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
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)
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.
34. C. Nutrition Therapy
1. Energy:
2. High protein not recommended;
accelerates kidney failure.
3. Fat:
4. Sodium:
35. 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
36. PATHOPHYSIOLOGY
• Microbial invasion of Renal Pelvis
• Inflammatory response
• Fibrosis or scar tissue formation
• Decreased tubular reabsorption & secretion
• Impaired renal function
39. 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.
40.
41. Clinical manifestations of chronic peylonephritis
• It does not have symptoms of infection
• Fatigue
• headache
• Poor appetite
• Polyuria
• Excessive thirst
• Weight loss
42. 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
43. 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
44. 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.
46. 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.
47. 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.
48. Chronic Kidney Disease
• Definition
• Chronic, irreversible loss of kidney function
attributable to loss of functional nephron
mass – pathophysiologic processes for more
than 3 months
49. 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
50. 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.
51. 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
52. 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
53. 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
54. 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
55. 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
56. 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
57.
58. 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
59. 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
63. 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.
64. • 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
65. 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
66. 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**
67. 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
69. 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
71. 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
72. Stress Incontinence: When to Refer?
• If incontinence causes decrease in quality of life
• Failed previous SUI treatment
• Failed Kegel exercises
73. 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
74. 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
75. 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
76. 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%
77. 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
78. 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.
79. 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
80. 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?
81. 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)
83. 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
84. 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.
85. 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
86. 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?
87. What to include in the referral?
• Urinalysis & Urine Culture
• Previous urologic/pelvic surgery
• Type of incontinence (UUI, SUI, Mixed)
• Attempted treatments
• ? Voiding diary
88. Refractory OAB
• >3 failed medical treatments
• Treatment Options:
–Intravesical Onabotulinum toxin A
–Sacral or peripheral nerve stimulation
–Bladder augmentation (rarely)
89. 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
90. 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
91. 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
92. 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)
