Nietrzymanie stresowe
Patofizjologia i mechanizm
Nietrzymanie stresowe moczu (SUI) charakteryzuje się mimowolnym wyciekiem moczu podczas wzrostu ciśnienia wewnątrzbrzusznego, gdy ciśnienie pęcherzowe (Pves) przekracza ciśnienie cewkowe (Pura), przy jednoczesnym niskim ciśnieniu wypieracza (Pdet bliskim zeru). Patomechanizm SUI obejmuje głównie nadmierną ruchomość cewki moczowej związaną z osłabieniem neuromięśniowego dna miednicy i uszkodzeniem tkanki łącznej podpierającej szyję pęcherza, a także niewydolność zwieracza wewnętrznego (ISD) wynikającą z dysfunkcji neuromięśniowej lub uszkodzeń pourazowych i pooperacyjnych. Kluczową rolę odgrywają mięsień dźwigacz odbytu oraz zewnętrzny zwieracz cewki moczowej, których dysfunkcja prowadzi do obniżenia ciśnienia zamykającego cewkę i utraty kontynencji.
- Patofizjologia nietrzymania stresowego
- Podstawowy mechanizm nietrzymania stresowego
- Anatomiczne czynniki patogenetyczne
- Rola mięśni dna miednicy
- Czynniki ryzyka i predysponujące
- Rola hormonów płciowych
- Patofizjologiczne aspekty nietrzymania moczu u mężczyzn
- Zaburzenia anatomiczne w nietrzymaniu stresowym
- Mechanizmy neuralne i mięśniowe
- Podsumowanie mechanizmów patofizjologicznych
Patofizjologia nietrzymania stresowego
Nietrzymanie stresowe (ang. stress urinary incontinence, SUI) to mimowolny wyciek moczu podczas aktywności zwiększających ciśnienie wewnątrzbrzuszne, takich jak kaszel, kichanie, śmiech czy wysiłek fizyczny. Występuje, gdy ciśnienie wewnątrz pęcherza przekracza zdolność cewki moczowej do pozostania zamkniętą, często w wyniku uszkodzenia mięśni zwieraczy odpowiedzialnych za utrzymanie kontynencji12. Patomechanizm nietrzymania stresowego jest złożony i wieloczynnikowy, a zrozumienie jego podstaw jest kluczowe dla optymalnego leczenia3.
Podstawowy mechanizm nietrzymania stresowego
Zgodnie z definicją Międzynarodowego Towarzystwa Kontynencji (ICS), nietrzymanie stresowe występuje, gdy ciśnienie pęcherzowe (Pves) jest większe niż ciśnienie cewkowe (Pura), przy jednoczesnym ustaleniu, że ciśnienie wypieracza (Pdet) jest bliskie zeru4. W warunkach prawidłowych ciśnienie w cewce moczowej musi być większe niż ciśnienie w pęcherzu zarówno w spoczynku, jak i podczas zwiększonego ciśnienia wewnątrzbrzusznego, aby utrzymać kontynencję5. Gdy ta równowaga zostaje zaburzona, dochodzi do utraty moczu w sytuacjach zwiększających ciśnienie wewnątrzbrzuszne6.
W prawidłowych warunkach wzrost ciśnienia wewnątrzbrzusznego jest jednakowo przenoszony na pęcherz i proksymalną część cewki moczowej. Kiedy cewka moczowa jest nadmiernie ruchoma, przenoszenie ciśnienia na ściany cewki może być zmniejszone, gdy obniża się ona i obraca pod kością łonową7. Nierównomierne przenoszenie ciśnienia i otwarcie szyi pęcherza prowadzi do mimowolnej utraty moczu podczas aktywności fizycznej, czyli nietrzymania stresowego8.
Anatomiczne czynniki patogenetyczne
Patogeneza nietrzymania stresowego jest związana głównie ze zmianami anatomicznymi struktur odpowiedzialnych za kontrolę oddawania moczu, w tym czynnikami anatomicznymi samej cewki moczowej, okolic okołocewkowych oraz unerwienia dna miednicy910.
Wyróżniamy dwa główne typy nieprawidłowości anatomicznych prowadzących do nietrzymania stresowego:
Nadmierna ruchomość cewki moczowej (hypermobilność)
Nadmierna ruchomość cewki moczowej wynika z osłabienia neuromięśniowego funkcjonowania dna miednicy w połączeniu z uszkodzeniem tkanki łącznej podpierającej cewkę moczową i szyję pęcherza11. W tym przypadku osłabienie struktur podporowych szyi pęcherza prowadzi do niedostatecznego zamknięcia szyi pęcherza, co powoduje zapadanie się tylnej ściany szyi pęcherza, przesunięcie szyi pęcherza w dół oraz zwiększenie lub nawet zniknięcie tylnego kąta pęcherzowo-cewkowego12.
Teoria „hamaka” (hammock theory) zaproponowana przez DeLanceya wyjaśnia ten mechanizm. Według niej, cewka moczowa spoczywa na podporze z tkanki łącznej i mięśni, która stanowi rodzaj hamaka. Gdy ta podpora jest osłabiona, cewka moczowa traci stabilność i nie jest w stanie wytrzymać zwiększonego ciśnienia wewnątrzbrzusznego1314.
Niewydolność zwieracza wewnętrznego
Niewydolność zwieracza wewnętrznego (ang. intrinsic sphincter deficiency, ISD) to stan, w którym zwieracz cewki moczowej nie jest w stanie się odpowiednio zamknąć i wytworzyć wystarczającego ciśnienia zamykającego, aby utrzymać mocz w pęcherzu1516. Mechanizm ten wynika z dysfunkcji zwieracza neuromięśniowego lub uszkodzenia spowodowanego wcześniejszymi operacjami miednicy, zaburzeniami neuropatycznymi i rdzeniowymi, urazami, zespołem ogona końskiego, złamaniami krzyżowymi i ciężkimi złamaniami miednicy, uszkodzeniem nerwów podczas operacji brzusznych, mielodysplazją, radioterapią miednicy lub powikłaniami po operacjach urologicznych, takich jak przezcewkowa resekcja prostaty lub radykalna prostatektomia17.
ISD jest spowodowana odnerwieniem i/lub odnerwieniem szyi pęcherza i proksymalnej cewki moczowej18. Nieodpowiedni opór ujścia pęcherza podczas aktywności fizycznej prowadzi do mimowolnej utraty moczu, określanej jako nietrzymanie stresowe typu III19.
Rola mięśni dna miednicy
Obecne rozumienie mechanizmu trzymania moczu u kobiet w warunkach stresowych przypisuje głównie rolę skoordynowanemu skurczowi mięśnia dźwigacza odbytu i zewnętrznego zwieracza cewki moczowej20. Uszkodzenie lub dysfunkcja mięśni dźwigacza odbytu (levator ani muscle, LAM) jest uważana za czynnik przyczyniający się do wystąpienia SUI21.
Mięsień dźwigacz odbytu oraz zewnętrzny zwieracz cewki moczowej odgrywają szczególnie ważną rolę wśród wielu czynników anatomicznych. Gdy te struktury są dysfunkcyjne, cewka moczowa nie może być silnie zamknięta, co prowadzi do nietrzymania moczu22. Badania włączone do przeglądu sugerują, że istnieją dowody neurofizjologiczne na uszkodzenie odnerwiające zewnętrznego zwieracza cewki moczowej u kobiet z SUI23.
Czynniki ryzyka i predysponujące
Etiologia nietrzymania stresowego jest wieloczynnikowa i obejmuje24:
- Utratę podparcia z mięśni dna miednicy i tkanki łącznej oraz nadmierną ruchomość cewki moczowej, co może wynikać z:
- Zaburzeń tkanki łącznej
- Przewlekłego kaszlu
- Otyłości
- Urazu dna miednicy
- Porodu pochwowego, szczególnie jeśli był traumatyczny
- Ciąży
- Operacji miednicy lub pochwy
- Zespołu genitourinary menopauzy lub innych stanów hipoestrogennych
- Przewlekłych zaparć
- Dźwigania ciężarów
- Palenia tytoniu
Czynniki ryzyka, takie jak wiek, poród, menopauza, otyłość, liczne porody drogą pochwową i inne, indukują zmiany w anatomicznych komponentach odpowiedzialnych za kontynencję26. Poród drogą pochwową jest uznawany za potencjalnie traumatyczny dla dna miednicy. Pierwszy poród może zapoczątkować uszkodzenie mechanizmu kontynencji w wyniku bezpośredniego uszkodzenia mięśni dna miednicy lub nerwów, lub obu tych struktur, podczas przejścia płodu27.
Rola hormonów płciowych
Funkcja cewki moczowej u kobiet jest pod wpływem estrogenów. Brak estrogenów w okresie menopauzy prowadzi do atrofii i zastąpienia podśluzówki (czyli splotu naczyniowego) przez tkankę włóknistą28. Częstość występowania nietrzymania stresowego zwiększa się po menopauzie z powodu obniżonego poziomu estrogenów29.
Niedobór estrogenów u kobiet po menopauzie powoduje atrofię warstwy śluzówki cewki moczowej, zmniejsza jej hermetyczne uszczelnienie i może przyczyniać się do wieloczynnikowej przyczyny nietrzymania stresowego30. Estrogeny zwiększają tonus mięśni cewki moczowej poprzez zwiększenie regulacji receptorów alfa-adrenergicznych w otaczającym obszarze i wzmacniają odpowiedź skurczową alfa-adrenergiczną w celu wzmocnienia mięśni miednicy, co jest ważne w podparciu cewki moczowej (tj. zapobiega nadmiernej ruchomości cewki moczowej)31.
Patofizjologiczne aspekty nietrzymania moczu u mężczyzn
U mężczyzn nietrzymanie stresowe rozwija się najczęściej po zabiegach na gruczole krokowym, takich jak radykalna prostatektomia32. Istnieje kilka przyczyn nietrzymania moczu po operacji. Głębokie szwy dna miednicy powodują bezpośrednie uszkodzenie zewnętrznego zwieracza lub jego unerwienia w przypadku krwawienia lub naciekania guza. Pooperacyjna nadmierna ruchomość cewki moczowej błoniastej została zidentyfikowana jako kolejny czynnik osłabienia zwieracza po radykalnej prostatektomii33.
Mechanizm leżący u podstaw trzymania moczu u mężczyzn jest istotny dla zrozumienia pooperacyjnego nietrzymania moczu po radykalnej prostatektomii (PPSUI). Trzymanie moczu u mężczyzn jest utrzymywane przez właściwe funkcjonowanie mięśnia wypieracza, proksymalnego zwieracza wewnętrznego w szyi pęcherza, zewnętrznego zwieracza cewki moczowej (EUS) oraz mechanizmu podwieszającego cewkę moczową (więzadeł łonowo-cewkowych)34.
Zaburzenia anatomiczne w nietrzymaniu stresowym
W świetle złożonych interakcji między morfologią tkanek, właściwościami mechanicznymi, perfuzją, unerwieniem i kontrolą motoryczną, kilka czynników może przyczyniać się do patofizjologii SUI, jednak dowody na wiele z tych czynników nie zostały systematycznie ocenione, a ich względne znaczenie jest w dużej mierze nieznane35.
Upośledzona struktura i podparcie cewki moczowej
Upośledzona struktura i podparcie cewki moczowej oraz szyi pęcherza, potwierdzone badaniami ultrasonograficznymi i MRI, okazały się być silnie związane z SUI u kobiet36. Rozszerzenie szyi pęcherza (lub lejkowanie) pojawiło się w metaanalizie jako wysoce rozpowszechnione u kobiet z SUI37.
Dominująca teoria sugeruje kombinację zaburzenia w tkankach łącznych podtrzymujących pęcherz i cewkę moczową oraz osłabienia struktur mięśniowych dna miednicy, szyi pęcherza i zwieraczy cewki moczowej, co prowadzi do zmniejszonego ciśnienia zamykającego cewkę moczową i niższego ciśnienia punktu przecieku (ALPP), co funkcjonalnie skutkuje SUI38.
Mechanizm wsparcia cewki moczowej
Mechanizm wsparcia cewki moczowej obejmuje wszystkie struktury zewnętrzne w stosunku do cewki moczowej, które oferują podporę, na której leżą proksymalna i środkowa część cewki moczowej. Wsparcie anatomiczne pochodzi bardziej ze struktur powięziowych niż z samego mięśniówki39.
Postulowano, że wydłużenie tylnych więzadeł łonowo-cewkowych może być istotnym czynnikiem przyczyniającym się do utraty podparcia cewki moczowej obserwowanego w przypadku nietrzymania stresowego40.
Mechanizmy neuralne i mięśniowe
Mikcja wymaga koordynacji kilku procesów fizjologicznych. Nerwy somatyczne i autonomiczne przenoszą informacje o objętości pęcherza do rdzenia kręgowego, a wynik motoryczny zaopatrujący wypieracz, zwieracz i mięśniówkę pęcherza jest odpowiednio dostosowywany41.
Zmiany w unerwieniu miednicy mogą wpływać na wewnętrzny gładki mięsień zwieracza i zwieracz prążkowany, a także na tonus dźwigacza i normalne odruchy4243. Uszkodzenie nerwów, mięśni i tkanki łącznej dna miednicy jest ważne w genezie nietrzymania stresowego, a poród prawdopodobnie jest najważniejszym mechanizmem44.
Poród drogą pochwową powoduje częściowe odnerwienie dna miednicy u większości pierwiastek, ale istnieją elektrofizjologiczne dowody na reinerwację po porodzie drogą pochwową u 80% z nich45.
Podsumowanie mechanizmów patofizjologicznych
Pięć najbardziej powszechnie akceptowanych teorii patofizjologii SUI, które wpłynęły na współczesne leczenie, to: pozycja proksymalnej cewki moczowej, niewydolność wewnętrznego zwieracza cewki moczowej, hipoteza hamaka, teoria integralna oraz uszkodzone więzadła pęcherzowo-cewkowe i łonowo-cewkowe46.
Aktualnie uznaje się, że patogeneza nietrzymania stresowego jest związana głównie ze zmianami związanymi z wiekiem, porodem, otyłością, zaparciami i innymi czynnikami ryzyka, które indukują zmiany w anatomicznych czynnikach kontroli oddawania moczu, w tym czynnikach anatomicznych samej cewki moczowej, czynnikach anatomicznych okolic okołocewkowych i czynnikach anatomicznych nerwu miednicy47.
U pacjentów z SUI mechanizm nietrzymania moczu obejmuje zwiększone ciśnienie pęcherzowe, które przekracza opór zwieracza, prowadząc do wydalenia moczu48. Może to być spowodowane nadmierną ruchomością cewki moczowej, niewydolnością wewnętrznego zwieracza lub kombinacją obu tych czynników49.
Zrozumienie patofizjologii nietrzymania stresowego na poziomie anatomicznym może pomóc w identyfikacji określonych defektów anatomicznych i ukierunkowaniu indywidualnego leczenia pacjentów cierpiących na nietrzymanie moczu50.
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Materiały źródłowe
- #1 Stress Urinary Incontinence – StatPearls – NCBI Bookshelfhttps://www.ncbi.nlm.nih.gov/books/NBK539769/
Stress urinary incontinence is characterized by the sudden involuntary leakage of urine during activities that increase intra-abdominal pressure, such as exertion, sneezing, coughing, laughing, or straining. […] The primary causes of stress urinary incontinence in women are the weakening of the pelvic floor muscles and connective tissues supporting the bladder and urethra. Intrinsic sphincter deficiency is the other major cause. […] Stress urinary incontinence occurs when the pressure inside the bladder exceeds the urethra’s ability to remain closed, often due to damage to the sphincteric muscles that maintain continence. […] The etiologies of stress urinary incontinence are multifactorial and include the following: Loss of support from pelvic floor musculature and connective tissue and urethral hypermobility: This involves the loss of pelvic support, which can originate from connective tissue disorders; chronic cough; obesity; pelvic floor trauma; vaginal delivery, especially if traumatic; pregnancy; pelvic or vaginal surgery; genitourinary syndrome of menopause or other hypoestrogenic states; chronic constipation; heavy lifting; and smoking.
- #2 Stress incontinence – Symptoms and causes – Mayo Clinichttps://www.mayoclinic.org/diseases-conditions/stress-incontinence/symptoms-causes/syc-20355727
Urinary incontinence is the loss of bladder control. Stress incontinence happens when movement or activity puts pressure on the bladder, causing urine to leak. […] Stress incontinence happens when certain muscles and other tissues linked to urinating weaken. These include the muscles that support the urethra, called the pelvic floor muscles, and the muscles that control the release of urine, called the urinary sphincter. […] The bladder expands as it fills with urine. Most often, valve-like muscles in the tube that carries urine out of the body, called the urethra, stay closed as the bladder expands. This keeps you from leaking urine until you reach a bathroom. […] But when those muscles weaken, anything that puts force on the stomach and pelvic muscles put pressure on your bladder. Sneezing, bending over, lifting or laughing hard, for instance, can cause urine leakage.
- #3 Pathophysiology of Stress Urinary Incontinencehttps://pmc.ncbi.nlm.nih.gov/articles/PMC1472873/
All cases of stress urinary incontinence (SUI) are not the same; urethral pressures, prolapse conditions, and congenital and acquired sphincteric dysfunction all contribute to SUI pathophysiology. […] In order to optimally manage SUI, a thorough understanding of the pathophysiology behind the condition is necessary. […] The condition stress incontinence exists when involuntary leakage is produced by an increase in total vesical pressure (Pves), a value that includes abdominal pressure (Pabd) and detrusor pressure (Pdet). […] To be genuine, stress incontinence must involve little or no Pdet component in the expulsive force. […] If the detrusor contracts or there is poor compliance, the expulsive force is not mainly Pabd but includes a significant Pdet component. […] Therefore, in any case when Pabd causes leakage and Pdet at the time is minimal, true stress incontinence is present.
- #4 Pathophysiology of Stress Urinary Incontinencehttps://pmc.ncbi.nlm.nih.gov/articles/PMC1472873/
Poor compliance is associated with symptoms that are similar to those of stress incontinence. […] The condition occurs as the rising Pdet begins to approach the closing pressure in the proximal sphincter, which creates a situation identical to intrinsic sphincteric deficiency (ISD), although the expulsive force is actually Pdet and not Pabd. […] According to the International Continence Society (ICS) definition, stress incontinence is present when Pves is greater than urethral pressure (Pura), when it is simultaneously determined that the detrusor pressure is nearly zero. […] These findings underscore the fact that, as far as the urethra is concerned, Pabd and Pdet are entirely different expulsive forces. […] Moreover, it is clear that the worst variety of urethral dysfunction and SUI occurs when proximal urethral sphincter function is lost or very weak, regardless of the function of the midurethral high-pressure zone.
- #5 PATHOPHYSIOLOGY OF STRESS INCONTINENCE | Abdominal Keyhttps://abdominalkey.com/pathophysiology-of-stress-incontinence/
The lower urinary tract provides continence by storing urine at low pressure until it is socially convenient and appropriate to void. This function is mediated by the presence of an expansible, low-pressure organ, the bladder, and a sphincter-controlled outlet mechanism. The outlet mechanism prevents urinary incontinence during an increase abdominal pressure by means of the sphincter and a complex pelvic support mechanism. Understanding the pathophysiology of stress incontinence at an anatomic level can help to identify specific anatomic defects and direct individualized treatment of patients suffering from incontinence. […] The urethral closure pressure must be greater than the bladder pressure at rest and during increases in abdominal pressure to maintain continence. The anatomic components necessary to meet this goal are a well-vascularized urethral mucosa and submucosa, a well-organized and functioning intrinsic urethral smooth muscle, a properly functioning striated sphincter with intact pudendal innervation (i.e., rhabdosphincter), and a stable, supportive hammock of surrounding muscular and fascial tissues.
- #6 Urinary incontinence – Wikipediahttps://en.wikipedia.org/wiki/Urinary_incontinence
The pressure inside the abdomen (from coughing and sneezing) is normally transmitted to both urethra and bladder equally, leaving the pressure difference unchanged, resulting in continence. When the sphincter is incompetent, this increase in pressure will push the urine against it, leading to incontinence.
- #7 Urinary Incontinence: Practice Essentials, Background, Anatomyhttps://emedicine.medscape.com/article/452289-overview
The loss of urethral and bladder neck support may impair urethral closure mechanisms during times of increased intra-abdominal pressure. […] Some hypothesize that under normal circumstances, any increase in intra-abdominal pressure is transmitted equally to the bladder and proximal urethra. […] When the urethra is hypermobile, pressure transmission to the walls of the urethra may be diminished as it descends and rotates under the pubic bone. […] A related way of describing the mechanism of hypermobility-related stress incontinence is the hammock theory posited by DeLancey. […] Intrinsic sphincter deficiency is a condition in which the urethral sphincter is unable to coapt and generate enough resting urethral closing pressure to retain urine in the bladder. […] Intrinsic sphincter deficiency is due to devascularization and/or denervation of the bladder neck and proximal urethra.
- #8 Incontinencehttps://www.csh.org.tw/dr.tcj/educartion/f/web/USI%201/index.htm
Stress urinary incontinence is defined as involuntary loss of urine coincident with increased intra-abdominal pressure in the absence of uninhibited detrusor contraction. […] Urethral hypermobility results from weakened anatomic support of the urethra, whereas intrinsic sphincter deficiency arises from a defect within the urethra proper. […] When there is loss of anatomic support, the proximal urethra and the bladder neck descend to rotate away and out of the pelvis at times of increased intra-abdominal pressure. […] Because the bladder neck and proximal urethra move out of the pelvis, more pressure is transmitted to the bladder. […] During this process, the posterior wall of the urethra shears off the anterior urethral wall to cause opening of the bladder neck. […] The uneven pressure transmission and the opening of the bladder neck results in involuntary urine loss during periods of physical activity, called Type II stress incontinence.
- #9 The Anatomical Pathogenesis of Stress Urinary Incontinence in Womenhttps://www.mdpi.com/resolver?pii=medicina59010005
Stress urinary incontinence is a common disease in middle-aged and elderly women, which seriously affects the physical and mental health of the patients. […] At present, it is believed that the pathogenesis of the disease is mainly due to changes related to age, childbirth, obesity, constipation and other risk factors that induce changes in the urinary control anatomy, including the anatomical factors of the urethra itself, the anatomical factors around the urethra and the anatomical factors of the pelvic nerve. […] Currently, it is believed that the pathogenesis of stress urinary incontinence is mainly due to changes related to age, childbirth, obesity, constipation and other risk factors that induce changes in the urinary control anatomical factors, including the anatomical factors of the urethra itself, the anatomical factors of periurethra and the anatomical factors of the pelvic nerve.
- #10 The Anatomical Pathogenesis of Stress Urinary Incontinence in Womenhttps://www.mdpi.com/resolver?pii=medicina59010005
The weakness of the supporting structure of the bladder neck can lead to the inadequate closure of the bladder neck, so that the posterior wall of the bladder neck collapses, the bladder neck moves downward, and the posterior vesicourethral angle increases or even disappears. […] The anatomical pathogenesis of SUI is very complex, involving the anatomical factors of urethra itself, the periurethra and the pelvic floor nerve. […] Among the many anatomical factors, the levator ani muscle and external urethral sphincter are particularly important. […] When the levator ani muscle and external sphincter of the urethra are dysfunctional, the urethra cannot be closed forcefully, resulting in urinary incontinence.
- #11 Urinary Incontinence: Practice Essentials, Background, Anatomyhttps://emedicine.medscape.com/article/452289-overview
The major cause of stress incontinence is urethral hypermobility due to impaired support from pelvic floor. A less common cause is an intrinsic sphincter deficiency, usually secondary to pelvic surgeries. In either case, urethral sphincter function is impaired, resulting in urine loss at lower than usual abdominal pressures. […] In women with stress urinary incontinence, either or both mechanisms may be present, although some authors hold that stress incontinence does not develop in patients with poor pelvic support unless intrinsic sphincter deficiency is also present. […] Urethral hypermobility is related to impaired neuromuscular functioning of the pelvic floor coupled with injury, both remote and ongoing, to the connective tissue supports of the urethra and bladder neck. […] Damage to the nerves, muscle, and connective tissue of the pelvic floor is important in the genesis of stress incontinence. Injury during childbirth probably is the most important mechanism.
- #12 The Anatomical Pathogenesis of Stress Urinary Incontinence in Womenhttps://www.mdpi.com/resolver?pii=medicina59010005
The weakness of the supporting structure of the bladder neck can lead to the inadequate closure of the bladder neck, so that the posterior wall of the bladder neck collapses, the bladder neck moves downward, and the posterior vesicourethral angle increases or even disappears. […] The anatomical pathogenesis of SUI is very complex, involving the anatomical factors of urethra itself, the periurethra and the pelvic floor nerve. […] Among the many anatomical factors, the levator ani muscle and external urethral sphincter are particularly important. […] When the levator ani muscle and external sphincter of the urethra are dysfunctional, the urethra cannot be closed forcefully, resulting in urinary incontinence.
- #13 Urinary Incontinence: Practice Essentials, Background, Anatomyhttps://emedicine.medscape.com/article/452289-overview
The loss of urethral and bladder neck support may impair urethral closure mechanisms during times of increased intra-abdominal pressure. […] Some hypothesize that under normal circumstances, any increase in intra-abdominal pressure is transmitted equally to the bladder and proximal urethra. […] When the urethra is hypermobile, pressure transmission to the walls of the urethra may be diminished as it descends and rotates under the pubic bone. […] A related way of describing the mechanism of hypermobility-related stress incontinence is the hammock theory posited by DeLancey. […] Intrinsic sphincter deficiency is a condition in which the urethral sphincter is unable to coapt and generate enough resting urethral closing pressure to retain urine in the bladder. […] Intrinsic sphincter deficiency is due to devascularization and/or denervation of the bladder neck and proximal urethra.
- #14https://link.springer.com/article/10.1007/s00192-020-04622-9
To evaluate the evidence for pathologies underlying stress urinary incontinence (SUI) in women. […] Deficits in urethral and bladder neck structure and support, neuromuscular and mechanical function of the striated urethral sphincter (SUS) and levator ani muscles all appear to be associated with SUI. […] The pathology of SUI is multifactorial, with strong evidence pointing to bladder neck and urethral incompetence. […] Prevailing theory suggests a combination of disruption in the supportive connective tissues of the bladder and urethra and weakening of the muscular structures of the pelvic floor, bladder neck and urethral sphincters all lead to reduced urethral closure pressure and lower ALPP, functionally resulting in SUI. […] Impaired anatomical support of the bladder neck and proximal urethra is associated with urethral hypermobility, which is thought to impede the transfer of loads induced by the descending pelvic structures to the urethra, resulting in less extrinsic closure force, and ultimately with urine leakage.
- #15 Stress Urinary Incontinence – StatPearls – NCBI Bookshelfhttps://www.ncbi.nlm.nih.gov/books/NBK539769/
Intrinsic sphincter deficiency: This is due to sphincteric neuromuscular dysfunction or damage from previous pelvic surgeries, neuropathic and spinal disorders, trauma, cauda equina, sacral and severe pelvic fractures, nerve injury from abdominal surgeries, myelodysplasia, radiation therapy of the pelvis, or complications of urological surgery such as transurethral resection of the prostate or radical prostatectomy. […] Current understanding mainly attributes stress urinary continence in women to the coordinated contraction of the levator ani muscle and the external urethral sphincter. […] Risk factors, such as age, childbirth, menopause, obesity, multiple vaginal births, and others, induce alterations in the anatomical components responsible for continence. […] Pelvic floor muscle weakness is a critical factor, often resulting from childbirth, increased abdominal pressure, pelvic surgery, connective tissue disorders, or neurological conditions.
- #16 Incontinencehttps://www.csh.org.tw/dr.tcj/educartion/f/web/USI%201/index.htm
Intrinsic sphincter deficiency is a condition in which the urethral sphincter is unable to coapt and generate enough resting urethral closing pressure to retain urine in the bladder. […] Inadequate bladder outlet resistance during times of physical activity result in involuntary urine loss, called Type III stress incontinence.
- #17 Stress Urinary Incontinence – StatPearls – NCBI Bookshelfhttps://www.ncbi.nlm.nih.gov/books/NBK539769/
Intrinsic sphincter deficiency: This is due to sphincteric neuromuscular dysfunction or damage from previous pelvic surgeries, neuropathic and spinal disorders, trauma, cauda equina, sacral and severe pelvic fractures, nerve injury from abdominal surgeries, myelodysplasia, radiation therapy of the pelvis, or complications of urological surgery such as transurethral resection of the prostate or radical prostatectomy. […] Current understanding mainly attributes stress urinary continence in women to the coordinated contraction of the levator ani muscle and the external urethral sphincter. […] Risk factors, such as age, childbirth, menopause, obesity, multiple vaginal births, and others, induce alterations in the anatomical components responsible for continence. […] Pelvic floor muscle weakness is a critical factor, often resulting from childbirth, increased abdominal pressure, pelvic surgery, connective tissue disorders, or neurological conditions.
- #18 Urinary Incontinence: Practice Essentials, Background, Anatomyhttps://emedicine.medscape.com/article/452289-overview
The loss of urethral and bladder neck support may impair urethral closure mechanisms during times of increased intra-abdominal pressure. […] Some hypothesize that under normal circumstances, any increase in intra-abdominal pressure is transmitted equally to the bladder and proximal urethra. […] When the urethra is hypermobile, pressure transmission to the walls of the urethra may be diminished as it descends and rotates under the pubic bone. […] A related way of describing the mechanism of hypermobility-related stress incontinence is the hammock theory posited by DeLancey. […] Intrinsic sphincter deficiency is a condition in which the urethral sphincter is unable to coapt and generate enough resting urethral closing pressure to retain urine in the bladder. […] Intrinsic sphincter deficiency is due to devascularization and/or denervation of the bladder neck and proximal urethra.
- #19 Incontinencehttps://www.csh.org.tw/dr.tcj/educartion/f/web/USI%201/index.htm
Intrinsic sphincter deficiency is a condition in which the urethral sphincter is unable to coapt and generate enough resting urethral closing pressure to retain urine in the bladder. […] Inadequate bladder outlet resistance during times of physical activity result in involuntary urine loss, called Type III stress incontinence.
- #20 Stress Urinary Incontinence – StatPearls – NCBI Bookshelfhttps://www.ncbi.nlm.nih.gov/books/NBK539769/
Intrinsic sphincter deficiency: This is due to sphincteric neuromuscular dysfunction or damage from previous pelvic surgeries, neuropathic and spinal disorders, trauma, cauda equina, sacral and severe pelvic fractures, nerve injury from abdominal surgeries, myelodysplasia, radiation therapy of the pelvis, or complications of urological surgery such as transurethral resection of the prostate or radical prostatectomy. […] Current understanding mainly attributes stress urinary continence in women to the coordinated contraction of the levator ani muscle and the external urethral sphincter. […] Risk factors, such as age, childbirth, menopause, obesity, multiple vaginal births, and others, induce alterations in the anatomical components responsible for continence. […] Pelvic floor muscle weakness is a critical factor, often resulting from childbirth, increased abdominal pressure, pelvic surgery, connective tissue disorders, or neurological conditions.
- #21https://link.springer.com/article/10.1007/s00192-020-04622-9
Damage to or dysfunction of the LAMs is thought to be a contributor to SUI. […] The SUS is considered part of the PFM complex, and it appears to be a major contributor to urinary continence control, along with the smooth muscle surrounding the urethra and bladder neck. […] In light of the complex interactions among tissue morphology, mechanical properties, perfusion, innervation and motor control, several factors may contribute to the pathophysiology of SUI, yet the evidence for many of these factors has not been systematically evaluated, and their relative importance is largely unknown. […] Impairments in urethral and bladder neck structure and support, evidenced through ultrasound imaging and MRI, emerged as being strongly associated with SUI in women. […] Bladder neck dilation (or funneling) emerged through meta-analysis as being highly prevalent in women with SUI. […] Studies included in this review suggest that there is neurophysiological evidence of denervation injury to the SUS in women with SUI.
- #22 The Anatomical Pathogenesis of Stress Urinary Incontinence in Womenhttps://www.mdpi.com/resolver?pii=medicina59010005
The weakness of the supporting structure of the bladder neck can lead to the inadequate closure of the bladder neck, so that the posterior wall of the bladder neck collapses, the bladder neck moves downward, and the posterior vesicourethral angle increases or even disappears. […] The anatomical pathogenesis of SUI is very complex, involving the anatomical factors of urethra itself, the periurethra and the pelvic floor nerve. […] Among the many anatomical factors, the levator ani muscle and external urethral sphincter are particularly important. […] When the levator ani muscle and external sphincter of the urethra are dysfunctional, the urethra cannot be closed forcefully, resulting in urinary incontinence.
- #23https://link.springer.com/article/10.1007/s00192-020-04622-9
Damage to or dysfunction of the LAMs is thought to be a contributor to SUI. […] The SUS is considered part of the PFM complex, and it appears to be a major contributor to urinary continence control, along with the smooth muscle surrounding the urethra and bladder neck. […] In light of the complex interactions among tissue morphology, mechanical properties, perfusion, innervation and motor control, several factors may contribute to the pathophysiology of SUI, yet the evidence for many of these factors has not been systematically evaluated, and their relative importance is largely unknown. […] Impairments in urethral and bladder neck structure and support, evidenced through ultrasound imaging and MRI, emerged as being strongly associated with SUI in women. […] Bladder neck dilation (or funneling) emerged through meta-analysis as being highly prevalent in women with SUI. […] Studies included in this review suggest that there is neurophysiological evidence of denervation injury to the SUS in women with SUI.
- #24 Stress Urinary Incontinence – StatPearls – NCBI Bookshelfhttps://www.ncbi.nlm.nih.gov/books/NBK539769/
Stress urinary incontinence is characterized by the sudden involuntary leakage of urine during activities that increase intra-abdominal pressure, such as exertion, sneezing, coughing, laughing, or straining. […] The primary causes of stress urinary incontinence in women are the weakening of the pelvic floor muscles and connective tissues supporting the bladder and urethra. Intrinsic sphincter deficiency is the other major cause. […] Stress urinary incontinence occurs when the pressure inside the bladder exceeds the urethra’s ability to remain closed, often due to damage to the sphincteric muscles that maintain continence. […] The etiologies of stress urinary incontinence are multifactorial and include the following: Loss of support from pelvic floor musculature and connective tissue and urethral hypermobility: This involves the loss of pelvic support, which can originate from connective tissue disorders; chronic cough; obesity; pelvic floor trauma; vaginal delivery, especially if traumatic; pregnancy; pelvic or vaginal surgery; genitourinary syndrome of menopause or other hypoestrogenic states; chronic constipation; heavy lifting; and smoking.
- #25 Stress Urinary Incontinence – StatPearls – NCBI Bookshelfhttps://www.ncbi.nlm.nih.gov/books/NBK539769/
Stress urinary incontinence is characterized by the sudden involuntary leakage of urine during activities that increase intra-abdominal pressure, such as exertion, sneezing, coughing, laughing, or straining. […] The primary causes of stress urinary incontinence in women are the weakening of the pelvic floor muscles and connective tissues supporting the bladder and urethra. Intrinsic sphincter deficiency is the other major cause. […] Stress urinary incontinence occurs when the pressure inside the bladder exceeds the urethra’s ability to remain closed, often due to damage to the sphincteric muscles that maintain continence. […] The etiologies of stress urinary incontinence are multifactorial and include the following: Loss of support from pelvic floor musculature and connective tissue and urethral hypermobility: This involves the loss of pelvic support, which can originate from connective tissue disorders; chronic cough; obesity; pelvic floor trauma; vaginal delivery, especially if traumatic; pregnancy; pelvic or vaginal surgery; genitourinary syndrome of menopause or other hypoestrogenic states; chronic constipation; heavy lifting; and smoking.
- #26 Stress Urinary Incontinence – StatPearls – NCBI Bookshelfhttps://www.ncbi.nlm.nih.gov/books/NBK539769/
Intrinsic sphincter deficiency: This is due to sphincteric neuromuscular dysfunction or damage from previous pelvic surgeries, neuropathic and spinal disorders, trauma, cauda equina, sacral and severe pelvic fractures, nerve injury from abdominal surgeries, myelodysplasia, radiation therapy of the pelvis, or complications of urological surgery such as transurethral resection of the prostate or radical prostatectomy. […] Current understanding mainly attributes stress urinary continence in women to the coordinated contraction of the levator ani muscle and the external urethral sphincter. […] Risk factors, such as age, childbirth, menopause, obesity, multiple vaginal births, and others, induce alterations in the anatomical components responsible for continence. […] Pelvic floor muscle weakness is a critical factor, often resulting from childbirth, increased abdominal pressure, pelvic surgery, connective tissue disorders, or neurological conditions.
- #27 PATHOPHYSIOLOGY OF STRESS INCONTINENCE | Abdominal Keyhttps://abdominalkey.com/pathophysiology-of-stress-incontinence/
It has been postulated that elongation of the posterior pubourethral ligaments may be a significant contributory factor to the loss of urethral support seen in stress incontinence. […] An important pathophysiologic factor is the contribution of pregnancy and childbirth to the development of urinary incontinence in women. […] Vaginal delivery has been recognized as being potentially traumatic to the pelvic floor. The first delivery may initiate injury to the continence mechanism as a consequence of direct damage to the pelvic floor muscles or nerves, or both, during the passage of the fetus. […] There are many mechanisms by which vaginal delivery can increase the risk of developing stress incontinence. […] Vaginal delivery causes partial denervation of the pelvic floor in most primiparous women, but there is electromyographic evidence of reinnervation after vaginal delivery in 80% of them.
- #28 Urinary Incontinence: Practice Essentials, Background, Anatomyhttps://emedicine.medscape.com/article/452289-overview
Female urethral function is influenced by estrogen. The lack of estrogen at menopause leads to atrophy and replacement of submucosa (ie, vascular plexus) by fibrous tissue. […] Stress incontinence on prolapse reduction (previously termed latent stress incontinence) is a term used to describe stress incontinence observed only after reduction of pelvic prolapse. […] In diagnosing occult incontinence, the goal is to avoid new-onset incontinence following surgical correction of prolapse.
- #29 Stress incontinence – Wikipediahttps://en.wikipedia.org/wiki/Stress_incontinence
Stress incontinence is the loss of small amounts of urine associated with coughing, laughing, sneezing, exercising or other movements that increase intra-abdominal pressure and thus increasing the pressure on the bladder. […] If this support is insufficient due to any reason, the urethra would not close properly at times of increased abdominal pressure, allowing urine to pass involuntarily. […] In women, pregnancy, childbirth, obesity, and menopause often contribute to stress incontinence by causing weakness to the pelvic floor or damaging the urethral sphincter, leading to its inadequate closure, and hence the leakage of urine. […] The incidence of stress incontinence increases following menopause, similarly because of lowered estrogen levels. […] Most stress incontinence in women results from the urethra dropping down toward the vagina. Therefore, common surgery for stress incontinence involves pulling the urethra up to a more normal position.
- #30 PATHOPHYSIOLOGY OF STRESS INCONTINENCE | Abdominal Keyhttps://abdominalkey.com/pathophysiology-of-stress-incontinence/
Intrinsic urethral function is the product of coaptation and compression along the length of the urethra, from the bladder neck to the proximal and mid-urethra. A robust anatomic support mechanism buttresses a competent bladder neck and functioning urethral mechanics and facilitates appropriate compression and pressure transmission during increases in abdominal pressure affecting the bladder outlet. […] The glandular secretions of the inner mucosa increase the surface tension, promoting its plasticity and increasing its ability to coapt. Estrogenic deficiency in postmenopausal women results in atrophy of this layer, reduces the hermetic seal of the urethra mucosal, and may contribute to the multifactorial cause of stress incontinence. […] The role of smooth muscle in the maintenance of female continence is still uncertain. The U-shaped loop of the detrusor smooth muscle surrounds the proximal urethra and favors its closure by creating a constant tone.
- #31 Urinary Incontinence Medication: Alpha-Adrenergic Agonists, Anticholinergic Agents, Antispasmodic Drugs, Tricyclic Antidepressants, Beta3 Agonists, Estrogens, Antidepressants, Serotonin/Norepinephrine Reuptake Inhibitors, Alpha-Adrenergic Blockers, Botulihttps://emedicine.medscape.com/article/452289-medication
In patients with stress incontinence, alpha agonist treatment results in contraction of the internal urethral sphincter and increases the urethral resistance to urinary flow. […] Sympathomimetic drugs, estrogen, and tricyclic agents increase bladder outlet resistance to improve symptoms of stress urinary incontinence. […] Estrogens increase the tone of urethral muscle by up-regulating the alpha-adrenergic receptors in the surrounding area, and they enhance alpha-adrenergic contractile response to strengthen the pelvic muscles, which is important in urethral support (ie, prevents urethral hypermobility). […] The result is an improved mucosal seal effect, which is important in urethral function (ie, it prevents intrinsic sphincter deficiency). […] Estrogen supplementation appears to be the most effective in postmenopausal women with mild-to-moderate incontinence. Both types of stress incontinence improve with estrogen fortification. There is also evidence however, estrogen use can exacerbate incontinence.
- #32 Medical Student Curriculum: Urinary Incontinence – American Urological Associationhttps://www.auanet.org/meetings-and-education/for-medical-students/medical-students-curriculum/urinary-incontinence
Overflow incontinence occurs at extreme bladder volumes or when the bladder volume reaches the limit of the urethral mechanism or the bladder’s viscoelastic properties. […] Although a diverse suite of pathophysiologic processes contribute to the symptoms of SUI, loss of pelvic floor anatomic support combined with dysfunction of the external urethral sphincter due to both structural and neuromuscular compromise often represent primary etiologies. […] Strategies for treatment of stress urinary incontinence are tailored to the amount of incontinence and how it affects the patient. […] Surgical therapy for stress incontinence is indicated when a patient doesn’t wish to pursue non-surgical therapy or when other treatments have failed. […] Men who are experiencing symptoms suggestive of SUI most commonly have a history of surgery for prostate cancer or benign prostatic hyperplasia.
- #33 Male Stress Urinary Incontinence: Diagnosis and Treatmenthttps://www.urology-textbook.com/male-stress-urinary-incontinence.html
Stress urinary incontinence is urine leakage, which is associated with increased abdominal pressure and insufficient urethral sphincter mechanism. […] There are several reasons for postoperative incontinence. Deep sutures of the pelvic floor cause direct damage to the external sphincter or its innervation in the case of bleeding or tumor infiltration. Postoperative hypermobility of the membranous urethra has been identified as another factor for sphincter weakness after radical prostatectomy. […] A pelvic fracture may lead to a distraction injury of the membranous urethra with stress urinary incontinence and erectile dysfunction. […] Age, immobility, neurological diseases, subvesical obstruction and aging processes of the urinary tract can lead to urinary incontinence in men. […] An intact urinary sphincter may soon compensate for the increased workload with the help of behavioral therapy (adjusting drinking habits and micturition), physiotherapy, and anticholinergic medication.
- #34 Contribution of pudendal nerve injury to stress urinary incontinence in a male rat model | Scientific Reportshttps://www.nature.com/articles/s41598-024-57493-1
Stress urinary incontinence (SUI), characterized by the involuntary leakage of urine during activities involving physical exertion, poses a significant challenge following radical prostatectomy (RP). […] The intricate mechanism underlying male urinary continence is essential to understand PPSUI. Urinary continence in men is maintained by proper function of the detrusor smooth muscle, the proximal intrinsic sphincter at the bladder neck, the external urethral sphincter (EUS), and the urethral suspensory mechanism (pubourethral ligaments). […] Despite the ubiquity of PPSUI, its etiology is multifaceted and is not fully understood. PPSUI is likely caused by a combination of nerve damage (PN, inferior hypogastric plexus, pelvic nerves, or sphincteric branches from the cavernous nerves), direct damage to the EUS, and a decrease in functional urethral length.
- #35https://link.springer.com/article/10.1007/s00192-020-04622-9
Damage to or dysfunction of the LAMs is thought to be a contributor to SUI. […] The SUS is considered part of the PFM complex, and it appears to be a major contributor to urinary continence control, along with the smooth muscle surrounding the urethra and bladder neck. […] In light of the complex interactions among tissue morphology, mechanical properties, perfusion, innervation and motor control, several factors may contribute to the pathophysiology of SUI, yet the evidence for many of these factors has not been systematically evaluated, and their relative importance is largely unknown. […] Impairments in urethral and bladder neck structure and support, evidenced through ultrasound imaging and MRI, emerged as being strongly associated with SUI in women. […] Bladder neck dilation (or funneling) emerged through meta-analysis as being highly prevalent in women with SUI. […] Studies included in this review suggest that there is neurophysiological evidence of denervation injury to the SUS in women with SUI.
- #36https://link.springer.com/article/10.1007/s00192-020-04622-9
Damage to or dysfunction of the LAMs is thought to be a contributor to SUI. […] The SUS is considered part of the PFM complex, and it appears to be a major contributor to urinary continence control, along with the smooth muscle surrounding the urethra and bladder neck. […] In light of the complex interactions among tissue morphology, mechanical properties, perfusion, innervation and motor control, several factors may contribute to the pathophysiology of SUI, yet the evidence for many of these factors has not been systematically evaluated, and their relative importance is largely unknown. […] Impairments in urethral and bladder neck structure and support, evidenced through ultrasound imaging and MRI, emerged as being strongly associated with SUI in women. […] Bladder neck dilation (or funneling) emerged through meta-analysis as being highly prevalent in women with SUI. […] Studies included in this review suggest that there is neurophysiological evidence of denervation injury to the SUS in women with SUI.
- #37https://link.springer.com/article/10.1007/s00192-020-04622-9
Damage to or dysfunction of the LAMs is thought to be a contributor to SUI. […] The SUS is considered part of the PFM complex, and it appears to be a major contributor to urinary continence control, along with the smooth muscle surrounding the urethra and bladder neck. […] In light of the complex interactions among tissue morphology, mechanical properties, perfusion, innervation and motor control, several factors may contribute to the pathophysiology of SUI, yet the evidence for many of these factors has not been systematically evaluated, and their relative importance is largely unknown. […] Impairments in urethral and bladder neck structure and support, evidenced through ultrasound imaging and MRI, emerged as being strongly associated with SUI in women. […] Bladder neck dilation (or funneling) emerged through meta-analysis as being highly prevalent in women with SUI. […] Studies included in this review suggest that there is neurophysiological evidence of denervation injury to the SUS in women with SUI.
- #38https://link.springer.com/article/10.1007/s00192-020-04622-9
To evaluate the evidence for pathologies underlying stress urinary incontinence (SUI) in women. […] Deficits in urethral and bladder neck structure and support, neuromuscular and mechanical function of the striated urethral sphincter (SUS) and levator ani muscles all appear to be associated with SUI. […] The pathology of SUI is multifactorial, with strong evidence pointing to bladder neck and urethral incompetence. […] Prevailing theory suggests a combination of disruption in the supportive connective tissues of the bladder and urethra and weakening of the muscular structures of the pelvic floor, bladder neck and urethral sphincters all lead to reduced urethral closure pressure and lower ALPP, functionally resulting in SUI. […] Impaired anatomical support of the bladder neck and proximal urethra is associated with urethral hypermobility, which is thought to impede the transfer of loads induced by the descending pelvic structures to the urethra, resulting in less extrinsic closure force, and ultimately with urine leakage.
- #39 PATHOPHYSIOLOGY OF STRESS INCONTINENCE | Abdominal Keyhttps://abdominalkey.com/pathophysiology-of-stress-incontinence/
The striated urogenital sphincter consists of two parts, the rhabdosphincter and the compressor urethra and the urethrovaginal sphincter distally. […] This part of the urethra is intrapelvic, immediately posterior to the pubic bone. In the past, it was suggested that when the urethra descended and lost this intra-abdominal position, intra-abdominal forces could no longer constrict it during straining, resulting in stress incontinence. […] If these postulates are correct, an appropriate contributory factor to female continence is provided by the bladder neck’s passive elastic tension, which is important in maintaining urethral closure. […] The urethral support mechanism comprises all the structures extrinsic to the urethra that offer a supportive back plate on which the proximal urethra and mid-urethra lie. The anatomic support is derived more from the fascial structures than from the musculature itself.
- #40 PATHOPHYSIOLOGY OF STRESS INCONTINENCE | Abdominal Keyhttps://abdominalkey.com/pathophysiology-of-stress-incontinence/
It has been postulated that elongation of the posterior pubourethral ligaments may be a significant contributory factor to the loss of urethral support seen in stress incontinence. […] An important pathophysiologic factor is the contribution of pregnancy and childbirth to the development of urinary incontinence in women. […] Vaginal delivery has been recognized as being potentially traumatic to the pelvic floor. The first delivery may initiate injury to the continence mechanism as a consequence of direct damage to the pelvic floor muscles or nerves, or both, during the passage of the fetus. […] There are many mechanisms by which vaginal delivery can increase the risk of developing stress incontinence. […] Vaginal delivery causes partial denervation of the pelvic floor in most primiparous women, but there is electromyographic evidence of reinnervation after vaginal delivery in 80% of them.
- #41 Urinary Incontinence: Practice Essentials, Background, Anatomyhttps://emedicine.medscape.com/article/452289-overview
Micturition requires coordination of several physiological processes. Somatic and autonomic nerves carry bladder volume input to the spinal cord, and motor output innervating the detrusor, sphincter, and bladder musculature is adjusted accordingly. The cerebral cortex exerts a predominantly inhibitory influence, whereas the brainstem facilitates urination by coordinating urethral sphincter relaxation and detrusor muscle contraction. […] Incontinence occurs when micturition physiology, functional toileting ability, or both have been disrupted. The underlying pathology varies among the different types of incontinence (ie, stress, urge, mixed, reflex, overflow, and functional incontinence). […] During episodes of stress incontinence, an increase in intra-abdominal pressure (eg, from laughing, sneezing, coughing, climbing stairs) raises pressure within the bladder to the point where it exceeds the urethras resistance to urinary flow. Leakage ceases when bladder pressure again falls below urethral pressure.
- #42 Volume 1, Chapter 85. Stress Urinary Incontinencehttps://glowm.com/resources/glowm/cd/pages/v1/v1c085.html
The muscular and fascial attachments of the urethrovaginal junction (UVJ) or bladder neck keep this crucial area in an intra-abdominal position. […] Alterations in pelvic innervation can affect the internal smooth muscle sphincter and the striated sphincter, as well as the levator tone and normal reflexes. […] A poorly functioning urethra can also contribute to or be the primary cause of SUI in patients. […] Importantly, patients may have some degree of a poorly functioning urethra working in concert with deranged anatomy or nerve injury, with all factors contributing to stress incontinence.
- #43 Volume 1, Chapter 85. Stress Urinary Incontinencehttp://www.glowm.com/resources/glowm/cd/pages/v1/v1c085.html
Alterations in pelvic innervation can affect the internal smooth muscle sphincter and the striated sphincter, as well as the levator tone and normal reflexes. Disruption of the normal anatomic supports of the hammock can allow excess rotation of the UVJ with physical stress, resulting in impaired transmission of pressure to this area. […] A poorly functioning urethra can also contribute to or be the primary cause of SUI in patients. Patients with this condition were previously described as having intrinsic sphincteric deficiency (ISD) or type III incontinence. An atrophic urethral mucosa, a scarred or fibrotic submucosal layer, a poor venous plexus, and/or impaired smooth muscle function can prevent normal apposition of the urethral mucosa.
- #44 Urinary Incontinence: Practice Essentials, Background, Anatomyhttps://emedicine.medscape.com/article/452289-overview
The major cause of stress incontinence is urethral hypermobility due to impaired support from pelvic floor. A less common cause is an intrinsic sphincter deficiency, usually secondary to pelvic surgeries. In either case, urethral sphincter function is impaired, resulting in urine loss at lower than usual abdominal pressures. […] In women with stress urinary incontinence, either or both mechanisms may be present, although some authors hold that stress incontinence does not develop in patients with poor pelvic support unless intrinsic sphincter deficiency is also present. […] Urethral hypermobility is related to impaired neuromuscular functioning of the pelvic floor coupled with injury, both remote and ongoing, to the connective tissue supports of the urethra and bladder neck. […] Damage to the nerves, muscle, and connective tissue of the pelvic floor is important in the genesis of stress incontinence. Injury during childbirth probably is the most important mechanism.
- #45 PATHOPHYSIOLOGY OF STRESS INCONTINENCE | Abdominal Keyhttps://abdominalkey.com/pathophysiology-of-stress-incontinence/
It has been postulated that elongation of the posterior pubourethral ligaments may be a significant contributory factor to the loss of urethral support seen in stress incontinence. […] An important pathophysiologic factor is the contribution of pregnancy and childbirth to the development of urinary incontinence in women. […] Vaginal delivery has been recognized as being potentially traumatic to the pelvic floor. The first delivery may initiate injury to the continence mechanism as a consequence of direct damage to the pelvic floor muscles or nerves, or both, during the passage of the fetus. […] There are many mechanisms by which vaginal delivery can increase the risk of developing stress incontinence. […] Vaginal delivery causes partial denervation of the pelvic floor in most primiparous women, but there is electromyographic evidence of reinnervation after vaginal delivery in 80% of them.
- #46 Evolution of stress urinary incontinence (SUI) outcomes assessment: a narrative review – Wu – Gynecology and Pelvic Medicinehttps://gpm.amegroups.org/article/view/10262/html
The anatomical pathogenesis of SUI is a complex topic that remains heavily debated to this day. […] The five most widely accepted theories of SUI pathophysiology that have influenced modern-day treatment are the position of the proximal urethra, intrinsic urethral sphincter deficiency, the hammock hypothesis, the integral theory, and damaged urethropelvic and pubourethral ligaments. […] The prevailing notion suggests the disturbance of supportive bladder and urethral fascia, coupled with the weakening of muscular structures within the pelvic floor, bladder neck, and urethral sphincters.
- #47 The Anatomical Pathogenesis of Stress Urinary Incontinence in Womenhttps://www.mdpi.com/resolver?pii=medicina59010005
Stress urinary incontinence is a common disease in middle-aged and elderly women, which seriously affects the physical and mental health of the patients. […] At present, it is believed that the pathogenesis of the disease is mainly due to changes related to age, childbirth, obesity, constipation and other risk factors that induce changes in the urinary control anatomy, including the anatomical factors of the urethra itself, the anatomical factors around the urethra and the anatomical factors of the pelvic nerve. […] Currently, it is believed that the pathogenesis of stress urinary incontinence is mainly due to changes related to age, childbirth, obesity, constipation and other risk factors that induce changes in the urinary control anatomical factors, including the anatomical factors of the urethra itself, the anatomical factors of periurethra and the anatomical factors of the pelvic nerve.
- #48 Stress urinary incontinence – Knowledge @ AMBOSShttps://www.amboss.com/us/knowledge/stress-urinary-incontinence/
Stress urinary incontinence (SUI) is a type of urinary incontinence characterized by the leakage of urine following activities that increase intra-abdominal pressure (e.g., coughing or sneezing). […] The underlying mechanism is an increase in bladder pressure that exceeds sphincter resistance, leading to urine being expelled. […] SUI in women is caused by a variety of conditions (e.g., pelvic muscle dysfunction and/or weakness, intrinsic sphincter deficiency); in men, it is most common secondary to prostate surgery. […] Pathophysiology: outlet incompetence […] Urethral hypermobility: loss of pelvic floor musculature and/or connective tissue support weak pelvic floor inability of the urethra to completely close. […] Intrinsic sphincter deficiency. […] Urine leakage during increased abdominal pressure confirms the diagnosis of SUI. […] Urethral mobility of 30 from the horizontal plane is associated with a higher degree of success for anti-incontinence surgery. […] Midurethral sling is the most effective treatment for SUI in female patients with urethral mobility 30.
- #49 Female Stress Urinary Incontinence | Melbourne Bladder Clinichttps://bladderclinic.com.au/conditions/bladder/female-stress-urinary-incontinence
Stress urinary incontinence (SUI) is often due to a combination of urethral hypermobility and intrinsic sphincter deficiency (ISD) in variable proportions. […] When there is a defect in the supporting pelvic floor, the urethra moves downwards from its resting position during activities such as laughing or coughing, and urine can leak through. This is called urethral hypermobility. […] ISD describes a urethral sphincter mechanism that lacks the co-aptation or normal closing pressure needed to prevent exertional leakage. […] In ISD, the bladder outlet is open at rest and urine can leak through even with lighter impact activities.
- #50 PATHOPHYSIOLOGY OF STRESS INCONTINENCE | Abdominal Keyhttps://abdominalkey.com/pathophysiology-of-stress-incontinence/
The lower urinary tract provides continence by storing urine at low pressure until it is socially convenient and appropriate to void. This function is mediated by the presence of an expansible, low-pressure organ, the bladder, and a sphincter-controlled outlet mechanism. The outlet mechanism prevents urinary incontinence during an increase abdominal pressure by means of the sphincter and a complex pelvic support mechanism. Understanding the pathophysiology of stress incontinence at an anatomic level can help to identify specific anatomic defects and direct individualized treatment of patients suffering from incontinence. […] The urethral closure pressure must be greater than the bladder pressure at rest and during increases in abdominal pressure to maintain continence. The anatomic components necessary to meet this goal are a well-vascularized urethral mucosa and submucosa, a well-organized and functioning intrinsic urethral smooth muscle, a properly functioning striated sphincter with intact pudendal innervation (i.e., rhabdosphincter), and a stable, supportive hammock of surrounding muscular and fascial tissues.