NEOPLASMS OF ESOPHAGUS
PRESENTER - DR. Dharmdev Yadav (assistant
professor IIMSR) ex senior resident kgmu lucknow
BENIGN TUMORS
• Mc – Leiomyoma (70%)
• 2nd Mc – Esophageal cysts (20%)
LEIOMYOMA
• Account for 2/3rd of all benign tumors of esophagus.
• Dysphagia occurs when tumor is more than 5 cm in diameter
• Diagnosis – esophagoscopy and barium swallow
• Biopsy is contraindicated – can cause perforation.
TREATMENT
• Enucleation
• Limited esophageal resection if tumor lies in lower esophagus and cannot be
enucleated.
ESOPHAGEAL CYSTS
• 2nd most common – 20% of benign esophageal tumors
• Congenital foregut cyst
• Acquired epithelial cyst
• Papilloma - associated with HPV and GERD, endoscopic excision
• Fibrovascular polyp – diagnosed with barium swallow, endoscopy, excision.
• Lipoma – usually asymptomatic and can be observed
• Fibroma – if symptomatic – enucleation.
• Hemangioma – it looks like esophageal varices – dysphagia, bleeding
Tx – observation, excision, radiotherapy.
CARCINOMA ESOPHAGUS
• Introduction
• Etiology
• Classification
• Spread
• Clinical features
• Investigations
• Diagnosis and Staging
• Treatment
• Prognosis
INTRODUCTION
• It is the 8TH most common cancer worldwide and is 6TH most common cause of cancer
related death.
• It most commonly presents in 6TH and 7TH decades of life.
• SCC and Adenocarcinoma are the most common cell types while other malignancies
such as melanoma and small cell carcinomas are rare.
• SCC is the predominant histological type.
• SCC remains steady, however in western countries, there has been an epidemiological
shift since the 1990s from SCC to adenocarcinoma such that incidence of
adenocarcinoma has surpassed that of SCC.
ANATOMICAL SPECIALTIES
• Lacks serosa
• Proximal 1/3 striated muscle and distal 2/3 smooth muscle.
• Segmental blood supply.
• Longitudinal arrangement of veins and lymphatics
• SCC most commonly occurs in middle 3rd of esophagus.
• Adenocarcinoma most commonly occurs in lower 3rd of esophagus
ETIOLOGY
• RISK FACTORS FOR SCC
 Alcohol
 Smoking
 Vit c deficiency
 Hot beverages
 Smoked fish and nitrosamine compounds
 Zinc, selenium, molybdenum deficiency
 HPV 16, 18
 Achalasia cardia
 Plummer vinson syndrome
 Tylosis
 Alkali injury
 Genetic predisposition
 Fanconi syndrome
RISK FACTORS OF ADENOCARCINOMA
Barrett’s esophagus
Obesity
Smoking
Scleroderma
Hiatus hernia
GERD
Scleroderma
Zollinger Ellison syndrome
SPREAD
• DIRECT SPREAD
Lack of serosa favors local extension.
It can spread through muscular layer and get adherent to left main bronchus, trachea,
recurrent laryngeal nerve( causes hoarseness), aorta or its branches(causes fatal hemorrhage).
Can perforate and cause mediastinitis.
broncho-esophageal, trachea-esophageal, esophageal-aortic fistulas can occur in advanced
cases.
• LYMPHATIC SPREAD
In the neck it spreads to the supraclavicular lymph nodes
Thorax – it spreads to para esophageal, tracheoesophageal and subdiaphragmatic
lymph nodes.
Abdomen – to the coeliac lymph nodes
• BLOOD spread to the liver, lungs, brain and bones
CLINICAL FEATURES
• Progressive dysphagia is the most common
symptom. Solids > liquids. More than 70
percent of lumen should be blocked to cause
significant dysphagia.
• Regurgitation
• Anemia
• Weight loss
• Halitosis
• Substernal or abdominal pain
• Hoarseness of voice when RLN is involved
• Aspiration and choking when tumor
obstruction is present or airway-esophageal
fistula
• Choking and cough on drinking water are
typical of fistula and associated hemoptysis is
common.
• Ascites due to liver secondaries
• Bronchopneumonia
INVESTIGATIONS
• 1ST / IOC – Endoscopy with biopsy
• IOC for Staging – PET-CT > CECT
• IOC for metastasis – 18 FDG PET
BARIUM SWALLOW
• Irregular filling defect • Shouldering sign
• Biopsy – for confirming diagnosis and histological type
• Chest x ray – to look for aspiration pneumonia
• Bronchoscopy / laryngoscopy – to see invasion in cases of upper 1/3rd growths
ENDOSCOPIC ULTRASONOGRAPHY
• To look for the depth of the tumor, involvement of nodes, cardia and left lobe of
liver. Nodes smaller than 5mm can be very well visualized by EUS which may be
missed in CT scan.
• It is the only imaging modality able to distinguish the various layers of esophagus
wall, usually seen as five alternating hyper and hypoechoic layers using 12-MHz
ultrasound.
• The drawback is that many advanced cancers do not permit passage of a
conventional echoendoscope.
CT SCAN
• To look for local extension, nodal status, peri esophageal, diaphragmatic,
pericardial vascular infiltration, obliteration of mediastinal fat and status of
tracheobronchial tree in case of upper third growth
FDG-PET
• SCC are FDG avid.
• Adenocarcinomas of OGJ sometimes show limited or absent FDG accumulation
regardless of tumor volume.
• It is mostly used for detecting regional and non regional nodes, as well as distant
metastasis.
• Change in uptake after neoadjuvant treatment is similarly useful in predicting
histological response and outcome
OTHER INVESTIGATIONS
• USG abdomen – to look for liver secondaries , lymph node status in abdomen.
• Chromoendoscopy using lugol’s iodine – normal mucosa is stained brown, while
dysplastic and early cancer are unstained.
• Laparoscopy – to see peritoneal spread, liver spread and nodal spread. Biopsy can
be taken from different places.
• Video assisted thoracoscopic approach – to stage esophageal carcinoma
STAGING
• Careful disease staging is essential to guide therapy.
• Current staging classification is according to American Joint Committee on
Cancer(AJCC)
TREATMENT
• CURATIVE
• PALLIATIVE
ENDOSCOPIC MUCOSAL RESECTION
• It is basically a diagnostic biopsy tool, but can be therapeutic in early and pre
malignant lesion.
• T1a tumors are resected by EMR as risk of lymph node metastasis is very low.
• It involves injection of saline (or other solutions such as glycerol or hyaluronic
acid) into the submucosal plane to raise the mucosal lesion.
• It is then sucked into a cap fitted onto tip of endoscope, looped by a snare wire
and cut by electrocautery.
• For larger lesions, piecemeal resection is needed.
ENDOSCOPIC SUBMUCOSAL DISSECTION
• It involves marking of margins of lesion, then submucosal injection, cutting the
mucosal edges along line of marking, submucosal dissection of tumor from its
bed and lastly hemostasis.
• It is more demanding than EMR.
• There is increased risk of post resection stricture formation if too much the
circumference of mucosa is removed.
• For early barrett’s , EMR and ESD can be done with additional ablation of whole
length of barrett’s using RFA.
PRINCIPLES
• Only 20 percent of esophageal cancers present early. In such early growths
confirmed with the absence of nodal spread, curative surgery is the main
approach– radical esophagectomy.
• Proximal extent of resection should be minimum of 10cm and distal extent
minimum 5 cm from the macroscopic tumor.
• Proximal stomach has to be removed in lower 1/3 tumors.
• If nodes are present, the multimodal treatment should be used – curative
treatment , chemo/radiotherapy.
• Outcome of surgery depends on location of tumor, number , location, size of
nodes, tumor grading.
• Neoadjuvant therapy prior to surgery may improve the survival.
• Aggressive chemoradiation may be used as curative therapy in some patients of
upper 1/3rd growths who are unfit for surgery.
• Palliative therapy is done for patients unfit for surgery, having metastasis. It is to
relieve pain and dysphagia, and also to prevent aspiration and bleeding.
UPPER 1/3RD GROWTH(SCC)
• Treated mainly by stereotactic radiotherapy with concomitant chemotherapy.
• Usually unresectable due to invasion of trachea, larynx and great vessels.
• Surgery is mostly reserved for salvage, when there is incomplete response or for
recurrent disease.
• In early and operable cases McKeown three phased esophagectomy and
anastomosis can be done.
MCKEOWN THREE PHASED ESOPHAGECTOMY
• It consist of
• Cervical component
• Thoracic component
• Abdominal component
MIDDLE 1/3RD GROWTH
• Ivor lewis operation( lewis – tanner two staged esophagectomy) – abdominal and
right thoracotomy.
• Partial esophagectomy and esophagogastric anastomosis is done in thorax.
• If growth is inoperable, palliative radiotherapy is given.
LOWER 1/3RD GROWTH (SCC AND
ADENOCARCINOMA)
• Left thoraco-abdominal approach ,partial esophagectomy is done with
esophagogastric anastomosis. Often jejunal roux-en-y anastomosis is done.
• Orringer approach i.e transhiatal blind total esophagectomy with anastomosis in
left side of neck
MINIMALLY INVASIVE PROCEDURES
• Traditional open procedures are increasingly replaced by minimally invasive
methods, by a combination of video – assisted thoracoscopy(VATS) and
laparoscopy or robotic techniques.
• Both thoracic and abdominal phases can be performed via minimally invasive
technique or one phase can be done by open surgery (HYBRID surgery).
ESOPHAGEAL CONDUITS
• Best – stomach
• Colon
• Jejunal roux loop
Routes
• Posterior mediastinal
• Retrosternal
• Subcutaneous
LYMPHADENECTOMY
• Two field dissection – mediastinal nodes and upper abdominal nodes around
coeliac trunk.
Mediastinal field –
• Standard – below tracheal bifurcation
• Extended – standard plus right paratracheal including those around right RLN.
• Total – extended plus nodes around left RLN.
 Three field lymphadenectomy – Two field plus bilateral cervical nodes including
supraclavicular nodes.
COMPLICATIONS
• Hemorrhage
• Atelectasis
• Pneumonia
• Atrial fibrillation
• Arrythmias
• Anastomotic leak
• Ischemia of conduit
• RLN injury
• Mediastinitis
• Chylothorax
• Stricture
CHEMOTHERAPY
CROSS REGIME
• Cisplatin
• 5-Flourouracil
MAGIC TRIAL
• Cisplatin , 5-FU , epirubicin
COMPLICATIONS
• Nephrotoxic, neurotoxic, ototoxic,
highly emetogenic
• Methotrexate
• Paclitaxel
• Etoposide
• Bleomycin
PALLIATIVE THERAPY
• 80% of patients have advanced tumor at time of presentation and they are only
amenable to palliative care.
• To relieve pain
• To relieve dysphagia
• To prevent bleeding
• To prevent aspiration
• Is done when patient is not fit for surgery, metastasis.
• Stenting – SEMS – self expanding metallic stents
• Radiotherapy
• Photodynamic therapy
• Cryotherapy
• Endoscopic laser
• Intubation
PROGNOSIS
Not good because of –
• Early spread
• Longitudinal lymphatics
• Difficult approach
• Late presentation
• 5 year survival rate in india is 15 - 20 %
THANK YOU

neoplasmsofoesophagus-230619112311-dfc34b23 (1).pptx

  • 1.
    NEOPLASMS OF ESOPHAGUS PRESENTER- DR. Dharmdev Yadav (assistant professor IIMSR) ex senior resident kgmu lucknow
  • 2.
    BENIGN TUMORS • Mc– Leiomyoma (70%) • 2nd Mc – Esophageal cysts (20%)
  • 4.
    LEIOMYOMA • Account for2/3rd of all benign tumors of esophagus. • Dysphagia occurs when tumor is more than 5 cm in diameter • Diagnosis – esophagoscopy and barium swallow • Biopsy is contraindicated – can cause perforation.
  • 5.
    TREATMENT • Enucleation • Limitedesophageal resection if tumor lies in lower esophagus and cannot be enucleated.
  • 6.
    ESOPHAGEAL CYSTS • 2ndmost common – 20% of benign esophageal tumors • Congenital foregut cyst • Acquired epithelial cyst
  • 8.
    • Papilloma -associated with HPV and GERD, endoscopic excision • Fibrovascular polyp – diagnosed with barium swallow, endoscopy, excision. • Lipoma – usually asymptomatic and can be observed • Fibroma – if symptomatic – enucleation. • Hemangioma – it looks like esophageal varices – dysphagia, bleeding Tx – observation, excision, radiotherapy.
  • 9.
    CARCINOMA ESOPHAGUS • Introduction •Etiology • Classification • Spread • Clinical features • Investigations • Diagnosis and Staging • Treatment • Prognosis
  • 10.
    INTRODUCTION • It isthe 8TH most common cancer worldwide and is 6TH most common cause of cancer related death. • It most commonly presents in 6TH and 7TH decades of life. • SCC and Adenocarcinoma are the most common cell types while other malignancies such as melanoma and small cell carcinomas are rare. • SCC is the predominant histological type. • SCC remains steady, however in western countries, there has been an epidemiological shift since the 1990s from SCC to adenocarcinoma such that incidence of adenocarcinoma has surpassed that of SCC.
  • 11.
    ANATOMICAL SPECIALTIES • Lacksserosa • Proximal 1/3 striated muscle and distal 2/3 smooth muscle. • Segmental blood supply. • Longitudinal arrangement of veins and lymphatics • SCC most commonly occurs in middle 3rd of esophagus. • Adenocarcinoma most commonly occurs in lower 3rd of esophagus
  • 13.
    ETIOLOGY • RISK FACTORSFOR SCC  Alcohol  Smoking  Vit c deficiency  Hot beverages  Smoked fish and nitrosamine compounds  Zinc, selenium, molybdenum deficiency  HPV 16, 18  Achalasia cardia  Plummer vinson syndrome  Tylosis  Alkali injury  Genetic predisposition  Fanconi syndrome
  • 14.
    RISK FACTORS OFADENOCARCINOMA Barrett’s esophagus Obesity Smoking Scleroderma Hiatus hernia GERD Scleroderma Zollinger Ellison syndrome
  • 16.
    SPREAD • DIRECT SPREAD Lackof serosa favors local extension. It can spread through muscular layer and get adherent to left main bronchus, trachea, recurrent laryngeal nerve( causes hoarseness), aorta or its branches(causes fatal hemorrhage). Can perforate and cause mediastinitis. broncho-esophageal, trachea-esophageal, esophageal-aortic fistulas can occur in advanced cases.
  • 17.
    • LYMPHATIC SPREAD Inthe neck it spreads to the supraclavicular lymph nodes Thorax – it spreads to para esophageal, tracheoesophageal and subdiaphragmatic lymph nodes. Abdomen – to the coeliac lymph nodes • BLOOD spread to the liver, lungs, brain and bones
  • 18.
    CLINICAL FEATURES • Progressivedysphagia is the most common symptom. Solids > liquids. More than 70 percent of lumen should be blocked to cause significant dysphagia. • Regurgitation • Anemia • Weight loss • Halitosis • Substernal or abdominal pain • Hoarseness of voice when RLN is involved • Aspiration and choking when tumor obstruction is present or airway-esophageal fistula • Choking and cough on drinking water are typical of fistula and associated hemoptysis is common. • Ascites due to liver secondaries • Bronchopneumonia
  • 19.
    INVESTIGATIONS • 1ST /IOC – Endoscopy with biopsy • IOC for Staging – PET-CT > CECT • IOC for metastasis – 18 FDG PET
  • 20.
    BARIUM SWALLOW • Irregularfilling defect • Shouldering sign
  • 23.
    • Biopsy –for confirming diagnosis and histological type • Chest x ray – to look for aspiration pneumonia • Bronchoscopy / laryngoscopy – to see invasion in cases of upper 1/3rd growths
  • 24.
    ENDOSCOPIC ULTRASONOGRAPHY • Tolook for the depth of the tumor, involvement of nodes, cardia and left lobe of liver. Nodes smaller than 5mm can be very well visualized by EUS which may be missed in CT scan. • It is the only imaging modality able to distinguish the various layers of esophagus wall, usually seen as five alternating hyper and hypoechoic layers using 12-MHz ultrasound. • The drawback is that many advanced cancers do not permit passage of a conventional echoendoscope.
  • 28.
    CT SCAN • Tolook for local extension, nodal status, peri esophageal, diaphragmatic, pericardial vascular infiltration, obliteration of mediastinal fat and status of tracheobronchial tree in case of upper third growth
  • 29.
    FDG-PET • SCC areFDG avid. • Adenocarcinomas of OGJ sometimes show limited or absent FDG accumulation regardless of tumor volume. • It is mostly used for detecting regional and non regional nodes, as well as distant metastasis. • Change in uptake after neoadjuvant treatment is similarly useful in predicting histological response and outcome
  • 31.
    OTHER INVESTIGATIONS • USGabdomen – to look for liver secondaries , lymph node status in abdomen. • Chromoendoscopy using lugol’s iodine – normal mucosa is stained brown, while dysplastic and early cancer are unstained. • Laparoscopy – to see peritoneal spread, liver spread and nodal spread. Biopsy can be taken from different places. • Video assisted thoracoscopic approach – to stage esophageal carcinoma
  • 33.
    STAGING • Careful diseasestaging is essential to guide therapy. • Current staging classification is according to American Joint Committee on Cancer(AJCC)
  • 35.
  • 36.
    ENDOSCOPIC MUCOSAL RESECTION •It is basically a diagnostic biopsy tool, but can be therapeutic in early and pre malignant lesion. • T1a tumors are resected by EMR as risk of lymph node metastasis is very low. • It involves injection of saline (or other solutions such as glycerol or hyaluronic acid) into the submucosal plane to raise the mucosal lesion. • It is then sucked into a cap fitted onto tip of endoscope, looped by a snare wire and cut by electrocautery. • For larger lesions, piecemeal resection is needed.
  • 38.
    ENDOSCOPIC SUBMUCOSAL DISSECTION •It involves marking of margins of lesion, then submucosal injection, cutting the mucosal edges along line of marking, submucosal dissection of tumor from its bed and lastly hemostasis. • It is more demanding than EMR. • There is increased risk of post resection stricture formation if too much the circumference of mucosa is removed. • For early barrett’s , EMR and ESD can be done with additional ablation of whole length of barrett’s using RFA.
  • 40.
    PRINCIPLES • Only 20percent of esophageal cancers present early. In such early growths confirmed with the absence of nodal spread, curative surgery is the main approach– radical esophagectomy. • Proximal extent of resection should be minimum of 10cm and distal extent minimum 5 cm from the macroscopic tumor. • Proximal stomach has to be removed in lower 1/3 tumors. • If nodes are present, the multimodal treatment should be used – curative treatment , chemo/radiotherapy.
  • 41.
    • Outcome ofsurgery depends on location of tumor, number , location, size of nodes, tumor grading. • Neoadjuvant therapy prior to surgery may improve the survival. • Aggressive chemoradiation may be used as curative therapy in some patients of upper 1/3rd growths who are unfit for surgery. • Palliative therapy is done for patients unfit for surgery, having metastasis. It is to relieve pain and dysphagia, and also to prevent aspiration and bleeding.
  • 42.
    UPPER 1/3RD GROWTH(SCC) •Treated mainly by stereotactic radiotherapy with concomitant chemotherapy. • Usually unresectable due to invasion of trachea, larynx and great vessels. • Surgery is mostly reserved for salvage, when there is incomplete response or for recurrent disease. • In early and operable cases McKeown three phased esophagectomy and anastomosis can be done.
  • 43.
    MCKEOWN THREE PHASEDESOPHAGECTOMY • It consist of • Cervical component • Thoracic component • Abdominal component
  • 45.
    MIDDLE 1/3RD GROWTH •Ivor lewis operation( lewis – tanner two staged esophagectomy) – abdominal and right thoracotomy. • Partial esophagectomy and esophagogastric anastomosis is done in thorax. • If growth is inoperable, palliative radiotherapy is given.
  • 46.
    LOWER 1/3RD GROWTH(SCC AND ADENOCARCINOMA) • Left thoraco-abdominal approach ,partial esophagectomy is done with esophagogastric anastomosis. Often jejunal roux-en-y anastomosis is done. • Orringer approach i.e transhiatal blind total esophagectomy with anastomosis in left side of neck
  • 49.
    MINIMALLY INVASIVE PROCEDURES •Traditional open procedures are increasingly replaced by minimally invasive methods, by a combination of video – assisted thoracoscopy(VATS) and laparoscopy or robotic techniques. • Both thoracic and abdominal phases can be performed via minimally invasive technique or one phase can be done by open surgery (HYBRID surgery).
  • 50.
    ESOPHAGEAL CONDUITS • Best– stomach • Colon • Jejunal roux loop Routes • Posterior mediastinal • Retrosternal • Subcutaneous
  • 52.
    LYMPHADENECTOMY • Two fielddissection – mediastinal nodes and upper abdominal nodes around coeliac trunk. Mediastinal field – • Standard – below tracheal bifurcation • Extended – standard plus right paratracheal including those around right RLN. • Total – extended plus nodes around left RLN.  Three field lymphadenectomy – Two field plus bilateral cervical nodes including supraclavicular nodes.
  • 54.
    COMPLICATIONS • Hemorrhage • Atelectasis •Pneumonia • Atrial fibrillation • Arrythmias • Anastomotic leak • Ischemia of conduit • RLN injury • Mediastinitis • Chylothorax • Stricture
  • 55.
    CHEMOTHERAPY CROSS REGIME • Cisplatin •5-Flourouracil MAGIC TRIAL • Cisplatin , 5-FU , epirubicin COMPLICATIONS • Nephrotoxic, neurotoxic, ototoxic, highly emetogenic • Methotrexate • Paclitaxel • Etoposide • Bleomycin
  • 56.
    PALLIATIVE THERAPY • 80%of patients have advanced tumor at time of presentation and they are only amenable to palliative care. • To relieve pain • To relieve dysphagia • To prevent bleeding • To prevent aspiration • Is done when patient is not fit for surgery, metastasis.
  • 57.
    • Stenting –SEMS – self expanding metallic stents • Radiotherapy • Photodynamic therapy • Cryotherapy • Endoscopic laser • Intubation
  • 58.
    PROGNOSIS Not good becauseof – • Early spread • Longitudinal lymphatics • Difficult approach • Late presentation • 5 year survival rate in india is 15 - 20 %
  • 59.