Материал: Oxford American Handbook of Urology ( PDFDrive )

522 CHAPTER 13 Neuropathic bladder

Management of hydronephrosis in the neuropathic patient

An overactive bladder (detrusor hyperreflexia) or poorly compliant bladder is frequently combined with a high-pressure sphincter (detrusorsphincter dyssynergia [DSD]). Bladder pressures during both filling and voiding are high.

At times the bladder pressure may overcome the sphincter pressure and the patient leaks small quantities of urine. For much of the time, however, the sphincter pressures are higher than the bladder pressures and the kidneys are chronically exposed to these high pressures. They are hydronephrotic on ultrasound, and renal function slowly, but inexorably, deteriorates.

Treatment options for hydronephrosis

Bypass the external sphincter

•IDC (indwelling catheter)

•ISC (intermittent self-catheterization) + anticholinergics

Treat the external sphincter

•Sphincterotomy: surgical incision via a cystoscope inserted down the urethra (electrically heated knife or laser), botulinum toxin injections into sphincter, urethral stent

•Deafferentation* + ISC or SARS

Treat the bladder

•Intravesical botulinum toxin + ISC

•Augmentation + ISC

•Deafferentation* + ISC or SARS

* Deafferentation converts the high-pressure sphincter into a low-pressure sphincter and the highpressure bladder into low-pressure bladder.

MANAGEMENT OF AUTONOMIC DYSREFLEXIA 523

Management of autonomic dysreflexia in the neuropathic patient

Autonomic dysreflexia (AD) is a unique and potentially life-threatening condition in spinal cord–injured patients. AD can cause rapid, extreme blood pressure elevation, headache, diaphoresis, bradycardia, sweating, nausea, and piloerection in patients with spinal cord lesions at and above the sixth thoracic level (T6).

Approximately 85% of quadriplegic and high paraplegic individuals are prone to AD in response to noxious stimuli. AD is more common in men than in women because of increased bladder outlet resistance. Stimuli, such as bladder distention, bowel distention, or pain, activate sympathetic neurons in the lateral horn of the spinal cord, causing unopposed reflex sympathetic activity.

Primary therapy should always be to remove the triggering stimulus (i.e., empty distended bladder or clear obstruction in Foley catheter). Rarely, acute episodes must be managed with intravenous nitrates or arterial dilators under closely monitored conditions. Chronic treatment with A-blockers may improve some symptoms of AD.

1 Vaidyanathan S, Soni BM, Sett P, et al. (1998). Pathophysiology of autonomic dysreflexia: longterm treatment with terazosin in adult and pediatric spinal cord injury patients manifesting recurrent dysreflexic episodes. Spinal Cord 36:761–770.

524 CHAPTER 13 Neuropathic bladder

Bladder dysfunction in multiple sclerosis, in Parkinson disease, after stroke, and in other neurological disease

Multiple sclerosis (MS)

MS is a neurological disease caused by focal demyelination of white matter in the brain and spinal cord. Urological manifestations are the presenting complaint in about 2.5% of MS patients.

Three-quarters of patients with MS have spinal cord involvement and, in these patients, bladder dysfunction is common. Detrusor hyperreflexia with urge incontinence is the most common GU symptom present in 78% of patients with voiding dysfunction.

DSD is present in 30% to 65% of patients, leading to poor emptying and possible upper tract damage.

Parkinson disease (PD)

PD is a cause of Parkinsonism, a clinical complex of tremor, rigidity, and bradykinesis, and is due to degeneration of dopaminergic neurons in the substantia nigra in the basal ganglia. Mild intellectual deterioration may occur, and frequency, urgency, and urge incontinence are common.1

The most common urodynamic abnormality is DH (the basal ganglia may have an inhibitory effect on the micturition reflex). L-dopa seems to have a variable effect on these symptoms and DH, improving symptoms in some and making them worse in others.

LUTS in Parkinson disease may simply be due to benign prostatic obstruction or to the PD itself. Many PD patients have coexisting detrusor overactivity with impaired bladder contractility.

Consider combining intermittent catheterization with antimuscarinic drugs initially (e.g., oxybutynin 5 mg PO tid or tolterodine LA 4 mg PO qd). Second-line medical therapy can include tricyclic antidepressants such as imipramine 10–25 mg PO bid/tid.

Traditionally, patients with PD have had a poorer outcome after TURP than those without PD, but if the patient has urodynamically proven BOO, TURP is a treatment option.

Multiple system atrophy (MSA; formerly Shy–Drager syndrome)

MSA is a cause of Parkinsonism characterized clinically by postural hypotension and detrusor areflexia. Loss of cells in the pons leads to DH (symptoms of bladder overactivity). Loss of parasympathetic neurons due to cell loss in the intermediolateral cell column of the sacral cord causes poor bladder emptying, and loss of neurons in Onuf nucleus in the sacral anterior horns leads to denervation of the striated sphincter causing incontinence.

1 Winge K. Skau AM. Stimpel H, et al. (2006). Prevalence of bladder dysfunction in Parkinson’s disease. Neurourol Urodyn 25(2):116–122.

526 CHAPTER 13 Neuropathic bladder

urinary retention. There is severe tetraparesis and bladder dysfunction, which often recovers to a substantial degree as the other neurological symptoms resolve.

Manage transient acute lower urinary tract dysfunction with CIC, anticholinergics, etc.6

Peripheral neuropathies

The autonomic innervation of the bladder makes it vulnerable to the effects of peripheral neuropathies such as those occurring in diabetes mellitus and amyloidosis. The picture is usually one of reduced bladder contractility (poor bladder emptying—i.e., chronic low pressure retention).

6 Ganesan V, Borzyskowski M (2001). Characteristics and course of urinary tract dysfunction after acute transverse myelitis. Dev Med Child Neurol 43(7):473–475.