The development of novel, less invasive therapies for stress urinary incontinence in women requires a thorough knowledge of the relationship between the pathophysiology of incontinence and anatomy. This article provides a review of the anatomy of the pelvic floor and lower urinary tract. Also discussed is the hammock hypothesis, which describes urethral support within the pelvis and provides an explanation of the continence mechanism.

Gastrointestinal (GI) symptoms are reported by up to 70% of endurance athletes. Although exercise leads to decreased gastrointestinal blood flow, GI-ischaemia is rarely reported as a cause. Mucosal ischaemia may result in nausea, abdominal cramps and bloody diarrhoea. After exercise, reperfusion damage and endotoxaemia may cause systemic symptoms as well. In three patients, two women aged 46 and 25 respectively and a man aged 40, with a heterogeneous presentation of exercise induced GI-symptoms, GI-ischaemia was demonstrated using gastric exercise tonometry. Gastric tonometry is mandatory for the diagnosis and follow-up. In the first patient, an isolated celiac artery stenosis was found; after incision of the left crus of the diaphragm, she was asymptomatic and the results of gastric tonometry improved. The other two patients had non-occlusive ischaemia associated with high exercise intensity. Reduction of the exercise intensity resulted in the complaints disappearing.

We report a case of acute gastrointestinal ischemia during a very stressful event in whom the diagnosis was made by 24-hour tonometry. This case report unequivocally links a stressful event with increased catecholamine release and subsequent severe symptomatic gastrointestinal ischemia. The role of ischemia as potential pathophysiological mechanism has never been studied in detail. The clinical significance of finding such an association is underscored by this case report, where a vasoactive drug normally used for hypertension treatment resulted in greatly improved abdominal symptoms. Copyright (c) 2007 S. Karger AG, Basel.

BACKGROUND:: The clinical relevance of splanchnic artery stenosis is often unclear. Gastric exercise tonometry enables the identification of patients with actual gastrointestinal ischaemia. A large group of patients with splanchnic artery stenosis was studied using standard investigations, including tonometry. METHODS:: Patients referred with possible intestinal ischaemia were analysed prospectively, using duplex imaging, conventional abdominal angiography and tonometry. All results were discussed within a multidisciplinary team. RESULTS:: Splanchnic stenoses were found in 157 (49.7 per cent) of 316 patients; 95 patients (60.5 per cent) had one-vessel, 54 (34.4 per cent) two-vessel and eight (5.1 per cent) had three-vessel disease. Chronic splanchnic syndrome was diagnosed in 107 patients (68.2 per cent), 54 (57 per cent) with single-vessel, 45 (83 per cent) with two-vessel and all eight with three-vessel stenoses. Treatment was undertaken in 95 patients, 62 by surgery and 33 by endovascular techniques. After a median follow-up of 43 months, 84 per cent of patients were symptom free. CONCLUSION:: Gastric exercise tonometry proved crucial in the evaluation of possible intestinal ischaemia. Comparing patients with single- and multiple-vessel stenoses, there were significant differences in clinical presentation and mortality rates. Copyright (c) 2006 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd.

Stenotic disorders of the splanchnic arteries are not rare, and it is generally assumed that symptoms are rare in patients with a single splanchnic stenosis, and even in patients with multiple-vessel stenoses. Currently, only gastric exercise tonometry aids the diagnostic evaluation, as it indicates actual ischaemia. Patients with stenotic disorders without complaints are referred to as having chronic splanchnic disease (CSD) and those with ischaemic complaints as having chronic splanchnic syndrome (CSS). The classical presentation of CSS, including the triad postprandial pain, weight loss and upper abdominal bruit, is also known as 'intestinal angina'. From the experience of our multidisciplinary working team on gastrointestinal ischaemia in 110 patients with stenoses of at least one splanchnic artery, two different clinical patterns were observed. In our series approximately 60% of patients with single-vessel stenoses, including the coeliac artery compression syndrome, have CSS. They have fewer complications, very low mortality, but most can be successfully treated by stenting or surgical treatment. Patients with multivessel splanchnic stenoses have more classical ischaemic complaints. Progression to a bowel infarction was seen in 34%, and mortality was 21%, mostly from bowel or myocardial infarction. Treatment should be tailored based upon perioperative risk assessment and local vascular anatomy. This may consist of autologous arterial bypass of one or two vessels, preferably antegrade. stenting or a combination of both. This differentiation between single- and multivessel splanchnic disease has considerable consequences for optimal work-up and treatment.

OBJECTIVE: The technical and clinical outcome of endovascular revascularization was analyzed in patients with suspicion of chronic splanchnic syndrome (CSS). METHODS: Medical history, duplex, angiography and exercise gastric tonometry suggested CSS in 97 patients. Twenty-seven of them were treated endovascular (one patient had 3-vessel, 12 patients had 2-vessels, 14 patients had 1-vessel CSS). Five patients received previous splanchnic revascularization. Twenty-three patients (85%) had severe co-morbidity: cardiac, pulmonary or cachexia. Endovascular treatment consisted of percutaneous transluminal angiography (PTA) of the coeliac artery (CA) or superior mesenteric artery (SMA) in three and primary balloon expandable stenting in 24 patients (13 CA and 10 SMA solitary, two CA and SMA both, 31 splanchnic arteries in total). RESULTS: Three patients showed procedure related complications (11%). Mean follow-up was 19, range 2-76 months. Two patients died during follow up, both not procedure or CSS related. Five patients had no improvement of symptoms, without evidence of re- or residual stenosis. The primary clinical success was 67%, secondary clinical success was 81%. The primary patency was 81% and secondary patency was 100%. CONCLUSION: Endovascular treatment of CSS has a reasonable outcome. It is an alternative to operative treatment, especially in patients with high co-morbidity or limited life expectancy.

BACKGROUND:: The effect on outcome of the introduction of endovascular techniques for the exclusion of abdominal aortic aneurysm (AAA) is largely unknown. The aim of the study was to contrast the early and mid-term outcome after open and endovascular AAA repair. METHODS:: Consecutive patients who underwent transfemoral endovascular aneurysm repair (EVAR; n = 93) between April 1998 and January 2003, or conventional open aneurysm repair in the time intervals before (n = 113) and after (n = 82) the introduction of EVAR were studied. All data were collected prospectively. All patients underwent elective and primary repair. Patient survival was calculated by the Kaplan-Meier method and the possible predictive value of more than 25 perioperative variables on five outcome variables (length of intensive care unit stay, morbidity, and 30-day, 6-month and overall mortality) was assessed by multivariate analysis. RESULTS:: There were no differences in risk profiles between the three groups. Selection for EVAR was based on anatomical grounds only. All five outcome variables were significantly better with EVAR than either former or recent open repair. The only significant predictors of failure were advanced age and the need to perform an additional procedure for former open repair; hypertension and the preoperative use of anticoagulants for recent open repair; and renal insufficiency and pulmonary insufficiency for EVAR. CONCLUSION:: EVAR offered considerable benefits compared with conventional open repair at early and mid-term follow-up, which was not explained by selection of patients with a favourable risk profile. In the current era, in which patients are selected for open repair as a consequence of unfavourable anatomy, morbidity and mortality rates following conventional open treatment of AAA have increased at early and mid-term, but not at long-term, follow-up.

INTRODUCTION: Open repair of ruptured abdominal aortic aneurysm (rAAA) still has a high mortality. Endovascular aortic repair (EVAR) may be the way to improve survival rates. However, it is not clear how many patients with rAAA will be suitable for acute EVAR. METHODS: Between October 2000 and April 2002 all patients with acute symptomatic or ruptured AAA were assessed for EVAR on an intention-to-treat basis with emergency computed tomographic angiography (CTA). Patient and logistic characteristics were analysed. We used two commercially available aorto uni-iliac devices with a maximum proximal diameter of 28 and 34 mm. RESULTS: Five out of 26 patients were excluded for CTA and EVAR because of severe and persistent hypotension (3 pts) or logistic reasons (2 pts, both eligible). Twelve patients were found not eligible for EVAR due to unsuitable infrarenal aortic neck length (3 pts), neck diameter (1 pt) or a combination of both (8 pts). The remaining six patients were treated with EVAR. After 6 months no graft failure or aneurysm related deaths were recorded in the EVAR group. CONCLUSION: A total of 28% of patients with symptomatic or ruptured AAA was treated with EVAR. A potential 42% of patients could have been suitable for EVAR, if the correct devices had been in stock and all patients had been properly assessed.

Budd-Chiari syndrome is a rare disease and, with or without treatment, the prognosis is usually poor. Percutaneous transluminal angioplasty of the hepatic vein in Budd-Chiari syndrome is a safe method, although recurrent stenosis makes it necessary to repeat it several times in most cases. Insertion of a wall-stent in the hepatic vein seems to be a more long-lasting treatment. Monitoring the blood flow through the wall-stent every 6 months is important because of the apparent obliteration of the wall-stent by intimal fibrosis of the hepatic vein. Further follow-up investigations of this method are necessary.

The microvascularisation of the male urethra was studied in neonates and infants by injection of agarised China ink into the circulation. The purpose of this study was to specify the angioarchitecture of each tunic of the urethral wall. The disposition of the microvascularisation networks varies depending on the urethral parts considered: only the mucous membrane networks are uniform throughout the entire urethra. The sub-mucous networks are significantly increased in the spongy part. The muscular networks disappear in the spongy part.

PURPOSE: Despite the prevalence of stress urinary incontinence in women there are no approved drugs for the disease. MATERIALS AND METHODS: Designing medical therapies requires a comprehensive understanding of how the internal and external sphincters are neurologically controlled. In this review recent advances in mapping storage and micturition reflexes, and the association of serotonergic and noradrenergic systems with these reflexes are discussed. RESULTS: Urine storage and micturition are controlled by a series of hard wired reflexes that are under the modulatory influence of serotonin and norepinephrine. Augmentation of the serotonergic and noradrenergic systems with duloxetine increases bladder capacity and urethral rhabdosphincter activity. The increase in sphincter activity is mediated by alpha1 adrenergic receptors and 5-hydroxytryptamine receptors. CONCLUSIONS: Increasing rhabdosphincter activity with duloxetine may offer a therapeutic benefit in women with stress urinary incontinence.

OBJECTIVE: To assess dynamic intraurethral sonography in the diagnostic evaluation of the function of the rhabdosphincter in female patients with urinary stress incontinence in relation to patient age. METHODS: Sixty-two patients with clinically proved urinary stress incontinence were investigated by means of intraurethral sonography with a 12.5-MHz endoluminal 9F catheter. The omega-shaped rhabdosphincter was visualized at rest and during voluntary contractions. Changes of muscle thickness and transducer-sphincter distance were measured and considered as parameters of muscle function. The intraurethral sonographic data were compared with results of standard urodynamic tests. RESULTS: Transducer-sphincter distance and sphincter muscle thickness showed a significant decrease with positive linear dependency on patient age (P <.001). Patients with grade III urinary stress incontinence had complete loss of sphincter contractility. A negative correlation was revealed between urethral closure pressure and patient age. CONCLUSIONS: We found an age-related decrease in rhabdosphincter function. Our results suggest that the rhabdosphincter is a substantial component of the continence mechanism in female urinary stress incontinence. Unlike urethral pressure profiles, which can only reveal zones of higher intraluminal pressure, transurethral sonography is highly specific for measurement of the function of the rhabdosphincter.

Urethral closure mechanisms during passive increments in intravesicular pressure (P(ves)) were investigated using microtip transducer catheters in urethane-anesthetized female rats. After a block of reflex bladder contractions by spinal cord transection at T8-T9, abruptly raising P(ves) to 20, 40, or 60 cmH(2)O for 2 min induced a bladder pressure-dependent contractile response in a restricted portion of the middle urethra (12.5-15 mm from the urethral orifice) that was abolished by cutting the pelvic nerves bilaterally. In pelvic nerve-intact rats, the bilateral transection of either the pudendal nerves, the nerves to the iliococcygeous/pubococcygeous muscles, or the hypogastric nerves significantly reduced (49-74%) the urethral reflex response induced by passive P(ves) increases, and combined transection of these three sets of nerves totally abolished the urethra-closing responses. In spinal cord-intact rats, similar urethral contractile responses were elicited during P(ves) elevation (20 or 40 cmH(2)O) and were also eliminated by bilateral pelvic nerve transection. After spinal cord and pelvic nerve transection, leak point pressures, defined as the pressure inducing fluid leakage from the urethral orifice during passive P(ves) elevation by either bladder pressure clamping in 2.5-cmH(2)O steps or direct compression of the bladder, were significantly lowered by 30-35% compared with sham-operated (spinal cord-transected and pelvic nerve-intact) rats. These results indicate that 1) passive elevation of P(ves) can elicit pelvic afferent nerve-mediated contractile reflexes in the restricted portion of the urethra mediated by activation of sympathetic and somatic nerves and 2) bladder-to-urethral reflexes induced by passive P(ves) elevation significantly contribute to the prevention of stress urinary incontinence.

Stress urinary incontinence (SUI) is a debilitating disorder caused by malfunctioning of the urethral sphincter. Anatomical and histological properties of the sphincter, its innervation and supporting structures are explained in relation to the closing mechanism of the bladder outlet. Urethral sphincter function is discussed from the passive concept of urethral pressure transmission to the 'hammock theory' and the role of the pubococcygeus muscles. SUI is caused by a combination of intrinsic sphincter deficiency and urethral hypermobility. The difficult interpretation of the parameters in urodynamic investigation to assess intrinsic sphincter deficiency (ISD) and/or urethral hypermobility is discussed. Electromyography (EMG) is valuable in the assessment of the overall urethral sphincter in relation to maneuvers (kinesiological EMG) and at the level of the muscle fiber (needle EMG). The diagnostic potential of circumferential surface EMG in the urethral sphincter is reviewed in relation to the EMG features of ISD.

Histological observations of semiserial sections obtained from the cadavers of 30 elderly Japanese women (aged 61-93 years) found that the urethral rhabdosphincter (URS) usually occurred as a ventrally localized structure instead of exhibiting the normal completely circular configuration. The superoinferior length, thickness and muscle fiber density of the URS area showed significant interindividual variation. A thick fascicle, extending posterolaterally from the URS and radiating to the lateral vaginal wall and other perineal tissues, was usually observed. A circular smooth muscle layer, which immediately surrounded the longitudinal smooth muscle layer, was consistently present in the proximal urethral but not in the bladder neck. These findings suggest that voluntary sphincteric action is weak or incomplete in elderly Japanese women. We therefore hypothesize that upward retraction of the midurethra by the URS, compression of the distal urethra by its posterolateral extensions, and tonus provided by the outer circular smooth muscle layer all contribute to maintaining continence in these women.

The anatomic structures that prevent stress incontinence, urinary incontinence during elevations in abdominal pressure, can be divided into 2 systems: a sphincteric system and a supportive system. The action of the vesical neck and urethral sphincteric mechanisms at rest constrict the urethral lumen and keep urethral closure pressure higher than bladder pressure. The striated urogenital sphincter, the smooth muscle sphincter in the vesical neck, and the circular and longitudinal smooth muscle of the urethra all contribute to closure pressure. The mucosal and vascular tissues that surround the lumen provide a hermetic seal, and the connective tissues in the urethral wall also aid coaptation. Decreases in striated muscle sphincter fibers occur with age and parity, but the other tissues are not well understood. The supportive hammock under the urethra and vesical neck provides a firm backstop against which the urethra is compressed during increases in abdominal pressure to maintain urethral closure pressures above rapidly increasing bladder pressure. The stiffness of this supportive layer is presumed to be important to the degree to which compression occurs. This supporting layer consists of the anterior vaginal wall and the connective tissue that attaches it to the pelvic bones through the pubovaginal portion of the levator ani muscle and also the tendinous arch of the pelvic fascia. Activation of the levator muscle during abdominal pressurization is important to this stabilization process. The integrity of the connection between the vaginal wall and tendinous arch also plays an important role.

The urethral closure mechanism under a stress condition induced by sneezing was investigated in urethane-anesthetized female rats. During sneezing, while the responses measured by microtip transducer catheters in the proximal and middle parts of the urethra increased, the response in the proximal urethra was almost negligible when the bladder response was subtracted from the urethral response or when the abdomen was opened. In contrast, the response in the middle urethra during sneezing was still observed after subtracting the bladder response or after opening the abdomen. These responses in the middle urethra during sneezing were significantly reduced approximately 80% by bilateral transection of the pudendal nerves and the nerves to the iliococcygeous and pubococcygeous muscles but not by transection of the visceral branches of the pelvic nerves and hypogastric nerves. The sneeze leak point pressure was also measured to investigate the role of active urethral closure mechanisms in maintaining total urethral resistance against sneeze-induced urinary incontinence. In sham-operated rats, no urinary leakage was observed during sneeze, which produced an increase of intravesical pressure up to 37 +/- 2.2 cmH2O. However, in nerve-transected rats urinary leakage was observed when the intravesical pressure during sneezing exceeded 16.3 +/- 2.1 cmH2O. These results indicate that during sneezing, pressure increases elicited by reflex contractions of external urethral sphincter and pelvic floor muscles occur in the middle portion of the urethra. These reflexes in addition to passive transmission of increased abdominal pressure significantly contribute to urinary continence mechanisms under a sneeze-induced stress condition.