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Author: Blue whale Xiaohu Diabetes is a chronic, systemic metabolic disease, diabetes prevalence rate of over 10%, including type 2 diabetes accounts for about 90% to 95%.
Diabetes has brought a huge economic burden to the medical system.
In 2011, my country's medical expenditure related to diabetes treatment reached 806 billion yuan.
Chronic hyperglycemia state has harmful effects on the functions of different cells and organs, and is an important factor leading to complications.
Diabetic cystopathy, also known as diabetic neurogenic bladder, is a common urological complication of diabetes, affecting more than 50% of patients.
In the past, diabetic bladder disease was thought to be a "triad" of decreased bladder sensation, increased bladder capacity, and poor bladder emptying.
In addition, diabetic patients often suffer from overactive bladder.
Therefore, the new definition of diabetic bladder disease includes a wide range of lower urinary tract symptoms (LUTS), including overactive bladder, urinary dysfunction, and urinary retention.
The incidence of diabetic bladder disease confirmed by urodynamic examination is about 25% to 90%.
A clinical study in 2011 showed that 22.
5% of diabetic patients had overactive bladder, and 48.
0% of them had urinary incontinence.
Clinical and urodynamic manifestations of diabetic bladder disease Traditionally, diabetic bladder disease is considered to be a manifestation of diabetic neuropathy, characterized by decreased bladder sensation, increased bladder volume, decreased detrusor contractility, and increased residual urine after urination .
Diabetic neuropathy is the cause of bladder dysfunction.
It is currently believed that diabetic bladder disease is a progressive disease, accompanied by a series of clinical symptoms and urodynamic manifestations, from overactive bladder to poor bladder contraction, including urine storage and urination abnormalities.
Diabetic bladder disease develops progressively, and can be divided into compensatory phase, decompensated phase, and end atonic phase according to disease progression and urodynamic performance.
The early stage of compensation mainly manifests as bladder storage dysfunction, and urodynamics finds overactive bladder; the later decompensation stage shows abnormal urination, and urodynamics shows loss of bladder tone.
Therefore, over time, the urodynamics changes from involuntary detrusor contraction to impaired detrusor contraction or loss of reflex, which can further lead to upper urinary tract dysfunction (bilateral hydronephrosis or renal failure) .
The etiology and pathophysiology of diabetic bladder disease The influence of diabetes on lower urinary tract function is multi-factorial.
Changes in detrusor physiology, neuronal damage and urothelial dysfunction play a major role.
Changes in detrusor physiology The mechanisms of changes in detrusor physiology include intercellular connections and excitability, changes in the density and distribution of muscarinic receptors, changes in intracellular signals and genetic changes, which have been shown to induce the formation and composition of bladder tissue.
Changes in compliance.
The detrusor smooth muscle contractility decreases after potassium chloride and carbachol stimulation, which is related to the duration and increase of hyperglycemia.
As the density of muscarinic receptors increases, the response of detrusor smooth muscles to muscarinic agonists also increases.
Neuronal damage The neuronal control of bladder function involves complex interactions between autonomic nerves, somatic afferent and efferent pathways.
Both physical and autonomic neuropathy mediate bladder dysfunction in diabetic patients.
Hyperglycemia exerts its toxic effects through neuronal damage.
Metabolic disorders lead to axon degeneration and nerve conduction disorders, which are manifested by hyposensitivity in the bladder.
Bladder filling causes the detrusor muscle to contract, and activation of afferent nerves is an important sensory mechanism that causes urination.
Decreased bladder fullness causes over-inflated bladder, and long-term over-inflated bladder in diabetic patients causes low bladder contractility.
Urothelial dysfunction The urothelium acts as a sensor to communicate with the underlying nerves, connective tissue, and muscle tissue, and to control bladder function.
The urothelium also releases mediators that affect afferent nerves and induces diabetic bladder disease.
Bradykinin and ATP can significantly increase the release of urothelial prostaglandin (PG) F2α and PGE2 under pathological conditions.
In addition, the increased density of urothelial muscarinic M2 and M3 receptors is the pathogenesis of excessive detrusor activity in diabetic patients.
Abnormal urothelium affects lower urinary tract function by changing the release of diabetic bladder media and the excitability of sensory nerve fibers, causing detrusor instability and changes in bladder capacity.
Urethral dysfunction The storage and release of urine requires coordination between the bladder and the external urethral sphincter.
In the course of disease progression, the afferent nerves of the urethra are over-excited, and long-term high blood sugar causes dysfunction of the external urethral sphincter, which increases the resistance of the urethral outlet and affects the relaxation of the urethral smooth muscle.
In diabetic patients, it is found that the detrusor-sphincter synergy is unbalanced, which leads to bladder remodeling and increased residual urine output after urination, which exacerbates the impact of impaired bladder contractility.
The treatment strategy of diabetic bladder disease The treatment of diabetic bladder disease depends on the main complaint of the individual patient, its severity, the degree of distress and its impact on the quality of life.
The choice of treatment depends on clinical symptoms and urodynamic abnormalities.
Urodynamic examination is the cornerstone of diagnosis and determines treatment strategies.
However, there is still a lack of practical guidelines to guide treatment.
The treatment goals of diabetic bladder disease include alleviating LUTS, promoting urinary control, and preserving renal function.
Management strategies include adjusting behavior patterns, medications, and surgery.
Non-invasive interventions are preferred in the early stage of treatment.
Lifestyle changes, including weight loss, diet and fluid intake adjustments, and bladder function exercise, can greatly improve LUTS in diabetic patients.
Weight loss can improve urinary incontinence in obese patients and is the initial step of conservative treatment of urinary incontinence.
Patients can be educated to minimize nocturia by limiting fluid intake, urinating before going to bed, and avoiding bladder irritants.
Regular urination, such as urinating once every 2-4 hours, can also help prevent urinary incontinence.
For patients with significantly impaired detrusor contraction, urinary dysfunction and severe upper urinary tract dysfunction, clean intermittent catheterization is an important means to empty the bladder and preserve renal function.
Antimuscarinic drugs, such as Tolterodine and Solinasine, are the drugs of choice for patients with overactive bladder.
However, the effect of drugs in the treatment of detrusor non-reflex is limited.
Patients with impaired detrusor contractility and poor behavioral and drug treatment should consider surgical intervention, with the goal of improving urinary control and restoring renal function.
Surgical interventions include bladder neck incision, selective pudendal nerve block, and sacral nerve electrical stimulation (also known as bladder pacemaker).
Summary Diabetes can cause a variety of LUTS, leading to diabetic bladder disease.
Careful examination of the nervous system and urodynamics is necessary for the diagnosis of diabetic bladder disease.
In addition, prostate hyperplasia often associated with diabetes may also lead to urinary dysfunction, which makes it difficult to assess the relationship between diabetes and urinary dysfunction.
The treatment of diabetic bladder disease includes lifestyle adjustment, medication and surgical treatment.
Finally, good blood sugar control can prevent complications in the urinary system, and it is also an important guarantee for any treatment to be effective.
References 1.
Yuan Z, Tang Z, He C, Tang W.
Diabetic cystopathy: A review.
J Diabetes.
2015 Jul;7(4):442-7.
2.
Powell CR.
Is the Diabetic Bladder a Neurogenic Bladder? Evidence from the Literature.
Curr Bladder Dysfunct Rep.
2014 Dec;9(4):261-267.
3.
Yang Z, Dolber PC, Fraser MO.
Diabetic urethropathy compounds the effects of diabetic cystopathy.
J Urol.
2007 Nov;178(5) :2213-9.
4.
Brown JS.
Diabetic cystopathy--what does it mean? J Urol.
2009 Jan;181(1):13-4.
5.
Lee WC, Wu HP, Tai TY, Yu HJ, Chiang PH Investigation of urodynamic characteristics and bladder sensory function in the early stages of diabetic bladder dysfunction in women with type 2 diabetes.
J Urol.
2009 Jan;181(1):198-203.
6.
Schulman JM, Gelber AC.
Diabetic Cystopathy with Bilateral Hydronephrosis.
Am J Med.
2018 Jun;131(6):e255-e256.
7.
Xu J, Xu H, Yu Y, He Y, Liu Q, Yang B.
Combination of Luteolin and Solifenacin Improves Urinary Dysfunction Induced by Diabetic Cystopathy in Rats.
Med Sci Monit.
2018 Mar 10;24:1441-1448.
8.
Goldstraw MA, Kirby MG, Bhardwa J, Kirby RS.
Diabetes and the urologist: a growing problem.
BJU Int.
2007 Mar;99(3):513-7.
Diabetes has brought a huge economic burden to the medical system.
In 2011, my country's medical expenditure related to diabetes treatment reached 806 billion yuan.
Chronic hyperglycemia state has harmful effects on the functions of different cells and organs, and is an important factor leading to complications.
Diabetic cystopathy, also known as diabetic neurogenic bladder, is a common urological complication of diabetes, affecting more than 50% of patients.
In the past, diabetic bladder disease was thought to be a "triad" of decreased bladder sensation, increased bladder capacity, and poor bladder emptying.
In addition, diabetic patients often suffer from overactive bladder.
Therefore, the new definition of diabetic bladder disease includes a wide range of lower urinary tract symptoms (LUTS), including overactive bladder, urinary dysfunction, and urinary retention.
The incidence of diabetic bladder disease confirmed by urodynamic examination is about 25% to 90%.
A clinical study in 2011 showed that 22.
5% of diabetic patients had overactive bladder, and 48.
0% of them had urinary incontinence.
Clinical and urodynamic manifestations of diabetic bladder disease Traditionally, diabetic bladder disease is considered to be a manifestation of diabetic neuropathy, characterized by decreased bladder sensation, increased bladder volume, decreased detrusor contractility, and increased residual urine after urination .
Diabetic neuropathy is the cause of bladder dysfunction.
It is currently believed that diabetic bladder disease is a progressive disease, accompanied by a series of clinical symptoms and urodynamic manifestations, from overactive bladder to poor bladder contraction, including urine storage and urination abnormalities.
Diabetic bladder disease develops progressively, and can be divided into compensatory phase, decompensated phase, and end atonic phase according to disease progression and urodynamic performance.
The early stage of compensation mainly manifests as bladder storage dysfunction, and urodynamics finds overactive bladder; the later decompensation stage shows abnormal urination, and urodynamics shows loss of bladder tone.
Therefore, over time, the urodynamics changes from involuntary detrusor contraction to impaired detrusor contraction or loss of reflex, which can further lead to upper urinary tract dysfunction (bilateral hydronephrosis or renal failure) .
The etiology and pathophysiology of diabetic bladder disease The influence of diabetes on lower urinary tract function is multi-factorial.
Changes in detrusor physiology, neuronal damage and urothelial dysfunction play a major role.
Changes in detrusor physiology The mechanisms of changes in detrusor physiology include intercellular connections and excitability, changes in the density and distribution of muscarinic receptors, changes in intracellular signals and genetic changes, which have been shown to induce the formation and composition of bladder tissue.
Changes in compliance.
The detrusor smooth muscle contractility decreases after potassium chloride and carbachol stimulation, which is related to the duration and increase of hyperglycemia.
As the density of muscarinic receptors increases, the response of detrusor smooth muscles to muscarinic agonists also increases.
Neuronal damage The neuronal control of bladder function involves complex interactions between autonomic nerves, somatic afferent and efferent pathways.
Both physical and autonomic neuropathy mediate bladder dysfunction in diabetic patients.
Hyperglycemia exerts its toxic effects through neuronal damage.
Metabolic disorders lead to axon degeneration and nerve conduction disorders, which are manifested by hyposensitivity in the bladder.
Bladder filling causes the detrusor muscle to contract, and activation of afferent nerves is an important sensory mechanism that causes urination.
Decreased bladder fullness causes over-inflated bladder, and long-term over-inflated bladder in diabetic patients causes low bladder contractility.
Urothelial dysfunction The urothelium acts as a sensor to communicate with the underlying nerves, connective tissue, and muscle tissue, and to control bladder function.
The urothelium also releases mediators that affect afferent nerves and induces diabetic bladder disease.
Bradykinin and ATP can significantly increase the release of urothelial prostaglandin (PG) F2α and PGE2 under pathological conditions.
In addition, the increased density of urothelial muscarinic M2 and M3 receptors is the pathogenesis of excessive detrusor activity in diabetic patients.
Abnormal urothelium affects lower urinary tract function by changing the release of diabetic bladder media and the excitability of sensory nerve fibers, causing detrusor instability and changes in bladder capacity.
Urethral dysfunction The storage and release of urine requires coordination between the bladder and the external urethral sphincter.
In the course of disease progression, the afferent nerves of the urethra are over-excited, and long-term high blood sugar causes dysfunction of the external urethral sphincter, which increases the resistance of the urethral outlet and affects the relaxation of the urethral smooth muscle.
In diabetic patients, it is found that the detrusor-sphincter synergy is unbalanced, which leads to bladder remodeling and increased residual urine output after urination, which exacerbates the impact of impaired bladder contractility.
The treatment strategy of diabetic bladder disease The treatment of diabetic bladder disease depends on the main complaint of the individual patient, its severity, the degree of distress and its impact on the quality of life.
The choice of treatment depends on clinical symptoms and urodynamic abnormalities.
Urodynamic examination is the cornerstone of diagnosis and determines treatment strategies.
However, there is still a lack of practical guidelines to guide treatment.
The treatment goals of diabetic bladder disease include alleviating LUTS, promoting urinary control, and preserving renal function.
Management strategies include adjusting behavior patterns, medications, and surgery.
Non-invasive interventions are preferred in the early stage of treatment.
Lifestyle changes, including weight loss, diet and fluid intake adjustments, and bladder function exercise, can greatly improve LUTS in diabetic patients.
Weight loss can improve urinary incontinence in obese patients and is the initial step of conservative treatment of urinary incontinence.
Patients can be educated to minimize nocturia by limiting fluid intake, urinating before going to bed, and avoiding bladder irritants.
Regular urination, such as urinating once every 2-4 hours, can also help prevent urinary incontinence.
For patients with significantly impaired detrusor contraction, urinary dysfunction and severe upper urinary tract dysfunction, clean intermittent catheterization is an important means to empty the bladder and preserve renal function.
Antimuscarinic drugs, such as Tolterodine and Solinasine, are the drugs of choice for patients with overactive bladder.
However, the effect of drugs in the treatment of detrusor non-reflex is limited.
Patients with impaired detrusor contractility and poor behavioral and drug treatment should consider surgical intervention, with the goal of improving urinary control and restoring renal function.
Surgical interventions include bladder neck incision, selective pudendal nerve block, and sacral nerve electrical stimulation (also known as bladder pacemaker).
Summary Diabetes can cause a variety of LUTS, leading to diabetic bladder disease.
Careful examination of the nervous system and urodynamics is necessary for the diagnosis of diabetic bladder disease.
In addition, prostate hyperplasia often associated with diabetes may also lead to urinary dysfunction, which makes it difficult to assess the relationship between diabetes and urinary dysfunction.
The treatment of diabetic bladder disease includes lifestyle adjustment, medication and surgical treatment.
Finally, good blood sugar control can prevent complications in the urinary system, and it is also an important guarantee for any treatment to be effective.
References 1.
Yuan Z, Tang Z, He C, Tang W.
Diabetic cystopathy: A review.
J Diabetes.
2015 Jul;7(4):442-7.
2.
Powell CR.
Is the Diabetic Bladder a Neurogenic Bladder? Evidence from the Literature.
Curr Bladder Dysfunct Rep.
2014 Dec;9(4):261-267.
3.
Yang Z, Dolber PC, Fraser MO.
Diabetic urethropathy compounds the effects of diabetic cystopathy.
J Urol.
2007 Nov;178(5) :2213-9.
4.
Brown JS.
Diabetic cystopathy--what does it mean? J Urol.
2009 Jan;181(1):13-4.
5.
Lee WC, Wu HP, Tai TY, Yu HJ, Chiang PH Investigation of urodynamic characteristics and bladder sensory function in the early stages of diabetic bladder dysfunction in women with type 2 diabetes.
J Urol.
2009 Jan;181(1):198-203.
6.
Schulman JM, Gelber AC.
Diabetic Cystopathy with Bilateral Hydronephrosis.
Am J Med.
2018 Jun;131(6):e255-e256.
7.
Xu J, Xu H, Yu Y, He Y, Liu Q, Yang B.
Combination of Luteolin and Solifenacin Improves Urinary Dysfunction Induced by Diabetic Cystopathy in Rats.
Med Sci Monit.
2018 Mar 10;24:1441-1448.
8.
Goldstraw MA, Kirby MG, Bhardwa J, Kirby RS.
Diabetes and the urologist: a growing problem.
BJU Int.
2007 Mar;99(3):513-7.
