Urinary retention, obstruction and hydronephrosis

Obstruction damages the kidney through a sequence of pressures, and each step can be measured. Urine is normally propelled by gentle peristaltic waves that generate only a few centimetres of water of pressure inside the renal pelvis, so the tubules downstream are never exposed to a significant hydrostatic load. When an obstruction appears, whether it is a prostatic enlargement, a calculus or a fibrous stricture, the fluid behind it becomes static. Because the tract is a closed space, the pressure generated by the collecting system is transmitted backwards, rising first in the ureter and then in the renal pelvis. The kidney responds with distension, which is hydronephrosis, but the visible swelling matters less than the pressure it represents, because that pressure is transmitted to the nephrons themselves. Within hours of an acute complete obstruction, the glomerular filtration rate falls substantially; the cause is a combination of reduced renal blood flow and a rising hydrostatic pressure in Bowman’s space that opposes filtration. Tubular function is impaired at the same time: the ability to transport sodium, potassium and protons, and to dilute or concentrate the urine, is severely reduced, so the kidney loses the fine control that keeps the internal environment steady. If the obstruction is relieved quickly, much of this recovers, but the depression of glomerular filtration can persist for weeks, and a kidney that has been subjected to repeated or prolonged episodes develops interstitial fibrosis as the muscular wall of the ureter is replaced by collagenous scar tissue and the renal parenchyma thins through pressure atrophy. This is why repeated high-pressure episodes cause permanent scarring and chronic kidney disease. Bilateral obstruction is far more dangerous than unilateral, because the unobstructed contralateral kidney can compensate for one damaged organ but not for two, and it is bilateral obstruction that produces azotaemia and, if untreated, uraemic complications.

Relieving a long-standing obstruction does not always end the problem. The distended kidney has been building and maintaining a salty medullary gradient so that it can reabsorb water from the collecting duct; when the pressure is suddenly removed, that gradient is washed out and the tubule can no longer conserve water. At the same time, the urea and sodium that accumulated during the obstruction are delivered to the tubule in large amounts and act as an osmotic diuretic, dragging water out with them. The result is post-obstructive diuresis: a large volume of dilute urine that can continue for hours to days. The clinical risk is that this fluid is lost from a patient who is already unwell, so plasma volume falls, electrolyte reserves are depleted, and the acute kidney injury that the catheter was meant to prevent can worsen. There is a clear threshold for action: patients producing more than 200 mL of urine per hour should have about half of that output replaced with intravenous fluid, and their urine output is monitored over the 24 hours after catheterisation. Not every patient needs this. The risk is concentrated in those with a very large residual volume, and volumes above about 1000 mL are seen only in acute-on-chronic retention, which is why the drained volume is recorded and not simply discarded. Nursing observation therefore has three parts: an hourly measurement rather than a 24-hour total, because the threshold is expressed per hour; a record of the colour and concentration, since dilute urine confirms the mechanism; and regular monitoring of renal function and electrolytes, particularly potassium and magnesium, because replacement fluid restores volume but not necessarily the solutes lost with it. Patients whose function is still impaired also keep their catheter, since a further retention episode would add damage on top of damage.

The site of an obstruction is often predictable from the patient’s age, and that pattern is a useful first question. In children, obstruction is due mainly to birth defects, and the classic example is posterior urethral valves, extra folds of tissue in the back part of the urethra that narrow the outflow before the child is ever toilet trained; other congenital constrictions narrow the ureter or the junction between the ureter and the renal pelvis. In young adults the commonest cause is a stone lodged in a kidney, a ureter or elsewhere, and because stones are mobile and irregular they typically produce the intermittent agony of renal colic rather than the silent distension of a slow obstruction. In older adults the balance shifts to benign prostatic hyperplasia and prostate cancer, together with tumours and stones, which is why obstruction is more common in men than in women overall. Beyond that age pattern the list is long: polyps in the ureter, a blood clot, a tumour pressing on the ureter from outside, disorders of the muscle or nerve of the ureter or bladder, fibrous tissue forming around the ureter after surgery, radiation therapy or certain drugs such as methysergide, a ureterocele, which is a bulging of the lower ureter into the bladder, tumours, abscesses and cysts of the bladder, cervix, uterus, prostate or other pelvic organs, and a large mass of faeces stuck in the rectum. In women two mechanisms are particular to them: as the uterus expands in pregnancy it can compress the ureters, and a prolapsed uterus or a cystocele, in which the bladder droops because the wall between bladder and vagina has weakened, can distort the outflow. The practical message is that obstruction in a woman or a child is not rare and is not always prostatic, so the assessment follows the anatomy rather than the stereotype.