INTRODUCTION

Obstruction of the urinary tract is a common medical condition and an important cause of reversible acute kidney injury. It affects all age groups. The cause of obstruction varies by age. Pediatric patients most commonly have anatomic abnormalities that lead to obstruction, such as stenoses of the ureter at the ureteropelvic or ureterovesicular junction, urethral valves, or strictures. Renal calculi are the most common cause of urinary tract obstruction in young adults, whereas in the elderly population, renal calculi remain a prominent cause, but benign prostatic hyperplasia (BPH) and neoplasm, as well as other pelvic carcinomas, are also important causes.

Urinary tract obstruction can be either unilateral or bilateral, partial or complete. An understanding of this is important because the presence of urine flow does not exclude obstruction. In the case of unilateral obstruction, the unobstructed kidney continues to function normally. With partial obstruction, urine flow can be decreased, normal, or even increased. The increased urine flow from a partially obstructed kidney results from tubular injury and loss of concentrating ability. Anuria most commonly results from profound shock or complete obstruction. Therefore, anuria in a patient who is hemodynamically stable should prompt an immediate search for obstruction.

With partial or unilateral obstruction, the decline in glomerular filtration rate (GFR) may be mild. Therefore, an elderly patient or a patient with a history compatible with obstruction and unexplained chronic kidney disease should be evaluated for obstruction. Acute kidney injury acquired in the hospital is rarely caused by obstruction; in some studies, however, the incidence is as high as 10%, thus evaluation of these patients should be done on a case-by-case basis.

PHYSIOLOGY OF MICTURITION

Normal Bladder Function

The bladder is a smooth muscle reservoir lined by transitional epithelium. When fully contracted, it is only a potential space. In the absence of obstruction or bladder dysfunction, there is no residual urine after voiding. The bladder fills at a rate of 1 mL/min. This gradual filling allows the bladder to slowly expand and accommodate the increasing volume by progressive relaxation. This allows intravesical pressure to remain between 0 and 10 cm H₂O during filling. When capacity is reached, approximately 400 mL, the ability to accommodate additional volume is exceeded and the intravesical pressure rises rapidly to 30 to 40 cm H₂O. This results in stimulation of pressure receptors in the trigone that send impulses to the micturition center in the spinal cord at S2-S4, which results in detrusor contraction, bladder neck opening, and relaxation of the external sphincter.

Multiple spinal cord levels are involved in bladder function. Nuclei within the sacral spinal cord innervate the bladder and striated sphincter. The micturition center transmits signals to the brain as an urge to void that can be activated or suppressed through facilitator or inhibitor pathways in spinal cord. Parasympathetic fibers at the level of S2 and S3 stimulate contraction of the detrusor muscle and empty the bladder. Contraction is inhibited by α-adrenergic sympathetic fibers. The sphincter controlling continence is composed of voluntary muscles in the perineum innervated by the pudendal nerve (S2, S3) and an inner sleeve of smooth muscle extending from the bladder neck through the prostatic and membranous urethra innervated by α-adrenergic sympathetic nerve fibers. The micturition center coordinates contraction of the detrusor muscle (parasympathetic activation) and relaxation of sphincter muscles (pudendal nerve and sympathetic inhibition). During voiding, intravesicular pressure rises to 40 to 50 cm H₂O, and urine is expelled at a flow rate of 25 mL/s.

KEY POINTS

SIGNS AND SYMPTOMS

Symptoms

Signs and symptoms experienced by the patient with urinary tract obstruction depend on the rapidity and degree of obstruction. If obstruction occurs suddenly as in nephrolithiasis, distension of the ureter, kidney, and surrounding fascia causes intense pain. The pain is associated with other visceral symptoms, such as nausea, vomiting, and diaphoresis. This is referred to as renal colic. If the onset of obstruction occurs slowly, as with prostate cancer, the patient may be asymptomatic. An important exception to this rule is the patient with partial obstruction. In this setting, a fixed amount of urine can bypass the obstruction without causing back pressure and hence distension of the renal pelvis and ureter. When urine flow increases, ureteral distension can occur proximal to the point of narrowing and result in symptoms similar to acute obstruction. A clinical example is in young adults with asymptomatic partial obstruction through adolescence. During college, beer consumption in large quantities leads to intermittent increases in urine flow and acute episodes of renal colic.

Renal colic is a sharp, pulsatile pain that waxes and wanes. The location of the pain, although not diagnostic of the site of obstruction, can provide clues to its location. Obstruction that occurs at the ureteropelvic junction or in the proximal ureter produces flank pain and tenderness. Obstruction in the distal ureter or at the ureterovesicular junction produces pain that radiates into the ipsilateral groin.

With chronic obstruction such as occurs with BPH symptoms can be either obstructive or irritative. Obstructive symptoms include decreased force of urination, hesitancy, intermittency, and postvoid dribbling. Postvoid dribbling occurs as a result of a loss of pressure at the end of detrusor contraction. Irritative symptoms are the result of the effects of obstruction on the detrusor muscle. These include frequency, urgency, urge incontinence, and nocturia. Frequency results from a loss of bladder compliance and decreased bladder capacity because of the retention of residual urine. Intravesicular pressure increases at low urine volumes and results in the sensation to void. Urgency is the result of hyperreactivity of the detrusor muscle. There is a sudden increase in the force of contraction that raises intravesicular pressure and an abrupt sensation of having to void ensues.

Signs

Only 2 entities—bilateral obstruction and profound shock—cause anuria. Therefore, anuria in a patient who is hemodynamically stable points almost exclusively to obstruction. The presence of normal to increased urine flow, however, does not rule out obstruction. In the case of unilateral complete obstruction, urine flow remains normal. With partial obstruction, urine flow may increase because of loss of concentrating ability that results in a form of nephrogenic diabetes insipidus. Finally, in some patients with partial obstruction there can be alternation between oligoanuria and polyuria.

Chronic kidney disease can result from obstruction. Renal failure can either be acute with a rapidly rising serum creatinine concentration suggesting near complete loss of renal function or mild suggesting a partial loss of kidney function. The latter is particularly important in the outpatient setting, as this may be the only indication that obstruction is present.

Hypertension may be a presenting sign of urinary tract obstruction. Acute unilateral obstruction can activate the renin-angiotensin-aldosterone system (RAAS) and cause a sudden and acute rise in blood pressure in a fashion similar to that by which renal artery stenosis causes hypertension. Bilateral obstruction does not activate the RAAS. The loss of ability to clear solutes, however, leads to volume overload and results in volume-mediated hypertension. It remains unclear why some patients with obstruction develop hypertension but others do not.

CAUSES OF URINARY TRACT OBSTRUCTION AND ITS DIAGNOSIS

Causes

When considering the causes of urinary tract obstruction it is helpful to distinguish between complete and partial obstruction. Complete obstruction primarily occurs at the level of the bladder and is caused by prostatic enlargement or an atonic bladder. Complete obstruction results from retroperitoneal or pelvic tumors that arise near the bladder and involve both ureters. Complete obstruction may also develop from any cause in the patient with a solitary kidney. Neuropathic or atonic bladder, as in a diabetic or a patient with spinal cord injury, can result in complete obstruction. Proper bladder function requires complex coordination between multiple levels of the spinal cord and the detrusor muscle and sphincters. A defect in any of these results in loss of detrusor contraction, bladder overdistension, and, finally, loss of muscle function. As bladder volume increases, pressure is transferred to the collecting system and causes a decrease in GFR. The most common cause of complete urinary tract obstruction is BPH. Consequently, complete urinary tract obstruction is primarily a problem of men and not women. BPH is characterized by an increased number of epithelial and stromal cells in the periurethral area of the prostate. Epithelial gland formation is normally seen only in fetal development. This observed increase in cell numbers may be the result of epithelial and stromal proliferation or of impaired programmed cell death leading to cellular accumulation. Possible causes of this process are androgens, estrogens, stromal–epithelial interactions, growth factors, and other neurotransmitters. Hyperplasia of the prostate causes increased urethral resistance and results in compensatory changes in bladder function. The elevated detrusor pressure required to maintain urinary flow in the presence of increased outflow resistance results in decreased bladder storage capacity. Therefore obstruction induces a change in bladder function that results in higher filling pressure and transmission of this pressure back to the renal parenchyma.

Partial obstruction of the urinary tract is caused most commonly by nephrolithiasis. Other causes are ureteral tumors, as well as pelvic tumors that involve 1 ureter. Less commonly, blood clots that result from pathology within the kidney, shed papillae from papillary necrosis, and fungal infections resulting in fungus balls cause unilateral ureteral obstruction. In young male children, congenital urethral strictures and posterior urethral valves are rare forms of obstruction that must be considered. Adult males acquire urethral strictures from infections and trauma from indwelling catheters.

Lastly, retroperitoneal fibrosis in some cases can cause partial obstruction of the urinary tract. This disease process is very rare with an incident rate ranging between 1 per 100,000 and 1 per 1,000,000. Because the disease process is very insidious, manifestations of kidney failure can occur slowly over long periods of time. Recently, this fibrosing disorder has been related to a group of diseases called immunoglobulin (Ig) G₄-related diseases. This disease constellation can present in multiple organs or be isolated to single sites such as the retroperitoneum (Figure 19.1). Discovery of this disease process has changed the landscape somewhat because IgG₄-related retroperitoneal fibrosis may be responsive to glucorticoids; consequently, when it is identified as the cause of acute or chronic kidney disease, a tissue diagnosis will help guide therapy.

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