGk6aJM3IU 

●       Free Download / Stream: https://alplus.io/halfway-through 

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’m Fernando, a GP in the UK. Today we are going to do an up-to-date review of the NICE guideline on the management of stable COPD in adults, always focusing on what is relevant in Primary Care only. If you wish to know about COPD diagnosis, please see the corresponding episode on this channel. The link is in the episode description.

Right, so let’s jump into it.

For COPD management, once we have offered smoking cessation advice and support, we will offer inhaled therapy.

Let’s have a look at the different types of inhalers. We have:

·      Short-acting beta2 agonists or SABAs, like salbutamol

·      Short-acting muscarinic antagonists or SAMAs, like ipratropium

·      Inhaled corticosteroids (ICS)

·      Long-acting muscarinic antagonists or LAMAs and

·      Long-acting beta2 agonists or LABAs

When do we use the different types of inhalers? Well, these are the general rules to follow:

·      We will use short-acting bronchodilators, that is, either SABAs or SAMAs, as necessary, to relieve breathlessness and exercise limitation. 

·      We will judge the effectiveness of bronchodilator therapy depending on symptom improvement, not just lung function alone.

·      We will not use oral corticosteroid reversibility tests to identify who should be prescribed inhaled corticosteroids, because oral steroids do not predict response to inhaled corticosteroid therapy. 

·      We will take into account the risk of side effects (including pneumonia) of inhaled corticosteroids for COPD

·      Inhaled combination therapy refers to combinations of a LAMA, a LABA and inhaled corticosteroids (ICS) and

·      Combination therapy is recommended in confirmed COPD with SOB or exacerbations despite short-acting bronchodilators

Let’s now look at the different combinations and when to recommend them.

We will offer a LAMA+LABA combination if there are no asthmatic features or features suggesting steroid responsiveness. This includes a previous diagnosis of asthma or of atopy, a higher blood eosinophil count, substantial variation of at least 400 ml in FEV1 over time or substantial diurnal variation of at least 20% in peak flow rate

On the other hand, we will consider a LABA+ICS combination if these asthmatic features or features suggesting steroid responsiveness, are present. 

And let’s stop for a moment to remark that the LAMA + ICS dual combination does not appear as a recommended option.

Now, what can be recommended after dual combination therapy is triple combination therapy with a LAMA+LABA+ICS. Triple therapy is recommended if:

·      they have a severe exacerbation, that is, requiring hospitalisation or

·      they have 2 moderate exacerbations, that is, requiring oral steroids and/or antibiotics, within a year, or if

·      they have significant symptoms. However, for those patients on a LAMA+LABA combination, that is, patients without asthmatic features or features suggestive steroid responsiveness, we will:

o  first give a trial of LAMA+LABA+ICS for 3 months only and then review:

§ if symptoms have not improved, we will revert to the LAMA+LABA combination but

§ if symptoms have improved, we will continue with the LAMA+LABA+ICS triple combination 

NICE has produced a one-page visual summary covering non-pharmacological management and use of inhaled therapies in COPD, which I will review at the end of this episode.

Now, let’s focus on inhaled therapy a bit more. What delivery systems can be used to deliver inhaled therapy?

·      Although alternatives can be offered, if necessary, in most cases a hand-held inhaler (including a spacer if appropriate) is best. In that case, 

o  We will give advice on spacer cleaning, telling them:

§ Not to clean the spacer more than monthly, washing it warm water and washing-up liquid, and allowing it to air dry.

§ This is to avoid build-up of static which can affect its performance.

·      We will consider nebuliser therapy if there are significant symptoms despite maximal inhaler therapy and we will continue only if there is symptomatic improvement. And

·      We will offer a choice between a facemask and a mouthpiece, unless the drug specifically requires a mouthpiece (for example, anticholinergic drugs). 

What oral therapy can be given in COPD? Well:

·      Long-term use of oral corticosteroid therapy in COPD is not normally recommended. Some people with advanced COPD may need long-term oral steroids if they cannot be stopped following an exacerbation. In these cases, the dose should be kept as low as possible.

o  We will monitor people on long-term oral steroid therapy and give them osteoporosis prophylaxis, if appropriate. However, we will start osteoporosis prophylaxis without the need for monitoring in patients over 65. 

·      We will consider mucolytic drug therapy for people with a chronic cough productive of sputum. 

·      Oral anti-oxidants and oral anti-tussive therapy are not recommended and

·      Before starting prophylactic antibiotics, we should seek specialist input is needed. 

o  Azithromycin, usually 250 mg 3 times a week can be given if certain conditions are met. Because we will normally by guided by secondary care, I will not go through all these conditions and precautions here.

o  For people who are taking prophylactic azithromycin and are still at risk of exacerbations, we can provide a non-macrolide antibiotic to keep at home as part of their exacerbation action plan, explaining that it is not necessary to stop prophylactic azithromycin during an acute exacerbation.

In this episode, I will not cover the management of pulmonary hypertension and co pulmonale and the use of:

·      Oral phosphodiesterase-4 inhibitors

·      Non-invasive ventilation

·      Oxygen therapy, either long-term, ambulatory or as short-bursts and

·      Oral theophylline, except for saying that we should reduce the dose prescribing drugs that interact with it such as macrolide or fluoroquinolone antibiotics

In terms of self-management, we will develop an individualised self-management plan including an exacerbation action plan if the patient is at risk of exacerbations. For this we will offer them a short course of oral steroids and antibiotics to keep at home as part of their exacerbation action plan if:

·      they have had an exacerbation within the last year, and remain at risk of exacerbations

·      they understand when and how to take them and

·      they inform their healthcare professional when they have used them, and ask for replacements

There is a separate guidance on the choice of antibiotics for acute COPD exacerbations. I will cover these recommendations in my next video on COPD exacerbation management.

For people who have used 3 or more courses of oral corticosteroids and/or oral antibiotics in the last year, we will investigate the possible reasons for this. 

We will offer pulmonary rehabilitation to those functionally disabled by COPD, usually with an MRC dyspnoea grade 3 and above. Pulmonary rehabilitation is not suitable for people who are unable to walk, who have unstable angina or who have had a recent myocardial infarction. 

We will offer pneumococcal vaccination and an annual flu vaccination to all people with COPD,

There is separate guidance on the use on antivirals to prevent and treat flu, which I will not cover here. I have put the link to it in the episode description.

We should consider physiotherapy for people have excessive sputum, so that they can be taught:

·      how to use positive expiratory pressure devices

·      active cycle of breathing techniques. 

We will monitor:

·      for the development of anxiety and depression and

·      Their nutritional state and BMI. Whilst the NICE guideline on obesity states that a healthy BMI is between 18.5 to 24.9 , this may not be appropriate for people with COPD, where it is recommended a BMI between 20 and 25. With that in mind, we will:

o  refer for dietetic advice if they have an abnormal BMI and

o  for people with a low BMI, we will give nutritional supplements and encourage them to exercise

We will regularly ask people with COPD about their ability to undertake daily activities and assess their need for occupational therapy. 

We will also consider referring people for assessment by social services if they have disabilities caused by COPD. 

When appropriate, palliative care for end-stage COPD, may include the following treatments for breathlessness that is unresponsive to other therapies:

·      Opioids

·      Benzodiazepines

·      Tricyclic antidepressants

·      Major tranquillisers and

·      Oxygen

During follow-up of all people with COPD we should:

·      Include smoking cessation

·      Record spirometric parameters and a loss of 500 ml or more over 5 years in FEV1 suggests rapidly progressing disease which may need specialist referral and investigation. 

During the clinical review we will cover the following issues:

In mild/moderate/severe COPD (stages 1 to 3) we will:

·      Review them at least annually

·      We will assess:

o  Smoking status

o  Symptom including breathlessness, exercise tolerance and exacerbation frequency

o  Need for pulmonary rehabilitation

o  Presence of complications and

o  Medication, including inhaler technique

·      We will measure FEV1, FVC, BMI and MRC dyspnoea score

In very severe COPD (stage 4) in addition to this, we will :

·      Review them at twice a year

·      We will assess:

o  The Presence of cor pulmonale

o  The need for long term oxygen therapy

o  The nutritional state

o  The presence of depression

o  The need for referral to social services, occupational therapy and for specialist input

As I mentioned earlier, NICE has produced a one-page visual summary covering non-pharmacological management and use of inhaled therapies. Let’s have a look at it now:

So, once we have confirmed the diagnosis of COPD

We will cover the fundamentals of COPD care, that is, we will offer treatment and support to stop smoking, pneumococcal and influenza vaccinations, pulmonary rehabilitation if appropriate, develop a personalised self-management plan and we will also optimise treatment for comorbidities

And we will revisit these plans at every review

Then we will start inhaled therapies only if, after doing all this, they are needed to relieve breathlessness and exercise limitation, as long as they can demonstrate satisfactory inhaler technique

And we will review the medication and assess inhaler technique and adherence regularly

So, we will offer a SABA or a SAMA inhaler to use on demand

And if the patient still has symptoms or has exacerbations despite treatment

We will see if there are asthmatic features or features of steroid responsiveness.

And let’s remember that these features in this context include any previous secure diagnosis of asthma or atopy, a higher blood eosinophil count, a substantial variation in FEV1 over time , that is, at least 400 ml, or a substantial diurnal variation in peak expiratory flow of at least 20%.

So, if these features are not present

We will offer the combination of a LAMA and a LABA

And if despite this, the patient’s symptoms are not adequately controlled

We will consider 3-month trial of triple therapy with a LAMA, a LABA and an ICS

Bearing in mind the increased risk of side effects of ICS (including pneumonia) and we will document in the clinical records the reason for continuing the ICS treatment.

But, if there is no improvement, we will revert to dual therapy with a LAMA + LABA

If the issue with the LAMA LABA combination is that the patient has 1 severe or 2 moderate exacerbations within a year

Then we will also consider triple therapy with a LAMA a LABA and an ICS. This is because ICS have been proven to help reduce exacerbations

On the other hand, if the patient on a SABA or SAMA has asthmatic features or features suggesting steroid responsiveness

Then we will offer treatment with a combination of a LABA and an ICS

And if the patient continues to have significant symptoms, or has 1 severe or 2 moderate exacerbations within a year

Then we will offer triple therapy with a LABA a LAMA and an ICS

And, for all these patients, if symptoms or exacerbations continue to be a problem, we will explore further treatment options, including referral.

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.

The video version of this podcast can be found here:

·      https://youtu.be/5aV0krXAuj8

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". 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 NICE.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I will go through new and updated guidelines published in June 2024 by the National Institute for Health and Care Excellence (NICE), focusing on those that are relevant to Primary Care only.

Because there were no updates relevant to Primary Care, instead in this episode I will go through the current four consultations open by NICE, also focusing on aspects that are relevant to Primary Care only.

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:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

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

The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The YouTube video on the management of headaches can be found here:

·      https://youtu.be/6AZttMzfFr0?si=yxPcoC4legE8zS_p

The Full NICE News bulletin for June 2024 can be found here:

·      https://www.nice.org.uk/guidance/published?from=2024-06-01&to=2024-06-30&ndt=Guidance&ndt=Quality+standard

The links to the current consultations can be found here:

Digital supported self-management technologies for adults with chronic obstructive pulmonary disease: early value assessment:

·      https://nice.us8.list-manage.com/track/click?u=7864f766b10b8edd18f19aa56&id=9f762dc422&e=03ed9b0dd0

12 SQ-HDM SLIT for treating allergic rhinitis and allergic asthma caused by house dust mites:

·      https://nice.us8.list-manage.com/track/click?u=7864f766b10b8edd18f19aa56&id=501af7f75a&e=03ed9b0dd0

Meningitis (bacterial) and meningococcal disease update:

·      https://nice.us8.list-manage.com/track/click?u=7864f766b10b8edd18f19aa56&id=4baddb7b5d&e=03ed9b0dd0

Asthma: diagnosis, monitoring and chronic asthma management:

·      https://nice.us8.list-manage.com/track/click?u=7864f766b10b8edd18f19aa56&id=d7e86c9fd8&e=03ed9b0dd0

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

Music provided by Audio Library Plus 

Watch: https://youtu.be/aBGk6aJM3IU 

Free Download / Stream: https://alplus.io/halfway-through 

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 were supposed to look at the NICE updates relevant to Primary Care published in June 2024. However, this month we have had no new guidance relevant to primary care, as they were all connected to secondary care such as surgical techniques, chemotherapy agents, and acute myeloid leukaemia, amongst others.

So, instead, we are going to look forward and review the guidelines that are under consultation, which will lead to new or updated guidance in the coming months. Because they are in draft form, we will only give them a quick overview. They are only four areas, so today will be a brief episode. 

So, let’s jump into it.

The first consultation is on House Dust Mite Sublingual Immunotherapy, for treating allergic rhinitis and allergic asthma caused by house dust mites.

This is referred to by NICE as 12 SQ HDM SLIT, which is a tablet, also known as Acarizax, which has already been authorised by European regulatory authorities. Let’s have a look at some key points:

It is recommended for:

HDM-Induced Allergic Asthma that is not well-controlled by inhaled steroids and

Mild to severe HDM Allergic Rhinitis but it’s only

Approved for adults aged 18 to 65 years of age

From a patient perspective these conditions can be debilitating, and they have an impact on daily life. Although there are other treatments available, their management can be challenging when triggers are unexpected or outside people’s control.

HDM SLIT (House Dust Mite Sublingual Immunotherapy) involves the administration of allergens (in this case, house dust mites) under the tongue to desensitise the immune system to these allergens, reducing symptoms over time.

It is done using a sublingual tablet that dissolves under the tongue. The goal is to gradually train the immune system to tolerate the allergen through desensitisation or tolerance induction.

The treatment typically lasts several months to a few years, depending on the patient's response and the specific protocol being followed.

Over time, patients usually experience a reduction in symptoms and long-lasting relief, even after the treatment has ended.

It is generally considered safe, with the most common side effects being oral itching or discomfort. Serious allergic reactions are rare but can occur, so initial close medical monitoring is recommended.

The effectiveness can vary depending on the person and it is an alternative to subcutaneous immunotherapy. The sublingual route is preferred because of convenience and a better safety profile due to lower risk of severe allergic reactions.

The next consultation is on new quality statements on bacterial meningitis and meningococcal disease. The statements that we should be aware of in Primary care are that people who have had bacterial meningitis or meningococcal disease should have:

·      An audiological assessment within 4 weeks of them being well enough for testing and

·      A follow-up appointment in secondary care within 6 weeks of discharge from hospital.

In the third consultation NICE evaluates various digital self-management technologies for adults with COPD. These technologies aim to support patients in managing their condition at home, potentially reducing symptoms and improving patient outcomes.

Some of the key technologies being assessed include digital platforms that offer:

·      Pulmonary rehabilitation

·      Remote monitoring

·      Weekly check-ins from healthcare professionals

·      Educational modules on exercises and medication and

·      Mindfulness exercises

NICE states that, although a digital technology will not replace face-to-face appointments, offering digital technologies as an option could improve access and reduce symptoms and exacerbations. Furthermore, there have been no safety concerns for this type of supported self-management.

And the final consultation is a very important one for us, because it is an update on asthma.

The draft guideline on the diagnosis, monitoring, and management of chronic asthma has been produced collaboratively by the British Thoracic Society, NICE, and the Scottish Intercollegiate Guidelines Network or SIGN. It will update the previous 2017 NICE guideline and 2019 BTS/SIGN guideline. It will not cover the management of acute asthma.

The update reviews questions like, for example, whether spirometry with bronchodilator reversibility should be routinely used in the diagnosis of asthma or whether the bronchodilator response (using peak flow or FEV1) should be calculated as a percentage change from the baseline result, as it is now, or change it to being related to the predicted FEV1

The draft document is large so I will not be able to summarise it here. Besides, it will be better to wait for the final guidance just in case the recommendations change at the last minute. But at least it gives us some awareness of what it is to come on that front.

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.