Micturition requires active opening of the posterior urethral wall by directional striated muscles

Abstract

Inability to adequately evacuate the bladder is a major source of repeated urinary infection and pathology. Catheter-associated urinary tract infection (UTI) is the most common nosocomial infection, accounting for >1 million cases in hospitals and nursing homes. The risk of UTI increases with increasing duration of catheterization. In non-institutionalized elderly populations, UTIs are the second most common form of infection, accounting for nearly 25% of all infections with a cost of 1 billion dollars p.a. The traditional view of the mechanism of micturition was described by Messelink et al: “The pelvic floor muscles must relax in order to remove the passive continence mechanisms, thereby favouring normal micturition”. A recent Review of voiding dysfunction shed little light on the problem. It stated, “There remains a lack of consensus regarding a precise diagnosis and definition of voiding abnormalities in women”. The Review’s statement of causation was limited to “detrusor underactivity and outflow obstruction which could be either physiological or iatrogenic”. Two studies reporting improvement of bladder emptying following cystocele and fascial repair were mentioned, but no anatomical explanations were forwarded as to why. We believe that the answer to these conundra is to be found in urethral resistance to urine flow which is exponentially determined and is instantaneously modified by an external striated muscle mechanism first described in 1990. Micturition Video: https://www.youtube.com/watch?v=eiF4G1 mk6EA&feature=youtu.be This mechanism, since validated with electromyography and video X-ray studies stretches open the posterior urethral walls during micturition, Figure 1 and 2, and is in turn ultimately dependent on competent posterior suspensory ligaments