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Urinary system disorders.pptx

  1. Urinary system disorders
  2. Functions of the Kidneys A. Homeostatic Functions 1. Waste excretion (urine formation) a. Nitrogenous end products: urea, creatinine, uric acid, etc. b. Metabolic degradation of peptide hormones: glucagon, insulin, PTH, growth hormone, FSH, and gastrin. 2. Fluid/electrolyte balance (Na+, K+, water) 3. Acid/base regulation: • kidneys generate and reclaim filtered bicarbonate, as well as secrete excess acid to maintain balance. 4. Balance of other electrolytes (Ca++, Mg++, Phosphate PO4 3-)
  3. B. Non-excretory functions 1. Renin-angiotensin mechanism to control BP a. Kidney senses decreased BP b. Secretes renin (enzyme), which converts Angiotensin I to angiotensin II c. Angiotensin II is a vasoconstrictor  increased BP d. Angiotensin II also stimulates aldosterone secretion e. Aldosterone increases Na+ and H2O reabsorption, increased plasma volume, and increased BP (aldosterone also stimulates potassium secretion into tubules)
  4. 2. Produces erythropoietin a. Stimulates erythropoiesis in bone marrow b. The anemia of CRF is primarily caused by impaired erythropoiesis c.  RBC formation is mainly due to  erythropoietin production in the diseased kidneys, although other compounds that accumulate in renal failure may also suppress erythropoiesis.
  5. 3. Maintains Calcium-Phosphorus bone homeostasis a. Activates Vitamin D (Hydroxylation of 25-OH-D3 to 1,25-OH-D3) in kidney disease, can supplement calcitriol, but very expensive Low vit. D  less Ca++ absorbed b. Inverse relationship between Ca++ and P, so when P is retained by diseased kidney, Ca++ levels decline (less calcium reabsorbed by the kidney). c. Low serum calcium  parathyroid gland releases PTH: Parathyroid Hormone: works to elevate serum Ca++ by pulling it from the bones  fragility, muscular weakness, decreased muscular tone, and general neuromuscular hypoexcitability.
  6. Assessment and Diagnostic Tests 1. Physical Characteristics & Measurements – appearance – color – odor – volume – specific gravity 2. Chemical Measurements – pH – protein; glucose – ketones – bilirubin; urobilinogen – leukocytes; nitrite – blood 3. Microscopic – cells (wbc, rbc, sperm) – casts – crystals – bacteria 4. Detection of Bacteriuria – nitrite test • qualitative or screening test – C & S • Colony Count, if done, make this a quantitative test • NOTE: Step 4, qualitatively, is done as part of step 2
  7. • Appearance – Clear = normal – Cloudy = ? Infection – If sediment = kidney disease – Dark = ?blood, ?bilirubin, ?concentrated • Color – Urochrome pigment = yellow • comes from breakdown of hemoglobin – Concentration • More Concentrated = Deeper Yellow – Change of Color From: • Meds – Vitamin = yellow • Diseases – Blood = red-brown – Liver = Orange • Foods – Rhubarb = red-brown • Odor – Normal = ammonia-like smell • from breakdown of urea – Unpleasant = ? infection • Quantity – Average per 24 hours = 1500 cc • 60 cc per hour • GFR = 125 cc/min – Thus, 7500 cc/ hour • Urine Made Per Hour = 60 cc • Urine GFR Per Hour = 7500 cc – KEY: 1 % of filtered urine remains urine; 99 % becomes reabsorbed back into blood – Oliguria = 100 - 400 cc per day – Anuria = less than 100 cc per day – Polyuria = diabetes, nerves, diuretics
  8. • Specific Gravity – Determines Concentration – Compares Test Liquid to H2O – Normal = 1010 - 1030 – First AM Specimen = > 1020 – In many kidney diseases, one loses the ability to concentrate urine – 3 ways to do it: 1. Reagent Strip 2. Refractometer 3. Urinometer • pH – Determines Acidity or Alkalinity – Normal = 6.0 – Range = 4.5 - 8.0 • Acidity example = diabetes • Alkaline example = UTI • Protein – OK to have a Trace in the urine – Benign Conditions: • exercise • exposure to cold •  protein consumption – Generally Means Kidney Disease • Glucose – Will only be in urine if exceed Renal Threshold (160 - 180 mg/dl) • Ketone (note Acetone is a Ketone) – Ketones are products of Fat Metabolism – If cant breakdown Sugars for energy, the body will begin using Fat – Seen in: • Uncontrolled Diabetes • Starvation • Hi-Fat Diet
  9. • Bilirubin & Urobilinogen Formation – When used-up RBC’s are broken down by Reticulo-Endothelial System, a by-product is Bilirubin – Bilirubin removed from blood by liver & excreted into intestine – Bacteria in intestine convert Bilirubin into Urobilinogen – Some Urobilinogen reabsorbed into blood • Of this amount reabsorbed some my be normally passed in urine • Bilirubin – Normally None in Urine – Found in urine if it can’t get from the liver into G-I tract • From Obstruction of Bile Ducts – Found in urine if have: • Liver Disease (hepatitis) • Blood Disease (hemolysis) • Urobilinogen – generally follows whatever happens to bilirubin – may get none in urine if on antibiotics (destruction of gut flora) – usually get small amount in urine • Blood – None is normal – But may see some if female is menstruating • Leukocytes – from inflammation of kidney or lower G-U tract • Nitrites – screening test for bacteriuria – bacteria convert nitrate to nitrite
  10. A. Inflammatory disorders (1) glomerulonephritis (2) nephrotic syndrome 3) Pyelonephritis B. Voiding dysfunction C. CKD D. Renal stone E. Renal failure Disorders
  11. Epidemiology of Chronic Kidney Disease (CKD) • Chronic Kidney Disease (CKD) affects about 26 million people in the US • Approximately 19 million adults are in the early stages of the disease – On the rise do to increasing prevalence of diabetes and hypertension • Total cost of end stage renal disease (ESRD) in US was approximately $40 billion in 2008 & $42 billion in 2013 • Prevalence is 11-13% of adult population in the US • Increases risk for all-cause mortality, CV mortality, kidney failure (ESRD), and other adverse outcomes. • 6 fold increase in mortality rate with DM + CKD
  12. Pathophysiology • Repeated injury to kidney
  13. Symptoms • Hematuria • Flank pain • Edema • Hypertension • Signs of uremia • Lethargy and fatigue • Loss of appetite • If asymptomatic may have elevated serum creatinine concentration or an abnormal urinalysis
  14. Primary Glomerular Diseases A variety of diseases can affect the glomerular capillaries, including acute and chronic glomerulonephritis
  15. Acute Glomerulonephritis • The term nephritis describes a group of inflammatory but NONINFECTIOUS disease characterized by wide-spread kidney damage. • Glomerulonephritis is a type of nephritis that occurs most frequently in children and young adults; however, it can affect individuals at any age. • It is an inflammation of the glomerular capillaries • Nephritic Syndrome: is a group of diseases characterized by glomerular inflammation (glomerulonephritis)
  16. Pathophysiology • Symptoms of acute glomerulonephritis appear about 1 to 2 weeks after a group A beta-hemolytic streptococci upper respiratory infection. • The relationship between the infection & acute glomerulonephritis is not clear; microorganisms are not present in the kidney when symptoms appear, but the glomeruli are acutely inflamed.
  17. Clinical features • About 50% are symptom free. • Occasionally the onset is sudden with pronounced symptoms such as fever, nausea, malaise, headache, generalized edema, or periorbital edema, puffiness around the eyes. • In some instances, the disorder is discovered during a routine physical examination. • More often, the client or family notices that the person’s face is pale and puffy and that slight ankle edema occurs in the evening. • Many other vague symptoms
  18. Medical Management • No specific treatment exists for acute glomerulonephritis and treatment is guided by the symptoms and their underlying abnormality. • Treatment may consist of bed rest, a sodium-restricted diet (if edema or HTN is present), and • Antimicrobial drugs to prevent a superimposed infection in the already inflamed kidney. • The client is not considered cured until the urine is free of protein and red blood cells for 6 months. • Return to full activity usually is not permitted until the urine is free of protein for 1 month.
  19. Nursing Management • First nurses should make nursing assessment and Dx- decide the nursing management depending on the DX • Generally, the following nursing management are common • Maintain bed rest when the blood pressure is elevated and edema is present • Collect daily urine specimens to assist with evaluating the client’s response to TX. • Assess the BP q 4 hours or prn • Encourage adequate fluid intake and measure I & O. • Encourage carbohydrate intake to prevent the catabolism of body protein stores (may be restricted in sodium and protein)
  20. Chronic Glomerulonephritis • Repeated attacks of acute Glomerulonephritis due to: • Hypertensive nephrosclerosis • Hyperlipidemia • Glomerular sclerosis • Clinically: • the kidneys shrinks • reduce its size • It has rough and irregular surface • Thickened renal artery Glomerular damage ESRD
  21. Chronic Glomerulonephritis • A slowly progressive disease characterized by inflammation of the glomeruli that causes irreversible damage to the kidney nephrons. • Some live for years with only occasional symptomatic episodes or none at all, or the disease may be rapidly fatal unless renal failure is treated with dialysis. Pathophysiology • The chronic inflammation leads to ever-increasing bands of scar tissue that replace nephrons, the vital functioning units of the kidney. • Decreased glomerular filtration can eventually lead to renal failure. • Chronic glomerulonephritis accounts for approx. 40% of people on dialysis.
  22. Clinical features • Some experience no symptoms of this disorder until renal damage is severe. • Generalized edema known as ANASARCA is a common finding. • Anasarca is due to the shift of fluid from the intravascular space to interstitial and intracellular fluid locations. • The fluid shift is due to depletion of serum proteins, albumin in particular, which is lost in the urine. • Clients remain markedly edematous for months or years. • The client may feel relatively well, but the kidney continues to excrete albumin. • The fluid burden and subsequent renal failure contribute to fatigue, headache, hypertension, dyspnea, and visual disturbances.
  23. Diagnostic Findings • Azotemia, accumulation of nitrogen waste products in the blood, is evidenced by elevated BUN, serum creatinine, and uric acid levels. • The urine contains protein (albumin), sediment, cast (deposits of minerals that break loose from the walls of the tubules), and red and white blood cells.
  24. Medical Management • Treatment is nonspecific and symptomatic • Management goals include • (1) controlling HTN with medications and sodium restriction • (2) correcting fluid and electrolyte imbalance, • (3) reducing edema with diuretic therapy • (4) preventing congestive heart failure • (5) eliminating urinary tract infections with antimicrobials. • May necessitate dialysis or kidney transplantation
  25. Nursing Management • Fluid Volume Excess Weigh daily at the same time on the same scale while wearing similar clothing. – Measure I & O – Monitor BP, HR, lung and heart sounds each shift – Assess for pitting edema, tight rings or shoes, clothes that do not fit comfortably – Educate on low sodium restriction – Administer prescribed diuretics • Fatigue & Activity Intolerance – Avoid clustering nursing tasks and physical activities – Provide periods of rest and promote uninterrupted sleep at night – Eliminate any activities of daily living that are not necessary. – Assist the client with activities when evidence of tachycardia or dyspnea is present.
  26. Nephrotic Syndrome • It is a primary glomerular disease characterized by the following: » Marked increase in protein in the urine » Decrease in albumin in the blood » Edema » High serum cholesterol
  27. Pathophysiology of nephrotic syndrome Damage glomerular capillary membrane Loss of plasma protein ”albumin” Stimulate synthesis of lipoproteins hyperlipedemia hypoalbuminemia Activation of renin-angiotensin system Sodium retention Edema
  28. Possible causes: 1. SLE, glomerulonephritis 2. Infections 3. diabetes mellitus 4. drugs/toxins 5. lipid nephrosis (more rare, seen in kids) lipid deposited in kidney tissue.
  29. Diagnostic Findings of nephrotic syndrome Needle biopsy of the kidney may be performed for histologic examination of renal tissue
  30. Characterized by: 1. Proteinuria (hallmark of nephrotic syndrome) – urinary protein loss of >3g/day (2’ increased capillary permeability) a. Hypoalbuminemia b. loss of immunoglobulins c. loss of transferrin d. loss of vitamin D binding protein 2. Edema 2’ 3. Hyperlipidemia 4. Also possible: • blood coagulation disorders or increased clotting (can  occlusions in lungs and legs)
  31. Complications of nephrotic syndrome • Infection ”low immune response” • Thromboembolism” renal vein” • Pulmonary emboli • Acute renal failure • Accelerated athrosclerosis ”due to hyperlipedemia”
  32. Management of Nephrotic Syndrome • Diuretics for edema • Immunosupprsant medications • Low salt diet • Protein in diet around 0.8 gm g/kg/day • Patients with nephrotic syndrome need instructions towards: » Dietary regimen » Referral system » medications
  33. C. Nutrition Therapy 1. Energy: 2. High protein not recommended; accelerates kidney failure. 3. Fat: 4. Sodium:
  34. Pyelonephritis Definition: • It is an bacterial infections that involves both the parenchyma and the pelvis of the kidney, it may affect one or both kidneys. • It is frequently secondary to ureterovesical reflux • It may be acute or chronic • when it is chronic, the kidneys are scarred, contracted and non- functioning
  35. PATHOPHYSIOLOGY • Microbial invasion of Renal Pelvis • Inflammatory response • Fibrosis or scar tissue formation • Decreased tubular reabsorption & secretion • Impaired renal function
  36. Pyelonephritis
  37. Chronic Pyelonephritis • Repeated attacks of acute pyelonephritis may lead to chronic pyelonephritis
  38. Pathophysiology of Chronic Pyelonephritis • The kidney shows atrophy of variable degree depending upon the severity of the involvement. • In minimal involvement, the kidney shows scarring in the renal surfaces while in extensive involvement, there is a fibrosis specially in the pelvic mucosa.
  39. Clinical manifestations of chronic peylonephritis • It does not have symptoms of infection • Fatigue • headache • Poor appetite • Polyuria • Excessive thirst • Weight loss
  40. Medical Management • Tx includes relieving the fever and pain and prescribing antimicrobial drugs such as Septra or Cipro for 14 days. • Antispasmodics and anticholinergics such as Ditropan & Pro- Banthine relax smooth muscles of the ureters and bladder, • promote comfort, and increase bladder capacity. • 4 weeks of drug therapy is prescribed
  41. Nursing Management • Obtain a complete medical, drug, & allergy history. • V/S ( temp or BP) • Any s/s of fluid retention such as peripheral edema and SOB. • Collect a clean-catch urine specimen for urinalysis and urine culture. • Measure I & O • Provide a liberal fluid intake of approx. 2,000 to 3,000 mL to flush the infectious microorganisms from the urinary tract. • LAB TEST: BUN, creatinine, serum electrolytes, and urine culture
  42. Family Teaching • Suggest consuming acid-forming foods such as meat, fish, poultry, eggs, grains, corn, • lentils, cranberries, prune, plums, and their juices to prevent calcium and magnesium phosphate stone formation. • Recommend avoiding alcohol and caffeine products if bladder spasms are present or until a clinical response to therapy is verified.
  43. Complications of Chronic Pyelonephritis • ESRD • Bacteremia • Hypertension • Renal stones • Renal failure
  44. Specific Nursing Care for chronic Pyelonephritis 1.The nurse must instruct the patient to continue antibiotic and antimicrobial therapy even after symptoms resolve. 2. Encourage the patient to drink 3 liters/day of fluids unless otherwise instructed. 3. Monitor urinary output and report if there is oliguria or intake more than output. 4. Weighing daily and instruct the patient to report immediately about weight gain. 5. Teach the patient measures to prevent infection and early seek for medical advice if there are signs of urinary infection. 6. Continue with medical follow-up and get follow-up urine cultures as instructed.
  45. Specific Nursing Care for peylonephritis 1.Health promotion and maintenance measures should be applied. 2.Early treatment for cystitis to prevent ascending infections. 3.Encourage the patient to drink at least 2000 ml of fluid everyday. 4.Antibiotic therapy according to results of urine cultures. 5.Serial urine cultures and other evaluation studies must be continued.
  46. Chronic Kidney Disease • Definition • Chronic, irreversible loss of kidney function attributable to loss of functional nephron mass – pathophysiologic processes for more than 3 months
  47. Pathophysiology of CKD • Final Common Pathway is loss of nephron mass Structural/ Functional Hypertrophy of remnant nephrons Sclerosis of remnant nephrons Loss of Nephron Mass Mediated by vasoactive molecules, cytokines and growth factors, renin angiotensin axis Diabetes Hypertension Chronic GN Cystic Disease Tubulointerstitial disease
  48. Risk Factors • Age of more than 60 years • Hypertension and Diabetes – Responsible for 2/3 of cases • Cardiovascular disease • Family history of the disease. • Race and ethnicity • Highest incidence is for African Americans • Hispanics have higher incidence rates of ESRD than non- Hispanics.
  49. CKD Risk Factors* Modifiable • Diabetes • Hypertension • History of AKI • Frequent NSAID use Non-Modifiable • Family history of kidney disease, diabetes, or hypertension • Age 60 or older (GFR declines normally with age) • Race/U.S. ethnic minority status
  50. Modification of Other CVD Risk Factors in CKD • Smoking cessation • Exercise • Weight reduction to optimal targets • Lipid lowering therapy – In adults >50 yrs, statin when eGFR ≥ 60 ml/min/1.73m2; statin or statin/ezetimibe combination when eGFR < 60 ml/min/1.73m2 – In adults < 50 yrs, statin if history of known CAD, MI, DM, stroke • Aspirin is indicated for secondary but not primary prevention
  51. Detect and Manage CKD Complications • Anemia – Initiate iron therapy if TSAT ≤ 30% and ferritin ≤ 500 ng/mL (IV iron for dialysis, Oral for non-dialysis CKD) – Individualize erythropoiesis stimulating agent (ESA) therapy: Start ESA if Hb <10 g/dl, and maintain Hb <11.5 g/dl. Ensure adequate Fe stores. – Appropriate iron supplementation is needed for ESA to be effective • CKD-Mineral and Bone Disorder (CKD-MBD) – Treat with D3 as indicated to achieve normal serum levels – 2000 IU po qd is cheaper and better absorbed than 50,000 IU monthly dose. – Limit phosphorus in diet (CKD stage 4/5), with emphasis on decreasing packaged products - Refer to renal RD – May need phosphate binders
  52. Detect and Manage CKD Complications • Metabolic acidosis o Usually occurs later in CKD o Serum bicarb >22mEq/L o Correction of metabolic acidosis may slow CKD progression and improve patients functional status1,2 • Hyperkalemia o Reduce dietary potassium o Stop NSAIDs, COX-2 inhibitors, potassium sparing diuretics (aldactone) o Stop or reduce beta blockers, ACEi/ARBs o Avoid salt substitutes that contain potassium
  53. Primary care • Recognize and test at-risk patients • Educate patients about CKD and treatment • Manage blood pressure and diabetes • Address other CVD risk factors • Evaluate and manage anemia, malnutrition, CKD, and other complications in at-risk patients • Refer to dietitian for nutritional guidance • Consider patient safety issues in CKD • Consult or refer the patient
  54. primary care • Evaluate and manage anemia, malnutrition, CKD-MBD, and other complications in at-risk patients • Refer to dietitian for nutritional guidance • Consider patient safety issues in CKD • Consult or team with a nephrologist (co-management) • Refer patient to nephrology when appropriate
  55. Urinary Incontinence Prevalence • Increases with age and affects women more than men (2:1) until age 80 • 15-30% in community dwellers age 65 and older • 60-70% in older adults age 65 and older in long term care • Significantly impairs quality of life
  56. What is Needed for Normal Bladder Function? 1. Filling - Efficient and low pressure 2. Storage - Low pressure, with perfect continence 3. Emptying - Periodic complete urine expulsion, at low pressure, when convenient The Bladder: Innervation • Bladder innervation – Sympathetic (Hypogastric nerve) – Parasympathetic (Pelvic Nerve) – Somatic (Pudendal Nerve) • Common disorders: – Classification – Stress Urinary Incontinence – Urge Incontinence/Overactive Bladder (OAB) – Neurogenic Bladder
  57. Normal Bladder Function: Bladder Filling NorE 2,3 Ach 2,3 1 NorE Sympathetic “On” Parasympathetic “Off” Striated Sphincter Bladder Neck Detrusor Hypogastric Nerve Pelvic Nerve Pudendal Nerve Voluntary
  58. Normal Bladder Function: Bladder Emptying NorE 2,3 Ach 2,3 1 NorE Parasympathetic “On” Striated Sphincter Bladder Neck Detrusor Hypogastric Nerve Pelvic Nerve Pudendal Nerve Voluntary 2,3 Sympathetic “Off” Parasympathetic “On” NorE NorE Ach 2,3 1 Hypogastric Nerve Pelvic Nerve Detrusor Bladder Neck
  59. Voiding Dysfunction: Functional Classification • Classification: – Failure to Store Bladder Outlet – Failure to Empty • Bladder • Outlet Striated Sphincter Bladder Neck Pelvic Nerve Bladder
  60. Incontinence: • Definition: "the complaint of any involuntary loss of urine". • Types • Stress incontinence: Loss of urine with exertion or sneezing or coughing. • Urge incontinence: Leakage accompanied by or immediately preceded by urinary urgency. • Mixed incontinence: Loss of urine associated with urgency and also with exertion, effort, sneezing, or coughing. • Overflow incontinence: Leakage of urine associated with urinary retention. • Total incontinence: Is the complaint of a continuous leakage.
  61. • Frequency: voiding too often • Urgency: sudden compelling desire to pass urine which is difficult to defer • Urge incontinence: involuntary loss of urine associated with or immediately preceded by urgency • Nocturia: waking one or more times per night to void Other Incontinence Terms: Definitions
  62. Incontinence History: Try to Classify the Incontinence  Stress Incontinence  Involuntary loss of urine with coughing or sneezing, or physical exertion  “Do you leak when you cough, sneeze, laugh, lift, walk, run, jump?”  Urgency Incontinence  involuntary loss of urine associated with or immediately preceded by urgency  “Do you get that feeling like you “really” have to pee before you leak?  Mixed Incontinence - both
  63. Incontinence History: Other Key Points • Use and number of incontinence pads • Lower urinary tract symptoms (LUTS) • Presence of neurologic disease • History of pelvic surgery or radiotherapy • Obstetrical history • Bowel and sexual function • Medication history • **Impact on quality of life**
  64. Physical Examination General examination Edema, Neurologic Abnormalities, Mobility, Cognition, Dexterity Abdominal examination Assess for palpable or distended bladder Pelvic exam - women, ? prolapse Do RectalE xam- men Cough test - observe urine loss
  65. Incontinence: Investigations • Urinalysis • Urine Culture • Voiding Diary – Type of incontinence – Number of episodes – Volume of leakage
  66. Incontinence in the Elderly: Try to identify and treat underlying reversible causes (DIAPPERS) • D – delirium (impaired cognition) • I – infection (UTI) • A – atrophic vaginitis/urethritis • P – psychological • P – pharmacologic (diuretics, narcotics, etc.) • E – endocrine (DM)/excessive urinary output • R – restricted mobility • S – stool impaction
  67. Stress Urinary Incontinence • “Loss of urine with exertion or sneezing or coughing”
  68. Stress Incontinence: Primary Care (Initial) Management  Risk Reduction Weight loss Smoking cessation Topical Estrogen  Behavioral techniques: Kegel exercises –Designed to strengthen pelvic floor muscles –Initial treatment for stress incontinence –Also helpful for urge incontinence
  69. Stress Incontinence: When to Refer? • If incontinence causes decrease in quality of life • Failed previous SUI treatment • Failed Kegel exercises
  70. Stress Incontinence: Other Treatment Options • Pelvic Floor Biofeedback • Pessary – Intra-vaginal insert to reduce prolapse and support the urethra • Urethral Bulking Agents: (collagen, etc.) – Minimally invasive – Less durable than surgery • Surgery – Urethral sling – Effective and durable
  71. Stress Incontinence: Surgery Mid-Urethral Sling • Day surgery • 20-30 minutes • Risks: – Bleeding – Infection – Too tight/retention – Mesh complications • Off work 2-4 weeks – No restrictions after 4 weeks
  72. Stress Incontinence Surgery: Mid-Urethral Slings  Limited vaginal dissection  Polypropylene mesh under midurethra without tension  No fixation of the tape  Operation can be done under local anaesthetic, sedation, GA, or SA
  73. Stress Incontinence Surgery: Does it Work? Success: 80-85% Not all bladder/women the same Treats stress incontinence, not OAB 30% of women will have improvements in OAB symtpoms Retention: 2-3%
  74. Urge Urinary Incontinence (UUI) /Overactive Bladder (OAB) • Urge Incontinence: – Involuntary leakage of urine accompanied by – or immediately preceded by urinary urgency • OAB: – A symptom complex of urgency, with or without urge incontinence, usually with frequency and nocturia Definition • Frequency: voiding too often • Urgency: sudden compelling desire to pass urine which is difficult to defer • Urge incontinence: involuntary loss of urine associated with or immediately preceded by urgency • Nocturia: waking one or more times per night to void
  75. Overactive Bladder: Prevalence: Incontinent versus Continent 37% WET 63% DRY OAB Stewart W et al. Prevalence of OAB in the US: results from the NOBLE program. Poster presented at WHO/ICI; July, 2001; Paris, France.
  76. Overactive Bladder: Etiology  Inappropriate contraction (or sensation) of detrusor muscle during bladder filling Idiopathic no identifiable cause ?related to aging (unclear mechanism) Neurogenic stroke, Parkinson’s disease, MS, Alzheimer’s disease, brain tumor
  77. Overactive Bladder: Important Questions on History • How often do you void during the day? – Give examples: q1hr, q2-3hr, etc. • When you want to go, do you go? • How many times do you get out of bed to void? • Do you leak urine? • Do you have to wear pads? Change clothes? • Do you have a strong or slow stream? • Feel like you empty?
  78. OAB/Urge Incontinence: Primary (Initial) Treatment • Most cases of OAB can be diagnosed and treated by primary health care providers. • Treat OAB and urge incontinence the same. • Treat for 6-8 weeks and reassess • Consider voiding diary (frequency volume chart for 3 days)
  79. Overactive Bladder: Treatment Options • Behavioral therapy • Medication (Anti-cholinergics, B3 Agonists) • Combined therapy1 • Minimally invasive therapy • Surgery 1. Burgio KL et al. J Am Geriatr Soc. 2000;48:370-374.
  80. Behavioral Therapy • Patients should implement the following program at home: – Regular pelvic floor muscle exercises – Specified voiding schedule aimed at avoiding emergencies – Reduce fluid intake to 1.5 litres per day – Avoid caffeine and alcohol
  81. Anti-cholinergic Medications • Investigational compounds Two antimuscarinic agents are available for the treatment of OAB: tolterodine (Detrol® LA) and oxybutynin (Ditropan XL® and Oxytrol™ patch). • The antidepressant duloxetine is currently being studied for the treatment of stress urinary incontinence but not for urge urinary incontinence.
  82. Follow-up Appointment • Review urinalysis and culture • Compare voiding diaries • “Did the treatment work?” • Any side effects? • Switch to another anti-cholinergic medications, or • Increase dose
  83. 1. Uncertain diagnosis/no clear treatment plan 2. Unsuccessful therapy for OAB – after 2-3 meds? 3. Neurological disease 4. Stress incontinence concurrently 5. Hematuria without infection 6. Persistent symptoms of poor bladder emptying 7. History of previous radical pelvic or anti- incontinence surgery When should you refer to a urologist?
  84. What to include in the referral? • Urinalysis & Urine Culture • Previous urologic/pelvic surgery • Type of incontinence (UUI, SUI, Mixed) • Attempted treatments • ? Voiding diary
  85. Refractory OAB • >3 failed medical treatments • Treatment Options: –Intravesical Onabotulinum toxin A –Sacral or peripheral nerve stimulation –Bladder augmentation (rarely)
  86. OAB/UUI: Key clinical points • Educate and reassure the patient • No anti-cholinergic better than another • Efficacy and side effects vary from individual to individual • OK to try different medications • Realistic expectations – not a cure • Be careful in geriatric patients – Trosec 20 mg daily or bid, Detrol 2mg or 4mg, Enablex, Vesicare
  87. Total Incontinence: Key Points • Total incontinence: The complaint of a continuous leakage.  This may be indicative of an abnormal communicating tract between urinary tract and other organ (commonly with the vagina) • i.e. vesicovaginal fistula • Inquire about past surgical history • Needs referral and further investigation
  88. Overflow Incontinence: Key Points • Overflow incontinence: Leakage of urine due to chronic urinary retention  Usually related to bladder outlet obstruction  BPH or Urethral Stricture  May also be related to a weak or “hypotonic” bladder • Treatment: – Relief of urinary obstruction – If due to a weak bladder - self-catherization
  89. Neurogenic Bladder • Failure of bladder function with loss of innervation • Normal bladder: – Holds 350-500mL – Senses fullness – Low pressure – Empties >80% efficiency • Innervation: – Parasympathetic (S2-4) – empties bladder (bladder contracts, sphincter relaxes) – Sympathetic (T10-L2) – fills bladder (bladder relaxes, sphincter contracts) • Classification: – Upper motor neuron (lumbar and higher) – Lower motor neuron (sacral and lower)
  90. Neurogenic Bladder • Upper motor lesion: – Detrsuor overactivity – Above pons – Detrusor overactivity & discoordinated sphincter – Spinal cord (thoracic & lumbar) • Treatment – Lower bladder pressure – Anticholinergics – Empty bladder – Intermittent self catheterization – Augment bladder (surgery) if high pressures persist • Lower motor lesion (sacral or lower): – Detrusor atony/areflexia – Treat with Clean Intermittent catheterization
  91. Autonomic Dysreflexia • Autonomic dysreflexia – Massive sympathetic release in response to stimulation below spinal cord lesion – Hypertension, headaches, bradycardia, flushing above – THIS IS A POTENTIALLY LIFE THREATENING EVENT – Treat with alpha-blockers, sublingual nifedipine
  92. Summary • Urinary incontinence is quite common • Basic evaluation – Classify incontinence on history – Urinalysis, Urine C&S – Voiding Diary • Excellent surgical options for stress incontinence but try Kegel exercises first • Urge incontinence/OAB try lifestyles measures and anti- cholinergic treatment
  93. General approach to Urinary Incontinence
  94. Lifestyle Management – Weight loss – Extreme fluid intake – Limit caffinated beverages – Limit alcohol – Limit evening fluid intake – Quit smoking (stress UI)
  95. • Overall Nursing diagnoses  Urinary elimination, impaired  Tissue perfusion: renal, ineffective  Pain, acute and chronic  Infection, risk for  Fluid volume excess  Sexuality patterns, ineffective  Knowledge, deficient Nursing Process