My name is Fernando Florido and I am a GP in the United Kingdom. In today’s episode I look at another random case of hypertension to see how the NICE guidelines could apply to it. By way of disclaimer, I am not giving medical advice; this video is intended for health care professionals, it is only my interpretation of the guidelines and you must use your clinical judgement. 

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

 ·      The NICE GP YouTube Channel: NICE GP - YouTube

 The NICE hypertension flowcharts can be found here:

 ·      Website: https://www.nice.org.uk/guidance/ng136/resources/visual-summary-pdf-6899919517

·      Download: https://1drv.ms/b/s!AiVFJ_Uoigq0lgKKs3AbARF_VLEI?e=KRIWrn

 The full NICE Guideline NG136 can be found here:

 ·      Website: https://www.nice.org.uk/guidance/NG136

·      Download: https://1drv.ms/b/s!AiVFJ_Uoigq0lgP6nFVHRypL9fdj?e=Jbtgus

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Transcript

Hello everyone and welcome. My name is Fernando Florido and I am a GP in the United Kingdom. 

 In today’s episode I look at another random case of hypertension to see how the NICE guidelines could apply to it, focusing on the pharmacological treatment. By way of disclaimer, I am not giving medical advice; this is for health care professionals and it is only my interpretation of the guidelines so you must use your own clinical judgement.

Remember that there is also a Youtube version of these episodes so have a look in the episode description. 

 Right, so let’s generate our random patient.

 OK, so we have a 45-year-old Caucasian man presenting in clinic with a BP of 180/65, so quite significant isolated systolic hypertension. He has two other co-morbidities, PVD and CKD and he is on treatment and therefore we will assume that he has already been diagnosed with hypertension. He is on 3 different antihypertensives, an alpha blocker, terazosin 10 mg daily, a calcium channel blocker, felodipine 2.5mg daily and spironolactone 25mg daily.

 So, what are my initial thoughts? Well, two really. The first one is that he is fairly young and he has significant hypertension despite being on 3 different medications. The second is that, on first impressions, his treatment looks rather strange and we will need to look into this in more detail.

 We will treat his clinic BP as accurate. NICE says that for people that have been diagnosed with hypertension, we can use clinic blood pressure measurements to monitor drug treatment so there is no need for ABPM or HBPM unless you suspect issues. For the purpose of this case, we will also that he is not under any form of stress and that his high clinic BP reading is like other readings that he has been getting on his home monitor. So, there is no concern about white coat hypertension.

 It is also worrying that, at 45, he already, has PVD and CKD and that makes me wonder whether there is something else going on here that we are missing. Could this patient have renovascular hypertension? He has PVD so we know that there is significant atherosclerosis. Could this be affecting his renal arteries? Also, he has CKD. Whilst one of the possible reasons for the drop in eGFR could simply be hypertensive nephropathy, could it also be due to a fall in renal perfusion secondary to bilateral renal artery stenosis? I think that this patient may very well warrant further investigations and referral.

 NICE says that we should consider further investigations and / or referral in people with signs and symptoms suggesting a secondary cause of hypertension. So, in this case, good ways to start would be auscultating the renal areas for the detection of bruits, checking for proteinuria or microalbuminuria and organising a doppler ultrasound of the kidneys.

 I would also look at his records and see when his hypertension was firstly diagnosed. NICE says that we need to consider referral for patients under 40 with hypertension, for the evaluation of secondary causes of hypertension. So if this patient’s hypertension started more than 5 years ago and he was never fully investigated, a referral would be really recommended.

 I will now look at his medication. Whilst his drug combination seems a little odd, let’s try and think of reasons why this could be the case.

 If we have a look at the NICE guidelines, we will see that the first drug of choice for a person under the age of 55 and not of Black African or Afro Caribbean family background is an ACE inhibitor or ARB. We also know that in the small print, NICE also tells us that for people with hypertension and CKD, we need to follow the NICE guideline on CKD, which also emphasises the need to prescribe an ACEI or ARB if there is microalbuminuria of 30 or more. And yet, this patient is not on an ACEI or ARB. Why could this be?

 Perhaps, if there is indeed renal artery stenosis, the previous initiation of an ACEI or ARB caused a significant and progressive deterioration of his renal function and this is why it was stopped. Remember that for the deterioration in renal function to be significant after an ACEI or ARB, the eGFR has to drop persistently by more than 25% or the creatinine has to increase persistently by more than 30%

 Another reason may be that the drugs were not tolerated, for example, because of a cough. A cough is a common side effect of ACEIs and it is normally managed by switching to an ARB. But, although much rarer, a cough can also be a side effect of ARBs so this could be a reason for not being on these drugs. If this was the reason, I would check if the side effect happened at lower or higher doses and I would see if a lower dose of an ACEI or ARB could be tolerated on the basis that a small dose of an ACEI/ARB is better than no ACEI/ ARB at all.

 Or was it because of hyperkalaemia? If so, did the hyperkalaemia happened when the patient was already on spironolactone? Perhaps it was the combination of these two drugs rather than the ACEI / ARB medication in isolation?

 Another reason could be the development of angioedema, which is not that uncommon with ACEIs. Normally, if this happens, you would switch the patient to an ARB but, although much rarer, angioedema can also be a side effect of ARBs.

 This patient is also on two other drugs, spironolactone and an alpha blocker that are usually reserved for step 4 treatment, when and the combination of an ACEI/ARB, a CCB and a thiazide like diuretic have failed to control the blood pressure.

 The patient is on a CCB but not a thiazide like diuretic. Why? I would check if it has been tried before and whether it could not be tolerated, for example because of gout. Although Bendroflumethiazide is the one typically associated with a rise in uric acid and worsening gout, it can also happen with other thiazide like diuretics such as indapamide and hydrochlorothiazide. Perhaps this is the reason why spironolactone was prescribed instead of the thiazide diuretic?

 And perhaps it is the issue of spironolactone that I am most uncomfortable with. Being a drug at step 4, I feel that it should not have been be initiated before the rest of his treatment has been optimised, especially in view that the history doesn’t give any other indications for it, such as chronic heart failure.

 And the issue or the alpha blocker needs looking into too. I would look to see if perhaps it was prescribed because the patient suffers from urinary outflow obstruction and it was thought that we could, so to speak, “kill two birds with one stone”. Remember that terazosin is licensed for both hypertension and benign prostatic hyperplasia.

 And finally, the dose of his CCB is low. Felodipine can go up to 10 mg daily and he is only on 2.5 mg OD. As long as he has not developed leg / ankle oedema as a side effect on higher doses in the past, increasing the dose could be an option.

 Right, having said all this, in order to progress with the case, we will say the following:

 ·      There are no signs of renal artery stenosis and that he has been fully investigated for secondary causes of hypertension and it has been concluded that he has essential or primary hypertension.

 ·      The reason for not being on an ACEI or ARB is because a cough developed with lisinopril 2.5mg OD and also when the dose of losartan went from 50mg to 100mg OD.

 ·      Felodipine has never been given at a higher dose than 2.5mg OD and currently there is no ankle oedema

 ·      A thiazide diuretic was not tolerated because of gout but since then the patient has been started on allopurinol so gout no longer seems to be a problem.

 ·      Terazosin was given in place of tamsulosin, which was recommended by his urologist for benign prostatic hyperplasia.

 ·      There is no other indication for spironolactone.

 So, what would I do?

 My interpretation is that, given that small doses of an ARB were tolerated before, I would try to restart losartan at 25mg OD increasing to 50mg OD to see if it is tolerated at lower doses without causing a cough. On doing this, I would stop spironolactone to minimise the risk of hyperkalaemia and also because there is no real indication for spironolactone at this stage.

 I would also, at the same time, increase felodipine to 5mg OD and possibly to 10 mg OD soon after depending on the response.

 And I would keep him on terazosin 10 mg OD for the benefit on his BPH.

 Remember that we want to treat him aggressively because of his age. According to NICE, the target BP for people under the age of 80 is <150/90 but <140/90 if the patient has CKD and <130/80 if the patient has CKD and an ACR >70. In his case we know that the target needs to be at least <140/90.

 If the BP is not controlled on the optimal tolerated doses of these 3 drugs, then we would say that he has resistant hypertension.

 And NICE says that before considering further treatment for a person with resistant hypertension:

·      We should confirm it using ambulatory or home blood pressure recordings.

·      We should assess for postural hypotension.

·      We should discuss adherence

And NICE also says that for people with confirmed resistant hypertension, we could consider adding a fourth antihypertensive drug as step 4 treatment or seeking specialist advice. 

If it came to that, what would I do?

I may be tempted to refer him because of his young age. But you could also argue in favour of adding a fourth drug. Which one would I choose in this case?

I might start by trying a thiazide diuretic, now that his gout is under control, as he may tolerate it now. Unfortunately, both indapamide and hydrochlorothiazide can potentially interact with allopurinol, increasing the risk of hypersensitivity reactions and, although the manufacturer makes no recommendations in this respect, it is a severe theoretical risk. In this situation I would consider changing the gout treatment from allopurinol to an alternative agent, something like Febuxostat and then add, for example, indapamide MR 1.5mg OD for his hypertension.

If the patient or you did not want to change his gout medication for a reason, the other two options would spironolactone and a betablocker. You could start spironolactone if the potassium levels are below 4.5 but watching the levels carefully as the combination of an ACEI or ARB and spironolactone can increase the risk of hyperkalaemia. If the potassium levels are above 4.5 the choice would be restricted to a betablocker. However, remember that betablockers are contraindicated in severe PVD so this may be a problem in this patient. However, when there is no alternative, sometimes a cardio selective betablocker may be used cautiously under specialist supervision if the PVD is not severe.

 But remember that this is only my interpretation so it is not necessarily the best option. 

 We have come to the end of this episode. I hope that you have found it useful. Thank you for listening and good-bye