Harrisons Manual of Medicine, 18th Ed.

CHAPTER 157. Urinary Tract Obstruction

Urinary tract obstruction (UTO), a potentially reversible cause of renal failure (RF), should be considered in all cases of acute or abrupt worsening of chronic RF. Consequences depend on duration and severity and whether the obstruction is unilateral or bilateral. UTO may occur at any level from collecting tubule to urethra. It is preponderant in women (pelvic tumors), elderly men (prostatic disease), diabetic pts (papillary necrosis), pts with neurologic diseases (spinal cord injury or multiple sclerosis, with neurogenic bladder), and individuals with retroperitoneal lymphadenopathy or fibrosis, vesicoureteral reflux, nephrolithiasis, or other causes of functional urinary retention (e.g., anticholinergic drugs).

CLINICAL MANIFESTATIONS

Pain can occur in some settings (obstruction due to stones) but is not common. In men, there is frequently a history of prostatism. Physical exam may reveal an enlarged bladder by percussion over the lower abdominal wall; bedside ultrasound assessment (“bladder scan”) can be helpful to assess the post-void bladder volume. Other findings depend on the clinical scenario. Prostatic hypertrophy can be determined by digital rectal examination. A bimanual examination in women may show a pelvic or rectal mass. The workup of pts with RF suspected of having UTO is shown in Fig. 157-1. Laboratory studies may show marked elevations of blood urea nitrogen and creatinine; if the obstruction has been of sufficient duration, there may be evidence of tubulointerstitial disease (e.g., hyperkalemia, non-anion-gap metabolic acidosis, mild hypernatremia). Urinalysis is most often benign or with a small number of cells; heavy proteinuria is rare. An obstructing stone may be visualized on abdominal radiography or helical noncontrast CT with 5-mm cuts.

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FIGURE 157-1 Diagnostic approach for urinary tract obstruction in unexplained renal failure. Circles represent diagnostic procedures and squares indicate clinical decisions based on available data.

Ultrasonography can be used to assess the degree of hydronephrosis and the integrity of the renal parenchyma; CT or IV urography may be required to localize the level of obstruction. Calyceal dilation is commonly seen; it may be absent with hyperacute obstruction, upper tract encasement by tumor or retroperitoneal fibrosis, or indwelling staghorn calculi. Imaging in retroperitoneal fibrosis with associated periaortitis classically reveals a periaortic, confluent mass encasing the anterior and lateral sides of the aorta. Kidney size may indicate the duration of obstruction. It should be noted that unilateral obstruction may be prolonged and severe (ultimately leading to loss of renal function in the obstructed kidney), with no hint of abnormality on physical exam and laboratory survey.

TREATMENT Urinary Tract Obstruction

Management of acute RF associated with UTO is dictated by (1) the level of obstruction (upper vs. lower tract), and (2) the acuity of the obstruction and its clinical consequences, including renal dysfunction and infection. Benign causes of UTO, including bladder outlet obstruction and nephrolithiasis, should be ruled out because conservative management, including Foley catheter placement and IV fluids, respectively, will usually relieve the obstruction in most cases.

Among more seriously ill pts, ureteral obstruction due to tumor is the most common and concerning cause of UTO. If technically feasible, ureteral obstruction due to tumor is best managed by cystoscopic placement of a ureteral stent. Otherwise, the placement of nephrostomy tubes with external drainage may be required. IV antibiotics should also be given if there are signs of pyelonephritis or urosepsis. In addition to ureteral stenting, pts with idiopathic retroperitoneal fibrosis are typically treated with immunosuppression (prednisone, mycophenolate mofetil, and/or tamoxifen).

Fluid and electrolyte status should be carefully monitored after obstruction is relieved. There may be a physiologic natriuresis/diuresis related to volume overload. However, there may be an “inappropriate” natriuresis/diuresis related to (1) elevated urea nitrogen, leading to an osmotic diuresis; and (2) acquired nephrogenic diabetes insipidus. Hypernatremia, sometimes of a severe degree, may develop.

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For a more detailed discussion, see Seifter JL: Urinary Tract Obstruction, Chap. 289, p. 2396, in HPIM-18.