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Moderators: Dr. P.Haricharan
Associate professor
Dr. koti reddy
Associate professor
Speaker: Dr K. Meena Reddy
II yr PG
CARCINOMA OF
STOMACH
EPIDEMIOLOGY
• Incidence:
more common in males
peak incidence in 7th decade
Second leading cause of cancer death worldwide
common in japan
most commonly distal gastric cancers
RISK FACTORS
• Familial-10%
1. Mutations of gene coding for cell adhesion molecules “e-
cadherin” -90% risk
2. Activation of proto oncogenes.eg: c-met, k-sam, c-erb B2
3. Inactivation of tumor suppressor genes-
P53(Li-Fraumeni syn), P16, BCL2, APC gene(25%)
4. Reactivation of telomerase and micro satellite instability-
HNPCC/Lynch syndrome(5-10%)
5. Over expression of different GF receptors
6. Blood group A, FAP-10-20% risk
7. Her2 over expression reported in 6%-35% of gastric
cancers
• Medical-
1. HELICOBACTER PYLORI infection:
- prevalence common in areas with less sanitation
- associated with distal gastric ca-intestinal type
- risk increases with cagA gene.
- Eradication of h pylori through
antibiotic treatment and bismuth
administration may prevent
both atrophic gastritis and
intestinal type gastric cancers
Mechanism: chronic inflammation
corpus gastritis
gastric atrophy
intestinal metaplasia
Dysplasia
Intestinal type of gastric cancer
2.Pre cancerous lesions:
Chronic atrophic gastritis
Pernicious anemia
Adenomatous gastric polyps >2cm,sessile
Intestinal metaplasia
Agammaglobulinemia
Benign gastric ulcer
Previous gastric surgery
Menetriers disease
3.Proton pump inhibitors- long term use
• Nutritional-Smoked,salted red meat and fish
high nitrate consumption
high complex carbohydrate consumption
low fruit and vegetable intake-low vit A &C
selenium is protective
• Environmental-smoking,alcohol,obesity
poor drinking water
lack of refrigeration
workers of rubber and coal industry
EB virus infection
• Social- low socio economic status-distal cancers
high socio economic status-proximal cancers
PATHOLOGICAL CLASSIFICATIONS
1. GROSS (macroscopic):
• Cauliflower
• Ulcerative
• Infiltrative/Flat
( extreme is Linitis plastica
“leather bottle stomach”)
• Environmental,H.pylori ,Old
age precancerous setting
• M>W
• Polypoidal Superficial, gland
formation with difinitive
cellular architecture
• well differentiated
• hematogenous spread
• favourable prognosis
• Familial
• Young females, blood group A
• W>M
• grossly Linitis plastica
Ulcerative growth
without gland formation
• Poorly differentiated
Signet type
• Early wall penetration
&lymphatic spread
• poor prognosis
2. LAUREN,S /DIO CLASSIFICATION:
DIFFUSE(33%) INTESTINAL(53%)
A. Early gastric cancer
involvement of
mucosa &/ submucosa
+ LN involvement
3.DEPENDING ON DEPTH OF INVASION
B.Advanced gastric carcinoma: involment of
muscularis &/ serosa + LN involvement
LINITIS PLASTICA / TYPE IV CARCINOMA
• Aggressive diffuse type
• Enormous proliferation of fibrous tissue involving
submucosa (mother of pearls appearance)
• Mucosa appears and feels normal
• Poorly differentiated type lacking glandular formation
• DIAGNOSIS by Barium meal & Endosonography
• Treatment by Total gastrectomy & Oesophagojejunal
anstomosis
WHO HISTOLOGICAL CLASSIFICATION
 Adeno carcinoma-commonest
papillary
tubular
mucinous
signet ring
 Adenosquamous ca.
 Squamous cell ca.
 Small cell ca.
 Undifferentiatd
 unclassified
Type I carcinoma barret’s
esophagus / true esophageal
adeno carcinoma (centre
located within between 1-5cm
above the anatomic OGJ)
extending to GE junction
Type II adenocarcinoma of
the real cardia (within 1cm
above and 2cm below the
OGJ)
Type III adenocarcioma of
the subcardial stomach (2-
5cm below OGJ)
PROXIMAL GASTRIC ADENOCARCINOMA
SIEWERT CLASSIFICATION
COMMON SITE OF OCCURRENCE
SPREAD
Direct:
• horizontal
• vertical
Lymphatic :
• permeation and embolisation through lymphatics
• retrograde spread
ZONES OF LYMPHATIC DRAINAGE IN
STOMACH
LYMPH NODE GROUPS
Group I- perigastric LNs
Group II-along root of major vessels
Group III-at the root of SMA & Hepato dudenal ligament
Group IV-distant LNs(virchow’s,sister mary joseph’s
nodes)
haematogenous spread:
liver(commonest)-hard nodules with umbilications
Lungs & Bones
transperitoneal spread:
Peritoneal seedling-ascitis
Krukenberg tumor in ovary(drop metastasis)
Blummer’s shelf on DRE
Transperitoneal spread is best identified and confirmed by
laparoscopy & biopsy
DIAGNOSIS & WORKUP
• Signs & Symptoms
a. asymptomatic
b. non specific symptoms- gastritis ,weight loss, early
satiety, anemia, haematemesis, malaena, jaundice
c. specific symptoms: Dysphagia-proximal ca
Obstruction-distal ca
Mass
Perforation
PARANEOPLASTIC SYNDROMES
• Acanthosis nigricans
• Polymyositis, Dermatomyositis
• Circinate erythemas, Pemphigoid
• Dementia and cerebellar ataxia
• Idiopathic venous thrombosis
• Cushing’s syndrome
• Leser-trelat sign(multiple seborrheic keratosis)
• Metastatic symptoms:
Liver mass,
Ovarian secondaries,
Peritoneal metastasis, ascites
sister mary joseph
nodes
virchow’s
node(troisier’s sign)
INVESTIGATIONS: FOR DIAGNOSIS &
STAGING
• Hb,Hct
• Barium meal study
BARIUM MEAL FINDINGS OF
CARCINOMA STOMACH
UPPER GI ENDOSCOPY &BIOPSY
• Detects >95% of gastric cancers
• Biopsy is accurate only in 80% of cases
• Positive cytology with no endoscopic abnormality
indicates superficial spreading gastric cancer
ENDOSCOPIC ULTRA SOUND
• Differentiation between
benign and malignant
changes in the wall is
often difficult
• 6 times more accurate
than CT in staging
• More useful in imaging
the cardia which is
difficult by CT
• Lymph node biopsies
can be obtained by
EUS guidance
ENDOSCOPIC ULTRA SOUND
Advantages Disadvantages
• U/S abdomen-liver metastasis, ascites,
• lymph nodes, ovarian secondaries
• CXR for lung metastasis and pleural effusion
• CECT abdomen,pelvis & chest : for locally
advanced disease, metastasis
• PET scan: to monitor response and recurrence
comparitively more useful for GE junction
cancers
• LFTs: to r/o liver failure and obstructive jaundice
• FNAC of supraclavicular LN
• LAPAROSCOPY: now a part of routine workup to
stage the disease and to avoid unnecessary
laparotomies, with sensitivity reaching>95%
STAGING :
• AJCC TNM Staging:
• R status : describe tumor status after resection
Ro-microscopic tumor margin neg.for disease
R1-removal of macroscopic disease,but positive microscopic
margins
R2-gross residual disease
• JAPANESE CLASSIFICATION for gastric cancer
staging system described anatomical locations of LNs
removed during gastrectomy
• 16 LN stations/echelons are routinely described
Depending on the location of the primary
tumor, invasion of these stations are
considered as N1,N2,N3 or M disease
TREATMENT
• Treatment strategy:
• Surgical resection is the only modality that is potentially
curative,and is recommended for all non metastatic
cancers
• Complete resection of tumor with wide margins of
normal stomach via laparotomy is the standard of care
for resection with curative intent.
• But early tumors with minimal invasion with no LNs can
be treated with minimally invasive techniques like
EMR, ESMR, Laparoscopy.
ENDOSCOPIC MUCOSAL RESECTION
• advantage-avoiding the need for gastrectomy
• disadvantage - incomplete resection because of tumor
size or unrecognized lymph node metastases
• guidelines for endoscopic resection of early gastric
cancer are :
• (1) tumor limited to the mucosa;
• (2) no lymphovascular invasion;
• (3) tumor smaller than 2 cm;
• (4) no ulceration
PROCEDURE
ENDOSCOPIC SUB MUCOSALRESECTION
• For larger tumors with SM1 invasion(<500µm)
• patients with tumors larger than 2 cm, with ulceration or
with any submucosal invasion, should be considered
for gastrectomy with lymph node dissection
• For cancers of the distal stomach including the body
and antrum, a distal gastrectomy with Billroth II
reconstruction is the appropriate operation
• proximal stomach is transected at the level of the
incisura at a margin of at least 6 cm, distal margin is
proximal duodenum
• For proximal lesions of the fundus or cardia, a total
gastrectomy with a Roux-en-Y esophagojejunostomy
is appropriate
• Operative techniques:
Distal gastrectomy
-upper midline or bilateral subcostal incision
-Step 1 is to identify the location of the tumor through
manual palpation, or for smaller lesions, visualization of
an endoscopically placed tattoo to determine the extent
of resection necessary to obtain an adequate resection
margin
-If frozen-section analysis available,sampling of para
aortic LNs done by giving an incision along lateral border
of 2nd part of duodenum to open retroperitoneum-if distal
nodal spread is excluded we can proceed for curative
resection
• The gastrocolic ligament is
detached from the transverse
colon along the avascular plane
using electrocautery
The anterior layer of the transverse mesocolon is sharply
dissected to the level of the inferior border of the
pancreas.
skeletonizing the mesocolonic vessels
right and left gastroepiploic vessels are ligated and
transected.
Dissection continued to the superior margin of the
pancreas exposing the celiac, splenic, and hepatic
arteries and their associated nodal beds.
• duodenum is divided 1–2 cm distal to tumor
involvement to obtain a microscopically negative
resection margin.(take care of vital structures)
• Point of proximal gastric
resection must be
determined based on the
location of the lesion.
• This requires resection of
the entire lesion with a
minimum 5-cm margin free
of cancer.
• The proximal resection
plane is created from
approximately 2 cm distal
to the esophagogastric
junction along the lesser
curvature to a point along
the greater curvature that
will allow for a 5-cm
resection margin.
• surgical approach for
a proximal gastric
lesion is very similar to
that outlined
previously for a distal
gastric lesion.
• dissection of the
omentum along the
greater curvature must
also be completed,
taking care to divide
the remaining short
gastric vessels close
to the spleen.
TOTAL GASTRECTOMY
• Proximal transaction
margin is identified on
the esophagus, just
proximal to the
gastroesophageal
junction and
Esophageal division is
completed and
removed en bloc
INTESTINAL RECONSTRUCTION
AFTER DISTAL GASTRECTOMY
BILLROTH II RECONSTRUCTION
technical ease,
reasonable long-term patency rate,
good functional outcome
• Procedure:
 Identifying the jejunal origin at the ligament of
Treitz, trace distally to identify the shortest amount of
jejunum necessary to create a tension-free
anastomosis, roughly 15 cm from the ligament of
Treitz.
 Next, decide whether to bring the jejunal limb to the
proximal gastric remnant through a retrocolic or
antecolic approach.
• Antecolic approach- jejunal limb can easily reach
gastric remnant, no risk of retrocolic internal
herniation.
• Retrocolic approach- if limb length is an issue as it
may shorten the distance involved for a tension-free
anastomosis.
• Gastro jejunal anastamosis done in Posterioro
inferior aspect in vertical, retrocolic, isoperistaltic
manner with no loop and no tension
ROUX-EN-Y RECONSTRUCTION
• advantage of eliminating bile reflux into the gastric
remnant
• disadvantages of two anastomoses and the possibility of
Roux stasis syndrome
• Procedure:
 identify origin of jejunum and trace distally
 create defect in jejunal mesentary and devide jejunum
 mesentery is divided enough to permit the limb to reach
to the gastric remnant while avoiding bowel
devascularization.
• proximal jejunal staple
line is anastomosed to
the distal jejunal
segment approximately
45–50 cm distal to the
gastrojejunostomy.
INTESTINAL RECONSTRUCTION
AFTER TOTAL GASTRECTOMY
• Total gastrectomy is associated with worse
postoperative weight loss and increased dumping
symptoms due to lack of a gastric reservoir
• So use of an inverted J pouch or S pouch in
conjunction with a Roux-en-Y reconstruction as a
means of improving postgastrectomy-associated
dumping, long-term weight loss, loss, and patient
quality of life
EXTENT OF LYMPH NODE DISSECTION
• D1 resection- when care is taken to completely dissect
and remove all of the N1 nodes with the surgical
specimen (include 1-7 stations)
• D2 resection- when all N1 and N2 nodes are completely
dissected and removed(upto 12a)
• D3 resection-N1,N2,N3 nodes removed(upto 16
• D4 resection-upto 18
COMPLICATIONS OF GASTRECTOMY
• caused by loss of reservoir function, interruption of the
pyloric sphincter mechanism, and vagal nerve
transection
• The GI and cardiovascular symptoms may result in
disorders collectively referred to as postgastrectomy
syndromes.
DUMPING SYNDROMES:
• Early
• Late
• GI symptoms include nausea and vomiting, a sense of
epigastric fullness, cramping abdominal pain, and often
explosive diarrhea
• The cardiovascular symptoms include palpitations,
tachycardia, diaphoresis, fainting, dizziness, flushing, and
occasionally blurred vision
• Dumping occurs because of the rapid passage of food of
high osmolarity from the stomach into the small intestine
• treatment -avoiding foods containing large amounts
of sugar, frequent feeding of small meals rich in
protein and fat, and separating liquids from solids
during a meal.
• long acting octreotide agonists
METABOLIC DISTURBANCES
• Anemia >30% of patients
combination of decreased iron intake
impaired iron absorption, and chronic blood loss
poor absorption of dietary B12 because of the lack of
intrinsic factor
• Osteoporosis and osteomalacia-calcium deficiency
AFFERENT LOOP SYNDROME
• As a result of partial obstruction of the afferent limb
• Accumulation of pancreatic and hepatobiliary
secretions within the limb, resulting in its distention,
which causes epigastric discomfort and cramping,
bilious vomiting followed by relief of symptoms
• Failure to visualize the afferent limb on upper
endoscopy is suggestive of the diagnosis
• Radionuclide studies
• Surgical correction is indicated
EFFERENT LOOP OBSTRUCTION
• Rare, more than 50% of cases present within the first
postoperative month
• Colicky left upper quadrant pain, bilious vomiting,
abdominal distention
• failure of barium to enter the efferent limb
ALKALINE REFLUX GASTRITIS
• severe epigastric abdominal pain accompanied by bilious
vomiting and weight loss.
• History, HIDA scan, UGI Endoscopy
• conversion of the Billroth II anastomosis into a Roux-en-
Y gastrojejunostomy
ADJUVANT AND NEOADJUVANT
THERAPY
• As gastric cancer remains a biologically aggressive
cancer, with high recurrence and mortality rates
• 3 preop cycles surgery 3 postop cycles (5-
fluorouracil and cisplatin)
PALLIATIVE THERAPY AND SYSTEMIC
THERAPY
• Patients with unresectable or metastatic gastric cancer
represent almost 50% of patients with the disease and
have only a 3- to 5-month median survival with the best
supportive therapy
• debilitating symptoms should be considered for surgical
therapy, even in the setting of metastatic disease.
• Chemotherapy- Cisplatin, 5-FU, Epirubicin, Adriamycin,
Mitomycin C
• epidermal growth factor receptor (EGFR) inhibitor
cetuximab, the human EGFR2 (HER2) antagonist
trastuzumab (Herceptin)
PALLIATIVE SURGICAL PROCEDURES
• Palliative partial gastrectomy is the best palliation
• Palliative anterior gastrojejunostomy with jejuno-
jejunostomy
• Devine’s exclusion procedure
• M-B tube/ Celestine tube insertion for proximal
stomach growths
• Endoscopic stenting /dilatation
• Laser recanalisation
Outcome:
• With curative resection 5yr survival rate is 25-60%
• Early gastric cancer cure rates>80%
• Advanced with distant metastasis-survival for 3-5 months
is only 4%
Reccurence: 40-80%
• Mostly with in 3 yrs
• As locoregional disease in remnant bed or regional LNs /
Distant metastasis
SURVEILLANCE
• Through Endoscopy, Blood counts , LFTs
• In 1st yr-every 4 months
• In next 2 yrs-every 6 months
• Anually thereafter
COMPLICATIONS OF GASTRIC
CANCER
• Bleeding- Endoscopic cautery, clipping, angiographic
coil embolisation
• Gastric outlet obstruction- Endoscopic dilatation with
stent, palliative bypass
• Perforation-Closure with omental patch
Carcinoma of stomach

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Carcinoma of stomach

  • 1. Moderators: Dr. P.Haricharan Associate professor Dr. koti reddy Associate professor Speaker: Dr K. Meena Reddy II yr PG CARCINOMA OF STOMACH
  • 2. EPIDEMIOLOGY • Incidence: more common in males peak incidence in 7th decade Second leading cause of cancer death worldwide common in japan most commonly distal gastric cancers
  • 3. RISK FACTORS • Familial-10% 1. Mutations of gene coding for cell adhesion molecules “e- cadherin” -90% risk 2. Activation of proto oncogenes.eg: c-met, k-sam, c-erb B2 3. Inactivation of tumor suppressor genes- P53(Li-Fraumeni syn), P16, BCL2, APC gene(25%) 4. Reactivation of telomerase and micro satellite instability- HNPCC/Lynch syndrome(5-10%) 5. Over expression of different GF receptors 6. Blood group A, FAP-10-20% risk 7. Her2 over expression reported in 6%-35% of gastric cancers
  • 4. • Medical- 1. HELICOBACTER PYLORI infection: - prevalence common in areas with less sanitation - associated with distal gastric ca-intestinal type - risk increases with cagA gene. - Eradication of h pylori through antibiotic treatment and bismuth administration may prevent both atrophic gastritis and intestinal type gastric cancers
  • 5. Mechanism: chronic inflammation corpus gastritis gastric atrophy intestinal metaplasia Dysplasia Intestinal type of gastric cancer
  • 6. 2.Pre cancerous lesions: Chronic atrophic gastritis Pernicious anemia Adenomatous gastric polyps >2cm,sessile Intestinal metaplasia Agammaglobulinemia Benign gastric ulcer Previous gastric surgery Menetriers disease 3.Proton pump inhibitors- long term use
  • 7. • Nutritional-Smoked,salted red meat and fish high nitrate consumption high complex carbohydrate consumption low fruit and vegetable intake-low vit A &C selenium is protective • Environmental-smoking,alcohol,obesity poor drinking water lack of refrigeration workers of rubber and coal industry EB virus infection • Social- low socio economic status-distal cancers high socio economic status-proximal cancers
  • 8. PATHOLOGICAL CLASSIFICATIONS 1. GROSS (macroscopic): • Cauliflower • Ulcerative • Infiltrative/Flat ( extreme is Linitis plastica “leather bottle stomach”)
  • 9. • Environmental,H.pylori ,Old age precancerous setting • M>W • Polypoidal Superficial, gland formation with difinitive cellular architecture • well differentiated • hematogenous spread • favourable prognosis • Familial • Young females, blood group A • W>M • grossly Linitis plastica Ulcerative growth without gland formation • Poorly differentiated Signet type • Early wall penetration &lymphatic spread • poor prognosis 2. LAUREN,S /DIO CLASSIFICATION: DIFFUSE(33%) INTESTINAL(53%)
  • 10. A. Early gastric cancer involvement of mucosa &/ submucosa + LN involvement 3.DEPENDING ON DEPTH OF INVASION
  • 11. B.Advanced gastric carcinoma: involment of muscularis &/ serosa + LN involvement
  • 12. LINITIS PLASTICA / TYPE IV CARCINOMA • Aggressive diffuse type • Enormous proliferation of fibrous tissue involving submucosa (mother of pearls appearance) • Mucosa appears and feels normal • Poorly differentiated type lacking glandular formation • DIAGNOSIS by Barium meal & Endosonography • Treatment by Total gastrectomy & Oesophagojejunal anstomosis
  • 13. WHO HISTOLOGICAL CLASSIFICATION  Adeno carcinoma-commonest papillary tubular mucinous signet ring  Adenosquamous ca.  Squamous cell ca.  Small cell ca.  Undifferentiatd  unclassified
  • 14. Type I carcinoma barret’s esophagus / true esophageal adeno carcinoma (centre located within between 1-5cm above the anatomic OGJ) extending to GE junction Type II adenocarcinoma of the real cardia (within 1cm above and 2cm below the OGJ) Type III adenocarcioma of the subcardial stomach (2- 5cm below OGJ) PROXIMAL GASTRIC ADENOCARCINOMA SIEWERT CLASSIFICATION
  • 15. COMMON SITE OF OCCURRENCE
  • 16. SPREAD Direct: • horizontal • vertical Lymphatic : • permeation and embolisation through lymphatics • retrograde spread
  • 17. ZONES OF LYMPHATIC DRAINAGE IN STOMACH
  • 18. LYMPH NODE GROUPS Group I- perigastric LNs Group II-along root of major vessels Group III-at the root of SMA & Hepato dudenal ligament Group IV-distant LNs(virchow’s,sister mary joseph’s nodes)
  • 19. haematogenous spread: liver(commonest)-hard nodules with umbilications Lungs & Bones transperitoneal spread: Peritoneal seedling-ascitis Krukenberg tumor in ovary(drop metastasis) Blummer’s shelf on DRE Transperitoneal spread is best identified and confirmed by laparoscopy & biopsy
  • 20. DIAGNOSIS & WORKUP • Signs & Symptoms a. asymptomatic b. non specific symptoms- gastritis ,weight loss, early satiety, anemia, haematemesis, malaena, jaundice c. specific symptoms: Dysphagia-proximal ca Obstruction-distal ca Mass Perforation
  • 21. PARANEOPLASTIC SYNDROMES • Acanthosis nigricans • Polymyositis, Dermatomyositis • Circinate erythemas, Pemphigoid • Dementia and cerebellar ataxia • Idiopathic venous thrombosis • Cushing’s syndrome • Leser-trelat sign(multiple seborrheic keratosis)
  • 22. • Metastatic symptoms: Liver mass, Ovarian secondaries, Peritoneal metastasis, ascites
  • 24. INVESTIGATIONS: FOR DIAGNOSIS & STAGING • Hb,Hct • Barium meal study
  • 25. BARIUM MEAL FINDINGS OF CARCINOMA STOMACH
  • 26. UPPER GI ENDOSCOPY &BIOPSY • Detects >95% of gastric cancers • Biopsy is accurate only in 80% of cases • Positive cytology with no endoscopic abnormality indicates superficial spreading gastric cancer
  • 28. • Differentiation between benign and malignant changes in the wall is often difficult • 6 times more accurate than CT in staging • More useful in imaging the cardia which is difficult by CT • Lymph node biopsies can be obtained by EUS guidance ENDOSCOPIC ULTRA SOUND Advantages Disadvantages
  • 29. • U/S abdomen-liver metastasis, ascites, • lymph nodes, ovarian secondaries • CXR for lung metastasis and pleural effusion • CECT abdomen,pelvis & chest : for locally advanced disease, metastasis
  • 30. • PET scan: to monitor response and recurrence comparitively more useful for GE junction cancers • LFTs: to r/o liver failure and obstructive jaundice • FNAC of supraclavicular LN • LAPAROSCOPY: now a part of routine workup to stage the disease and to avoid unnecessary laparotomies, with sensitivity reaching>95%
  • 31. STAGING : • AJCC TNM Staging:
  • 32.
  • 33. • R status : describe tumor status after resection Ro-microscopic tumor margin neg.for disease R1-removal of macroscopic disease,but positive microscopic margins R2-gross residual disease • JAPANESE CLASSIFICATION for gastric cancer staging system described anatomical locations of LNs removed during gastrectomy • 16 LN stations/echelons are routinely described
  • 34.
  • 35. Depending on the location of the primary tumor, invasion of these stations are considered as N1,N2,N3 or M disease
  • 37. • Surgical resection is the only modality that is potentially curative,and is recommended for all non metastatic cancers • Complete resection of tumor with wide margins of normal stomach via laparotomy is the standard of care for resection with curative intent. • But early tumors with minimal invasion with no LNs can be treated with minimally invasive techniques like EMR, ESMR, Laparoscopy.
  • 38. ENDOSCOPIC MUCOSAL RESECTION • advantage-avoiding the need for gastrectomy • disadvantage - incomplete resection because of tumor size or unrecognized lymph node metastases • guidelines for endoscopic resection of early gastric cancer are : • (1) tumor limited to the mucosa; • (2) no lymphovascular invasion; • (3) tumor smaller than 2 cm; • (4) no ulceration
  • 40. ENDOSCOPIC SUB MUCOSALRESECTION • For larger tumors with SM1 invasion(<500µm)
  • 41. • patients with tumors larger than 2 cm, with ulceration or with any submucosal invasion, should be considered for gastrectomy with lymph node dissection • For cancers of the distal stomach including the body and antrum, a distal gastrectomy with Billroth II reconstruction is the appropriate operation • proximal stomach is transected at the level of the incisura at a margin of at least 6 cm, distal margin is proximal duodenum • For proximal lesions of the fundus or cardia, a total gastrectomy with a Roux-en-Y esophagojejunostomy is appropriate
  • 42. • Operative techniques: Distal gastrectomy -upper midline or bilateral subcostal incision -Step 1 is to identify the location of the tumor through manual palpation, or for smaller lesions, visualization of an endoscopically placed tattoo to determine the extent of resection necessary to obtain an adequate resection margin -If frozen-section analysis available,sampling of para aortic LNs done by giving an incision along lateral border of 2nd part of duodenum to open retroperitoneum-if distal nodal spread is excluded we can proceed for curative resection
  • 43. • The gastrocolic ligament is detached from the transverse colon along the avascular plane using electrocautery
  • 44. The anterior layer of the transverse mesocolon is sharply dissected to the level of the inferior border of the pancreas. skeletonizing the mesocolonic vessels right and left gastroepiploic vessels are ligated and transected. Dissection continued to the superior margin of the pancreas exposing the celiac, splenic, and hepatic arteries and their associated nodal beds.
  • 45. • duodenum is divided 1–2 cm distal to tumor involvement to obtain a microscopically negative resection margin.(take care of vital structures)
  • 46.
  • 47. • Point of proximal gastric resection must be determined based on the location of the lesion. • This requires resection of the entire lesion with a minimum 5-cm margin free of cancer. • The proximal resection plane is created from approximately 2 cm distal to the esophagogastric junction along the lesser curvature to a point along the greater curvature that will allow for a 5-cm resection margin.
  • 48. • surgical approach for a proximal gastric lesion is very similar to that outlined previously for a distal gastric lesion. • dissection of the omentum along the greater curvature must also be completed, taking care to divide the remaining short gastric vessels close to the spleen. TOTAL GASTRECTOMY
  • 49. • Proximal transaction margin is identified on the esophagus, just proximal to the gastroesophageal junction and Esophageal division is completed and removed en bloc
  • 50. INTESTINAL RECONSTRUCTION AFTER DISTAL GASTRECTOMY BILLROTH II RECONSTRUCTION technical ease, reasonable long-term patency rate, good functional outcome • Procedure:  Identifying the jejunal origin at the ligament of Treitz, trace distally to identify the shortest amount of jejunum necessary to create a tension-free anastomosis, roughly 15 cm from the ligament of Treitz.  Next, decide whether to bring the jejunal limb to the proximal gastric remnant through a retrocolic or antecolic approach.
  • 51. • Antecolic approach- jejunal limb can easily reach gastric remnant, no risk of retrocolic internal herniation. • Retrocolic approach- if limb length is an issue as it may shorten the distance involved for a tension-free anastomosis. • Gastro jejunal anastamosis done in Posterioro inferior aspect in vertical, retrocolic, isoperistaltic manner with no loop and no tension
  • 52.
  • 53. ROUX-EN-Y RECONSTRUCTION • advantage of eliminating bile reflux into the gastric remnant • disadvantages of two anastomoses and the possibility of Roux stasis syndrome • Procedure:  identify origin of jejunum and trace distally  create defect in jejunal mesentary and devide jejunum  mesentery is divided enough to permit the limb to reach to the gastric remnant while avoiding bowel devascularization.
  • 54. • proximal jejunal staple line is anastomosed to the distal jejunal segment approximately 45–50 cm distal to the gastrojejunostomy.
  • 55. INTESTINAL RECONSTRUCTION AFTER TOTAL GASTRECTOMY • Total gastrectomy is associated with worse postoperative weight loss and increased dumping symptoms due to lack of a gastric reservoir • So use of an inverted J pouch or S pouch in conjunction with a Roux-en-Y reconstruction as a means of improving postgastrectomy-associated dumping, long-term weight loss, loss, and patient quality of life
  • 56.
  • 57. EXTENT OF LYMPH NODE DISSECTION • D1 resection- when care is taken to completely dissect and remove all of the N1 nodes with the surgical specimen (include 1-7 stations) • D2 resection- when all N1 and N2 nodes are completely dissected and removed(upto 12a) • D3 resection-N1,N2,N3 nodes removed(upto 16 • D4 resection-upto 18
  • 58. COMPLICATIONS OF GASTRECTOMY • caused by loss of reservoir function, interruption of the pyloric sphincter mechanism, and vagal nerve transection • The GI and cardiovascular symptoms may result in disorders collectively referred to as postgastrectomy syndromes.
  • 59. DUMPING SYNDROMES: • Early • Late • GI symptoms include nausea and vomiting, a sense of epigastric fullness, cramping abdominal pain, and often explosive diarrhea • The cardiovascular symptoms include palpitations, tachycardia, diaphoresis, fainting, dizziness, flushing, and occasionally blurred vision • Dumping occurs because of the rapid passage of food of high osmolarity from the stomach into the small intestine
  • 60. • treatment -avoiding foods containing large amounts of sugar, frequent feeding of small meals rich in protein and fat, and separating liquids from solids during a meal. • long acting octreotide agonists
  • 61. METABOLIC DISTURBANCES • Anemia >30% of patients combination of decreased iron intake impaired iron absorption, and chronic blood loss poor absorption of dietary B12 because of the lack of intrinsic factor • Osteoporosis and osteomalacia-calcium deficiency
  • 62. AFFERENT LOOP SYNDROME • As a result of partial obstruction of the afferent limb • Accumulation of pancreatic and hepatobiliary secretions within the limb, resulting in its distention, which causes epigastric discomfort and cramping, bilious vomiting followed by relief of symptoms • Failure to visualize the afferent limb on upper endoscopy is suggestive of the diagnosis • Radionuclide studies • Surgical correction is indicated
  • 63. EFFERENT LOOP OBSTRUCTION • Rare, more than 50% of cases present within the first postoperative month • Colicky left upper quadrant pain, bilious vomiting, abdominal distention • failure of barium to enter the efferent limb ALKALINE REFLUX GASTRITIS • severe epigastric abdominal pain accompanied by bilious vomiting and weight loss. • History, HIDA scan, UGI Endoscopy • conversion of the Billroth II anastomosis into a Roux-en- Y gastrojejunostomy
  • 64. ADJUVANT AND NEOADJUVANT THERAPY • As gastric cancer remains a biologically aggressive cancer, with high recurrence and mortality rates • 3 preop cycles surgery 3 postop cycles (5- fluorouracil and cisplatin)
  • 65. PALLIATIVE THERAPY AND SYSTEMIC THERAPY • Patients with unresectable or metastatic gastric cancer represent almost 50% of patients with the disease and have only a 3- to 5-month median survival with the best supportive therapy • debilitating symptoms should be considered for surgical therapy, even in the setting of metastatic disease. • Chemotherapy- Cisplatin, 5-FU, Epirubicin, Adriamycin, Mitomycin C • epidermal growth factor receptor (EGFR) inhibitor cetuximab, the human EGFR2 (HER2) antagonist trastuzumab (Herceptin)
  • 66. PALLIATIVE SURGICAL PROCEDURES • Palliative partial gastrectomy is the best palliation • Palliative anterior gastrojejunostomy with jejuno- jejunostomy • Devine’s exclusion procedure • M-B tube/ Celestine tube insertion for proximal stomach growths • Endoscopic stenting /dilatation • Laser recanalisation
  • 67. Outcome: • With curative resection 5yr survival rate is 25-60% • Early gastric cancer cure rates>80% • Advanced with distant metastasis-survival for 3-5 months is only 4% Reccurence: 40-80% • Mostly with in 3 yrs • As locoregional disease in remnant bed or regional LNs / Distant metastasis
  • 68. SURVEILLANCE • Through Endoscopy, Blood counts , LFTs • In 1st yr-every 4 months • In next 2 yrs-every 6 months • Anually thereafter
  • 69. COMPLICATIONS OF GASTRIC CANCER • Bleeding- Endoscopic cautery, clipping, angiographic coil embolisation • Gastric outlet obstruction- Endoscopic dilatation with stent, palliative bypass • Perforation-Closure with omental patch