Neurogenic Bladder
When the nerves controlling the bladder are damaged, the bladder misbehaves in a way that predicts from the level of the lesion — and the goals of management are always the same: protect the kidneys, keep the patient continent and infection-free, and empty the bladder safely.
The big picture
When the nerves controlling the bladder are damaged, the bladder misbehaves in a way that predicts from the level of the lesion — and the goals of management are always the same: protect the kidneys, keep the patient continent and infection-free, and empty the bladder safely. The unifying idea (built on the neurophysiology lesson) is that lesions above the sacral cord tend to make the bladder overactive, while lesions at or below the sacral cord make it underactive/flaccid. Layered on top is the danger of detrusor–sphincter dyssynergia and the emergency of autonomic dysreflexia.
The framework: classify by lesion level (suprapontine, suprasacral spinal, sacral/infrasacral), understand the resulting bladder behaviour, recognise dyssynergia and autonomic dysreflexia, and apply the protect-the-kidney management principles.
Mechanism pathway
Tap any step to see why it happens.
Interactive — where is the lesion?
Diagnostic algorithm
Each step answers one question. Tap to expand.
Board traps
Above the sacral cord → overactive bladder; at/below the sacral cord → flaccid/areflexic bladder.
Suprasacral spinal lesions cause detrusor–sphincter dyssynergia → high pressures → upper-tract damage (the key danger).
Acute spinal cord injury first causes spinal shock (flaccid bladder) before overactivity emerges.
Autonomic dysreflexia (SCI above ~T6) is a hypertensive emergency — a distended bladder is a classic trigger; drain it.
The overriding goal is protecting the kidneys — keep storage pressures low (anticholinergics + CIC).