Neurogenic Bladder (Neurogenic Lower Urinary Tract Dysfunction, NLUTD)

Autonomic dysreflexia is the headline - With a cord lesion at or above T6, a noxious stimulus below the level produces unopposed sympathetic outflow: severe throbbing headache, flushing and sweating above the lesion, pale cold skin below it, and a hypertensive spike with reflex bradycardia. About 85% of the time the trigger is urological — a distended bladder, a blocked Foley, or a UTI. Lesions below T10 rarely do this.

Know the baseline blood pressure - Many cord-injured patients are hypotensive at baseline. An episode is a systolic rise of at least 25 mmHg above that baseline; a systolic over 150 mmHg or more than 40 mmHg above baseline is significant. Without the baseline number on the chart you cannot call it.

Treat dysreflexia in order - Pause the surgery and remove the stimulus, which usually means draining or irrigating the bladder; deepen with propofol or a volatile agent; 100% oxygen; raise the head of the bed; then a vasodilator. Keep watching afterward, because one episode makes another within 24 hours more likely.

Anesthesia is the prophylaxis - General, spinal, and regional anesthesia are all preventive for stimulating procedures. Do not let a cystoscopy or urodynamic study proceed awake just because the patient has no sensation there. Urodynamics on an at-risk patient needs hemodynamic monitoring and drugs for extreme hypertension in the room.

What the hypertension can do - Hemorrhagic stroke, intracranial hemorrhage, pulmonary edema, left ventricular dysfunction, retinal detachment, seizures, atrial fibrillation or flutter, and myocardial infarction where there is coronary disease. The bradycardia can go all the way to arrest.

Check the upper tracts and renal function - Creatinine with an estimated GFR, plus renal ultrasound or abdominal CT. Sustained detrusor or detrusor leak-point pressures over 40 cm H2O greatly raise the risk of upper tract deterioration, and it progresses silently.

Assume colonized urine - Catheter-associated bacteriuria develops at 3% to 10% per day of catheterization, and infection is itself a dysreflexia trigger. A urine dipstick is the first test for new urinary symptoms: 98% negative predictive value but only 50% positive predictive value, so a positive one needs a culture.

Their bladder drugs - Anticholinergics are first-line for detrusor overactivity and cut maximal detrusor pressure by 30% to 40%; beta-3 agonists, alpha-blockers, and onabotulinumtoxinA injections repeated every 6 to 9 months are also common. Botulinum patients may be catheter-dependent until bladder function returns.

Handle a suprapubic tube carefully - Suprapubic tubes are preferred over urethral catheters for long-term drainage, and if one falls out it must be replaced urgently or the cystostomy tract closes.

Expect orthostatic swings - Over half of patients with autonomic dysreflexia also have orthostatic hypotension, on top of a low baseline pressure. Position changes and induction will exaggerate it, so have a vasopressor drawn up.

Normal micturition depends on the central nervous system coordinating sympathetic, parasympathetic, and somatic input to the detrusor and to the internal and external urethral sphincters. Break that coordination anywhere — spinal cord injury, multiple sclerosis, spina bifida, Parkinson disease, stroke, diabetes — and you get a neurogenic bladder: a failure to store, a failure to empty, or both, frequently with detrusor-sphincter dyssynergia.

It is common in the populations that fill urology lists: 70% to 84% of spinal cord injury patients, 40% to 90% of multiple sclerosis patients, 37% to 72% of Parkinson patients, and 15% of stroke patients. Sustained detrusor or leak-point pressures above 40 cm H2O push urine back up the ureters and destroy the upper tracts without symptoms. The perioperative headline is autonomic dysreflexia, since bladder distension is by far its most common trigger.