Bladder Outlet Obstruction
Regulation of prostate growth and development of benign prostatic hyperplasia (BPH)
BPH is characterized by an increase in epithelial and stromal cell numbers (hyperplasia) in the peri-urethral area of the prostate. New epithelial gland formation is normally only seen during foetal development. The development of new glands in the adult prostate has given rise to the concept of ‘reawakening’ of the inductive effect of the prostatic stroma on the prostatic epithelium.
The increase in prostate cell number could reflect proliferation of epithelial and stromal cells, impairment of programmed cell death, or a combination of both. During the early phases of development of BPH, cell proliferation occurs rapidly. In established BPH, cell proliferation slows down and there is impairment of programmed cell death (androgens and oestrogens actively inhibit cell death).
The role of androgens in BPH
Testosterone can bind directly to the androgen receptor or may be converted to a more potent form, dihydrotestosterone (DHT), by the enzyme 5α-reductase (5AR). There are two isoforms of 5AR, type I or ‘extraprostatic’ 5AR (which is absent in prostatic tissue and present in, for example, skin and liver) and type II or ‘prostatic’ 5AR (which is found exclusively on the nuclear membrane of stromal cells, but not within prostatic epithelial cells). Type I 5AR is not inhibited by finasteride whereas type II 5AR is. Dutasteride inhibits both types I and II 5AR. Finasteride reduces serum DHT by about 70% and dutasteride by about 95%. Finasteride reduces prostatic DHT (type II) by about 80% and dutasteride by about 94%. We do not know whether these differences translate into differences in clinical efficacy since neither drugs has been compared against the other.
Testosterone diffuses into prostate and stromal epithelial cells. Within epithelial cells, it binds directly to the androgen receptor. In prostate stromal cells, a small proportion binds directly to the androgen receptor, but the majority binds to 5AR (type II) on the nuclear membrane, is converted to DHT, and then binds (with greater affinity and, therefore, greater potency than testosterone) to the androgen receptor in the stromal cell. Some of the DHT formed in the stromal cells diffuses out of these cells and into nearby epithelial cells (a paracrine action). The androgen receptor/testosterone or androgen receptor/DHT complex then binds to specific binding sites in the nucleus, thereby inducing transcription of androgendependent genes and subsequent protein synthesis.
It is thought that stromal/epithelial interactions may be mediated by soluble growth factors—small peptides that stimulate or inhibit cell division and differentiation. Growth stimulating factors include basic fibroblastic growth factor (bFGF), epidermal growth factor (EGF), keratinocyte growth factor (KGF), and insulin-like growth factor (IGF). Transforming growth factors (e.g. TGFβ) normally inhibit epithelial cell proliferation and it is possible that in BPH, TGFβ is downregulated.
Pathophysiology and causes of bladder outlet obstruction (BOO) and BPH
The principal cause of BOO in men is BPH. Less common causes are urethral stricture and malignant enlargement of the prostate. BOO in women is altogether less common, the causes including pelvic prolapse (cystocele, rectocele, uterine), the prolapsing organ directly compressing the urethra; urethral stricture; urethral diverticulum; post-surgery for ‘stress’ incontinence; Fowler’s syndrome (impaired relaxation of external sphincter occurring in premenopausal women, often in association with polycystic ovaries); and pelvic masses (e.g. ovarian masses). In either sex, neurological disease (spinal cord injury, spina bifida, multiple sclerosis (MS)) can cause failure of relaxation of the external sphincter during voiding (detrusor sphincter dysynergia, DSD).
The pathophysiological basis of BOO due to benign prostatic enlargement (BPE) secondary to BPH (benign prostatic obstruction, BPO) has been studied more than any other type of obstruction. BPO has dynamic and static components:
Dynamic component of BPO: 1-adrenoceptor-mediated prostatic smooth muscle contraction. Smooth muscle accounts for approximately 40% of the area density of the hyperplastic prostate and human prostate contracts following administration of alpha adrenergic agonists. This effect is the rationale for α-adrenoceptor blocker treatment for symptomatic BPO.
Pathophysiological consequences of BOO
John Hunter (1786), who founded the Royal College of Surgeons of England, noted that ‘The disease of the bladder arising from obstruction alone is increased irritability and its consequences, by which it admits of little distension, becomes quick in its action, and thick and strong in its coats’. BOO causes thickening of the wall of the bladder. Microscopically, smooth muscle cells enlarge and there is an increase in connective tissue (collagen and elastin) between the smooth muscle bundles. In some cases, this may lead to poor compliance, with development of high bladder and intrarenal pressures. Progressive hydronephrosis can develop, with impairment of renal function and even renal failure (high-pressure chronic urinary retention).
Experimentally created BOO causes development of bladder overactivity (unstable bladder contractions during bladder filling). This may be due to prolonged increased intravesical pressure during voiding, causing ischaemia and leading to ischaemic damage to neurons within the bladder (i.e. denervation). Symptomatically, many patients with BOO develop frequency, urgency, and urge incontinence.
Benign prostatic obstruction (BPO): symptoms and signs
Clinical practice guidelines
Developed to standardize the approach to diagnosis (and treatment) of men presenting with symptoms suggestive of BPH.1 Every guideline agrees that a history should be taken, an examination performed, and that the severity of urinary symptoms should be formally assessed using the IPSS. This includes a measure of the ‘bother’ caused by the patient’s symptoms (i.e. the degree to which the symptoms are troubling).
Urinary symptoms—what do they mean?
During the 1990s, the classic ‘prostatic’ symptoms of frequency, urgency, nocturia, hesitancy, poor flow, intermittent flow, and terminal dribbling— traditionally said to indicate the presence of BOO due to BPE—were shown to bear little relationship to prostate size, flow rate, residual urine volume, or indeed, urodynamic evidence of BOO. Age-matched elderly men and women have similar symptom scores (IPSS), despite the fact that women have no prostate and rarely have BOO.
Prostatism vs LUTS vs LUTS/BPH
‘Prostatism’ has, therefore, been replaced by the expression ‘LUTS’, which avoids any implication about the cause of these symptoms. More recently, the expression ‘LUTS/BPH’ has been used to describe the symptoms of BPH. It doesn’t really matter whether you use ‘prostatism’, ‘LUTS’, or ‘LUTS/BPH’, as long as you remember that urinary symptoms may have non-prostatic causes. Try to avoid treating the prostate when the problem may lie elsewhere.
Ask specifically about the presence of:
Bedwetting: suggests the presence of high-pressure chronic retention (look for distension of the abdomen due to a grossly enlarged bladder that is tense on palpation and dull to percussion).
Marked frequency and urgency, particularly when also combined with bladder pain: look for carcinoma in situ of the bladder (urine cytology, flexible cystoscopy, and bladder biopsy).
Macroscopic haematuria: sometimes due to a large vascular prostate, but exclude other causes (bladder and kidney cancer and stones) by flexible cystoscopy and upper tract imaging.
Back pain and neurological symptoms (sciatica, lower limb weakness, or tingling): rarely, LUTS can be due to neurological disease.
Websites for BPH clinical practice guidelines
WHO (International Consensus Committee) guidelines. M http://www.who.int/ina-ngo/ngo/ngo048.htm.
Australian guidelines. M http://www.health.gov.au/nhmrc/publications/pdf/cp42.pdf.
German guidelines. M http://dgu.springer.de/Leit/pdf/3_99.pdf.
Singapore guidelines. M http://www.urology-singapore.org.html/guidelines_BPH.htm.
Malaysian guidelines. M http://www.mohtrg.gov.my/guidelines/BPH98.pdf.
UK guidelines. M http://www.rcseng.ac.uk/publications/.
1 Irani J, Brown CT, van der Meulen J, Emberton M (2003) A review of guidelines on benign prostatic hyperplasia and lower urinary tract symptoms: are all guidelines the same? BJU Int 92:937-42.
Diagnostic tests in men with LUTS thought to be due to BPH
Clinical practice guidelines
Developed as an attempt to standardize the approach to diagnosis and treatment of men presenting with symptoms suggestive of BPH.1 All agree that a history should be taken, an examination performed, and all recommend assessment of symptom severity using the IPSS. This includes a measure of the ‘bother’ caused by the patient’s symptoms. There is considerable variation between guidelines in terms of recommended diagnostic tests. High-quality guidelines (e.g. based on results of randomized trials) recommend few diagnostic tests2—urine analysis, completion of a voiding diary (frequency-volume chart) to detect the presence of polyuria and nocturnal polyuria (which may be the cause of a patient’s increased frequency or nocturia), and measurement of serum creatinine. They regard flow rate measurement and assessment of residual urine volume as optional tests.
DRE and PSA
Done to detect nodules that may indicate an underlying prostate cancer and to provide a rough indication of prostate size. Size alone is not an indication for treatment, but if surgical treatment is contemplated, marked prostatic enlargement can be confirmed by transrectal ultrasound scan (prostate volume in the order of 100mL or more increases the likelihood of an open prostatectomy). Discuss the pros and cons of PSA testing with the patient.
Serum creatinine
Baseline measure of renal function and to detect renal failure secondary to high-pressure urinary retention.
Post-void residual urine volume (PVR)
Varies considerably (by as much as 600mL between repeat measurements) on the same or different days.3 It cannot predict symptomatic outcome from TURP. Along with serum creatinine, it indicates whether watchful waiting is safe. It is safe not to operate where the PVR volume is <350mL,4, 5 since the majority of men show no worsening of creatinine, no increase in PVR, no worsening of symptoms, and do not require TURP.
Flow rate measurement
This is variously regarded as optional, recommended, and obligatory prior to undertaking surgical treatment for BPH. Like PVR, measurement of flow rate varies substantially on a given day,6 cannot distinguish between BOO and a poorly contractile bladder, and is not good at predicting the likelihood of a good symptomatic outcome after TURP.
Pressure flow studies
Reasonably good at predicting symptomatic outcome after TURP. However, most patients without obstruction have a good outcome and the time, cost, and invasiveness of pressure flow studies is perceived by most urologists as not justifying their routine use. The AUA Guidelines on the management of BPH (
http://www.auanet.org) regards pressure flow studies as optional since they are unable to reliably predict treatment failure in the individual patient (treatment failure is somewhat higher in the absence of obstruction, but unobstructed individuals still have a reasonable chance of improvement with TURP). The AUA Guidelines specifically state that ‘If interventional therapy is planned without clear evidence of the presence of obstruction, the patient needs to be informed of possible higher failure rates of the procedure’.
http://www.auanet.org) regards pressure flow studies as optional since they are unable to reliably predict treatment failure in the individual patient (treatment failure is somewhat higher in the absence of obstruction, but unobstructed individuals still have a reasonable chance of improvement with TURP). The AUA Guidelines specifically state that ‘If interventional therapy is planned without clear evidence of the presence of obstruction, the patient needs to be informed of possible higher failure rates of the procedure’.Renal ultrasonography
To detect hydronephrosis if serum creatinine is elevated. The percentage of patients having upper tract dilatation on ultrasound according to serum creatinine is: creatinine <115mmol/L: 0.8%; creatinine 115-130mmol/L: 9%; and creatinine >130mmol/L: 33%.7
1 Roehrborn CG, Bartsch G, Kirby R, et al. (2001) Guidelines for the diagnosis and treatment of benign prostatic hyperplasia: a comparative international overview. Urology 58:642-50.
2 Irani J, Brown CT, van der Meulen J, Emberton M (2003) A review of guidelines on benign prostatic hyperplasia and lower urinary tract symptoms: are all guidelines the same? Br J Urol Int 92:937-42.
3 Dunsmuir WD, Feneley M, Corry DA, et al. (1996) The day-to-day variation (test-retest reliability) of residual urine measurement. Br J Urol 77:192-3.
4 Bates TS, Sugiono M, James ED, et al. (2003) Is the conservative management of chronic retention in men ever justified? Br J Urol Int 92:581-3.
5 Wasson JH, Reda DJ, Bruskewitz RC, et al. (1995) A comparison of transurethral surgery with watchful waiting for moderate symptom of benign prostatic hyperplasia. The Veterans Administration Cooperative Study Group on Transurethral Resection of the Prostate. N Engl J Med 332:75-9.
6 Reynard JM, Peters TJ, Lim C, Abrams P (1996) The value of multiple free-flow studies in men with lower urinary tract symptoms. Br J Urol 77:813-18.
7 Koch WF, Ezz el Din KE, De Wildt MJ, et al. (1996) The outcome of renal ultrasound in the assessment of 556 consecutive patients with benign prostatic hyperplasia. J Urol 155:186-9.
The management of LUTS in men: NICE 2010 Guidelines
(
www.nice.org.uk/CG97)
www.nice.org.uk/CG97)For those practising in the UK, the NICE 2010 LUTS Guidelines provide a helpful summary of diagnostic and treatment options for men with LUTS. Like guidelines in general, they are not written in stone—there is no absolute requirement to follow them to the letter; you may ‘step outside’ the guidelines as long as your rationale for doing so has a logical (reasonable) basis. Differences exist between those aspects of the NICE Guidelines that cover BPH-related LUTS and the AUA 2010 Guidelines on the management of BPH (
http://www.auanet.org) and these differences are highlighted where relevant.
http://www.auanet.org) and these differences are highlighted where relevant.Initial assessment (i.e. primary care)
Assess general medical history to identify possible causes of LUTS and comorbidities; examine abdomen, genitals, DRE; dipstick urine for blood, glucose, protein, leucocytes, nitrites; complete FVC; serum creatinine and eGFR only if suspected renal impairment.
Offer information, advice, and time to decide if they wish to have PSA testing if LUTS are suggestive of BOO secondary to BPE or abnormal feeling of prostate on DRE or patient concerned about prostate cancer.
Do not routinely offer cystoscopy, flow rate, or residual urine volume measurement.
Offer lifestyle advice (e.g. advice on fluid intake); mild or moderate bothersome LUTS—discuss active surveillance* (reassurance, lifestyle advice, no immediate treatment, regular follow-up) or active intervention (conservative management, drugs, surgery).
Conservative management
Storage symptoms: If overactive bladder (OAB) suspected, offer supervised bladder training, advice on fluid intake, lifestyle advice and, if needed, containment products, i.e. pads or sheaths; offer supervised pelvic floor exercises for stress incontinence caused by—continue for at least 3 months before considering other options.
Voiding symptoms: offer intermittent self-catheterization (ISC) before indwelling or suprapubic catheterization if less invasive means fail to correct LUTS; tell men with proven BOO that bladder training is less effective than surgery; for post-micturition dribbling, explain how to do urethral milking.
Drug treatment
Offer drug treatment where conservative options are unsuccessful or inappropriate; take account of comorbidities and current treatments; do not offer homeopathy, phytotherapy, or acupuncture (Table 4.1).
Nocturnal polyuria: exclude other medical causes—diabetes mellitus and insipidus, adrenal insufficiency; hypercalcaemia; liver failure; polyuric renal failure; chronic heart failure; obstructive sleep apnoea, dependent oedema; chronic venous stasis; calcium channel blockers; diuretics; selective serotonin reuptake inhibitor antidepressants.
Consider a late afternoon loop diuretic. Consider offering oral desmopressin—measure serum sodium 3 days after first dose; stop if sodium falls below normal reference range.
Table 4.1 Drug treatment | ||||||||||||||||||
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Refer for specialist assessment
Specialist assessment
(i.e. secondary care—‘health care professional with specific training in managing LUTS in men’). A summary of surgical treatment options, based on prostatic size, for voiding symptoms is shown in Table 4.2 and for storage symptoms in Table 4.3.
Table 4.2 Voiding symptoms | ||||||||||
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Offer the following only as part of a randomized controlled trial (RCT): prostatic botox injection; laser vaporization techniques; bipolar TUVP; TUVRP (monopolar or bipolar transurethral vaporization resection of the prostate).
Transurethral needle ablation of the prostate (TUNA); transurethral microwave thermotherapy of the prostate (TUMT); high intensity focused ultrasound (HIFU); laser coagulation; transurethral ethanol ablation of the prostate (TEAP) (AUA 2010 Guidelines include TUNA and TUMT as treatment options for the patient with moderate to severe LUTS, i.e. IPSS 8 or more).
Table 4.3 Storage symptoms | ||||||||||
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Why do men seek treatment for their symptoms?
Men seek treatment for their LUTS for several reasons:
The symptoms may be bothersome.
They may fear that the symptoms are a warning that acute urinary retention will develop.
They may be concerned that their symptoms indicate that they have prostate cancer.
Establish what the patient wants from his consultation with you. Once reassured that the likelihood of urinary retention and prostate cancer is low, he may not want treatment for symptoms that, on the surface, may appear quite bad and he may be happy to adopt a policy of watchful waiting.
Goals of treatment
To improve bothersome symptoms.
To prevent symptom progression.
To reduce long-term complications (urinary retention, renal insufficiency).
Management options include watchful waiting, lifestyle modification, drug treatments (α-adrenergic blockers, 5α-reductase inhibitors, anticholinergics, plant extracts), minimally invasive surgery, TURP, open prostatectomy. The choice of treatment is determined by the patient based on his perception of how bad (bothersome) his symptoms are, balanced against the perceived benefit and risks of the various options. Drug treatments have the least impact on symptoms, but are generally safe. Minimally invasive surgery has a somewhat greater impact, with a higher risk of side effects. TURP and open prostatectomy have the greatest impact on symptoms, but at the risk of potentially serious complications.
Bothersome symptoms
Bothersomeness does not necessarily equate with symptom severity as assessed by symptom scores. Thus, a man with a low symptom score may find his symptoms very bothersome and may want treatment, whereas another man with a high symptom score may not be bothered and may want no treatment. If one symptom is particularly bad, but the other six symptoms in the 7-symptom score are minimal, overall symptom score will obviously be relatively low, but the patient may find that one symptom very bothersome (e.g. urgency and nocturia tend to be more bothersome than hesitancy or poor flow).
‘Are my symptoms due to prostate cancer?’
No particular LUTS are specific for prostate cancer. Even if it later turns out that he does have prostate cancer, a patient’s symptoms might be due to coexistent BPH or some other LUT pathology. If he is concerned about the possibility of prostate cancer, counsel him with regard to PSA testing and prostate biopsy.
‘Am I likely to develop retention of urine?’
Many patients are understandably concerned that their urinary symptoms may be a harbinger for the development of acute urinary retention.
This may influence their decision to seek help for symptoms, which they may perceive as indicating a risk of subsequent retention and it may affect the type of treatment they choose. Table 4.4 can help give the patient some idea of his risk of developing urinary retention.
This may influence their decision to seek help for symptoms, which they may perceive as indicating a risk of subsequent retention and it may affect the type of treatment they choose. Table 4.4 can help give the patient some idea of his risk of developing urinary retention.
Table 4.4 Yearly risk of retention according to age and symptom score (i.e. number of men experiencing an episode of retention every year)* | ||||||||||||
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* AUA 2010 Guidelines use the terms ‘watchful waiting’ and ‘active surveillance’ interchangeably; it defines ‘watchful waiting’ as ‘a management strategy in which the patient is monitored by his physician, but currently receives no active intervention’. Watchful waiting is recommended for patients with mild symptoms (AUA-SI <8) and patients with AUA-SI of 8 or more who are not bothered by their LUTS.
1 Jacobsen SJ, Jacobson DJ, Girman CJ, et al. (1997) Natural history of prostatism: risk factors for acute urinary retention. J Urol 158:481-7.
Watchful waiting for uncomplicated BPH
A number of studies have shown that in a substantial proportion of men, symptoms do not progress, even for those with severe symptoms.
Ball:1 a total of 107 men followed with watchful waiting over 5y. In none was there an absolute indication for surgery. Half of the patients were obstructed on urodynamic testing. A third of the patients got better, just under a half stayed the same, a quarter got worse (of whom eight underwent TURP); 2% went into retention.
PLESS study (Proscar long-term efficacy and safety study):2 a total of 1500 men with moderate to severe symptoms were randomized to placebo (and a similar number to active drug). Those on placebo had an average fall in symptom score of 1 point at 4y.
Wasson study of watchful waiting versus TURP:3 for men with moderate symptoms, the risk of progression to retention, worsening symptoms, or need for TURP was relatively low in those who chose watchful waiting; 40% noticed an improvement in their symptoms, 30% got worse, and TURP was required in about a quarter.
Five centres’ study:4 a total of 500 men referred by their family doctors for consideration for TURP were managed non-operatively after viewing an educational programme. Over the following 4y period, a proportion of the men chose drug treatment or surgery. For men with mild, moderate, or severe symptoms, 10%, 24%, and 39%, respectively, had undergone surgery at the end of 4y. For the same symptom categories, 63%, 45%, and 33% were still not receiving any treatment at the end of 4y. Almost a quarter of men who initially presented with severe symptoms noted an improvement in their symptoms to mild or moderate.
On the basis of these studies, we can say that symptoms, even if severe, do not necessarily get worse, even over fairly long periods of time. This forms the foundation of watchful waiting as an option for many patients, even if the symptoms at baseline are severe. The IPSS measures both symptom ‘severity’, but more importantly, the bother that the symptoms cause the patient. Thus, if a patient has a high symptom score (severe symptoms), but is not bothered by these symptoms, there is no indication for treatment. Some patients, on the other hand, have a low symptom score, but may find even this degree of symptoms very bothersome. Treatment is indicated in such cases (usually starting with medical therapy such as an alpha blocker or 5α-reductase inhibitor).
1 Ball AJ, Feneley RC, Abrams PH (1981) Natural history of untreated ‘prostatism’. Br J Urol 53:613-16.
2 McConnell JD, Bruskewitz R, Walsh PC, et al. (1998) The effect of finasteride on the risk of acute urinary retention and the need for surgical treatment among men with benign prostatic hyperplasia (PLESS). N Engl J Med 338:557-63.
3 Wasson JH, Reda DJ, Bruskewitz RC, et al. (1995) A comparison of transurethral surgery with watchful waiting for moderate symptoms of benign prostatic hyperplasia. The Veterans Affairs Cooperative Study Group on Transurethral Resection of the Prostate. N Engl J Med 332:75-9.
4 Barry MJ, Fowler FJJ, Bin L, et al. (1997) The natural history of patients with benign prostatic hyperplasia as diagnosed by North American urologists. J Urol 157:10-4.
Medical management of BPH: alpha blockers
The rationale for blocker therapy in BPH
As described earlier, BPO is caused partly by α1-adrenoceptor-mediated prostatic smooth muscle contraction and this is the rationale for α-adrenoceptor blocker treatment for symptomatic BPO.
There are two broad subtypes of α-adrenoceptor (AR)—α1 and α2. Molecular cloning studies have identified three α1-AR subtypes—α1a (predominant in human stroma and, therefore, mediates prostate smooth muscle contraction), α1b (predominant in human prostate epithelium), and α1L (believed to be a conformational state of the α1a-AR). The AR subtypes mediating efficacy and side effects of α-adrenoceptor blocking drugs are unknown.
Alpha blocker classification
Alpha blockers are categorized by their selectivity for the AR and by their elimination half-life.
Non-selective: phenoxybenzamine—effective symptom control, but high side effect profile.
α1: prazosin, alfuzosin, indoramin.
Long-acting α1: terazosin, doxazosin, alfuzosin SR.
Subtype selective: tamsulosin—relatively selective for α1a-AR subtype compared to the α1b subtype.
No study has directly compared one alpha blocker with another in terms of efficacy or side effects. Terazosin and doxazosin require dose titration to minimize dizziness and syncope at the start of treatment.
Indications for treatment
Bothersome LUTS where watchful waiting has failed or the patient wishes to have treatment.
Efficacy
Percentage of patients who respond to alpha blockers
Patients are able to perceive a 4-point improvement in IPSS. If ‘response’ is defined as >25% improvement in symptoms relative to placebo, most studies describe response rates of 30-40%.1 The mean probability for improvement in symptom score after TURP is in the order of 80% (i.e. 8 out of 10 men will notice an improvement in their symptoms after TURP). For those men who respond, the alpha blockers have a much more rapid onset than do the 5α-reductase inhibitors. Their effect will be maximal within a month of starting treatment.
Improvements in symptom score in men who ‘respond’ to alpha blockers
The average improvement in symptom score after TURP is about 85%.2 While some of this may represent a placebo response, this improvement is considerably better than that seen with the alpha blockers, which result in a 10-30% improvement in symptom score relative to placebo.3 This equates to a 4-5 points’ improvement in symptom score over placebo.
Side effects
A substantial proportion of men stop taking their medication either because of side effects (15-30% report some constellation of side effects) or because of a perceived lack of effectiveness (approximately 50% of men stop taking an alpha blocker within 3y because of a perception that it has not worked).4 Side effects include asthenia (weakness in 5%), dizziness (2-14%), headache (2%) and postural hypotension (1%), and retrograde ejaculation (8%). There is little data on the safety of concomitant use of the alpha blockers with drugs for erectile dysfunction.1
Intraoperative floppy iris syndrome (IFIS) and alpha blocker use
A triad of progressive intraoperative miosis (constriction of the pupil) despite preoperative dilation, billowing of a flaccid iris, and iris prolapse toward the incision site during cataract surgery lead to complications such as posterior capsule rupture with vitreous loss and post-operative intraocular pressure spikes (visual acuity outcomes appeared preserved). The original report linked this condition with the preoperative use of tamsulosin; iris dilator smooth muscle inhibition has been suggested as a potential mechanism.5, 6
Risk of IFIS among men taking tamsulosin is substantial (43-90% in ten retrospective and prospective studies).7 The risk of IFIS appears to be lower with older, generic alpha blockers such as terazosin and doxazosin (0-25%).7
Whether stopping alpha blocker treatment at any time before surgery mitigates the risk of IFIS is unclear. The AUA 2010 BPH Guidelines7 recommend that men with LUTS secondary to BPH where alpha blocker therapy is planned should be asked about planned cataract surgery. Those with planned cataract surgery should avoid the initiation of alpha blockers until their cataract surgery is completed.
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