The normal micturition process requires the proper function of both bladder and urethra. Normal functionality of detrusor muscle and physiologically competent internal and external urethral sphincters is necessary to maintain healthy urinary continence. The micturition process is controlled by the central nervous system, which collaborates the sympathetic and parasympathetic nervous system activity with the somatic nervous system to maintain urinary continence.
Bladder dysfunctions can better be understood if we know the basic neuroanatomy and neurophysiology of the upper and lower urinary tract system. The voluntary micturition process consists of bladder filling, storage, and emptying. The kidneys excrete nearly 1L/day of fluid as urine. It passes through the ureter into the bladder and stores here for a while unless it exceeds the bladder storage capacity i.e., 400 to 500cc.
Anatomically, the bladder divides into two parts: the dome and the base. The dome of the bladder is made up of smooth muscle, and the base consists of a trigone and neck that are closely connected to the pelvic floor. There are two urethral sphincters at the bladder outlet that are necessary for normal voluntary micturition. The internal urethral sphincter is in the bladder neck and proximal urethra, while the external sphincter is present at the membranous part of the urethra. Any disturbance to the normal functionality of the structures mentioned above as a result of trauma or disease can cause bladder dysfunction.
There are multiple conditions in which neurogenic bladder can develop. Some of these appear in the list below:
The mean age of neurogenic bladder patients is 62.5 (standard deviation 19.6) years. In the U.S, the neurogenic bladder is a finding in 40 to 90% of persons with multiple sclerosis (detrusor hyperreflexia in 50 to 90% of cases), 37 to 72% in patients with Parkinson disease, and 15% in stroke patients.
Research shows that 70 to 84% of patients with spinal cord injuries have neurogenic bladder dysfunction at some point in their life. In spina bifida patients, bladder dysfunction of any time is present most of the time. Vesicoureteral reflux is present in up to 40% of the cases in children by the age of 5 and up to 60.9% of adults with spina bifida experience urinary incontinence.
The clinical findings typically correlate with the location of the lesion along the efferent (motor) or afferent (sensory) portions of the sacral arc pathway, alone or in combination. Classic presentations include patients who have a preserved sensation of bladder fullness and an inability to empty (motor neurogenic bladder) and patients who can void but have decreased sensation (sensory neurogenic bladder). The patients with former lesion have an injury of the efferent sacral nerves or a conus medullaris lesion that selectively spares afferent transmission to supraspinal centers, and the patients with the latter type of injury are expected to have a pure afferent lesion.
In clinical practice, patients usually have a mixture of symptoms that involve both pathways. Patients with sacral or infrasacral lesions often complain of alterations in erectile function. Reflexogenic erections, like bladder and external sphincter contractility, rely on the somatic function of the pudendal nerve and the autonomic function of the pelvic nerve. These pathways may become disrupted in patients with infrasacral or CONUS lesions, but 95% of patients with suprasacral lesions have reflexogenic erections. The physical examination of patients with lesions at or below the conus medullaris typically reveals skeletal muscle flaccidity of the lower extremities. A number of reflexes reflect the status of the sacral cord and nerves 52 through S4 (Table 2).
The status of these reflexes provides significant information regarding detrusor and external sphincter function because the pudendal nerve and the preganglionic parasympathetic motor fibers originate from these levels as well. The absence of a sacral reflex is highly suggestive of a neurologic lesion involving the conus medullaris, cauda equina, or a peripheral nerve. The presence of a sacral reflex, however, does not exclude such a lesion, and when present in a patient with an areflexic bladder suggests an incomplete lower motor neuron lesion.’ Patients with isolated lesions of the conus medullaris or the pudendal nerve may have areflexic bladders and absent sacral reflexes, but the Achilles deep tendon reflex (L5-S2) and the knee-jerk reflex (L2-L4) should be present because these reflex arcs originate more rostral on the cord.
A thorough history is always the first step to evaluate the neurogenic bladder. The first line evaluation is always based on simple steps. We should also rule out external factors (i.e., medications, associated diseases) while evaluating this. A questionnaire about voiding habits should be used for all patients (frequency, number of voiding episodes, voiding volume, sense of incomplete evacuation or not, symptoms of UTI ( burning, associated fever), anorectal symptoms(constipation, stool impaction).
As an initial test, "urine dipstick" is recommended for all the patients with new bladder symptoms. It has a very high negative predictive value (i.e., 98%) but a low positive predictive value (i.e., 50%), so it is best to rule out the disease. It is also necessary to inquire about urinary retention and post-void residual (PVR) urine volume by ultrasonography or by catheterization must be done.
When urinary symptoms are present in tests mentioned above, other tests are necessary, including a three-day voiding chart, an ultrasound of the urinary tract, urine bacteriology, a urodynamic study a urine creatinine clearance, and impact of urinary symptoms on a quality of life scale( which is usually based on the specific and validated Qualiveen Questionnaire in multiple sclerosis and spinal cord injury). When high-risk factors are present, e.g., high vesicle pressure during the filling phase or voiding, then specific radiologic investigations must be performed (CT scan, cystourethrography, and sometimes renal scintigraphy when creatinine clearance is abnormal).
The primary goal of the treatment of neurogenic bladder is to protect the upper urinary tract from damage. The second goal is to maintain urinary continence, but all the while improving the patient's quality of life. The treatment also depends on the etiology causing the neurogenic bladder. Clean intermittent catheterization is the gold standard for neurogenic bladder and detrusor overactivity. it is combined with anti-muscarinic agents. Beta-3 receptor agonists have also been recently used for overactive bladder, but there is only limited clinical experience in neuro-urologic patients.
Nonselective and selective alpha-blockers are partially successful in the neurogenic bladder as they decrease bladder outlet resistance, residual volume, and autonomic dysreflexia. Sacral neuromodulation is another treatment option for NB. Patients can get benefit from neuromodulation of the sacral spinal nerve (S3). It does not resolve all urinary symptoms but may prove to be a good option in combination with other treatment options. Pudendal neuromodulation is another potential treatment of neurogenic bladder overactivity, especially immediately after spinal cord injury.
Percutaneous tibial nerve stimulation is also a treatment option that is minimally invasive and has fewer side effects. The surgical procedures include augmentation enterocystoplasty and artificial urinary sphincter in refractory cases.
The timely diagnosis of neurogenic bladder is crucial, and it has a significant impact on patient outcomes. The neurogenic bladder can have various differentials, most important of which is spinal cord injury. Any injury to the spinal cord, including blunt, degenerative, developmental, vascular, infectious, traumatic, and idiopathic injury can disturb normal micturition and can result in urinary incontinence. Other causes of urinary dysfunction can be the following:
History and review of systems play a key role in identifying the cause of the neurogenic bladder in addition to the physical exam with a thorough neurologic examination. Laboratory evaluation is also necessary to reach the final diagnosis.
The goal of the treatment of neurogenic bladder is to preserve continence and renal function. Medical management by clean intermittent catheterization and anticholinergics is sufficient to maintain urinary continence and to preserve renal function in about 90% of the patients with neurogenic bladder. But the management requires long term follow to check the graphs of renal function and urinary habits.
A detailed follow up is also useful in assessing the previously given treatment regimen is effective in managing the patient's condition or not. In patients with neurogenic bladder sphincter dysfunction, no recommended guidelines exist on how renal function can ideally undergo evaluation. In clinical practice, radiologic imaging, GFR are used to assess the urinary and renal function.
Complications of the neurogenic bladder usually fall into two categories, i.e., short term complications and long term complications. When the neurogenic bladder is left untreated, then it can lead to repeated bouts of pyelonephritis and complete loss of bladder compliance. Long term complications include renal stones, refractory urinary incontinence, and sometimes it can also result in malignancy.
There should be consultations to the following departments according to the need:
The patient with a neurogenic bladder who is on catheter should receive education about catheter care and urinary output monitoring. If a patient is on clean intermittent catheterization (CIC), it is crucial to teach proper techniques of CIC use to prevent complications. Those who are on suprapubic catheters should also follow appropriate measures of catheter care and keep the suprapubic site clean and also avoid urine leakage to prevent dermatitis. In case of complications, patients may need proper followup home care and education.
Patients who have associated benign prostatic hyperplasia (BPH) should receive counsel regarding a trial without catheterization and necessary follow-up care. The surgical options require discussion with the patient, along with their risks and complications. If the condition is amenable to management with medications, patients should have counsel about the side effects of the drug, and the potential need to find an alternative.
The health outcomes can be improved by thorough history taking, using the questions recommended by the American Urological Association. Any neurological disorder must be ruled out by taking a proper medication review and performing a detailed physical examination. Patients should also receive education regarding catheter use and proper antiseptic techniques. The nursing team should have enough knowledge of the contraindications of catheter placement and should be able to recognize them.
In patients who have acute retention and are unable to pass a urethral catheter, the urology team should be consulted to provide suprapubic catheter placement. If a urologist is not available immediately, and the patient is in extreme discomfort, the clinician should have enough expertise to pass suprapubic needle drainage or temporary catheter drainage to relieve the patient’s discomfort. The patient and the patient’s family should receive appropriate training regarding CIC. They should also be educated regarding medication compliance and on medications used to treat benign prostatic hyperplasia.
There should be proper coordination between primary care doctors, urologists, nephrologists, and emergency room doctors. Urology nurses counsel patients, monitor their condition and provide updated information to the interprofessional team. By following the above measures, healthcare outcomes can improve significantly.
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