Pelvic floor disorders are a wide-ranging group of potentially disabling, embarrassing, and often painful conditions that can greatly affect a person’s quality of life. The pelvic floor consists of the muscles, fascia, and ligaments that support the pelvic organs and help to provide control for bodily functions. Pathology within the musculoskeletal and neurologic structures of the deep pelvis can lead to the development of pelvic pain, dyspareunia, voiding dysfunction including urinary incontinence or urinary urgency, fecal incontinence (FI), constipation, and pelvic organ prolapse.
Both women and men can develop pelvic floor disorders, although women are at increased risk compared with men because of their unique anatomy and biomechanics. A more broad and shallow female pelvis requires greater muscular and ligamentous stiffness to provide support to the bony pelvic girdle. Women are also more likely to have injury to the pelvic floor as a result of pregnancy and childbirth. As a result, abnormal biomechanics of the pelvic floor muscles (PFMs) may lead to changes in contraction, relaxation, muscle strength, and myofascial pain. In a 2008 study, the prevalence of symptomatic pelvic floor disorders in the United States was estimated to be approximately 24%.
People with pelvic floor disorders often benefit from an interdisciplinary rehabilitation approach to improve function and reduce pain. Physiatrists, with experience in acute and chronic pain, neurologic and musculoskeletal conditions, and neurogenic bowel/bladder management, are well suited to direct the patient’s care. The role of the physiatrist is to summarize the musculoskeletal findings of the history, physical examination, and diagnostic testing and to provide a specific physical therapy (PT) prescription. This prescription allows the physiatrist to convey impressions and suggest specific interventions for the pelvic floor as well as other related musculoskeletal structures (e.g., lumbar spine, pelvis, and hip). The rehabilitation provider must be aware of when to consult obstetrics-gynecology, urogynecology, urology, colorectal surgery, gastroenterology, and psychology specialists to provide additional specialist care ( Table 38-1 ). In this chapter, we will review the anatomy and physical examination of the pelvic floor, discuss the definitions and epidemiology of pelvic floor disorders, and explain the rehabilitation approach to treating these common disorders.
| Gynecologic | Gastrointestinal/Genitourinary | Musculoskeletal | Psychological |
|---|---|---|---|
| Vulvodynia | Interstitial cystitis | Low back pain | Anxiety |
| Dysmenorrhea | Urgency/frequency syndrome | Lumbar radiculopathy | Depression |
| Endometriosis | Levator ani syndrome | Sacroiliac joint dysfunction | History of abuse |
| Fibroids | Bowel/bladder incontinence | Coccydynia | |
| Organ prolapse | Hip disorders |
Pelvic Floor Neuromusculoskeletal Anatomy
The pelvic floor is composed of muscles, ligaments, and fascia that act as a sling to support the bladder, reproductive organs, and rectum. This sling of soft tissue is enclosed by the bony scaffolding of the pelvis, formed from the ilium, ischium, and pubis, which articulate with the sacrum posteriorly and each other anteriorly ( Figure 38-1 ). Extending from the sacrum is the coccyx, which acts as an important ligamentous and tendinous anchor.
The stability of the articulating surfaces of the pelvis is thought to arise through mechanisms termed “force closure” and “form closure.” Force closure is achieved through the interlocking of the ridges and grooves of the bony joint surfaces in the pelvis, whereas form closure is achieved through the compressive forces of the muscles, ligaments, and fascia providing passive stability. In the posterior pelvic ring there are two sacroiliac joints (SIJs). The anterior sacroiliac ligaments, comprising the anterior longitudinal ligament, the anterior sacroiliac ligament, and the sacrospinous ligament, stabilize the joint by resisting upward movement of the sacrum and lateral movement of the ilium. The posterior sacroiliac ligaments are made up by the short and long dorsal sacroiliac ligaments, the supraspinous ligament, the iliolumbar ligament, and the sacrotuberous ligament. These ligaments function to resist downward and upward movement of the sacrum and medial motion of the ilium. Anteriorly, the pubic symphysis is a cartilaginous joint between the two pubic bones reinforced by superior, inferior, anterior, and posterior ligaments. Functionally it resists tension, shearing, and compression, and is subject to great mechanical stress as it widens during pregnancy.
The superficial PFMs are the bulbospongiosus, ischiocavernosus, and superficial and deep transverse perineal muscles. The deep PFMs that line the inner walls of the pelvis are the levator ani and coccygeus, which along with the endopelvic fascia comprise the pelvic diaphragm ( Table 38-2 ). The levator ani is composed of three muscles: the puborectalis, pubococcygeus, and iliococcygeus ( Figure 38-2 ). The pubococcygeus is located most anteriorly. It originates from both the posterior pubic bone and the anterior portion of the arcus tendineus; it inserts into the anococcygeus ligament and the coccyx. The iliococcygeus is the posterior part of the levator ani. It originates from the posterior part of the arcus tendineus and ischial spine and attaches along the anococcygeal raphe and coccyx. Lastly, the puborectalis is located below the pubococcygeus and forms a U-shaped sling around the rectum. Its sphincterlike action pulls the anorectal junction forward, contributing to continence. The coccygeus muscle is triangular in shape, reinforcing the posterior pelvic floor by arising from the ischial spine and inserting on the lower sacral-coccygeal bones and is contiguous with the sacrospinous ligament. The perineal body or central perineal tendon is located between the vagina and anus. This is a site where the pelvic muscles and sphincters converge to provide support to the pelvic floor. Rupture of this entity during childbirth can lead to pelvic organ prolapse. The PFMs function to support the pelvic organs by coordinated contraction and relaxation. At rest, the pelvic floor provides active support through muscular activity and passive support from the surrounding connective tissue and fascia. With an increase in intraabdominal pressure, the PFMs contract with upward movement and closure of the vagina, urethral, and anal sphincters. This action is important for maintaining continence. Pelvic floor relaxation returns the muscles to their resting state and allows for normal micturition and defecation. Lining the lateral walls of the pelvis, the piriformis arises from the anterior sacrum, with the sacrotuberous ligament and attaches on the superior border of the greater trochanter. When the sacrum is fixed, the piriformis laterally rotates an extended thigh or abducts a flexed thigh. If the femurs are fixed it can retrovert the pelvis. The obturator internus, another lateral rotator of the thigh, arises from the pelvic surfaces of the ilium, ischium, and obturator membrane. It also attaches just distally to the piriformis on the greater trochanter.
| Muscle | Origin | Insertion | Innervation | Function |
|---|---|---|---|---|
| Puborectalis | Pubic symphysis | Pubic symphysis | S3 to S5, direct innervation from sacral nerve roots | Raises the pelvic floor |
| Pubococcygeus | Posterior pubic bone and arcus tendineus | Anococcygeus ligament and coccyx | S3 to S5, direct innervation from sacral nerve roots | Maintains floor tone in upright position |
| Iliococcygeus | Ischial spine and arcus tendineus | Anococcygeal raphe and coccyx | S3 to S5, direct innervation from sacral nerve roots | Voluntary control of urination |
| Coccygeus | Ischial spine | Lower sacral and upper coccygeal bones | S3 to S5, direct innervation from sacral nerve roots | Support of fetal head |
| Piriformis | Anterior sacrum | Posterior surface of greater trochanter | S1 to S2 via nerve to piriformis | Lateral rotation, abduction of thigh; retroversion of pelvis |
| Obturator Internus | Pelvic surface of ilium, ischium, and obturator membrane | Posterior surface of greater trochanter | L5, S1 to S2 via nerve to obturator internus | Lateral rotator of thigh |
The PFMs receive innervation through somatic, visceral, and central pathways. Skin innervation of the lower trunk, perineum, and proximal thigh is mediated through the iliohypogastric, ilioinguinal, and genitofemoral nerves (L1 to L3). Perhaps the most clinically relevant nerve to this chapter is the pudendal nerve and its branches ( Figure 38-3 ). Arising from the ventral branches of S2 to S4 of the sacral plexus, the pudendal nerve passes between the piriformis and coccygeal muscle as it traverses through the greater sciatic foramen, over the spine of the ischium, and back into the pelvis through the lesser sciatic foramen. It courses along the lateral wall of the ischiorectal fossa, where it is contained in a sheath of the obturator fascia termed the pudendal (or Alcock) canal. There are three main terminal branches of the pudendal nerve: the inferior rectal nerve (which typically originates proximal to the Alcock canal), the perineal nerve, and the dorsal nerve of the penis/clitoris. The pudendal nerve innervates the penis/clitoris, the bulbospongiosus and ischiocavernosus muscles, the anterior portions of the levator ani muscles, the perineum, the anus, the external anal sphincter, and the urethral sphincter. This nerve contributes to external genital sensation, continence, orgasm, and ejaculation. Muscles of the levator ani are thought to have direct innervation from sacral nerve roots S3 to S5.
Overview of Terminology
In 2005, the International Continence Society (ICS) presented a standardized terminology for PFM function and dysfunction. The PFMs function by coordinated contraction and relaxation as a unit. Voluntary contraction occurs when the patient can contract the PFMs on demand; voluntary relaxation occurs when the patient can relax the PFMs on demand after a contraction. Involuntary contraction of the PFMs occurs during a rise in intraabdominal pressure to prevent incontinence, such as during a cough. Involuntary relaxation occurs during a strain or Valsalva maneuver to allow for normal micturition or defecation.
Contraction and relaxation can be observed during the pelvic floor physical examination, as described later in this chapter. Based on examination of the PFMs, the following conditions have been defined by the ICS: Normal PFMs refer to muscles that can voluntarily and involuntarily contract with normal strength and relax completely. Overactive PFMs (also termed nonrelaxing PFMs) do not relax and may paradoxically contract when relaxation is needed, such as during micturition or defecation. Underactive PFMs (also called noncontracting PFMs) cannot voluntarily contract when desired. Nonfunctioning PFMs refer to no palpable PFM action and can be based on a noncontracting, nonrelaxing pelvic floor where the muscles are both weak and hypertonic. These categories can be helpful for generating a differential diagnosis for possible etiologies of pelvic floor dysfunction (see Table 38-1 ).
Pelvic Floor Physical Examination
A thorough musculoskeletal examination of the lumbar spine, hips, pelvic girdle, lower limbs, and PFMs will guide the differential diagnosis. The pelvic floor examination consists of vaginal and rectal examination of the PFM function and a neurologic examination of the lower sacral segments. A musculoskeletal pelvic floor examination does not obviate the need for gynecologic, urologic, or colorectal evaluation because visceral structures are not typically evaluated. Verbal consent from the patient is required. The examination should occur in a private examination or treatment room.
The examination begins with external inspection for swelling, cysts, scars, and lesions that may necessitate appropriate referral to another specialist. Next, the examiner visualizes the lift of the perineal body with a voluntary contraction (termed a Kegel contraction) and involuntary contraction (cough), as well as normal descent of the perineal body with voluntary relaxation and then involuntary relaxation (Valsalva maneuver). In women, the vaginal vestibule is evaluated for any visible organ prolapse. The Q-tip test for vulvodynia is performed by lightly touching a cotton swab inside the vestibule to elicit any pain or allodynia. The examiner proceeds to an external sensory examination of the S2 to S5 sacral dermatomes (see Figure 38-3 ). An anal wink reflex is obtained near the anus to test the sacral reflex arc. The superficial PFMs are palpated for any tenderness.
Next, the examiner moves on to the internal pelvic floor examination; both vaginal and rectal examinations can be performed. It is best to use a flat examination table without stirrups. The vaginal examination is performed in hook lying position, supine with the knees bent, and ankles hip-width apart. The rectal examination is typically performed in a left lateral decubitus position.
One lubricated, gloved finger is inserted into the vaginal introitus or anal canal to palpate the PFMs internally. A clock face diagram is useful to correctly identify the anatomic positions of the PFMs with the pubic bone at 12 o’clock and the anus and coccyx at 6 o’clock ( Figure 38-4 ). The levator ani can be palpated on both vaginal and rectal examinations from 1 to 5 o’clock on the left and 7 to 11 o’clock on the right, with the pubococcygeus located more anteriorly and the iliococcygeus located more posteriorly. The obturator internus is located just above 3 o’clock on the left and 9 o’clock on the right, and is separated from the levator ani by locating the arcus tendineus, which feels similar to a guitar string on palpation (see Figure 38-2 ). The obturator internus can also be identified by having the patient externally rotate the hip to activate the muscle causing it to bulge medially, which can be appreciated with internal digital palpation. Rectal examination affords the ability to additionally assess anal sphincter tone as well as the coccygeus, piriformis, and puborectalis muscles. The puborectalis can be easily appreciated, forming the innermost portion of the anal canal. The coccyx can be examined intrarectally to assess for tenderness, mobility, and anterior or lateral deviation. The PFMs are palpated for tenderness, taut bands, and referring trigger points. The presence of intramuscular scar tissue should be noted. PFM tone can be assessed as either an increased or decreased resting state of the muscle. A Tinel sign can be obtained by tapping over the pudendal nerve as it courses inferior to the ischial spine and may provoke pelvic floor or perineal paresthesias.
Voluntary contraction of the PFMs is felt as a tightening, lifting, and squeezing action under the examining finger that occurs upon demand. Voluntary contraction is graded with the Modified Oxford scale. Similar to manual muscle testing for limb muscles, the scale ranges from 0/5 signifying “absent” contraction to 5/5, which implies that the patient is able to “lift, tighten, and maintain for 10 seconds” ( Table 38-3 ). Strength testing should be performed in four quadrants, especially in patients with neurologic deficits, such as hemiplegia. Voluntary relaxation of the PFMs is felt as a termination of the contraction as the muscles return to their resting state. The examiner then has the patient cough to look for presence or absence of involuntary contraction , and then perform a Valsalva maneuver to look for presence or absence of involuntary relaxation . It is important to assess for dyssynergia or inappropriate contraction of the PFMs during attempts at Valsalva. Endurance is tested by asking the patient to hold a full contraction for 10 seconds. Coordination is tested by performing “quick flicks” or asking the patient to contract and relax the PFMs rapidly.
| Grading | Contraction | Lift or Tighten |
|---|---|---|
| 0/5 | No | No |
| 1/5 | Flicker | No |
| 2/5 | Weak | No |
| 3/5 | Moderate | Some lifting/tightening, contraction visible |
| 4/5 | Good | Holds for 5+ seconds |
| 5/5 | Strong | Holds for 10+ seconds |
Types of Pelvic Floor Dysfunction
Urinary Incontinence
Definitions and Etiology
Urinary incontinence, defined as the involuntary leakage of urine, can be divided into three main types. Stress urinary incontinence (SUI) is the loss of urine with increased intraabdominal pressure, such as during coughing, laughing, sneezing, or physical exertion. SUI occurs where there are deficiencies in the PFMs, urethra, bladder, and/or sphincter such that it is difficult to maintain urethral closure pressures. The etiology is multifactorial and has been shown to be related to pregnancy, vaginal delivery, pelvic surgery, pelvic organ prolapse, neurologic causes, active lifestyle, obesity, and aging. Urge urinary incontinence (UUI) is involuntary leakage accompanied by or immediately preceded by the sudden onset of an urge to void that cannot be deferred easily. UUI can be caused by an involuntary detrusor contraction that overcomes the sphincter mechanism or poor bladder compliance that results from loss of the viscoelastic features of the bladder. The cause of UUI may be neurogenic or idiopathic. Neurologic processes that can cause low bladder compliance include spinal cord injury, spinal stenosis, multiple sclerosis, and stroke. Nonneurogenic etiologies are usually processes that change the bladder tissue, such as radiation. Mixed urinary incontinence (MUI) occurs when a patient experiences both SUI and UUI symptoms.
Epidemiology
Urinary incontinence is by far more common in women. A survey of 45,000 households in the United States with a mixed respondent population (82% women) found a 34% prevalence of urinary incontinence. The prevalence of urinary incontinence has been shown to increase in both men and women with age. Prevalence rates by age group were found to be 15% for ages 18 to 24 years and 46% for ages 60 to 64 years. Reported risk factors for urinary incontinence include race, hormonal status, obesity, history of pregnancy or childbirth, and chronic disease, such as diabetes. The prevalence of urinary incontinence also increases with smoking, body mass index, and increased parity. One study, which looked at vaginal delivery and its effect on the prevalence of different types of urinary incontinence in women, found a 15.3% rate of SUI, a 6.1% rate of UUI, and a 14.4% rate of MUI. High-level female athletes are also at an increased risk of developing incontinence; one recent study indicated an SUI prevalence in this population of 41.5%. Other risk factors not consistently reported include constipation and family history.
Diagnosis and Physical Examination
Physiatrists often discover urinary incontinence as part of screening questions for back pain or on review of systems. This is essential because fewer than 50% of those suffering from this condition will seek out treatment. If a patient admits to this condition, it is important to review their medical history, noting any neurologic disease. The physician should determine whether the patient has SUI, UUI, or MUI with questions regarding timing of accidents and relation to activity and urgency symptoms. If a patient with urinary incontinence has presented to the office because of back pain, it is necessary to rule out surgical emergencies, such as cauda equina syndrome. Patients who do not have neurologic deficits should be further examined by a physiatrist who is comfortable performing a pelvic floor examination or referred to a urologist for additional workup.
A thorough neurologic, lower extremity, and pelvic floor physical examination can help distinguish between neurogenic causes and PFM contributions to incontinence. For urinary incontinence, pelvic floor examination should focus on inspection of the vulva and perineum, sensory testing of S2 to S5 dermatomes, tone and strength testing of the PFMs, and assessment for a gross pelvic organ prolapse (POP). It is important to note POP in a patient with back pain and incontinence because this may be a source of vague, achy low back pain. The PFMs are usually found to be underactive and weak in SUI and overactive in UUI. The integrity of the vaginal mucosa should also be noted because menopausal hypoestrogenic state has been associated with urinary incontinence. Determination of when to refer for advanced testing, such as cystoscopy, postvoid residuals, and urodynamics, should be made on an individual basis.
Treatment
Management for urinary incontinence includes pharmacologic, surgical, behavioral, and exercise-based treatments. Conservative treatment for urinary incontinence often results in improvement of symptoms, but the initial severity usually dictates the amount of success. Treatment options vary for SUI and UUI, but both respond well to behavioral modifications and rehabilitation interventions.
Behavioral and lifestyle alterations include changes in diet, regulating fluid intake, and bladder training. Reduction of more than 5% body weight has led to a 47% decrease in incontinence episodes versus 28% with education alone. Bladder training usually consists of two parts, timed voiding and urge suppression techniques, and can take approximately 12 weeks to see improvement. The overall goals of bladder training are to prolong the time between voids and to void before experiencing a sense of urgency or UUI. Using a bladder diary to identify the shortest interval between voids, patients are instructed to increase this time by approximately 15 to 30 minutes until there is approximately 3 hours between voids. Urge suppression can temporarily reduce the intensity of a bladder contraction by causing reflex inhibition of the parasympathetic nerves acting on the detrusor muscle. When one feels an urge, they should stop and/or sit, perform five to six quick voluntary PFM (or Kegel) contractions, take a deep breath, relax until the urge passes, and then walk to the restroom normally.
PFM contraction (or Kegel) exercises can be used to strengthen the PFMs and reduce episodes of SUI. The majority of people who try to perform a proper PFM (or Kegel) contraction are unable to do so. As such, patients should be taught how to perform these exercises with a pelvic floor expert. Biofeedback therapy with or without electrical stimulation is often used to improve a patient’s ability to perform a PFM contraction ( Figure 38-5 ). A strengthening program for the PFMs increases support for the bladder and urethra and helps maintain the urethral closure pressures. As strength improves, patients can be taught to make a PFM contraction an automatic response when anticipating increase in intraabdominal pressure (such as with a sneeze), and to perform them during functional activities. The long-term effect of PFM strengthening for SUI symptom improvement ranges from 41% to 85%.
Pharmacologic management of UUI focuses on medications for overactive bladder (OAB) (see the following section). There are currently no approved drugs for SUI in the United States. The mainstay of pharmacologic management of OAB and UUI are anticholinergic medications that decrease urgency and detrusor instability by blocking parasympathetic nerves of the bladder. However, their use and efficacy are often limited by side effects, such as constipation, drowsiness, and dry mouth.
When conservative measures have failed, botulinum toxin and neuromodulation can be used to decrease detrusor muscle contractility and treat UUI. When botulinum toxin is injected into the detrusor muscle, daily frequency, urgency, and incontinence can be reduced by 29%, 3%, and 59%, respectively. Neuromodulation by stimulation of S3 sacral nerve root can lead to effective control of UUI and symptoms of urgency and frequency.
Other forms of therapy for SUI include urethral bulking agents and surgery. Urethral bulking agents increase the compressive force on the urethral lumen by augmenting the submucosal layer. The most common surgery for SUI has become the placement of midurethral slings. These slings are thought to improve urethral support, create resistance to increases in abdominal pressure, and restore the normal forces on the urethra.
Urinary Urgency and Frequency
Definitions and Etiology
Urinary urgency is defined as “the complaint of a sudden compelling desire to pass urine which is difficult to defer” by the ICS. Frequency of urination more than every 2 to 3 hours can be considered abnormal. The symptoms of urgency and frequency are similar to those of UUI that were discussed earlier. Urinary urgency associated with or without incontinence, daytime frequency, and nocturia is termed OAB. As its name describes, the diagnosis of OAB should be reserved for cases that are clearly of bladder origin, namely detrusor muscle overactivity. There are also neurogenic, medical, and muscular causes of urgency/frequency symptoms.
The pathophysiology of neurogenic urgency and frequency is usually attributable to detrusor overactivity as a result of disruption to the complex micturition reflex at the cerebral, pons or corticospinal level. Such neurologic causes include stroke, Alzheimer disease, Parkinson disease, or multiple sclerosis. Lower motor neuron causes or peripheral neuropathies can also cause voiding dysfunction.
Medical causes of urinary urgency and frequency include urinary tract infections in which increased inflammation in the bladder leads to sensory afferent upregulation, ultimately causing detrusor muscle instability. Similarly, estrogen deficiency can lead to vaginal and urethral irritation, which may bring on increased infections and OAB. The normal aging process also leads to increased bladder contractility and decreased bladder compliance resulting in urgency and frequency, respectively.
Patients with urinary urgency and frequency in the absence of bladder or neurologic pathology may have these symptoms as a result of overactive PFMs. Those in this category will have dysfunctional voiding with a sense of urgency and/or frequency resulting from increased external pressure around the urethra. Patients can describe a constant need or an exaggerated urge to void. Patients with hypertonic PFMs can have difficulty with voluntary relaxation or can have involuntary contractions during voiding. Other symptoms of pelvic floor dysfunction resulting from overactive PFMs includes postvoiding pain, urethral pain, hesitancy, or incomplete bladder emptying. Patients with functional constipation or bowel impaction (discussed later) should be screened for urinary urgency and frequency because both can be a result of overactive pelvic floor dysfunction. Development of overactive PFMs with urinary dysfunction is often attributable to holding behaviors developed during childhood or as a result of circumstances that may cause one to suppress the urge to void for many hours (such as working as a taxi driver, teacher or nurse, or having a fear of voiding in public restrooms). Overactive pelvic floor dysfunction is also associated with a history of sexual abuse or those with severe anxiety disorders.
Diagnosis and Physical Examination
Patients presenting with pure urinary urgency and frequency symptoms need to be initially evaluated by a urologist for a complete workup of their voiding dysfunction, including postvoid residuals and urodynamic testing. Men should have a thorough prostate examination. As with urinary incontinence, a thorough evaluation of patients with urinary frequency and urgency includes a full medical history and physical examination to assess for medical or neurogenic causes. Diagnosis of overactive PFMs can be made during a musculoskeletal pelvic floor examination. Externally, minimal movement of the perineal body when patients are asked to do voluntary PFM contraction or relaxation should lead the examiner to consider a hypertonic state. On the internal (vaginal or rectal) assessment, attention is focused on the stiffness and length of the levator ani muscles. Patients are likely to have shortened levator ani muscles that feel weak when tested for strength. These patients often have pain in the PFMs as a result of chronic hypertonicity. Again, minimal movement of the muscles during the internal part of the examination will help diagnose hypertonic or overactive PFM dysfunction.
Treatment
The underlying etiology of the voiding dysfunction should be treated, if possible. Patients who have idiopathic or pure muscular causes of urinary frequency and urgency can be treated conservatively with pelvic floor PT. The goal of this treatment program is to teach patients how to relax the PFMs during voiding. PFM training focuses first on developing an awareness of muscle contraction versus relaxation with biofeedback. The focus should then turn to teaching volitional relaxation of the PFMs in the context of voiding. Perineal, rectal, or vaginal biofeedback can be especially useful for bringing muscle tension to a conscious level. In addition, to facilitate relaxation patients can be taught to relax the muscle for a longer period of time compared with a contraction, usually in a 1 : 2 ratio. Patients with urgency and frequency voiding dysfunction should be taught urge suppression techniques with bladder training (as described earlier). Lifestyle modifications and education about fluid management, bladder irritants, and weight loss should also be stressed.
Fecal Incontinence
Definitions and Etiology
Fecal incontinence (FI) is defined as the involuntary loss of liquid or solid stool that is a social or hygienic problem. A related term is anal incontinence (AI), which is defined as the involuntary loss of liquid or solid stool, mucus, or flatus. FI is strongly associated with aging. Other risk factors include nursing home residence, obesity, poor general health, physical limitations, and neurologic disease. Patients with gastrointestinal disorders, such as irritable bowel syndrome or inflammatory bowel disease, have a higher likelihood of FI. FI is more common in patients who have weakness or injury to the anal sphincter. Obstetric factors are likely to play a large role: sphincter laceration, use of forceps, midline episiotomy, and intrapartum pudendal nerve damage have all been shown to contribute to the development of subsequent FI. Pelvic surgeries can also predispose to the development of this disorder. FI has been reported as a complication in 33% of hemorrhoidectomies, 11% of sphincterotomies, and 9% to 32% of radical prostatectomies. Pelvic radiation can lead to the development of FI in 14% to 46% of patients.
Epidemiology
Prevalence has been reported at 2% to 24% of the adult population, with 1% to 2% experiencing significant impact on daily activities. A survey study of over 10,000 respondents found that 5.7% of women and 6.2% of men over 40 years of age report some degree of FI, with prevalence increasing with age. FI is also prevalent in high-level athletes, although to a lesser extent than SUI. One study of 393 female athletes found a prevalence of AI of 14.9% and reported that 8% of all high-level athletes needed to wear a pad for protection as a result of significant FI. It is estimated that less than 30% of the people who struggle with FI discuss the problem with their health care providers.
Diagnosis and Physical Examination
As with urinary incontinence, it is important for the physician to enquire about the presence of FI, because patients are often reluctant to discuss the subject. It is important to determine whether there is loss of liquid or solid stool, mucus, or flatus. The timing and frequency of episodes, the volume of stool loss, and the ability of the patient to sense the involuntary passage of anal contents are all necessary elements of the history. The physical examination should include a thorough neurologic and spine examination, as well as a digital rectal examination to assess for sphincter tone, sphincter defects, PFM tone, strength, and endurance are important. Diagnostic tools for FI include anorectal manometry, which measures the strength and endurance of the anal sphincter at rest and with contraction. Pudendal nerve terminal motor latency testing can be performed as part of electrodiagnostic testing. Endoanal ultrasound is a very effective tool for the evaluation of the integrity of the internal and external anal sphincters.
Treatment
Treatments include conservative measures such as dietary modifications, medications, and pelvic floor rehabilitation, as well as more invasive approaches such as the use of perianal injectable bulking agents, sacral nerve stimulation, or surgery. Many patients prefer to avoid the risk of interventions, and a stepwise approach to treatment has been advocated to minimize injury to patients.
Pelvic floor rehabilitation has been used successfully in the treatment of FI and can produce significant functional and quality of life benefits for patients. Most of the reported literature in this area has been in the form of case reports and nonrandomized prospective trials. In fact, more than 70 such uncontrolled studies have been published, with the majority reporting a response range of 50% to 90%. There have been a smaller number of randomized controlled trials (RCTs) on pelvic floor rehabilitation for FI, less than 30 in total of high quality, according to two recently published Cochrane reviews on the topic. Most RCTs also demonstrated successful improvement of FI symptoms in 50% to 80% of participants.
Pelvic floor rehabilitation techniques for the treatment of FI include bowel management education and retraining, PFM training, biofeedback therapy, the use of electrical stimulation, manual myofascial release, and connective tissue mobilization techniques. The different rehabilitation techniques can be used independently, but more frequently are used in conjunction with one another in a multimodal approach to produce the maximum benefit for the patient. The primary goal of all forms of pelvic floor rehabilitation is to improve pelvic floor and anal sphincter muscle strength, tone, endurance, and coordination to effect a positive change in function with a decrease in symptoms. Additional goals include increasing the patient’s awareness of their own muscles, improving rectal sensitivity, and reducing scar burden to allow for improved muscle function.
There are three main approaches for the use of biofeedback as a part of pelvic floor rehabilitation for FI. Biofeedback therapy is most commonly used to improve strength and endurance of the PFMs and/or external anal sphincter. It has been theorized that this training is effective because it enables the patient to hold the stool within the rectal vault for a longer period of time, allowing them to make it to the restroom with less accidents. The second treatment modality is to use biofeedback to improve rectal sensitivity or compliance. This type of treatment is typically done with sequentially inflated rectal balloons. The rationale behind sensory retraining is to allow the patient to detect smaller volumes of stool at an earlier time, again making it possible for them to reach the restroom before an accident occurs. The third biofeedback approach deals with coordination training for the anal sphincter.
The incorporation of lifestyle education into the therapeutic treatment program is of vital importance for patients with FI. It is important to instruct patients about optimal fluid intake; dietary adjustments can be important in certain patient populations. Patients with irritable bowel syndrome and FI, for example, often find that regulating dairy, gluten, and fiber can be an important component of controlling their stool leakage. It is generally recommended that all patients with FI increase their fiber intake, as Bliss et al. were able to demonstrate that fiber supplementation significantly reduced the rate of FI. Behavior modification can also be explored with patients, including training on the establishment of a predictable pattern of bowel evacuation, timing of defecation relative to activities to limit incontinent episodes, techniques to reduce straining, proper defecation posture when sitting on the toilet, and fecal urge suppression techniques. Weight reduction is typically encouraged.
There have only been a few studies that have looked at which types of patients will most likely benefit from a rehabilitation approach to treatment for FI. Good sphincter function and mild to moderate symptomatology are considered as more favorable prognostic factors. Disruption of the anal sphincter, spinal cord injury or other neurogenic disorders, severe impairment of rectal sensory function, cognitive impairments, severe depression or other mental illness, and age less than 6 years are all thought to be predictors of poor response to biofeedback and other rehabilitation treatments.
Functional Constipation
Definitions and Etiology
Functional constipation, as defined by the Rome III diagnostic criteria must include two or more of the following: straining during at least 25% of defecations, lumpy or hard stools in at least 25% of defecations, sensation of incomplete evacuation for at least 25% of defecations, sensation of anorectal obstruction/blockage for at least 25% of defecations, manual maneuvers to facilitate at least 25% of defecations (e.g., digital evacuation, support of the pelvic floor), and fewer than three defecations per week. Loose stools are rarely present without the use of laxatives and patients should not meet the criteria for irritable bowel syndrome.
Functional constipation is further subdivided into normal transit constipation, slow transit constipation, and outlet constipation. Normal transit constipation occurs when there is a self-reported perception of constipation with normal stool movement through the colon. Slow transit constipation occurs when there is prolonged transit time through the colon, confirmed with a motility study. Outlet constipation (also called dyssynergia, disordered defecation, or nonrelaxing puborectalis syndrome) occurs as a result of pelvic floor dysfunction, when there is a defect in the coordination that is needed for stool evacuation. Most often, this incoordination occurs because of the failure of the PFMs to relax appropriately during evacuation efforts. Other causes of outlet dysfunction constipation may include rectocele, enterocele, peritoneocele, and intrarectal intussusception. Common features of outlet constipation include prolonged or excessive straining, soft stools that are difficult to pass, and rectal discomfort. The etiology of outlet constipation is unclear.
Epidemiology
Chronic constipation has been reported to affect approximately 15% of the general population, including all ages and both sexes, with estimates ranging from 2% to 27%. Constipation significantly decreases the quality of life of those affected.
Diagnosis and Physical Examination
When taking a history from a patient with constipation, it is important to ask about the number of bowel movements per week, stool consistency, the presence of straining, and the presence of bleeding or mucus. Hard, small, pellet-shaped stools are indicative of poor colonic transit or significant time in the rectal vault. Pencil-shaped stools are a common finding with a nonrelaxing puborectalis syndrome, also termed overactive PFMs. The physician should ask about the use of manual maneuvers to facilitate defecation and the use of over-the-counter laxatives and fiber. The physical examination should include abdominal examination and digital rectal examination to assess the sphincter tone and the PFMs. When asked to strain as if having a bowel movement or to attempt to expel the examiner’s finger, the examiner should appreciate relaxation of the anal sphincter and relaxation of the puborectalis muscle with decent of the perineum. Additionally, when the patient contracts the PFMs, the examiner should appreciate a lift of the PFMs. Absence of these findings suggests pelvic floor dysfunction.
Diagnostic testing for functional constipation includes anorectal manometry, Sitz study, and defecography. Anorectal manometry can be used to determine if anal sphincter pressures rise with attempts at defecation or rectal balloon expulsion, hallmarks of dyssynergia. Digital rectal examination is reasonably accurate relative to manometry for assessing anal resting tone and squeeze function and for identifying dyssynergia. A Sitz study can be performed to assess colonic motility. The patient is asked to swallow a capsule containing 25 radiopaque markers and an abdominal plain film is obtained 5 days later at which time a majority of the markers should no longer be visible. Sitz markers scattered throughout the colon indicate a problem of slowed colonic transit. Sitz markers clustered in the rectum and sigmoid colon indicate a problem of outlet dysfunction or dyssynergia. Defecography is another important tool in the diagnosis of constipation, because it can distinguish between the many causes of outlet dysfunction constipation including PFM dyssynergia, rectocele, and intrarectal intussusception. Defecography can be done via plain films but magnetic resonance (MR) defecography is emerging as the modality of choice because of its superior image quality.
Treatment
The treatment of functional constipation depends greatly on the cause. Slow transit constipation can benefit from increasing fluid intake, fiber supplementation, magnesium supplementation, and stool softener or laxative use. Nonstimulant laxatives, such as polyethylene glycol, are preferred to stimulant laxatives, such as bisacodyl and senna, because stimulant laxatives have been shown to cause dependency and decreased bowel function over time. Prescription medications for constipation include lactulose, lubiprostone, and linaclotide. Laxative enemas and intrarectal suppositories can also be of benefit. If such measures are not effective for severe slow transit constipation, surgical options include subtotal or total colectomy with ileoanal anastomosis or colostomy.
Dyssynergia is ideally treated with pelvic floor PT. Treatment should include biofeedback and pelvic floor relaxation training. Biofeedback therapy can be used to teach the patient how to perform evacuation by relaxing and paring outward the abdominal and PFMs. Protocols of five to six training sessions lasting 30 to 60 minutes, spaced 2 weeks apart, have been shown to be beneficial. The goals of therapy include education about disordered defecation, coordination of increased intraabdominal pressures with pelvic floor relaxation during evacuation, and therapist-assisted practiced defecation simulation with an intrarectal balloon. Techniques employed may also include diaphragmatic breathing, intrarectal and intravaginal myofascial release, visceral mobilization, abdominal wall and colonic massage/stimulation techniques, or the use of anal dilators. The therapist will typically ensure that the patient is using proper defecatory posture while sitting on the toilet, and often will instruct the patient to prop their feet up on a stool and lean forward slightly during defecation to allow for maximum relaxation of the PFMs. Options are limited for patients with severe dyssynergia or anismus who do not respond to pelvic floor PT. Botox to the puborectalis (typically done under endoanal ultrasound guidance) can be considered, but the risk of development of subsequent FI must be taken into careful consideration. The only surgical option is colostomy.
Patients with a symptomatic rectocele can be taught to splint intravaginally with their thumb pressing backward to facilitate stool expulsion. Patients with a significant enterocele, peritoneocele, or intrarectal intussusception often need surgical intervention such as a resection rectopexy.
Pelvic Floor Myofascial Pain
Definitions and Etiology
Pelvic floor myofascial pain is characterized by muscular pain, taut bands, and trigger points that cause pain referral with pressure, usually resulting from underlying overuse or weakness. Myofascial trigger points can develop from functional events through overuse, repetitive strains, motion injuries, or dysfunctional posturing as well as a result of a viscerosomatic reflex. Pelvic floor myofascial dysfunction refers to abnormal muscle activation patterns of the PFMs. Pelvic floor myofascial pain and dysfunction can contribute to the symptom of dyspareunia, or painful sexual intercourse, and to chronic pelvic pain (CPP), but there are many other causes of these conditions with significant overlap.
Epidemiology
PFM pain was found on vaginal physical examination in 22% of women with CPP (ages 14 to 79 years), 70% of women with pregnancy-related pelvic girdle pain (PGP) in the second trimester, and 52% of postpartum women with chronic lumbopelvic pain that began during pregnancy. CPP affects 25% of community-dwelling adult women.
Diagnosis and Physical Examination
The diagnosis of pelvic floor myofascial pain and dysfunction is made clinically by a combination of a focused history and pelvic floor physical examination. Patients with pelvic floor myofascial pain will report pain that is “deep” and internal. They may report associated symptoms of dysuria, dyschezia, dysmenorrhea, or dyspareunia, but often must be prompted with direct questioning because of the intimate nature of pelvic floor pain. Pelvic floor myofascial pain and dysfunction are often related to painful bladder syndrome/interstitial cystitis, urinary urgency/frequency syndrome, vulvar vestibulitis, and chronic prostatitis. A history of related pelvic visceral disorders, such as infection, endometriosis, or fibroids, should be ascertained as these can be related to pelvic floor pain and dysfunction via the viscerosomatic reflex. History of birth trauma, instrumentation (forceps), prolonged labor, or perineal tears during vaginal delivery may point to injury to the PFMs. A history of abuse (physical, sexual, or emotional) can manifest later in life as pelvic pain with PFM overactivity. Finally, a poor response to traditional therapy and treatments for hip and low back pain can often indicate an underlying pelvic floor disorder.
During internal examination of the PFMs, myofascial pain is identified by pain on palpation of the levator ani and obturator internus muscles with taut bands and trigger points that refer pain with pressure. Making note of underactive and overactive PFM tone is useful to direct further intervention. A complete neurologic and musculoskeletal examination of the spine and lower extremities is important to evaluate for other contributing spine, pelvis, or hip pathology.
Diagnostic imaging can also be useful to aid in ruling out other musculoskeletal causes of lumbopelvic pain. Typically, a conventional pelvic and lumbar radiograph is useful to evaluate the structural integrity of the spine and pelvis; based on physical examination findings, the physician may consider the addition of hip radiographs. Magnetic resonance imaging (MRI) of the spine, hip, or pelvis may be useful to rule out serious causes of pelvic pain, including herniated lumbosacral disk or sacral fracture. Ultrasound is an emerging imaging technique, with increasing musculoskeletal applications to evaluate soft tissue, superficial joints, and neural structures.
Treatment
Pelvic floor PT is a mainstay of rehabilitation treatment for pelvic floor myofascial pain and dysfunction. The goals of pelvic floor PT are to restore muscle imbalances, improve function, and reduce pain. Therapeutic options for myofascial pain are based on myofascial release techniques combined with neuromuscular reeducation to inactivate trigger points. Soft tissue mobilization can address adhesions, diminish trigger points, and desensitize tissue. Manual techniques for myofascial trigger points include manual release, acupressure, muscle energy, and strain-counterstrain. Because the PFMs are intimately related to the anatomic structures of the pelvic girdle, hip, spine, and core musculature, exercises are also prescribed to restore normal movement patterns, joint range of motion, and muscle strength. Adjuvant treatments include the use of biofeedback to improve muscle firing patterns in both underactive and overactive PFMs by providing the patient with objective feedback about muscle activation at rest and with activities of daily living (see Figure 38-5 ). Electrical stimulation can be used to increase PFM activity in underactive muscles or provide pain relief in overactive muscles by the use of surface electrodes or vaginal/rectal probes.
Medication use in pelvic floor myofascial pain and dysfunction is aimed at reducing pain, treating anxiety, and restoring restful sleep. Medications, such as nonsteroidal antiinflammatory drugs (NSAIDs), are often used for acute pain but are limited from long-term use by gastrointestinal side effects and the risk of bleeding. Tricyclic antidepressants (TCAs) (e.g., nortriptyline) and related mediations, such as trazodone and cyclobenzaprine, may be used to address pain, mood, and sleep in myofascial pain syndromes, but can cause anticholinergic side effects, such as dry mouth, constipation, or urinary retention. If there is a neurogenic or central sensitization component, antiepileptics (e.g., gabapentin or pregabalin) or serotonin norepinephrine reuptake inhibitors (SNRIs) (e.g., duloxetine or venlafaxine) may also be useful. SNRIs may be better tolerated than antiepileptics because of less sedating side effects. Muscle relaxants (e.g., cyclobenzaprine) may be helpful, especially for painful nighttime muscle spasms, but are limited by the side effect of sedation and are not recommended for long-term use. Care should be taken to avoid long-term use of narcotic pain medications. Topical medications are often a helpful adjuvant treatment option, including estrogen creams and topical anesthetics (e.g., lidocaine cream). Antispasmodic medications, such as valium or baclofen, may be used as an intravaginal suppository or made into a compounded cream. It is often helpful to use intravaginal valium or baclofen before pelvic floor PT, before sexual intercourse, or before going to sleep at night.
When the previously mentioned rehabilitation treatment interventions do not provide adequate relief from pelvic floor myofascial pain, injections can be used to reduce pain and increase participation in therapeutic exercises. Combining trigger point injections with manual techniques in PT may provide additional, longer lasting relief. Specific medical management techniques for myofascial trigger points include local anesthetic, botulinum toxin, corticosteroid injections, as well as dry needling. The use of botulinum toxin for trigger point injections remains an off-label indication. If the patient also complains of posterior pelvic pain, a trial of an ultrasound-guided piriformis muscle trigger point injection may be indicated. Cadaveric studies demonstrate that the piriformis and obturator internus muscles are fused in approximately 40% of people, and the combination of piriformis and obturator internus injection provided substantial relief in patients with posterior pelvic pain. Additionally, fluoroscopic-guided SIJ, pubic symphysis, or hip intraarticular steroid injections may be additional targets to reduce pain and improve function, given the anatomic relationships described earlier. Injection treatment should be guided by a detailed history and musculoskeletal physical examination to identify potential pain generators. Injection interventions should not be used in isolation, but as part of a comprehensive rehabilitation plan to aid in diagnosis, progress goals in therapy, reduce pain, and improve function.
Pregnancy and Postpartum Pelvic Floor Dysfunction
Definitions and Etiology
Many musculoskeletal changes occur during pregnancy to accommodate for the growing fetus and prepare the woman’s body for childbirth. In addition to the increase in body mass, the abdominal muscles lengthen, there is an increase in lumbar lordosis, an increase in the anterior pelvic tilt, an increase in the pelvic width, and the center of gravity shifts anteriorly as the fetus grows. Hormonal changes also increase joint laxity. All of these changes lead to an increased demand being placed on the hip extensors, hip abductors, ankle plantar flexors, and the PFMs.
Musculoskeletal pain during pregnancy can arise from numerous areas, including the pelvic girdle, lumbar spine, hip, and PFMs. It is important to remember that anything that occurs in the nonpregnant woman can also occur during pregnancy. Although pain can arise from multiple locations, PGP is the most common cause of back and pelvic pain in pregnancy. PGP is pain experienced between the posterior iliac crest and the gluteal fold, particularly in the region of the SIJs. The pain may radiate to the posterior thigh. PGP may include pubic symphysis pain, which may radiate to the anterior thigh. Women with PGP have a diminished endurance capacity. To diagnose PGP, lumbar causes of pain must be excluded and the pain must be reproducible by specific clinical tests.
Several etiologies have been proposed with regard to PGP, including mechanical, hormonal, inflammatory, collagen abnormalities, and neural. It has been shown that women with PGP are more likely to have deep PFM tenderness in both the levator ani and obturator internus. Joint laxity has also been studied in patients with PGP. No relationship has been shown between increased SIJ laxity and pelvic pain during pregnancy; however, there was a correlation between asymmetric laxity of the SIJs and pain during pregnancy.
Relaxin, a hormone produced by the corpus luteum that relaxes the uterine musculature and allows for an increase in pelvic expansion, has been studied in PGP. Relaxin elevates during the first trimester of pregnancy and then remains stable throughout the rest of the pregnancy. The levels then decline sharply after delivery. There have been multiple studies showing a correlation between relaxin levels and PGP, whereas other studies have shown no correlation. These differences may be explained by study method variation because different studies had different methods of measuring joint laxity, some measured laxity in nonpelvic joints and used varying definitions of PGP. Marnach et al. looked at several different hormone levels in pregnancy and found that cortisol, estradiol, and progesterone all substantially increase with each trimester. Women with joint complaints were more likely to have higher levels of estradiol and progesterone and lower levels of relaxin. Hormones may change the elasticity of ligaments by affecting collagen metabolism, which may contribute to the laxity of the joints during pregnancy. Kristiansson et al. demonstrated that serum concentrations of a collagen turnover marker were significantly correlated with pelvic pain in pregnancy.
Epidemiology
PGP is estimated to affect approximately 20% of pregnant women. Risk factors for development of PGP include a history of low back pain and previous trauma to the pelvis. Probable risk factors include parity and workload. The use of oral contraceptive pills, time interval since last pregnancy, height, weight, smoking, and age are not risk factors.
PGP can be further subdivided into four groups of pain patterns, defined by the locations of the painful joint(s) in the pelvis. Double-sided SIJ syndrome, the most common of the four groups, affects approximately 6.3% of pregnant women. Pelvic girdle syndrome affects approximately 6% of pregnant women and is diagnosed in women with daily pain in all three pelvic joints. One-sided SIJ syndrome is the next most common, affecting 5.5% of pregnant women, and finally, symphysiolysis or pubic symphysis pain affects 2.3% of pregnant women.
Diagnosis and Physical Examination
History and physical examination are the primary diagnostic tools for evaluation of the pregnant patient. A pain history should focus careful attention to previous history of low back pain or pelvic trauma. PGP is typically unilateral or bilateral posterior pelvic pain near the SIJs, but may also involve the lower abdominal area near the pubic symphysis. Radicular leg pain or paresthesias, groin pain, difficulty with weight bearing, and new onset bowel or bladder symptoms may be red flags of other underlying pathology.
Physical examination should include a general examination, neurologic examination of the lower extremities, and musculoskeletal examination of the pertinent areas of the patient’s complaints, generally including the spine, pelvis, and hips. The external pelvic examination should focus on the SIJs and the pubic symphysis. The external pelvic examination should include palpation of the long dorsal ligament and pubic symphysis. Provocative pain testing for the SIJs should include the Patrick (FABER) test, posterior pelvic pain provocation (P4 or PPPP), and the Gaenslen test. Pain provocation testing of the pubic symphysis can be done using the modified Trendelenburg test. Functional stability testing should also be performed with the active straight leg raise test. Rectal examination can be performed if there is concern for coccydynia or pelvic floor disorder; however, vaginal examination of the pelvic floor should be avoided during pregnancy unless approved by the patient’s obstetrician.
Treatment
The mainstay of treatment for PGP is individualized PT that includes realignment and stabilizing exercises. Pelvic floor PT, especially with external biofeedback or intrarectal treatments, can be performed with the obstetrician’s permission if the patient has PFM overactivity. Pelvic manipulations and SIJ belts have been beneficial for symptomatic relief but do not alter the course of the disease. There is no evidence for massage, specific pillow use, education apart from PT treatment, or bed rest in the treatment of PGP. Ice and acetaminophen are also often used in this patient population. Lidoderm patches and cyclobenzaprine are pregnancy class B and can be used for symptomatic relief. Low-dose opioids are generally considered safe and may be necessary when severe pain does not respond to other rehabilitation treatments. NSAIDs are not thought to be safe for use during pregnancy, but may be resumed in the postpartum period, even when breastfeeding. Approximately 6 weeks after delivery, the postpartum patient can be further evaluated and treated with both pelvic girdle and pelvic floor PT if there is remaining pelvic floor myofascial pain and/or dysfunction (as discussed earlier).
Pelvic Nerve Injuries
Definitions and Etiology
Neural injury can be a source of CPP and can coexist with pelvic floor dysfunction and pelvic floor myofascial pain. The iliohypogastric, ilioinguinal, genitofemoral, and pudendal nerves most commonly contribute to pelvic pain symptoms. Pudendal neuropathy has also been implicated as a potential cause of urinary incontinence and FI, as well as sexual dysfunction. The anatomy of these nerves has been reviewed earlier.
The iliohypogastric and ilioinguinal nerves are particularly susceptible to injury if a Pfannenstiel or low transverse incision is dissected too far laterally beyond the edge of the rectus abdominis muscles. Neuroma formation is common after such nerve damage and can be a source of chronic pain. The genitofemoral nerve can be damaged via compression during gynecologic surgery, often by poor placement of self-retaining retractors. All three of these nerves are thought to be common causes of chronic groin pain after surgery for inguinal hernia repair.
Injury to the pudendal nerves during vaginal delivery has been well reported in the literature, and pudendal neuropathy has been implicated as a possible contributing factor to new onset postpartum urinary incontinence and FI. The pudendal nerve can also be injured in pelvic surgeries (particularly with the use of vaginal mesh), in cases of pelvic trauma, with bicycle riding, with chronic straining to defecate, and during anal intercourse.
Epidemiology
Overall incidence of ilioinguinal and/or iliohypogastric nerve injury after a Pfannenstiel incision has been estimated at 2% to 4%. The incidence of chronic groin pain after hernia repair attributable to injury of one of these three nerves is thought to be as high as 16%, with 6% to 8% of all patients after herniorrhaphy having moderate-to-severe, disabling symptoms.
Reported incidence of pudendal neuralgia in the general population has ranged from 1% to 4%. Allen et al. recruited a group of 75 women who agreed to pudendal nerve terminal motor latency testing and needle electromyography (EMG) of the external anal sphincter at 36 weeks’ gestation and again at 2 months’ postpartum. While pregnant, pudendal neurophysiology testing was normal, but EMG evidence of pelvic floor reinnervation potentials were seen in 80% of the postpartum women.
Diagnosis and Physical Examination
Having a high index of suspicion is the key to diagnosing a pelvic nerve injury. The history is often more helpful than the physical examination. The symptoms of iliohypogastric and ilioinguinal neuralgia typically include pain in the lower abdomen, groin, or pubis. There can be accompanying numbness. Genitofemoral neuralgia is also often described as pubic or groin pain, but can also be appreciated as labial or scrotal/testicular pain. If the femoral branch of the genitofemoral is involved, there can be pain in the upper anterior thigh. Symptoms of pudendal neuralgia include perineal pain and pain medial to the ischial tuberosity. Symptoms are most often unilateral. The pain is most often described as burning, with occasional numbness or paresthesia. Pain is worse with sitting, dyspareunia is common, and patients may report a sensation of a foreign body in the rectum or perineum.
Many patients with pelvic nerve injury will also have pelvic floor myofascial dysfunction; it can be difficult to determine on physical examination whether the muscles or the nerves are the source of the pain. Many patients with pudendal neuralgia are thought to have significant PFM overactivity, which in turn compresses the small, infiltrating branches of the pudendal tree, producing the characteristic burning sensation even in the absence of a true pudendal nerve lesion or entrapment. It should be noted that, despite the anatomic function of the pudendal nerve, in many cases of pudendal neuralgia, there is no objective sensory loss and anal sphincter tone, and other neurologic examination testing may be normal in all but the most severe cases. The Nantes criteria are a validated set of clinical conditions which, when met, make it likely that the patient has pudendal neuralgia.
The iliohypogastric, ilioinguinal, genitofemoral, and pudendal nerves can be evaluated electrophysiologically via a number of different methods. Unfortunately, these nerves are technically difficult to study; therefore these studies are not routinely used. Pudendal nerve terminal motor latency can be obtained through the use of a St. Mark electrode, with nerve stimulation at the ischial spine and recording of muscle contraction response at the external anal sphincter. The usefulness of pudendal nerve terminal motor latency has been questioned, because it has been shown to have a high rate of interobserver and intraobserver variability. Needle EMG of the external anal sphincter or bulbospongiosus muscles can be performed. The bulbocavernosus reflex latency can also be obtained by stimulating at the clitoris or penis. Electrodiagnostic testing for pudendal neuropathy may be less well tolerated than standard nerve conduction studies and needle EMG of the extremities.
Diagnostic nerve blocks are a potentially good option for diagnosis. A positive response to infiltration of a local anesthetic around the iliohypogastric, ilioinguinal, and genitofemoral nerves is thought to be a reliable indicator of etiologic correlation. It is less clear that a positive response to a pudendal block is definitively correlated with true pathology. It is always preferable to use ultrasound, pulsed radiofrequency, or ideally computed tomography (CT) guidance for better accuracy when performing these diagnostic injections.
Ultrasound, in general, is not particularly useful for evaluating nerve injuries about the hip and pelvis, because these nerves are typically too deep to allow for long segment exploration and good visualization. MR neurography technology is rapidly becoming recognized as one of the most effective diagnostic tools for nerve injury and is thought to be far superior for nerve visualization than standard MRI. MR neurography of the lumbosacral plexus is often able to demonstrate injury to the iliohypogastric, ilioinguinal, genitofemoral, and pudendal nerves. Figure 38-6 shows MR neurography images of a left genitofemoral neuropathy.
