Carcinoma Cervix Ppt
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Transcript of Carcinoma Cervix Ppt
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CARCINOMA CERVIX
INCIDENCE 4-15 in developedcountries 30-40/lac in developing countriesAccounts for 60% of malignancies in developed &80% in developed countries .Life time risk 1.9( USA), 2.2(india)
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Magnitude of the problem
Incidence is decreasing in developed countries
Pap smear has reduced incidence by 80%& death by 70%
Preventable disease- availability screening, diagnostic, therapeutic procedures.
1 million fresh cases/year across the globe Most common CA in developing countries
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ICMR REPORT
II nd commonest cancer in women Relative proportion varies – 14-24 Causes- economic factor, sexual behavior &
degree of effective mass screening
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Risk factors
Early intercourse(<16yrs) Early age of pregnancy Too many/ too frequent pregnancy LES Multiple sexual partners STD’s HPV 16,18,33,35 HIV Death of wife due to ca cx OCPills smoking
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Pathogenesis
Cx epithelium-> infection->hpv dna integration to human genome-> up regulation of viral oncogenes-> expression of E6&E7 oncoproteins ->interference with tumor suppressor genes-> host cell immortalization, HPV induced euplastic transformation
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HPV TRIAGE
Pap smear test -> atypical -> Hpv testing- high risk positive Colposcopy This strategy highly effective in diagnosing
CIN II & III lesions reduces load on colposcopy clinic
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Gross pathology
Ecto-cervix- 80%, endocx- 20% Naked eye exopytic- from ectocx & forms friable
masses filling upper vagina Ulcerative- lesion excavates the cx often
involves vaginal fornices Infiltrative- found in endocervical growth->
expansion of cx -> barrel shaped cx
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HISTOPATHOLOGY
Squamous cell carcinoma is the commonest (80-90%)
Well differentiated, moderately differentiated, poorly differentiated
Source- SCJ, healing erosion, squamous metaplasia of columnar epithelium, squamous cell rests in ectocx
SCC-> i) large cell keratinising ii) large cell non keratinising iii) small cell type
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HISTOPATHOLOGY
Adenocarcinoma (10-15%) develops from endocervical canal- from lining epithelium/glands
Occurs at young age 80% purely endocervical type Others- endometroid, clear, adenosquamous, or
mixed Adenoma malignum- well differentiated
adenocarcinoma with favourable prognosis
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Mode of spread
Direct – adjacent structures-, uterus, vagina, parametrium, paracervical, paravaginal tissues. Through-> rectum, pubocervical-> bladder
Lymphatics- parametrial,obturator,internal iliac external iliac, sacral nodes
Secondary nodes- common iliac, inguinal, para-aortic nodes Sentinal node 85% drainage to single node detected by
methylene blue injection in to tumour, lymphoscintigraphy Blood spread- veins- lungs,liver,bones Direct implantion
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Involvement of lymphnodes in different stages
stage Pelvic nodes% Paraaortic %
0 0 0
Ia1 0-0.5 0
Ia2 5 <1
Ib 16 2
II 30 15
III 44 30
IV 55 40
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STAGING
For determining prognosis To formulate line of treatment To compare results
FALLACIES
-difficult to assess lymph node involvement on clinical examination – adversely affects prognosis
- Difficulty in assessing parametrium(inflammatory/malignant induration)
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BASIS
CLINICAL EXAMINATION Pelvic examination- p/s,p/v,p/r- under anesthesia Supplemented by Cxr, IVP, cystoscopy, proctoscopy In case of infection antibiotic to be given prior to staging Final stage cannot be changed once therapy has begun Choose lower stage if in doubt CT,MRI,PET, lymphangiography- detect LN,&
parametrium .MRI- tumour volume, parametrial extension.but these donot change FIGO stage
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FIGO staging of carcinoma cervix
Preinvasive carcinoma Stage-0 carcinoma in situ
Invasive carcinoma Stage-I strictly confined to cx Stage-Ia- preclinical diagnosed only on microscopy Stage-Ia1 minimally microscpically invasive <3mm Stage-Ia2 invasion>3mm<5mm, width<7mm, Stage-Ib greater than Ia2 Stage-Ib1 <4cm in size Stage-Ib2 >4cm in size
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FIGO STAGING
Stage-II extends beyond cervix but not to pelvic wall, involves vagina but not lower 1/3rd
Stage-IIa no obvious parametrial involve ment
Stage-IIb obvious parametrial involvement
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FIGO STAGING
Stage-III carcinoma extends to pelvic wall,
involves lower 1/3rd of vagina,
hydronephrosis/nonfunct kidney Stage-IIIa no extension to pelvic wall but
to lower 1/3rd Stage-IIIb extension to pelvic wall&/
hydronephrosis/nonfunct kidney
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FIGO STAGING
Stage IV extension beyond true pelvis, or clinically has involved mucosa of bladder/rectum
Stage IVa spread to adjacent organs Stage IVb distant metastasis
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prognosis
Stage Site- endocervical dangerous Depth<1 cm, <LN -> ^ survival Differentiation Age Paraaortic node involvement< survival by
50% Hpv
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Diagnosis
early ca – limited to cx Survival I=80-100%,II=55-70% Preclinical- biopsy/cytology-
colposcopy/schiller’s guided biopsy- diagnostic conisation- depending on depth of stroma staging done
Stage 0, stage Ia, stage Ib
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Diagnosis
Stage 0 – BM intact stage Ia – BM disrupted Mean age 38-42 Majority asymptomatic- diagnosis by
conisation Stage Ib symptoms- menstrual abnormalities, white
discharge
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diagnosis
p/s-> erosion/ nodular growth, ulcer Bleeds to touch. p/v-> indurated, friable, bleeding to touch p/r-> parametrium free Confirmation by biopsy
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Advanced carcinoma
Symptoms: irregular/continuos bleeding Offensive discharge Pelvic pain Leg edema Bladder symptoms Rectal symptoms Ureteral obstruction
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Advanced carcinoma
p/s-> ulcerative / fungating growth p/v -> induration / extent of growth p/r-> parametrium/ extention to lateral wall/rectal
involvement Smooth induration- infetion, nodular- malignancy Confimation of diagnosis- biopsy
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Differential diagnosis
Cervical tuberculosis Syphilitic ulcer Cx ectopy Incomplete abortion Fibroid polyp
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complications
Haemorrhage Ureteric colic-> pyelitis, pyelonephritis,
hydronephrosis Pyometra VVF RVF
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Causes of death
Uremia Hemorrhage Sepsis Cachesia Metastases-> lung-36%, LN-> 30%, bone-
>16% , abdominal cavity-> 7%
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management
Prevention-> high risk male/female Use of condom Hysterectomy-(stump ca 1%) Recombinant vaccination Secondary prevention by screening Down staging screening(WHO 1986)-> diagnosis by p/s Normal cx-> pink,smooth, round, does not bleed to touch Abnormal cx-> reddish,red/white area of patch, bleeds to touch
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curative
Treat ment decision should be made by gynaecologist and radiotherapist
Improve general health , anemia, malnutritionModalities
Primary surgery Primary radio therapy Chemotherapy Combination therapy
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surgery
Radical hysterectomy abdominal->Wertheim vienna 1898, okabayashi
1921, meigs usa-1944 Vaginal-> schauta of vienna-1902, mithra india- 1957 Structures removed- uterus, tubes, ovaries,upper
half of vagina, parametrium, primary lymphnodes Limited to early stages
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Advantage of surgery over RT
Better staging stage+LN=> better survival Ovarian function preserved Transpositioning of ovaries possible Normal Vagina maintained Psychological benefit
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Special indications
PID-acute/chronic Pelvic kidney Fibroid,prolapse,ovarian tumour,vvf Young patient Vaginal stenosis Recurrance after RT adenoCA, adenosquamousCA
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Post op complications
Major- per op- hemorrhage,injury,anaesthetic Post op- shock,urinary, pyrexia, Vvf,uvf,bladder
dysfunction,pyelonephritis,rectal dysfunction Lymphocyst, dyspareunia& recurrance Mortality<1%
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Pelvic exenteration
Ultraradical surgery- brunschwig Stage IVa Central pelvic recurrent CA Resectable tumour mass Absence of ureteral obstruction,sciatic
pain,unilateral edema Woman ready to accept stomas Contra indications- distant metastasis
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TYPES
Anterior Posterior Complete/total Laparoscopic radical hysterectomy
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Primary radiotherapy
First malignancy to be treated- by margaret cleves 1903
Chemoradiation – IIb- Iva External photon beam radiation,
brachytherapy Advantages- wider applicability,survival-
85%,less primary mortality/morbidity,individualisation possible
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Early stages
Brachy therapy – radium 226Ra, cesium 137 Cs or cobalt 60Co
Tandems-uterine cavity, ovoids& colpostats-vaginal vault under GA
Methods- paris, manchester- strength small exposure time more
Stockholm- large high intensity- less exposure time Remote after loading –fletcher suit
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Draw backs of RT
Strictures Fistulas Vaginal fibrosis, stenosis rad- menopause,
fibrosis of bowel / bladder Ovarian trans position
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Calculation of dose
Point A 2cm above & lateral to ext os Point B 2cm above 5cm lat to same plane Point A- 7000-8000 cGy Point B-2000 cGy EBRT- 4000 cGy IMRT Advanced cases- hyper baric oxygenation recurrent CA- EBRT Ca after TAH- EBRT 4500cGy Stump CA- tandem+ EBRT
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Combination therapy
Surgery followed by RT Positive LN Accidental diag of CA after TAH Positive tissue resection margin + RT followed by surgery Endocervical Ca barrel CX Bulky tumour Neoadjuant chemotherapy LARVH,radical vaginal trachelectomy
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Planning of treatment
Early- Ia- Ia1- TAH,conisation, Ia1(3mm inv)- extrafascial hysterectomy(type 1),
Ia2- radical hysterectomy Ia1/Ia2- lymphovascular invasion- type II
radical Ib,IIa- typeIII, EBRT if nodes+ / primaryRT
with platinum chemo therapy Radical trachelectomy
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Relatively advanced disease
Stage IIb- RT+ cisplatin Advanced disease IIa-IVa= primary chemoradiation+cisplatin
based chemotherapy disseminated: IV a- chemo/palliative radiation
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Palliative therapy
Symptomatic therapy Foul smelling discharge- antimicrobial cream Bleeding- palliative radiation(180-200cGy/day),
packing with monsel’s solution Pain- NSAIDS, p.radiation- 3000cGy Diazepam/amitryptyaline Neuropathic pain - blocks
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pregnancy
Diagnosis – cone biopsy Micro invasive- follow up Advanced- Ist tri – same as non pregnant Late- classical cs followed by radical
surgery/RT Stage the imp for prognosis
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Results
stage 5yr survival
IIa 76.0
IIb 73.3
IIIa 50.5
IIIb 46.4
IV a 29.6
IVb 22.0
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Recurrent cervical cancer
M.c. site- pelvic side wall Follow up – majority of recurrancies- 2 yrs Interval 3-4 months
stump carcinoma
1%
Radical parametrectomy/ EBRT