The lazy bladder syndrome: a possible urodynamic evolution in patients with idiopatic detrusor and pelvic floor...

To correlate the urge syndrome due to bladder overactivity and the lazy bladder syndrome, demonstrating that, at least in some cases, the lazy bladder may be the final stage of the evolution of an overactive bladder when associated with overactivity of the pelvic floor during micturition.

From January 1998 to December 1999, 38 children, 30 females and 8 males, 5 to 16 yrs. old (median 7.4 yrs), presenting with urge symptoms and never treated before, have been evaluated with repeated urodynamic investigations. At presentation all the patients underwent complete baseline urodynamics including evaluation of free flow, EMG, cystometrogram, subtracted detrusor pressure and flow/pressure studies. Flow/EMG was repeated every four months during the treatment period and full urodynamic investigation every year.

The first urodynamic study showed that 17 patients were affected by pure detrusor overactivity with good detrusor-sphincter co-ordination, while 21 presented both detrusor and pelvic floor muscles overactivity. All the patients have been treated with oxibutinin (0.3-0.5 mg/Kg. in 3 divided doses) and a timed voiding program with the help of a frequency-volume chart. At the end of the study 16 out of the 17 children with pure overactive bladder were cured (94%), while only 12 of the 21 patients with both bladder and sphincter overactivity were clinically and urodinamically normal Nine girls showed a progressive shift towards the development of a lazy bladder syndrome (capacious, hypocontractile bladder with large post-voiding residual and a non relaxing sphincter during micturition). Clinically this shift was signalled by recurrent urinary tract infections.

The transition from an overactive bladder to a hypocontractile one has been reported previously, but it has not been extensively investigated in children and its causes are largely hypothetical. In our cases this phenomenon occurred only in girls that, initially showed both detrusor urethral sphincter overactivity, therefore we can reasonably conceive that, at least in some cases, the lazy bladder syndrome may be due to prolonged and repeated high pressure bladder contractions opposed by a non relaxing sphincter that may lead to a progressive loss of the contractile properties of detrusor muscle fibres. The rather rapid shift observed in our patients might have been favoured by the use of anticholinergic medications.