title: Chronic pelvic ischemia: etiology, pathogenesis, clinical presentation and management.
abstract: Overactive bladder (OAB) and bladder pain syndrome (BPS) although common, are vaguely defined and difficult to diagnose and manage etiologies of storage-type lower urinary tract symptoms (LUTS). The lack of optimal management options is a direct consequence of deficient understanding of the pathophysiologic mechanisms underlying these conditions. These conditions are especially prevalent in females, and cumulative contemporary epidemiological, clinical and laboratory evidence implicates ischemia as one of the key players in the pathophysiologic foundation of both these disorders. Taken together they make up "the" diagnostic as well as therapeutic black-hole in urologic practice. Much akin to chronic ischemic heart disease, chronic ischemia-reperfusion has been shown to cause degenerative changes at cellular and subcellular level in the bladder mucosa, smooth muscle fibers, and vesical neural and microvascular structures leading to a hypersensitive, hyperactive bladder initially, which with time invariably progresses into a failed, fibrotic and pressurized bladder. Diagnosis and management of these diseases are currently symptom focused and remains a source of much frustration. Consideration of role of ischemia connotates hope and could lead to a paradigm shift in the management of these patients with a completely new therapeutic armamentarium attacking the pathology itself. The aim of the current review is to provide a clinical thought perspective on the etiology/pathophysiology of chronic pelvic ischemia and its role as a precursor to the aforementioned conditions, and shed some light upon the potential management strategies to consider.
authors.affiliation: Department of Surgery, Maulana Azad Medical College, New Delhi, India - asood1@hfhs.org.
authors.forename: H
authors.initials: H
authors.lastname: Kapoor
authors.forename: E
authors.initials: E
authors.lastname: Gupta
authors.forename: A
authors.initials: A
authors.lastname: Sood
mesh_terms: D000368:Aged; D000818:Animals; D050197:Atherosclerosis / Q000150:complications / Q000175:diagnosis / Q000188:drug therapy; D002118:Calcium / Q000378:metabolism; D015687:Cell Hypoxia; D059350:Chronic Pain / Q000209:etiology; D004195:Disease Models, Animal; D004967:Estrogens / Q000627:therapeutic use; D005260:Female; D005609:Free Radicals / Q000378:metabolism; D006801:Humans; D006984:Hypertrophy; D007511:Ischemia / Q000150:complications / Q000175:diagnosis / Q000209:etiology / Q000473:pathology / Q000503:physiopathology / Q000628:therapy; D019194:Ischemic Preconditioning; D015227:Lipid Peroxidation; D008297:Male; D008333:Mandelic Acids / Q000627:therapeutic use; D008875:Middle Aged; D018727:Muscarinic Antagonists / Q000627:therapeutic use; D009130:Muscle, Smooth / Q000503:physiopathology; D009569:Nitric Oxide / Q000502:physiology; D011312:Pressure; D015427:Reperfusion Injury / Q000209:etiology / Q000503:physiopathology; D012727:Sex Characteristics; D014524:Urethral Obstruction / Q000150:complications; D001743:Urinary Bladder / Q000098:blood supply* / Q000294:innervation / Q000473:pathology; D001745:Urinary Bladder Diseases / Q000209:etiology; D053201:Urinary Bladder, Overactive / Q000188:drug therapy / Q000209:etiology
chemical_list: D004967:Estrogens; D005609:Free Radicals; D008333:Mandelic Acids; D018727:Muscarinic Antagonists; D009569:Nitric Oxide; C005419:oxybutynin; D002118:Calcium