Cheen Lum, PharmD

• Clinical Specialist in Behavioral Care, Community Hospital North
• Ambulatory Care Pharmacist�Behavioral Care, Community Health Network, Indianapolis, Indiana

Most of these symptoms may be a consequence of the normal anatomic and physiological changes that occur in pregnancy; however allergy treatment acupuncture rhinocort 200mcg free shipping, superimposed on these changes may be further pathological changes as a consequence of tissue damage allergy virus symptoms order rhinocort with paypal, from either pregnancy or labor allergy medicine comparison chart cheap rhinocort online visa, resulting in persistent symptoms allergy grocer order rhinocort uk. The distinction between normal physiological changes and transient or permanent pathophysiology is often not clear and may be a continuum allergy testing long island generic 100 mcg rhinocort otc. Anatomic and Physiological Changes the urinary tract undergoes both structural and functional changes during pregnancy and after delivery allergy be gone best purchase for rhinocort. These changes may be specific in response to pregnancy and, in some women, may be compounded by pathological changes that persist after delivery. In normal pregnancy, the kidneys increase by 1 cm in length due to an increase in vascular volume and interstitial space. Dilation of the ureters is a well-known phenomenon in pregnancy and hydroureter is noted in approximately 90% of pregnant women by the third trimester. This dilation is more marked on the right compared to the left side, probably related to the relative dextrorotation of the uterus. As a result, plasma creatinine, urea, and urate values are lower than the normal range for nonpregnant women. The bladder is passively drawn upward and anteriorly as the uterus enlarges, resulting in lengthening of the urethra [51]. The urethral mucosa becomes more hyperemic and congested in pregnancy in response to the increase in circulating estrogen levels. After delivery, cystoscopy of the bladder shows changes such as mucosal congestion, submucosal hemorrhage, and capillary oozing, especially around the bladder neck, trigone, and ureteric orifices. These changes have been seen in association with a decrease in bladder sensation and tone [52] and are most marked in those who underwent vaginal delivery [53]. Studies assessing bladder capacity have revealed conflicting results, with most early studies using simple cystometry only. Muellner [54] reported an increase in bladder capacity to an average of 1300 mL in the third trimester due to bladder hypotonia, with a return to normal values postpartum. However, other investigators found no change in bladder capacity in the first trimester and a reduced bladder capacity in the third trimester in association with increased detrusor irritability, rather than bladder hypotonia [55]. Dual-channel cystometry studies have found that all urodynamic variables, such as first sensation and maximum bladder capacity, are lower in pregnancy and postpartum compared to a nonpregnant population, and this may account for symptoms of frequency, nocturia, and urgency [56]. Normal nonpregnant 917 women void between four and six times per day and rarely at night. Using a definition of frequency as at least seven daytime voids and one nighttime void, Francis [55] studied the voiding habits in 400 healthy women during and after an uncomplicated pregnancy and compared them with 50 healthy nonpregnant patients of similar age. Frequency was reported by 59% in early pregnancy, 61% in midpregnancy, and 81% in late pregnancy. Parboosingh and Doig [57] defined nocturia as at least three nighttime voids and, following the questioning of 873 healthy antenatal patients, found that nearly 66% experienced nocturia by the third trimester. The cause of frequency was not related to bladder capacity or the effect of posture, but due to the polydipsia and polyuria of pregnancy [57]. Both fluid intake and output rise rapidly in the first trimester, remaining constant until the third trimester, when a decrease in sodium excretion leads to a decrease in output. Despite this, frequency persists related to the pressure on the bladder by the uterus. There was no correlation between the maximum voided volumes and diurnal frequency and nocturia. Parboosingh and Doig also measured mean urine flow and solute excretion in 24 hour and overnight collections in 100 normal and nonpregnant women. An increase in sodium excretion was the major reason for increased nighttime voiding as well as the mobilization of dependent edema at night in the recumbent position. Voiding Difficulties Urinary hesitancy may be found in up to 27% of patients in the first two trimesters [59]. Fischer and Kittel [60] assessed flow rates in 290 women during pregnancy and found that there was a significant increase in peak flow rates in the second and third trimesters compared to controls and early pregnancy, but these higher flow rates were associated with larger voided volumes. Urinary retention can occur in pregnancy associated with the enlargement of a retroverted uterus with subsequent entrapment of the fundus below the sacral promontory. This retention usually resolves by 16 weeks gestation as the uterus grows out of the pelvis and can be managed in the interim with either bladder drainage or intermittent selfcatheterization. Alternatively, manual reduction of the uterus can be performed or a Hodge pessary may be inserted to maintain uterine position and relieve the obstruction on the bladder neck. Risk factors include a first labor, instrumental delivery epidural analgesia, and a longer duration of labor (800 minutes) [62]. Studies have looked at sensation after delivery [63] and found that the bladder can take up to 8 hours to regain sensation after the last top-up of an epidural. Overdistension of the bladder may occur during this period, leading to permanent detrusor dysfunction. Urinary Incontinence Incontinence is a common symptom associated with pregnancy and has been reported in up to 85% of women [64]. Francis [63] found that in the first trimester of pregnancy 16% of women complained of stress incontinence and 34% in the second half of pregnancy. Viktrup and Lose [8] interviewed 305 primiparae and found that 39% had stress incontinence before, during, or after pregnancy and 7% developed de novo stress incontinence after delivery. The association with these obstetric risk factors was lost by 3 months postpartum. However, in a subsequent follow-up study of the original cohort of 278 women, they reported a prevalence of stress incontinence of 30% at 5 years. In those without symptoms after the first delivery, the incidence was 19%; however, in those who reported stress incontinence 3 months after the first delivery, there was a 92% risk of having stress incontinence 5 years later [8]. A prospective cohort study of 949 women undertaken to find risk factors for postpartum stress incontinence at 3 months 918 found that urinary incontinence was experienced by 22. New onset urinary incontinence was more common in parous compared to nulliparous women. This study highlights the high proportion of women who suffer from urinary incontinence as 15. It confirms previous data that have found that the presence of antenatal and prepregnancy stress incontinence seems to increase the risk of future stress incontinence [66,67]. The pattern of the development of incontinence during pregnancy, with rapid postpartum recovery followed by a steady decline of continence over time, suggests a dual mechanism of nerve and tissue damage. The evidence regarding the contribution of obstetric factors to the development of stress incontinence is conflicting. The data are unclear whether it is pregnancy or the birth itself that is the major contributor to postpartum incontinence. Some investigators have found a relationship with the duration of the second stage of labor [68,69] and birth weight [1]. However, most of these studies are relatively small population studies that differ widely in their questioning techniques and definition of stress incontinence. Thus, pregnancy itself rather than the mode of delivery may also be an etiological factor in the development of urinary incontinence. Epidural analgesia has been reported to be more protective than pudendal block against postpartum stress incontinence [90]. However, this has not been supported by other research that has found a higher incidence of stress incontinence in those who received epidural analgesia than those who did not [92]. Changes in the Lower Urinary Tract and Pelvic Floor Related to the Development of Incontinence the exact etiological mechanism of stress incontinence is unclear and probably multifactorial, related to nerve damage and/or physiological and structural changes of the lower urinary tract. Functional Changes Iosif and Ulmsten [72] compared urethral pressure profile measurements in pregnant women with stress incontinence with continent healthy women from an earlier study. The maximum urethral closure pressure increased to 93 cmH2O at 38 weeks and then dropped to prepregnancy values of 69 cmH2O postpartum. These changes were not seen in women complaining of incontinence and are postulated to be a mechanism whereby continence is maintained despite an increase in intravesical pressure in pregnancy. This corresponds with other studies that have shown evidence of low urethral pressure in nonpregnant women with stress incontinence [59,73]. This increase in urethral closure pressure may be the result of an increase in urethral sphincter volume from increased blood flow. There is also an increase in the amplitude of vascular pulsations recorded from the urethral wall, especially in the first 16 weeks of pregnancy, which may be related to an increase in blood volume in pregnancy. Pregnant women with urodynamic stress incontinence showed a decrease in the amplitude of vascular pulsations in the periurethral plexus compared to continent women, suggesting that this affects urethral closure pressure [74]. Three-dimensional imaging of the urethral sphincter after vaginal delivery shows a reduction in sphincter volume, which has been implicated in the development of stress incontinence [75]. The mean values for urodynamic variables in the third trimester and postpartum were lower than the values defined in a nonpregnant population and not related to obstetric or neonatal variables (Table 58. However, despite the high prevalence of symptoms in this study, there was poor correlation between symptoms and urodynamic findings, which agrees with data in nonpregnant women [76]. Therefore, these observed changes in bladder function were consistent with a pressure effect of a gravid uterus and not related to mode of delivery or neonatal factors. Nerve Damage Patients with urodynamic stress incontinence have been shown to have abnormal conduction in the perineal branch of the pudendal nerve, which innervates the periurethral striated muscle and pubococcygeus muscle [77,78]. This damage is likely to lead to a loss of striated muscle of the urethral sphincter [79]. The degree of pudendal nerve damage was greater in multiparous women and correlated with the use of forceps and a longer second stage of labor [77,78]. In 60% of these women, pudendal nerve latency had returned to normal at 2 months postpartum [12]. Using concentric needle electromyography and pudendal nerve conduction tests, Allen et al. Electromyography of the right and left pubococcygeus muscle has shown that childbirth induces both qualitative and quantitative changes, demonstrating sphincter weakness can be attributed to not only the loss of motor units but also the asynchronous activity in those units that remain [80]. Structural Changes Ultrasound studies have shown changes in bladder neck position and the urethral sphincter in relation to delivery. Alterations in the urethral sphincter closure mechanism have previously been described in association with stress incontinence. They found that vaginal delivery was related to an increased bladder neck mobility and 920 larger levator hiatus, with both antenatal and postpartum mobility greater in women who delivered vaginally. These results are interesting but their long-term consequences are unclear as the findings were not related to symptoms. The authors postulated that the larger sphincter volume in pregnancy was a function of the tissue and hormonal effects of pregnancy. This supports previous observations that increased bladder neck mobility is associated with vaginal delivery. It has been suggested that there may be a group of women at an inherent increased risk of developing incontinence due to abnormalities in collagen [83], as the collagenous component of the connective tissue contributes to structural support of the bladder neck. In pregnancy, the tensile properties of the connective tissue are reduced, with a reduction in total collagen content and increase in glycosaminoglycans [57]. Changes in collagen may result in greater mobility of the bladder neck resulting in stress incontinence. In a study of 116 primigravidae, perineal ultrasound was used to assess bladder neck mobility. Approximately 50% of this group reported stress incontinence at 3 months postpartum [84]. This estimate for fecal incontinence is conservative, as it did not inquire about incontinence of flatus that is probably more common and has been reported to be as high as 29% at 9 months after delivery in one study of 349 primiparous women [87]. Despite the high number of women with incontinence, only a few had sought medical advice. Changes in the Anal Canal and Pelvic Floor Related to Anal Incontinence the etiology of postpartum anal incontinence is complex and both nerve and mechanical trauma have been implicated. Nerve Damage Denervation injury of the pelvic floor may occur from traction and straining during vaginal delivery, similar to the mechanism of nerve damage reported in patients with chronic constipation, which may result in anorectal incontinence [89]. In 80% of women with idiopathic anorectal incontinence, there is histological evidence of denervation of the striated pelvic floor muscle, particularly the puborectalis and external anal sphincter muscles [90]. Serial measurements of pudendal nerve terminal motor latencies in patients with idiopathic anorectal incontinence show progressive damage from recurrent stretch injury during straining at stool [91]. The presence of neuropathy has been found to be related to the length of the second stage of labor, size of the baby, and instrumental delivery [92]. However, no relationship between abnormal neurophysiology and symptoms of anal incontinence was shown. These allow the detection of differences in touch, temperature, and pain in the anal canal. The rectum has a configuration of nerve plexuses that serve as specialized sensory receptors for distension for perception of fullness, urgency to defecate, and pain [94,95]. It is believed that sensory information is critical to the preservation of continence, and in patients with fecal incontinence, there is a significant reduction in the ability to perceive electrical and other forms of stimulation [96]. In pregnancy, however, the role of anal sensation is unclear as deficits in anal canal sensation appear to be transient and unrelated to the development of incontinence [97].

The theory of potassium cycling allergy testing cpt rhinocort 200mcg discount, developed from this allergy testing lynchburg va cheap rhinocort american express, suggests that potassium diffuses into the bladder interstitium once the epithelium permeability is impaired allergy report austin purchase 200mcg rhinocort free shipping. A patient with no symptoms who has a normal bladder epithelium would not be experiencing any symptoms when potassium is instilled gluten allergy symptoms joint pain purchase rhinocort in india, while a patient with impaired bladder epithelium will experience symptoms with potassium instillation [32] allergy medicine urinary retention order rhinocort us. This may be associated with daytime as well as nighttime frequency zocor allergy symptoms discount rhinocort 100 mcg with mastercard, nocturia, and urgency. The disease may be progressive but often presents in cycles of flares and remission. Flares may be provoked by a number of factors including sexual activity, hormonal fluctuations, and physical and emotional stress [31,37]. It impairs quality of life and causes depression, sleep deprivation, and difficulties with sexual intercourse [25,50]. A history should be taken to establish the duration of symptoms and elucidate if there are other associated symptoms that would suggest an alternative diagnosis. A previous history of bladder disease, pelvic surgery, or other medical illnesses including irritable bowel syndrome and autoimmune disease should also be established. Examination is often more helpful in excluding other conditions that can cause similar symptoms. Women who complain of vaginal or vulval pain should be examined with pain mapping of the vulval region and for tenderness in the urethra, bladder, and levator and adductor muscles of the pelvic floor [53]. Urine Studies Urine culture is essential to exclude simple urinary tract infection as well as atypical infections caused by Ureaplasma urealyticum, Mycoplasma hominis, or Chlamydia trachomatis. Cytology is recommended if hematuria is present or if there are risk factors for bladder cancer (smoking, age, family history, and occupational exposure to certain industrial chemicals such as aromatic amines). If there is sterile pyuria, culture for tuberculosis and fastidious organisms should be performed. It does, however, address some quality of life issues unlike the other two questionnaires and could therefore prove to be clinically useful. It does not, however, address the relationship between these symptoms and sexual activity or more general issues. It includes questions on frequency, urgency, and pain in both the bladder and pelvis and tries to assess the amount of bother caused to the patient by these symptoms. As yet, none of the questionnaires has been shown to be of value in terms of diagnosis [21]. Fluid intake and output is recorded by the patient in the diary for initial evaluation. Voiding diaries help to assess the degree of frequency, nocturia, and volumes voided at each episode. They are also useful in the identification of polydipsia and polyuria, which cause urinary frequency. They help to ascertain the highest functional capacity, which is usually the maximum voided amount and patient sensation at each void. It is not performed routinely if the diagnosis is certain from the history but is reserved for select cases where the diagnosis is uncertain. Cystoscopy Cystoscopy and biopsy is used to exclude diagnosis of bladder cancer or urethral diverticulum in those with risk factors or suggestive symptoms. Glomerulations have been identified in the bladders of patients without bladder disease or bladder pain [10,55]. This is often difficult to achieve as the etiology of the disease is not well understood. The available treatment strategies can be classified into conservative, bladder instillation therapy, medical, and surgical. Treatment strategies should proceed using more conservative therapies first; surgical treatments are generally reserved for intractable disease that has not responded to other treatment modalities. They should be made aware of the fact that no single treatment is curative and that symptom control may require a trial of multiple therapeutic options (including combination therapy) before it is achieved [43]. For selected group of highly motivated patients in whom the predominant complaint is urinary frequency, behavioral modification in the form of timed voiding, controlled fluid intake, keeping a bladder diary, pelvic floor muscle training, and bladder retraining may be beneficial. Dietary Manipulation Avoidance of certain foods appears in some patients to improve their symptoms. Although the clinical data are lacking many, patients have reported benefit from dietary alteration. Caffeinated or alcoholic drinks, spicy foods, and citrus fruits have all been reported to aggravate symptoms. Where possible, the stress-inducing factor should be removed or reduced as much as possible. Cystoscopy and Hydrodistension under Anesthesia this is considered to be both diagnostic and therapeutic. It is also thought to be therapeutic as it has been shown to provide symptomatic relief in some patients. Its effects are, however, only short lasting and so it is not considered first-line treatment [7,29]. Oral Therapy Amitriptyline this is a tricyclic antidepressant commonly used for pain management. Its analgesic effect is thought to be due to its ability to inhibit serotonin and noradrenaline reuptake in the central nervous system. Side effects including fatigue, weight gain, and dry mouth are a common reason for patients to stop treatment. It is available in oral formulation and given at dosage of 100 mg three times daily. Intravesical Treatments Intravesical treatments involve direct administration of the drug into the bladder. They are usually used alone as second-line treatment or in conjunction with oral therapy and other forms of conservative management. Botulinum Toxin A this is a potent neurotoxin derived from the bacterium Clostridium botulinum. Until further evidence from larger trials become available, botulinum toxin is not recommended for use outside of carefully controlled clinical trials. Other intravesical treatments that have been used include resiniferatoxin, capsaicin, lignocaine, and oxybutynin. Neuromodulation Sacral nerve stimulation is often used in the management of patients with detrusor overactivity. It is a minimally invasive procedure that involves stimulation of the S3 or S4 nerve root by a mild electric current. Surgery Surgery is reserved for severe cases that have refractory to all other treatment options. Available surgical treatments include bladder augmentation cystoplasty, cystectomy, and urinary diversion. Patients typically complain of pain in the bladder or pelvic area associated with urinary frequency or urgency. Diagnostic adjuncts such as urinary analysis, urodynamics, and cystoscopy aid the diagnosis and exclusion of other confusable diseases. Management should commence with conservative measures such as behavioral modification and dietary modification followed by medical management with oral or intravesical therapy, which aims to provide symptomatic relief for pain and irritable bladder symptoms. More invasive treatments such as surgery should be reserved for refractory cases as they are associated with more morbidity. There is a limited role currently in clinical practice for neuromodulation and botulinum toxin. Although the results of available studies are promising, larger trials are required on the efficacy of these therapies. The standardisation of terminology of lower urinary tract function: Report from the standardisation sub-committee of the international continence society. Activated mast cells in proximity to colonic nerves correlate with abdominal pain in patients with irritable bowel syndrome. Prevalence of symptoms of bladder pain syndrome/interstitial cystitis among female adults in the United States. Are patient symptoms predictive of the diagnostic and/or therapeutic value of hydrodistension Sacral neuromodulation for the symptomatic treatment of refractory interstitial cystitis: A prospective study. Evidence for a mechanism of bacterial toxin action that may lead to the onset of urothelial injury in the interstitial cystitis bladder. Glomerulation observed during transurethral resection of the prostate for patients with lower urinary tract symptoms suggestive of benign prostatic hyperplasia is a common finding but no predictor of clinical outcome. Summary of the National Institute of Arthritis, Diabetes, Digestive and Kidney Diseases Workshop on Interstitial Cystitis. Potassium sensitivity test for painful bladder syndrome/interstitial cystitis: con. Bladder Pain Syndrome Committee of the International Consultation on Incontinence. Percutaneous sacral nerve root neuromodulation for intractable interstitial cystitis. Interstitial cystitis: Characterisation and management of an enigmatic urologic syndrome. Psychosocial phenotyping in women with interstitial cystitis/painful bladder syndrome: A case control study. Mast cell and substance p-positive nerve involvement in a patient with both irritable bowel syndrome and interstitial cystitis. Interstitial cystitis: Clinical manifestations and diagnostic criteria in over 200 cases. Prostatitis, interstitial cystitis, chronic pelvic pain and urethral syndrome share a common pathophysiology: Lower urinary dysfunctional epithelium and potassium recycling. A quantitatively controlled method of study prospectively interstitial cystitis and demonstrate the efficacy of pentosan polysulfate. Intravesical potassium sensitivity in patients with interstitial cystitis and urethral syndrome. Intravesical bacillus Calmette-Guerin and dimethyl sulfoxide for treatment of classic and nonulcer interstitial cystitis: A prospective, randomized double-blind study. The efficacy of intravesical bacillus Calmette-Guerin in the treatment of interstitial cystitis: Long-term follow up. Trigonal injection of botulinum toxin A in patients with refractory bladder pain syndrome/interstitial cystitis. Practical use of the New American Urological Association Interstitial Cystitis Guidelines. Mast cell involvement in interstitial cystitis: A review of human and experimental evidence. A prospective, randomised, placebo controlled, double blind study of amitriptyline for the treatment of interstitial cystitis. Cystoscopic findings consistent with interstitial cystitis in normal women undergoing tubal ligation. This chapter does not discuss upper tract infections, as knowledge on this subject is normally obtained during training in obstetrics. Cystitis is the general term used to describe inflammation of the urinary bladder. Bacterial cystitis is an inflammatory response to bacterial infection of the lower urinary tract. Bacterial cystitis may be acute, chronic, or recurrent as well as being simple or complex. The natural history is dependent on the type and virulence of the urinary pathogen, resistance to antimicrobial agents, and host defenses. Diagnosis in most simple cases is based on clinical symptoms, urine dipstick testing (which is controversial), preferably with laboratory confirmation by microscopy and/or culture. Management comprises identification of the causative organism and, based on the results of urine culture and sensitivity, at the same time prescription of an appropriate antimicrobial agent for a suitable length of time. In those women with recurrent or complex infections, more detailed strategies may be needed. When assessing the results of urine cultures, the clinician must distinguish between true bacteriuria and contamination of the urine as it passes through the distal urethral and introitus. The term "significant bacteriuria" was first defined in the late 1950s by Kass, a Harvard nephrologist. His goal was to determine a quantitative threshold that would accurately distinguish true bacteriuria (which he defined as "actual residence of bacteria within the urine of the urinary tract") from bacterial contamination ("the adventitious entry of bacteria into the urine during the collection of the specimen") [1]. Bacteria cultured from the "low-count" group frequently showed commensal organisms and a repeat urine sample taken from them rarely matched the original specimen. In contrast, counts of >105 were more consistent on repeat testing and known urinary pathogens were commonly isolated. He concluded that "patients with more than 105 bacteria per mL of urine may be regarded as having true bacteriuria" [1,2].

Similarly allergy testing bees rhinocort 200mcg overnight delivery, it can be very helpful for some patients to restrict fluids for a time when toilet access will be limited allergy research group buy genuine rhinocort on line, such as before a church service allergy chest pain purchase rhinocort online now. Women using such targeted fluid restriction should be reminded to compensate for these missed fluids earlier or later to ensure that their total daily fluid intake is adequate allergy treatment side effects discount rhinocort 200mcg fast delivery. In patients who consume an abnormally high volume of liquids allergy symptoms due to weather cheap rhinocort amex, fluid restriction is often appropriate allergy symptoms of low blood pressure 200 mcg rhinocort visa. Some patients maximize their fluid intake deliberately in the belief that they need to "flush" their 649 kidneys, to avoid dehydration, or in an effort to lose weight. It is not uncommon to see women carry a water bottle throughout the day taking frequent drinks for health reasons. In these cases, reducing excess fluids can relieve problems with sudden bladder fullness and urgency. Caffeine Reduction Caffeinated beverages in particular can exacerbate incontinence because in addition to its diuretic effect, caffeine is a bladder irritant for many people. Research has demonstrated that caffeine increases detrusor pressure [58] and that it is a risk factor for detrusor instability [59,60]. Although it is very difficult for most coffee drinkers to completely eliminate it from their diet, provided with the knowledge that caffeine may be aggravating their incontinence, many will be willing to reduce their intake or to eliminate it for a few days as a trial. Reducing caffeine intake can be done gradually by mixing decaffeinated beverages with caffeinated beverages in increasing increments. Avoiding Bladder Irritants Many clinicians recommend, even as a first-line approach, restricting certain foods and beverages that are believed to irritate the bladder, including sugar substitutes, citrus fruits, spicy foods, and tomato products. Although there is little scientific evidence on dietary factors, there are many cases in which these substances appear to be aggravating incontinence, and reducing or eliminating them has provided clinical improvement. A diary of food and beverage intake can sometimes be useful in identifying which substances are irritants for individual patients. Rather than recommending that all patients restrict their intake of these substances, a diary or trial restriction can help to identify which patients are sensitive and may chose to reduce their intake. Women with higher body mass index are not only more likely to develop incontinence, but they also tend to have more severe incontinence than women with lower body mass index. Research on the relationship between body mass index and incontinence reports that each five-unit increase in body mass index increases the risk of daily incontinence by approximately 60% [64,65]. Similarly, significant improvements in continence status have been demonstrated with as little as 5% weight reduction in more traditional weight loss programs [69]. Both groups received a booklet describing a step-by-step self-administered behavioral program to reduce incontinence. The weight loss program, which resulted in a mean weight loss of 8%, showed significantly greater reductions in number of incontinence episodes compared to the control group, which had a mean weight loss of 1. Because moderate weigh loss is an achievable goal for many women, it is rationale to recommend weight loss as a first-line treatment or as part of a comprehensive program to treat incontinence in overweight and obese women. Bowel Management Fecal impaction and constipation have been cited as factors contributing to urinary incontinence in women, particularly in nursing home populations [71]. In severe cases, fecal impaction can be an irritating factor in overactive bladder or obstruct normal voiding, causing incomplete bladder emptying and overflow incontinence. Disimpaction relieves symptoms for some patients, but it can recur in the absence of a bowel management program. Bowel management may consist of recommendations for a normal fluid intake and dietary fiber (or supplements) to maintain normal stool consistency and regular 650 bowel movements. When hydration and fiber are not enough, stool softeners or enemas may be used to stimulate a regular daily bowel movement, preferably after a regular meal such as breakfast to take advantage of postprandial motility. This reliance on patient behavioral change is perhaps the main limitation of this treatment approach. Like any new habit or skill, changing daily bladder habits and learning new skills require effort and persistence over time. It can be challenging for women to remember to use their muscles strategically in daily life as well as to maintain a regular exercise regimen for strength and skill. A key ingredient in addressing this challenge is to maintain contact with the patient during this period of time when her benefit is not yet appreciable. In addition, when initiating behavioral treatment, it is important to make it clear to the patient that her improvement, as with any new skill, will likely be gradual, with good days and bad days, and that it will depend on her consistent practice. The patient who expects this course of treatment will be better prepared to persist over time so that results can be achieved and maintained long term. Most patients who engage actively with behavioral treatment for incontinence experience some degree of improvement, yet there is considerable variation in outcomes. Little is known to help us predict which patients will respond best to behavioral treatment. Most studies examining predictors of success have found that outcomes are not related to the type of incontinence or urodynamic diagnosis [13,52,55,75,76]. Some studies show that patients with more severe incontinence have greater improvements [52,72], but others conclude that patients with more severe incontinence have poorer outcomes [22,72,76] or no relationship between severity and outcome [24,55,75,77]. Current evidence indicates that outcomes are not associated with patient race, parity, body mass index, cystocele, uterine prolapse, hysterectomy, hormone therapy, use of diuretics, or urodynamic parameters [76]. There is little information in the usual clinical evaluation of a patient with incontinence that would indicate the likelihood of her success or failure with behavioral treatment. Thus, given that behavioral therapies are virtually without risk and most adherent patients experience symptom improvement, offering behavioral treatment as first-line therapy is appropriate for any woman with urinary incontinence. Moore K, Dumoulin C, Bradley C, Burgio K, Chambers T, Hagen S, Hunter K, Imamura M, Thakar R, Williams K. Progressive resistance exercise in the functional restoration of the perineal muscles. Urinary incontinence in the elderly: Bladder-sphincter biofeedback and toileting skills training. A comparison of effectiveness of biofeedback and pelvic muscle exercise treatment of stress incontinence in older community-dwelling women. Efficacy of biofeedback when included with pelvic floor muscle exercise treatment for genuine stress incontinence. Efficacy of pelvic floor muscle exercises in women with stress, urge, and mixed urinary incontinence. Single blind randomized controlled trial of pelvic floor exercises, electrical stimulation, vaginal cones, and no treatment in management of genuine stress incontinence in women. A randomized controlled trial of pelvic floor muscle exercises to treat postnatal urinary incontinence. Postnatal incontinence: A multicenter, randomized controlled trial of conservative treatment. Conservative management of persistent postnatal urinary and faecal incontinence: A randomized controlled trial. Effect of postpartum pelvic floor muscle training in prevention and treatment of urinary incontinence: A one-year follow-up. Effect of behavioral training with or without pelvic floor electrical stimulation on stress incontinence in women: A randomized controlled trial. Behavioral versus drug treatment for urge incontinence in older women: A randomized clinical trial. Evidence for benefit of transversus abdominus training alone or in combination with pelvic floor muscle training to treat female urinary incontinence: A systematic review. Adherence to behavioral interventions for urge incontinence when combined with drug therapy: Adherence rates, barriers, and predictors. Adherence to behavioral interventions for stress incontinence: Rates, barriers, and predictors. Comparisons of approaches to pelvic floor muscle training for urinary incontinence in women. An assessment of the Frewen regime in the treatment of detrusor dysfunction in females. A controlled trial of bladder drill and drug therapy in the management of detrusor instability. The management of urinary incontinence due to primary vesical sensory urgency by bladder drill. Assessment and treatment of female urinary incontinence by cystometrogram and bladder retraining programs. Oxybutynin and bladder training in the management of female urinary urge incontinence: A randomized study. Comparative efficacy of behavioral interventions in the management of female urinary incontinence. Reliability assessment of the bladder diary for urinary incontinence in older women. Dietary caffeine intake and the risk for detrusor instability: a case-control study. The effect of behavioral therapy on urinary incontinence: A randomized controlled trial. Predictors of outcome in the behavioral treatment of urinary incontinence in women. Effects of pelvic floor muscle training on strength and predictors of response in the treatment of urinary incontinence. In Western countries approximately 10% of all adult women report leakage at least weekly [1]. Others report a prevalence of any urinary incontinence of 22% [4] to 29% [1] in older women, severe urinary incontinence in 7% [1]. Urinary incontinence is associated with nursing home admission from the community [6]. The annual incidence of "monthly" or "any" urinary incontinence varies between 1% and 19%, for "weekly" urinary incontinence between 1. Mainly due to shame, taboo, and unawareness of treatment possibilities, only a minority of people suffering from incontinence seek professional help [9,10]. In daily general practice, patients usually go for help when the loss of urine leads to mental, physical, or social problems or discomfort for the patient or his or her social environment. Because of more and better patient information, in the Netherlands now about half of the women suffering from urinary incontinence consult a medical doctor [10]. Symptoms of the latter are urgency, frequent micturition, nocturia, and/or urgency incontinence [11]. Combinations of the aforementioned symptoms of stress and urgency incontinence are considered to reflect mixed incontinence [12]. A patient suffering from stress incontinence usually has a normal voiding frequency (less or equal than eight times in 24 hours) and bladder volume and has mean micturitions between 200 and 400 cc/void, but with neither urgency nor micturition. A patient with urgency incontinence usually loses more urine (up to the complete content of the bladder) than a patient with stress incontinence. On the other hand, the patient may void less than 150 mL urine during micturition, suggesting a reduced functional capacity of the bladder. Incontinence has several treatment options such as physiotherapy, drug treatment, and surgical procedures. For the time being, little is known about the implementation of these guidelines and their use in daily practice [16]. For patients with incontinence, physiotherapy is often considered as first-line treatment due to its noninvasive character, the results in terms of symptom relief, the possibility of combining physiotherapy with other treatments, the low risk of side effects, and the moderate to low costs. Important restrictions are that the success depends on the motivation and perseverance of both the patient and the physiotherapist and the time needed for therapy [16]. In this chapter, we review and discuss the diagnosis, analysis, evaluation, and therapeutic possibilities of physiotherapy for stress incontinence, urgency incontinence, and mixed incontinence. How many times in the last 7 days have you had an accidental leakage of urine onto your clothing, underwear, or pad during an activity such as coughing, sneezing, laughing, running, exercising, or lifting How many times in the last 7 days have you had an accidental leakage of urine onto your clothing, underwear, or pad with such a sudden strong need to urinate (United States)/pass water (United Kingdom) that you could not reach the toilet in time Specialists, like the urologist or the gynecologist may fall back on specific diagnostic tests such as urodynamic evaluation. However, because of its invasive character and doubts about its usefulness, reliability, and validity, the need for urodynamic testing is currently being discussed. A metaanalysis of primary care diagnostic methods of urinary incontinence (initial management) showed a sensitivity of 0. Moreover, the symptoms of incontinence may be vague and less clear-cut as compared to that which is written in textbooks. Altogether, this may impair the reliability of history taking and physical examination [13]. But in the initial management of urinary incontinence in women, in a lot of cases, the presumed medical diagnosis lacks accuracy, confronting the physiotherapists with heterogeneity or complexity of indications and unclear grade of severity, which might result in a minor degree of success or even failure. After a childbirth, stress incontinence sometimes goes together with a total denervation of the pelvic floor muscles or with great damage to surrounding connective and structural tissue. Next to pregnancy and birth dysfunction, incontinence can also develop as a result of a neurological problem and/or a trauma. For the majority, the pathophysiology of the health problem(s) determine(s) prognosis and result of treatment [36,37]. Also, other etiological and prognostic factors such as age, hysterectomy, estrogen depletion during menopause, chronic diseases such as diabetes mellitus, immobility, obesity, and number, duration, and mode of delivery play a role in incontinence [43]. If, and to what extent, there is a causal relationship between these factors and the incidence of incontinence is by far not clear yet [49,50].

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Diseases

• Hyperostosis cortical infantile
• Cerebellar hypoplasia endosteal sclerosis
• Lopes Gorlin syndrome
• Laryngeal neoplasm
• Myoglobinuria dominant form
• Photosensitive epilepsy
• Colobomata unilobar lung heart defect
• Leishmaniasis
• Polyneuritis