Testicular Tumours

TESTICULAR TUMOUR
1% of all Malignant Tumour Affects young adults - 20 to 40 yrs - when Testosterone Fluctuations are maximum 90% to 95% of all Testicular tumours from germ cells 99% of all Testicular Tumours are malignant. Causes Psychological & Fertility Problems in young

Survival in Testicular Tumours

Improved overall survival in last 15 to 20 years due to Better understanding of Natural History and Pathogenesis of disease Reliable Tumour Markers Cis-platinum based chemotherapy

CROSS SECTION OF TESTIS

Testis Stroma Seminiferous Tubules (200 to 350 tubules)

Interstitial Cells Leydig (Androgen)

Supporting or Sertoli Cell

Spermatogonia

EPIDEMIOLOGY
Incidence : 1.2 per 100,000 (Bombay) 3.7 per 100,000 (USA) Age : 3 Peaks - 20-40 yrs. Maximum - 0 - 10 yrs. - After - 60 yrs.

Bilaterality :

2 to 3% Testicular Tumour

CLASSIFICATION
I. Primary Neoplasma of Testis. A. Germ Cell Tumour B. Non-Germ Cell Tumour Secondary Neoplasms.

II.

III. Paratesticular Tumours.

I. PRIMARY NEOPLASMS OF TESTIS

A.
Germinal Neoplasms : (90 - 95 %) 1. Seminomas - 40% (a) Classic Typical Seminoma (b) Anaplastic Seminoma (c) Spermatocytic Seminoma 2. Embryonal Carcinoma - 20 - 25% 3. Teratoma - 25 - 35% (a) Mature (b) Immature 4. Choriocarcinoma - 1% 5. Yolk Sac Tumour

I. PRIMARY NEOPLASMS OF TESTIS

B. 1. Nongerminal Neoplasms : ( 5 to 10% ) Specialized gonadal stromal tumor (a) Leydig cell tumor (b) Other gonadal stromal tumor Gonadoblastoma Miscellaneous Neoplasms (a) Adenocarcinoma of the rete testis (b) Mesenchymal neoplasms (c) Carcinoid (d) Adrenal rest tumor

2. 3.

II. SECONDARY NEOPLASMS OF TESTIS

A. B.
III.

Reticuloendothelial Neoplasms Metastases

PARATESTICULAR NEOPLASMS

A. B. C. D. E.

Adenomatoid Cystadenoma of Epididymis Mesenchymal Neoplasms Mesothelioma Metastases

AETIOLOGY OF TESTICULAR TUMOUR

1. Cryptorchidism
2. 3. Carcinoma in situ Trauma

4. Atrophy

CRYPTORCHIDISM & TESTICULAR TUMOUR

Risk of Carcinoma developing in undescended testis is 14 to 48 times the normal expected incidence

Clinical Staging of Testicular Tumour

Staging A or I Staging B or II - Tumour confined to testis. - Spread to Regional nodes.

IIA - Nodes <2 cm in size or < 6 Positive Nodes IIB - 2 to 5 cm in size or > 6 Positive Nodes IIC - Large, Bulky, abd.mass usually > 5 to 10 cm

Staging C or III - Spread beyond retroperitoneal Nodes or Above Diaphragm or visceral disease

Requirements for staging

To properly Stage Testicular Tumours following are pre-requisites: (a) Pathology of Tumour Specimen

(b)
(c) (d) (e)

History
Clinical Examination Radiological procedure - USG / CT / MRI / Bone Scan Tumour Markers - HCG, AFP

TNM Staging of Testicular Tumour

T0 T1s T1 T2 = = = = No evidence of Tumour Intratubular, pre invasive Confined to Testis Invades beyond Tunica Albuginea or into Epididymis Invades Spermatic Cord Invades Scrotum Single < 2 cm Multiple < 5 cm / Single 2-5 cm Any node > 5 cm

T3 T4
N1 N2 N3

= =
= = =

Epididymis or Scrotal skin Lymph drainage to Inguinal Nodes

Pathogenesis & Natural History of Testicular Tumour

Course of Spread of Germ Cell Tumours are predictible once Histology of Tumour cofirmed Lymphatic Spread has a set pattern depending on side of Tumour Seminoma may have non-seminomatous metastasis High Grade Tumours spread by both Vascular invasion & via Lymphatics

Investigation
1. 2. 3. 4. Ultrasound - Hypoechoic area Chest X-Ray - PA and lateral views CT Scan Tumour Markers - AFP - HCG - LDH - PLAP

CLINICAL FEATURES

Painless Swelling of One Gonad

Dull Ache or Heaviness in Lower Abdomen 10% - Acute Scrotal Pain

10% - Present with Metatstasis

- Neck Mass / Cough / Anorexia / Vomiting / Back Ache/ Lower limb swelling 5% - Gynecomastia Rarely - Infertility

DICTUM FOR ANY SOLID SCROTAL SWELLINGS

All patients with a solid, Firm Intratesticular Mass that cannot be Transilluminated should be regarded as Malignant unless otherwise proved

Tumour Markers
TWO MAIN CLASSES Onco-fetal Substances : AFP & HCG

Cellular Enzymes : LDH & PLAP

( AFP - Trophoblastic Cells HCG - Syncytiotrophoblastic Cells )

AFP ( Alfafetoprotein )
NORMAL VALUE: Below 16 ngm / ml HALF LIFE OF AFP 5 and 7 days Raised AFP : Pure embryonal carcinoma Teratocarcinoma Yolk sac Tumour Combined Tumour
REMEMBER: AFP Not raised is Pure Choriocarcinoma or Pure Seminoma

HCG ( Human Chorionic Gonadotropin )

Has and polypeptide chain
NORMAL VALUE: < 1 ng / ml HALF LIFE of HCG: 24 to 36 hours RAISED HCG 100 % - Choriocarcinoma 60% - Embryonal carcinoma 55% - Teratocarcinoma\ 25% - Yolk Cell Tumour 7% - Seminomas

ROLE OF TUMOUR MARKERS

Helps in Diagnosis - 80 to 85% of Testicular Tumours have Positive Markers
Most of Non-Seminomas have raised markers

Only 10 to 15% Non-Seminomas have normal marker level

After Orchidectomy if Markers Elevated means Residual Disease or Stage II or III Disease Elevation of Markers after Lymphadenectomy means a STAGE III Disease

ROLE OF TUMOUR MARKERS cont...

Degree of Marker Elevation Appears to be Directly Proportional to Tumour Burden Markers indicate Histology of Tumour: If AFP elevated in Seminoma - Means Tumour has Non-Seminomatous elements Negative Tumour Markers becoming positive on follow up usually indicates Recurrence of Tumour Markers become Positive earlier than X-Ray studies

PRINCIPLES OF TREATMENT
Treatment should be aimed at one stage above the clinical stage
Seminomas Radiotherapy. Radio-Sensitive. Treat with

Non-Seminomas are Radio-Resistant and best treated by Surgery

Advanced Disease or Metastasis - Responds well

to Chemotherapy

PRINCIPLES OF TREATMENT
Radical INGUINAL ORCHIDECTOMY is Standard first line of therapy
Lymphatic spread initially goes to

RETRO-PERITONEAL NODES
Early hematogenous spread RARE Bulky Retroperitoneal Tumours or Metastatic Tumors Initially DOWN-STAGED with CHEMOTHERAPY

Treatment of Seminomas
Stage I, IIA, ?IIB
Radical Inguinal Orichidectomy followed by radiotherapy to Ipsilateral Retroperitonium & Ipsilateral Iliac group Lymph nodes (2500-3500 rads)

Bulky stage II and III Seminomas Radical Inguinal Orchidectomy is followed by Chemotherapy

Treatment of Non-Seminoma
Stage I and IIA: RADICAL ORCHIDECTOMY followed by RETROPERITONEAL LYMPH NODES DISSECTION Stage IIB: RPLND with possible ADJUVANT CHEMOTHERAPY

Stage IIC and Stage III Disease: Initial CHEMOTHERAPY followed by SURGERY for Residual Disease

STANDARD CHEMOTHERAPY FOR NON-SEMINOMATOUS GERM CELL TUMOURS

Chemotherapy
BEP Bleomycin
Etoposide (VP-16)

Toxicity
Pulmonary fibrosis Myelosuppression Alopecia Renal insufficiency (mild) Secondary leukemia Renal insufficiency Nausea, vomiting Neuropathy

Cis-platin

Left

Right

Axial CT Section demonstarating - Left Hydronephrosis, due to large Para-Aortic Nodal Mass from a Germ cell tumour

Limits of Lymph Nodes Dissection For Right & Left Sided Testicular Tumours

THERAPY OF PATIENT WITH SEMINOMA

Stage I, IIA, ? IIB Stage IIB, IIC, III
B - Bleomycin E - Etoposide (VP-16) 4 cycles P - cis-platin

Abdominal Radiotherapy

Follow Up

Stable/Regress F/U

Relapse/Growth
? RPLND ? Chemotherapy ? XRT

Therapy of Nonseminomatous Germ Cell Testicular Tumours

Radical Inguinal Orchidectomy

Stage I, II (minimum) RPLND Stage I, II B1
Observe

Stage II B2
BEP 2 cycles
Bleomycin Etoposide Cis-platin

Therapy of Nonseminomatous Germ Cell Testicular Tumours Radical Inguinal Orchidectomy Stage II C (advanced) / III
Complete Response Observe Cancer
V-Vinblastine I-Ifosfamide P-cis-platin

BEP 4 cycles Partial Response RPLND

Progress

VIP or Autologous Bone marrow Transplant Teratoma / Fibrosis

OBSERVE

PROGNOSIS
Seminoma Stage I 99% Nonseminoma 95% to 99%

Stage II

70% to 92%

90%

Stage III

80% to 85%

70% to 80%

CONCLUSION
Improved Overall Survival of Testicular Tumour due to Better Understanding of the Disease, Tumour Markers and Cisplatinum based Chemotherapy
Current Emphasis is on Diminishing overall Morbidity of Various Treatment Modalities

Carcinoma Penis

Introduction
Incidence worldwide is roughly 1% of the total cancers in male Social stigma and reluctant patient delayes the presentation Early detection can prevent major morbidity and mortality

CLINICAL PRESENTATION
Middle aged male with or without a precancerous condition Most patients present with mass and ulceration and / or induration 50% patients have inguinal adenopathy at initial presentation

DIAGNOSING Ca PENIS
Histology forms the cornerstone of diagnosis Incisional biopsy of the lesion is the preferred modality Biopsy provides opportunity to grade the tumor at the time of initial diagnosis

IMAGING MODALITIES
Recommended for :
Staging the disease Follow up of patient To assess spread and resectability

IMAGING MODALITIES
USG:
To assess extent and resectability of T4 disease Assessment of lymph nodes

CT SCAN:
Assessment of lymph nodes Limited utility in primary lesion

MRI:
Most accurate in detecting primary and nodal disease

IMAGING MODALITIES
FLUOROSCENCE STUDIES:
For accurate planning of treatment plan for laser ablation

Lymphoscintigraphy:
Most accurate in identifying need of LN dissection

STAGING Ca PENIS: JACKSONS SYSTEM

Jackson classification for SCC of the penis
Stage I - Tumor confined to the glans or the prepuce Stage II - Invasion into the shaft or the corpora; no nodal or distant metastases Stage III - Tumor confined to the penis; operable metastases of the inguinal nodes Stage IV - Tumor involves adjacent structures; inoperable inguinal nodes and/or distant metastasis or metastases

STAGING Ca PENIS: TNM SYSTEM

Tumor
Tis - Carcinoma in situ (Bowen disease, erythroplasia of Queyrat) Ta - Noninvasive verrucous carcinoma T1 - Tumor invading the subepithelial connective tissue T2 - Tumor invading the corpus spongiosum or cavernosum T3 - Tumor invading urethra or prostate T4 - Tumor invading other adjacent structures

Node

Metastasis

N1 - Involvement of a single superficial inguinal node N2 - Involvement of multiple or bilateral superficial inguinal nodes N3 - Involvement of deep inguinal or pelvic nodes, unilateral or bilater M1 - Distant metastasis present M1a - Occult metastasis (biochemical and/or other tests) M1b - Single metastasis in a single organ M1c - Multiple metastasis in a single organ M1d - Metastasis in multiple organ sites

STAGING Ca PENIS: INVESTIGATIONS

Biopsy
Depth of invasion Histological grading

USG abdomen

Assessment of lymph nodes Detectable metastases

CT Scan

Lymph nodes Metastases

MRI

OTHER INVESTIGATIONS
Routine blood investigations:
Anaemia Raised ESR Leucocytosis

CXR Others depending on metastatic suspicion

INVESTIGATIONS FOR METASTATIC DISEASE

CXR / CT Scan chest
LFT CT Head Bone scan

TREATMENT OPTIONS
SURGICAL TREATMENT
MINIMALY INVASIVE SURGERY LASER THERAPY RADIOTHERAPY CHEMOTHERAPY

SURGICAL TREATMENT OF PRIMARY DISEASE

Surgery forms the cornerstone of therapy Length of healthy stump is the most important determinant in deciding the extent of resection Urinary diversion (Perineal Urethrostomy) should accompany total amputation

SURGICAL TREATMENT OF PRIMARY DISEASE

INDICATIONS OF LYMPH NODE DISSECTION

All patients with palpable non responding adenopathy All patients with cytologically proven disease All patients with T2 disease or more should undergo prophylactic dissection Minimum dissection is bilateral superficial inguinal group dissection

MANAGEMENT OF NODAL DISEASE

Bilateral superficial inguinal node dissection is the treatment of choice Deep nodes to dissected on the side where the superficial nodes are positive Iliac nodes to be dissected if deep nodes are positive Para-aortic adenopathy contraindicates lymph node dissection

PRODUCTION OF BILIRUBIN

STRUCTURE OF BILIRUBIN
Terra - Pyrrole ring structure
Extensive hydrogen bonds: Water insoluble

Exposure to light: converts into more polar form

LYMPH NODE DISSECTION: COMPLICATIONS AND CONTRAINDICATIONS

COMPLICATIONS:
Lower limb lymphoedema Flap necrosis Seroma Infections

CONTRAINDICATIONS
Para-aortic lymphadenopathy Verrucous carcinoma Metastatic disease Major surgery contraindicated

ROLE OF RADIOTHERAPY
INDICATIONS:
Small exophytic lesion if patient does not want surgery Inguinal node irradiation if surgery is not planned

External beam irradiation or mould may be used

Circumcision should be done prior to radiation Stenosis and fistula are the major complications

ROLE OF CHEMOTHERAPY
Topical 5 FU may be used for very superficial lesions Systemic chemotherapy (VBM) has limited role after node dissection to prevent metastases Neo adjuvant therapy is being investigated for advanced lesions with unresectable or fixed nodes

MINIMALLY INVASIVE THERAPY

Laser therapy
Mohs micrographic surgery Cryotherapy

CONCLUSION
Surgery is the mainstay of treatment of carcinoma penis Histological confirmation is the easiest and most effective mode of diagnosis Nodal dissection improves survival and is hence indicated

Chemotherapy and radiotherapy have limited indications

Penile reconstructive procedures may be offered to young males with good prognosis

Carcinoma Prostat

Definition

Relevance Incidence Mortality

Most common noncutaneous malignancy in men Nearly 200,000 new cases per year in U.S.

Morbidity

32,000 deaths in the United States each year Second most common cause of cancer death in men2 Single histologic disease Ranges

From indolent, clinically irrelevant To virulent, rapidly lethal phenotype.

Epidemiology

Prostate-specific antigen (PSA) assay has affected incidence of prostate cancer Incidence
Prior to PSA 1993 1996
84,000

19,000 new cases / year in US

Since 1996

300,000

200,000 per year A number that more closely estimate the true annual incidence of clinically detectable disease

Epidemiology

Death rate
Declined by about 1% per year since 1990 Greatest decrease in men younger than age 75 years Men older than 75 years still account for two thirds of all prostate cancer deaths Due to
Early detection (screening) or to improved therapy?

Epidemiology
Risk factors
Increasing age Family history African-American Dietary factors.

Nutritional factors have protective effect against prostate cancer

Reduced fat intake Soy protein Lycopene Vitamin E Selenium

Race

Genetics

Incidence doubled in African Americans compared to white Americans. Common among relatives with early-onset prostate cancer Susceptibility locus (early onset prostate cancer) An abnormality at this locus occurs in less than 10% of prostate cancer patients.
Chromosome 1, band Q24

Pathophysiology
Adenocarcinoma
95% of prostate cancers

Rare histopathologic types of prostate carcinoma

Occur in approximately 5% of patients Include
Small cell carcinoma Mucinous carcinoma Endometrioid cancer (prostatic ductal carcinoma) Transitional cell cancer Squamous cell carcinoma Basal cell carcinoma Adenoid cystic carcinoma (basaloid) Signet-ring cell carcinoma Neuroendocrine cancer

Developing in the acini of prostatic ducts

Pathophysiology

Peripheral zone (PZ)

70% of cancers

Transitional zone (TZ)

20% Some claim
TZ prostate cancers are relatively nonaggressive PZ cancers are more aggressive
Tend to invade the periprostatic tissues.

Clinical Manifestations

Early state (organ confined)

Asymptomatic

Locally advanced
Obstructive voiding symptoms
Hesitancy Intermittent urinary stream Decreased force of stream

May have growth into the urethra or bladder neck Hematuria Hematospermia

Advanced (spread to the regional pelvic lymph nodes)

Edema of the lower extremities Pelvic and perineal discomfort

Clinical Manifestations

Metastasis
Most commonly to bone (frequently asymptomatic)
Can cause severe and unremitting pain

Bone metastasis
Can result in pathologic fractures or Spinal cord compression

Visceral metastases (rare) Can develop pulmonary, hepatic, pleural, peritoneal, and central nervous system metastases late in the natural history or after hormonal therapies fail.

Detection and Diagnosis

PSA level

Helpful in asymptomatic patients

A palpable nodule on digital rectal examination

Next most common clinical presentation Prompts biopsy Advanced disease

> 60% of patients with prostate cancer are asymptomatic Diagnosis is made solely because of an elevated screening PSA level

Much less commonly, patients are symptomatic

Obstructive voiding symptoms Pelvic or perineal discomfort Lower extremity edema Symptomatic bone lesions.

Staging
Stage T1

Nonpalpable prostate cancer Detected only on pathologic examination

Incidentally noted after
Transurethral resection for benign hypertrophy (T1a and T1b) or On biopsy obtained because of an elevated PSA (T1c-the most common clinical stage at diagnosis)

Nodal metastases

Distant metastases

Can be microscopic and can be detected only by biopsy or lymphadenectomy, or they can be visible on imaging studies Predominantly to bone Occasional visceral metastases occur.

Stage T2

Stage T3

Palpable tumor Appears to be confined to the prostatic gland (T2a if one lobe, T2b if two lobes)
Tumor with extension through the prostatic capsule (T2a if focal, T2b if seminal vesicles are involved)

Stage T4

Invasion of adjacent structures

Bladder neck External urinary sphincter The rectum The levator muscles The pelvic sidewal

Small, E., Cecil Textbook of Medicine, Prostate Cancer, 2004, WB Saunders, an Elsevier imprint

Treatment

Surgery
Traditional Robotic

Radiation
Brachytherapy External beam

Cryotherapy Androgen Deprivation Watchful waiting

Prognosis
Prognosis correlates with histologic grade and extent (stage) of disease Adenocarcinoma Grading
> 95% of prostate cancers Multifocality is common
Ranges from 1 to 5

Gleason score
Definition
Ranges

Sum of the two most common histologic patterns seen on each tissue specimen From 2 (1 + 1) To 10 (5 + 5) Well-differentiated (Gleason scores 2, 3, or 4) Intermediate differentiation (Gleason scores 5, 6, or 7) Poorly differentiated (Gleason scores 8, 9, or 10).

Category

Prognosis

PROGNOSIS

Gleason
2-4

10-year PSA progression-free survival is 70 to 80% Treated with radiation therapy or surgery 50 to 70% 15 to 30%

Climbing PSA after radical prostatectomy

Prognostic variables
Time to detectable PSA Gleason score at the time of prostatectomy PSA doubling time

5-7

8-10

Benign Prostatic Hyperplasia

Benign Prostatic Hyperplasia

Benign Prostatic Hyperplasia

Generalised disease of the prostate due to hormonal derangement which leads to enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms

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BPH Proposed Etiologies

Cause not completely understood Reawakening of the urogenital sinus to proliferate Change in hormonal milieu with alterations in the testosterone/estrogen balance Induction of prostatic growth factors Increased stem cells/decreased stromal cell death Accumulation of dihydroxytestosterone, stimulation by estrogen and prostatic growth hormone actions

BPH facts
Occurs in 50% of men over 50 and in 80% of men over 80 have BPH BPH progresses differently in every individual Many men with BPH may have mild symptoms and may never need treatment BPH does not predispose to the development of prostate cancer

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Benign Prostatic Hyperplasia

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BPH Pathophysiology
Normal BPH

BLADDER

PROSTATE URETHRA

Hypertrophied detrusor muscle

Obstructed urinary flow

Kirby RS et al. Benign prostatic hyperplasia. Health Press, 1995.

BPH Pathophysiology

Slow and insidious changes over time Complex interactions between prostatic urethral resistance, intravesical pressure, detrussor functionality, neurologic integrity, and general physical health. Initial hypertrophydetrussor decompensation poor tonediverticula formationincreasing urine volumehydronephrosisupper tract dysfunction

Complications
Urinary retention UTI Sepsis secondary to UTI Residual urine Calculi Renal failure
Hematuria Hernias, hemorroids, bowel habit change
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Clinical manifestations
Voiding symptoms
decrease in the urinary stream Straining

Dribbling at the end of urination

Intermittency Hesitancy Pain or burning during urination Feeling of incomplete bladder emptying
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Clinical manifestations
Irritative symptoms
urinary frequency urgency dysuria bladder pain nocturia incontinence symptoms associated with infection
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Benign Prostatic Hyperplasia

Leading to symptom bother and worsened QOL

Other Relevant History

GU History (STD, trauma, surgery) Other disorders (eg. neurologic, diabetes) Medications (anti-cholinergics) Functional Status

Diagnostic Tests
History & Examination
Abdominal/GU exam Focused neuro exam

Digital rectal exam (DRE) Validated symptom questionnaire. Urinalysis Urine culture BUN, Cr

Prostate specific antigen (PSA) Transrectal ultrasound biopsy Uroflometry Postvoid residual

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AUA Symptom Score Sheet

Not at all

Less than 1 time in 5

Less than half the time

About half the time

More than half the time

Almost always

Your score

Incomplete emptying
Over the past month, how often have you had a sensation of not emptying your bladder completely after you finish urinating?

0 0 0 0 0 0
None

1 1 1 1 1 1
1 time

2 2 2 2 2 2
2 times

3 3 3 3 3 3
3 times

4 4 4 4 4 4
4 times

5 5 5 5 5 5
5 times or more Your score

Frequency
Over the past month, how often have you had to urinate again less than two hours after you finished urinating?

Intermittency
Over the past month, how often have you found you stopped and started again several times when you urinated?

Urgency
Over the last month, how difficult have you found it to postpone urination?

Weak stream
Over the past month, how often have you had a weak urinary stream?

Straining
Over the past month, how often have you had to push or strain to begin urination?

Nocturia
Over the past month, many times did you most typically get up to urinate from the time you went to bed until the time you got up in the morning?

4
Mostly dissatisfied

Quality of life due to urinary symptoms

If you were to spend the rest of your life with your urinary condition the way it is now, how would you feel about that?

Delighted

Pleased

Mostly satisfied

Mixed about equally satisfied and dissatisfied

Unhappy

Terrible

Total score: 0-7 Mildly symptomatic; 8-19 moderately symptomatic; 20-35 severely symptomatic.

DRE

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BPH Danger Signs on DRE

Firm to hard nodules Irregularities, unequal lobes Induration Stony hard prostate Any palpable nodular abnormality suggests cancer and warrants investigation

Optional Evaluations and Diagnostic Tests Urine cytology in patients with:

Predominance of irritative voiding symptoms. Smoking history Flow rate and post-void residual Not necessary before medical therapy but should be considered in those undergoing invasive therapy or those with neurologic conditions Upper tract evaluation if hematuria, increased creatinine Cystoscopy

PSA
Elevated levels of PSA
0 4 ng/ml
Prostatic pathology

Correlates with tumor mass Some men with prostate cancer have normal PSA levels

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Treatment Options
Mild to severe symptoms with little bother
Manage with watchful waiting.
Risk of therapy outweighs the benefit of medical or surgical treatment

Moderate to severe symptoms with bother

Management options include watchful waiting, medical management and surgical treatment.

Therapy
Watchful waiting and behavioral modification Medical Management
Alpha blockers 5-alpha reductase inhibitors Combination therapy

Surgical Management
Office based therapy OR based therapy

Urethral stents

Watchful Waiting and Behavioral Modification

is the preferred management technique in patients with mild symptoms and minimal bother AUA score < 7, 1/3 improve on own.

Watchful Waiting and Behavioral Modification

Decrease caffeine, alcohol )diuretic effect( Avoid taking large amounts of fluid over a short period of time Void whenever the urge is present, every 2-3 hours Maintain normal fluid intake, do not restrict fluid Avoid bladder irritants to include dairy products, artificial sweeteners, carbonated beverages Limit nighttime fluid consumption BPH symptoms can be variable, intermittent