Urinary tract infections (UTI) occur when bacteria, often from the skin or rectum, ascend the urethra and infect the urinary tract. In the United States, the urinary tract is the most common source of infection of patients presenting in septic shock, with an associated mortality of 10% to 20%.

UTI describes an inflammatory response of the urothelium to microorganisms in the urinary tract, resulting in clinical symptoms that include dysuria, frequency, urgency, hematuria, and suprapubic or costovertebral angle discomfort. The diagnosis of a UTI requires the presence of urinary-specific symptoms or signs in a patient who has bacteriuria and no other identified source of infection. Bacteriuria is the presence of bacteria in the urine but is not considered to represent a UTI in the absence of clinical manifestations. Bacteriuria accompanied by symptoms should be treated, whereas bacteriuria in the absence of symptoms should be treated only in select patients (e.g., pregnant women, immunosuppressed patients).

UTIs are classified as lower (confined to the bladder) or upper (involving the ureters or kidneys) and as uncomplicated or complicated. An uncomplicated infection occurs in a nonpregnant individual with a structurally and functionally normal urinary tract. A complicated UTI is a heterogeneous term that may be associated with an underlying functional or structural abnormality, history of urinary instrumentation or organ transplantation, or systemic disease, such as renal insufficiency, diabetes, and immunodeficiency. UTIs in men are generally categorized as complicated given the higher incidence of associated urologic abnormalities. However, men can experience a UTI without an underlying structural or functional abnormality. Complicated UTIs often require a prolonged course of antibiotic therapy and a more in-depth approach to testing and anatomic evaluation.

The term urethritis refers to the inflammation of the urethra secondary to an infection or trauma. Frequently, urethritis may be a manifestation of a sexually transmitted infection (STI), such as gonococcal urethritis in Neisseria gonorrhoeae infection, but may occur in other clinical scenarios as well. Cystitis generally refers to inflammation of the bladder resulting in increased urinary frequency, urgency, dysuria, and suprapubic pain. The causes of cystitis can be separated into bacterial and nonbacterial (e.g., radiation) categories. Acute pyelonephritis is a UTI involving the renal parenchyma and collecting system, manifesting with the clinical syndrome of fever, chills, and flank pain. Management and disposition of patients with acute pyelonephritis depend on whether the infection is simple or complicated.

In women, the urethra is short and opens close to the vulvar and perirectal areas. This contributes to the much higher incidence of UTI in women. The route of infection in men is also usually ascending, from the urethra to the prostate to the bladder and then to the kidney. Risk factors for cystitis and pyelonephritis include sexual intercourse, use of spermicides, previous UTI, new sex partner, and history of UTI in a first-degree female relative suggestive of possible inherited urethral anatomic pathology.

UTIs arise when urinary pathogens from the bowel or vagina colonize the periurethral mucosa and ascend through the urethra and into the collecting system. Infrequently, bacterial infection of the urinary tract arises from hematogenous or lymphatic sources. This is frequently the pathologic mechanism in debilitated and chronically ill patients who are immunosuppressed. Obstruction from any cause, with resultant stasis of urine, is a common contributor to infection. Urinary calculi may cause obstruction and increased susceptibility to the development of a UTI. Likewise, numerous abnormalities of the urinary tract may interfere with its innate ability to resist infection.

Subgroups of patients who are more susceptible than the normal population to UTIs include diabetics, pregnant women, elders, patients who are unable to empty their bladder completely, patients with indwelling urinary catheters, and those with immunodeficiency disorders. Lower UTIs are more common in aging men in the setting of prostatic enlargement or obstruction.

Escherichia coli is responsible for approximately three-quarters of cases of UTI in men and women. Other less common bacteria that may be responsible for infection include Staphylococcus saprophyticus and other members of the Enterobacteriaceae family ( Klebsiella pneumonia and Proteus mirabilis ). Unusual microorganisms may be found in institutionalized or hospitalized populations. Such settings and conditions predispose the patient to alterations in the normal gastrointestinal (GI) flora, leading to complex UTIs. The uropathogens in these patients include more resistant strains of Escherichia, Klebsiella, Proteus, and Enterobacter, as well as Pseudomonas, Enterococcus, Staphylococcus, Providencia, Serratia, Morganella, Citrobacter, Salmonella, Shigella, and Haemophilus spp., Mycobacterium tuberculosis, and fungi.

UTI is usually manifested as dysuria, with or without frequency, urgency, hematuria, or suprapubic discomfort. Symptoms of dysuria, frequency, hematuria, nocturia, and urgency all increase the probability of UTI, whereas vaginal discharge decreases the likelihood of UTI. The probability of cystitis is greater than 90% in women who have dysuria and frequency without vaginal discharge or irritation.

Symptoms of UTI in men may also represent storage or voiding disturbances that are common in aging men (e.g., prostatic enlargement). Commonly, men with lower UTIs have symptoms of urinary urgency, frequency, dysuria, hematuria, and suprapubic pain. If fever and chills are present in association with irritative symptoms and difficulty voiding, acute bacterial prostatitis should be strongly considered. A digital rectal examination of the prostate gland with attention to size, shape, and consistency can identify prostatic enlargement, inflammation, or cancer.

Clinical signs and symptoms suggestive of pyelonephritis include fever, chills, flank pain, costovertebral angle tenderness, and nausea or vomiting, with or without symptoms of cystitis. The presentation of UTI and pyelonephritis can be particularly challenging in those who are debilitated and elders because they may not be able to verbalize their symptoms and can present without fever; these patients may present with nonspecific complaints such as altered mental status, lethargy, abdominal pain, or generalized weakness.

Bacterial UTI is the most common cause of dysuria. Differential considerations include acute urethritis or acute vaginitis from STI, as well as mechanical trauma or irritation ( Table 85.1 ). In the ED setting, UTI is often overdiagnosed and associated with missed STI diagnoses. In general, if historical information includes contact with multiple sexual partners, recent change in sexual partners, or sexual partner with dysuria or discharge, Chlamydia trachomatis and N. gonorrhoeae infection should be strongly considered. Because the diagnosis of UTI is rarer in men, a high suspicion for an STI such as gonococcal or nongonococcal urethritis should be maintained. Trauma, calculi, chemical irritation, candidal infections, psychogenic disorders, neoplasm, and malformations or space-occupying lesions compressing the distal genitourinary tract can also cause dysuria.

Most patients with acute cystitis or pyelonephritis do not need emergency imaging of the urinary tract. Imaging is reserved for patients with a clinical suspicion for underlying structural abnormalities or complicating factors such as abscess, urolithiasis, or emphysematous pyelonephritis. Patients with pyelonephritis who have severe or worsening illness or persistent fever 48 to 72 hours after the initiation of appropriate antimicrobial treatment should undergo imaging to exclude renal stones, abscesses, or obstruction.

Ultrasonography is indicated to assess for potential urinary obstruction. Ultrasound is a sensitive tool for detecting postvoid residual bladder volume, intrarenal and perinephric abscess, and presence of hydroureter and hydronephrosis ( Figs. 85.1 and 85.2 ). Ultrasound can also detect the presence of pyelonephritis and congenital anomalies. Regardless of patient age, this procedure is relatively inexpensive and avoids the hazards of contrast and radiation exposure. A suggestion of obstruction based on clinical suspicion or lack of response to medical therapy necessitates performance of an abdominal ultrasound or noncontrast CT scan.

Ultrasound Image Demonstrating Hydronephrosis With a Dilated Collecting System.

Courtesy Dr. Peter Croft.

Ultrasound Image Demonstrating a Normal Kidney.

Courtesy Dr. Peter Croft.

A contrast CT scan of the abdomen is the most comprehensive test for assessing the kidneys, ureters, and bladder. It has a high sensitivity for detecting abscess, obstruction, and acute inflammation. Imaging with an abdominal CT scan is recommended for those with pyelonephritis and known functional or anatomic abnormalities, recent instrumentation, immunosuppression, or concern for obstruction. Its disadvantages include radiation exposure, cost, and potential to induce contrast reactions.

Hospitalization is required in the presence of clinical toxicity (e.g., fever, tachycardia, hypotension, vomiting), inability to take oral medications, an immunocompromised state, third-trimester pregnancy, failure of oral outpatient therapy, urologic abnormalities, or patients with significant comorbid conditions, including heart failure and renal insufficiency. Patients who don’t fall into these categories often benefit from short-term treatment in the ED or observation unit with IV hydration, pain and fever control, and the first dose of an IV fluoroquinolone. If these patients improve clinically, and can tolerate food and drink, they can be safely discharged home on a 10- to 14-day course of an oral fluoroquinolone, with close primary physician follow up. Urine culture with sensitivity testing and further diagnostic evaluation are not necessary in this patient population.

UTI during pregnancy represents a special situation. Although the incidence of UTI in pregnancy is approximately the same as in nonpregnant women, pyelonephritis is more common during pregnancy. This is likely a result of the physiologic changes that occur within the urinary tract of pregnant women, which include ureteral and renal pelvis dilation. Factors associated with a higher risk of bacteriuria include a history of prior UTI, preexisting diabetes mellitus, increased parity, and low socioeconomic status.

Unlike bacteriuria in nonpregnant females, bacteriuria in pregnant women, even if they are asymptomatic, should be treated. Untreated bacteriuria in pregnancy is associated with premature labor, low birth weight, perinatal mortality, maternal anemia, and maternal pyelonephritis. Like nonpregnant women, E. coli is the most common uropathogen. The symptoms of UTI and pyelonephritis are also the same as in nonpregnant patients; however, urinary frequency and urgency may be symptoms of a normal pregnancy. Specimen collection and diagnostic strategies are also similar. A urine culture specimen should be obtained, along with a follow-up culture as a test of cure.

Options for empirical treatment for UTI include amoxicillin-clavulanate, cefpodoxime, nitrofurantoin, fosfomycin, and TMP-SMX ( Table 85.6 ). The evidence regarding an association between the nitrofuran and sulfonamide classes of antibiotics and birth defects is mixed. Previous American College of Obstetricians and Gynecologists (ACOG) recommendations were to avoid TMP-SMX and nitrofurantoin during the first trimester. Current recommendations state that it is appropriate to prescribing sulfonamides or nitrofurantoin in the first trimester when no other suitable alternative antibiotics are available.

During the second and third trimesters, sulfonamides and nitrofurantoins may be used as first-line agents for the treatment of UTIs. Fluoroquinolones should be avoided in pregnancy.

Hospital admission should be considered for patients in their last trimester, who appear ill, or who have evidence of pyelonephritis and would benefit from treatment with parenteral antibiotics and IV fluids. Parenteral regimens for the empirical treatment of pyelonephritis are similar to those for nonpregnant patients, except the use of fluoroquinolones, and include ceftriaxone, cefepime, aztreonam, and piperacillin-tazobactam ( Table 85.7 ). Nitrofurantoin and fosfomycin do not achieve tissue levels adequate to treat pyelonephritis appropriately. Hospitalized pregnant patients who are afebrile for 48 hours can be discharged on oral antibiotics, directed by culture susceptibility results, to be completed in 10 to 14 days.

Catheter-associated UTI (CAUTI) is defined as urine containing greater than 1000 CFU/ml of one or more bacterial species in a catheterized patient with suggestive symptoms, such as pelvic discomfort, flank pain, fever, rigors, malaise, altered mental status or lethargy with no other identified cause, costovertebral angle tenderness, or acute hematuria.

Screening for or treating asymptomatic bacteriuria in patients with indwelling catheters is not indicated. Antibiotic treatment results in the development of resistant microorganisms, whereas removal of the catheter leads to the spontaneous elimination of bacteria in many patients. Treatment of patients with a UTI in whom permanent removal of the catheter is contraindicated includes antibiotic therapy and urine culture and sensitivity. Replacement of the catheter and strong consideration for hospitalization is indicated in those who exhibit altered vital signs, systemic symptoms, or a toxic appearance.

Many patients with indwelling urinary catheters who present to the ED are older and not able to verbalize their symptoms or lack clinical signs of infection. Given that a catheter-associated UTI is a common cause of subsequent bacteremia and mortality, empirical antimicrobial therapy, in addition to replacement or removal of the catheter, is often appropriate in such patients. Urine culture with antibiotic sensitivity testing will help guide antibiotic therapy in this patient population. The most important risk factor for bacteriuria is the duration of catheterization. The most effective strategy for addressing CAUTIs is to prevent the infection from occurring by placing urinary catheters only when necessary and considering the use of intermittent catheterization and condom catheters, when appropriate.

Males with cystitis often have involvement of the prostate. Prostatitis encompasses four distinct clinical processes—acute bacterial prostatitis, chronic bacterial prostatitis, chronic prostatitis–chronic pelvic pain syndrome, and asymptomatic inflammatory prostatitis.

Acute bacterial prostatitis generally affects men between the ages of 20 and 40 years, with a second peak in men older than 60 years. Acute prostatitis is caused by a bacterial infiltration that is usually precipitated by reflux of urine infected by E. coli, Klebsiella, Enterobacter, Proteus, or Pseudomonas spp.

Chronic bacterial prostatitis is a persistent bacterial infection of the prostate lasting more than 3 months. Approximately 10% of acute bacterial prostatitis cases develop into chronic bacterial prostatitis. This can be caused by undertreated acute bacterial prostatitis or highly virulent strains. Like acute bacterial prostatitis, gram-negative bacteria are responsible for most cases of chronic prostatitis.

Whereas acute and chronic bacterial prostatitis have clear bacterial etiologies and are managed as infectious diseases, chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is characterized by chronic pelvic pain and voiding symptoms in the absence of a clear bacterial etiology. CPPS is defined as urologic pain in the pelvic region associated with urinary symptoms or sexual dysfunction lasting for at least 3 of the previous 6 months. Symptoms of chronic bacterial prostatitis may not differ from those of CP/CPPS. It is a heterogeneous condition with broad diagnostic criteria and uncertain cause, making it difficult to determine an effective treatment regimen reliably.

Asymptomatic inflammatory prostatitis is a painless inflammation of the prostate gland in the absence of infection. It is a common finding in men with benign prostatic hyperplasia and a diagnosis of exclusion in the ED.

Patients with acute prostatitis often report UTI symptoms such as fever, chills, dysuria, urinary frequency or urgency, and/or perineal and low back pain. A rectal examination will reveal an exquisitely tender and swollen prostate gland in more than 90% of patients. There is no evidence that performing a rectal examination induces clinically significant bacteremia.

Clinical manifestations of chronic prostatitis vary widely, making recognition difficult. Most patients report some degree of voiding symptoms (e.g., frequency, urgency, dysuria), low back and perineal pain and, occasionally, myalgias. Fever and chills are uncommon except during an acute exacerbation of the chronic infection. Findings on the physical examination, including examination of the prostate, often are unremarkable. The diagnosis is based on history, physical examination, and positive urine culture.

Acute bacterial prostatitis is a clinical diagnosis. A urine Gram stain and culture are recommended to identify causative organisms and guide treatment. Blood cultures are recommended for patients with acute prostatitis and fever who have not yet received antibiotics. Although acute bacterial prostatitis is usually caused by typical urinary pathogens, an STI such as chlamydia and gonorrhea should be considered, especially in sexually active patients. Urethral swabs or first-voided urine, with subsequent culture or DNA amplification, should be obtained if a STI is suspected.

The most common complications of acute prostatitis are acute urinary retention (AUR) and prostatic abscess. Approximately 10% of men with acute prostatitis will have some urinary retention, which can be diagnosed using bedside ultrasound. Transrectal ultrasound or CT can detect prostatic abscess and should be considered in patients who fail to improve with antibiotics ( Fig. 85.3 ).

Prostate Abscess.

B, Bladder; P, prostate; R, rectum.

From Vandover JC, Patel N, Dalawari P. Prostatic abscess. J Emerg Med . 2011;40:e83–e85.

Outpatient therapy can be used if the patient is not systemically ill, can tolerate oral medications, and does not have urinary retention. General support measures for outpatients should include bed rest, analgesics, nonsteroidal antiinflammatory drugs (NSAIDs), hydration, and stool softeners. Alpha blocker therapy is also recommended for obstructive voiding symptoms related to prostatitis (see Table 85.5 ).

There is no consensus regarding an optimal treatment regimen, so regional patterns of antibiotic resistance should be considered. Few antimicrobial agents are able to penetrate the prostrate and achieve sufficient concentrations to eradicate infection. Fluoroquinolones, such as ciprofloxacin or levofloxacin, achieve the highest concentrations in the prostate and are the first-line agents in the treatment of bacterial prostatitis. Empirical parenteral antibiotics such as ciprofloxacin, levofloxacin, or ceftriaxone are recommended until fever and other symptoms have subsided. After improvement, oral antibiotics are recommended for at least 4 weeks ( Table 85.8 ). Hospitalization for parenteral antibiotics is recommended for patients who appear systemically ill, cannot tolerate oral medications, or have urinary retention as determined by ultrasound or catheterization. Antibiotic options include ciprofloxacin 400 mg IV every 12 hours, levofloxacin 500 mg IV every 24 hours, or ceftriaxone 2 g IV every 24 hours. Following clinical improvement, the patient may be transitioned to an oral regimen, such as a fluoroquinolone. The duration of treatment should be a minimum of 2 weeks, although 4 to 6 weeks may be necessary.

The treatment of chronic bacterial prostatitis consists of antibiotics for 4 to 12 weeks. Of the researched treatments, α-adrenergic receptor blockers and antibiotics used alone or in combination result in the greatest improvement in symptoms (see Tables 85.5 and 85.8 ). Anti-inflammatories may also be beneficial. Patients thought to have chronic prostatitis or CPPS should be referred to a urologist.

Treatment of prostatic abscess consists of broad-spectrum intravenous antibiotics (e.g., ciprofloxacin, 400 mg IV every 12 hours) and urologic consultation for perineal drainage or surgical debridement.

Urolithiasis affects about 12% of the world population and occurs approximately twice as much in men than women. Multiple pathogenic factors interact to cause the formation of renal calculi. Risk factors include older age, male gender, obesity, and family history ( Box 85.2 ). Its incidence depends on geographic, ethnic, dietary, and genetic factors. Approximately 50% of patients will have a recurrence within 5 years.

Most ureteral calculi originate in the kidney and then pass into the collecting system. The chemical composition of urinary tract stones is the key factor for determining optimal management. Stones are generally composed of calcium, struvite, or uric acid. Most stones (75%) are composed of calcium oxalate, alone or in combination with calcium phosphate. The hyperexcretion of calcium is a major contributor to stone formation; its most common identified cause is hyperparathyroidism. Other medical conditions that lead to increased calcium levels include hypercalcemia of malignancy, sarcoidosis, and excessive calcium ingestion or increased absorption from the gut. The other major component of calcium stones, oxalate, is influenced by diet. Hyperoxaluria occurs in the presence of small bowel disease, bariatric surgery, Crohn disease, ulcerative colitis, and radiation enteritis.

Magnesium ammonium phosphate (struvite) stones account for approximately 15% of all renal calculi. Struvite stones occur almost exclusively in patients with UTIs and are sometimes referred to as infection stones. They form as a result of the presence of urea-splitting organisms, such as Proteus, Providencia, Klebsiella, Pseudomonas, and Staphylococcus. Patients with anatomic abnormalities that predispose them to recurrent UTIs are at increased risk of developing struvite stones. Most staghorn calculi—stones that fill the greater part of the collecting system—are composed of struvite.

Uric acid stones account for 10% of all stones in the United States. Approximately 15% of patients with symptomatic gout have uric acid calculi, and the incidence of uric acid stones increases with the use of uricosuric agents. In addition to hyperuricosuria, aciduria is considered necessary because the precipitation of uric acid is unlikely at a higher urine pH. A distinctive feature of uric acid stones is their radiolucency.

Impaction along the genitourinary tract is a serious complication of renal calculi and can cause several physiologic changes. Once obstruction occurs, a rapid redistribution of renal blood flow results in a decrease in the glomerular filtration rate (GFR). As glomerular and tubular function decrease, renal excretion shifts to the unaffected kidney. Obstruction also causes a rapid decrease in ureteral peristaltic activity. In the presence of infection, renal and ureteral function may be impaired. Complete obstruction of the ureters may lead to loss of renal function with an increased incidence of irreversible damage after 1 to 2 weeks. Partial obstruction is associated with a lower likelihood of renal injury but may still result in irreversible damage.

Although calculus size and location are important determinants of the degree of disease, the major cause of progressive renal damage is associated infection. The stone behaves as a foreign body and leads to stasis and obstruction, decreasing host resistance and increasing the incidence of infection. Subsequent infectious complications include pyelonephritis, perinephric abscess, and gram-negative bacterial sepsis.

The three primary predictors of stone passage without the need for surgical intervention are calculus size, location, and degree of patient pain. The most important factor that relates to passage of a calculus though the genitourinary tract is its size. Approximately 90% of stones smaller than 5 mm pass spontaneously within 4 weeks. This percentage decreases to 15% for stones 5 to 8 mm in size. Up to 95% of stones larger than 8 mm become impacted along the genitourinary tract, and lithotripsy or surgical removal is usually required. Surgical intervention can be performed on an outpatient basis, provided the patient is able to tolerate oral intake and has adequate pain control unless the stone is infected, renal damage is considerable, there are bilateral obstructing stones, or there is obstruction of a solitary or transplanted kidney. Spontaneous passage is more frequent with stones located below the midureter than those located above the midureter.

Renal calculi seldom cause complete obstruction. There are five sites along the ureter at which calculi are likely to become impacted ( Fig. 85.4 ). First, a stone may lodge in the calyx of the kidney or pass into the renal pelvis and become lodged at the ureteropelvic junction. Second, the relatively large renal pelvis (1 cm) narrows abruptly at its distal portion, where it is equal in diameter to its adjoining ureter (2 to 3 mm). The third region is near the pelvic brim, where the ureter arches over the iliac vessels posteriorly into the true pelvis. The most constricted area along the ureter, and a common location for impaction, is the ureterovesicular junction. This is the site at which the ureter enters the muscular coat of the bladder (intramural ureter). At the time of diagnosis, up to 75% of stones are located in the distal third of the ureter. Finally, calculi may become lodged in the vesical orifice.

Variations in Caliber of the Ureter.

Fr, French catheter size.

Adapted from Eisendrath, Rolnick. Lich R Jr, et al. Childhood disorders and diseases. In: Harrison JH, Gittes RF., eds. Campbell’s Urology . Vol. 1. 4th ed. Philadelphia: WB Saunders; 1978.

The onset of pain usually is abrupt, with a crescendo of extreme pain that begins in the flank, extends laterally around the abdomen, and radiates into the groin. Pain may radiate to the testicles in men and the labia majora in women. A constant, underlying dull ache in the flank is common between episodes of colic. The cause of colicky, severe flank pain is hyperperistalsis of the smooth muscle of the calyces, pelvis, and ureter, whereas the cause of a dull ache can be acute obstruction and renal capsular tension. GI symptoms of nausea and vomiting are common.

One-third of patients experience gross hematuria, with or without blood clots in the urine. Symptoms of urinary urgency and frequency often develop as the stone nears the bladder. A history of fever and chills strongly suggests superimposed infection; these cases should be regarded as true urologic emergencies.

A patient with renal colic often is in severe pain and paces or writhes in pain on the stretcher, unable to find a comfortable position. The abdomen should be auscultated and palpated in search of bruits and thrills over the abdominal aorta and iliac vessels because the clinical manifestations of aortic abdominal aneurysms (AAAs) may mimic those of renal colic. Patients commonly have intermittent pain that may nearly resolve between episodes of severe discomfort.

A number of clinical diseases can produce pain similar to that of renal colic ( Box 85.3 ). Potentially serious or life-threatening alternate diagnoses include pulmonary embolism, ectopic pregnancy, biliary disease, bowel obstruction, incarcerated inguinal hernia, pancreatitis, appendicitis, AAA, renal vein thrombosis, and renal malignancies and infarction.

BOX 85.3

Differential Diagnosis for Pain Associated With Urolithiasis

Urologic Disease

Upper Urinary Tract

• Renal infarct

• Renal parenchymal tumors

• Urothelial tumors

• Papillary necrosis

• Pyelonephritis

• Hemorrhage (blood clot)

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