Health and Prostate

The indications for surgery in benign prostatic hypertrophy are essentially the symptoms confirmed by signs of prostatism. More absolute indications are those of secondary renal failure, recurrent infection, and of course, urinary retention. These factors must be considered in conjunction with the patient’s age and state of health.’

I think it important that the family physician understand some aspects of the surgical technique and possible complications, in order to reassure both patient and family at the time of referral and in subsequent follow-up. Essentially, the surgical techniques are either transurethral or open (supra-pubic or retropubic) and both procedures remove the adenoma down to the level of the capsule if properly performed. The transurethral procedure is preferable, but the open technique may be necessary in the presence of a particularly large adenoma. The urologist must decide on the basis of his own ability whether or not he can adequately resect the gland transurethrally within the allotted time. If he feels the gland is too big for this, it should be approached via the open route. However, the open procedure is not more complete than the transurethral one, if the latter is done properly. In both situations, the capsule remains and neither procedure prevents the subsequent development of carcinoma.

One problem which often causes patients to delay seeing their doctor is their concern about subsequent sexual function. Many patients have the idea that prostatectomy means the end of their sexual life. In this area, the family doctor can be particularly reassuring. Prostatectomy for benign disease by either the transurethral or open routes (except for the seldom used perineal route) does not lead to impotence. Usually the only abnormality seen may be a degree of retrograde ejaculation. After a prostatectomy, the bladder neck may not close completely at the time of ejaculation allowing the ejaculate to pass into the bladder in retrograde fashion. This is then simply passed with the next voiding. The patient should experience normal orgasm, but if not prepared, may be concerned about the lack of emission. Once reassured, this should not affect sexual activity, although it would obviously result in infertility.

At the time of discharge, many patients will still be complaining of urgency, frequency and dysuria. This is related to inflammation in the bladder secondary to the catheterization, and also to the rawness of the prostatic cavity. Many physicians mistakenly assume these symptoms to be related to urinary tract infection, on the basis of pyuria and hematuria visualized on routine microscopy. In the post-prostatectomy period, these microscopic findings are associated with the surgery and the raw prostatic capsule. The diagnosis of infection can only be made on the basis of a proper urine culture with a significant bacterial count.

Another postoperative concern is related to urinary control. Shortly after the procedure, many patients develop urgency incontinence, again related to the inflammmation in the bladder and prostatic fossa. The physician must reassure his patient that control will return to normal once the inflammation settles down and the prostatic fossa reepithelializes. On the other hand, total incontinence is a dreaded complication of prostatectomy and is not likely to improve greatly. Some urologists feel that stress incontinence is related to slight sphincter damage, but this improves with time and does not tend to be a prolonged problem.

Finally, it is important that the physician follow the post-prostatectomy patient with regular rectal examinations in order to pick up the development of carcinoma in its early stages.

Initial management of a patient in the prostatic age group presenting in urinary retention involves insertion of a urinary catheter. However, certain preventive measures might be kept in mind when dealing with a patient in this age group. Many of these patients get along reasonably well in bladder balance until some situation tips them over into retention. This may be a sudden increase in fluid intake (i.e. a drinking bout or diuretics) which results in rapid bladder filling, distending the bladder beyond the critical diameter to generate the pressure necessary to overcome the increased outlet resistance associated with prostatic obstruction (Laplace’s Law). Prolonged car trips or other situations which delay voiding, allowing the bladder to distend beyond that critical volume, may also result in urinary retention. The use of belladonna derivatives such as Atropine or Probanthine may inhibit the detrussor muscle, resulting in retention. As well, other drugs such as sedatives, which decrease the patient’s ability to respond to a full bladder, result in retention. By keeping these situations in mind when dealing with elderly patients, physicians can often prevent the development of urinary retention and caution patients against situations such as long motor trips without frequent stops.

When retention has developed, however, the initial management involves proper aseptic catheterization. The use of drugs such as Carbachol or Urecholine in this situation is to be condemned, since the problem is essentially one of obstruction rather than detrussor failure. Use of these drugs will only result in increased discomfort for the patient and delay the inevitable catheterization. If the patient has had a previous history of very significant prostatic symptoms, an indwelling catheter should be inserted and prostatectomy should be considered.

If on the other hand, he has been getting along reasonably well, but has developed symptoms following catheterization or the use of drugs, then it is probably reasonable to remove the catheter and give him a trial of voiding. He should be closely watched and investigated with a view to prostatectomy at a later and perhaps more convenient time. If the catheter is removed, the patient must also be closely watched for urinary infection. Although prostatic patients carry a residual urine, this is usually sterile until contaminated. The bladder that does not empty well does not handle infection well, but does not predispose to infection until contaminated. The few bacteria introduced with catheterization might be handled well by the normal bladder defense mechanisms in a young patient, but can be disastrous in an elderly patient with a residual urine. Should this type of patient develop bacteriuria and subsequent bacteremia with sepsis, it may be necessary to catheterize him to ‘drain the abcess’ in order to control the septic process, if he does not respond to the usual doses of antibiotics.

Often difficulty may occur in attempting to catheterize a patient with significant prostatic hypertrophy. This difficulty is usually associated with poor technique and a misunderstanding of that area’s anatomy. The usual indwelling catheter used is a #16 F. or #18 F. Remember that the catheter is not being threaded through a small hole in the prostatic urethra, but rather is being forced between the two large lateral obstructing lobes and possibly up and over a large median lobe. If catheterization proves difficult, one should resort to a Tieman type of catheter which is stiffer and has a coudecurved tip which tends to take the catheter through the bladder lobes, directing it up and over the median lobe. It is important not to try a smaller catheter, if the obstruction is truly the prostate, since the smaller French sizes tend to be not as stiff and less likely to force the lateral lobes apart.

If catheterization proves impossible, and expert urological assistance is not available, the patient who is truly in retention can be easily managed with percutaneous insertion of a suprapubic tube. This should be inserted in the midline just above the symphysis pubis. If a specially prepared percutaneous suprapubic tube is not available, the large intravenous intracath will often suffice. Because the distended bladder tends to sweep the peritoneum up and away from this area, there is no danger of sticking the needle into any intraperitoneal structures. This will then manage the acute situation until the patient can be transferred for definitive urological treatment.

In the past, much concern has been placed on decompressing the bladder slowly because of the complications of hematuria and significant renal failure. More recently, however, it has become apparent that slow decompression does not prevent these complications. The hematuria appears to be secondary to the sudden release of pressure in the collecting system, resulting in rupture of many of the small veins lining that system. This is predominantly seen in the bladder, but can also occur in the upper collecting system. In order to maintain flow in the presence of increased intravesical pressures, these thin walled veins must develop a significantly increased intra-luminal pressure. The sudden removal of pressure in the bladder with catheterization results in a loss of support for the thin walled veins and they may burst, resulting in significant hematuria. Unfortunately, this complication is not prevented by prolonged decompression. Pressure studies have shown that the pressure in the bladder essentially returns to normal and the patient’s discomfort usually disappears with the removal of 10-50 ml of urine. Therefore, decompression beyond this point is obviously of no value and simply prolongs the bladder emptying, possibly leading to confusion in monitoring the patient’s output.

The post-obstructive pathological diuresis with subsequent vascular collapse and renal failure described in textbooks and the earlier literature is now better understood and is in fact believed to be a physiological diuresis. This is usually seen in patients with early renal failure (BUN greater than 70 mg %) and is due to an increased total body exchangeable sodium. Many of these patients will have some edema and perhaps development of early hypertension secondary to this increased volume. Renal failure is often reversible with relief of obstruction and the patient simply undergoes a physiological diuresis until his volume returns to normal. However, on noting this diuresis, physicians tend to set up a IV and try and match input with output — as in the diuresis seen with the recovery phase of ATN. This results in a prolonged diuresis until the physician finally slows down the IV. The better approach would be to set up an IV and monitor the patient closely with a view to instilling intravenous saline at the first signs of volume contraction. The typical patient at risk for this type of problem is usually the elderly confused patient presenting in chronic retention. The confusion is often due to early uremia and will revert to normal with catheter drainage. Therefore, when seeing a patient in chronic urinary retention with signs of confusion, mild hypertension and/or edema, BUN, creatinine, and electrolytes should be obtained at the time of catheterization so that his subsequent course can be properly monitored.

Having obtained the symptoms suggestive of outlet obstruction, the diagnosis should then be confirmed by the signs of outlet obstruction. On physical examination, the bladder may or may not be palpable. Rectal examination should normally reveal an enlarged prostate. However, it is the periurethral portion of the gland which initially enlarges; it is possible for this to cause very little overall enlargement of the gland. Usually, enlarged glands are more likely to be associated with obstruction, but it is possible to have

significant outlet obstruction in the presence of a relatively small gland palpable rectally. If the symptoms suggest prostation, the patient should be further investigated.

Urinalysis and urine culture should always be performed to rule out infection, diabetes and other renal and bladder problems which might contribute to the symptoms mentioned above.

Blood work should consist of indices of renal failure such as BUN and creatinine, plus serum acid and alkaline phosphatase. An elevated serum acid phosphatase in the absence of Paget’s disease or other problems associated with a tremendously high alkaline phosphatase suggests stage D carcinoma of the prostate, which may influence both investigation and treatment of the patient’s symptoms. However, the acid phosphatase is normally elevated only when the cancer has spread beyond the confines of the gland and only in a well differentiated tumor (a poorly differentiated cell cannot manufacture this complicated protein). An acid phosphatase is therefore not a screening test for prostatic carcinoma.

An IVP with a post-void film may be particularly useful. The pyelogram itself will show evidence of upper tract problems secondary to obstruction such as hydroureters and hydronephrosis. As well, an enlarged prostate can often be seen elevating the bladder base and even bulging into the bladder. The bladder film may also reveal evidence of cellules and diverticuli secondary to outlet obstruction and increased bladder pressures. The post-void film is most useful, however, in obtaining an assessment of residual urine without contaminating the bladder by instrumentation. On the other hand, one must keep in mind that elderly patients often find the hustle and bustle of a modern radiology department somewhat disconcerting and are not always able to relax enough to void properly. This can result in falsely increased residual urines, but a negative residual urine under these circumstances is most significant and suggests another cause for the patient’s symptoms.

If the above investigation suggests that the patient does suffer from prostatic hypertrophy or if the diagnosis is still somewhat confused, the patient should be referred for cystoscopy. This examination will not only assess the lower urinary tract, but will confirm whether or not the gland is obstructive. Also, examination of the bladder should show significant signs of obstruction, such as a high residual urine, trabeculation and cellule formation. This will be particularly useful information in the patient with a small gland but symptoms of obstruction. It may also be helpful in ruling out the patient with prostatitis who certainly would not benefit by surgery and might in fact be made worse. As mentioned earlier, the differentiation between true obstruction and prostatitis can be most difficult in the presence of an enlarged gland. Even at cystoscopy, the true nature of the problem may not be obvious and often on visualizing some obstruction and a little trabeculation the surgeon has been led into an operation which he subsequently regrets.

The commonest symptom associated with prostatism is frequency and in particular, nocturia. The most objective of these is nocturia, since every patient remembers getting up at night and exactly how many times. It is usually this which brings him to his doctor. Day time frequency is less objective, since it often relates to other influences such as lunch hours and coffee breaks, and is less likely to inconvenience the patient. Frequency of prostatic hypertrophy is related to a relative decrease in functioning bladder capacity. The patient carries a large residual urine which actually gives him an increased bladder capacity, but because most of the urine remains behind as a residual, the functioning capacity is quite small. If the bladder does not empty completely, it does not take as long to fill up again and give the patient the urge to void.

Many other situations, however, can also lead to frequency and may be confused with prostatic hypertrophy. A small contracted bladder, as seen with radiotherapy or tuberculosis, will produce frequency. Bladder irritability secondary to inflammation such as infection, stone or tumor will also lead to frequency. A patient with an indwelling catheter develops a significant inflammatory response in the bladder and upon removal of the catheter will be cured with frequency until the secondary inflammation disappears. In particular, patients with chronic prostatitis (bacterial or not) will present with frequency secondary to irritation. These cases are often very difficult to differentiate from true prostatic hypertrophy and obstruction, since on rectal examination the prostate may feel somewhat enlarged.

However, most patients with frequency from irritation usually have associated dysuria, which is not a common finding in patients with pure obstruction, unless their residual urine has been contaminated. Polyuria may also lead to frequency; it is often seen in patients taking diuretics and those having chronic renal tubular diseases with poor concentrating ability. Late onset diabetes may also initially present with frequency secondary to the osmatic diuretic affect of glycosuria. A neurogenic bladder can also lead to frequency, as in a diabetic with neuropathy and a secondary-type neurogenic bladder. This patient often does not appreciate bladder fullness until he notes abdominal discomfort. As a result, he leaves behind a large residual urine even though he initially has relatively normal muscular activity.

Prostatism also includes the symptoms of hesitancy and a small stream. Both of these symptoms may not be as obvious to the patient as one might expect. The decreasing stream occurs over a long period of time and most patients accept this simply as a symptom of old age. Hesitancy also develops over a long period of time and often has to be quite dramatic before the patient will actually volunteer this complaint.

Urgency and urgency incontinence often bring the patient to his physician, because they will interrupt his normal daily routine. Incontinence can be associated with overflow in a patient in chronic retention, or may consist simply of persistent post-void dribbling.

Beware, however, of ‘silent’ prostatism, where symptoms may be absent or minimal in the face of far advanced bladder decompensation — the patient may present with symptoms related to renal failure and other sequelae of long standing obstruction.

It is important to obtain details of the patient’s drug intake, in particular anticholinergics or tranquillizers which may inhibit the bladder, leading to some of the above mentioned symptoms.

Prostatism is the clinical syndrome consisting of the symptoms associated with outlet obstruction at the bladder neck. By far the commonest cause of this syndrome is benign prostatic hypertrophy, but other entities such as bladder neck stenosis and urethral strictures can produce these symptoms as well.

Prostatic hypertrophy is in fact a hyperplasia of epithelial and fibromuscular elements arranged in multicentric nodules and originating in the periurethral part of the gland. As the hyperplastic process continues, the nodules coalesce into lobes which compress the outer prostate into a false or ‘surgical’ capsule. The surgery for benign prostatic disease (open or transurethral) involves removal of these lobes down to the level of this capsule, but does leave the outer prostate behind and therefore does not prevent subsequent development of carcinoma.

Although eight anatomic types of prostatic obstruction have been described, for practical purposes most obstruction consists of lateral lobe hypertrophy plus or minus median lobe involvement. Cystoscopically, this is visualized as two large lobes coming in from both sides laterally and as the instrument goes beyond, it may or may not have to go up over a prominent median lobe before entering the bladder. This anatomical information is of some significance when trying to catheterize a patient with prostatic obstruction.

The prostate can be palpated rectally. It is normally rubbery, firm and because of the usual lateral lobe involvement, the median sulcus is normally preserved. The apex (distal portion) is usually narrower than the base (bladder neck area) and normally the benign gland is relatively symmetrical — but asymmetry does not necessarily mean malignancy. Normal adult prostate size would be roughly two centimeters in diameter. Most urologists, however, describe prostatic size as a measure of volume by weight. This may seem a little strange, but relates to the pathologist’s initial description of the surgically removed gland in grams; thus a normal adult size prostate would be 10-20 grams in size. Commonly, benign prostatic hypertrophy involves a gland of approximately 30 to 40 grams in size, but certainly adenomas removed at open prostatectomies have been weighed at over 200 grams.