Voluntary emptying of the bladder is achieved by a command transmitted to the bladder via the splanchnic nerves. The splanchnic nerves are bilateral, but their participation (dominance) may be unbalanced. They can be affected both by the endometriosis nodule (infiltration, compression, irritation, in which case symptoms precede surgery) and by the surgical procedure. During surgery, the very fragile splanchnic nerves may be removed en bloc with the nodule, or sectioned.
Even when preserved, splanchnic nerves can be affected by heat diffusion from the energies used to coagulate vessels, or stretched during dissection, leading to neuropraxia. The term neuropraxia is used to describe moderate nerve damage resulting in temporary impairment of nerve function, and corresponds to a temporary loss of the nerve's myelin sheath, without any associated axonal damage. This demyelination slows the speed of conduction of the electrical impulse within the nerve, and consequently impairs the transmission of information through the nerve.
The prognosis is favorable, with complete recovery usually within a few weeks or months, due to reformation of the myelin sheath. The clinical result is difficulty in emptying the bladder, which permanently retains a variable quantity of urine. If the volume of urine remaining in the bladder at the end of a micturition (post-micturition residue or PMR) exceeds 100ml, patients must use small bladder catheters to empty the bladder several times a day (usually 5 or 6 times), at set times, and after attempting voluntary micturition. Bladder function improves progressively, over 4-6 weeks post-operatively, and self-catheterization can be discontinued when RPM consistently falls below 100ml.
When self-catheterization is indicated, it is taught before discharge from the clinic. Patients are asked to regularly record the volumes evacuated by catheterization (voiding calendar) and to communicate these to the surgeon.
The incidence of bladder atony requiring systematic self-catheterization is around 25% at discharge, decreasing to around 5% one year after surgery. Recovery of bladder function is explained by the regression of neuropraxia, edema and local inflammation due to surgery.