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Editorials

Prostate artery embolisation for benign prostatic hyperplasia

BMJ 2018; 361 doi: https://doi.org/10.1136/bmj.k2537 (Published 19 June 2018) Cite this as: BMJ 2018;361:k2537

Re: Prostate artery embolisation for benign prostatic hyperplasia

Dear Sirs,

I would like to give a patient’s point of view of the exciting curative opportunity PAE can offer, compared with surgery or long term drugs.

I had a PAE in June 2017. Previously, I had had 5 years of mild LUTS, controlled by lifestyle. But over two months I progressed to an IPSS score of 30+ and found myself in AUR. The pre-PAE MRI reported prostate volume at 116cc; no suspicion of carcinoma.

I was offered HoLEP but the downsides were 3 – 3 ½ hours under general anaesthetic; 3% need for repeat; 5% risk of a stricture (I was now catheterised); an outside chance of pulmonary embolism and/or stroke, and a 100% chance I would never ejaculate normally forwards again, I didn’t fancy the op.

I talked to a urologist with experience of 100+ PAEs. His advice: PAE fails in about 20% of cases but since I was actually in AUR, my chance of success was 50%. However, if I PAE failed, my worst case was that I would just have to do the HoLEP anyway; if PAE worked, I would have avoided HoLEP and its side effects and risks. I’d know within 3 weeks of doing a PAE whether PAE was working; I could go for a HoLEP if it wasn’t.

So, for me, PAE was what snooker players call “a shot to nothing”. If PAE worked, I’d retain, as a young and athletic 62 year old, full sexual function and avoid taking the risk a stricture or stroke/pulmonary embolism.

My interventional radiology (experienced in 50+ PAEs) advised after CT that I had simple vascular anatomy; access to my prostate would be easy; and my prostate was “adenomatous dominant”, a factor in recent successes: see the Little et al paper cited below.

I decided to give PAE go for three months. My urologist changed my urethral catheter to superpubic, to put me in control of continuous trials for voiding. Cystoscopy photos showed I did not have middle lobe, nor a “ball valve” problem; these are other factors in recent PAE successes.

My GP checked out the radiation risk I would expose myself to. In simple terms, it was calculated in my case as five summers in England, which I thought was very acceptable.

Intolerant to alpha blockers, I did the PAE without using them, the first such documented case, I was told. From my viewpoint, there was a tiny scratch in an artery. I lay back and listened to music on my headphone. Within 45 minutes, full bilateral embolization was successfully accomplished, using the “PErFecTED technique”. It was all very pleasant.

Within 2 hours, I was voiding naturally. I went home that afternoon. There were a few hours of searing pain, until the prostatic nerves, deprived of blood, died, but they soon switched off like a light – there was no pain at all after that. I never looked back from the first day, voiding 2 ½ litres. It was tough going until an aperture widened. But within three weeks I was voiding completely normally and freely without any feeling of discomfort. My GP checked every few days for urine infections, since PAE works by necrotising internal tissue. We were onto the two I got straight away, so they were not a problem. We used the charts in the Gao paper, cited below, to monitor progress; they detail a timescale for measured improvements in IPSS and flow seen in other cases.

Within a month, my IPSS score was zero where it has remained; my peak flow was 20mm/sec. The superpubic catheter was removed. Within 6 months, a second MRI showed that my prostate volume was 53cc, as compared with 116cc before the PAE, a reduction of 54%.

Here I am, therefore, a documented case of someone in AUR, who escaped AUR through a PAE with no surgery and no drugs, has an IPSS score of zero, is asymptomatic, and retains full sexual function. How many others who have had LUTS can say that?

Why did the PAE work for my type of LUTS? KT Foo (see citation) has been explaining that some types of LUTS are primarily caused by adenomas, not prostatic size per se. Imagine internal adenomas as if they were marbles inside a tennis ball (the prostate) and you can imagine how, when all the adenomas expand, the prostatic cap resists and a reverse force is exerted back to compress the uethra. Or imagine two large adenomas as if croquet balls side by side growing so as to “squeeze” the urethra. Or imagine one large adenoma growing to as to kink the urethra, as if an “oxbow” bend in the channel of a river. A PAE can attack such adenomas, resolving the problem directly.

An MRI generated picture of an example of an “oxbow bend” case of a steep kink in a urethra induced by an enormous prostatic adenoma has been produced by Dr Mark Little in his Oxford Surgery video lecture cited below (minutes 31 – 36). The urethra is later straightened out after the patient has a PAE that destroys the adenoma, enabling the urethra to straighten.

This is why I suggest alpha blockers might not resolve this type of LUTS problem. They work by relaxing the sphincter. But, if the real cause of this type of LUTS is adenomatous in nature, alpha blockers might not address the root of that problem. PAE does.

PAE is going to be very popular. Lots of men will want to preserve full sexual function and avoid stricture, or other, risks. But it is not yet fully appreciated is LUTS drugs can have some tedious side effects and PAE may offer men at least the chance of avoiding drugs in cases where the true nature of the LUTS is adenoma-generated.

References:

Gao et al, Radiology 2014 Mar, 270(3): 920-928.
Foo, Asian J Urology 2017 Jul: 4(3): 152-157.
Little et al, Cardiovasc Interv Radiology 2017, May 40(5): 682-689.
Oxford Surgical Lecture “Prostate Artery Embolization in the Management of LUTS” https://www.youtube.com/watch?v=bcricbWiq1M

Competing interests: No competing interests

20 June 2018
Brian W Dye
Patient
None
Sevenoaks, UK