Testicular Tumours

TESTICULAR TUMOUR1% of all Malignant TumourAffects young adults - 20 to 40 yrs - when Testosterone Fluctuations are maximum90% 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 TumoursImproved overall survival in last 15 to 20 years due to - Better understanding of Natural History and Pathogenesis of diseaseReliable Tumour Markers Cis-platinum based chemotherapy

CROSS SECTION OF TESTIS Testis

StromaSeminiferous Tubules (200 to 350 tubules)

Interstitial Cells Supporting SpermatogoniaLeydig or(Androgen) Sertoli Cell

EPIDEMIOLOGYIncidence :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

CLASSIFICATIONI.Primary Neoplasma of Testis.A.Germ Cell Tumour B.Non-Germ Cell Tumour

II.Secondary Neoplasms.

III.Paratesticular Tumours.

I. PRIMARY NEOPLASMS OF TESTISA.Germinal Neoplasms : (90 - 95 %)1.Seminomas - 40%(a)Classic Typical Seminoma(b)Anaplastic Seminoma(c)Spermatocytic Seminoma2.Embryonal Carcinoma - 20 - 25%3.Teratoma - 25 - 35%(a)Mature(b)Immature4.Choriocarcinoma - 1%5.Yolk Sac Tumour

I. PRIMARY NEOPLASMS OF TESTISB.Nongerminal Neoplasms : ( 5 to 10% )1.Specialized gonadal stromal tumor(a)Leydig cell tumor(b)Other gonadal stromal tumor2.Gonadoblastoma3.Miscellaneous Neoplasms(a)Adenocarcinoma of the rete testis(b)Mesenchymal neoplasms(c)Carcinoid(d)Adrenal rest tumor

A.AdenomatoidB.Cystadenoma of EpididymisC.Mesenchymal NeoplasmsD.MesotheliomaE.MetastasesII. SECONDARY NEOPLASMS OF TESTISA.Reticuloendothelial NeoplasmsB.MetastasesIII.PARATESTICULAR NEOPLASMS

AETIOLOGY OF TESTICULAR TUMOUR1.Cryptorchidism

2.Carcinoma in situ

3.Trauma

4.Atrophy

CRYPTORCHIDISM & TESTICULAR TUMOURRisk of Carcinoma developing in undescended testis is

14 to 48 times the normal expected incidence

Clinical Staging of Testicular TumourStaging A or I- Tumour confined to testis.

Staging B or II- Spread to Regional nodes.

IIA - Nodes 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

To properly Stage Testicular Tumours following are pre-requisites: (a)Pathology of Tumour Specimen(b)History(c)Clinical Examination(d)Radiological procedure - USG / CT / MRI / Bone Scan(e)Tumour Markers - HCG, AFPRequirements for staging

TNM Staging of Testicular TumourT0=No evidence of TumourT1s=Intratubular, pre invasiveT1=Confined to TestisT2=Invades beyond Tunica Albuginea or into EpididymisT3=Invades Spermatic CordT4=Invades Scrotum

N1=Single < 2 cmN2=Multiple < 5 cm / Single 2-5 cmN3=Any node > 5 cmEpididymis 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

Investigation1.Ultrasound - Hypoechoic area2.Chest X-Ray - PA and lateral views3.CT Scan4.Tumour Markers- AFP- HCG- LDH- PLAP

CLINICAL FEATURESPainless Swelling of One GonadDull Ache or Heaviness in Lower Abdomen10% - Acute Scrotal Pain10% - Present with Metatstasis- Neck Mass / Cough / Anorexia / Vomiting / Back Ache/ Lower limb swelling5% - GynecomastiaRarely - Infertility

DICTUM FOR ANY SOLID SCROTAL SWELLINGSAll patients with a solid, Firm Intratesticular Mass that cannot be Transilluminated should be regarded as Malignant unless otherwise proved

Tumour MarkersTWO MAIN CLASSESOnco-fetal Substances : AFP & HCGCellular Enzymes : LDH & PLAP ( AFP - Trophoblastic Cells HCG - Syncytiotrophoblastic Cells )

AFP ( Alfafetoprotein )NORMAL VALUE: Below 16 ngm / mlHALF LIFE OF AFP 5 and 7 days

Raised AFP : Pure embryonal carcinomaTeratocarcinoma 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 Tumour7% - Seminomas

ROLE OF TUMOUR MARKERSHelps in Diagnosis - 80 to 85% of Testicular Tumours have Positive Markers Most of Non-Seminomas have raised markersOnly 10 to 15% Non-Seminomas have normal marker level After Orchidectomy if Markers Elevated means Residual Disease or Stage II or III DiseaseElevation 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 BurdenMarkers indicate Histology of Tumour: If AFP elevated in Seminoma - Means Tumour has Non-Seminomatous elementsNegative Tumour Markers becoming positive on follow up usually indicates -Recurrence of TumourMarkers become Positive earlier than X-Ray studies

PRINCIPLES OF TREATMENT

Treatment should be aimed at one stage above the clinical stage Seminomas - Radio-Sensitive. Treat with Radiotherapy.Non-Seminomas are Radio-Resistant and best treated by SurgeryAdvanced Disease or Metastasis - Responds well to Chemotherapy

PRINCIPLES OF TREATMENTRadical INGUINAL ORCHIDECTOMY is Standard first line of therapyLymphatic spread initially goes to RETRO-PERITONEAL NODESEarly hematogenous spread RAREBulky 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-SeminomaStage I and IIA: RADICAL ORCHIDECTOMYfollowed by RETROPERITONEAL LYMPH NODES DISSECTION

Stage IIB: RPLND with possible ADJUVANT CHEMOTHERAPYStage IIC and Stage III Disease:Initial CHEMOTHERAPY followed by SURGERY for Residual Disease

Chemotherapy Toxicity

BEP -BleomycinPulmonary fibrosis

Etoposide (VP-16) MyelosuppressionAlopeciaRenal insufficiency (mild)Secondary leukemia

Cis-platinRenal insufficiencyNausea, vomitingNeuropathySTANDARD CHEMOTHERAPY FOR NON-SEMINOMATOUS GERM CELL TUMOURS

LeftRight

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 SEMINOMAStage I, IIA, ? IIBStage IIB, IIC, III

B - BleomycinAbdominal RadiotherapyE - Etoposide (VP-16) 4 cyclesP - cis-platin

Follow UpStable/RegressRelapse/Growth

F/U? RPLND? Chemotherapy? XRT

Therapy of Nonseminomatous Germ Cell Testicular TumoursRadical Inguinal Orchidectomy

Stage I, II (minimum)

RPLND Stage I, II B1Stage II B2

ObserveBEP 2 cyclesBleomycinEtoposideCis-platin

Radical Inguinal Orchidectomy

Stage II C (advanced) / III

BEP 4 cyclesComplete Response Partial ResponseProgress

Observe RPLNDVIP orAutologousBone marrowTransplantCancerTeratoma / Fibrosis

V-VinblastineI-IfosfamideOBSERVEP-cis-platinTherapy of Nonseminomatous Germ Cell Testicular Tumours

PROGNOSISSeminoma Nonseminoma

Stage I99% 95% to 99%

Stage II 70% to 92%90%

Stage III80% to 85%70% to 80%

CONCLUSIONImproved Overall Survival of Testicular Tumour due to Better Understanding of the Disease, Tumour Markers and Cis-platinum based ChemotherapyCurrent 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 PRESENTATIONMiddle 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 PENISHistology 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 MODALITIESRecommended for :

Staging the disease

Follow up of patient

To assess spread and resectability

IMAGING MODALITIESUSG:To assess extent and resectability of T4 diseaseAssessment of lymph nodes

CT SCAN:Assessment of lymph nodesLimited utility in primary lesion

MRI:Most accurate in detecting primary and nodal disease

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

Lymphoscintigraphy:Most accurate in identifying need of LN dissection

STAGING Ca PENIS:JACKSONS SYSTEMJackson classification for SCC of the penisStage I - Tumor confined to the glans or the prepuceStage II - Invasion into the shaft or the corpora; no nodal or distant metastasesStage III - Tumor confined to the penis; operable metastases of the inguinal nodesStage IV - Tumor involves adjacent structures; inoperable inguinal nodes and/or distant metastasis or metastases

STAGING Ca PENIS:TNM SYSTEMTumor 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 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 bilateralMetastasis 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:INVESTIGATIONSBiopsy Depth of invasionHistological grading

USG abdomenAssessment of lymph nodesDetectable metastases

CT ScanLymph nodesMetastases

MRI

OTHER INVESTIGATIONSRoutine blood investigations:AnaemiaRaised ESRLeucocytosis

CXR

Others depending on metastatic suspicion

INVESTIGATIONS FOR METASTATIC DISEASECXR / CT Scan chest

LFT

CT Head

Bone scan

TREATMENT OPTIONSSURGICAL TREATMENT

MINIMALY INVASIVE SURGERY

LASER THERAPY

RADIOTHERAPY

CHEMOTHERAPY

SURGICAL TREATMENT OF PRIMARY DISEASESurgery 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 DISSECTIONAll 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 DISEASEBilateral 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 BILIRUBINTerra - Pyrrole ring structure

Extensive hydrogen bonds: Water insoluble

Exposure to light: converts into more polar form

LYMPH NODE DISSECTION: COMPLICATIONS AND CONTRAINDICATIONSCOMPLICATIONS:Lower limb lymphoedemaFlap necrosisSeroma Infections

CONTRAINDICATIONSPara-aortic lymphadenopathyVerrucous carcinomaMetastatic diseaseMajor surgery contraindicated

ROLE OF RADIOTHERAPYINDICATIONS:Small exophytic lesion if patient does not want surgeryInguinal 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

Sterility and Priapism may also occur

ROLE OF CHEMOTHERAPYTopical 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 THERAPYLaser therapy

Mohs micrographic surgery

Cryotherapy

CONCLUSIONSurgery 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

DefinitionRelevanceMost common noncutaneous malignancy in menIncidenceNearly 200,000 new cases per year in U.S.Mortality32,000 deaths in the United States each yearSecond most common cause of cancer death in men2MorbiditySingle histologic disease Ranges From indolent, clinically irrelevant To virulent, rapidly lethal phenotype.

EpidemiologyProstate-specific antigen (PSA) assay has affected incidence of prostate cancerIncidencePrior to PSA 19,000 new cases / year in US199384,000 1996 300,000 Since 1996200,000 per yearA number that more closely estimate the true annual incidence of clinically detectable disease

EpidemiologyDeath rateDeclined by about 1% per year since 1990Greatest decrease in men younger than age 75 yearsMen older than 75 years still account for two thirds of all prostate cancer deathsDue toEarly detection (screening) or to improved therapy?

EpidemiologyRisk factorsIncreasing ageFamily historyAfrican-AmericanDietary factors. Nutritional factors have protective effect against prostate cancerReduced fat intakeSoy proteinLycopeneVitamin ESelenium RaceIncidence doubled in African Americans compared to white Americans. GeneticsCommon among relatives with early-onset prostate cancerSusceptibility locus (early onset prostate cancer)Chromosome 1, band Q24An abnormality at this locus occurs in less than 10% of prostate cancer patients.

PathophysiologyAdenocarcinoma95% of prostate cancers Developing in the acini of prostatic ductsRare histopathologic types of prostate carcinoma Occur in approximately 5% of patientsInclude Small cell carcinomaMucinous carcinomaEndometrioid cancer (prostatic ductal carcinoma)Transitional cell cancerSquamous cell carcinomaBasal cell carcinomaAdenoid cystic carcinoma (basaloid)Signet-ring cell carcinomaNeuroendocrine cancer

PathophysiologyPeripheral zone (PZ)70% of cancers Transitional zone (TZ)20% Some claim TZ prostate cancers are relatively nonaggressivePZ cancers are more aggressive Tend to invade the periprostatic tissues.

Clinical ManifestationsEarly state (organ confined)AsymptomaticLocally advancedObstructive voiding symptoms HesitancyIntermittent urinary streamDecreased force of streamMay have growth into the urethra or bladder neck Hematuria HematospermiaAdvanced (spread to the regional pelvic lymph nodes)Edema of the lower extremitiesPelvic and perineal discomfort

Clinical ManifestationsMetastasis Most commonly to bone (frequently asymptomatic)Can cause severe and unremitting painBone metastasis Can result in pathologic fractures or Spinal cord compressionVisceral 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 DiagnosisPSA levelHelpful in asymptomatic patients> 60% of patients with prostate cancer are asymptomaticDiagnosis is made solely because of an elevated screening PSA levelA palpable nodule on digital rectal examinationNext most common clinical presentationPrompts biopsyMuch less commonly, patients are symptomaticAdvanced diseaseObstructive voiding symptomsPelvic or perineal discomfortLower extremity edemaSymptomatic bone lesions.

StagingStage T1 Nonpalpable prostate cancer Detected only on pathologic examinationIncidentally 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)Stage T2 Palpable tumor Appears to be confined to the prostatic gland (T2a if one lobe, T2b if two lobes)Stage T3 Tumor with extension through the prostatic capsule (T2a if focal, T2b if seminal vesicles are involved)Stage T4 Invasion of adjacent structuresBladder neckExternal urinary sphincterThe rectumThe levator musclesThe pelvic sidewalNodal metastases Can be microscopic and can be detected only by biopsy or lymphadenectomy, or they can be visible on imaging studiesDistant metastases Predominantly to boneOccasional visceral metastases occur.

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

TreatmentSurgeryTraditionalRoboticRadiationBrachytherapyExternal beamCryotherapyAndrogen DeprivationWatchful waiting

PrognosisPrognosis correlates with histologic grade and extent (stage) of diseaseAdenocarcinoma> 95% of prostate cancers Multifocality is commonGradingRanges from 1 to 5Gleason scoreDefinitionSum of the two most common histologic patterns seen on each tissue specimenRanges From 2 (1 + 1) To 10 (5 + 5)CategoryWell-differentiated (Gleason scores 2, 3, or 4)Intermediate differentiation (Gleason scores 5, 6, or 7)Poorly differentiated (Gleason scores 8, 9, or 10).

Prognosis PROGNOSISGleason2-410-year PSA progression-free survival is 70 to 80% Treated with radiation therapy or surgery5-750 to 70% 8-1015 to 30%

Climbing PSA after radical prostatectomyPrognostic variablesTime to detectable PSAGleason score at the time of prostatectomyPSA doubling time

Benign Prostatic Hyperplasia

Benign Prostatic Hyperplasia

**Benign Prostatic HyperplasiaGeneralised 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

BPHProposed EtiologiesCause not completely understoodReawakening of the urogenital sinus to proliferateChange in hormonal milieu with alterations in the testosterone/estrogen balanceInduction of prostatic growth factorsIncreased stem cells/decreased stromal cell deathAccumulation of dihydroxytestosterone, stimulation by estrogen and prostatic growth hormone actions

**BPH factsOccurs in 50% of men over 50 and in 80% of men over 80 have BPHBPH progresses differently in every individualMany men with BPH may have mild symptoms and may never need treatmentBPH does not predispose to the development of prostate cancer

**Benign Prostatic Hyperplasia

BPH PathophysiologyNormalBPHHypertrophied detrusor muscleObstructed urinary flowPROSTATEBLADDERURETHRAKirby RS et al. Benign prostatic hyperplasia. Health Press, 1995.

BPH PathophysiologySlow and insidious changes over timeComplex 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

**ComplicationsUrinary retentionUTISepsis secondary to UTIResidual urineCalculiRenal failureHematuriaHernias, hemorroids, bowel habit change

**Clinical manifestations

Voiding symptomsdecrease in the urinary streamStrainingDribbling at the end of urinationIntermittencyHesitancy Pain or burning during urinationFeeling of incomplete bladder emptying

**Clinical manifestationsIrritative symptomsurinary frequencyurgencydysuriabladder painnocturiaincontinencesymptoms associated with infection

Benign Prostatic Hyperplasia

Leading to symptom bother and worsened QOL

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

**Diagnostic TestsHistory & ExaminationAbdominal/GU examFocused neuro examDigital rectal exam (DRE)Validated symptom questionnaire.Urinalysis Urine cultureBUN, Cr

Prostate specific antigen (PSA)Transrectal ultrasound biopsyUroflometryPostvoid residual

AUA Symptom Score SheetInternational prostate symptom score (IPSS) Name:Date:

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

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

Not at allLess than 1 time in 5Less than half the timeAbout half the timeMore than half the timeAlmost alwaysYour scoreIncomplete emptying Over the past month, how often have you had a sensation of not emptying your bladder completely after you finish urinating?012345FrequencyOver the past month, how often have you had to urinate again less than two hours after you finished urinating?012345IntermittencyOver the past month, how often have you found you stopped and started again several times when you urinated?012345UrgencyOver the last month, how difficult have you found it to postpone urination?012345Weak streamOver the past month, how often have you had a weak urinary stream?012345StrainingOver the past month, how often have you had to push or strain to begin urination?012345

None1 time2 times3 times4 times 5 times or moreYour scoreNocturia 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?012345

Quality of life due to urinary symptomsDelightedPleasedMostly satisfiedMixed about equally satisfied and dissatisfiedMostly dissatisfiedUnhappyTerribleIf you were to spend the rest of your life with your urinary condition the way it is now, how would you feel about that?0123456

**DRE

BPHDanger Signs on DRE

Firm to hard nodulesIrregularities, unequal lobesIndurationStony hard prostateAny palpable nodular abnormality suggests cancer and warrants investigation

Optional Evaluations and Diagnostic TestsUrine cytology in patients with:Predominance of irritative voiding symptoms.Smoking historyFlow rate and post-void residualNot necessary before medical therapy but should be considered in those undergoing invasive therapy or those with neurologic conditionsUpper tract evaluation if hematuria, increased creatinineCystoscopy

**PSAElevated levels of PSA 0 4 ng/mlProstatic pathologyCorrelates with tumor massSome men with prostate cancer have normal PSA levels

Treatment OptionsMild to severe symptoms with little botherManage with watchful waiting.Risk of therapy outweighs the benefit of medical or surgical treatment

Moderate to severe symptoms with botherManagement options include watchful waiting, medical management and surgical treatment.

TherapyWatchful waiting and behavioral modificationMedical ManagementAlpha blockers5-alpha reductase inhibitorsCombination therapy Surgical ManagementOffice based therapyOR based therapyUrethral stents

Watchful Waiting and Behavioral Modificationis the preferred management technique in patients with mild symptoms and minimal bother

AUA score < 7,

1/3 improve on own.

Watchful Waiting and Behavioral ModificationDecrease caffeine, alcohol )diuretic effect(Avoid taking large amounts of fluid over a short period of timeVoid whenever the urge is present, every 2-3 hoursMaintain normal fluid intake, do not restrict fluidAvoid bladder irritants to include dairy products, artificial sweeteners, carbonated beveragesLimit nighttime fluid consumptionBPH symptoms can be variable, intermittent

*

Fig 1