STUDY - Technical - New Dacian's Medicine
Urinary
Disorders, Incontinence and Bladder Pain
Translation Draft
As we announce you are at sea (Corbu, Constanta). I occupied the position for this post but I will only realize it on Monday because here there is no power source to use the laptop more time.
I'm going to start with the mymitating disorders. Normal bladder filling depends on the unique elastic properties of the bladder wall, which allow it to increase the volume to a pressure lower than that of the neck and urethra (otherwise incontinence would occur). Despite provocative manoeuvres, such as coughing or jumping on the heels, voluntary bladder contractions do not occur. Emptying is dependent on the integrity of a complex neuromuscular network that causes the ureteral sphincter to relax a few milliseconds before the detrusor (the bladder muscle) is reduced.
Under the conditions of a normal, sustained contraction of the detrusor, the bladder completely emptys. A bladder that can fill and empty in this manner has a normal detrusor muscle and is described, in accordance with current terminology, as stable.
Because voluntary control of motion depends on neural connections between the cerebral cortex and the brain stem, disruption of these paths (brain tumors, strokes, head trauma, Parkinson's disease) affects the ability to suppress and control bladder contractions. A bladder contraction "without the owner's permission" characterizes an unstable bladder. The instability of the bladder or detrusor of neurological origin is called hyperreflection of detrusor.
On the other hand, the detrusor muscle that cannot be contracted during discharge is called non-contractile or subreactive, and the subreactivity of the detrusor due to damage to the sacral marrow or pelvic nerves is called detrusor are called areflexia. These terms characterizing the function of the detrusor muscle and urethra have replaced the terms as atonic, hypotonic, autonomic or flasc, which refer to etiologies of dysfunction sometimes difficult to establish with certainty.
Contrary to the usual belief, the center that controls normal shrinkage is not located in the spinal cord but in the brain stem. Proper coordination (synergy) between the detrusor and the urethral sphincters requires intact neural communication (vegetative and somatic nervous systems) between the bladder and the urethra. Damage to the upper spinal cord, for example, can cause dyssynergy between the bladder and urethra, which results in incontinence, residual urine retention, changes in the bladder wall (traberculation and fibrosis) and possibly renal failure.
A simple way to classify exhaust dysfunctions is to determine whether we mainly have a storage failure or a emptying failure, given two milestones: 1. exhaust dysfunction is due to the bladder or orifice (vescal neck or urethra) - storage failure or 2. is the neurologically free patient - emptying failure. Problems of bladder storage and emptying may coexist in the same individual and may cause similar lower urinary tract (STUI) symptoms.
The most common cause of STUI in middle-aged and elderly men is prostatic hyperplasia, which causes obstruction of urinary flow by occupying the urethral lumen. Histologically, 50-80% of the prostate volume is composed of stromal tissue (smooth muscle), and what remains is glandular tissue. The transitional area, which is responsible for benign prostate growth, comprises 10-15% of the prostate at the end of puberty, but increases in volume after the age of 40.
However, enlargement of the prostate is not always accompanied by symptoms because the direction of growth can be external, so small changes in urinary flow (at least up to a certain prostate volume) may occur. In contrast, men with early histological signs of prostatic hyperplasia may experience significant evacuation symptoms. The reason for the latter phenomenon is believed to be an increased tone of the smooth prostate muscle, possibly due to an increase in the number of alpha-adrenergic receptors (in this situation, increased prostate tension inside an undistenible prostate capsule can cause obstruction).
In response to obstruction, smooth bladder muscle cells hypertrophate to generate more pressure required for evacuation, and increased bladder muscle mass leads to low elasticity or compliance and low bladder capacity. Detrusor dysfunction due to obstruction of the bladder cervix may cause any combination of STUI described above. When obstruction progresses, the infiltration of the extracellular matrix between the smooth muscle bundles of the bladder wall may cause the appearance of a hypocontractile or acontractile bladder (vescal insufficiency).
During the course of an obstructive process, other complications may develop, such as urinary tract infections or bladder stones secondary to large postmytional residues (stasis) and upper tract conditions (hydronephrosis, reflux). Although prostatic hyperplasia is the most common cause of bladder obstruction in men, other sources of obstruction include prostate cancer, urethral strictures and lack of adequate sphincteral relaxation (neurological cause).
Nonobstructive causes of STUI include diabetic neuropathy, which can affect the parasympathetic nerves of the bladder. Decrease in the sensation of bladder filling leads to incomplete emptying and overdistension of the bladder and as such to increased frequency of shrinkage and nocturia due to bladder overflow (these symptoms are frequently worsened by polydipsia/ polyuria in diabetes mellitus). Sometimes storage symptoms can be caused by other neurological causes, such as strokes, multiple sclerosis or Parkinson's disease.
The international score for prostate symptoms (SISP) is routinely used in assessing the severity of STUI. This score is determined by "collecting" and evaluating the answers to a series of questions as follows: 1. low force of the jet (in the last month, often you had a weak urinary jet), 2. intermittance (in the last month, how often you have stopped and restarted several times during urination), 3. incomplete emptying (in the last month, how often have you felt that you have not completely emptied the bladder after you have finished urinating), 4. straining (in the last month, how often you had to strain to urinate).
The impact of storage symptoms is also assessed in sISP: 1. frequency (in the last month, how often you urinated again within 2 hours of the previous motion), urgency (in the last month, how difficult it was for you to postpone the motion) and 3. nocturia (in the last month, how many times you had to urinate between the time you went to bed and waking up in the morning - interval: never up to five or more times). With the exception of nocturia, answers take values between 0 (not at all) and 5 (almost always). A score below 8 indicates minimal discharge dysfunction (a score of 13 or more is usually required to recruit patients for pharmacological studies to treat benign prostate hyperplasia - HPB; in symptom score above 23 suggests a significant obstruction of the bladder outlet). Since similar symptoms may be the result of neurological causes, the SISP questionnaire cannot be used to diagnose prostate hyperplasia, but is used only as an index of severity and response to treatment.
In women, urethral obstruction is a rare cause of STUI. A careful biannual examination and the introduction of a urinary probe are sufficient to exclude urethral stenosis, which is usually secondary to previous instrumental maneuvers or a surgical procedure and urethral cancer. Urinary tract infection (cystitis) is much more common in women and should be excluded by urinary tests, and multiple sclerosis should be considered in middle-aged women with frequency, imperiousness or incontinence.
In addition, compared to the many similar conditions that cause evacuation symptoms in men, estrogen deficiency, frequency-imperiosity syndrome and interstitial cystitis (CI) with minimal pain should be taken into account. The cystocele and pelvic prolapse may cause mictional frequency secondary to damage to bladder emptying.
Men and women with STUI and concomitant neurological disease should undergo a complete urodynamic assessment. In the absence of a neurological disease, men with STUI most commonly have prostate hyperplasia. However, it is necessary to exclude prostate cancer, especially if there is a positive family history, abnormal rectal cough or a high level of specific prostate antigen (PSA). In both sexes, bladder cancer may give symptoms of storage and is suggested by microscopic hematuria and/ or abnormal urinary cytology.
Usually, a detailed genitourinary history, a symptom assessment, a careful neurological examination including rectal cough and evaluation of the bulbocavernos reflex, determinations of urinary flow and residual urinary volume after emptying (by bladder ultrasound) and limited laboratory measurements (urinary analyses, urinary cultures, PSA levels, urinary cytology, urea/ creatinine levels, as appropriate) should be sufficient to direct therapy. Sometimes more complex investigations of the lower urinary tract (cystoscopy, myctional cystography, urodynamic analyses) and upper urinary tract (pielography or ultrasound) are indicated.
It's the "turn" of incontinence. This is a condition in which involuntary loss of urine is actually demonstrated and is a social or hygiene problem. A common variant, stress incontinence, denotes involuntary loss of urine during physical exertion (cough, sneezing, sports, sexual activity). Impulse incontinence is an involuntary loss of urine associated with a strong desire to urinate, and overflow incontinence is an involuntary loss of urine when increasing intravescal pressure with overfilling or relaxation of the bladder exceeds the maximum urethral pressure. Loss of urine through channels other than the urethra is rare (ectopic ureter, fist) but causes total or continuous incontinence.
Urinary incontinence affects hundreds of millions of women, the number cannot be estimated due to the impossibility of obtaining a relevant statistic. Of women 60 years of age or older, non-institutionalized, 25-30% have incontinence daily or weekly, and about half of institutionalized women have incontinence more than once a day (annual costs for the care of people with incontinence being tens of billions of dollars). Urinary stress incontinence (IUS) is secondary to urethral hypermobility or, less commonly (less than 10%), intrinsic sphincteral impairment (CSI).
In female continents, the bladder and proximal urethra are supported by the anterior vaginal wall and its lateral grip to the lator muscles. Relaxation of the anterior vaginal wall causes urethral hypermobility, usually due to aging and/ or oestrogen deficiency, previous traumatic birth or pelvic surgery. Paradoxically, the woman may have clinical signs of urethral hypermobility, but without stress urinary incontinence. Some women have a bladder neck and a normal anatomical urethra, but still have IUS due to damage to the internal sphincter (fixed, rigid or "in pipe pipe"), caused by anti-incontinence surgery, pelvic irradiation or trauma or neurological diseases with urethra denervation. Urethral hypermobility and DSI may coexist in some patients and may cause persistence (or rapid recurrence) of incontinence after a simple suspension of the bladder cervix that remedyes hypermobility but leaves the sphincter untreated.
Impulse incontinence may be present alone or in combination with IUS (mixed incontinence). The cause of non-suppressible or uninhibited bladder contractions is usually idiopathic, but bacterial cystitis, bladder tumors, bladder opening obstruction and neurological bladder should be excluded. Overflow incontinence is due to either obstruction of the bladder outlet (rare in women), an acontractile bladder (diabetic neuropathy, multiple sclerosis), excessive relaxation of smooth muscles due to drugs (anticolinergics), or psychogenic retention.
In men, incontinence is less common than obstruction, but urgency and impulse incontinence can occur as a result of obstruction of the bladder outlet hole (as in prostatic hyperplasia), which damages the function of the smooth detrusor muscle and leads to instability of the detrusor. Men with neurological bladder (diabetic neuropathy, multiple sclerosis, Parkinson's disease, strokes) may develop impulse incontinence. Other causes, such as bacterial cystitis or bladder tumours, should be excluded. IUS in men is usually the result of radical prostatectomy for prostate cancer.
Transient urinary incontinence is common in the elderly (old). A mnemotechnic formula of Resnick describes its many causes, namely delirium, infection, atrophic urethritis, pharmacological, psychological, excessive urinary excretion (hyperglycaemia, congestive heart failure), restricted mobility and the effect of defecation (DIAPPERS). Impulse incontinence is the second most common condition in this age group and is attributed to the progressive loss of modulating influences of the frontal lobes of the cortex on the centers of motion in the brain stem.
The assessment of urinary incontinence in women should include: assessment of history and quality of life, a journal of urination, physical examination including a pelvic examination, analyses and urinary cultures and measurement of postmictional residual volume. For a patient with a blurred history or after previous pelvic anti-incontinence intervention, evaluation may include cytoscopy, urodynamic evaluation and imaging studies (lower and/ or higher urinary tract). History should define the onset, duration, evolution and triggering events of urinary loss.
Previous drug treatments, frequent motion schedules and exercise regimens should be noted. The severity of urinary incontinence is given by the recording of the number and type of tampons used per day or night and how incontinence affects daily activities (the questionnaire for the impact of incontinence). Information should be obtained about the amount and type of fluids consumed, sexual history (hormonal status, births, venereal diseases), gastrointestinal function (fecal incontinence, constipation) and urological history (bed watering, surgery).
Physical examination should place special emphasis on abdominal, genital, pelvic (associated prolapse) and neurological examination. IUS should be demonstrated by having the patient cough, strain or stand or squat. While leaks during a coughing fit confirm the IUS, the leakage after cough is due to bladder instability (stress-induced instability). IUS in the absence of urethral hypermobility raises the suspicion of a sphincter defect.
More complex tests are needed to determine whether the anatomy of the urethra is normal (assessment of urethral mobility, lateral visualization of the urethra in myctional cystourography, cytoscopy), whether urethral function is normal with proper closure (leak pressure point, urethral profilerometry, videourodynamic studies) or whether bladder function is normal (vescal volume based on a home-kept log, filling cystometrogram).
From a treatment point of view, mild stress incontinence can be treated non-surgically with drugs, hormonal supplements or biofeedback techniques. Ways such as urethral plugs and prostheses for the anterior vaginal wall are under investigation. Moderate to severe stress incontinence responds to surgical procedures focused on supporting the anterior vaginal wall (vaginal, laparoscopic or abdominal operations) or on increased urethral closure when stress incontinence is secondary to internal sphincter deficiency (periuretral injection of Teflon or collagen or insertion of an artificial urethral sphincter).
Impulse incontinence responds to the treatment of its cause, for example removal of the obstruction of the outlet. When it is due to neurological or idiopathic causes, anticholinergic agents are partially effective, although side effects such as dry mouth, blurred vision or constipation may limit their usefulness. Restricting fluid consumption (which should only be recommended with great caution) and bladder re-education through biofeedback can be helpful. In the absence of neurological diseases, more aggressive interventions such as bladder enlargement or urinary deviations are rarely necessary.
I will complete this long post with the presentation of some elements related to bladder pain. Painful bladder disease is a general term for any pathology that causes suprapubic, urethral or pelvic pain. Interstitial cystitis (CI) is the most common cause of bladder pain, but endometriosis, bacterial cystitis and obstructions of the outlet that cause bladder instability can mimic the symptoms of CI. CI is a chronic, severe bladder condition that causes frequent urination, nocturia and suprapubic pain. The disease usually affects women and is rare in the black race. Routine urinary cultures are uniformly negative, and symptoms do not respond to antibiotic therapy.
Etiology is probably multifactorial, with current assumptions including autoimmune reactions against bladder antigens, deficiencies in the glycosaminoglican layer on the bladder surface that allow supposed "toxins" to penetrate the mucosa, infiltration of mast cells and their activation, leading to the release of histamine and local damage to the bladder wall by "cryptic" bacteria. There are no universally accepted criteria for making the diagnosis, this being one of exclusion - infection, irradiation cystitis, urethral diverticules, herpes simplex infection and malignant diseases should be excluded.
Cytoscopy under anesthesia can join glomeulations (submucous vascular abnormalities) or the rare Encountered Hunner ulcer suggestive of CI (makes it possible to estimate bladder capacity - an important guide for treatment, allows biopsy of the bladder wall, when it is indicated and sometimes provides a therapeutic benefit with reduced pain and urinary frequency levels up to 6 months, rarely longer).
From an evaluation point of view, the frequency of urination and chronic bladder pain affect the quality of life to an extreme degree, although most patients have an undulating evolution (only 10% of patients have a constant progression of symptoms). The evaluation should include a detailed history, physical examination for the exclusion of neurological and gynecological pathology, myctional cystogram to exclude urethral defects and urodynamic tests to remove the neurological bladder, bladder instability or obstruction of the outlet and to document sensory instability.
It may be advisable to refer to specialists to exclude the pathology of the appendages, endometriosis or intestinal dysfunctions or to use modern pain treatment techniques in order to prevent drug dependence.
And finally, something about treatment... The empirical treatments that have been used include oral medication (amitriptyline, hydroxyzine) and intravescal agents (dimethylsulfoxide, chlorpactin and heparin). These measures may improve urinary symptoms and occasionally reduce pain, but do not alter long-term development. Surgery (augmentation cytoplasty, urinary derivatives) is indicated in less than 5% of cases because it is a chronic disease with occasional spontaneous remissions that do not threaten life. "Last-resort" interventions, such as excision of the bladder and urethra, are not a guarantee of success because some patients continue to have pelvic pain after that.
As we announce you are at sea (Corbu, Constanta). I occupied the position for this post but I will only realize it on Monday because here there is no power source to use the laptop more time.
I'm going to start with the mymitating disorders. Normal bladder filling depends on the unique elastic properties of the bladder wall, which allow it to increase the volume to a pressure lower than that of the neck and urethra (otherwise incontinence would occur). Despite provocative manoeuvres, such as coughing or jumping on the heels, voluntary bladder contractions do not occur. Emptying is dependent on the integrity of a complex neuromuscular network that causes the ureteral sphincter to relax a few milliseconds before the detrusor (the bladder muscle) is reduced.
Under the conditions of a normal, sustained contraction of the detrusor, the bladder completely emptys. A bladder that can fill and empty in this manner has a normal detrusor muscle and is described, in accordance with current terminology, as stable.
Because voluntary control of motion depends on neural connections between the cerebral cortex and the brain stem, disruption of these paths (brain tumors, strokes, head trauma, Parkinson's disease) affects the ability to suppress and control bladder contractions. A bladder contraction "without the owner's permission" characterizes an unstable bladder. The instability of the bladder or detrusor of neurological origin is called hyperreflection of detrusor.
On the other hand, the detrusor muscle that cannot be contracted during discharge is called non-contractile or subreactive, and the subreactivity of the detrusor due to damage to the sacral marrow or pelvic nerves is called detrusor are called areflexia. These terms characterizing the function of the detrusor muscle and urethra have replaced the terms as atonic, hypotonic, autonomic or flasc, which refer to etiologies of dysfunction sometimes difficult to establish with certainty.
Contrary to the usual belief, the center that controls normal shrinkage is not located in the spinal cord but in the brain stem. Proper coordination (synergy) between the detrusor and the urethral sphincters requires intact neural communication (vegetative and somatic nervous systems) between the bladder and the urethra. Damage to the upper spinal cord, for example, can cause dyssynergy between the bladder and urethra, which results in incontinence, residual urine retention, changes in the bladder wall (traberculation and fibrosis) and possibly renal failure.
A simple way to classify exhaust dysfunctions is to determine whether we mainly have a storage failure or a emptying failure, given two milestones: 1. exhaust dysfunction is due to the bladder or orifice (vescal neck or urethra) - storage failure or 2. is the neurologically free patient - emptying failure. Problems of bladder storage and emptying may coexist in the same individual and may cause similar lower urinary tract (STUI) symptoms.
The most common cause of STUI in middle-aged and elderly men is prostatic hyperplasia, which causes obstruction of urinary flow by occupying the urethral lumen. Histologically, 50-80% of the prostate volume is composed of stromal tissue (smooth muscle), and what remains is glandular tissue. The transitional area, which is responsible for benign prostate growth, comprises 10-15% of the prostate at the end of puberty, but increases in volume after the age of 40.
However, enlargement of the prostate is not always accompanied by symptoms because the direction of growth can be external, so small changes in urinary flow (at least up to a certain prostate volume) may occur. In contrast, men with early histological signs of prostatic hyperplasia may experience significant evacuation symptoms. The reason for the latter phenomenon is believed to be an increased tone of the smooth prostate muscle, possibly due to an increase in the number of alpha-adrenergic receptors (in this situation, increased prostate tension inside an undistenible prostate capsule can cause obstruction).
In response to obstruction, smooth bladder muscle cells hypertrophate to generate more pressure required for evacuation, and increased bladder muscle mass leads to low elasticity or compliance and low bladder capacity. Detrusor dysfunction due to obstruction of the bladder cervix may cause any combination of STUI described above. When obstruction progresses, the infiltration of the extracellular matrix between the smooth muscle bundles of the bladder wall may cause the appearance of a hypocontractile or acontractile bladder (vescal insufficiency).
During the course of an obstructive process, other complications may develop, such as urinary tract infections or bladder stones secondary to large postmytional residues (stasis) and upper tract conditions (hydronephrosis, reflux). Although prostatic hyperplasia is the most common cause of bladder obstruction in men, other sources of obstruction include prostate cancer, urethral strictures and lack of adequate sphincteral relaxation (neurological cause).
Nonobstructive causes of STUI include diabetic neuropathy, which can affect the parasympathetic nerves of the bladder. Decrease in the sensation of bladder filling leads to incomplete emptying and overdistension of the bladder and as such to increased frequency of shrinkage and nocturia due to bladder overflow (these symptoms are frequently worsened by polydipsia/ polyuria in diabetes mellitus). Sometimes storage symptoms can be caused by other neurological causes, such as strokes, multiple sclerosis or Parkinson's disease.
The international score for prostate symptoms (SISP) is routinely used in assessing the severity of STUI. This score is determined by "collecting" and evaluating the answers to a series of questions as follows: 1. low force of the jet (in the last month, often you had a weak urinary jet), 2. intermittance (in the last month, how often you have stopped and restarted several times during urination), 3. incomplete emptying (in the last month, how often have you felt that you have not completely emptied the bladder after you have finished urinating), 4. straining (in the last month, how often you had to strain to urinate).
The impact of storage symptoms is also assessed in sISP: 1. frequency (in the last month, how often you urinated again within 2 hours of the previous motion), urgency (in the last month, how difficult it was for you to postpone the motion) and 3. nocturia (in the last month, how many times you had to urinate between the time you went to bed and waking up in the morning - interval: never up to five or more times). With the exception of nocturia, answers take values between 0 (not at all) and 5 (almost always). A score below 8 indicates minimal discharge dysfunction (a score of 13 or more is usually required to recruit patients for pharmacological studies to treat benign prostate hyperplasia - HPB; in symptom score above 23 suggests a significant obstruction of the bladder outlet). Since similar symptoms may be the result of neurological causes, the SISP questionnaire cannot be used to diagnose prostate hyperplasia, but is used only as an index of severity and response to treatment.
In women, urethral obstruction is a rare cause of STUI. A careful biannual examination and the introduction of a urinary probe are sufficient to exclude urethral stenosis, which is usually secondary to previous instrumental maneuvers or a surgical procedure and urethral cancer. Urinary tract infection (cystitis) is much more common in women and should be excluded by urinary tests, and multiple sclerosis should be considered in middle-aged women with frequency, imperiousness or incontinence.
In addition, compared to the many similar conditions that cause evacuation symptoms in men, estrogen deficiency, frequency-imperiosity syndrome and interstitial cystitis (CI) with minimal pain should be taken into account. The cystocele and pelvic prolapse may cause mictional frequency secondary to damage to bladder emptying.
Men and women with STUI and concomitant neurological disease should undergo a complete urodynamic assessment. In the absence of a neurological disease, men with STUI most commonly have prostate hyperplasia. However, it is necessary to exclude prostate cancer, especially if there is a positive family history, abnormal rectal cough or a high level of specific prostate antigen (PSA). In both sexes, bladder cancer may give symptoms of storage and is suggested by microscopic hematuria and/ or abnormal urinary cytology.
Usually, a detailed genitourinary history, a symptom assessment, a careful neurological examination including rectal cough and evaluation of the bulbocavernos reflex, determinations of urinary flow and residual urinary volume after emptying (by bladder ultrasound) and limited laboratory measurements (urinary analyses, urinary cultures, PSA levels, urinary cytology, urea/ creatinine levels, as appropriate) should be sufficient to direct therapy. Sometimes more complex investigations of the lower urinary tract (cystoscopy, myctional cystography, urodynamic analyses) and upper urinary tract (pielography or ultrasound) are indicated.
It's the "turn" of incontinence. This is a condition in which involuntary loss of urine is actually demonstrated and is a social or hygiene problem. A common variant, stress incontinence, denotes involuntary loss of urine during physical exertion (cough, sneezing, sports, sexual activity). Impulse incontinence is an involuntary loss of urine associated with a strong desire to urinate, and overflow incontinence is an involuntary loss of urine when increasing intravescal pressure with overfilling or relaxation of the bladder exceeds the maximum urethral pressure. Loss of urine through channels other than the urethra is rare (ectopic ureter, fist) but causes total or continuous incontinence.
Urinary incontinence affects hundreds of millions of women, the number cannot be estimated due to the impossibility of obtaining a relevant statistic. Of women 60 years of age or older, non-institutionalized, 25-30% have incontinence daily or weekly, and about half of institutionalized women have incontinence more than once a day (annual costs for the care of people with incontinence being tens of billions of dollars). Urinary stress incontinence (IUS) is secondary to urethral hypermobility or, less commonly (less than 10%), intrinsic sphincteral impairment (CSI).
In female continents, the bladder and proximal urethra are supported by the anterior vaginal wall and its lateral grip to the lator muscles. Relaxation of the anterior vaginal wall causes urethral hypermobility, usually due to aging and/ or oestrogen deficiency, previous traumatic birth or pelvic surgery. Paradoxically, the woman may have clinical signs of urethral hypermobility, but without stress urinary incontinence. Some women have a bladder neck and a normal anatomical urethra, but still have IUS due to damage to the internal sphincter (fixed, rigid or "in pipe pipe"), caused by anti-incontinence surgery, pelvic irradiation or trauma or neurological diseases with urethra denervation. Urethral hypermobility and DSI may coexist in some patients and may cause persistence (or rapid recurrence) of incontinence after a simple suspension of the bladder cervix that remedyes hypermobility but leaves the sphincter untreated.
Impulse incontinence may be present alone or in combination with IUS (mixed incontinence). The cause of non-suppressible or uninhibited bladder contractions is usually idiopathic, but bacterial cystitis, bladder tumors, bladder opening obstruction and neurological bladder should be excluded. Overflow incontinence is due to either obstruction of the bladder outlet (rare in women), an acontractile bladder (diabetic neuropathy, multiple sclerosis), excessive relaxation of smooth muscles due to drugs (anticolinergics), or psychogenic retention.
In men, incontinence is less common than obstruction, but urgency and impulse incontinence can occur as a result of obstruction of the bladder outlet hole (as in prostatic hyperplasia), which damages the function of the smooth detrusor muscle and leads to instability of the detrusor. Men with neurological bladder (diabetic neuropathy, multiple sclerosis, Parkinson's disease, strokes) may develop impulse incontinence. Other causes, such as bacterial cystitis or bladder tumours, should be excluded. IUS in men is usually the result of radical prostatectomy for prostate cancer.
Transient urinary incontinence is common in the elderly (old). A mnemotechnic formula of Resnick describes its many causes, namely delirium, infection, atrophic urethritis, pharmacological, psychological, excessive urinary excretion (hyperglycaemia, congestive heart failure), restricted mobility and the effect of defecation (DIAPPERS). Impulse incontinence is the second most common condition in this age group and is attributed to the progressive loss of modulating influences of the frontal lobes of the cortex on the centers of motion in the brain stem.
The assessment of urinary incontinence in women should include: assessment of history and quality of life, a journal of urination, physical examination including a pelvic examination, analyses and urinary cultures and measurement of postmictional residual volume. For a patient with a blurred history or after previous pelvic anti-incontinence intervention, evaluation may include cytoscopy, urodynamic evaluation and imaging studies (lower and/ or higher urinary tract). History should define the onset, duration, evolution and triggering events of urinary loss.
Previous drug treatments, frequent motion schedules and exercise regimens should be noted. The severity of urinary incontinence is given by the recording of the number and type of tampons used per day or night and how incontinence affects daily activities (the questionnaire for the impact of incontinence). Information should be obtained about the amount and type of fluids consumed, sexual history (hormonal status, births, venereal diseases), gastrointestinal function (fecal incontinence, constipation) and urological history (bed watering, surgery).
Physical examination should place special emphasis on abdominal, genital, pelvic (associated prolapse) and neurological examination. IUS should be demonstrated by having the patient cough, strain or stand or squat. While leaks during a coughing fit confirm the IUS, the leakage after cough is due to bladder instability (stress-induced instability). IUS in the absence of urethral hypermobility raises the suspicion of a sphincter defect.
More complex tests are needed to determine whether the anatomy of the urethra is normal (assessment of urethral mobility, lateral visualization of the urethra in myctional cystourography, cytoscopy), whether urethral function is normal with proper closure (leak pressure point, urethral profilerometry, videourodynamic studies) or whether bladder function is normal (vescal volume based on a home-kept log, filling cystometrogram).
From a treatment point of view, mild stress incontinence can be treated non-surgically with drugs, hormonal supplements or biofeedback techniques. Ways such as urethral plugs and prostheses for the anterior vaginal wall are under investigation. Moderate to severe stress incontinence responds to surgical procedures focused on supporting the anterior vaginal wall (vaginal, laparoscopic or abdominal operations) or on increased urethral closure when stress incontinence is secondary to internal sphincter deficiency (periuretral injection of Teflon or collagen or insertion of an artificial urethral sphincter).
Impulse incontinence responds to the treatment of its cause, for example removal of the obstruction of the outlet. When it is due to neurological or idiopathic causes, anticholinergic agents are partially effective, although side effects such as dry mouth, blurred vision or constipation may limit their usefulness. Restricting fluid consumption (which should only be recommended with great caution) and bladder re-education through biofeedback can be helpful. In the absence of neurological diseases, more aggressive interventions such as bladder enlargement or urinary deviations are rarely necessary.
I will complete this long post with the presentation of some elements related to bladder pain. Painful bladder disease is a general term for any pathology that causes suprapubic, urethral or pelvic pain. Interstitial cystitis (CI) is the most common cause of bladder pain, but endometriosis, bacterial cystitis and obstructions of the outlet that cause bladder instability can mimic the symptoms of CI. CI is a chronic, severe bladder condition that causes frequent urination, nocturia and suprapubic pain. The disease usually affects women and is rare in the black race. Routine urinary cultures are uniformly negative, and symptoms do not respond to antibiotic therapy.
Etiology is probably multifactorial, with current assumptions including autoimmune reactions against bladder antigens, deficiencies in the glycosaminoglican layer on the bladder surface that allow supposed "toxins" to penetrate the mucosa, infiltration of mast cells and their activation, leading to the release of histamine and local damage to the bladder wall by "cryptic" bacteria. There are no universally accepted criteria for making the diagnosis, this being one of exclusion - infection, irradiation cystitis, urethral diverticules, herpes simplex infection and malignant diseases should be excluded.
Cytoscopy under anesthesia can join glomeulations (submucous vascular abnormalities) or the rare Encountered Hunner ulcer suggestive of CI (makes it possible to estimate bladder capacity - an important guide for treatment, allows biopsy of the bladder wall, when it is indicated and sometimes provides a therapeutic benefit with reduced pain and urinary frequency levels up to 6 months, rarely longer).
From an evaluation point of view, the frequency of urination and chronic bladder pain affect the quality of life to an extreme degree, although most patients have an undulating evolution (only 10% of patients have a constant progression of symptoms). The evaluation should include a detailed history, physical examination for the exclusion of neurological and gynecological pathology, myctional cystogram to exclude urethral defects and urodynamic tests to remove the neurological bladder, bladder instability or obstruction of the outlet and to document sensory instability.
It may be advisable to refer to specialists to exclude the pathology of the appendages, endometriosis or intestinal dysfunctions or to use modern pain treatment techniques in order to prevent drug dependence.
And finally, something about treatment... The empirical treatments that have been used include oral medication (amitriptyline, hydroxyzine) and intravescal agents (dimethylsulfoxide, chlorpactin and heparin). These measures may improve urinary symptoms and occasionally reduce pain, but do not alter long-term development. Surgery (augmentation cytoplasty, urinary derivatives) is indicated in less than 5% of cases because it is a chronic disease with occasional spontaneous remissions that do not threaten life. "Last-resort" interventions, such as excision of the bladder and urethra, are not a guarantee of success because some patients continue to have pelvic pain after that.
Enjoy life and always have
understanding, love and gratitude!
Dorin, Merticaru