Immediate Management of Serious and Life-Threatening Conditions
It is helpful to categorize the mechanism as prerenal (eg, resulting from decreased or abnormal renal perfusion), renal (eg, resulting from intrinsic renal disease), or postrenal (eg, disease of the urinary collecting system distal to the renal parenchyma). Prerenal and postrenal causes are often suggested by the history and physical examination. Additionally, it is be helpful to determine the presence and extent of acute kidney injury (AKI) that frequently accompanies oliguria and anuria.
Prerenal causes include hypovolemia, sepsis, and heart failure.
Renal causes include tubular, glomerular, vascular, or interstitial disease.
Supravesical obstruction rarely causes oliguria or anuria, because bilateral disease is required to reduce decreased urine flow. There are two types of supravesical obstruction: (1) ureteral obstruction (usually tumor) and (2) ureteropelvic or ureterovesical obstruction.
Intravesical or infravesical obstruction is more common than supravesical obstruction and may be from many causes (Table 39–1).
| Cause | Frequency of Occurrence | Results of History and Physical Examination | Laboratory Tests and Other Studies |
|---|---|---|---|
| Prostatic hypertrophy | Common | Gradually increasing difficulty in voiding, often with abrupt worsening. Enlarged prostate on rectal examination is common | Urethral catheterization may be difficult. |
| Urethral strictures or valves | Uncommon | Often previous attacks of urethritis or urethral trauma. Onset may be gradual or abrupt | Urethral catheterization often difficult. Urethrogram or urethroscopy is diagnostic |
| Bladder stones or tumor | Uncommon | Hematuria is common. Obstruction may be intermittent | Urethral catheter is passed without difficulty. Cystogram or cystoscopy is diagnostic |
| Neuropathic bladder | Very common | Onset may be gradual and painless or abrupt and painful. Look for associated neurologic abnormalities (sacral dermatomal hypesthesia, poor rectal sphincter tone, neuralgic pain) | Urethral catheter passed without difficulty. Cystometrogram is diagnostic |
| Traumatic urethral injury | Uncommon | Male; history of trauma, prostatic dislocation, urethral bleeding | Do not pass catheter. Retrograde urethrogram and percutaneous cystogram are diagnostic |
Differentiate between reduced urine output (with normal or nearly normal voiding patterns) and oliguria associated with difficult in voiding, feeling of incomplete voiding, and diminished urinary stream. The latter findings suggest obstruction.
Ask about coexisting cardiac, pulmonary, renal, or other underlying disease that might contribute to renal or prerenal oliguria.
The patient’s medications might cause problems with urination or be nephrotoxic. Anticholinergics and sympathomimetics are most often the culprits of urinary retention.
Obtain a complete set of vital signs. Correct volume depletion, if present (Chapter 11).
Focus on signs of cardiac, pulmonary, renal, or hepatic disease that might contribute to oliguria of a prerenal or renal origin. Look for signs of volume depletion, such as dry mucous membranes or poor skin turgor.
Palpate the lower abdomen to determine whether a suprapubic mass, consistent with a distended bladder, is present. A distended bladder is manifested as a firm (but not hard) mass that is adjacent to the symphysis pubica and is dull to percussion.
Examine the prostate for masses, prostatic hypertrophy, prostatic tenderness, or prostatic dislocation (associated with trauma).
Bladder outlet obstruction (complete or partial) is strongly suggested by a palpable bladder in a patient who is unable to void or who has a weak urinary stream or a feeling of incomplete voiding. Severe lower abdominal pain is more likely to be present with acute obstruction and rapid bladder distention than gradually progressive obstruction.
The diagnosis may be confirmed by calculating postvoid residual using either catheter drainage, ultrasonography, or CT scanning immediately after the patient’s attempt to completely empty their bladder. Diagnostic features of some of the common causes of bladder outlet obstruction are set forth in Table 39–1.
Oliguria and anuria are frequently accompanied by AKI. A standardized definition as well as objective grading system for AKI has been developed to help predict outcomes and aid in treatment (Table 39–2). It is important to note that laboratory markers of AKI such as serum creatinine usually lag behind oliguria or anuria.
| AKIN Stage | Serum Creatinine | Urine Output |
|---|---|---|
| 1 | Increased by 1.5–2 times baseline or by ≥0.3 mg/dL | <0.5 mL/kg/hr for 6 hrs |
| 2 | Increased between 2 and 3 times baseline | <0.5 mL/kg/hr for 24 hrs |
| 3 | Increased by >3 times baseline or to ≥4mg/dL with an acute rise of ≥0.5 mg/dL | <0.3 mL/kg/hr for 24 hrs |
If the patient appears to be acutely ill, in shock, septic, in decompensated heart failure or has other serious coexisting conditions that might cause prerenal oliguria, these disorders must be evaluated and treated before those of the urinary tract.
Draw blood for complete blood count (CBC), electrolyte determination, and blood urea nitrogen and serum creatinine measurements.
Try to pass an indwelling urethral (Foley) catheter. If this maneuver is successful, drain the bladder, record the volume of urine obtained, and send a specimen for urinalysis and culture. Monitor the patient for postobstructive diuresis. Gradual bladder draining is not a proven method of decreasing bladder atony or mucosal hemorrhage. If bladder outlet obstruction is relieved by passage of a Foley catheter and is apparently due to a transient cause (eg, drugs), the catheter may be removed and the patient observed for ability to void after the effects of any drugs are presumed to have dissipated. In patients with fixed bladder outlet obstruction (eg, benign prostatic hypertrophy), leave the catheter in place, and obtain urologic consultation within 1 week. If a standard Foley catheter cannot be passed secondary to prostatic hypertrophy, reattempt passage using a coudé catheter (which has a curved tip that usually allows passage beyond the enlarged prostate). Inability to pass the catheter beyond the proximal urethra is suggestive for urethral stricture.
If the coudé catheter is unsuccessful and a urologist is not available, insert a suprapubic catheter for temporary drainage (Chapter 7). A large (16-gauge) needle-clad catheter (eg, Intracath) will provide satisfactory emergency bladder drainage.
See Dysuria section, below.
Hospitalize patients who have systemic symptoms (fever, rigors, intractable emesis) and those who need additional diagnosis and treatment (eg, for management of postobstructive diuresis, azotemia, sepsis, or electrolyte abnormalities).
If the patient can void on command but continues to have subjective or objective evidence of a weak urinary stream or if the patient experiences a feeling of incomplete voiding, partial bladder outlet obstruction is likely.
Draw blood for CBC, electrolyte, blood urea nitrogen, and serum creatinine measurements. Send a urine specimen for urinalysis and culture. Treat cystitis or prostatitis, if present. If blood chemistry results and urinalysis are normal, refer the patient to a urologist. The presence of azotemia or electrolyte abnormalities indicates severe or long-standing obstructive uropathy, and the patient likely requires hospitalization.
Consider the following in the differential diagnosis (1) intrinsic renal disease, (2) occult prerenal disease (unlikely, because most causes would be obvious on brief physical examination), (3) occult bladder outlet obstruction, or (4) supravesical obstructive uropathy (rare).
Draw blood for CBC; serum glucose, electrolyte, calcium, and phosphorus; and tests of renal and hepatic function. Obtain chest and abdominal X-rays to help evaluate the size of the kidneys and bladder. Ultrasonography is the best noninvasive test for evaluating kidney and bladder size.
Ensure adequate hydration. In an adult without obvious volume overload (eg, pulmonary or peripheral edema), give 1–2 L of fluid orally or intravenously, and observe the patient for 1–2 hours. In an individual with normal kidneys, this amount should produce a brisk flow of urine.
If anuria persists despite adequate hydration and if the bladder is not distended, the cause of the anuria is likely to be proximal to the bladder (prerenal, renal, or, rarely, bilateral ureteral obstruction). Bladder catheterization, with strict adherence to sterile technique, should be performed to confirm the lack of urine output. Hospitalize the patient for further evaluation.
Hospitalization is required for patients with persistent unexplained anuria or severe oliguria (<500 mL/d), those with systemic symptoms, and those with markedly abnormal electrolytes or renal function.
Patients with partial bladder outlet obstruction (ie, weak urinary stream, with or without palpable bladder) should be referred to a urologist if renal function is normal or nearly normal. Asymptomatic patients with an indwelling urethral catheter should be reexamined or referred to a urologist within 1 week.
See Table 39–3.
| History | Physical Examination | Urinalysis Results | Other Laboratory Studies | Treatment and Disposition | |
|---|---|---|---|---|---|
| Trauma | History of injury | Scrotal hematoma | Variable; may have hematuria | Sonogram | Obtain urologic consultation (Chapter 24) |
| Urolithiasis | Antecedent flank or back pain; occasionally abdominal pain | Testicle minimally tender or nontender | Hematuria | Stones on excretory urogram | Obtain urologic consultation |
| Viral (eg, mumps) orchitis | Gradual onset, coexisting mumps parotitis common | Tender testicles (unilateral or bilateral); epididymis rarely involved | Normal | Viral cultures (throat, stool) if available; characteristic fourfold rise in serum antibody titer. | Elevate and immobilize testicle (eg, athletic supporter), give analgesics, and discharge for follow-up care. |
| Incarcerated hernia | Gradual onset; crampy pain | Fluid rushes heard in scrotum (early); abdominal tenderness consistent with intestinal obstruction | Normal | Characteristically abnormal results on ultrasound studies; abdominal X-ray results often abnormal (intestinal obstruction) | Obtain general surgical consultation; hospitalize |
| Epididymitis | Gradual onset; history of urethritis or urinary tract infection common; older men (>age 25 yrs) | Tender epididymis (often unilateral) with normal testicle early in course; pain relieved by elevating scrotum. | Leukocytes; bacteriuria in some cases (coexisting urinary tract infection) | Normal results on Doppler and ultrasound studies; nuclide scan shows uptake in epididymis |
|
| Testicular torsion | Abrupt onset (minutes to hours); history of testicular pain in some; boys and young men (< age 25 yrs) | Tender testicle, often elevated and horizontally displaced; normal epididymis (if palpable) | Normal | Characteristically abnormal results on Doppler examination and radionudidescan | Obtain emergency urologic consultation; hospitalize for surgery. Attempt manual detorsion (see text) |
| Torsion of testicular appendage | Abrupt onset | Firm nodule with point tenderness on upper anterior pole of testis; testicle normal | Normal | Transillumination may reveal affected appendage as “blue dot,” normal results on Doppler ultrasound and radionuclide studies. |
|
- Trauma is a common cause
- Infection accounts for orchitis and epididymitis
- Flank pain, hematuria, and scrotal pain usually indicates urolithiasis
- Incarcerated hernias cause scrotal pain
- Testicular torsion requires urgent diagnosis to salvage the testicle. A torsed testis may be high riding or horizontally lying; ultrasound will show diminished blood flow to the torsed testis
(See also Chapter 26) Trauma commonly causes testicular or scrotal pain. Careful questioning may be required to elicit the circumstances under which the trauma occurred.
Mumps virus and the enteroviruses may cause acute unilateral or bilateral orchitis. In orchitis due to mumps virus, associated parotitis is usually present.
Rarely, patients with urolithiasis present with pain localized mainly in the scrotum; however, in most cases, back or flank pain has preceded the scrotal pain, or a history of nephrolithiasis is present. In such cases, the testicle and epididymis are normal to palpation. Hematuria is an important diagnostic clue.
Inguinal hernias incarcerated in the scrotum may cause scrotal pain that may be confused with testicular pain. Bowel sounds are heard in the scrotum early in incarceration; if the hernia strangulates, bowel sounds are no longer audible. Intestinal hernia into the scrotum is almost always associated with clinical findings of intestinal obstruction (Chapter 15). Ultrasonography is diagnostic.
(See Table 39–3) Torsion of a testicular appendage, epididymitis, and testicular torsion are the three most common causes of acute scrotal pain and account for approximately 85–90% of cases. Because of the urgency to diagnose and treat testicular torsion within 6 hours to prevent loss of the testis, testicular torsion must be promptly ruled out in all patients with scrotal pain. It may be difficult to distinguish from epididymitis or torsion of testicular appendages as edema and inflammation progress to involve the entire scrotal sac and contents.
Testicular torsion tends to occur in young men and is rare in men older than 30 years; however, it can and does occur at all ages and a smaller peak also occurs in the first year of life. There is often a history of episodes of similar scrotal pain representing torsion with spontaneous repositioning of the testicle. The pain is abrupt in onset, severe, unilateral, and often associated with nausea and vomiting. Tenderness is initially noted only in the testicle; however, with persistent torsion and the resulting testicular hypoxia, pain and tenderness spread to involve contiguous intrascrotal structures.
Examination early in the illness shows an elevated testicle that is apt to have a horizontal lie (Bell clapper deformity). The epididymis may be felt in an abnormal position (eg, anteriorly) in the early stages. Later, the entire scrotal contents become swollen and tender, making the examination extremely difficult and less informative because the epididymis becomes indistinguishable from the testis on palpation.
Epididymitis tends to occur in sexually active men older than 20 years and is the most common misdiagnosis for testicular torsion. There may be a history of urinary tract infection or urethritis. Pain begins gradually and is less severe than in testicular torsion. The Prehn’s sign is present if the pain is reduced when the scrotum is elevated. This finding is not specific to epididymitis nor is it a reliable discriminating clinical sign. Physical examination reveals a tender epididymis, often unilateral and often with erythema and edema of the scrotal skin. Early on, the testicle may be normal or minimally tender. However, as edema worsens, the epididymis becomes indistinguishable from the testicle on palpation, and a reactive hydrocele may develop, making it difficult to differentiate epididymitis from testicular torsion. Urinalysis frequently shows pyuria and possibly bacteriuria if a concomitant urethritis or urinary tract infection is present. Doppler ultrasound shows increased blood flow to the affected testis, in contrast to the decreased blood flow seen in testicular torsion.
Of the four appendages, the appendix testis, located on the anterosuperior pole of the testis, is the most frequently (92%) torsed appendage followed by the appendix epididymis (7%), located on the head of the epididymis. Pain is usually sudden in onset and can be severe, with nausea and vomiting. Physical examination occasionally (21%) reveals a small, tender, firm nodule (“blue dot” sign), representing the infarcted appendage in the anterosuperior pole of the testis. The scrotal skin and testicle are usually normal and minimally tender. In advanced cases, marked edema and appearance of a reactive hydrocele may obscure the diagnosis of testicular torsion.
These tests should not delay emergency urologic consultation and surgical treatment of patients with high probability of testicular torsion (ie, patients younger than 18 years with acute unilateral testicular pain and no signs or recent history of urinary tract infection).
Color-flow Doppler ultrasonography is the diagnostic study of choice in most institutions. It is widely available and has a sensitivity of 86–100% and a specificity of 100% as compared with a sensitivity of 80–100% and a specificity of 86–100% for radionucleotide imaging. The most frequent sonographic finding is absent or diminished blood flow to the affected testis, compared with the unaffected side. If the diagnosis is still unclear, then a nuclear study should be pursued. Ultrasound is more advantageous than nuclear scanning for elucidating other scrotal pathology including varicoceles, hydroceles, hernias, and masses.
In epididymitis, scanning of the scrotum after intravenous injection of technetium-99m sodium pertechnetate reveals increased scrotal uptake on the affected side, whereas torsion shows decreased uptake.
