Presentation is loading. Please wait.

Presentation is loading. Please wait.

Urology Back to Basics The “Nuts” and Bolts

Similar presentations


Presentation on theme: "Urology Back to Basics The “Nuts” and Bolts"— Presentation transcript:

1 Urology Back to Basics The “Nuts” and Bolts
James Watterson, MD FRCSC Assistant Professor, University of Ottawa Director, Ottawa Lithotripsy and Stone Program Endourology and Laparoscopic Urological Surgery Division of Urology, The Ottawa Hospital

2 References The Medical Council of Canada www.mcc.ca
Objectives for the Qualifying Examination MCC Objectives.doc University of Toronto Notes Campbell’s Urology

3 Objectives The Medical Council of Canada Abdominal Mass Adrenal Mass
Blood in Urine (Hematuria) Gynecomastia Ambiguous Genitalia Infertility Incontinence, Urine Incontinence, Urine, Pediatric (Enuresis) Impotence, Erectile Dysfunction Acute and Chronic Renal Failure (Post-renal / Obstruction) Scrotal Mass / Scrotal Pain Urinary Tract Injuries Dysuria and / or Pyuria Urinary Obstruction / Hesitancy / Prostatic Cancer

4 Objectives The Medical Council of Canada Abdominal Mass Adrenal Mass
Blood in Urine (Hematuria) Gynecomastia Ambiguous Genitalia Infertility Incontinence, Urine Incontinence, Urine, Pediatric (Enuresis) Impotence, Erectile Dysfunction Acute and Chronic Renal Failure (Post-renal / Obstruction) Scrotal Mass / Scrotal Pain Urinary Tract Injuries Dysuria and / or Pyuria (UTI) Urinary Obstruction / Hesitancy / Prostatic Cancer

5 Blood in Urine (Hematuria)
Key Objective (s): Differentiate red or brown urine from hematuria, transient from persistent, and glomerular from extraglomerular hematuria

6 Hematuria Objectives Through efficient, focused, data gathering
Determine whether the patient has true hematuria Diagnose the presence of urinary tract infections Differentiate between glomerular and extraglomerular hematuria by examination of urine sediment List and interpret critical clinical and laboratory findings which are key in the processes of exclusion, differentiation, and diagnosis Interpret reported urinalysis findings Outline significance of patient’s age, gender and life style on diagnostic possibilities Conduct an effective plan of management for a patient with hematuria Select treatment for patients with UTI appropriate for gender, lower, and upper urinary tract Outline a plan for investigation of patients with recurrent nephrolithiasis Formulate a management plan (non-Rx) for prevention of recurrent nephrolithiasis Discuss possible strategies for the detection and prevention of urinary tract tumors

7 Hematuria Objectives Through efficient, focused, data gathering
Determine whether the patient has true hematuria Diagnose the presence of urinary tract infections Differentiate between glomerular and extraglomerular hematuria by examination of urine sediment List and interpret critical clinical and laboratory findings which are key in the processes of exclusion, differentiation, and diagnosis Interpret reported urinalysis findings Outline significance of patient’s age, gender and life style on diagnostic possibilities Conduct an effective plan of management for a patient with hematuria Select treatment for patients with UTI appropriate for gender, lower, and upper urinary tract Outline a plan for investigation of patients with recurrent nephrolithiasis Formulate a management plan (non-Rx) for prevention of recurrent nephrolithiasis Discuss possible strategies for the detection and prevention of urinary tract tumors

8 Hematuria Considerations
Pseudohematuria Menses Dyes (ie. Anthrocyanin in beets, rhodamine B in drinks, candy and juices) Hemoglobinuria (hemolytic anemia) Myoglobinuria (rhabdomyolysis) Drugs (rifampin, phenazopyridine) Porphyria (brownish urine) Laxatives (phenolphthalein) Urine dipstick – if positive, indicates hematuria, hemoglobinuria, or myoglobinuria Microscopy distinguishes hematuria from Hgburia or Mgburia

9 Hematuria Objectives Through efficient, focused, data gathering
Determine whether the patient has true hematuria Diagnose the presence of urinary tract infections Differentiate between glomerular and extraglomerular hematuria by examination of urine sediment List and interpret critical clinical and laboratory findings which are key in the processes of exclusion, differentiation, and diagnosis Interpret reported urinalysis findings Outline significance of patient’s age, gender and life style on diagnostic possibilities Conduct an effective plan of management for a patient with hematuria Select treatment for patients with UTI appropriate for gender, lower, and upper urinary tract Outline a plan for investigation of patients with recurrent nephrolithiasis Formulate a management plan (non-Rx) for prevention of recurrent nephrolithiasis Discuss possible strategies for the detection and prevention of urinary tract tumors

10 UTI Limited sensitivity History & P/E Inspection of urine – Turbid
Irritative voiding symptoms (dysuria, freq, urg, suprapubic pain, hematuria) Fever Flank pain Inspection of urine – Turbid May be secondary to excessive phosphates Urinalysis Dipstick Leukocyte esterase Nitrites Microscopic analysis False-negative (low numbers bacteria), false-positive (normal vaginal flora; NB squamous epithelial cells indicate contamination) > 2 WBCs/HPF correlates with presence of bacteriuria RBCs lack sensitivity (40-60% cases of cystitis) but highly specific Urine culture mid-stream vs. catheterized specimen Traditionally, > 105 cfu/mL In dysuric patients, 102 cfu/mL of a known pathogen significant Limited sensitivity

11 Hematuria Objectives Through efficient, focused, data gathering
Determine whether the patient has true hematuria Diagnose the presence of urinary tract infections Differentiate between glomerular and extraglomerular hematuria by examination of urine sediment List and interpret critical clinical and laboratory findings which are key in the processes of exclusion, differentiation, and diagnosis Interpret reported urinalysis findings Outline significance of patient’s age, gender and life style on diagnostic possibilities Conduct an effective plan of management for a patient with hematuria Select treatment for patients with UTI appropriate for gender, lower, and upper urinary tract Outline a plan for investigation of patients with recurrent nephrolithiasis Formulate a management plan (non-Rx) for prevention of recurrent nephrolithiasis Discuss possible strategies for the detection and prevention of urinary tract tumors

12 Hematuria MCC Causal Conditions
Transient Urinary tract infections Exercise induced Stones/Crystals Trauma Endometriosis Thromboembolism Anticoagulants (similar incidence of hematuria in non-anticoagulated patients) Persistent Extraglomerular (Urological) Renal Tumors Tubulointerstitial diseases (e.g polycystic kidneys, pyelonephritis) Vascular (e.g. papillary necrosis, sickle cell disease) Collecting system Stones Lower urinary tract Glomerular Isolated (e.g. IgA nephropathy, thin membrane disease) Post-infections (e.g. post-streptococcal) Systemic involvement (e.g. vasculitis, SLE)

13 Figure 3-7 Evaluation of nonglomerular renal hematuria (circular erythrocytes, no erythrocyte casts, and proteinuria). CT, computed tomography; IgA, immunoglobulin A; IVU, intravenous urography; PT, prothrombin time; PTT, partial thromboplastin time; R/O, rule out.

14 Figure 3-6 Evaluation of glomerular hematuria (dysmorphic erythrocytes, erythrocyte casts, and proteinuria). ANA, antinuclear antibody; ASO, antistreptolysin O; Ig, immunoglobulin.

15 Hematuria Diagnostic Evaluation: Is it? True or False
Extraglomerular vs. Glomerular Dysmorphic RBCs Casts (RBC, WBC) Proteinuria (> mg/dL or 2+ to 3+ on dipstick) Gross or Microscopic > 3 RBC / HPF Further Urological Questions Location- Renal/Ureter/Bladder/ Prostate/Urethra Painful/Painless Part of Stream- Initial/Terminal/Throughout ??? Clots – shape of clots

16 Investigations for Hematuria
History and P/E Smoking Other risk factors for urothelial malignancy Urine Urinalysis / Microscopy / C & S Cytology Upper tract Microscopic Renal U/S Gross CT urogram Lower tract cystoscopy

17 Hematuria DDx VINDICATE Renal/Ureter/Bladder/Prostate/Urethra
Neoplasm.. Neoplasm.. Neoplasm Stone Trauma Infection

18 Hematuria Objectives Through efficient, focused, data gathering
Determine whether the patient has true hematuria Diagnose the presence of urinary tract infections Differentiate between glomerular and extraglomerular hematuria by examination of urine sediment List and interpret critical clinical and laboratory findings which are key in the processes of exclusion, differentiation, and diagnosis Interpret reported urinalysis findings Outline significance of patient’s age, gender and life style on diagnostic possibilities Conduct an effective plan of management for a patient with hematuria Select treatment for patients with UTI appropriate for gender, lower, and upper urinary tract Outline a plan for investigation of patients with recurrent nephrolithiasis Formulate a management plan (non-Rx) for prevention of recurrent nephrolithiasis Discuss possible strategies for the detection and prevention of urinary tract tumors

19 UTI Treatment Principles of Antimicrobial Therapy
Effective antimicrobial therapy must eliminate bacterial growth Antimicrobial resistance is increasing because of excessive utilization Antimicrobial selection should be influenced by efficacy, safety, cost and compliance Lower Tract UTI – cystitis; most occur in women; 10% incidence Bacteria – E.coli causative organism in 75 – 90% of acute cystitis in young women Drug choices TMP-SMX DS BID 3 days Nitrofurantoin 100mg BID 3 days Norfloxacin 400mg BID 3 days Ciprofloxacin 500mg BID 3 days

20 UTI Treatment Recurrent Lower Tract UTI in Women
Self-start Rx Post-coital single dose Low dose prophylaxis 3-6 months Upper Tract UTI (Acute Pyelonephritis) E.coli accounts for 80% of cases Blood cultures positive in 25% Consider U/S or CT if failure to respond after 72 hrs of therapy Rx Uncomplicated – Cipro 500mg BID PO, Levofloxacin 500mg QD PO x 7 – 10 days Complicated – Parenteral Cipro, Levo, Amp + Gent x 7 – 10 days

21 Hematuria Objectives Through efficient, focused, data gathering
Determine whether the patient has true hematuria Diagnose the presence of urinary tract infections Differentiate between glomerular and extraglomerular hematuria by examination of urine sediment List and interpret critical clinical and laboratory findings which are key in the processes of exclusion, differentiation, and diagnosis Interpret reported urinalysis findings Outline significance of patient’s age, gender and life style on diagnostic possibilities Conduct an effective plan of management for a patient with hematuria Select treatment for patients with UTI appropriate for gender, lower, and upper urinary tract Outline a plan for investigation of patients with recurrent nephrolithiasis Formulate a management plan (non-Rx) for prevention of recurrent nephrolithiasis Discuss possible strategies for the detection and prevention of urinary tract tumors

22 Risk Factors for Stone Disease
Diet, Diet, Diet Dehydration High protein intake High salt intake Certain foods high in oxalate Occupation Inflammatory Bowel Disease, Gout, Hyperparathyroidism Genetics Rarely Recurrent nephrolithiasis Refer to urologist or nephrologist Metabolic evaluation Serum chemistry (Lytes, BUN, Cr, Ca, Urate, PTH) 24 hour urine (Lytes, Ca, Oxalate, Uric acid, citrate, Mg, cystine)

23 Dysuria and/or Pyuria Key Objective (s):
Differentiate between urinary tract infections and conditions outside the urinary tract with similar presentation; determine which infections require treatment, and select the appropriate treatment. In patients with recurring urinary tract infections, determine whether a predisposing condition may be present (e.g., stasis from obstruction, reflux).

24 Dysuria and/or Pyuria Through efficient, focused, data gathering:
Interpret urinalysis and clinical findings in order to diagnose problems external to urinary tract. Evaluate examination findings so that problems involving the urethra or prostate are identified. Determine whether cystitis or pyelonephritis is the more likely diagnosis. List and interpret critical clinical and laboratory findings which were key in the processes of exclusion, differentiation, and diagnosis: Outline significance of patient's age, gender, and life style on diagnostic possibilities. Select findings which are best for differentiating cystitis from pyelonephritis. Describe the collection of samples to be sent for culture and sensitivity; interpret results. Conduct an effective plan of management for a patient with urinary frequency, dysuria, and/or pyuria: Determine which patients require additional investigation and/or referral. Determine which patients require hospitalization. Determine which patients should be on prophylactic treatment and the type of treatment. Select the most appropriate treatment for the underlying condition. List conditions which predispose to urinary tract infections. Outline strategies for prevention of recurrent urinary tract infections.

25 Dysuria and/or Pyuria Dysuria = painful urination
Usually caused by inflammation Commonly referred to the urethral meatus Start: may indicate urethral End (stranguria): usually bladder origin Usually accompanied by frequency and urgency Pyuria = presence of white blood cells (WBCs) in urine Generally indicative of infection and an inflammatory response of the urothelium to the bacterium Bacteriuria without pyuria is generally indicative of bacterial colonization without infection Pyuria without bacteriuria warrants evaluation for TB, stones, or cancer

26 Dysuria and/or Pyuria DDx
Dysuria / Freq / Urgency >> Vesical vs. Extravesical Extravesical Urological Urethral diverticulum / CA Prostatitis Urethritis Lower ureteral stone Gyne Vulvovaginitis Herpes Endometriosis Ovarian / Uterine / Cervical CA Bowel Diverticulosis Fistula Crohn’s Colon CA Vesical Bacterial cystitis Bladder tumor / CIS Bladder stone TB cystitis Radiation cystitis Nonbacterial cystitis Cyclophosphamide / ASA / NSAID / Allopurinol

27 Dysuria and/or Pyuria Evaluation
Dysuria / Freq / Urgency >> Vesical vs. Extravesical History Age, Gender, Smoking History LUTS PMHx (Gyne, IBD, divertic), PSHx (pelvic), PGUHx (UTI, STD, Tumor, Stone, Hematuria) Physical examination Suprapubic tenderness Genital exam Rectal exam (prostate, rectum) Pelvic exam Investigations Urine (U/A, C&S, cytology) Ultrasound - pelvic Cystoscopy

28 Urinary Obstruction / Hesitancy / Prostatic Cancer
Key Objective (s): Determine whether a patient has an acute obstruction any time the complaint is complete anuria or unexplained renal insufficiency

29 Urinary Obstruction / Hesitancy / Prostatic Cancer
Objective (s): Through efficient, focused, data gathering: Determine whether the obstruction is acute or chronic, duration, complete or partial, and unilateral or bilateral, and site. Ask whether pain is present, site of pain (e.g., suprapubic for bladder distention, flank for renal capsule), whether it is colicky and radiates to ipsilateral testicle or labia (renal or ureteral colic), or occurs after a fluid load that increases urine output (e.g., beer drinking). Examine for tenderness, hydronephrosis, hypertension, and palpable bladder. List and interpret critical clinical and laboratory findings which are key in the processes of exclusion, differentiation, and diagnosis: Select ultrasonography as the diagnostic imaging tool to diagnose obstruction. List indications for other types of diagnostic imaging. Select and interpret tests of renal function; outline indications for prostate cancer screening. Conduct an effective plan of management for a patient with urinary tract obstruction: Perform catheterization of the bladder for both therapeutic and diagnostic reasons. Select patients for referral to specialized care.

30 Definitions Uremia = clinical signs and symptoms seen as a result of renal failure Azotemia = elevation of blood urea (BUN) Obstructive Uropathy = reversible or irreversible renal dysfunction due to the effects of impaired urine drainage Hydronephrosis = dilation of the renal pelvis and calyces

31 Urinary Tract Obstruction Classification
Supravesical vs. Infravesical Acute vs. Chronic Unilateral vs. Bilateral Anatomical site Intrarenal Ureter Bladder Prostate Urethra Extraluminal (LN, mass) vs. Intraluminal (stone, blood clot, fungus ball) vs. Intramural (TCC, polyp)

32 Diagnosis Clinical features Flank pain/renal colic
Urinary retention or overflow incontinence Anuria or oliguria Uremia Stones Recurrent UTI Asymptomatic

33

34 Pathophysiology Factors Influencing Severity of Renal Dysfunction
Complete or partial obstruction Duration; >30 days of complete obstruction results in irreversible loss of renal function Unilateral or bilateral Presence of infection

35 Urinary Tract Obstruction Major Sequelae
Loss of renal function Urinary tract infection / sepsis Stones

36 Urinary Tract Obstruction Diagnosis
Clinical features Laboratory investigations Imaging studies

37 Urinary Tract Obstruction Diagnosis
Laboratory investigations Elevated BUN and Cr with bilateral ureteral or bladder outlet obstruction Abnormal urinary indices

38 Urinary Tract Obstruction Diagnosis
Imaging studies Renal ultrasound Intravenous pyelogram (IVP) CT Scan Retrograde pyelogram Lasix renogram

39 Hydronephrosis may not develop if acute obstruction or if presence of perinephric fibrosis

40

41

42 Urinary Tract Obstruction Temporary Measures
Bypass the cause of obstruction Bladder outlet obstruction Foley catheter Renal or ureteral obstruction Ureteral stent Nephrostomy tube

43 Percutaneous Nephrostomy
Ureteral Stenting

44 Urinary Tract Obstruction Definitive Treatment
Remove the cause of obstruction BPH Pharmacotherapy (alpha-blockers) Surgical (TURP) Stone ESWL, ureteroscopy, percutaneous stone removal

45 Prostate Cancer Most common solid tumor in U.S. males
Second leading cause of male cancer deaths Lifetime risk 1/6 Lifetime risk of a 50 year old: 50%, risk of dying 3% Risk factors Family history: 1st degree relative (2x) blacks High dietary fat Histologic Incidence rates 10-30% > 50 50% > 80

46 Presentation Asymptomatic (75%) h PSA abN DRE Locally Advanced
LUTS (uncommon without met) Hematuria Hematospermia Renal failure Metastatic Disease Bony pain (osteoblastic) DDx Prostatic Nodule Prostate Cancer (30%) BPH Prostatits Prostatic Infarct Prostatic Calculus Tuberculous Prostatitis

47 PSA Enzyme produced by epithelial cells of prostate gland to liquify the ejaculate Elevated in: Prostate cancer Prostatitis BPH Trauma catheterization Ejaculation

48 Screening DRE PSA Hypothenar eminence = benign CCFP - not recommended
US FP + Urologist – recommended “normal” < 4 but 30% have PCa Age 50 unless 1st degree relative or black male >>>40-45 yrs Screen between ages 50-70/75 years

49 Screening Probability of Finding Cancer on Biopsy According to a Man’s DRE Result and PSA Level PSA (NG/ML) 2-4 4-10 >10 15% 25% 50% 20% 45% >75% DRE N AbN

50 If abN DRE +/ h PSA.. AND > 10 YR LIFE EXPECTANCY…
TRUS + BIOPSY

51 Scrotal Mass Key Objective (s):
Differentiate testicular tumor from a mass of inguinal origin (not possible to get above it, may reduce), cystic lesion (trans-illuminates), and a varicocele (easier to palpate with patient erect)

52 Scrotal Mass Objective (s):
Through efficient, focused, data gathering: In boys, ask about pain, trauma, change in scrotal size, difficulty voiding Elicit history of undescended testicle, infertility, previous testicular tumor, and breast enlargement / tenderness Differentiate from condition that presents primarily with pain Perform abdominal exam including inguinal areas, and an examination of the male genitalia (erect and supine, testes, epididymis, cord, scrotal skin) including rectal examination to assess the prostate and seminal vesicles, transilluminate List and interpret critical clinical and laboratory findings which are key in the processes of exclusion, differentiation, and diagnosis: Select patients requiring ultrasound, CT and explain reason; order beta human chorionic gonadotrophin and alpha-fetoprotein Conduct an effective plan of management for a patient with scrotal mass: Outline management options for masses which are not testicular tumors.

53 Approach to Scrotal Masses
Painful vs. painless Benign vs. malignant Etiology varies with age of patient DDX differs between adults and children >>>Anatomical Approach

54 Anatomy Scrotal Contents: Testes Epididymis Spermatic Cord:
Tunica albuginea Tunica vaginalis Epididymis Spermatic Cord: Vas deferens Arteries: Testicular Cremasteric Artery to the Vas Veins: Pampiniform plexus Nerves: Ilioinguinal Genital br. Of Genitofemoral Sympathetics

55 History Risk Factors Age of patient HPI Recent trauma Infection
Onset (acute, insidious) Painful vs. painless Radiation Aggravating Factors Relieving Factors LUTS PMHx PSHx Risk Factors Recent trauma Infection Instrumentation of the urinary tract Congenital anomalies Prior history of neoplasm

56 Physical Examination Vital Signs Skin Abdominal exam Inguinal Penis
Temp Skin Abdominal exam Inguinal Hernia (may reduce, unable to get above) Lymph Nodes Masses Penis malignancy Scrotum Skin Testes: 3.5 cm Mass Hydrocele Transillumination Varicocele Valsalva DRE

57 Differential Diagnosis
Painful Trauma Contusion, rupture Epididymo-orchitis Hernia Incarcerated, strangulated Torsion Testes Appendages Painless Tumor Intratesticular Paratesticular Varicocele Hydrocele Spermatocele Scrotal wall malignancies SCC, sarcomas

58 Testicular Torsion Intravaginal (all age groups, puberty)
Extravaginal (prenatal, neonatal) Hx: Acute Painful scrotum N & V Rx to groin / abdomen None or minimal trauma Px: Patient appears unwell Tender, swollen testicle High riding, transverse lie Scrotal erythema No cremasteric reflex

59 Testicular Torsion If suspected clinically, surgical exploration indicated Orchidectomy Orchidopexy of contralateral side INV: Transcrotal Ultrasound Duplex Doppler Nuclear testicular blood flow scan

60 Torsion of Appendix Testis / Epididymis
Appendix Testis: 2-3 mm embryol. remnant near upper pole of testis may twist on stalk --> pain O/E: local tenderness, blue dot sign

61 Epididymitis / Orchitis
Hx: More insidious onset Fever Recent instrumentation Sexual activity LUTS Px: Painful epididymis +/- testis Testis in normal position Urethral discharge + Prehn’s sign INV: CBC U/A, C&S, Urethral Swab for GC / Chlamydia TB >>May Resemble Torsion!

62 Epididymitis / Orchitis
Causative <35 years: N.gonorrhea, C.trachomatis, E.coli >35 years: E.coli Homosexual: E.coli Mumps orchitis: 30% of patients with mumps Risk of infertility Rx: Antibiotics Bed rest Analgesics / Anti-inflammatories Scrotal elevation Specific Recommendations: GC: ceftriaxone 250 mg IM Cipro 500 mg PO NonGC: Azithromycin 1 g PO Doxycycline 100 mg BID x 7 days E.coli: IV antibiotics if severe Fluoroquinolone x days

63 Hydrocele A collection of serous fluid in some part of the processus vaginalis, usually in the tunica More common in childhood 1% of adult males Congenital: Processus vaginalis does not close after testicular descent Acquired: Primary (idiopathic) vs. secondary to disease of the testis Defective absorption, increased production, lymphatic obstruction

64 Hydrocele Hx: Px: INV: Painless (unless large)
Change during day (suggests communication) Other symptoms (secondary hydrocele) Px: Transilluminates Palpate testes Hernia ? INV: Transcrotal ultrasound if testis not palpable

65 Hydrocele Rx: Specifics: Adults: Children: Surgical Aspiration
Symptomatic Cosmesis Underlying testicular pathology Children: Most will resolve in 1st year If persists, repair of hernia may be indicated Specifics: Surgical Aspiration Sclerotherapy

66 Spermatocele Painless mass Contains fluid and spermatozoa
4th / 5th decades Region of caput Usually can palpate the testis separately from spermatocele Obstruction of efferent duct Mass may transilluminate

67 Spermatocele Rx: Conservative Spermatocelectomy
Surgery may have negative consequences >>> delay if reproductive age

68 Varicocele Dilation of the veins of the pampiniform plexus of the spermatic cord due to absent competent venous valves in the spermatic vein 15% of males, 30% of subfertile males (multiple theories) Elevated intratesticular temperature widely accepted Most Left-sided; May be bilateral; Right-sided only>> be suspicious! Rare prior to puberty

69 Varicocele Hx: Px: Scrotal Ultrasound
Painless vs. dull ache; pain never present on awakening Discomfort increases with standing / activity over long period of time Exaggerated with Valsalva Infertility Px: “Bag of Worms”, “vascular thrill” Gr.I: Palpable with valsalva Gr.II: Palpable without Valsalva Gr.III: Visible Abdominal mass Scrotal Ultrasound

70 Varicocele Rx: Surgical options: Sx’s Cosmesis Infertility
Ipsilateral testicular atrophy Surgical options: Retroperitoneal Inguinal Subinguinal Laparoscopic Transvenous embolization

71 Testicular Tumors Testis CA most common malignancy in males 15 to 35 years Incidence: 3.7 / 100,000 (whites), 0.9 / 100,000 (blacks) R>L, 2-3% bilateral Risk factors: Age (<10, 15-35, >60) Race Cryptorchidism Atrophy

72 Testicular Tumors Germ Cell tumors Gonadal Stromal Paratesticular
Seminoma Non-Seminomatous Embryonal carcinoma Choriocarcinoma Yolk Sac tumor Teratoma Mixed Gonadal Stromal Leydig-cell Sertoli-cell Gonadoblastoma Paratesticular Secondary RES Leukemia Lymphoma Metastases

73 Testicular Tumors Hx: Px:
Painless intratesticular mass (pain if hemorrhage) May present with metastatic disease (SOB, cough, hemoptysis, abdominal bloating, GI complaints, lower limb edema) Px: Chest (pleural effusion, wheezing, gynecomastia) Abdominal exam (mass) Genital exam Nodal exam (inguinal, supraclavicular)

74 Testicular Tumors INV: Rx: Scrotal U/S CXR Tumor markers
BHCG AFP LDH CT Chest / Abdo / Pelvis Rx: Radical orchiectomy

75 Testicular Tumors Rx: Dependent upon: Options: Clinical stage
Pathological stage Histology Options: Surveillance XRT RPLND Chemotherapy

76 Urinary Tract Injuries
Key Objective (s): Suspect trauma to bladder or posterior urethra in patients with pelvic fracture Examine for bleeding at the external urethral meatus after trauma; urethral injury necessitating urgent ascending urethrogram may be present.

77 Urinary Tract Injuries
Objective (s): Through efficient, focused, data gathering: Elicit history about the nature of the injury, difficulty voiding, and blood in urine or at meatus; differentiate straddle injury from sexual abuse (straddle injuries typically are unilateral and superficial and involve the anterior portion of the genitalia in both boys and girls Examine for swelling, bruising, in males’ displacement of prostate on rectal List and interpret critical clinical and laboratory findings which are key in the processes of exclusion, differentiation, and diagnosis: List the most appropriate investigations used to determine the nature and severity of urinary tract injuries (e.g. retrograde urethrogram for urethral injury, CT scan for renal injury) Conduct an effective plan of management for a patient with urinary tract obstruction: Outline initial management of anterior urethral injury (e.g. 7 to 10 days of urethral catheterization and antibiotic therapy)

78 GU Trauma Accounts for 10% of ER trauma visits
Associated with multi-system trauma Subtle presentations, easily overlooked Diseased GU organs susceptible to injury

79 Trauma Evaluation Airway with C-spine control Breathing
Circulation (2 large bore IVs) Disability (brief neurologic exam) Expose (general survey)

80 Renal Trauma Most commonly injured organ GU tract
Often in association with multi-system organ injury Blunt 80% Penetrating <20%

81 Renal Trauma

82 Renal Trauma Presentation
Hematuria (gross or microscopic) May be absent Shock (hypotension, tachycardia, oliguria) Flank mass Flank pain/tenderness

83 Imaging Need both anatomic and functional information
CT Scan (with contrast) – gold standard IVP Angiography

84

85 Indications for Imaging in Scenario of Possible Renal Injury
Penetrating injuries Blunt injuries in association with Gross hematuria Shock (SBP<90 systolic) Children regardless of degree of hematuria

86 Renal Trauma - Classification
AAST Renal Injury Grading Scale

87 Renal Trauma Management
ABCs Conservative for 85% of blunt trauma Admission, bedrest, serial vital signs, CBC Indications for surgical exploration Hemodynamic instability Penetrating injuries Extensive urine extravasation “Shattered kidney” Pedicle injury

88 Bladder Trauma

89 Bladder Trauma Classified by site Contusion
Hematuria and normal cystogram Intraperitoneal rupture 30% Extraperitoneal rupture 60% Combined 10% Concommitant urethral injury 10%

90 Bladder Trauma Clinical presentation
Extra 2X > Intraperitoneal ruptures Suprapubic pain and tenderness Inability to void Pelvic fracture + gross hematuria 98% of bladder injuries have gross hematuria Mortality 20%, d/t associated injuries

91 Bladder Trauma Cystogram: Study of choice! IVP: CT:
300 cc of contrast 3 films: plain, full (300cc), drainage (+/- oblique) IVP: Poor; may demonstrate only 15% of bladder ruptures CT: Bladder filled with 300cc contrast prior to CT Difficult to assess bladder neck competence The severity of bladder injury cannot be determined by the amount of extravasation seen on any Xray study

92 Bladder Trauma - Management
Extraperitoneal Foley catheter x days Selective Exploration and Repair Bladder neck, prostatic urethra Laparotomy Hemorrhage / clots Urethral catheter cannot be placed Penetrating Open repair to rule out BN injury

93

94 Bladder Trauma - Management
Intraperitoneal Open surgical repair Lower midline incision Avoid dissection in perivesical areas Vertical anterior cystotomy to assess bladder neck Debridement Closure in 2 layers: water-tight Suprapubic catheter Drain Postop Antibiotics Foley x days Cystogram before catheter removal

95

96 Urethral Trauma

97 Urethral Trauma Proper management crucial
Majority caused by blunt injury 5% of pelvic fractures have associated posterior urethral injury 90% of posterior urethral injuries have associated pelvic fractures 10-29% of prostatomembranous urethral ruptures have bladder injury

98 Urethral Trauma Common mechanisms Classification
Pelvic crush – membranous urethra disruption Straddle injury – bulbous urethra Penile fracture – pendulous urethra Iatrogenic – false passages Classification Anterior: pendulous, bulbous urethra Posterior: membranous, prostatic urethra

99 Urethral Trauma Haematuria
Inability to void or difficulty with voiding Blood at urethral meatus Sensitivity % Perineal ecchymosis (classically in a “butterfly” pattern) Full bladder High riding prostate on DRE (posterior), bony fragments Pelvic fracture: esp. rami #’s

100 Urethral Trauma - Diagnosis
Retrograde urethrogram: Gold standard Oblique position Sterile technique Slight penile stretch 8F foley in fossa navicularis, 2cc in balloon 10-20 cc slow continuous injection Fluoroscopy preferred Peri-catheter if foley previously placed

101

102 Posterior Urethral Injury Presentation
Pelvic # Blood at the urethral meatus “High riding” prostate Scrotal swelling/ecchymosis Inability to void If potential for urethral injury exists, do not insert urethral catheter

103

104

105 Urethral Trauma - Management
Goal: control urinary drainage and minimize long-term complications Anterior: Primary repair: penetrating injury, penile fracture Suprapubic cystotomy: complete, blunt Urethral catheter: partial, blunt

106 Urethral Trauma - Management
Posterior: Open SPT + Delayed primary repair 3 – 6 months Primary catheter realignment Open vs.Endoscopic BN laceration: intrinsic sphincter mechanism crucial for continence after membranous urethra disruption (site of external sphincteric mechanism) Rectal laceration: pelvic abscess or fistula Long separation of prostate and bulbous urethra: difficult delayed repair

107 Impotence / Erectile Dysfunction
Key Objective (s): Recognize that a psychogenic component is present in all cases. Recognize that testosterone deficiency is an uncommon cause of erectile dysfunction.

108 Impotence / Erectile Dysfunction
Objective (s): Through efficient, focused, data gathering: Determine if an organic cause for impotence is likely by a medical, sexual, and social history. Exclude decreased libido, ejaculatory disorders, performance anxiety, and depression. Identify reveersible causes (recent medications – antihypertensives, antidepressants, etc) Examine for signs of vascular disease and diabetic complications (BP postural change, ankle-brachial index, pulses); examine for gynecomastia, lack of male hair distribution, small testes. List and interpret critical clinical and laboratory findings which are key in the processes of exclusion, differentiation, and diagnosis: Order screening tests for unrecognized systemic disease (e.g. diabetes) If hormonal cause is likely, order testosterone, LH, prolactin.

109 Impotence / Erectile Dysfunction
Objective (s): Conduct an effective plan of management for a patient with urinary tract obstruction: Treat associated medical conditions; suggest lifestyle changes (smoking cessation, exercise, weight loss, diet, stress reduction) Determine therapy for impotence based on the underlying cause (e.g. if testosterone is low and LH is high, consider testosterone therapy / exclude prostate; if prolactin high, pituitary imaging/referral). Outline the effectiveness of inhibitors of phosphodiesterase type V and contraindications. Describe the role of injectable, transurethral, and vacuum devices. Select patients in need of specialized care (e.g., failed medical therapy, penile anatomic disease, pelvic/perineal trauma, vascular/neurologic assessment, endocrinopathies, psychiatric, etc.). Counsel and educate patient (+/- partner). Determine the therapy for impotence based on the underlying cause. Describe the role of specific injectable and oral medications in patients with erectile dysfunction.

110 Impotence / Erectile Dysfunction
KEY POINTS: PENILE COMPONENTS AND THEIR FUNCTION DURING ERECTION Corpora cavernosa Support corpus spongiosum and glans Tunica albuginea (of corpora cavernosa) Contains and protects erectile tissue Promotes rigidity of the corpora cavernosa Participates in veno-occlusive mechanism Smooth muscle Regulates blood flow into and out of the sinusoids Ischiocavernosus muscle Pumps blood distally to hasten erection Provides additional penile rigidity during rigid erection phase Bulbocavernosus muscle Compresses the bulb to help expel semen Corpus spongiosum Pressurizes and constricts the urethra lumen to allow forceful expulsion of semen Glans Acts as a cushion to lessen the impact of the penis on female organs Provides sensory input to facilitate erection and enhance pleasure Facilitates intromission because of its cone shape

111 Impotence / Erectile Dysfunction
Normal Erection Innervation: Autonomic (SNS, PNS): cavernous nerves Somatic (sensory, motor): sensation, contraction of bulbocavernosus/ischiocavernous muscles Nitric oxide (NO) released from nonadrenergic, noncholinergic neurotransmission and from the endothelium 1) Relaxation of smooth muscles 2) Dilation of the arterioles and arteries, increasing blood flow 3) Trapping of the incoming blood by the expanding sinusoids 4) Stretching of the tunica to its capacity, which occludes the emissary veins between the inncer circular and outer longitudinal layers and further decreases venous outflow to a minimum 5) increase in intracavernous pressure (100 mm Hg) leading to full erection “P(arasymp) to Point, S(ymp) to Shoot”

112 Erection: A Neurovascular Event
In 1999, a national survey of adults aged 45 years and older was conducted for the AARP.1 Only 10% of 639 men with sexual problems who responded to the questionnaire reported that they had either sought or received medicines, hormones, or other treatments to improve sexual function and activity.1,2 Half of those who had sought or received treatment (5% of the survey population) had tried or were currently using sildenafil.1 The AARP findings are consistent with those of a smaller Australian general medical practice study in which only 11.6% (55) of 488 men with ED reported having received treatment. Intracavernosal injection therapy was the predominant treatment used by more than half (33) of these men.3 1. AARP/Modern Maturity Sexuality Study. Washington, DC: AARP; 1999. 2. McKinlay JB. Int J Impot Res. 2000;12(suppl 4):S6-S11. 3. Chew KK et al. Int J Impot Res. 2000;12:41-45.

113

114 Sexual response involves a balance between inhibitory input from the sympathetic nervous system and excitatory input from the parasympathetic system. In the absence of arousal, the penis is kept flaccid by impulses from portions of the sympathetic nervous system that limit blood flow. Arousal as the result of fantasy or visual, auditory, olfactory, or tactile stimulation of the central nervous system can trigger excitatory signals that originate in the brain and trigger an erection via the parasympathetic nervous system. Release of oxytocin by the paraventricular nucleus in the brain activates the excitatory nerve pathways connecting this center and the penis. During an erection, specialized tactile receptors in the penis send signals to the spinal cord and brain, where they affect nerve pathways. Goldstein I and the Working Group for the Study of Central Mechanisms in Erectile Dysfunction. Sci Am. August 2000:70-75.

115 With normal erectile function, penile/sexual stimulation triggers the release of NO into the corpora cavernosa from the vascular endothelium and the NANC autonomic nerves of the parasympathetic system (Paths A, B, and C).1,2 NO activates the enzyme guanylate cyclase, which catalyzes the conversion of GTP to cGMP.2 Accumulation of cGMP triggers a cascade of intracellular biochemical events leading to a decrease in intracellular calcium and ultimately relaxation of vascular smooth muscle in the corpora cavernosa.1-4 Additionally, new findings have identified that eNOS regulation can occur because of acute increase in shear stress of blood flow permitting a sustained NO release.5 Dilation of the penile arteries markedly increases blood flow into the corpora cavernosa, which fill with blood. This compresses the penile venules and veins, trapping blood in the penis, rapidly increasing intracavernosal pressure, and resulting in penile rigidity and erection.1,6 In men with ED, the PDE5 isoenzymes appear to degrade cGMP before accumulation of intracellular concentrations sufficient to produce rigidity and erection.7 When a PDE5 inhibitor is present, sexual stimulation triggers the same cascade of biochemical events. However, sildenafil, tadalafil, and vardenafil block degradation of cGMP by inactivating the PDE5 isoenzyme. In this way, the PDE5 inhibitors act synergistically with NO to markedly increase concentrations of cGMP within the cavernosal smooth muscle, facilitating relaxation of penile smooth muscle.6 If there is no sexual stimulation, PDE5 inhibitors will have no effect on the penis, because in the flaccid state, levels of NO and cGMP are low.7 Kloner RA. Hosp Pract. 2001;36:41-51. Sáenz de Tejada I et al. In: Jardin A et al, eds. Erectile Dysfunction. Plymouth, UK: Health Publication Ltd; 2000: Miller TA. Am Fam Physician. 2000;61: Boolell M et al. Int J Impot Res. 1996;8:47-52. Burnett AL. J Androl. 2002;23:S20-S26. Corbin JD, Francis SH. J Biol Chem. 1999;274: Lue TF. N Engl J Med. 2000;342:

116 The penis contains 3 cylindrical structures: the corpus spongiosum, which surrounds the urethra, and 2 erectile bodies, the corpora cavernosa.1   The corpora cavernosa are composed of a meshwork of interconnecting cavernosal spaces lined by vascular endothelium, and are surrounded by the tunica albuginea, a tough fibroelastic covering.1,2 There is an incomplete septum between the corpora cavernosa, which lets them function as a single unit.1   A central artery runs through the cavernosal tissue, and postcavernous venules are located beneath the tunica albuginea. These venules merge to form large emissary veins that penetrate the tunica albuginea and then drain into the deep dorsal vein.1  Miller TA. Am Fam Physician. 2000;61:95-104, Boolell M et al. Int J Impot Res. 1996;8:47-52.

117 A complex series of dynamic neural and vascular interactions are necessary for healthy erectile function. When the penis is in a flaccid state, there is a balance between blood inflow and outflow in the corpora cavernosa. Venules are not compressed and arterial vessels are constricted.1 Sexual stimulation triggers the release of nitric oxide (NO) into the corpora cavernosa from nonadrenergic-noncholinergic (NANC) autonomic nerves in the cavernosal tissue and sinusoids and from the vascular endothelium.1,2 NO stimulates the enzyme guanylyl cyclase to produce the intracellular mediator cyclic guanosine monophosphate (cGMP).1,2 Increases in intracellular cGMP decrease intracellular calcium and cause relaxation of vascular smooth muscle in the arteries, arterioles, and sinusoids of the corpora cavernosa.2,3 Relaxation of the penile vasculature markedly increases blood flow into the corpora cavernosa and these erectile bodies then fill with blood, like a sponge filling with water.1,2 Entry of blood into the corpora cavernosa compresses the venules and veins under the fibroelastic covering, trapping blood in the penis.1,2 The combination of increased inflow and decreased outflow of blood leads to a rapid increase in intracavernosal pressure, resulting in penile rigidity and erection.1 Following ejaculation, release of catecholamines and rapid breakdown of cGMP by the phosphodiesterase type 5 (PDE5) isoenzyme returns the penis to a flaccid state.2,4 Miller TA. Am Fam Physician. 2000;61:95-104, Corbin JD, Francis SH. J Biol Chem. 1999;274: Boolell M et al. Int J Impot Res. 1996;8:47-52. Lue TF. N Engl J Med. 2000;342:

118 Sexual response involves a balance between inhibitory input from the sympathetic nervous system and excitatory input from the parasympathetic system. In the absence of arousal, the penis is kept flaccid by impulses from portions of the sympathetic nervous system that limit blood flow. Arousal as the result of fantasy or visual, auditory, olfactory, or tactile stimulation of the central nervous system can trigger excitatory signals that originate in the brain and trigger an erection via the parasympathetic nervous system. Release of oxytocin by the paraventricular nucleus in the brain activates the excitatory nerve pathways connecting this center and the penis. During an erection, specialized tactile receptors in the penis send signals to the spinal cord and brain, where they affect nerve pathways. Goldstein I and the Working Group for the Study of Central Mechanisms in Erectile Dysfunction. Sci Am. August 2000:70-75.

119 Impotence / Erectile Dysfunction
Inability to achieve or maintain an erection sufficient for satisfactory sexual relations Organic (90%) vs. Psychgenic Vascular Disease (70%) Medications (10%) Surgical (10%) Neurologic (5%) Endocrine (3%) Trauma (2%)

120 Erectile Dysfunction Evaluation

121 Erectile Dysfunction Evaluation – IIEF 15

122 Advancing age; the presence of chronic disease such as heart disease, hypertension, diabetes, LUTS, or depression; medications, such as thiazide diuretics and beta-blockers; and unhealthy behaviors, such as cigarette smoking, alcohol or drug abuse, obesity, or a sedentary lifestyle, increase the likelihood of erectile dysfunction.1-4 Feldman HA et al. J Urol. 1994;151:54-61. Lewis RW et al. In: Lue TF et al, eds. Sexual Medicine: Sexual Dysfunctions in Men and Women. Paris, France: Health Publications; 2004:37-72. Rosen R et al. Eur Urol. 2003;44: Esposito K et al. JAMA. 2004;291:

123 In most cases, the sexual history provided by the patient can suggest whether the primary cause is psychogenic or organic.  ED primarily of psychogenic origin is characterized by a sudden onset, and complete and immediate loss of sexual function. However, morning erections are present. In addition, the condition seems to vary according to the partner and circumstances in which sexual relations are attempted.  ED primarily of organic origin typically has a gradual onset and progresses incrementally. A characteristic finding is a lack of morning erections and lack of erections under sexually stimulating circumstances.  Ralph D et al. BMJ. 2000;321:

124 Vascular disease is a prominent cause of ED1,2 and is most often the result of medical disorders that affect the arterial system.1,3  Among men older than 50 years, atherosclerotic disease causes an estimated 40% of cases of ED.4 Men with lipid abnormalities may experience ED before significant vascular stenosis occurs in penile arteries. Risk factors associated with atherosclerotic disease, such as smoking, diabetes, dyslipidemia, and hypertension, are also risk factors for ED.1,5,6  Other vasculogenic causes of ED include vascular surgery3 and venous leaks3 that are sometimes related to degenerative changes as the result of Peyronie’s disease, increasing age, or diabetes mellitus.5,7  Other vascular causes of ED include traumatic pelvic and perineal injury, which affect approximately 600,000 men in the United States. Over a period of 9.5 years, the incidence and pattern of venous drainage was evaluated in 131 men with erectile function changes associated with blunt pelvic or perineal trauma. Results of cavernosonography and arteriography showed corporeal veno-occlusive dysfunction in 62% of patients and cavernous arterial insufficiency in 70%. Compared with perineal trauma, pelvic trauma was associated with significantly more abnormal sites of venous drainage.8  In addition, perineal arterial compression during bicycling has been associated with ED. A crossover study that used penile oxygen pressure measurements (pO2) evaluated penile blood flow in 46 male cyclists before, during, and after cycling in an upright and reclining position. Because it was concluded that cycling in an upright position significantly (P<.05) decreases pO2, riding in a reclining position was recommended to avoid reduction in penile blood flow due to compression of the penile arteries near the pubic bone.9 Miller TA. Am Fam Physician. 2000;61:95-104, Azadzoi KM et al. J Urol. 1998;160: NIH Consensus Development Panel on Impotence. JAMA. 1993;270:83-90. Kaiser FE et al. J Am Geriatr Soc. 1988;36: Lue TF. N Engl J Med. 2000;342: McVary KT et al. J Urol. 2001;166: DePalma RG et al. J Vasc Surg. 1989;10: Munarriz RM et al. J Urol. 1995;153: Sommer F et al. Eur Urol. 2001;39:

125 Nerve damage as the result of radical pelvic surgery, prostatectomy, spinal cord injuries, multiple sclerosis or other demyelinating conditions, or neuropathies from diabetes or chronic alcoholism can lead to ED by interrupting somatic nervous pathways.1-3 This, in turn, may impair reflex erections and interrupt the tactile sensations that help maintain psychogenic erections.2 Injury to the pudendal nerve leading to ED is often seen in cyclists as the result of trauma from the cycle seat or middle bar on the cycle, which can be prevented if the cyclist changes position frequently.4,5 Nerve conduction studies in a 44-year-old male cyclist with transient penile numbness showed pudendal neuropathy. In addition to changing positions frequently, cross-training and/or use of ergonomically designed saddles are recommended for cyclists who ride more than 200 miles a week and experience genital numbness.6 ED may also be caused by neurologic disorders, such as stroke, Alzheimer’s disease, and Parkinson’s disease, that decrease libido or prevent the initiation of an erection.1 Lue TF. N Engl J Med. 2000;342: NIH Consensus Development Panel on Impotence. JAMA. 1993;270:83-90. Kloner RA. Hosp Pract. 2001;36:41-51. Lewis RW. Urol Clin North Am. 2001;28: Cherington M. Semin Neurol. 2000;20: Ricchiuti VS et al. J Urol. 1999;162:

126 Most hormonal abnormalities that cause ED are related to dysfunction of the hypothalamic-pituitary-gonadal axis and are associated with insufficient testosterone or excess prolactin.1-5 Hypogonadism, defined as a free testosterone level below the lower limit of normal for young adults, occurs in some men as they age. Secondary hypogonadism may be caused by suppression of the central axis as the result of any major illness or surgical procedure. Pituitary tumors may cause hypogonadism by destroying pituitary tissue or causing oversecretion of prolactin.1 Occasionally, clinicians administer testosterone injections when levels are low; however, in general, further tests are needed to establish an accurate diagnosis.  Overproduction of prolactin from any cause (eg, medications, hypothyroidism with increased thyrotropin, chest wall injuries, compression of the pituitary stalk) can result in both reproductive and sexual dysfunction.1,3,4 Problems with libido or erection may also occur as the result of hyperthyroidism, adrenal insufficiency, or excessive levels of adrenal corticosteroids.1  Low libido, headache, and visual disturbances are common clinical clues to hormonal imbalance.2 AACE Male Sexual Dysfunction Task Force. Endocr Pract. 2003;9:77-95. Morales A, Heaton JP. Urol Clin North Am. 2001;28: Lue TF. N Engl J Med. 2000;342: Johri AM et al. Int J Impot Res. 2001;13: Lewis RW et al. In: Lue TF et al, eds. Sexual Medicine: Sexual Dysfunctions in Men and Women. Paris, France: Health Publications; 2004:37-72.

127 Penile injury or disease can cause ED
Penile injury or disease can cause ED.1-3 In addition, a history of penile trauma (eg, penile fracture) or priapism may result in Peyronie’s disease, which can cause degenerative changes in the tunica albuginea.2,3 Furthermore, anatomic abnormalities of the penis and structural changes of the cavernous smooth muscle and endothelium may cause ED.3,4 Lewis RW et al. In: Lue TF et al, eds. Sexual Medicine: Sexual Dysfunctions in Men and Women. Paris, France: Health Publications; 2004:37-72. Chun J, Carson CC. Urol Clin North Am. 2001;28: Lue TF. N Engl J Med. 2000;342: Miller TA. Am Fam Physician. 2000;61:95-104,

128 Jackson G et al. Int J Clin Pract. 1999;53:445-451.
A number of prescription and over-the-counter (OTC) drugs have been linked to ED.1-11  Antihypertensive agents, particularly thiazide and thiazide-like diuretics, are associated with ED.1-5 However, in an analysis that adjusted for the effects of comorbidities and health behaviors, only nonthiazide diuretics and benzodiazepines remained significantly associated with ED.6 Selective serotonin-reuptake inhibitors (SSRIs) are commonly used for the treatment of depression and are associated with sexual side effects, such as delayed ejaculation and absent or delayed orgasm. Less common sexual side effects possibly caused by SSRIs include decreased libido and problems with arousal. The effects of SSRIs on sexual functioning appear to be dose-related and vary with different agents depending on their serotonin and dopamine reuptake mechanisms, induction of prolactin release, anticholinergic effects, inhibition of NO synthase, and likelihood of accumulation with long-term administration.7 A variety of cardiac agents, such as digoxin, ACE inhibitors, and calcium-channel blockers, are associated with ED.2,4 Other findings suggest that there is an inverse relationship between ED and ACE inhibitor therapy.8 The antihyperlipidemic agents clofibrate and gemfibrozil have been associated with ED; the statins (eg, simvastatin, pravastatin) appear to have a lower risk.3 Hormonal agents, including antiandrogens, luteinizing hormone-releasing hormone analogues, and estrogens, also increase the risk of ED.3 Other prescription and OTC drugs associated with ED include protease inhibitors (eg, ritonavir, saquinavir, indinavir),9 cytotoxic agents,10,11 and H2-receptor antagonists (eg, cimetidine, ranitidine, famotidine).2,3 Lue TF. N Engl J Med. 2000;342: Jackson G et al. Int J Clin Pract. 1999;53: Ralph D et al. BMJ. 2000;321: Burchardt M et al. J Urol. 2000;164: Grimm RH Jr et al. Hypertension. 1997;29:8-14. Lewis RW et al. In: Lue TF et al, eds. Sexual Medicine: Sexual Dysfunctions in Men and Women. Paris, France: Health Publications; :37-72. Rosen RC et al. J Clin Psychopharmacol. 1999;19:67-85. Rosas SE et al. Kidney Int. 2001;59: Schrooten W et al. AIDS. 2001;15: Chatterjee R et al. Bone Marrow Transplant. 2000;25: Lewis RW. Urol Clin North Am. 2001;28:

129 The diagnosis of erectile dysfunction (ED) is based on the patient’s self-reported problems and on a targeted medical, sexual, and psychosocial history.1 At the initial visit, it is important to query the patient regarding use of prescription, over-the-counter (OTC), or recreational drugs; prior surgery; or pelvic trauma. The sexual history should elicit information regarding not only erectile function but also penile sensation and/or pain. When taking the patient history, it is also important for the clinician to determine if ED is the actual diagnosis or if the problem is with another part of the male sexual cycle (eg, libido, ejaculation).2 Physical examination of the genitalia, which is frequently overlooked, is important because common findings in patients who either are developing or already have ED include plaques, fibrosis, and sometimes shortening of the penis. The exam should also include an approximate measurement of the testes, recognizing that normal size is generally thought to be >2 cm. Furthermore, clinicians should evaluate the cremasteric and bulbocavernosal reflexes.3 A complete examination should also include identification of secondary sexual characteristics, such as body hair and fat distribution.4 Laboratory tests for ED should be individualized and should include fasting blood sugar and a lipid profile. Complete blood count (CBC), urinalysis, and thyroid function tests may be included for a more complete exam; however, they have not proven beneficial for ED screening. Serum testosterone should be considered with evidence of decreased libido.1-3 The results of these initial assessments will characterize the problem and its duration and severity and help the clinician determine the need for additional testing. At this point, the clinician has the option of proceeding with the overall management of the patient, adopting a multidisciplinary approach involving clinicians from other disciplines, or referring the patient to a specialist for further diagnosis and management.1-3 The Process of Care Consensus Panel. Int J Impot Res. 1999;11:59-74. Miller TA. Am Fam Physician. 2000;61:95-104, Kuritzky L. J Am Osteopath Assoc. 2002;102(suppl 4):S7-S11. Rosen R et al. In: Lue TF et al, eds. Sexual Medicine: Sexual Dysfunctions in Men and Women. Paris, France: Health Publications; 2004:

130 When the patient’s presenting complaint is ED, it is possible to obtain a targeted medical, sexual, and psychosocial history in 4 to 6 minutes.1 Physical examination of the genitalia, with attention to secondary sexual characteristics, can be done adequately in 2 to 4 minutes.1 It is also important to assess CV risk. If the patient exercises regularly at the equivalent of 1 mile in 15 minutes and remains asymptomatic, a treadmill test probably is not necessary.2 The laboratory tests being ordered can be reviewed with the patient in 1 to 2 minutes.1 Therefore, as a presenting complaint, ED can be assessed in about 12 minutes.1 Kuritzky L. J Am Osteopath Assoc. 2002;102(12 suppl 4):S7-S11. Kuritzky L, Miner M. Prim Care Spec Ed. 2005;9:37-41.

131 The “doorknob” consultation, when the patient raises the issue of sexual problems as the clinician has his or her hand on the door, can be one of the most challenging concerns for PCCs. The clinician may reward the patient for the inquiry by telling him that therapies are available. The clinician then can reassure the patient by explaining that ED is a common problem in men of his age group, as well as for men who have diabetes, HTN, or in men who smoke. ED is a risk factor for CVD, and it is important to closely monitor a patient’s other modifiable risk factors. If the patient is not taking any nitrates, the clinician can dispense a sample PDE5 inhibitor and provide a prescription for more. Selected laboratory tests may be obtained at this visit. A targeted history, physical examination, and any additional laboratory tests can be done at a follow-up visit 3 to 4 weeks later. At that time, the patient can discuss with the clinician the PDE5 inhibitor course of treatment. Kuritzky L, personal communication, 2004.

132 The targeted medical history will help determine whether the patient’s primary complaint is ED or another sexual issue. If the complaint is ED, the clinician may determine whether ED is a problem for the patient and his partner. The patient history can identify whether ED is psychogenic or organic and point to underlying causes.1 Psychogenic ED may be associated with problems such as depression, which is a common comorbidity.2 A question such as “Do you sometimes feel blue or down in the dumps?” can be helpful for diagnosis.3 In addition, ED, primarily of psychogenic origin, is characterized by a sudden onset and complete and immediate loss of sexual function, although morning erections are present. The psychogenic ED also seems to vary according to the partner and the circumstances in which sexual relations are attempted.4 Organic ED can be caused by medications (implicated in up to 25% of cases of ED), hypogonadism, or vasculopathy, especially in patients with diabetes or HTN.3-6 In addition, ED primarily of organic origin typically has a gradual onset and progresses incrementally. A characteristic finding is a lack of morning erections and lack of erections under sexually stimulating circumstances.4 It also is essential to determine whether the patient or anyone else in the household is taking nitrates, because PDE5 inhibitors are contraindicated in patients receiving nitrates of any form.7-9 Rosen R et al. In: Lue TF et al, eds. Sexual Medicine: Sexual Dysfunctions in Men and Women. Paris, France: Health Publications; 2004: Shabsigh R et al. Urology. 1998;52: Sadovsky R et al. Am J Manag Care. 1999;5: Ralph D et al. BMJ. 2000;321: Kuritzky L. J Am Osteopath Assoc. 2002;102(12 suppl 4):S7-S11. Slag MF et al. JAMA. 1983;249: Cialis® (tadalafil) prescribing information. Lilly ICOS LLC: Indianapolis, Ind and Bothell, Wash; 2005. Levitra® (vardenafil) prescribing information. Bayer Pharmaceuticals Corp: West Haven, Conn; 2005. Viagra® (sildenafil) prescribing information. Pfizer Inc: New York, NY; 2005.

133 The male sexual cycle of desire (libido), excitement, orgasm, and resolution forms the basis for questions regarding the patient’s sexual history. When obtaining the sexual history, questions should reflect problems with libido, arousal/erection, and orgasm/ejaculation.1 For example, the patient may be asked whether he is in the mood for sex and has desire, sexual thoughts, or fantasies.1 It is also important to ascertain whether the patient has trouble getting or keeping an erection or both; whether he loses the erection before he ejaculates; if he feels that he ejaculates too quickly or that it takes him too long to ejaculate; and how his partner reacts to their sexual encounters.2 Sadovsky R et al. Am J Manag Care. 1999;5: Rosen R et al. In: Lue TF et al, eds. Sexual Medicine: Sexual Dysfunctions in Men and Women. Paris, France: Health Publications; 2004:

134 The patient’s social history is very important, because sexual problems are often related to anxiety-related changes such as job problems, relationship problems (including poor communication/discord), financial worries, or moral values.1,2 PCCs should also be alert for substance abuse, including alcohol or cigarettes.2 It is important to consider cultural, social, ethnic, and religious perspectives because they may significantly influence patient needs, expectations, priorities, and treatment preferences.3 Tiefer L, Schuetz-Mueller D. Urol Clin North Am. 1995;22: Sadovsky R et al. Am J Manag Care. 1999;5: Lue TF et al. J Sex Med. 2004;1:6-24.

135 Physical examination of the patient with ED should include measurement of blood pressure, examination of the genitalia, and a neurologic examination. Physical examination of the genitalia, which is frequently overlooked, is important because common findings in patients who are either developing or already have ED include plaques, Peyronie’s disease, and sometimes shortening of the penis. The exam should include an approximate measurement of the testes, recognizing that normal size is generally thought to be  2 cm. Furthermore, clinicians should evaluate perineal sensations, rectal tone, and cremasteric and bulbocavernosal reflexes. Kuritzky L. J Am Osteopath Assoc. 2002;102(12 suppl 4):S7-S11.

136 The patient who is not taking nitrates and is able to walk at the rate of 1 mile in 15 minutes or less without shortness of breath or chest pain is at low CVD risk and probably does not need to undergo treadmill testing.1 The Princeton Consensus Panel recommendations can be used to further stratify patients’ CV status.2 Exertion is measured clinically as the metabolic equivalent of energy expenditure (ie, oxygen consumption), where 1 MET equals the resting state.3 A study in healthy young married men and their wives showed that the energy expended during sexual activity is equivalent to that of walking 2 to 3 miles per hour on a level surface.2,3 Kuritzky L. In: Seftel AD, ed. Male and Female Sexual Dysfunction. New York, NY: Mosby Publishers; 2004: Kostis JB et al. Am J Cardiol. 2005;96: Fox SM 3rd et al. Ann Clin Res. 1971;3:

137 Laboratory tests for ED should be individualized, based on the patient’s history, physical examination, complaints, and risk factors.1 Measurement of the morning free serum testosterone level should be considered if there is evidence of decreased libido or hypogonadism or if ED is present at a younger age.2 If the patient has not had a prostate-specific antigen (PSA) test in the past year or 2, it should be considered, particularly if there is a family history of prostate cancer, or if testosterone treatment is being considered.2 However, the role of routine PSA screening remains controversial. The American Academy of Family Practice does not recommend routine PSA screening,3 and the US Preventive Services Task Force (USPSTF) found that the evidence was insufficient to recommend for or against routine PSA screening.4 According to the USPSTF, the specificity of the test for prostate cancer is only 59%, and the overall positive predictive value of PSA is only 32% to 40%. There is a high rate of false-positive results because benign prostatic hyperplasia,3 which is seen with increasing prevalence in men after 45 years of age,5 often increases PSA levels. However, the American Urological Association endorses the American Cancer Society’s recommendation that PSA should be offered annually, beginning at age 50 years, to men who have a life expectancy of at least 10 years.6,7 If testosterone treatment is being considered, it is advisable to obtain a PSA level to evaluate prostate size and whether a tumor is present.2 A CVD risk burden profile consisting of fasting high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and blood glucose or HbA1c should be obtained for each patient. Measurement of homocysteine is optional.1 Kuritzky L. J Am Osteopath Assoc. 2002;102(12 suppl 4):S7-S11. Sadovsky R et al. Am J Manag Care. 1999;5: Prostate Specific Antigen. Family Practice notebook.com. Available at: Accessed November 22, 2005. US Preventive Services Task Force. Screening for prostate cancer: recommendations and rationale. Rockville, Md: Agency for Healthcare Research and Quality; AHRQ publication A. Boyle P et al. In: Chatelain C et al, eds. Benign Prostatic Hyperplasia. Plymouth, UK: Health Publication Ltd; 2001:19-68. American Urological Association. Early detection of prostate cancer. Available at: statements/services.cfm. Accessed May 20, 2003. American Cancer Society. Prostate cancer screening guideline. Available at: Accessed February 24, 2004.

138 Erectile Dysfunction Treatment

139 Penile Disorders Tx: Oral (phosphodiasterase type-5 inhibitors)
Penile Injection (PGE2, papavarine, phentolamine) Intraurethral pellet (MUSE): PGE2 Vacuum Erection Device Penile implant

140 Components of first-line therapy include lifestyle and drug therapy modifications that may impact erectile dysfunction (ED); psychosocial counseling and education about sexual techniques and normal age-related changes; androgen replacement therapy if a documented deficiency is present; and oral therapy such as phosphodiesterase type 5 (PDE5) inhibitors. Recommendations of the 1st International Consultation on Erectile Dysfunction. In: Jardin A et al, eds. Erectile Dysfunction. Plymouth, UK: Health Publication Ltd; 2000:

141 Unhealthy lifestyle may contribute to development of ED
Unhealthy lifestyle may contribute to development of ED. It is recommended, therefore, that patients modify behaviors that may increase ED risk.1-3 The following lifestyle modifications should be encouraged: smoking cessation,1,2 avoidance of alcohol1 and drug abuse, eating a healthy diet,2 and proper exercise.3 Lue TF et al. In: Lue et al, eds. Sexual Medicine: Sexual Dysfunctions in Men and Women. Paris, France: Health Publications; 2004: Feldman HA et al. Prev Med. 2000;30: Derby CA et al. Urology. 2000;56: Lewis RW et al. In Lue TF et al, eds. Sexual Medicine: Sexual Dysfunctions in Men and Women. Paris, France: Health Publications; 2004:37-72.

142 A growing body of evidence indicates an association between ED and a number of modifiable lifestyle factors, including smoking,1,2 lack of exercise or a sedentary lifestyle,3,4 and obesity.1 Data suggest that sedentary men may be able to reduce their risk of ED by exercising regularly.1,4 Interventions such as smoking cessation, weight loss, or a change in drinking habits in middle age have not consistently been shown to affect ED.3,4 However, there is some evidence to indicate that modification of risk factors such as tobacco and alcohol abuse, and better control of concomitant medical conditions such as diabetes mellitus (DM) or hyperlipidemia, may reverse ED and also possibly enhance the success rate with oral therapy.2,5 Despite the lack of strong clinical evidence for an effect on ED, changes such as smoking cessation, limiting or avoiding alcohol, and following a healthy diet constitute good clinical practice and should be recommended for the patient’s general well-being. Moreover, results of an anonymous, self-administered questionnaire completed by 104 hypertensive male patients showed that the 70.6% who suffered from ED had a significantly higher prevalence of cardiovascular complications (P<.05).6 Because these findings suggest that ED can be considered a marker for cardiovascular complications in hypertensive patients, lifestyle interventions are particularly important in this patient group. However, it is important to advise patients with ED that lifestyle changes alone may not reverse ED. Feldman HA et al. Prev Med. 2000;30: Guay AT et al. Endocr Pract. 1998;4:23-26. Derby CA et al. Urology. 2000;56: Esposito K et al. JAMA. 2004;291: Guay AT et al. J Androl. 2001;22: Burchardt M et al. Int J Impot Res. 2001;13:

143 Antihypertensive agents, mainly thiazides and thiazide-like diuretics,1-7 and, to a lesser extent, beta-blockers5,6 and calcium-channel blockers,6,7 have been reported to adversely affect sexual function. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin-receptor blockers are less likely to affect sexual function.8 The SSRIs are another category of drugs commonly associated with sexual side effects, such as delayed ejaculation and absent or delayed orgasm. Less common sexual side effects include decreased libido and problems with arousal, although a specific association between these complaints and SSRIs has not been found consistently.9 Hormonal chemotherapeutics, particularly the antiandrogens, also increase the risk of ED.10,11 Other drugs that interfere with the endocrine system, such as H2-receptor antagonists, contribute to ED. The H2-receptor antagonist most often associated with ED is cimetidine, which binds to androgen receptors. There have been few reports of ED with the newer proton pump inhibitors.7 If a patient receiving treatment with any of these agents complains of ED, he should be switched to an alternative therapeutic regimen whenever possible. 1. Grimm RH Jr et al. Arch Intern Med. 1985;145: 2. Chang SW et al. Arch Intern Med. 1991;151: 3. Curb JD et al. JAMA. 1985;253: 4. Wassertheil-Smoller S et al. Arch Intern Med. 1991;114: 5. Grimm RH Jr et al. Hypertension. 1997;29:8-14. 6. Suzuki H et al. J Hypertens. 1988;6(suppl):S649-S651. 7. Lundberg PO, Biriell C. Int J Impot Res. 1993;5: 8. Rosas SE et al. Kidney Int. 2001;59: 9. Rosen RC et al. J Clin Psychopharmacol. 1999;19:67-85. 10. Ralph D et al. BMJ. 2000;321: 11. Jackson G et al. Int J Clin Pract. 1999;53:

144 Psychosocial counseling may be used alone to manage ED or may be used as an adjunct to other treatment options. Psychosocial therapy addresses 4 main areas: anxiety reduction and desensitization, cognitive-behavioral interventions, sexual stimulation techniques, and interpersonal assertiveness with couples’ communication training.1 In addition, educating the patient and partner about what creates a normal sexual response and what contributes to ED can help overcome sexual difficulties.2 When psychological causes, such as those related to distress or adjustment (eg, depression, major life stress), are thought to be contributing to ED, one or more of these interventions typically is employed.1 However, outcomes research in this area is limited and the success of specific therapeutic techniques has not been well documented.2 Rosen RC. Urol Clin North Am. 2001;28: Althof SE et al. In: Lue TF et al, eds. Sexual Medicine: Sexual Dysfunctions in Men and Women. Paris, France: Health Publications; 2004:

145 AACE Male Sexual Dysfunction Task Force. Endocr Pract. 2003;9:77-95.
For men with a documented deficiency (eg, androgen deficiency and hypogonadism), hormone replacement therapy is appropriate. However, androgen replacement therapy may not necessarily improve ED, and the long-term health risks of such therapy, particularly with regard to cardiovascular and prostate disease, are not known.1 The most widely used form of testosterone replacement therapy in the United States is the transdermal gel, which can be applied daily to the shoulder, upper arm,2,3 or abdomen.2 The gel delivers a continuous amount of testosterone for 24 hours. A recent comparative trial in 227 hypogonadal men showed that the testosterone gel improved sexual function and mood, increased lean mass and muscle strength, and was associated with less skin irritation and fewer discontinuations than a permeation-enhanced testosterone patch.4 There are 2 transdermal testosterone patches for daily application to various nonscrotal body sites.5,6 Both formulations provide continuous release of testosterone and have central drug-delivery reservoirs that deliver physiologic amounts of testosterone so that circulating levels of hormone mimic the normal circadian rhythm of healthy young men. Until recently, the standard treatment for androgen deficiency was a depot IM injection of testosterone enanthate or cypionate (200 mg or 300 mg, respectively) every 2 or 3 weeks. Because smaller dosages and more frequent injections (50-mg to 150-mg IM at 7- to 14-day intervals) maintain normal levels of circulating testosterone more effectively, the current approach is to administer 100 mg on days 1, 11, and 21 of each month.1 Long-acting testosterone pellets for subcutaneous implantation are also available. Each pellet contains 75 mg of testosterone and provides a slow release of hormone for 3 to 6 months. The subcutaneous dosage for replacement in androgen deficiency is 150 mg to 450 mg.7 Although androgens were advocated in the past to enhance male sexual function, more effective treatments are available today. Use of testosterone should be discouraged when ED is not associated with hypogonadism.8 Oral testosterone preparations are contraindicated for use in the United States because of possible hepatotoxicity (cholestasis, hepatitis, benign or malignant tumors).8 AACE Male Sexual Dysfunction Task Force. Endocr Pract. 2003;9:77-95. AndroGel® 1% (testosterone gel) prescribing information. Unimed Pharmaceuticals Inc: Deerfield, Ill; 2001. Testim® 1% (testosterone gel) prescribing information. Auxilium Pharmaceuticals Inc: Norristown, Pa; 2003. Wang C et al. J Clin Endocrinol Metab. 2000;85: Testoderm® (testosterone transdermal system) prescribing information. Alza Pharmaceuticals: Palo Alto, Calif; 1998. Androderm® (testosterone transdermal system) prescribing information. Watson Pharma Inc: Corona, Calif; 1999. Testopel® (testosterone) pellets prescribing information. Bartor Pharmacal Co. Inc: Rye, NY; 1992. Lue TF. N Engl J Med. 2000;342:

146 Oral therapies currently available for treatment of ED are sildenafil, tadalafil, and vardenafil.1-3
Viagra® (sildenafil) prescribing information. Pfizer Inc: New York, NY; 2005. Cialis® (tadalafil) prescribing information. Lilly ICOS LLC: Indianapolis, Ind and Bothell, Wash; 2005. Levitra® (vardenafil) prescribing information. Bayer Pharmaceuticals Corp: West Haven, Conn; 2005.

147 Ernst E, Pittler MH. J Urol. 1998;159:433-436.
A number of substances that either enhance or block various neurotransmitters, such as nitric oxide (NO), dopamine, serotonin, norepinephrine, and acetylcholine, may act centrally to promote the initiation of erection or peripherally by causing relaxation of corporal smooth muscle.1 Although these agents are not as widely used as the peripherally acting agents sildenafil, tadalafil, and vardenafil, clinicians may encounter a patient who has used or is currently using one of these options for the treatment of ED. Phentolamine acts peripherally, while yohimbine and apomorphine act centrally.1 The alpha-adrenergic blocker yohimbine is thought to act at the brain centers involved in libido and penile erection.2 A recent meta-analysis of 7 randomized, controlled trials in men with ED found yohimbine to be superior to placebo for ED due to all causes combined, and especially for ED due to nonorganic causes. However, since yohimbine’s effect is marginal in organic ED, it is recommended only for nonorganic ED.3 Side effects most often reported include palpitation, fine tremor, elevated blood pressure (BP), and anxiety.2 Oral phentolamine has been reported to improve erections.2 Although not approved by the US FDA for the treatment of ED,2 it is available in Mexico, where drugs are often obtained by many US residents. Apomorphine SL, a sublingual formulation, is a centrally acting agent that acts on central dopaminergic receptors. It has good tolerability and modest efficacy in mild ED. It is not FDA approved for use in the United States, but has been approved and used in Europe since It is associated with moderate nausea and rare vasovagal syndrome.1 Over-the-counter herbal agents such as ginseng and Ginkgo biloba have received considerable attention in the media as ED remedies.4 The efficacy of these agents in humans has yet to be established in randomized, placebo-controlled trials. A 3-month, randomized trial compared Korean red ginseng (1,800 mg/d), trazodone (25 mg at bedtime), and placebo in 90 Korean patients with nonorganic ED. Results of monthly patient interviews showed more partial responses, defined as improved erections but not satisfactory for intercourse, in the ginseng-treated patients than in the other 2 groups.5 Lue TF et al. In: Lue TF et al, eds. Sexual Medicine: Sexual Dysfunctions in Men and Women. Paris, France: Health Publications; 2004: Lue TF. N Engl J Med. 2000;342: Ernst E, Pittler MH. J Urol. 1998;159: Moyad MA et al. Semin Urol Oncol.1999;17: Choi HK et al. Int J Impot Res. 1995;7:

148 Erectile Dysfunction Treatment

149 Second-line therapies, though generally more invasive, are local rather than systemic (ie, oral medications) therapy.1 These local therapies include vacuum constriction devices (VCDs), intracavernosal injection,1,2 transurethral therapy,1-4 and topical treatments.1,5,6 VCD is a second-line therapy option for men who are not interested in drug therapy or have specific contraindications to the available options.1 Intracavernosal injection, as well as transurethral or topical therapies, are options for men reluctant to use oral therapy, those who do not respond, have specific contraindications, or who experience AEs with oral therapy.2-6 Intracavernosal injections usually are alprostadil (prostaglandin E1) or, less often, a mixture of papaverine, phentolamine, and alprostadil (trimix). The trimix formulation is not currently approved by the FDA but is used in Europe.1 Alprostadil Medicated Urethral System for Erection (MUSE®) is generally considered less effective than intracavernosal injection and can cause vaginal irritation in female partners.1-4 Topical gels and creams (intrameatal) applications are alprostadil and a dermal permeation enhancer.1,4-7 Although approved for use in some Asian countries, intrameatal alprostadil is currently in phase 3 trials in the United States.7 Lue TF et al. In: Lue et al, eds. Sexual Medicine: Sexual Dysfunctions in Men and Women. Paris, France: Health Publications; 2004: Lue TF. N Engl J Med. 2000;342: Padma-Nathan H et al. N Engl J Med. 1997;336:1-7. Lewis R. Int J Impot Res. 2000;12(suppl 4):S86-S90. Goldstein I et al. Urology. 2001;57: McVary KT et al. J Urol. 1999;162: Becher E. Expert Opin Pharmacother. 2004;5:

150 VCDs are considered a second-line option for men who are not interested in drug therapy or those who have specific contraindications to the available pharmacologic options.1,2 By applying negative pressure to the penis, the VCD draws blood into the cavernosal spaces. The blood is then retained by application of an elastic band to the base of the penis.1,2 Penile pain, numbness, bruising, and retarded ejaculation are the main side effects associated with VCD therapy.1,2 Many patients prefer VCD therapy because it is available for on-demand use, lacks contraindications, and is less costly over time than other treatment options.1,2 Lue TF et al. In: Lue TF et al, eds. Sexual Medicine: Sexual Dysfunctions in Men and Women. Paris, France: Health Publications; 2004: Lewis JL. Am J Nurs. 2003;103:48-87.

151 Intracavernosal injection therapy is the preferred second-line treatment option after oral therapy.1 It is appropriate for those in whom oral therapy is contraindicated, those who are intolerant to or who fail to respond to oral therapy, those who have adverse reactions to the oral drugs, and those who object to oral medications.1,2 Office trials of intracavernosal injection therapy are done initially to titrate the dose and instruct the patient on self-administration. After the patient has become comfortable with the injection technique, at-home therapy can be prescribed. A follow-up examination is scheduled several weeks after starting home therapy; subsequent follow-up visits are scheduled 2 or 3 times a year.3 Advantages of intracavernosal injection therapy are that it is relatively safe and highly effective, producing more reliable, rapid (5 to 20 minutes),1 and predictable erections.2 Intracavernosal injection is associated mainly with local side effects, including pain, priapism, and fibrotic changes (eg, palpable nodules or plaques) on or within the tunica albuginea.2,3 Intracavernosal therapy is contraindicated in patients with sickle cell anemia and other conditions that predispose one to priapism.2 Shabsigh R et al. Urology. 2000;55: Lue TF et al. In: Lue TF et al, eds. Sexual Medicine: Sexual Dysfunctions in Men and Women. Paris, France: Health Publications; 2004: Leungwattanakij S et al. Urol Clin North Am. 2001;28:

152 An alternative to injection therapy is transurethral application of alprostadil with or without a penile constriction device.1,2 Like injection therapy, transurethral alprostadil is appropriate for those who fail to respond to oral therapy and for those who have adverse reactions to specific oral drugs or in whom oral drugs are contraindicated.1 It is also another option for men in whom a penile prosthesis has failed3 and for those who have failed injection therapy.4 Transurethral therapy is less invasive than injections and produces more rapid (5 to 10 minutes), predictable erections.5 However, it is significantly less effective than intracavernosal injection.1,2 Penile pain is a common complaint of patients who use transurethral alprostadil.1,2 In addition, symptomatic hypotension and syncope have been reported.1,5 This therapy can also cause vaginal irritation if the some of the pellet gets into the partner’s vagina.1 Transurethral alprostadil is contraindicated in men with abnormal penile anatomy and sickle cell anemia. 5 Lue TF et al. In: Lue TF et al, eds. Sexual Medicine: Sexual Dysfunctions in Men and Women. Paris, France: Health Publications; 2004: Shabsigh R et al. Urology. 2000;55: Benevides MD, Carson CC. J Urol. 2000;163: Engel JD, McVary KT. Urology. 1998;51: MUSE® (alprostadil) urethral suppository prescribing information. Vivus Inc: Mountain View, Calif; 1998.

153 The final treatment option for patients with ED who are intolerant to or who fail to respond to other treatment modalities is implantation of a penile prosthesis.1 This treatment option is particularly helpful for patients with irreparably damaged erectile tissue and those with specific concomitant medical conditions such as vascular or neurologic disease, chronic renal disease, and genital trauma (eg, Peyronie’s disease).2-4 Lue TF et al. In: Lue TF et al, eds. Sexual Medicine: Sexual Dysfunctions in Men and Women. Paris, France: Health Publications; 2004: Carson CC et al. J Urol. 2000;164: Carson CC, Patel MP. Adv Renal Replacement Ther. 1999;6: Carson CC. Int J Impot Res. 2000;12(suppl 4):S122-S126.

154 Currently, multicomponent, inflatable penile prostheses are the type most frequently used.1
A retrospective US multicenter study to determine longevity, morbidity, and patient satisfaction examined the medical records of 372 men who underwent implantation with the AMS 700CX from 1987 to 1996, and obtained telephone interviews with 207 patients.2 Mechanical reliability of the AMS 700CX prosthesis was 86% after 5 years. Erections suitable for sexual intercourse were reported by 91% of 172 men who had a valid questionnaire. In addition, 86.5% of the men stated that they would undergo penile prosthesis implantation again, and 88.2% said that they would recommend the procedure to a friend or relative with ED.2 Another retrospective study reviewed the medical records for 273 men with ED who underwent primary penile prosthesis implantation with the AMS 700CXM from January 1991 to April A telephone interview assessed the functional status of the prosthesis and found the mechanical reliability to be 90.4% after 5 years.3 Similar mechanical reliability after 5 years (92.6%) was seen with first-time implantation of the enhanced Mentor Alpha I penile prosthesis.4 Jhaveri FM et al. Int J Impot Res. 1998;10: Carson CC et al. J Urol. 2000;164: Choi YD et al. J Urol. 2001;165: Wilson SK et al. J Urol. 1999;162:

155 Incontinence, Urine Key Objective (s):
Contrast between the two most common causes of incontinence, stress incontinence and urgency incontinence.

156 Incontinence, Urine Objectives
Through efficient, focused, data gathering Determine duration, characteristics, frequency, timing, and amount; elicit other lower urinary tract symptoms, precipitants, fluid intake patterns, changes in bowel habits or sexual function. Differentiate between stress (small amounts of leakage with exertion), urgency (involuntary associated with urge to urinate), reflex (associated neurologic deficit), and overflow incontinence (associated with urinary retention) Perform an abdominal exam, a pelvic exam, and rectal exam for prostate size List and interpret critical clinical and laboratory findings which are key in the processes of exclusion, differentiation, and diagnosis Perform urinalysis, estimate post-void residual urine. Select patients in need of cystoscopy and other specialized tests. Conduct an effective plan of management for a patient with hematuria Outline a plan of management for cystitis and urethritis. Counsel patients with stress incontinence about possible pelvic muscle exercises. For urge incontinence, discuss trial of anticholinergic medication (e.g. oxybutynin, tolterodine) Select patients for referral (e.g. neurologic conditions, genital prolapse, abnormal post-void)

157 Lower Urinary Tract Group of inter-related structures
>> efficient and low pressure bladder filling >> low pressure urine storage with perfect continence >> periodic voluntary urine expulsion at low pressure Functional, physiologic, and pharmacologic considerations Many different classifications >> will present a functional and practical approach

158 Normal Lower Urinary Tract Function
2 phase concept of function Filling / Storage Emptying

159 Normal Lower Urinary Tract Function
Bladder Filling / Storage Accomodation of increasing volumes of urine at low pressures with appropriate sensation Bladder outlet that is closed at rest and remains so during increases in intra-abdominal pressure Absence of involuntary bladder contractions

160 Normal Lower Urinary Tract Function
Bladder Emptying Coordinated contraction of bladder smooth musculature of adequate magnitude Lowering of resistance at the level of the smooth and striated sphincter Absence of anatomic (as opposed to functional) obstruction

161 Voiding Dysfunction Any type of voiding dysfunction must result from an abnormality of one or more of the previous factors The Functional classification Failure to Store Because of the bladder Because of the outlet Failure to Empty

162 The Functional Classification
Failure to Store Because of the Bladder Detrusor Hyperactivity Suprasacral neurologic dz BOO Idiopathic Inflammation Aging Decreased Compliance Neurologic dz (denervation) Fibrosis / inflammation Detrusor Hypersensitivity Neurologic Infectious Inflammation (I.C.) Psychologic Because of the Outlet Stress Incontinence (Hypermobility) Nonfunctional bladder neck/proximal urethra (ISD) Neurologic Trauma Surgery Obstetrical/Gynecologic Aging

163 The Functional Classification
Failure to Empty Because of the Bladder Neurologic (sacral / peripheral nerves, pain, Herpes, DM, Tabes Dorsalis, pelvic surgery) Myogenic (overdistention, infection, meds, fibrosis) Psychogenic Idiopathic Pharmacologic Because of the Outlet Anatomic Prostatic obstruction Bladder neck contracture Urethral stricture Urethral Compression Functional Smooth Sphincter Dyssynergia (SCI above T6) Striated Sphincter Dyssynergia

164 Evaluation of Voiding Dysfunction
History Physical Urinalysis Urodynamics Radiography Cystoscopy Videourodynamics

165 Evaluation of Voiding Dysfunction
History Urologic Lower urinary tract symptoms Storage vs. Emptying symptoms Irritative, obstructive, pain, hematuria, incontinence (stress, urge, unconscious, continuous) Ob/Gyn Neurologic Medical / Surgical Social / Psychologic Radiation Pelvic Trauma

166 Evaluation of Voiding Dysfunction
Incontinence History “involuntary loss of urine” Symptom – statement of involuntary loss Sign – objective demonstration of urine loss Condition – pathophysiology underlying incontinence Characterization of incontinence Stress – loss during coughing, sneezing, physical exertion Urge – sudden, strong urge to void Unconscious – unaccompanied by stress or urge Continuous Overflow Length and severity of symptoms Impact on quality of life Associated bowel problems

167 Evaluation of Voiding Dysfunction
Physical Exam Systemic vaginal and pelvic exam Condition of mucosa Urethral hypermobility Demonstration of incontinence / SUI Vaginal prolapse Use of bottom half of small speculum Bimanual exam Standing position in females with SUI / prolapse Neurologic exam Mental status Mobility Lumbar and sacral sensory and motor BC reflex, anal wink, knee and ankle DTR’s, perineal / perianal sensation

168 Evaluation of Voiding Dysfunction
Simple Ancillary Tests Voiding and intake diary Time, input, output, types of beverages Incontinence Diary Stress, urge U/A – rule out hematuria, UTI C & S, cytology when indicated Post void residual Pad Test Endoscopy Not recommended as a routine in the evaluation of incontinence May be useful when clinically indicated Hematuria Refractory incontinence Anatomic abnormalities Prior surgery Etc.

169 Transient vs. Established Incontinence
Delirium Infection Atrophic urethritis/ vaginitis Pharmaceuticals Psychological Endocrine Restricted mobility Stool Impaction

170 Transient vs. Established Incontinence
Delirium Infection Atrophic urethritis/ vaginitis Pharmaceuticals Psychological Endocrine Restricted mobility Stool Impaction

171 Treatment of Voiding Dysfunction


Download ppt "Urology Back to Basics The “Nuts” and Bolts"

Similar presentations


Ads by Google