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Anatomy, Abdomen and Pelvis, Bladder Detrusor Muscle

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Last Update: November 13, 2018.

Introduction

The walls of the bladder are mainly formed of detrusor muscle which allows the bladder to contract to excrete urine or relax to hold urine. At the inferior end of the bladder, the detrusor muscle is continuous with the internal urethral sphincter. The combination of detrusor contraction and urethral sphincter relaxation leads to urination. The detrusor muscle is under control from the autonomic system and is composed of smooth muscle. Detrusor muscle pathology can lead to urinary retention, incontinence or a combination of both. Abnormalities of the detrusor muscle if left untreated, can lead to deterioration of the upper urinary tracts.[1][2]

Structure and Function

The main function of the detrusor muscle is to contract during urination to push the urine out of the bladder and into the urethra. The detrusor will relax to allow urine to be stored in the urinary bladder.

Embryology

The bladder is initially derived from the upper segment of the urogenital sinus in the fetus and connected with the allantois. However, the allantois is eventually obliterated to become the urachus leaving just the bladder. Detrusor smooth muscle is of mesoderm and neural crest origin.

Blood Supply and Lymphatics

The upper portion of the urinary bladder is supplied primarily by the superior vesical artery (a branch of the hypogastric artery). The lower portion is supplied by the vaginal and inferior vesicular arteries in female and male respectively. There is minor supply via the inferior gluteal and obturator arteries. The venous system is drained via the vesical venous plexus, which drains into the vesical veins which eventually leads to the internal iliac veins. The lymphatics of the bladder mostly drain to the external iliac lymph nodes.

Nerves

The detrusor muscle is under autonomic control. The parasympathetic nervous system stimulates the muscarinic stretch receptors in the bladder through the pelvic nerve fibers. When urine fills the bladder, the M3 receptors located within the bladder are stretched and stimulated, which lead to contraction of the detrusor muscle for urination. At the same time, the parasympathetic fibers inhibit the internal urethral sphincter, which causes relaxation allowing for bladder emptying. During ejaculation, the sympathetic response leads to contraction of the internal urethral sphincter, to prevent reflux of semen into the bladder. This response also prevents urine from passing during ejaculation. The most sensitive region of the bladder for the stretch receptors is the trigone. When the bladder is emptied of urine, the stretch fibers are inactivated, and the sympathetic nervous system is stimulated to activate the beta-3 receptors through adenylyl cyclase-cAMP pathway in the bladder through the hypogastric nerve to cause relaxation of the detrusor muscle. Newer beta-3 agonists utilize this pathway to treat bladder overactivity. Sensory fibers detect pain from overdistention. The center for coordinating urination is located in the pons.[3][4]

Muscles

The detrusor muscle is located within the walls of the bladder and is composed of smooth muscle fibers that are longitudinal and circular. The layers of the detrusor muscle start longitudinally in the inner layer which becomes circular in the middle layer and then longitudinal again in the outer layer. The muscle is continuous with the internal urethral sphincter, which is also composed of smooth muscle. The ureter passes obliquely through the detrusor muscle to prevent back reflux of urine into the kidney as the bladder fills. If this ureteral tunnel is not oblique, or short, then urine can reflux into the kidney causing infections, renal scarring, and renal damage.

Physiologic Variants

Pediatric detrusor muscle has less contractility and has more passive stiffness compared to adult detrusor muscles. This is most likely due to a greater connective tissue to smooth muscle ratio in children. This is known as bladder compliance (change in bladder pressure/change in bladder volume). Poor (decreased) bladder compliance is associated with upper urinary tract damage.

Surgical Considerations

Pelvic surgery may lead to bladder dysfunction. Some pelvic surgeries that have reported complications of bladder dysfunction include but are not limited to radical prostatectomy, perineal resection, radical hysterectomy, and proctocolectomy. Surgeons should take caution during pelvic surgery to avoid damage to any nerves, vessels, or structures of the bladder or urinary system.[5][6]

Clinical Significance

Patients with urinary retention usually present with difficulty voiding, a sensation of incomplete emptying, urinary retention, frequent voiding, and overflow incontinence. Diabetes mellitus and other neurologic conditions such as a stroke are the main causes of detrusor nerve control degeneration. Detrusor areflexia is the inability for the bladder to contract, which is typically neurologic in origin. Some causes of detrusor areflexia include spinal cord injury, fractures, herniated disc, and infections. Damage to the detrusor muscle from chronic overdistention can lead fibrosis of the muscle with weakness in contraction of the muscle. This is often referred to as a myogenic bladder. A common cause of chronic bladder distension is benign prostatic hypertrophy in males and less commonly severe pelvic organ prolapse in females. Whether the issue is of nerve or muscle origin, they both can lead to poor emptying ability. A subset of women may have detrusor overactivity with poor contractility, which can lead to overflow incontinence. This is common in the aging female population. Detrusor overactivity is often associated with urgency incontinence. Urgency incontinence is the sudden urge to urinate which may lead to leakage. Urgency incontinence is common in older women with other comorbid diseases. Treatment of the underlying disease is the most effective treatment. Usually, the first steps in treatment involve conservative options with lifestyle modifications, pelvic floor exercises, and bladder training. However, if these initial conservative therapies do not improve symptoms, there are other pharmacologic and surgical therapies. The 2 medication classes commonly used are antimuscarinics such as oxybutynin and tolterodine or beta 3-adrenergic such as mirabegron. Antimuscarinics have side effects such as dry mouth, constipation, blurry vision, drowsiness and cognitive issues. Sacral nerve stimulation and Botox are other options. More invasive therapies include surgery with augmentation cystoplasty or detrusor myectomy which improves compliance of the bladder to limit or prevent upper tract damage due to high bladder pressures.[2][7][8]

Other Issues

Bladder cancer is one of the most common cancers of the urinary system. Patients present with painless hematuria with frequency, urgency, or dysuria in an older patient. Bladder cancer is diagnosed and staged by doing a cystoscopy with biopsy. The depth of invasion of the cancer is a key factor in determining therapy and prognosis. When cancer spreads to the submucosa or lamina propria, it is considered a T1 lesion. There are multiple therapies for T1 bladder cancers that include transurethral resection, intravesical therapy, and surveillance. However, when cancer invades past the submucosa to the detrusor muscle, it will be considered a T2 lesion. These are considered muscle-invasive bladder cancer. This is a very important distinction when it comes to therapies because T2 lesions have an increased risk of nodal and distant metastasis. Thus, when cancer invades the detrusor muscle, the standard of therapy is the removal of the urinary bladder (radical cystectomy) and divert the urine. Urinary diversion involves the creation of a bowel conduit or neobladder by harvesting a bowel segment. Finally, T3 lesions are when tumor extends past the muscle into the perivesical fat, and T4 lesions occur when the tumor extends to nearby organs.[9]

Questions

To access free multiple choice questions on this topic, click here.

Detrusor muscle

Figure

Detrusor muscle. Image courtesy S Bhimji MD

References

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Fitz F, Sartori M, Girão MJ, Castro R. Pelvic floor muscle training for overactive bladder symptoms - A prospective study. Rev Assoc Med Bras (1992). 2017 Dec;63(12):1032-1038. [PubMed: 29489983]
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Andersson KE. On the Site and Mechanism of Action of β3-Adrenoceptor Agonists in the Bladder. Int Neurourol J. 2017 Mar 24;21(1):6-11. [PMC free article: PMC5380826] [PubMed: 28361520]
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Purves JT, Spruill L, Rovner E, Borisko E, McCants A, Mugo E, Wingard A, Trusk TC, Bacro T, Hughes FM. A three dimensional nerve map of human bladder trigone. Neurourol. Urodyn. 2017 Apr;36(4):1015-1019. [PubMed: 27265789]
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Iguchi N, Malykhina AP, Wilcox DT. Early life voiding dysfunction leads to lower urinary tract dysfunction through alteration of muscarinic and purinergic signaling in the bladder. Am. J. Physiol. Renal Physiol. 2018 Nov 01;315(5):F1320-F1328. [PMC free article: PMC6293296] [PubMed: 30089034]
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Yoshida M, Yamaguchi O. Detrusor Underactivity: The Current Concept of the Pathophysiology. Low Urin Tract Symptoms. 2014 Sep;6(3):131-7. [PubMed: 26663593]
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Radadia KD, Farber NJ, Shinder B, Polotti CF, Milas LJ, Tunuguntla HSGR. Management of Postradical Prostatectomy Urinary Incontinence: A Review. Urology. 2018 Mar;113:13-19. [PubMed: 29031841]
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Aoki Y, Brown HW, Brubaker L, Cornu JN, Daly JO, Cartwright R. Urinary incontinence in women. Nat Rev Dis Primers. 2017 Jul 06;3:17042. [PMC free article: PMC5878864] [PubMed: 28681849]
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El-Achkar A, Souhami L, Kassouf W. Bladder Preservation Therapy: Review of Literature and Future Directions of Trimodal Therapy. Curr Urol Rep. 2018 Nov 03;19(12):108. [PubMed: 30392150]
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Bookshelf ID: NBK482181PMID: 29489195

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