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Benign prostatic hyperplasia

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Benign prostatic hyperplasia

  2. 2. Presentation layout • • • • • • • • Relevant anatomy Etiology Pathophysiology Symptoms Complications of BPH Diagnosis Treatment References
  3. 3. Prostate Gland Anatomy • • • • • • Male sex gland Pear-shape,wt7-16gm Size of a walnut Helps control urine flow Produces fluid component of semen Produces Prostate Specific Antigen (PSA
  4. 4. Development • The prostatic part of the urethra develops from the urogenital sinus (endodermal origin). • It grows into the surrounding mesenchyme • The glandular epithelium of the prostate differentiates from these endodermal cells • Mesenchyme differentiates into the dense stroma and the smooth muscle of the prostate • The prostate glands arises by the 9th week of embryonic life • Condensation of mesenchyme, urethra and Wolffian ducts gives rise to the adult prostate gland, a composite organ made up of several glandular and non-glandular components tightly fused.
  5. 5. Arterial supply • From the anterior division of the internal iliac artery Inferior vesical artery, Middle rectal artery Internal pudendal artery originates (hypogastric) artery. • The capsular artery is the second main branch of the prostate. Supply the glandular tissue.
  6. 6. Venous drainage • Prostatic plexus of veins • Valveless communication exists between the prostatic and vertebral plexus through which prostatic carcinoma spread to vertebral column and to skull
  7. 7. • Innervations  from pelvic plexuses formed by the parasympathetic, visceral, efferent, and preganglionic fibers that arise from the sacral • levels(S2-S4)  sympathetic fibers from the thoracolumbar levels (L1L2).  The pudendal nerve is the major nerve supply leading to • Somatic innervations of the striated sphincter and the levator • ani. The preprostatic sphincter and the vesicle neck or internal sphincter is under alpha-adrenergic control.
  8. 8. Lymphatic drainage • Obturator and the internal iliac lymphatic channels. • External iliac, presacral, and the para-aortic lymph nodes.
  9. 9. ETIOLOGY Role of Androgens • Androgens do not cause BPH • The development of BPH requires the presence of testicular androgens • Patients castrated before puberty or who are affected by a variety of genetic diseases that impair androgen action or production do not develop BPH.
  10. 10. ETIOLOGY Dihydrotestosterone and Steroid 5α-Reductase • Intraprostatic DHT concentrations are maintained but not elevated in BPH • DHT is a more potent androgen than testosterone because of its higher affinity for the AR • Moreover, the DHT-receptor complex may be more stable than the testosterone receptor complex.
  11. 11. • Two types of steroid 5α-reductase have been discovered, each encoded by a separate Type 1 5α-reductase, the predominant enzyme in extraprostatic tissues, such as skin and liver, is normally expressed in the 5αreductase deficiency syndrome Type 2 5α-reductase is the predominant prostatic 5α-reductase, although it is also expressed in extraprostatic tissues
  12. 12. ETIOLOGY Role of Estrogens • There is animal model evidence to suggest that estrogens play a role in the pathogenesis of BPH • The role of estrogens in the development of human BPH, however, is less clear • There are at least two forms of ER ER-α is expressed by prostate stromal cells ER-β is expressed by prostate epithelial cells
  13. 13. ETIOLOGY Regulation of Programmed Cell Death • Programmed cell death (apoptosis) is a physiologic mechanism crucial to the maintenance of normal glandular homeostasis • This is impaired in BPH
  14. 14. ETIOLOGY Stromal-Epithelial Interaction • Prostatic stromal and epithelial cells maintain a sophisticated paracrine type of communication • Thus BPH may be due to a defect in a stromal component that normally inhibits cell proliferation, resulting in loss of a normal “braking” mechanism for proliferation
  15. 15. ETIOLOGY Growth Factors • Interactions between growth factors and steroid hormones may alter the balance of cell proliferation versus cell death to produce BPH • GF implicated in prostate growth. bFGF (FGF-2) acidic FGF (FGF-1) Int-2 (FGF-3) KGF, FGF-7) β (TGF-β EGF • TGF-β (transforming ) is a potent inhibitor of proliferation in normal epithelial cells in a variety of tissues
  16. 16. ETIOLOGY Other Signaling Pathways • The early growth response gene-1 (EGR1) • α2-macroglobulin • IL-2, IL-4, IL-7, IL-17, interferon-γ (IFN-γ) • Genetic and Familial Factors
  17. 17. PATHOPHYSIOLOGY • The pathophysiology of BPH is complex • BPH increases urethral resistance, resulting in compensatory changes in bladder function • Elevated detrusor pressure is required to maintain urinary flow in the presence of increased outflow resistance
  18. 18. LUTS Voiding (obstructive) symptoms • Hesitancy • Weak stream • Straining to pass urine • Prolonged micturition • Feeling of incomplete bladder emptying • Urinary retention Storage (irritative or filling) symptoms • Urgency • Frequency • Nocturia • Urge incontinence LUTS is not specific to BPH – not everyone with LUTS has BPH and not everyone with BPH has LUTS
  19. 19. Common Symptoms n decrease in the urinary stream n Dribbling or leaking after urination n Intermittency n Hesitancy n Pain or burning during urination n Feeling that the bladder never completely empties
  20. 20. Complications Mortality • 10 per 100,000 Bladder Stones • bladder stone development is small Urinary Tract Infections • 0.1/100 patient-years Bladder Decompensation • progression from normal mucosa to advancing trabeculation, diverticula and detrusor muscle failure
  21. 21. Complications Urinary Incontinence • complications from surgical intervention for BPH • secondary to overdistention of the bladder (overflow incontinence) • Due to detrusor instability (urge incontinence) Acute Urinary Retention • Long-term outcome resulting from BPH
  22. 22. Diagnosis of BPH • History and Examination • Digital rectal examination(DRE) • inaccurate for size but can detect shape and consistency • Ultrasonography • Urodynamic analysis • Measurement of prostate-specific antigen (PSA) – high correlation between PSA and PV, specifically TZV 1 – men with larger prostates have higher PSA levels – PSA is a predictor of disease progression and screening tool for CaP – as PSA values tend to increase with increasing PV and increasing age, PSA may be used as a prognostic marker for BPH
  23. 23. Other investigations • • • • • • Serum Creatinine Measurement Urinalysis Postvoid Residual Urine Volume Pressure-Flow Studies Filling Cystometry (Cystometrography) Urethrocystoscopy
  24. 24. TREATMENT BPH needs to be treated ONLY IF: n The symptoms are severe enough to bother patient and affect the quality of life n Renal insufficiency n Frequent urinary tract infections
  25. 25. TREATMENT • Medical • Minimally Invasive and Endoscopic • Surgical approaches
  26. 26. TREATMENT •First line of defense against bothersome urinary symptoms –Manage the condition - don’t fix it •Two major types: •(Alpha-1-blocker) - relax the prostate and provide a larger urethral opening (prazosin,terazosin) •Shrink the prostate gland (5-alpha reductase inhibitor) (finasteride)
  27. 27. TREATMENT • Combination therapy with both an αadrenergic receptor blocker and a 5αreductase inhibitor has been demonstrated to be the most effective • Antimuscarinic agents are useful adjuncts for patients with “storage” symptoms or ED
  28. 28. Minimally Invasive and Endoscopic Temporary Stents • Temporary stents are tubular devices that are made of either a nonabsorbable or a biodegradable material • designed for short-term use, to relieve bladder outlet obstruction (BOO)
  29. 29. Temporary Stents • Spiral Stents- e.g Urospiral,stent should remain in the prostatic urethra for longer than 12 months • Polyurethane Stents • Biodegradable Stents
  30. 30. Permanent Stents • were introduced as a definitive treatment for prostatic obstruction, particularly for patients unfit for prostatic surgery • Patients were able to void satisfactorily in most cases, but complications were relatively high • UroLume endourethral prosthesis
  31. 31. TRANSURETHRAL NEEDLE ABLATION OF THE PROSTATE (TUNA) • Heat treatment inducing necrosis of prostatic tissue • The aim is to increase prostatic temperature to in excess of 60° C • Uses low-level radiofrequency (RF) energy that produces localized necrotic lesions in the hyperplastic tissue.
  32. 32. Deployment of radiofrequency needles in transurethral needle ablation
  33. 33. TRANSURETHRAL MICROWAVE THERAPY • These cover heat changes and differential blood flow in the prostate • Damages the sympathetic nerve endings • Induction of apoptosis
  34. 34. The Prostatron antenna, treating the prostatic transition zone.
  35. 35. LASERS • “laser” stands for light amplification by the stimulated emission of radiation • There are four types of laser that can be used to treat the prostate 1. Neodymium : Yttrium-Aluminum-Garnet Laser 2. Potassium-Titanyl-Phosphate Laser 3. Holmium : Yttrium-Aluminum-Garnet Laser 4. Diode Laser
  36. 36. LASERS The energy from lasers can be delivered as follows: • End firing Bare tip Sculptured tip Sapphire tip • Side firing Metal or glass reflector Prismatic internal reflector
  37. 37. TRANSURETHRAL RESECTION OF THE PROSTATE (TURP) • Gold Standard” of care for BPH • Uses an electrical “knife” to surgically cut and remove excess prostate tissue • Effective in relieving symptoms and restoring urine flow
  38. 38. TURP Operation is performed through a modified cystoscope • Prostatic tissue is resected using an electrically energized wire loop • • Prostatic capsule is usually preserved. Continuous irrigation is necessary to distend the bladder and to wash away blood and dissected prostatic tissue. •
  40. 40. IRRIGATION FLUID Ideally the irrigation solution should be: • Isotonic • electrically inert • Nontoxic • Transparent • inexpensive • • Nonhemolytic Nonmetabolized
  41. 41. COMPLICATIONS •TURP can be associated with a number of complications: •TURP Syndrome (2%) •Hemorrhage •Bladder perforation (1%) •Hypothermia •Septicemia (6%) •DIC •The main challenges are blood loss and TURP Syndrome due to excessive absorption of irrigant fluid
  42. 42. TURP SYNDROME • • TURP syndrome: constellation of signs and symptoms caused by the absorption of large volumes of isotonic irrigating fluids through prostatic veins or breaches in the prostatic capsule. The syndrome is characterized by • hypervolemia, • hyponatremia • hypo-osmolarity
  43. 43. TURP SYNDROME: RISK FACTORS TURP syndrome is more likely to occur: 1. The hydrostatic pressure of the irrigation solution is high. 2. An excessively distended bladder 3. Prostatic gland is large. 4. The Prostatic Capsule is violated during surgery. 5. Duration of surgery (>60mins)
  44. 44. Retropubic Prostatectomy • Proper Positioning of the Patient • Once anesthesia has been induced the patient is positioned on the operating table in a supine position • Trendelenburg position without extension
  45. 45. Retropubic prostatectomy. The space of Retzius has been opened and the periprostatic adipose tissue has been dissected free from the superficial branch of the dorsal vein complex. The endopelvic fascia is incised bilaterally
  46. 46. A 2-0 chromic suture on a 58-inch circle-tapered needle is passed in the avascular plane between the urethra and the dorsal vein complex at the apex of the prostate. A tie is grasped and tied around the dorsal vein complex. B, With 2-0 chromic suture material on a CTX needle, a figure-ofeight suture is placed through the prostatovesicular junction just above the level of the seminal vesicles to control the main arterial blood supply to the prostate gland. When placing this suture, care must be taken to avoid entrapment of the neurovascular bundles located posteriorly and slightly laterally
  47. 47. Retropubic prostatectomy. A, With the superficial branch of the dorsal vein complex secured proximally and distally, a No. 15 blade on a long handle is used to make the transverse capsulotomy. B, Metzenbaum scissors are used to develop the plane anteriorly between the prostatic adenoma and the prostatic capsule.
  48. 48. Retropubic prostatectomy. A, With blunt dissection with the index finger, the prostatic adenoma is dissected free laterally and posteriorly. B, Metzenbaum scissors are used to divide the anterior commissure to visualize the posterior urethra and verumontanum. C, The index finger is then used to fracture the urethral mucosa at the level of the verumontanum. With this last maneuver, extreme care is taken not to injure the external sphincteric mechanism
  49. 49. Retropubic prostatectomy. A, After removal of the left lateral lobe of the prostate, the right lateral lobe is excised with the aid of a tenaculum and Metzenbaum scissors. B, Lastly, the median lobe is removed under direct vision
  50. 50. Retropubic prostatectomy. A, View of the prostatic fossa and posterior urethra after enucleation of all the prostatic adenoma. Note that the verumontanum and a strip of posterior urethra remain intact. B, After placement of a urethral catheter and, if needed, a Malecot suprapubic tube, the transverse capsulotomy is closed with two running 2-0 chromic sutures. The two sutures are tied first to themselves and then to each other across the midline to create a watertight closure of the prostatic capsule.
  51. 51. Suprapubic Prostatectomy • Proper Positioning of the Patient • After anesthesia has been induced, the patient is positioned on the operating table in a supine position. • The table is placed in a mild Trendelenburg position without extension • 22-Fr catheter is inserted into the bladder. After residual urine is drained, 250 mL of saline is instilled into the bladder and the catheter is clamped.
  52. 52. Suprapubic prostatectomy. A, A lower midline incision is made from the umbilicus to the pubic symphysis. B, After developing the prevesical space, a small, longitudinal cystotomy is made with an electrocautery
  53. 53. With adequate exposure of the bladder neck, a circular incision in the bladder mucosa is made distal to the trigone, using an electrocautery
  54. 54. Starting at the bladder neck posteriorly, Metzenbaum scissors are used to develop the plane between the prostatic adenoma and the prostatic capsule (lateral view). B, Anterior view of the same maneuver
  55. 55. Using the index finger, the prostatic adenoma is enucleated from the prostatic fossa (lateral view). B, Anterior view of the same maneuver. With extreme large prostate glands, the left, right, and median lobes should be removed separately
  56. 56. After enucleation of the entire prostatic adenoma, a 0-chromic suture is used to place two figure-of-eight sutures to advance bladder mucosa into the prostatic fossa at the 5- and 7-o’clock positions at the prostatovesicular junction to ensure control of the main arterial blood supply to the prostate.
  57. 57. suprapubic tube, the cystotomy is closed in two layers using a running 2-0 Vicryl suture, enforced by tying of multiple interrupted 3-0 Vicryl stay sutures. A closed Davol suction drain is placed on one side of the bladder and exits via a separate stab incision
  58. 58. REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9. Abrams P, Chapple C, Khoury S, et al. Evaluation and treatment of lower urinary tract symptoms in older men. J Urol 2009;181(4):1779–87. Berry SJ, Coffey DS, Walsh PC, Ewing LL. The development of human benign prostatic hyperplasia with age. J Urol 1984;132(3):474–9. Garraway WM, Collins GN, Lee RJ. High prevalence of benign prostatic hypertrophy in the community. Lancet 199124;338(8765):469–71. Hutchison A, Farmer R, Verhamme K, et al. The efficacy of drugs for the treatment of LUTS/BPH, a study in 6 European countries. Eur Urol 2007;51(1):207–15; discussion 215–206. Jacobsen SJ, Jacobson DJ, Girman CJ, et al. Natural history of prostatism: risk factors for acute urinary retention. J Urol 1997;158(2):481–7. Kohler T, McVary K. The relationship between erectile dysfunction and lower urinary tract symptoms and the role of phosphodiesterase type 5 inhibitors. Eur Urol 2009;55(1):38–48. Madersbacher S, Alivizatos G, Nordling J, et al. EAU 2004 guidelines on assessment, therapy and follow-up of men with lower urinary tract symptoms suggestive of benign prostatic obstruction (BPH guidelines). Eur Urol 2004;46(5):547–54. McConnell JD, Roehrborn CG, Bautista OM, et al. The long-term effect of doxazosin, finasteride, and combination therapy on the clinical progression of benign prostatic hyperplasia. N Engl J Med 2003;349(25):2387–98. McNeill SA, Hargreave TB, Roehrborn CG. Alfuzosin 10 mg once daily in the management of acute urinary retention: results of a double-blind placebo-controlled study. Urology 2005;65(1):83–9; discussion 89–90.