In Depth review of the Surgical management of esophageal carcinoma including management overview, endoscopic management, Type of surgeries, Open, and minimally invasive, Extent of lymphadenectomy. Literature review of evidence for type of surgery and complications
In Depth review of the Surgical management of esophageal carcinoma including management overview, endoscopic management, Type of surgeries, Open, and minimally invasive, Extent of lymphadenectomy. Literature review of evidence for type of surgery and complications
A multidisciplinary approach that includes surgery, medical oncology, and radiation oncology is required for optimal treatment of patients with rectal cancer
A multidisciplinary approach that includes surgery, medical oncology, and radiation oncology is required for optimal treatment of patients with rectal cancer
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
2. Epidemiology and incidence
• Esophageal cancer is the eighth most common cancer worldwide
• Incidence of 160/100,000 in parts of South Africa and China and 540/100,000 in
Kazakhstan.
• India 8-20 / 100,000 , 6th most common in males
• Squamous cell carcinoma still accounts for most esophageal cancers diagnosed.
• M:F – 3:1 (SCC) .. …..15:1 (adeno)
• Adeno – whites …..SCC – african American
Globocan 2018
3. Anatomy
• The esophagus is a thin-walled, hollow tube approximately 25 cm in length.
• It is lined with stratified keratinized squamous epithelium, extending from the
cricopharyngeus muscle at the level of the cricoid cartilage superiorly to the
gastroesophageal junction inferiorly.
• The esophageal wall is composed of three layers: the mucosa, submucosa, and
muscularis propria
• The mucosal layer contains the epithelium(M1), lamina propria(M2), and muscularis
mucosae(M3).
• The epithelium is separated from the lamina propria by a basement membrane. In the
portion of the esophagus containing columnar-type epithelium, the muscularis mucosae
may consist of two layers.
• Similarly, the submucosal layer may be divided into inner (SM1), middle (SM2), and
outer(SM3) layers. The muscularis propria consists of a circular inner layer and
longitudinal outer layer.
• The adventitia (periesophageal connective tissue) lies directly on the muscularis propria.
• No serosa is present, facilitating extraesophageal spread of disease.
• AJCC 8th 4 Parts : cervical , upper thoracic ,middle thoracic ,lower thoracic
4. Siewert’s classification
• Type I : From >1 cm up to 5 cm above
the gastroesophageal junction (Z line),
the tumor is classified as a carcinoma
of the distal esophagus
• Type II : Within 1 cm cephalad to 2 cm
caudad to the gastroesophageal
junction.
• Type III :Tumor center is located >2
cm below the gastroesophageal
junction
AJCC 8th
• Cancers with an epicenter in the
lower thoracic esophagus or
gastroesophageal junction or within
the proximal 2 cm of the stomach
(i.e.,cardia) and extending up to the
GE junction or esophagus are staged
as a carcinoma of the esophagus.
• If the epicenter is >2 cm distal to the
gastroesophageal junction, these are
classified as stomach cancers.
9. Lymphatics
• The esophagus has an extensive, longitudinal
interconnecting system of lymphatics. The
esophageal lymphatic network is primarily
located within the submucosa .However,
channels are also present within the lamina
propria, facilitating spread of even superficial
cancers of the esophagus involving the
mucosa.
• In addition to these longitudinal lymphatics,
intramural lymphatics may traverse the
muscularis propria, facilitating tumor spread to
regional lymphatic channels and
paraesophageal nodes.
• Lymph can travel the entire length of the
esophagus before draining into lymph nodes,
the entire esophagus is at potential risk for
lymphatic involvement.
• Up to 8 cm or more of “normal” tissue can
exist between gross tumor and
micrometastases “skip areas”.
• Lymphatics of the esophagus drain into nodes
that usually follow arteries,including the
inferior thyroid artery, the bronchial and
esophageal arteries, and the left gastric artery
(celiac axis).
10. LN Status
• Depth of tumor penetration (T stage)
affects lymph node involvement (LNI)
• Intramucosal T1 lesions (18% LNI)
• submucosal T1 lesions (55% LNI)
• T2 lesions (60% LNI)
• T3 lesions (80% LNI)
• Chance if LN <50% - conservative eso
resection and limited lymph node dissection
• LN>50% - neoadjuvant therapy followed by
resection
11. Natural history and pattern of spread
• Squamous cell carcinoma is characterized by
extensive local growth and proclivity to lymph node
metastases.
• Because the esophagus has no covering serosa,
direct invasion of contiguous structures may occur
early.
• Lesions in the upper esophagus can impinge on or
invade the recurrent laryngeal nerves,carotid
arteries, and trachea. If extraesophageal extension
occurs in the mediastinum, tracheoesophageal or
bronchoesophageal fistula may occur.
• Tumors in the lower one-third of the esophagus can
invade the aorta or pericardium, resulting in
mediastinitis, massive hemorrhage, or empyema.
12. Histology • Squamous and adeno -95% of all carcinomas
• Psuedosarcoma – spindle cell carcinoma (SCC
variant)
• Adenoca variants –Adenoid cystic
,mucoepidermoid poorer prognosis
• Small cell carcinoma – arise from argyrophilic
cells paraneoplastic syndromes !!
(ADH,hypercalcemia) , similar to SCLC
• Nonepithelial origin – very rare
• Malignant melanoms –MS 7months
• Lymphoma –mostly extension , as primary very
rare
13. SCC
• Squamous cell carcinomas arise from the squamous mucosa - native to the
esophagus - 70% - upper and middle thirds
• Most common type of esophageal ca in India (90%)
• Smoking and alcohol are common eitiologic factors (5 fold increase in risk)
• Combined increase risk from 25 - 100 folds
• Dietary
• Nitrosamines (pickled foods ,
smoked food)
• long term ingestion of hot liquids
• Micronutrient deficiency (Vit. A,
B12, C, E).
• Trace Element deficiency (Cobalt,
Copper & Selenium)
• Acquired
• Cigarette smoking
• Alcohol.
• Chronic esophagitis.
• Chronic Dysphagia
• Caustic ingestion
• Radiation exposure
• Plummer – vinson
syndrome
• Tylosis(40%)
• Achalasia (16 -fold)
• Esophageal strictures
and diverticula
• p53
• Premalignant conditions
14. Adenocarcinoma
• almost 70 % - United States and Western countries.
Etiology :
• Increasing incidence of GERD
• Western diet
• Increased use of acid-suppression medications
Histologically it is from :
• Submucosal glands of the esophagus
• Heterotopic islands of columnar epithelium
• Malignant degeneration of metaplastic columnar epithelium (Barrett’s esophagus) – 40
fold increased risk
15. Barret’s esophagus
• Traditionally - the presence of columnar mucosa extending at
least 3 cm into the esophagus.
• Recently - the specialized, intestinal-type epithelium
(presence of goblet cells) found in the Barrett’s mucosa is the
only tissue predisposed to malignant degeneration - the
diagnosis of BE is presently made given any length of
endoscopically identifiable columnar mucosa that is proven
on biopsy.
• 10 % of GERD pts develop – BARRETS
• Approx 1 in every 100 patient years of followup of barrets
develop adenocarcinoma (40 fold increased risk)
16. Clinical manifestations
• Early - asymptomatic – mimic GERD (3-4 months before diagnosis)
• Dysphagia >90% (mc) > 2/3rds of lumen has to be obstructed (lack of serosa)
• Weight Loss (40-70%) -most common symptoms
• Vomiting/Regurgitation
• Pain.
• Cough , choking , asp.pneumonia (TEF)
• Hoarseness.(left.RLN , vocal cords)
• Dyspnoea
• In high-incidence areas where screening is practice,the most prominent early symptom is
pain on swallowing rough or dry food
• Systemic disease – jaundice ,excessive pain ,bone pain,respiratory symptoms
Perez & Brady 7E
18. Esophagoscopy :
• Good 1st test – dysphagia & suspecting ca
esophagus
• Can differentiate intra luminal from
intramural & intrinsic from extrinsic
• Dx of esophageal ca is best made by
endoscopic biopsy
Critical points :
• Location of lesion
• Nature of lesion (polypoid etc)
• Extent & relationship to cricophayngeus ,GEJ
Apple core
appearance
19. :
CT
• Imp for staging.
• Chest and abdomen – Length , thickness, LN Liver
and lung mets , T4
• Accuracy 57%- T 74%- N , 83%- M
• Many unresectable tumors by CT scan are deemed
resectable at the time of surgery.
20. PET :
• FDG –PET:
• Evaluates Primary mass LN ,Mets
• Sensitivity and specificity slightly greater than CT
• Not reliable as single Dx tool
• Value in evaluating response to chemo and RT
• N staging imitations :periesophageal ln difficult to distinguish from primary mass , infections
• Detect distant metastasis in 20% pts
• (which was Not detected on CT )
• PET + CT – improve accuracy of detecting
• -stage III by 23%
• -stage IV by 18%
Figure Distant lymph node metastases of esophageal
cancer detected by integrated CT PET. A, Integrated CT
PET demonstrates para-aortic lymph node metastases
showing increased FDG uptake (arrowheads). B,
Corresponding CT image shows lymph nodes
(arrowheads) measuring 5 to 8 mm in diameter. Based
on size criteria, these lymph nodes may be considered
benign on CT scan
21. MRI
• Not done routinely
• To identify involvement of vascular & neural
• Accurately detects T4 and mets
• But overstages T & N status
22. EUS(Endoscopic Ultrasonography)
• More accurately assess
-periesophageal & celiac LN involvement
-transmural extent of ds.
• Limitation :
-less significant accuracy following neoadjuvant therapy d/t not
discriminate tumor from postradiation inflammation & fibrosis
• Overall accuracy for Local nodal (N) staging 75% to 80%
• Overall accuracy for Tumor staging (T) 85% to 90%
23.
24. EMR :
• double-channel endoscope with a soft plastic cap at its tip. The cap is placed over
the top of the lesion, suction is applied, and a snare is brought down over the top of
the lesion
• A biopsy specimen of 1 to 1.5 cm will contain mucosa and submucosa
• may also be used as a therapeutic modality for premalignant and early
malignant conditions
25. Minimal invasive surgical modalities for
staging:
• Includes bronchoscopy ,Thoracoscopy and Laparoscopy.
• Highly accurate in evaluating N & M Status.
26. Molecular considerations
• HER2/neu oncogene : overexpressed in 15% to 30% of adenocarcinomas and 5% to
13% of SCC , Both IHC and FISH to be done , associated with tumor invasion,
lymph node metastases, and poor prognosis.
• EGFR :Overexpression of EGFR on IHC testing occurs in approximately 80% of
patients with adenocarcinoma and SCC , research for targeted therapies ongoing,
poor prognosis in terms of decreased survival.
• (VEGF) expression levels: poor prognosis , targeted therapy (ramucirumab)
• COX-2:Inhibition of COX-2 activity results in enhanced radiosensitization of tumor
tissue but not normal tissue.
31. Endoscopic methods
• Endoscopic Mucosal Resection-
• CONSIDERED as essential diagnostic, staging and therapeutic option for patient having high
grade dysplasia, superficial esophageal tumor
• Procedure – injection of fluid in submucosal layer or use the suction to trap the lesion into
cylinder followed by tissue retrieval by snare or endoscopic knife
• Complete local remission rate – 99-100%
• 5 yr survival rate – 98%
33. CERVICAL ESOPHAGUS
Proximal esophageal tumors are treated with DEFINITIVE
CHEMORADIOTHERAPY
Total esophagectomy with resection of pharynx, larynx, thyroid gland is
required (Total pharyngo-laryngo-esophagectomy) – high morbidity with loss
of function.
34. THORACIC ESOPHAGUS
IVOR LEWIS OPERATION
Abdomen opened first and stomach mobilized
And then Right thoracotomy -Oesophagogastric anastomosis
2 stage approach
McKeown OPERATION
3 incisions
Abdominal, right posterolateral thoracotomy
and left cervical incision
35. TRANSHIATAL ESOPHAGECTOMY without thoracotomy
( ORRINGER’S OPERATION )
Avoidance of thoracotomy incision
Avoidance of mediastinitis
Shorter Duration of operation
Poor visualization of upper and
middle esophageal tumors
Anastomotic leak
Chylothorax
Recurrent laryngeal nerve injury
DisadvantagesAdvantages
36. Lymph node dissection
• En Bloc resection is the best treatment with
removal of all lymph nodesEn
bloc esophagectomy involves resection of
middle and lower esophageal tumors with an
envelope of adjacent tissue that includes the
mediastinal pleura laterally, the pericardium
anteriorly, and the azygos vein and thoracic
duct posterolaterally with the surrounding
periesophageal tissue and lymph nodes
37. Transhiatal vs transthoracic approach
Transhiatal approach Transthoracic approach
Thoracotomy not required Required
Distal esophagus Middle or distal esophagus
Less pulmonary complications more
Anastmotic leak high low
Disease free survival 1.4yr 1.7yr
Overall survival 1.8yr 2.0yr
5 yr survival rate 34% 36%
In hospital mortality 2% 4%
• Conclusion- either the transhiatal or transthoracic procedure can be performed with
acceptable mortality and morbidity , with either technique the outcome is almost
similar
38. Surgery Alone as Treatment
• 5 yr survival rate 28% , compared to 10% in patients treated medically.
• Locoregional failure rate 32-45%
• Need for adjuvant therapy
• Conclusion- as relapse rate is high and long term survival is poor ,
integration of adjuvant or neoadjuvant chemoradiation approaches in
treatment is rational and indicated.
• Optimum time for surgery ? (After NACRT)
Traditional 4-6 weeks Vs >12 weeks
Perez and Brady’s 7th edition
39. Radiation
Pre op RT
Pre op CT RT
Post op RT
Radical RT
Radical CT RT
Palliative
Brachytherapy
40. Role of Preoperative Radiation Therapy
• In various trials comparing surgery alone vs
preoperative radiation followed by surgery it was
found that there is no clinical benefit of using
preoperative radiation.
• No significant survival benefit
• Local control rate was improved but non
significant.
• Conclusion- preoperative radiation therapy is not
recommended
• Dosage - 41.4-50.4 Gy/ 1.8-2.0 Gy per fraction/
23-28 Fr
41. Role of Preoperative Chemoradiation
• It is most common approach for resectable
esophageal cancer
• Benefits
downstaging of disease
increase rate of complete resection of disease
with negative margins
eradicate occult micrometastatic disease
• Improves local control
• Absolute Survival benefit 2yr - 13%
5yr - 6.5%
42.
43. Median Survival was 49 months as compared to 24
months in surgical arm – DOUBLED !!
44. Regimens
• Paclitaxel+carboplatin (cat-1)
Paclitaxel 50mg/m2 I V &+ Carboplatin AUC 2 Day-1 Wkly x 5 wk
• Cisplatin+ Fluorouracil (cat-1)
Cisplatin 75-100 mg /m2 D1&D29 + Fluorouracil 750-1000 mg /m2 IV infusion
over 24 hours daily on D1- 4 & D 29–32 {35day cycle} OR
Cisplatin 15 mg /m2 D1 - 5 + Flourouracil 800 mg /m2 IV infusion over 24 hours
daily on D1-5- 21days cycle x 2
• Fluorouracil+Oxaliplatin
Oxaliplatin 85 mg /m2 IV on D1 + Leucovorin 400 mg /m2 D1+ FU 400 mg /m2 IV
Push D1 and 800 mg /m2 IV continuous infusion over 24 hrs daily on D1 & D2
14 days cycle x 3 with radiation and 3 after radiation
45. Radiotherapy Alone as Treatment
• Indications- inoperable disease
- medical contraindication of surgery
- as palliative treatment
• Median survival – 6-12 month
• 5 yr survival - <10%
(I- 20%, II- 10%, III- 3%, IV- 0%)
• When compared to chemoradiation the 3 yr survival rate in radiation therapy alone
group was found 0%
• Conclusion- treatment with radiation therapy alone for esophageal cancer is palliative
in majority of patients and for radical treatment it should be used in conjunction with
other modalities.
46. Definitive Chemoradiation
Indications :-
• In squamous cell carcinoma
-cT1b-cT4a, N0-N+
- Cervical esophagus
- If patient refuses surgery
- cT4b
• In adenocarcinoma esophagus
- cT1b-cT4a, N0-N+
- If patient refuses surgery
- cT4b
47. Definitive Chemoradiation
• In comparison to radiation therapy alone –
Improved median survival 14 vs 9 months
Improved 5 yr survival rate 27 % vs none
• When compared to surgery alone in a resectable esophageal tumor no
difference in survival rate, local failure, treatment related mortality.
• 5 yr survival rate – 27%
• Radiation Dose – 50-50.4 Gy/ 1.8-2.0 Gy per fraction/25-28 Fr
48. CHEMOTHERAPY REGIMENS USED IN DEFINITIVE CHEMORADIATION
• Cisplatin+ Fluorouracil 5-FU (cat-1)
( Cisplatin 75-100 mg /m2 D1 + 5-FU 750-1000 mg /m2 IV infusion over 24 hours
daily on D1- 4 {28 day cycle} x 4) 2 cycles with RT F/b 2 cycles without RT
• Oxaliplatin + 5FU (cat-1)
Oxaliplatin 85 mg/m2 D1+ Leucovorin 400 mg/m2 IV D1
+ 5-FU 400 mg/m2 IV D1 + 5-FU 800 mg/m2 IV over 24 hours D1 & D2 2weekly -
3cycles with RT f/b 3cycles without RT
OR
Oxaliplatin 85 mg/m2 IV on D1,D15,D29 for 3 doses
Fluorouracil 180 mg/m2 IV Daily on D1-33
49. Post operative radiation therapy
• No survival advantage
• May decrease time to local recurrence particularly in cases with involved margins
• no significant decrease in local or distal failure rates
• Dosage - 45-50.4 Gy/ 1.8-2.0 Gy per fraction/ 25-28 Fr
Post operative Chemoradiation (in case of R1 ,Node positive(adeno carcinoma), pT3
,pT4a)
• When compared to surgery alone, surgery followed by chemoradiation group showed
• 5FU +Leucovorin based chemotherapy
• Significant decrease in local failure – 19% vs 29%
• Significant survival advantage – 27 vs 36 months
• Long term followup (>10yr) – continued to show survival advantage
• Conclusion- it is appropriate to advise adjuvant chemoradiation in view of improved local
control and survival
50. RADIOTHERAPY TECHNIQUES
PATIENT POSITIONING & IMMOBILISATION :
• Cervical /upper third :
Supine with arms by the side with straight cervical spine &
parallel to couch top + Immobilisation of jaw ,neck & upper
thorax
• Middle and lower third:
Supine with arms above their head + Vertebral column should
be as parallel to couch as possible
GEJ tumours and involving stomach fasting 2 hours before
simulation for reproducibility.
51. Upper Esophagus Radiation Field
• .Superior: 5 cm proximal to tumor +
supraclavicular LN + upper mediastinal
LN
Inferior: 5 cm distal to tumor
Lateral: Tumor + 2.5 –3 cm + mediastinal
LN + 2/3 of clavicle for SCF LN
52. Middle esophagus Radiation field
Superior: 5 cm proximal to
tumor + upper mediastinal LN
Inferior: 5 cm distal to tumor +
mediastinal LN
Lateral: tumor + 2.5–3 cm +
mediastinal LN
53. Lower esophagus RT
Superior: 5 cm proximal to tumor
+ mediastinal LN
Inferior: 5 cm distal to tumor +
mediastinal LN + celiac LN (until
L1–2 vertebrae)
Lateral: tumor + 2.5–3 cm +
mediastinal LN
54. Fields commonly used:-
• AP/PA fields followed by AP/Right posterior oblique(RPO)/Left posterior
oblique(LPO) with or without boost
• AP/PA approach followed by Right anterior oblique(RAO)/LPO fields with
or without boost
• 3-field technique (AP/PA with left lateral or oblique field)
• 45 Gy by AP/PA field followed by additional 5.4 Gy using oblique or lateral
fields –mc used.
56. Nodal basins to be covered under CTV:-
• Cervical & Upper Esophagus – lower cervical and supraclavicular to subcarinal lymph nodes + upper
paraesophageal lymph nodes
• Middle Esophagus – Complete coverage of paraesophageal lymph nodes ( individualized field design)
• Lower Esophagus – Subcarinal to left gastric and common hepatic artery/celiac lymph node inferiorly
• Adenocarcinoma – similar to lower thoracic esophagus but paraesophageal lymph nodes also to be
included
• Middle and lower paraesophageal lymph nodes should be included in Type 1 ,Type 2 tumor with T2-T4
• Splenic and common hepatic artery nodes can be spared in Type 1 T2 tumor
• GTV– primary gross tumor + nodal gross disease based on diagnostic studies
• CTV– to cover subclinical disease
3-5 cm proximal and distal margins covers 94-100% subclinical disease.
2 cm radial margin
• PTV– CTV + 1cm radial, 1.5cm distal , 1cm proximal margin (as per departmental protocols)
IMRT
NCCN 2019
58. Brachytherapy in Carcinoma
Esophagus
• Iridium 192 is used – high dose rate
brachytherapy is used most commonally
• Insertion- Transnasal or transoral route
• 1cm proximal and 1 cm distal margin is taken
based on pretreatment tumor length.
59. Ca Esophagus -Brachytherapy indications
Good candidates Poor candidates Contraindications
Primary tumor length ≤
10 cm length
Primary tumor length>
10 cm length
TE fistula
Tumor confined to
esophageal wall
Extra –esophageal
extension
Cervical esophagus
location
Thoracic esophagus
location
Regional
Lymphadenopathy
Stenosis which cannot
be bypassed
No nodal / systemic
metastasis
Tumor involving EGJ or
cardia
61. Palliation
• 60 -80% rate of relief from dysphagia with radiation.
• MC received shedules were 20Gy/5# , 30Gy/10# , 35Gy/15# (with conc cisplatin or
FU) better relief of dysphagia in CRT group.
• Palliation by brachytherapy
• Stent placement –inferior compared to radiation /chemotherapy
62. Treatment sequale
• Esophagitis , dysphagia >75% , other usual symptoms nausea , vomiting , weight
loss
• Cytopenias with 2 drug chemoregimens are more pronounced.
• Chemoradiation patients grade 3 – grade 4 toxities as high as 40%.
• Late side effects :Stricture formation 14- 30% ,stenosis 60%
• Rare – radiation pneumonitis (14% -grade 2) , cardiac toxicity 10% (pericardial
effusion , IHD , HF)
• TEF – 5-10% ( advised stenting , excision , bypass or intubation) , MS -10 weeks!
64. Role of Preoperative Chemotherapy
• In resectable esophageal cancer
(adenocarcinoma of esophagus and GE
junction)
• Benfits - Downstaging of disease to facilitate
resection
-Improvement of local control
-Relief of dysphagia
• The limiting thing is delay in definitive
treatment with risk of further spread of disease
specially in non responders
• Response rate – 50%
• Improve overall survival
• Absolute benefit – 2 yr survival – 7%
5 yr survival - 4%
65. Regimens
• Only for adenocarcinoma of thoracic esophagus- 2 cycles 21 days apart with
• Fluorouracil – 1000 mg/m2 IV continuous infusion over 24 hr daily on D1-
D4
• Cisplatin – 80 mg/m2 IV on Day 1
66. Postoperative Chemotherapy
• Based on various trials no survival benefit was found
• Disease free survival rate was improved speacially in patients who had R0
esection and was found nodepositive and can be considered for these patients
• No benefit in in patients with R0 resection and N0 node
Regimen
• Capecitabine and Oxaliplatin
Capecitabine 1000mg/m2 PO BID D1-14
Oxaliplatin 130mg/m2 IV D1
21 days cycle
67. Systemic Therapy for Recurrent or Metastatic disease
• First line therapy -Two drug regimen is preferred (lower toxicity)
• Three drug regimen reserved for medically fit patients with good
performance status
• Trastuzumab should be added in first line chemotherapy for HER 2
overexpressing metastatic adenocarcinoma
Drug -Single agents Response rate
Cisplatin 19 to 35 %
Paclitaxel 25 to 35 %
Docetaxel, 100 mg/m2 20-25%
Irinotecan 15%
Methotrexate less than 5%
Etoposide less than 5%
Ifosamide less than 5%
Carboplatin less than 5%
68. Regimens used as combination chemotherapy
First line therapy:-
Cisplatin and fluoropyrimidines (cat1)
• Cisplatin 75-100 mg /m2 IV D1 + Fluorouracil 750-1000 mg /m2 IV
continuous infusion over 24 hours daily on D1-4 – 28 DAY CYCLE
• Cisplatin 50 mg /m2 IV D1 + Fluorouracil 2000 mg /m2 IV continuous
infusion over 24 hours daily on D1+ Leucovorin 200 mg /m2 IV on D1 (14 day
cycle)
• Cisplatin 80 mg /m2 IV on D1+Capecitabine 1000 mg /m2 PO BID on D1-14
(21 days cycle)
69. Fluoropyrimidine and Oxaliplatin:-
• Oxaliplatin 85 mg /m2 IV D1 + Leucovorin 400 mg /m2 IV D1 +
Fluorouracil 400 mg /m2 IV push on D1 and 1200 mg /m2 IV continuous
infusion over 24 hr on D1&2 – (14 days cycle)
• Oxaliplatin 85 mg /m2 IV D1 + Leucovorin 200 mg /m2 IV D1 +
Fluorouracil 2600 mg /m2 IV continuous infusion over 24 hr on D1 –
(14 days cycle)
• Capecitabine 1000 mg /m2 PO BID D1-14 + Oxaliplatin 130 mg /m2 IV
D1 (-21 days cycle)
OTHER REGIMENS – DCF modifications-
Docetaxel + cisplatin+ fluorouracil (OR) Docetaxel + oxaliplatin+ fluorouracil
(OR) Docetaxel + carboplatin+ fluorouracil
Paclitaxel with cisplatin or carboplatin
Epirubicin + cisplatin + fluorouracil
70. TRASTUZUMAB
• Used as first line therapy in recurrent or metastatic adenocarcinoma
esophagus overexpressing HER2
• When compared with 1st line combination chemotherapy, survival advantage
(13.8 vs 11.1 months) and response rate (47 vs 35%).
• Dosage – with chemotherapy
• 8 mg/kg IV loading dose on D1 of cycle 1 then 6mg/kg IV every 21 DAYS
OR
• 6mg/kg IV loading dose on D1 of cycle 1 then 4mg/kg every 14 DAYS
71. Second line therapy
• Ramucirumab + Paclitaxel ( Cat 1 for EGJ adenocarcinoma )
(Ramucirumab 8mg/kg IV on D1&15 + Paclitaxel 80 mg /m2 IV on D1,8,15 – 28
days cycle)
• Ramucirumab (Cat1 foe EGJ adenocarcinoma) – 8mg/kg IV on D1 – 14 days cycle
• Docetaxel – 75-100 mg /m2 IV on D1 – 21 days cycle
• Paclitaxel – 135-250 mg /m2 on D1 – 21 days cycle
• Paclitaxel – 80 mg /m2 IV on D1,8,15 cycled every 28 days
• Other regimens – irinotecan , irinotecan+fluorouracil, irinotecan +cisplatin,
docetaxel + irinotecan
72. Follow up and Surveillance
Tumor
classification
Therapy used Recommendations
Tis Endoscopic
resection(ER)/Ablat
ion
EGD X 6mnthly for 1-2 yr, then annually for 3 more yrs.
Esophagectomy EGD based on symptoms. If incomplete resection then EGD
every 6 mnths for 1-2 yr
T1a with or
without BE
ER/Ablation EGD every 3 mnthlyx1yr then every 4-6 mnths for 2nd yr then
annually for 3 more yrs
T1a Esophaegctomy EGD based on symptoms. If incomplete resection then
ablation f/b EGD every 3 mnthlyx1yr then every 4-6 mnths
for 2nd yr then annually for 3 more yrs
T1b , N0 ER/Ablation EGD every 3 mnthlyx1yr then every 4-6 mnths for 2nd yr then
annually for 3 more yrs. Further surveillance will depend on
relapse. PET-CT OR CT chest & abdomen yearly x 3yrs and
then if needed clinically
73. Follow up and Surveillance
T1b ANY N Esophagectomy PET-CT or CT chest and abdomen with contrast every 6
mnthly x 3yrs, then if clinically warranted. If incomplete
resection then ablation f/b EGD every 3 mnthlyx1yr then
every 4-6 mnths for 2nd yr then annually for 3 more yrs
Chemoradiation (non
surgical candidates)
EGD 6-12 months x 2 yrs then annually x3 yrs
PET-CT OR CECT chest and abdomen every 6-9 months x
2yrs then annually upto 5 yrs
Chemoradiation
(cadidate of salvage
esophagectomy)
EGD 6-12 months x 2 yrs then annually x3 yrs
PET-CT OR CECT chest and abdomen every 6-9 months x
2yrs then annually upto 5 yrs
T2-T4,N0-
N+,T4b
Bimodality therapy
(chemoradiation)
EGD every 3-4 mnthly x2 yr, every 6 monthly for 3rd yr , then
as clinically warranted. PET-CT OR CECT chest and abdomen
every 6-9 months x 2yrs then annually upto 5 yrs
T2-T4,N0-
N+,T4b
Trimodality therapy Imaging (PET-CT,CECT) every 4-6 monthly X 1 yr then 6-9
monthly for next 2 yr.
74. SUMMARY
• Often diagnosed in late stages, so poorer outcomes.
• Multimodality treatment is recommended and essential for carcinoma
esophagus.
• Pattern of failure - ~50% local failures needs improved local treatment .
• 75% succumb to distant metastasis as well , Molecular markers and newer
targeted therapies under study.