Health and Prostate

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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.

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