Primary Care Guidelines

The video version of this podcast can be found here:

·      https://youtu.be/k6amIFy84Bc

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 the NICE guideline on acute kidney injury, NG148, focusing on what is relevant to Primary Care only, covering the diagnosis, and investigations, as well as the recommendations on the use of contrast media.

In the next episode we will cover the management recommendations by NICE, and the Primary Care flowchart on AKI by Barnsley Hospital NHS Trust and King’s College Hospital NHS Trust, so stay tuned.

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.  

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 

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 guidance covered in this episode can be found here:

Acute kidney injury: prevention, detection and management (NG148):

·      https://www.nice.org.uk/guidance/ng148

The 1-page visual summary on assessing the risk of acute kidney injury in adults having iodine-based contrast media: outpatient, non-urgent inpatient and community settings:

·      https://www.nice.org.uk/guidance/ng148/resources/visual-summary-pdf-13551376429

The algorithm for early identification of acute kidney injury, endorsed by NHS England:

·      https://www.england.nhs.uk/akiprogramme/aki-algorithm/

The Management of acute kidney injury in adults in Primary Care by Barnsley Hospital NHS Trust:

·      https://best.barnsleyccg.nhs.uk/media/hruaaymn/best-december-2015-barnsley-aki-primary-careguidance-pathway.pdf?form=MG0AV3

The Adult Acute Kidney Injury Care Pathway for Primary Care by King’s College Hospital NHS Trust:

·      https://www.kch.nhs.uk/wp-content/uploads/2023/01/mi-169.2-adult-acute-kidney-injury-care-pathway.pdf

A calculator for the National Early Warning Score (NEWS):

·      https://www.mdcalc.com/calc/1873/national-early-warning-score-news

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 will go through the NICE guideline on acute kidney injury focusing on what is relevant in Primary Care only. In this episode, we will cover the diagnosis, and investigations, as well as the recommendations on the use of contrast media. In the next episode we will cover the management recommendations by NICE, and the Primary Care flowchart on AKI by Barnsley Hospital NHS Trust and King’s College Hospital NHS Trust, so stay tuned.

Right, let’s jump into it.

In order to identify acute kidney injury, we will check serum creatinine and compare it with baseline. AKI is most often seen during episodes of acute illness so we should do this screening in people with acute illness if there is:

• Pre-existing CKD (or eGFR less than 60)
• heart failure
• liver disease
• diabetes
• history of acute kidney injury
• oliguria (that is, a urine output less than 0.5 ml/kg/hour)
• neurological or cognitive impairment or disability, which may mean limited access to fluids
• hypovolaemia
• use of certain drugs such as NSAIDs, aminoglycosides, ACE inhibitors, ARBs and diuretics within the past week, especially if hypovolaemic
• use of iodine-based contrast media within the past week
• symptoms or risk of urological obstruction,
• sepsis
• deteriorating early warning scores and
• young age or age 65 years or over 

In addition, for children and young people we should also screen for AKI if there is:

• severe diarrhoea (particularly bloody diarrhoea)
• symptoms or signs of nephritis (such as oedema or haematuria)
• haematological malignancy and
• hypotension

However, AKI can also happen in the absence of an acute illness. So, if there is a rise in serum creatinine, we should still consider AKI rather than a worsening of their chronic disease if there is:

• CKD, especially if eGFR is less than 45
• urological disease or symptoms
• symptoms suggesting complications of acute kidney injury, like fluid overload, oliguria, hypertension, electrolyte imbalance or hypertension and finally
• symptoms of a multi‑system disease, such as, for example a purpuric rash 

There is a small but increased risk of acute kidney injury associated with an eGFR less than 30 when having iodine-based contrast media. Iodine contrast media is commonly used in a variety of investigations such as CT scans, angiography, and intravenous urography.

So, how do we assess the risk of AKI in these patients?

Well, before requesting a non-urgent CT scan with contrast, we should assess whether the person has pre-existing kidney disease. 

If available, we will use an eGFR measurement from the past 6 months. If the person has been acutely unwell or clinically unstable since their last eGFR test, we should request a more recent eGFR. 

If no eGFR is available from the past 6 months, we will ask the following screening questions:

• do they have kidney disease or a kidney transplant?
• have they seen or are waiting to see a nephrologist or urologist?
• do they have symptoms of acute illness likely to cause acute kidney injury such as diarrhoea, vomiting, fever, hypovolaemia, infection or difficulty passing urine? 

If the answer to any of the screening questions is yes, then we should request a new eGFR. However, if the screening questions do not indicate a problem and the person is clinically stable, NICE says that we could consider proceeding without the need for further blood tests before the scan. However, in practice and as a safety measure, it is likely that we will request the eGFR anyway, just in case.

In order to prevent and reduce the risk of AKI, we will encourage oral hydration before and after procedures using intravenous iodine-based contrast media. In addition, we will consider temporarily stopping ACE inhibitors and ARBs if they have CKD with an eGFR less than 30. NICE has produced a 1-page visual summary on assessing the risk of AKI in adults having iodine-based contrast media and I have put the link to it in the episode description.

Now, how do we prevent deterioration in people with AKI or at high risk of it?

Well, we will obviously use our clinical judgement, follow prescribing recommendations in our electronic clinical systems and consider optimising medication, such are stopping nephrotoxic drugs and adjusting doses according to renal function.

We should also consider temporarily stopping ACE inhibitors and ARBs in people with diarrhoea, vomiting or sepsis until they have improved. 

So, we screen for AKI by checking renal function on a blood test. But, how do we actually diagnose acute kidney injury?

Well, we will use any of the following criteria:

• a fall in urine output to less than 0.5 ml/kg/hour for more than 6 hours in adults and more than 8 hours in children and young people
• a rise in creatinine of 26 micromol/litre or greater within 48 hours
• a 50% or greater rise in creatinine known or presumed to be within the past 7 days or
• a 25% or greater fall in eGFR in those aged under 18 years within the past 7 days. 

There is also an algorithm that we can follow for early identification of acute kidney injury. However, it is fairly complex so I will not go through it here. You can find a link to it in the episode description.

We will obviously monitor creatinine regularly in those with AKI or at risk of it. The frequency of monitoring should vary according to clinical need. 

In terms of investigations, in order to identify the cause of AKI, NICE recommends that:

·      We should do a urine dipstick for urinalysis as soon as possible and take appropriate action when results are abnormal. For example, we should think about a diagnosis of acute nephritis when there is no obvious cause and the urine dipstick shows haematuria and proteinuria, without a UTI or trauma due to catheterisation. 

·      We should not routinely request an ultrasound scan if the cause of the AKI is known. However, if there is no identified cause for the AKI or the patient is at risk of urinary tract obstruction, the patient should have an urgent ultrasound within 24 hours, so, in practice, these patients are likely to need referral to the emergency department. This is even more so when pyonephrosis (that is, an infected and obstructed kidney) is suspected, given that the ultrasound should be performed within 6 hours in these cases.

So that is it, a review of the NICE guideline on AKI covering the diagnosis, and initial investigations. Make sure not to miss the next episode where we will cover the management recommendations.

We have come to the end of this episode. Remember that this is not medical advice but 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/hN5JRXItBJ4

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 October 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.   

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 

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 October 2024 can be found here:

·      https://www.nice.org.uk/guidance/published?from=2024-10-01&to=2024-10-31&ndt=Guidance&ndt=Quality+standard

The links to the guidance covered in this episode can be found here: 

Digital technologies for assessing attention deficit hyperactivity disorder (ADHD):

·      https://www.nice.org.uk/guidance/dg60

Acute kidney injury: prevention, detection and management:

·      https://www.nice.org.uk/guidance/ng148

The 1-page visual summary on assessing the risk of acute kidney injury in adults having iodine-based contrast media: outpatient, non-urgent inpatient and community settings:

·      https://www.nice.org.uk/guidance/ng148/resources/visual-summary-pdf-13551376429

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 October 2024, focusing on what is relevant in Primary Care only.  

Although most of the updates do not really relate to Primary Care, there were two areas that I found particularly interesting and relevant to us, ADHD and acute kidney injury.

Right, let’s get started. 

We will start with digital technologies for assessing ADHD.  

Let’s remember that attention deficit hyperactivity disorder (or ADHD) is a neurodevelopmental condition characterised by a persistent pattern of hyperactivity, impulsivity, and inattention that interferes with daily and occupational functioning.

As a result, people with ADHD may make important decisions hastily without considering the long-term consequences.

Treatment may be non-pharmacological, including psychoeducation, ADHD coaching, or environmental changes. Pharmacological treatment may include stimulant or non-stimulant medication.

There is a perception that recently there has been a huge increase in the demand for ADHD services because of an increased awareness of this condition. The global prevalence of ADHD in children is estimated to be around 5% and, in the UK, the prevalence of ADHD in adults is estimated to be between 3% and 4%, being more commonly diagnosed in males than females.

Following the current care pathway, people with suspected ADHD are referred to secondary care for assessment, which is based on clinical judgement, relying on information obtained from a range of sources. However, information from these sources may often be incomplete or contradictory, and the diagnosis may be further complicated due to an overlap with other disorders and mental health conditions, which usually causes an extended delay in reaching a diagnostic decision.

This is why, many digital technologies have been developed to assist in the diagnosis, which could reduce patient waiting lists and free up NHS resources. And it is precisely these digital technologies that have been assessed by NICE.

And one of these technologies is called the QbTest.

What is the QbTest?

Well, the QbTest has certain elements comparable to a computer game which measures the core symptoms of ADHD, that is, attention, impulsivity, and hyperactivity. Results from the test are compared with people without ADHD and the results are available within minutes. Trial evidence suggests that QbTest could reduce the time that it takes to make the diagnosis.

So, NICE has concluded that using QbTest alongside a standard clinical assessment was a cost-effective use of NHS resources for assessing ADHD in children and young people. However, because of lack of evidence, it is not recommended for the diagnosis in adults, or to evaluate response to treatment for those already with an ADHD diagnosis. For them, further research has been recommended.  

Right, let’s move to our next area, acute kidney injury.  

The actual update in the acute kidney injury guideline refers to the recommendations for people having iodine-based contrast scans. I will go through this section today, but given that acute kidney injury is such an important issue, I will dedicate the next episode to it, so stay tuned.

We need to be aware that there is a small but increased risk of acute kidney injury associated with an eGFR less than 30 when having iodine-based contrast media. Iodine contrast media is commonly used in a variety of investigations such as, for example, CT scans, angiography, and intravenous urography.

So, how do we assess the risk of AKI in these patients?

Well, before requesting a non-urgent iodine-based contrast media CT scan, we should assess whether the person has pre-existing kidney disease. 

If available, we will use an eGFR measurement from the past 6 months. However, if the person has been acutely unwell or clinically unstable since their last eGFR test, we should request a more recent eGFR. 

If no eGFR is available from the past 6 months, we will ask the following screening questions:

• do they have kidney disease or a kidney transplant?
• have they seen or are waiting to see a nephrologist or a urologist?
• do they have symptoms of acute illness likely to cause acute kidney injury such as diarrhoea, vomiting, fever, hypovolaemia, infection or difficulty passing urine? 

If the answer to any of the screening questions is yes, then we should request an eGFR. However, if the screening questions do not indicate a problem and the person is clinically stable, NICE says that we could consider proceeding without the need for further blood tests before the scan. However, in practice, and as a safety measure, it is likely that we will request the eGFR anyway, just in case.

In order to prevent and reduce the risk of AKI, we will encourage oral hydration before and after procedures using this type of contrast, especially if they are at increased risk of contrast-associated acute kidney injury.

In addition, we will consider temporarily stopping ACE inhibitors and ARBs in people having iodine-based contrast media if they have CKD with an eGFR less than 30. 

NICE has produced a 1-page visual summary on assessing the risk of acute kidney injury in adults having non-urgent iodine-based contrast media. I have put a link to it in the episode description but let’s quickly have a look at it.

Firstly, a reminder that this is for non-urgent cases, where a delay in the investigation is unlikely to be clinically significant.

Then, we will assess whether the patient has pre-existing kidney disease, and discuss the pros and cons, being aware that there is a small risk of AKI when eGFR is less than 30.

Then we will check if we have an eGFR value within 6 months

And if so,

We will use this value for our decision

But bearing in mind that if the person has been unwell or unstable, we should consider repeating the test.

However, if we don’t have an eGFR value within 6 months

We will ask our screening questions about kidney disease, renal transplant, referral to urology or nephrology and any symptoms of acute illness

And if there are any risk factors for AKI

We will consider checking eGFR before proceeding.

But if there are no risk factors for AKI

We will be able to proceed without needing to request further blood tests, although in practice we will probably request a new eGFR anyway.

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.

For the introductory video on cardiovascular risk reduction and lipid modification:

·      https://youtu.be/jIhlkmOcsiI 

For the second video on cardiovascular risk reduction and lipid modification:

·      https://youtu.be/QyN3toBGCNU 

For the NICE guidance on cardiac chest pain video: 

·      https://youtu.be/so97zARpmME 

For the NICE management of stable angina video: 

·      https://youtu.be/BtWs0VHjp00  

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 review the NICE guideline “Cardiovascular disease: risk assessment and reduction, including lipid modification” [NG238], published on 14 December 2023, focusing on what is relevant in Primary Care only. I cover statins for both primary and secondary prevention, assessing response to treatment, optimising therapy and what to do when statins are contraindicated or not tolerated.  

If you have not already done so, I recommend my previous introductory video on the subject covering CVD risk assessment, recommendations for specialist referral and considerations before starting statin therapy. The link is shown above. 

For a refresher on the NICE guidance on cardiac chest pain and the management of stable angina, please refer to the corresponding episodes on this channel. The links are shown above. 

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

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 

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 NICE guideline “Cardiovascular disease: risk assessment and reduction, including lipid modification” [NG238] Published: 14 December 2023 can be found here:

·      https://www.nice.org.uk/guidance/ng238

The online version of QRISK3 can be found here:

·      https://qrisk.org/

The QRISK3-lifetime tool can be found here:

·      https://qrisk.org/lifetime/index.php

The NICE guideline on familial hypercholesterolaemia can be found here:

·      https://www.nice.org.uk/guidance/cg71

The Simon Broome criteria for the diagnosis of familial hypercholesterolaemia can be found here:

·      https://www.nice.org.uk/guidance/cg71/evidence/full-guideline-appendix-f-pdf-241917811

The Dutch Lipid Clinic Network (DLCN) criteria for the diagnosis of familial hypercholesterolaemia can be found here:

·      https://www.mdcalc.com/calc/3818/dutch-criteria-familial-hypercholesterolemia-fh

Transcript

If you're 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’ll look at the NICE guideline on cardiovascular risk reduction and lipid modification, or NG238, which was published in December 2023, focusing on what is relevant in Primary Care only. In this episode we are going to cover statins for both primary and secondary prevention, assessing response to treatment, optimising therapy and what to do when statins are contraindicated or not tolerated.  

If you have not already done so, I recommend that you listen to the previous introductory episode on the subject covering CV risk assessment, recommendations for specialist referral and considerations before starting statin therapy. The link is in the episode description. 

If you’d like a refresher on the NICE guidance on cardiac chest pain and the management of stable angina, please refer to the corresponding episodes on this channel. The links are also in the episode description. 

Right, let’s jump into it. 

We are going to start reviewing the prescribing of statins for the primary prevention of cardiovascular disease. 

And, before offering a statin, we will discuss the benefits of lifestyle changes and optimise the management of all other modifiable CVD risk factors if possible. Then, if lifestyle changes are not sufficient, we will offer statin treatment. 

Equally, before starting statins, we will treat comorbidities and secondary causes of dyslipidaemia, which include, for example, excess alcohol, uncontrolled diabetes, hypothyroidism, liver disease and nephrotic syndrome. 

Is there a cholesterol target for primary prevention?

And the answer is yes. For primary prevention of CVD, we should aim for a greater than 40% reduction in non-HDL cholesterol. 

So, who should get statins for primary prevention?

Well, we will offer atorvastatin 20 mg for the primary prevention of CVD to people with and without type 2 diabetes who have a 10‑year QRISK3 score of 10% or more. However, NICE states that we should not rule out statins just because the QRISK3 score is less than 10% if there is a patient preference for taking it or there is concern that risk may be underestimated. 

Let’s remember that we do not estimate QRISK3 for people already with an increased CV risk, that is those aged 85 and older, people with type 1 diabetes and people with CKD. What do we do with them?

Well, for those aged 85 and older, we should also consider treatment with atorvastatin 20 mg because they are at increased risk because of age alone, obviously being aware that there may factors that may make treatment inappropriate

For the second group, that is, those with type 1 diabetes, NICE makes a distinction as to when we must definitely offer a statin and when we should simply consider it. But in summary, atorvastatin 20mg daily should be considered for everyone with type 1 diabetes over the age of 18, irrespective of the duration of their diabetes. This advice is even more emphatic if:

• they are over 40 or
• they have had diabetes for more than 10 years or
• they have established nephropathy or
• they have other CVD risk factors. 

Although it may be simpler for us to remember that all people with type 1 diabetes over the age of 18 would benefit from atorvastatin 20 mg. 

And for the third group, that is, for people with CKD, we will review their guidance a little later. This is because the management in CKD is the same for both primary and secondary prevention and it will be better to discuss it after we go through the recommendations for secondary prevention.

So, what are the recommendations for secondary prevention of cardiovascular disease?

Well, these recommendations apply to those with pre-existing cardiovascular disease both with and without type 1 and 2 diabetes. However, they do not apply to people with CKD, which we will discuss separately.

What is the lipid target in secondary prevention?

Well, we should aim for LDL levels of 2.0 mmol per litre or less, or non-HDL cholesterol levels of 2.6 mmol per litre or less. 

And to achieve this, we will offer atorvastatin 80 mg, whatever their cholesterol level, although we would offer a lower dose if:

• it could react with other drugs
• there is a high risk of adverse effects or
• the person would prefer to take a lower dose. 

We will discuss lifestyle changes at the same time but we should not delay statin treatment because of it. 

Also, in primary prevention we were advised to treat comorbidities and secondary causes of dyslipidaemia before starting statins. However, in secondary prevention, we will do this at the same time as starting statin treatment.

If the person is taking the maximum tolerated dose and intensity of statin but the lipid target for secondary prevention of CVD is not met, we should consider additional lipid-lowering treatments and for this we should consider ezetimibe as well as injectables such as alirocumab, evolocumab and inclisiran, each one of which has their own NICE guidance.

However, we can consider ezetimibe in addition to the maximum tolerated statin dose to reduce CVD risk further, even if the lipid target for secondary prevention of CVD is met. This is because studies have shown that the combination is effective in reducing CV events and ezetimibe is cost effective regardless of cholesterol levels.

So now let’s look at our special group, people with CKD but excluding those on renal replacement therapy. For both primary and secondary prevention of cardiovascular disease in CKD we will offer atorvastatin 20 mg. If the lipid target for primary or secondary prevention of CVD is not met and eGFR is 30 ml per minute per 1.73 m2 or more, we will increase the dose of atorvastatin. However, if the eGFR is less than 30 ml per minute per 1.73 m2, we will discuss with the renal team. 

When it comes to optimising treatment for people on statins, for everyone else other than for people with CKD, if the lipid target for primary or secondary prevention of CVD is not met:

• we will reinforce adherence and lifestyle advice, and
• we will consider increasing the statin intensity and / or dose if the person is not currently taking the maximum tolerated dose of a high intensity statin. 

And let’s remember that the only doses of statins that are considered high intensity, based on the percentage reduction in LDL cholesterol they can produce are:

• atorvastatin: 20 mg to 80 mg
• rosuvastatin: 10 mg to 40 mg.

Lower doses as well as the rest of the other statins will fall in the medium or low-intensity statins.

If the person reports adverse effects when taking a high-intensity statin, we will discuss the following:

• stopping the statin and trying again when the symptoms have resolved to check if the symptoms are related to the statin
• changing to a different statin in the same intensity group (for example, rosuvastatin if already receiving atorvastatin) or
• reducing the dose or
• changing to a lower-intensity statin, explaining that any statin at any dose reduces CVD risk. 

If statins are contraindicated or not tolerated for secondary prevention we will offer ezetimibe instead. This applies whatever the person's cholesterol level.

If the person is taking ezetimibe but the lipid target for secondary prevention is not met, we should consider alternatives or additional lipid-lowering treatments such as oral bempedoic acid and injectables such as alirocumab, evolocumab and inclisiran, each one of which has their own NICE guidance.

How do we assess response to treatment?

Well, we should measure liver transaminase and full lipid profile at 2 to 3 months after starting or changing lipid-lowering treatment. We will then measure liver transaminase at 12 months, but not again unless clinically indicated. 

We should also advise people on statins to seek medical advice if they develop unexplained muscle symptoms (pain, tenderness or weakness). If this occurs, we will measure creatine kinase. 

If creatine kinase level is less than 5 times the upper limit of normal, we will reassure them that their symptoms are unlikely to be due to the statin and explore other possible causes. 

However, we will not measure creatine kinase levels in asymptomatic people who are being treated with a statin. 

When checking glucose or HbA1c, we will not stop statins because of an increase in blood glucose level or HbA1c.

And we will remind the person to restart the statin if they stopped taking it because of drug interactions or to treat intercurrent illnesses. 

Patients on lipid-lowering treatment should have an annual medication review, offering an annual full lipid profile to inform discussions, encouraging adherence, lifestyle changes and addressing CVD risk factors.

We should also discuss with people who are stable on a low-intensity statin or medium‑intensity statin the likely benefits and potential risks of changing to a high-intensity statin and agree whether a change is needed. 

Right, so we have looked at the lipid lowering treatments that can be recommended, primarily statins and ezetimibe followed by alirocumab, evolocumab, inclisiran and bempedoic acid if necessary and meeting their individual NICE guidance.

On the other hand, lipid-lowering treatments that should not be recommended for primary and secondary prevention, including people with diabetes and CKD are:

·      Fibrates

·      Nicotinic acid

·      Bile acid sequestrants and

·      Omega 3 fatty acid compounds with the exception of icosapent ethyl, which has its own guidance for people with raised triglycerides

However, these treatments not recommended do not apply to people with familial hypercholesterolaemia, which has got its own guidance and for whom fibrates and other agents may be prescribed.

And that is it, the second part of the NICE guideline on CVD risk reduction in primary care. Make sure to check the previous introductory episode if you have not already done so. 

As always, remember that this is not medical advice, but only my summary and my interpretation of the guidelines. You must always use your clinical judgement. 

Thank you for watching and goodbye. 

Thank you for listening and goodbye.

For the introductory video on cardiovascular risk reduction and lipid modification:

·      https://youtu.be/jIhlkmOcsiI 

For the NICE guidance on cardiac chest pain video: 

·      https://youtu.be/so97zARpmME 

For the NICE management of stable angina video: 

·      https://youtu.be/BtWs0VHjp00  

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 review the NICE guideline “Cardiovascular disease: risk assessment and reduction, including lipid modification” [NG238], published on 14 December 2023, focusing on what is relevant in Primary Care only. I cover CV risk assessment, recommendations for specialist referral and considerations before starting statin therapy. In the next episode I will cover the rest of the guideline including primary and secondary prevention, assessing response to treatment, optimising therapy and what to do when statins are contraindicated or not tolerated.  

For a refresher on the NICE guidance on cardiac chest pain and the management of stable angina, please refer to the corresponding episodes on this channel. The links are shown above. 

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

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 NICE guideline “Cardiovascular disease: risk assessment and reduction, including lipid modification” [NG238] Published: 14 December 2023 can be found here:

·      https://www.nice.org.uk/guidance/ng238

The online version of QRISK3 can be found here:

·      https://qrisk.org/

The QRISK3-lifetime tool can be found here:

·      https://qrisk.org/lifetime/index.php

The NICE guideline on familial hypercholesterolaemia can be found here:

·      https://www.nice.org.uk/guidance/cg71

The Simon Broome criteria for the diagnosis of familial hypercholesterolaemia can be found here:

·      https://www.nice.org.uk/guidance/cg71/evidence/full-guideline-appendix-f-pdf-241917811

The Dutch Lipid Clinic Network (DLCN) criteria for the diagnosis of familial hypercholesterolaemia can be found here:

·      https://www.mdcalc.com/calc/3818/dutch-criteria-familial-hypercholesterolemia-fh 

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're 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’ll look at the NICE guideline on cardiovascular risk reduction and lipid modification, or NG238, which was published in December 2023, focusing on what is relevant in Primary Care only. In this episode we are going to cover CV risk assessment, recommendations for specialist referral and considerations before starting statin therapy. Stay tuned because in the next episode we will cover the rest of the guideline including primary and secondary prevention, assessing response to treatment, optimising therapy and what to do when statins are contraindicated or not tolerated.  

If you’d like a refresher on the NICE guidance on cardiac chest pain and the management of stable angina, please refer to the corresponding episodes on this channel. The links are also in the episode description. 

Right, let’s jump into it.

For people without established cardiovascular disease, we are now advised to use QRISK3 instead of QRISK2 to calculate the CV risk within the next 10 years. We will do this for those aged between 25 and 84, including those with type 2 diabetes.

Because QRISK2 is currently embedded in the electronic clinical systems that most of us use in the UK, NICE accepts that, until the clinical software systems are updated with QRISK3, it may be necessary to continue using QRISK2.

However, when assessing the CV risk for people taking steroids or atypical antipsychotics or people with SLE, migraine, erectile dysfunction or severe mental illness, we are advised to use the online version of QRISK3, because QRISK2 does not take these risk factors into account and may underestimate the risk. A link to the online version of QRISK3 is in the episode description.

So, what is the difference between QRISK2 and QRISK3?

Well, QRISK3 was introduced in 2017 as an update to QRISK2 and it includes all the factors in QRISK2, but adds new risk factors to make it more accurate. These factors are:

• Some medications which are known to increase CVD risk such as:
• Atypical antipsychotics and
• Corticosteroid
• Some diagnoses which have been linked to increased cardiovascular risk, such as:
• Chronic inflammatory conditions (for example, SLE)
• Severe mental illness (understood as a diagnosis of schizophrenia, bipolar disorder or other psychoses)
• Migraine and
• Erectile dysfunction
• And examination findings such as considering systolic blood pressure variability, because fluctuations in blood pressure have been found to be an independent risk factor for cardiovascular disease. This means that even if someone’s average blood pressure is normal, large swings in systolic pressure over time can increase the CV risk.

Is there anyone that is not suitable for the QRISK3 assessment tool? Well, we should not use it for those who are already at high risk of CVD, including people with:

• Pre-existing cardiovascular disease, that is, secondary prevention
• familial hypercholesterolaemia
• type 1 diabetes
• CKD, that is, either an eGFR less than 60 ml per minute per 1.73 m2 and/or albuminuria and finally
• Those aged 85 and older. As we know, we are advised to use QRISK3 in people aged 25 to 84 so we should not assess QRISK3 for those aged 85 or older, but instead, we should consider them to be at increased risk of CVD because of age alone. 

In addition, there are certain CV risk factors that are not fully considered in the assessment tools, like, for example, people treated for HIV or with drugs that can cause dyslipidaemia, such as, for example, immunosuppressants. 

Although we should offer patients information about their CV risk within the next 10 years, we should also consider using a lifetime risk tool such as QRISK3-lifetime to inform discussions and to motivate lifestyle changes, particularly for people with a 10‑year QRISK3 score less than 10%, and people under 40 who have CVD risk factors. The link to the QRISK3-lifetime tool is in the episode description.

It goes without saying that we will offer lifestyle advice for both the primary and secondary prevention of cardiovascular disease in the form of:

·      Healthy eating

·      A cardioprotective diet where saturated fats are replaced by mono‑unsaturated and polyunsaturated fats. 

·      Increased physical activity

·      Weight management and

·      Smoking cessation and alcohol advice

But we will not recommend either:

·      Aspirin for primary prevention of cardiovascular disease or

·      Plant stanols and sterols in any situation

Right, so now that we know who we are going to target and how we are going to assess them, let’s see how to interpret the results.

For the initial lipid measurement, we should check a full lipid profile, measuring both total and HDL cholesterol as well as triglycerides. And, depending on the results, there will situations where we should refer patients to a lipid clinic.

So, let’s have a look at the referral recommendations.

But, before making a referral, we should exclude and manage possible secondary causes of dyslipidaemia such as, for example, excess alcohol, uncontrolled diabetes, hypothyroidism, liver disease and nephrotic syndrome. 

Right, once we have excluded secondary causes, we will need to refer the patient primarily for two reasons:

1.   Because of suspected familial hypercholesterolaemia or

2.   Because of significantly raised triglycerides

Let’s look at familial hypercholesterolaemia first.

In order to judge the likelihood of a familial lipid disorder, we are advised to consider clinical findings, a full lipid profile and family history, rather than using strict lipid cut-off values alone. I have put the link to the guideline on familial hypercholesterolaemia in the episode description but, in summary, we should suspect it if:

• the total cholesterol is greater than 7.5 mmol/l or
• there is a personal or family history of premature coronary heart disease (that is, an event before 60 years in an index individual or first-degree relative). 

To diagnose familial hypercholesterolaemia in Primary Care, we will need to use the Simon Broome criteria or the Dutch Lipid Clinic Network (DLCN) criteria and apply them to those whom we suspect to have the condition. This should be done by someone competent in using the criteria, so we should seek advice if necessary. I have put links to the criteria in the episode description. If the criteria are met, we will make a clinical diagnosis of familial hypercholesterolaemia and we will refer them accordingly for consideration of genetic testing and family screening.

However, NICE recommends direct specialist referral without having to apply these criteria if

·      total blood cholesterol is more than 9.0 mmol per litre or

·      non-HDL cholesterol is more than 7.5 mmol per litre

and this is even in the absence of a first-degree family history of premature coronary heart disease. 

Let’s now look at when to refer when triglycerides are significantly raised.

For those with triglycerides of more than 20 mmol per litre that is not a result of excess alcohol intake or poor glycaemic control, we will refer them for urgent specialist review. This is because such elevated levels increase the risk of acute pancreatitis.

For those with triglycerides between 10 mmol and 20 mmol per litre:

• we will repeat the triglycerides with a fasting test (after an interval of 5 days, but within 2 weeks) and
• we will refer if the triglyceride level remains at more than 10 mmol per litre and secondary causes have been excluded 

Those with triglycerides between 4.5 mmol and 9.9 mmol per litre do not necessarily need referral but we need to be aware that QRISK may underestimate the CV risk in these cases.

Right, let’s assume that the patient has a high CV risk. The main way to reduce the CV risk in both primary and secondary prevention is with statins. What general information should we give to patients before starting them?

We should advise that the risk of muscle pain, tenderness or weakness associated with statin use is small and the rate of severe muscle adverse effects (or rhabdomyolysis) because of statins is extremely low. 

We should also advise that:

• other drugs, some foods (for example, grapefruit juice) and some supplements may interfere with statins and
• they should always check the risk of interactions when starting other drugs or thinking about taking supplements. 

Next, before starting statins we should:

Assess the patient, including smoking, alcohol, BP and BMI and

Perform blood tests including:

• a full lipid profile
• fasting glucose or HbA1c
• renal and liver function tests and
• thyroid function tests including TSH for those with symptoms of underactive or overactive thyroid. 

We will not routinely exclude from statin treatment people who have high liver transaminase levels which are less than 3 times the upper limit of normal. 

Also, before offering a statin, we should ask if they have had persistent generalised unexplained muscle symptoms (like pain, tenderness or weakness), and, if so, we will measure creatine kinase levels. If creatine kinase levels are:

• more than 5 times the upper limit of normal, we will recheck it after 7 days and if still 5 times the upper limit of normal, we will not start statin therapy. However, if CK levels are
• raised but less than 5 times the upper limit of normal, we can start statin treatment but we will do so at a lower dose. 

We obviously need to be aware that statins are contraindicated in pregnancy and that:

• statins should be stopped if pregnancy is a possibility
• statins should be stopped 3 months before attempting to conceive
• statins should not be restarted until breastfeeding is finished. 

And that is it, an introduction to CVD risk reduction in primary care. Make sure not to miss the next episode where we will cover the rest of the guideline including statins for both primary and secondary prevention. 

As always, remember that this is not medical advice, but only my summary and my interpretation of the guidelines. You must always use your clinical judgement. 

Thank you for listening and goodbye.

For the PSA video:

·      https://youtu.be/64vGSs6WLws

For the NICE management of male LUTS video:

·      https://youtu.be/fgQcv01YJg0

My name is Fernando Florido, and I am a General Practitioner in the United Kingdom. In this episode, I review the latest guidance on PSA testing as outlined in the PSA Consensus 2024, available through Prostate Cancer UK and also featured in the British Journal of General Practice. I will also discuss recommendations from Public Health England, along with key aspects of the NICE guidelines on prostate cancer (NG12 and NG131) and the Pan London urology cancer referral pathways. You can find links to all of these resources below.

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 any of the institutions.

I am not giving medical advice; this video is intended for health care professionals; it is only my summary and my interpretation of the information consulted. You must always 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 resources consulted can be found here:

Guidance updated on PSA testing for prostate cancer by Public Health England can be found here:

·      https://phescreening.blog.gov.uk/2020/01/20/psa-testing-guidance/

The PSA Consensus 2024 for health professionals available in Prostate Cancer UK can be found here:

·      https://prostatecanceruk.org/for-health-professionals/guidelines/psa-consensus-2024

The article published in the British Journal of General Practice: “Optimising the use of the prostate- specific antigen blood test in asymptomatic men for early prostate cancer detection in primary care: report from a UK clinical consensus” can be found here:

·      https://bjgp.org/content/74/745/e534

The leaflet on PSA testing and prostate cancer advice for men without symptoms of prostate disease aged 50 and over can be found here:

·      https://assets.publishing.service.gov.uk/media/64c3c279331a650014934e2c/PCRMP_patient_info_sheet_update_March_2022_v2.pdf

The NICE guideline on prostate cancer: diagnosis and management [NG131] can be found here:

·      https://www.nice.org.uk/guidance/ng131

The NICE guideline on Suspected cancer: recognition and referral [NG12] can be found here:

·      https://www.nice.org.uk/guidance/ng12/chapter/Recommendations-organised-by-site-of-cancer#urological-cancers

The Pan-London suspected cancer referral forms can be found here:

·      https://www.transformationpartners.nhs.uk/programmes/cancer/early-diagnosis/two-week-wait-referral-repository/suspected-cancer-referrals/

The information leaflet recommended by Public Health England for well men aged 50 and over containing a summary of the potential benefits and risks of PSA can be found here:

·      https://www.gov.uk/government/publications/prostate-specific-antigen-testing-description-in-brief

The NICE management of male LUTS video:

·      https://youtu.be/fgQcv01YJg0

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're 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’ll look at the latest guidance on PSA testing, as outlined in the PSA Consensus 2024, available through Prostate Cancer UK and also featured in the British Journal of General Practice. We’ll also cover recommendations from Public Health England, some aspects of the NICE guidelines on prostate cancer (NG12 and NG131), and the Pan London urology cancer referral pathways, focusing on what is relevant in Primary Care only. You can find links to all of these in the episode description.

If you’d like a refresher on the NICE guidance for managing male LUTS, please refer to the corresponding episode on this channel. The link is also in the episode description.

Right, let’s jump into it.

Although the PSA Consensus 2024 focuses on PSA testing in asymptomatic men, we’ll also cover testing in symptomatic patients.

So let’s start with patients with symptoms.

While many people with prostate cancer are asymptomatic, we should suspect it if there are unexplained symptoms. Possible prostate cancer symptoms can be non-specific, such as:

• Anorexia or weight loss,
• Lethargy, or
• Lower back or bone pain.

or urological symptoms, such as:

• Erectile dysfunction,
• haematuria, or
• Any lower urinary tract symptoms (LUTS), including nocturia, urinary frequency, hesitancy, urgency, or retention.

Even though male LUTS alone do not necessarily suggest prostate cancer or automatically warrant PSA testing, the NICE cancer guideline (NG12) recommends checking PSA and performing a digital rectal examination when these symptoms are present or whenever there’s any suspicion of prostate cancer.

We will make an urgent referral on the cancer pathway if a DRE reveals a suspicious prostate or PSA levels exceed age-specific thresholds. These thresholds are:

• 40–49: above 2.5 ng/mL
• 50–59: above 3.5 ng/mL
• 60–69: above 4.5 ng/mL
• 70–79: above 6.5 ng/mL
• For those aged under 40 or over 79, we will use our clinical judgement.

In addition, the Pan London cancer referral pathway states that the raised PSA should be in the absence of a UTI, or when the PSA levels remain elevated at least 8 weeks after a UTI has been treated. On the other hand, if the PSA exceeds 20 ng/mL, an urgent cancer referral can be made even if a UTI is present.

Right, so, we've covered what to do for symptomatic patients. Now, let’s look at the recommendations for PSA testing in asymptomatic patients.

Currently in the UK, PSA testing is freely available to anyone aged 50 and over who requests it. This includes anyone with a prostate, including trans women and non-binary people. Patients who request the PSA test should receive balanced information on the pros and cons of testing. Public Health England recommends a patient information leaflet, outlining the potential benefits and risks of PSA testing. A link to this leaflet is available in the episode description.

However, Public Health England also advises that GPs should not proactively raise the topic of PSA testing with asymptomatic people. This is due to the potential harms of overdiagnosis and overtreatment of slow-growing prostate cancers, which are common and may not cause symptoms or shorten life expectancy.

Additionally, PSA is not a perfect test. Although most patients have a PSA level below 3 ng/mL, around 75% of men with a PSA above this threshold do not have cancer. On the other hand, about 15% of men with a low PSA will later be found to have prostate cancer.

PSA levels can also be elevated for various reasons other than prostate cancer, including UTIs, benign prostatic hyperplasia, prostatitis, as well as recent ejaculation or vigorous exercise.

Therefore, before performing a PSA test, we should ensure the patient does not have:

• A UTI, or has not had one within the last 6 weeks,
• That they have not ejaculated or engaged in vigorous exercise within the past 48 hours, or
• That they have not undergone any urological interventions in the past 6 weeks.

We should also consider that medications like finasteride, can also increase PSA levels.

Now that we’ve reviewed the current recommendations, let’s look at the new guidance in the PSA Consensus 2024. This consensus was developed because current testing guidelines are based on an outdated diagnostic pathway, where a biopsy typically followed a raised PSA. The current pathways are more accurate, using MRIs and thus reducing the risk of overtreatment. Moreover, existing guidelines do not offer clear advice for men who are at higher risk of prostate cancer.

Another reason was to address potential health inequalities. While PSA tests are freely available through the NHS, GPs are instructed not to proactively raise the issue, meaning that the more health-literate and affluent patients are more likely to request testing, leaving men in deprived areas with lower testing rates.

Whilst the consensus still recommends that asymptomatic men should be provided with balanced information on PSA testing and should have access to it starting at age 50, in order to address all these concerns, it also recommends a more proactive approach for men who are at higher risk of prostate cancer, even though it does not go as far as recommending general screening.

Therefore, the consensus states that we should proactively discuss prostate cancer risk and PSA testing with those at higher risk, which includes:

• Black men aged 45 and over (as Black ethnicity alone confers a higher risk),
• Men aged 45 and over with a family history of prostate cancer, and
• Men with confirmed genetic risk factors, such as a BRCA2 gene variation.

The responsibility for raising awareness about prostate cancer in primary care lies with all trained healthcare professionals, not just GPs, and patients should still be provided with balanced information on PSA testing.

There was no consensus on PSA threshold values for asymptomatic patients due to insufficient evidence for age-specific thresholds. Currently, the referral threshold for asymptomatic men is a PSA level of 3.0 ng/mL or higher.

However, questions were raised regarding the rationale behind this threshold, especially for men aged 50–79. Let’s remember that, for symptomatic patients, NICE recommends different thresholds based on age: 3.5 ng/mL for those in their 50s, 4.5 ng/mL for those in their 60s, and 6.5 ng/mL for those in their 70s. Concerns were raised that using the lower threshold of 3.0 ng/mL in asymptomatic patients could lead to overtreatment. However, since no alternative thresholds were agreed upon, we will have to use our clinical judgement in order to decide whether to investigate further or refer.

Also, while DRE is still valuable in symptomatic patients, there is uncertainty over its usefulness in asymptomatic people so, if a referral is needed because of a high PSA, a DRE prior to referral was not strictly necessary especially evidence suggests that DRE can act as a barrier for some men seeking help. This is also the case in patients with normal PSA levels, even when risk factors like family history or Black ethnicity are present. The low positive predictive value of DRE and inconsistent results between primary and secondary care were cited as concerns. However, if a DRE is performed and the findings are suspicious, referral should then be made, even with a low PSA.

There was no agreement on whether DRE prior to testing increases PSA levels, so its impact on PSA results remains uncertain.

The frequency of repeat PSA testing should be based on individual risk factors. There was no consensus on specific intervals for repeat testing due to insufficient evidence and concerns about the burden on primary care. However, it’s likely that PSA testing will be required at least annually, potentially more often for high-risk patients or those with fluctuating PSA levels.

There is also a role for the use of PSA velocity in determining whether to refer to secondary care, but again, no specific guidance was given about this.

What is PSA velocity?

PSA velocity refers to how quickly the PSA increases over time. A rapid increase in PSA (even if the total PSA level is not very high) can be an indicator of an underlying prostate issue.

A PSA velocity of more than 0.75 ng/ml per year has been used as a threshold in some clinical settings to prompt further investigation. So, although PSA velocity is not officially incorporated into NICE guidance for asymptomatic patients, it can still be considered if there are concerns, always taking into account that PSA velocity has limitations, so it should always be interpreted in the context of the overall clinical picture.

Although there was no consensus on broader screening for asymptomatic patients due to the risk of overdiagnosis and overtreatment, there is agreement on the following points:

• The PSA blood test is the first step in the prostate cancer diagnostic pathway, identifying men who may benefit from further testing, typically an MRI and
• The balance of benefits and harms is shifting in favour of screening, but further research is still needed.

In summary, current guidelines recommend that GPs do not proactively raise the issue of PSA testing with asymptomatic men. However, the PSA Consensus 2024 challenges this, advising primary care professionals to have proactive discussions with men aged 45 and over who are at higher-than-average risk, including those of Black ethnicity, with a family history of prostate cancer, or with genetic risk factors. However, it did not recommend proactive conversations for all at-risk men — that is, aged ≥50 years without other risk factors.

This consensus reflects changes in policy in other countries. For example, EU member states are considering stepwise implementation of organised prostate cancer screening programmes, and a U.S. expert panel recently recommended annual PSA screening for Black men starting at age 40.

This shift is likely to prompt a review of UK guidelines in the near future.

And that is it, a review of PSA testing for early prostate cancer detection in primary care.

As always, remember that this is not medical advice, but 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/BnwK2Vts3gY

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 September 2024 by the National Institute for Health and Care Excellence (NICE), focusing on those that are relevant to Primary Care only. I also cover the guideline on Adrenal insufficiency published on 28th August 2024.

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 September 2024 can be found here:

·      https://www.nice.org.uk/guidance/published?from=2024-09-01&to=2024-09-31&ndt=Guidance&ndt=Quality+standard

The links to the guidance covered in this episode can be found here:

Vibegron for treating symptoms of overactive bladder syndrome:

·      https://www.nice.org.uk/guidance/ta999

Adrenal insufficiency: identification and management:

·      https://www.nice.org.uk/guidance/ng243

The Imperial Centre for Endocrinology prednisolone withdrawal regimen can be found here:

·      https://www.impendo.co.uk/prednisolone/prednisolone-withdrawal

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 September 2024, focusing on what is relevant in Primary Care only.

We are going to cover just two areas, the treatment of overactive bladder and the guideline on adrenal insufficiency, which was published late in August 2024 and did not make it into last month’s episode.

Right, let’s get started.

The first area is a technology appraisal on Vibegron for treating the symptoms of overactive bladder syndrome in adults. It is very similar to the technology appraisal on mirabegron.

Before looking at the recommendation, let’s have a quick overview of Overactive bladder syndrome. It is a condition characterized by a frequent and urgent need to pass urine, sometimes with urinary incontinence. It is often caused by involuntary contractions of the bladder wall.

Treatment for OAB involves lifestyle changes, behavioural therapies, and medications. NICE recommends that bladder training and lifestyle advice should be offered as first-line treatments. Then an antimuscarinic drug should be offered second-line and beta 3 agonists should be offered third line.

So, let’s look at the two types of drug treatment:

1. Antimuscarinic Agents (or Anticholinergics) are the most commonly prescribed drugs and they work by blocking muscarinic receptors in the bladder, reducing the involuntary contractions of the detrusor muscle.

• Examples are:
• Oxybutynin
• Tolterodine
• Solifenacin
• Darifenacin and
• Fesoterodine
• Since muscarinic receptors are also found in other parts of the body (e.g., the salivary glands, eyes, and intestines), antimuscarinic agents can cause side effects such as dry mouth, constipation, blurred vision, and cognitive dysfunction, especially in elderly patients.

1. Beta-3 Adrenergic Agonists are drugs like mirabegron and vibegron which offer an alternative to antimuscarinics. These drugs specifically stimulate beta-3 receptors on the detrusor muscle, causing the muscle to relax. This increases the bladder’s capacity and reduces the urgency and frequency of urination.

• Beta-3 agonists tend to have fewer side effects compared to antimuscarinic agents. Some common side effects are mild increases in blood pressure, arrythmias, headache, and urinary tract infections.

So, in summary, the main difference between these Drug Classes are that Antimuscarinics work by reducing involuntary bladder contractions whereas Beta-3 agonists relax the bladder, improving bladder storage.

Vibegron, as a beta 3 agonist, works in a similar way to mirabegron and an indirect comparison suggests that it is equally effective at a lower cost. So, vibegron is recommended if antimuscarinic medicines are not suitable, do not work well enough or have unacceptable side effects.

The next section is a brand-new guideline on adrenal insufficiency.

And before we look into it, let’s give a very brief overview on the subject.

Adrenal insufficiency is a disorder where the adrenal glands do not produce sufficient amounts of cortisol, and sometimes aldosterone. It's classified into primary, secondary, and tertiary, each with different causes and pathophysiology.

• Primary adrenal insufficiency is caused by a problem in the adrenal glands. Possible causes include autoimmune conditions, infection, and malignancy. The autoimmune condition Addison's disease is the most common cause in adults, and congenital adrenal hyperplasia is the most common cause in children
• Secondary adrenal insufficiency is caused by a problem in the pituitary gland which limits the secretion of ACTH, leading to reduced adrenal stimulation. Possible causes include pituitary tumours, and damage to the pituitary gland secondary to trauma, surgery or radiation.
• And Tertiary adrenal insufficiency is caused by a problem in the hypothalamus which reduces the levels of corticotropin-releasing hormone (or CRH). Possible causes include tumours in the hypothalamus or adjoining structures, or more commonly the use of prolonged glucocorticoids which suppress the hypothalamic-pituitary-adrenal axis.

The physiopathology in each case is also different:

• In primary adrenal insufficiency, the adrenal cortex is unable to produce both glucocorticoids, and mineralocorticoids, leading to cortisol and aldosterone deficiency.
• In secondary and tertiary adrenal insufficiency, the adrenal glands themselves are functional, but low levels of ACTH and / or corticotropin-releasing hormone (or CRH) impair the production of cortisol. However, mineralocorticoid production is usually preserved because it is regulated primarily by the renin-angiotensin system, not ACTH.

Adrenal insufficiency requires treatment with glucocorticoids and, in primary adrenal insufficiency, mineralocorticoids too. Failure to manage it can lead to life-threatening adrenal crises, especially during stress.

NICE states that we should suspect adrenal insufficiency when there are unexplained suggestive symptoms, bearing in mind that many of these symptoms are non-specific. They include:

• weight loss and lack of appetite
• nausea, vomiting or diarrhoea
• dizziness, hypoglycaemia and hypotension
• salt craving, hyponatraemia and hyperkalaemia and
• lethargy, and muscle weakness

We should also suspect adrenal insufficiency in people with unexplained hyperpigmentation, although hyperpigmentation may not be seen on black or brown skin. In these cases, we should ask the person if they have noticed a change in their skin colour and we should assess the buccal mucosa or any surgical scars.

When do we get this hyperpigmentation? This only happens in the case of primary adrenal insufficiency, when ACTH levels are high. ACTH and melanocyte-stimulating hormone (of MSH) share the same precursor, so when ACTH levels are high, MSH levels also increase with the subsequent increase in melanin.

One common cause of adrenal insufficiency occurs due to adrenal suppression in people who have recently stopped prolonged glucocorticoids by any route. Prolonged means 4 weeks in adults and 3 weeks in children.  However, it can also happen to those who are still taking steroids and have had an episode of physiological stress

Considering this, how should we taper off steroids to prevent adrenal insufficiency?

Well, the first thing that we need to understand is the concept of physiological equivalent dose, which is the dose of glucocorticoid that is equivalent to the amount that a healthy adrenal gland would normally produce. For adults this is a total daily dose of 3 mg to 5 mg of prednisolone, or of 0.5 mg of dexamethasone. In children the calculation requires the use of a complex formula.

So, for someone taking steroids for more than 4 weeks (or 3 weeks in the case of children), in order to taper off the dose safely, we should first reduce the dose gradually to a daily physiological equivalent dose. Then, we should give that dose every other day for 2 weeks, then then twice a week for 2 weeks and then stop, always taking into account that this decision should be made by the clinical team who initiated the treatment for whichever condition the steroids were prescribed for.

However, for people taking steroids for more than 12 weeks, a slower dose-tapering regimen is recommended. For example, for people taking prednisolone, once the daily dose is 3 mg, we are advised to follow the Imperial Centre for Endocrinology prednisolone withdrawal regimen. I have put the link to this in the episode description but the regimen looks like this, where we give patients, a schedule indicating what dose to take each day of the week depending on whether they are in week 1, 2, 3, etc. It takes 7 weeks to reduce the dose from 3 mg to 2 mg using this schedule and, similarly, thereafter, so a total of 21 weeks to reduce from 3 mg to zero. If the starting dose is 5 mg of prednisolone, then a slightly different regimen is followed where the reduction of the dose to zero is over 24 weeks.

As the initial investigations for adrenal insufficiency, we will offer an 8 am to 9 am serum cortisol test, bearing in mind that we should not do this test if taking oral glucocorticoids at physiological equivalent doses or above, because the cortisol levels will be suppressed.

In addition, other routes such as inhaled, intramuscular or topical steroids, may also cause a low cortisol level.

People taking oral oestrogen will have a falsely elevated cortisol so we should stop oral oestrogens for 6 weeks before checking it. If the oral oestrogen is taken for HRT, we will be able to switch to a transdermal preparation.

Once we get the results, if the cortisol level is:

Below 150 nmol/L, then the person may have adrenal insufficiency and we should refer them to endocrinology, urgently in the case of children.

If it is between 150 nmol/L and 300 nmol/L, then the probability of adrenal insufficiency is uncertain and we should repeat the test. If it remains at this level, we will seek specialist advice.

If it is above 300 nmol/L then adrenal insufficiency is very unlikely

The Routine pharmacological management is with Corticosteroid replacement, offering hydrocortisone or prednisolone, and we will add a mineralocorticoid like fludrocortisone for people with primary adrenal insufficiency or congenital adrenal hyperplasia. We will be seeking specialist advice so I will not cover any more of the treatment here.

If there are symptoms of adrenal insufficiency while tapering the dose below a physiological equivalent dose, we will prescribe double the physiological equivalent glucocorticoid dose daily until symptoms resolve, then we will reduce to a daily physiological equivalent dose for 1 week and then use a slower tapering regimen. If symptoms still develop using this slower regimen, then we will need further investigations such as checking serum cortisol levels.

Patients with adrenal insufficiency should be given an emergency kit containing an intramuscular hydrocortisone injection for emergency use in the case of a suspected adrenal crisis.

People having an adrenal crisis should immediately go to hospital by ambulance without needing a referral.

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/ivCRpRFs3cg

For the non-visible haematuria video:

·      https://youtu.be/SaizjWg7Fng

For the non-visible haematuria podcast:

·      https://youtu.be/bIKhn43o7ZI

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode, I go through the interpretation and initial management of sterile pyuria, always focusing on what is relevant in Primary Care only. The information is based on based on published medical articles in the British Journal of General Practice as well as the New England Journal of Medicine. The link to them can be found below. 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 any of the institutions.

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

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:

Sterile pyuria: a practical management guide - British Journal of General Practice 2016; 66 (644): e225-e227:

·      https://bjgp.org/content/66/644/e225

Sterile Pyuria – Review article NEJM - N Engl J Med 2015; 372:1048-1054:

·      https://www.nejm.org/doi/10.1056/NEJMra1410052?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200www.ncbi.nlm.nih.gov

The non-visible haematuria video can be found here:

·      https://youtu.be/SaizjWg7Fng

The non-visible haematuria podcast can be found here:

·      https://youtu.be/bIKhn43o7ZI

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 interpretation and initial management of sterile pyuria, always focusing on what is relevant in Primary Care only.

The information is based on two relevant medical publications in the British Journal of General Practice as well as the New England Journal of Medicine. The links to them are in the episode description.

If you want a reminder on how to manage non-visible haematuria, please watch the corresponding episode on this channel. The link is in the episode description too.

Right, so let’s jump into it.

Sterile pyuria is not an uncommon finding in clinical practice. Nine per cent of patients with lower urinary symptoms, and who are suspected of a UTI, are found to have sterile pyuria. It can be higher in specific populations and sterile pyuria is more common among women because of the higher incidence of pelvic infection.

Sterile pyuria continues to pose a diagnostic conundrum because there are no guidelines on its management. Furthermore, no agreed definition for sterile pyuria exists. It is simply the presence of white blood cells in the urine, in the absence of infection. Some authors have defined it as the presence of 10 or more white cells per cubic millimetre of urine, 3 or more white cells per field on microscopy, or a urinary dipstick test that is positive for leucocytes, all of this in the absence of positive urine cultures.

Sterile pyuria can also be associated with haematuria, proteinuria, and casts, complicating the diagnosis.

(Causes)

Looking at the cause, broadly speaking, sterile pyuria may be classified as infectious or non-infectious.

Let’s look at the infectious causes first. Simple bacterial UTIs are extremely common. However, a recently treated UTI, usually within 2 weeks, or even after a single dose of antibiotics, can present as sterile pyuria. Therefore, we should check whether a recent course of antibiotics has been given and, if we are treating a UTI and requesting a urine culture, we should ensure that we advise patients to collect the urine sample before taking the first dose of antibiotics.

When considering UTIs, we also need to take into account that, although colony counts greater than 100,000 colony-forming units per millilitre of urine (CFU/ml) have historically been used to diagnose a UTI, bacterial colony counts as low as 1000 colony-forming units per millilitre (CFU/ml) can be a sign of bacteriuria. So, it is important to consider that lower bacterial counts can still be associated with a urinary tract infection, even though the urine culture may be reported as negative, so repeating the cultures may be necessary.

Sexually transmitted infections should be considered in the younger, sexually active population. Chlamydia is the most common cause, but others are also possible such as, for example, gonorrhoea, mycoplasma, trichomonas, genital herpes and HPV. Therefore, a sexual history should always be sought in young patients presenting with urinary symptoms.

In the older population, prostatitis, cystourethritis, and balanitis may also present as sterile pyuria. Furthermore, common viruses such as adenovirus and parasitic infections such as schistosomiasis can also be a potential cause, so we should enquire about foreign travel.

In patients with chronic sterile pyuria, atypical infection should be considered, in particular renal tuberculosis. We should suspect it in patients coming from endemic regions, the immunocompromised, and those presenting with unintentional weight loss. Genitourinary tuberculosis is the most common form of non-pulmonary tuberculosis after lymphadenopathy.

And finally, fungal infections can also be a cause of sterile pyuria.

Pyuria has also been noted in the absence of infection, so let’s have a look now at the non-infectious causes. Some obvious causes include:

·      Pelvic inflammation secondary to, for example, appendicitis.

·      Radiotherapy involving the pelvis and urinary tract

·      Instrumentation like, for example, a cystoscopy and

·      Indwelling catheters and ureteric stents. However, when there is not a clear cause we must consider other causes such as

·      Local disease, including malignancy

·      Systemic disease, and

·      medication. Let’s look at these causes in a little bit more detail:

Sterile pyuria can be found in patients with local disease, from benign conditions like renal stones to malignancy. When presenting with either visible or non-visible haematuria, we should always investigate the cause, referring the patient if appropriate. Possible causes of sterile pyuria with haematuria are:

·      Malignancy

·      Polycystic kidney disease and

·      Renal papillary necrosis, which can be typically seen in patients with diabetes, sickle cell disease, and long-term analgesic use.

Systemic conditions that can cause sterile pyuria include SLE, Kawasaki disease, diabetes, sarcoidosis, and malignant hypertension.

There are also physiological causes such as post-menopausal changes and pregnancy. Therefore, repeated sterile pyuria with negative cultures during antenatal checks could be physiological, although we should always exclude other conditions too.

Finally, medications are also a common cause of sterile pyuria. Olsalazine and mesalazine, used to treat inflammatory bowel disease, and nitrofurantoin have been reported to cause sterile pyuria. Additionally, penicillin-based antibiotics, non-steroidal anti-inflammatory drugs, aspirin, PPIs, and diuretics have also been involved in acute drug reactions, causing tubulointerstitial nephritis with sterile pyuria.

Let’s summarise all this by looking at this algorithm published in the British Journal of general Practice:

So, the common causes include infectious and non-infectious.

Infectious causes include STIs, as well as parasitic and atypical infections

And examples are unresolved UTIs, prostatitis, cystourethritis, balanitis, post antibiotic pyuria, chlamydia, gonorrhoea, schistosomiasis, and adenoviruses.

In the non-infectious causes

If there is unintentional weight loss

We will think of malignancy or renal tract TB.

If there is a history of previous surgical procedures or pelvic radiotherapy

Then, the cause could be indwelling catheters, ureteric stents, cystoscopy and post intrabdominal surgery or pelvic radiation.

If there is haematuria

We will think of renal calculi, malignancy, polycystic kidney disease, renal papillary necrosis and interstitial nephritis.

I we are thinking of systemic conditions,

We will consider SLE, Kawasaki, diabetes, pregnancy, malignant hypertension, post-menopausal changes and interstitial cystitis.

And, finally, if we are thinking of drugs

We will check for the use of NSAIDs, steroids, olsalazine, penicillin, vancomycin, and PPIs.

(MANAGEMENT)

How do we manage sterile pyuria?

First of all, we will start with a detailed clinical history and examination to help us identify a possible cause.

General findings like hypertension, skin rashes, and oedema, can be signs of more serious underlying pathology.

Abdominal and pelvic examination, including a digital rectal examination and vaginal examination in females may be necessary.

Then we will move to carry out some investigations, generally in the form of urine tests, blood tests and imaging of the urinary tract.

As urine tests, urinalysis and urine cultures are the prime investigations for sterile pyuria. Importantly, sterile pyuria is not always sterile, so, as mentioned earlier, repeating urine cultures often yields a positive result on subsequent testing. Contamination, especially with vaginal leucocytes in females, is common, and samples should always be collected as a midstream sample.

If sterile pyuria is detected during routine screening tests sending a urine sample for culture is recommended, with onward review for further investigation.

For sexually active patients, a urine test or, in some cases, swabs for Chlamydia and Gonorrhoea are also recommended.

Other investigations to be considered are routine blood tests including a full blood count, renal, and liver function tests.

Eosinophilia is an important marker of drug-induced interstitial nephritis, but may also be seen in parasitic infections such as schistosomiasis.

Finally, if imaging is required, the type depends on the presentation. A renal tract ultrasound scan or CT is recommended when renal stones, masses, or nephritis are differential diagnoses. Other procedures such as a cystoscopy are recommended if tumours are suspected, although they also have the advantage of diagnosing and treating benign pathologies such as bladder stones.

The NEJM has proposed a flow chart on how to manage patients presenting with sterile pyuria. Let’s have a look at it.

If a patient presents with sterile pyuria, we will review the clinical presentation.

If the symptoms are primarily local, like pelvic pain, urinary or urethral symptoms

Then we will investigate for conditions like, for example, STDs, prostatitis and pelvic inflammatory disease.

And if these are not detected we will consider alternative diagnoses like urinary stones, foreign bodies, interstitial cystitis, bladder tumours and schistosomiasis, particularly if the patient has travelled to a high-risk area such as Africa.

On the other hand, if the symptoms are primarily systemic, like fever, other systemic and urinary symptoms or back, abdominal or pelvic pain

We will reassess for bacterial infection by repeating bacteriological studies and cultures.

And if bacteria are found, then we will treat accordingly.

And if bacteria are not detected

We will consider alternative diagnoses such as tuberculosis or fungal infections, especially if they are immunocompromised or they have been in endemic or high-risk areas.

And if no infection is detected, then appropriate referral will be the next step.

And that is it, a brief review of the causes and initial management of sterile pyuria.

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/j1mnA-jOi1A

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 go through the guidelines on hyponatraemia produced by North Bristol NHS Trust, Royal United Hospitals Bath NHS Trust and Royal Cornwall Hospitals NHS Trust, focusing on what is relevant to Primary Care only. Other guidance has also been consulted and links to all of them 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 here:

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 

·      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 further assessment and management of hyponatraemia, 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. If you have not already done so, I recommend that you look at the previous episode on hyponatraemia, its classification, clinical presentation, pathophysiology and causes, which will give you a good introduction.

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

Let’s have a look at the management of hyponatraemia.

·      As we have know, acute or severe hyponatraemia can be a medical emergency and we should admit for hospital treatment anyone with either symptoms or severe hyponatraemia, understood to be a sodium below 125.

·      People with asymptomatic mild hyponatraemia, that is, a sodium of between 130 and 135, can be investigated and initially managed in Primary Care.

·      But, what do we do with people who are asymptomatic and who have moderate hyponatraemia, that is, a sodium of between 125 and 129? Well, these people need careful assessment because there may be a risk of the sodium falling quickly. So, in these cases, we should seek specialist advice in respect of admission or referral.

Let’s now look at the management in Primary Care.

And as a precaution, all patients with new onset hyponatraemia should have a repeat sodium checked after one week to exclude a rapidly decreasing level.

We should then assess the volume status to see if there is fluid overload or hypovolaemia. We will look at a useful flowchart later which will give us more information in that respect.

We should then review the medication and, if it could be the cause, if possible, we will stop it and repeat the sodium levels in 1-2 weeks. If the sodium level remains low after stopping the medication, we should seek specialist advice.

Of course, if the medication cannot safely be stopped, then we will discuss with the prescribing consultant.

We should also look for and investigate disorders that may cause hyponatraemia. So:

·      We will look for symptoms of possible intercurrent illnesses that could play a part such as chest infections, gastrointestinal disease or UTIs.

·      We will ask about fluid intake and nocturnal polyuria that could point towards primary polydipsia.

·      We will enquire about possible cancer symptoms, especially lung and gastrointestinal, and arrange a chest X-ray and additional investigations if necessary. This is because these malignancies, particularly small cell lung cancer and pancreatic and colorectal cancers, are known to produce ectopic antidiuretic hormone.

·      We will consider further blood tests such as:

o  Renal function tests including eGFR and urinalysis to exclude renal disease

o  Liver function tests to exclude liver disease

o  Thyroid function tests to exclude hypothyroidism

9AM serum cortisol if Addison's disease is suspected.

BNP if heart failure is suspected. 

o  Total serum protein and serum electrophoresis as well as urine Bence-Jones protein if myeloma is suspected

·      And Finally, a paired serum osmolality and urine osmolality and sodium. It is essential that both the serum and urine are sent on the same day. Let’s see what these investigations mean:

o  Serum osmolality will determine whether the hyponatraemia is:

§ Pseudo-hyponatraemia, when the serum osmolality is normal

§ Hypertonic, like in hyperglycaemia, when the serum osmolality is high and

§ Hypotonic, like in true hyponatraemia, when the serum osmolality is low. In this case we will have to look at the urine results to assess further.

o  Urine osmolality will determine how concentrated the urine is:

§ If the urine is very diluted and urine osmolality is <100, then ADH is not acting, like seen in primary polydipsia or high beer intake or potomania

§ If the urine osmolality is >100, then ADH is acting and we will have to look at urinary sodium to categorise it further.

o  Urinary sodium will determine whether sodium is being appropriately regulated in the kidneys. So, if urine osmolality is >100 and:

§ If urinary sodium is low, that is, <30, then the kidneys are reabsorbing sodium correctly. If the patient is hypovolaemic, we will look at extrarenal losses of sodium like, for example. in excessive vomiting, diarrhoea, sweating or extensive burns. If the patient is hypervolaemic, we will consider conditions like, for example, heart failure, liver disease or nephrotic syndrome.

§ If both urine osmolality and urinary sodium are high, then it means that the kidneys are not reabsorbing sodium appropriately, like for example in Addison’s disease, salt wasting diseases and syndrome of inappropriate secretion of antidiuretic hormone. But the issue becomes more complicated depending on whether the patient is on diuretics or has CKD, so these patients are best referred for further specialist assessment.

And we should normally refer any patient in which we suspect:

·      Cancer

·      Primary polydipsia

·      An endocrinology cause or

·      Suspected Syndrome of inappropriate secretion of antidiuretic hormone.

So, let’s try and make sense to all of this by looking at this flowchart by Royal United Hospitals Bath.

So, when we find hyponatraemia

We will review the fluid status and medication and consider pseudo hyponatraemia and other possible confounding factors such as hyperglycaemia, hypertriglyceridaemia and paraproteinaemia.

If the patient is hypovolaemic

We will expect to find the typical clinical signs such as Postural hypotension, Tachycardia, Dry mucus membranes, a decreased Skin turgor, Sunken eyes and a raised urea.

And if the urinary sodium is low, that is, below 30

We will consider Extra Renal loss like, for example, Diarrhoea and vomiting, Burns, Bowel obstruction or Pancreatitis

However, if the urinary sodium is high, that is, above 30

We will consider Renal Loss, like for example, Diuretics, AKI, Renal disease, Addison’s, Congenital adrenal hyperplasia and Cerebral salt wasting disease.

In which case, admission and specialist treatment may be required. 

If the patient is hypervolaemic, like in oedematous disorders

We will consider conditions like, for example, CCF, Ascites, Liver failure. Nephrotic syndrome and Low albumin states

In which case, we will treat the underlying condition, which is also likely to require specialist referral.

If the patient is euvolaemic,

We will carry out investigations such as TFTs and 9 am serum cortisol as well as Paired Serum osmolality & Urine osmolality and sodium

If the thyroid function tests are abnormal or the 9AM serum cortisol is low

We will consider hypothyroid state or Addison’s disease

And we will refer them urgently to endocrinology, as the treatment is disease specific.

On the other hand, if Serum Osm is low, Urine Osm is high and the Urinary sodium is also high, with a normal cortisol and TFTs and without contributing drugs such as diuretics

We will think of syndrome of inappropriate secretion of antidiuretic hormone

But by then we will have concluded that referral for further specialist assessment and management is needed.

So that is it, a review of the further assessment and management of hyponatraemia 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/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 

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 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 
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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 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.