Diagnosis and assessment of NGB

Appropriate management relies on an accurate diagnosis. In some patients with NGB, the original cause of their symptoms may be misdiagnosed, resulting in failure of initial therapy.9 Assessment includes a comprehensive medical and voiding history, a physical examination, laboratory tests, computed tomography urogram or renal ultrasound (as indicated), endoscopic examination (as indicated), and uro­dynamic studies (Table 1).8

Presenting symptoms can be roughly divided into failure to empty or failure to store. Typical symptoms of disrupted bladder emptying include feelings of fullness and difficulty emptying the bladder, such as a slow stream while straining to void. Other patients report hesitancy, an interrupted or diminished stream, a sensation of incomplete emptying, lower abdominal discomfort, nocturia, and recurrent UTIs.7

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Failure to store usually presents as frequency, urgency, and UI. Depending on the level and severity of the neurologic lesion, patients may not have any bladder sensation; symptoms therefore may not be a reliable indicator of significant NGB dysfunction in certain patients.

Issues related to NGB include childhood urologic history, prior surgical procedures, and other medical conditions. Current medication use should be evaluated, as certain drugs can impact bladder function. In addition, issues related to bowel and sexual function are commonly seen in patients with NGB and may have to be addressed.

Loss of genitourinary and gastrointestinal function are important sequelae 
of SCI.10 Constipation can affect voiding function, leading to incontinence or retention. When taking a history, it is important to realize that some patients may have coexisting problems such as stress UI or benign prostatic hyperplasia, in addition to lower urinary tract dysfunction from NGB.

Physical examination should include a focused neurourologic evaluation. In addition to standard evaluation of the abdomen, back, rectum, pelvis, and genitalia, clinicians need to evaluate the sacral dermatomes, including perianal sensation and anal sphincter tone. The neurologic evaluation should be primarily focused at the sacral 2-4 level and assess the bulbocavernosus reflex, voluntary external sphincter control, and reflexes in the sacral dermatome levels. Deep tendon reflexes in the lower extremities, clonus, and plantar responses should be included.7,8

A urinalysis, with or without a urine culture,8 should be done to rule out UTI, glucosuria indicative of diabetes, and blood or protein in the urine that might indicate renal disease. If the results suggest an associated condition, the patient may need further diagnostic testing.

Urodynamic assessment can help determine the underlying neurologic issue, categorize the vesicourethral dysfunction, and provide a basis for appropriate therapy. In fact, clinical evaluation is often unable to identify the type of bladder dysfunction; therefore, optimal therapy is dependent on an appropriate urodynamic evaluation, as follows:6,11

Uroflow rate—the volume of urine voided per unit of time. It is primarily used to screen for bladder outlet obstruction.

Postvoid residual volume—considered part of the basic evaluation for UI. A high rate suggests acontractile bladder or bladder outlet obstruction.

Cystometrogram (with or without electromyogram)—a filling cystometrogram evaluates bladder capacity, compliance, and the presence of detrusor overactivity, while a voiding test records voiding detrusor pressure along with the rate of urinary flow. 

Electromyography—can help determine the presence of coordinated or uncoordinated voiding, and allows for an accurate diagnosis of detrusor sphincter dyssynergia that is common in suprasacral SCIs.

Videourodynamic study (multichannel with fluoroscopy)—combines the radiographic findings of voiding cystourethrogram with multichannel urodynamics.