Transcript Gastric Cancer

Gastric Cancer
Surgery”B” Department
“Meir” Hospital
Kfar-Saba
Gastric carcinoma
Malignant Gastric Neoplasm
* Adenocarcinoma (90%- 95% of all
malignant tumors)
* Lymphoma (NHL, MALT)
* GIST (various sarcomas)
* Neuroendocrine tumors (Carcinoid tumors)
Gastric carcinoma
• Epidemiology: 4-7/100,000 in US, yet a
leading killer (2.5% of all Ca)
• Incidence varies widely:
- High: Japan, China, Costa Rica, Chile,
Colombia, Iceland, Scotland, Finland,
Portugal ...
- Low: U.S., England, Canada, Australia,
N.Z., Sweden ...
- Overall incidence decreasing, but still a
major problem
Gastric carcinoma
Incidence
Gastric carcinoma
Risk factors
• Diet - Nitrites , smokers, lack of fresh vegetables
• Host factors:
- Chronic atrophic gastritis (ACHLORHYDRIA)
- H. pylori infection - a cofactor
- Prior partial gastrectomy
- Gastric adenomas
• Genetic factors - probably minor
- Blood group A
- Family history
- Race
Gastric carcinoma
CLASSIFICATION
• Depth of invasion
– EARLY GASTRIC CA - mucosa & submucosa
– ADVANCED GASTRIC CA - into or through
muscularis propria
• Macroscopic growth pattern
– Expanding
– Infiltrative - "linitis plastica"
• Histologic subtype
– Intestinal
– Diffuse (gastric); poorly differentiated; "signet
ring" cells
Gastric cancer
The current 5- year survival rates have not
shown a great deal of improvement.
Gastric cancer
Prognosis
• Overall, diffuse/infiltrative type is more
aggressive (higher stage, mets); often
occurs in young women (30's - 40's)
• Early gastric cancer - 5 yr. survival 90 95%
(only slightly less with positive lymph
nodes)
• Advanced cancer - 10% @ 5 yrs.
Gastric cancer
Metastases
• Regional nodes (supraclavicular =
Virchow's node)
• Liver, lungs
• Peritoneal surface
• Ovary - "Krukenberg tumor" (signet ring
cell type)
H. Pylori and Gastric Cancer?
H. Pylori and Gastric Cancer?
Displasia/ Metaplasia
Carcinoma
H. Pylori and Gastric Cancer?
The link between HP and precursors lesions
(displasia, metaplasia..) has been found in
nearly all countries with high rate of gastric
cancer.
More than 65% of Japanese of age > 50
are infected with HP
Gastric Cancer
Is presumed that Gastric Cancer develops as
multistep process in which multiple factors:
- genetic ( inherited and acquired)
- environmental insults
are acting over a period of time.
Precursors of Gastric Cancer
•
•
•
•
•
Adenomatous polyps
Chronic atrophic gastritis
Pernicious gastritis
Menetries’s disease
Previous gastric surgery for non- cancerous
conditions
Gastric cancer
“ Its primary concern is which the problem
of surgical cure of the all to frequent
carcinoma of the stomach against which
all internal therapy was proven ineffective”
Prof. Th. Billroth
(1881 –open letter to Vienna
Medical Weekly)
Surgical treatment of Gastric cancer
Surgical resection is the only
curative treatment
Gastric Cancer
The choice of therapy depends on the tumor
stage, at the beginning of any cancer therapy
the tumor stage must be evaluated.
TUMOR-STAGE-ADAPTED
THERAPY
TNM staging for gastric cancer
The American joint committee on cancer (AJCC)
Primary tumor (T)
TX-Primary tumor cannot be assessed ;T0- No evidence of primary tumor
Tis- intraepithelial,without invasion of lamina propria ;T1- tumor invades lamina
propria or submucosa; T2- tumor invades the muscularis propria;T3- tumor
penetrates the serosa without invading adjacent structures ;T4- Tumor invades
adjacent structures
TNM staging
Regional lymph nodes (N)
NX-regional lymph nodes cannot be assessed
N0- no regional lymph node metastasis
N1- metastasis in 1-6 regional LN
N2- metastasis in 7-15 regional LN
N3- metastasis in more than15 regional LN
Distant metastasis(M)
MX – cannot be assessed
M0 – no distant metastasis
M1- distant metastasis
Histopathologic Grade
G1
G2
G3
G4
Well differentiated
Moderately differentiated
Poorly differentiated
Undifferentiated
Pathologic Classifications
Borrmann’s
Gross Morphology
Lauren’s Histopathology (cohesiveness)
WHO
Histopathology (grade and growth)
Ming
Histopathology (growth and pattern)
Goeski
Histhopathology (atypia &
mucin)
Borrmann’s classification
I. Mainly exophytic growth.
II. Carcinoma with a central, bowl-shaped ulceration,
elevated margins, the carcinoma being relatively
sharply delineated from its surroundings.
III. Centrally ulcerating carcinoma without ridged,
elevated margins and indistinctly delineated from
its surroundings.
IV. Diffuse and infiltrating.
Lauren’s classification
1.Intestinal type- glandular pattern
polypoid /fungating
2. Diffuse – “signet-ring cells”
ulcerative/infiltrating
WHO of Gastric Cancer classification
Classification based on morphologic features
* Adenocarcinoma – divided according to the growth
pattern in:
- papillary
- tubular
- mucinous
- signet ring
* Adenosquamous cell carcinoma
* Squamous cell carcinoma
* Undifferentiated
* Unclassified
Gastric cancer
In 26% of the pts. disagreement between of the pre- and
post operative histopathological type.
World J Surg. Vol. 26, No2
February 2002
Gastric Cancer
Facts
- The risk of finding peritoneal implants (M1disease) at
the time of laparotomy is 25-37% after an otherwise
unremarkable CT.
- Few patients with M1 disease develop surgical
bleeding or significant gastric outlet obstruction prior
the death.
- Selected pts.with locally advanced disease (T3 and
T4) with high risk of recurrence may benefit from
neoadjuvant treatment – metastatic disease must
be excluded prior the treatment.
How to improve the pre-operative
staging?
Endoscopic Ultrasound (EUS)
A small, high frequency ultrasound transducer
incorporated into the distal end of the
endoscope.
Normal GI Wall
Endoscopic Ultrasound
Advantages:
- superior resolution.
- image not compromised by intervening
gases.
- lesion as small as 2-3 mm in diameter can
be imaged.
Endoscopic Ultrasound
Image / Drawing
Endoscopic Ultrasound
T1 lesion
Endoscopic Ultrasound
T2 lesion
Endoscopic Ultrasound
T3 lesion
Endoscopic Ultrasound
T4 lesion
Endoscopic Ultrasound
The overall accuracy for T staging is of 80%.
A major problems are:
- limited penetration depth of only 4-6 cm
- distinction between T2 and T3 lesions because of
peri- tumoral desmoplastic reaction (uT3 still
can be a pathologic T2).
- differentiation between T1m and T1sm (miniprobe)
Endoscopic Ultrasound
N stage
Low accuracy of EUS in assessment of LN
invasion ( correct in 50-80% of the cases).
CT
Role of CT in staging of gastric
carcinoma
* disappointing for recognition for neoplasm's
confined to mucosa and submucosa -diagnostic
accuracy of only 23-56%
* High accuracy for more advance stages,
88-95% for T4
Role of CT in staging of gastric
cancer
Diagnosis of lymph node involvement
Metastasis was noted in:
5% of LN < 5mm
21% of LN 5-9 mm
23% of LN 10-14%
Conclusion: Diagnosis of metastasis is
difficult in LN < 14 mm
Role of CT in staging of gastric
carcinoma
Accuracy of CT in diagnosis of :
- Hepatic metastasis is 79% -96% (will miss
the majority of meta <1cm)
- Peritoneal metastasis is 73 -80%
MRI
Role of MRI in staging of gastric
carcinoma
- better than CT in accurate diagnosis of T1
gastric cancer.
- better than CT in the identification of an
eventual intra-peritoneal diffusion.
- is equal to CT in evaluating lymph nodes.
PET scan
Cyclotron for synthesis of
radiopharmaceuticals
The PET scanner
FDG-PET scan
Tracer: flurodeoxyglucose –similar in
structure to glucose that is form in
complex apparatus- cyclotron
Role of PET scan in staging of gastric
cancer
- superior for diagnosis of LN metastasis.
- change in FDG uptake after chemiotherapic
treatment is correlated with prolonged survival.
J Tschmelitsch – Memorial Sloan Kettering
Surg Oncol 2000 Jul; 9(1)
Staging Laparoscopy
Role of laparoscopy in staging of
gastric cancer
No category I evidence (based on prospective
randomized trials) but good category II/III
evidence data.
Role of laparoscopy in staging of gastric
cancer
- Laparoscopic contact ultrasound (LCU)
overcomes the to major limitations of
laparoscopy:
* inspection is limited only to the surface of
the organs.
* lake of tactile palpation of the structures
- Staging laparoscopy makes possible abdominal
lavage for cytologic, immunohistochemical or
molecular biologic detection.
Role of laparoscopy in staging of
gastric cancer
Laparoscopic inspection is better than
laparotomy for diagnosis of small
metastatic nodes in subphrenic space
and Douglas pouch.
Role of Laparoscopy in staging of
gastric cancer
Preoperative staging laparoscopy is currently
included at Memorial Sloan Kattering in the
diagnostic algorithm.
37% - considered to have localized disease by
CT and EUS had metastatic disease
(accuracy of 94%)
Role of laparoscopy in staging of
gastric cancer
* benefit and risks must be evaluated
(mortality, morbidity, port site metastasis)
* timing: separate procedure? immediately
before the planned curative surgery?
* extent of the procedure: inspection only?
biopsy of suspicious lesions? extensive
dissection?
* routine use of LUS & peritoneal cytology
sampling?
Role of peritoneal cytology in staging of
gastric cancer
- cytology is positive only in 1/3 of patients with
advance cancer- fewer that might be expected
(low sensitivity)
- survival- poorer of one stage or more
- 5-year survival rate with positive cytology was only
2% - worst that in patients with macroscopic
dissemination
Positive CYTOLOGY is independent prognostic factor
and can add accuracy in the stage classification
Role of peritoneal cytology in staging of
gastric cancer
How to improve insensitivity of the sampling
technique?
- addition of serosal brush cytology/ imprinting
cytology
- immunocytology with monoclonal antibody Bar- Ep4
- reverse transcriptase –polimerase chain reaction
- measurement of the CEA level in peritoneal washes
- use of molecular biology
Therapeutic questions for Gastric
carcinoma
* extent of primary resection
* extent of lymphadenectomy
* efficacy of postoperative radiation
* efficacy of chemotherapy or radiation or
both as adjuvant treatment
* more recently, the potential benefit of
neoadjuvant chemotherapy
Surgical treatment of Gastric
carcinoma
Radical surgery was a well established
procedure at MSKCC in the 1960s.
Surgical treatment of Gastric
carcinoma
The radical surgery was abandoned by most
surgeons in the US and Europe because of its
high morbidity and mortality and unclear
survival benefit.
MSKCC is one of the few centers in the US in
which lymph node dissection (D2) is performed
routinely.
Gastric carcinoma in Japan and in the
West
Instead in Japan lymph node dissection up to
the N2 lymph nodes became a routine
together with screening program to identify
earlier lesions .
What are the factors that might
explain better treatment results in
Japan?
Different factors that has been suggested are:
- higher frequency of early stage lesions
(better screening?)
- less obese patients
- greater use of extended lymph node
dissection with more accurate staging
- different location of the tumor
- different type of gastric tumors
The Japanese Research Society for Gastric
Cancer
The 16 lymph node locations were classified
into 4 concentric groups: N1, N2, N3, N4
Periepigastric
Extraepigastric
N-1 perigastric LN - closest to the tumor
Lt. and Rt. cardiac
Greater
curvature
Supra-pyloric
Lesser
curvature
Sub-pyloric
N-2 lymph nodes- located along the course of
feeding arteries
Coeliac artery LN
Common hepatic
artery LN
Lt gastric
artery LN
Splenic hilum &
splenic artery
N-3 and N-4 Lymph nodes
There are lymph nodes in groups not
associated with the normal drainage pattern
of lymph from stomach.
- hepato-duodenal ligament LN
- retro-pancreatic LN
N3
- rout of mesentery
- LN along meddle colic artery
N4
- para-aortic LN
What must be extent of the
lymphadenectomy in relation to
the location of the primary tumor?
Stomach 4 zone of lymphatic drainage
I – 2/3 lesser curvature & large part of the
body Lt gastric nodes  Celiac nodes
II – distal part of lesser curvature & pylorus
 Rt. gastric nodes  Supra-pyloric
nodes  Hepatic nodes Celiac & Aortic LN
Stomach 4 zones of lymphatic drainage
III- lt. part of greater curvature LGE nodes
Pancreatic –Lineal nodes  Celiac
IV- rt. part of the greater curvature and pylorus  RGE
nodes  Pyloric nodes ( ant. surface of the pancreas)
 Supra-pyloric ( along gastro-duodenal artery) 
Hepatic nodes
What is the ideal extent of
lymphadenectomy ?
D0- removes less than all relevant N1 nodes
D1- removes N1 nodes only
- Lt and Rt cardiac
- Lt and Rt gastro-epiploic
- Sub and Supra pyloric
D2- removes all N1 and N2 nodes
- Lt gastric
- Common hepatic
- Celiac
- Splenic hilum and along splenic artery
D3- removes all N2 and N3 nodes
Variation according to the location of
primary tu
Antral Ca- include supra and sub-pyloric LN
but need not include cardia LN
Fundus Ca- include cardia LN but resection pyloric
LN are optional
The residual tumor (R) classification
The absence or presence of demonstrable residual
tumor after conclusion of the treatment (UICC)
R0 resection -no demonstrable residual tumor
R1 resection- microscopically demonstrable
residual tumor (e.g. diseased
residual margin)
R2 resection – macroscopically visible tumor
Distinction between primary palliative intervention
(R1&R2) vs. potentially curative ones (R0)
Survival after gastric resection
The profound impact on survival of leaving a
microscopic and macroscopic disease behind.
R0 resection
How much of a gastrectomy is
enough?
Gastric Carcinoma
The extent of gastric resection depends on:
- tumor size
- location
- depth of invasion
- histological type
Sub- total Gastrectomy
Total Gastrectomy
Total Gastrectomy
End to end anastomosis
Total Gastrectomy
End –to side anastomosis
Total Gastrectomy
Reconstruction using the EEA staplers
Total Gastrectomy
The creation of pouch ( rarely necessary)
Proximal Gastrectomy
Extent of resection for distal tumors
Randomized Controlled trials:
* Gouzi Jl.et al Ann Surg 209;162-6 1989
( French prospective controlled study)
- 169 pts. with antral cancers randomized to
subtotal vs. total gastrectomy
* Bozzetti F. et al Ann Surg 230;2:170-8 1999
(Italian trial – Italian Gastrointestinal Study group)
- 648 pts.with distal gastric cancers
randomized to subtotal vs. total gastrectomy
Extent of resection for distal tumors
Morbidity
Mortality
Authors n DST TG
DST TG
Gouzi 169 34% 32% 3.2% 1.3%
1989
Bozzetti 624 9% 13%
1% 2%
1999
Extent of resection for distal tumors
Authors n
Gouzi 169
1989
Bozzetti 648
1999
5%- Year Survival
DST
TG
48%
48%
64%
62%
Distal Subtotal Gastrectomy
Looking back at a number of retrospective studies,
the general sense is that DSG gives:
* Better nutritional function
* Improved quality of life
* No decrease in survival
Extent of resection for distal tumors
Conclusion:
Total gastrectomy offered no benefit over subtotal gastrectomy in patients treated with
curative intent.
Total gastrectomy should be reserved for
extensive gastric cancers and most proximal
cancers.
Extent of Gastrectomy
* What is an adequate margin?
- No randomized trial
- 5-6 cm margin recommended
* Intra-operative margin assessment
What is the ideal extent of
lymphadenectomy?
What is the ideal extent of
lymphoadenectomy?
There have been 4 prospective randomized trials
comparing D1 vs. D2 resection.
- Dutch trial – Benenkamp (1999)
- British MRC randomized controlled trial
(1996)
- Hong Kong trial – (1994)
- South African trial – Capetown -Dent (1993)
Dutch Trail
Benenkamp et al.
New England Journal of Medicine340; 12:908 1999
Multi-center trail – 80 Dutch hospitals
711 randomized patients
- 380 in the D-1 group
- 331 in the D-2 group
Dutch Trial
* D-2 group had higher rate of complications
43% vs. 25% P< 0.001
* D-2 higher number of postoperative deaths
10% vs. 4% P= 0.004
* D-2 longer hospital stays
median 16 vs. 14 days P< 0.001
British MRC Trial
Cuschieri et al Lancet 347; 9007: 995, 1996
400 pts.
( D-1 200; D-2 200)
Randomized controlled trail
* D-2 resection had higher rate of complications
46% vs. 28% P< 0.001
* D-2 higher number of postoperative deaths
13% vs. 6.5%
* Hospital stay the same (medium 14 day)
D-2 lymphadenectomy
The excess of morbidity and mortality in
Dutch and MRC trail was associated with
distal pancreatico-splenectomy or
splenectomy
South African trial
Dent et al. Br J Surgery - 1993
D1 versus D2 lymph dissection
- small trial ( lack of statistical power) : 66 patients
- median follow –up of 6.1 years
Conclusion: no survival difference
longer operation time
longer postoperative stay
more re-operations for complications
D-2 lymhadenectomy
In all the randomized controlled trails there is
no difference in overall survival.
Autor
Patients 5-year surv
P
Dent
D-1 n = 35
D-2 n = 31
Robertson D-1 n = 25
D-2 n = 30
Benenkamp D-1 n = 380
D-2 n = 331
Cuschieri D-1 n = 200
D-2 n = 200
68%
67%
45%
35%
45%
47%
35%
45%
NS
NS
NS
NS
Extent of Lymhadenectomy
Based on the available data:
* D-1 lymphadenectomy is associated with
less morbidity and mortality than a D-2
lymph node dissection at no apparent
diminution in survival.
* The D-1 dissection should be considered as
an acceptable minimum standard of care.
Extent of Lymphadenectomy
Way the D-1 lymphadenectomy is
a minimum standard of care?
Lymph node involvement impact on
survival
N-0 no positive LN ; N-1 1-6 positive LN
N-2 7-14 positive LN ; N-3 > 15 positive LN
Truly LN negative patients have significantly
better prognosis: 80% - 5 year survival
69% - 10 year survival
Number of examined LN and prognosis in
gastric cancer
Not only number of involved LN has impact on
prognosis.
Number of examined LN have significant
impact on prognosis!
- 5.4 % of pts. had metastasis in group 2 nodes while
group 1 nodes were unaffected (skip metastasis)
- prophylactic LN dissection (D2)- better staging
Lymph node Staging
The UICC / AJCC requirement
- To be staged as “N0” at least 15 lymph
nodes must be examined
Survival vs. number of examined lymph
nodes in N1 group
.
Survival vs. number of examined
lymph nodes in N2 group
Results of Immunohistochemical
LN examination
Higher recurrence rate in pts. with EGC and NO
after D1 than D2 and D3 dissection.
Micrometastasis in negative lymph nodes,
undetected by normal hystopathological
examination ?
24% cytokeratine-positive cancer cells in pts.
with negative LN.
Yashihiko, Surgery- 2002; 131s85-91
What operation you do?
D-1 if the number of LN
is less than 15
D-1 plus if the number
of LN is about 15
(taking some of N-2
nodes but not all of them)
D-2 if the mean number
of LN was 26
Summery
* R0 resection is the goal
* Distal subtotal gastrectomy is the procedure
of choice for the curative treatment of
distal tumors.
* Splenectomy and pancreatectomy increase
morbidity and mortality without
increasing survival
* The surgical procedure and pathologic
exam. should ensure that at least 15 lymph
nodes are examined (for adequate end
stage)
Early Gastric Cancer
Early Gastric Cancer
Early Gastric Cancer
Mass screening programs in Japan established
the concept of early gastric cancer.
Definition: tumor invasion is limited to
mucosa and sub-mucosa
regardless of presence of lymph
node metastasis
Early Gastric Cancer
The incidence of EGC among all gastric
cancer :
In Western countries 6-16%
In Japan > 50%-60%
In Korea from 14.9% (1974-1992) to 30% 40% today
Reasons for high proportion
of EGC in Japan
- asymptomatic patient are screened
- gastroscopy in Japan is more careful
procedure. ( indigo carmine, simeticone,
hyoscine is part of the routine)
GUT 2001 11/81 in UK with advance gastric
cancer had previous gastroscopy within two
years!
- West “high grade dysplasia” is in Japan “
intra-mucosal carcinoma”
Early Gastric Cancer
Survival
With appropriate resection
> 90% - 5year survival
> 80% - 10 year survival
Early Gastric Cancer
Macroscopic types
Early Gastric Cancer Type I
Macroscopic type I- protuberant (nodular polypoid
lesion)
Early Gastric Cancer Type II a
Macroscopic type II a – fungating and can have
ulceration on the dome
Early Gastric Cancer Type II b
Macroscopic type II b – flat type
Early Gastric Cancer Type II c
Macroscopic type II c – superficial depressed
Early Gastric Cancer Type III
Macroscopic type III – ulcerated tumor with a
penetrating ulcer base
Early Gastric Cancer
Prognostic factors
1% (16 /1589) recurrent cases after D1 &D2 of
EGC (1963-1989) Namieno,World J Surg
Risk factors for recurrence:
- submucosal (1.6%) vs. mucosal (0.29%)
- type IIb and III
Early Gastric Cancer
Prognostic factors
1051 pts. after D1&D2 resection for EGC
(Shimada ; Surgery 2001)
Mucosal (M) tumors
- lesions with ulceration or with scar even
smaller than 1.5 cm LN metastasis high
rate of metastasis( 4.8%)
- no correlation between the size and
histological type of carcinoma and LN
metastasis.
- all LN metastasis in N1
Early Gastric Cancer
Prognostic Factors
Sub-mucosal (SM) tumors
- LN metastasis (19.8%) including to N2
nodes(3.7%)
- the size and histological type correlates with LN
Early Gastric Cancer
Prognostic factors
The overall 5-years survival
without LN meta - 96.7%
with
LN meta - 75.9%
Early Gastric Cancer
Wang- suggests another classification based on
excellent prognosis rather than the depth on
invasion.
Only node negative pT1 gastric cancer should be
called EGC
Prognosis of node –positive pT1 and node negative
pT2 gastric cancer would be not favorable enough
to be categorizes as EGC
Early Gastric Cancer
Less invasive treatment?
The trends in the management of EGC are
different between Japan and the West.
Aggressive
Conservative
Early Gastric cancer
Less invasive treatment?
Trends in treatment for EGC at National
Cancer Hospital - Tokyo
Early Gastric Cancer
Less invasive treatment?
* Endoscopic mucosal resection (EMR)
* Local resection with regional lymphadenectomy
* Laparoscopic wedge resection with lesion
lifting method or laparoscopic intragastric
mucosal resection.
* Proximal gastrectomy with jejunal pouch
interposition
* Pylorus preserving gastrectomy (PPG)
Endoscopic mucosal resection
The method was introduced 15 years ago (in 1987)
There are still unsolved problems with regard to its:
- indications
- techniques
- preoperative evaluation of curability (EUS,
Laparoscopy..)
- method of follow up
Endoscopic Mucosal Resection
Diameter of the tumor ?
< 3cm
> 3cm well or moderately differentiated
superficially elevated and or depressed
(typs I, IIa, and IIc) but without
ulceration
Some cases of 8 cm EGC resection in pts. unfit for
surgery.
In lesion > 3 cm complete resection was achieved
only in 38%
Endoscopic Mucosal Resection
Margins of the resection ?
- Complete resection – local recurrence 2%
- Complete resection not confirm or resection
done in multiple fragments – local recurrence
of 18% after follow up of 4 month.
In recurrent cases: surgery/laser/reresection –all
remain disease free during median follow up of
38 month.
Endoscopic Mucosal Resection
What to do with pts.with submucosal invasion
after EMR?
Conservative resection?
D1 or D2 resection?
Follow up?
Local resection with regional
lymphadenectomy for EGC
Procedure can be done by Laparotomy or Laparoscopy
- Endoscopic sub - mucosal injection of dye
- Dissection of the perigastric nodes in dye area
(sentinel nodes) and sampling of LN in other sites
- LN FS - analysis
- In LN+  conventional gastrectomy
- In LN-  local resection
Laparoscopic intragastric mucosal
resection
- lesions in posterior wall of the stomach, near
the cardia and pylorus.
- tree balloon trocars are placed in the
stomach.
- the stomach is insufflated with CO2 and
surgical instruments are introduced
- mucosal and sub-mucosal layers around the
lesion is are resected
More surgical procedures for the
treatment of EGC
- Proximal gastrectomy with interposition of
double jejunal pouch between the esophagus
and the remnant stomach.
- Pyloric preservation gastrectomy: preservation
of a pyloric cuff of 2 cm and removal of
distal 2/3 of the stomach with Billroth I
reconstruction
- Laparoscopic assisted total or distal
gastrectomy with lymph node dissection
Conclusions of EGC treatment
Nowadays
Limited surgery is recommended only in mucosal
EGC( low rate of LN involvement)
In sub-mucosal EGC extended lymphadenectomy
appears to prolong the survival
- higher rate of LN involvement (11-19%)
- 7% of skip metastasis in extraperigastric LN
- micrometastasis
In Europe and USA- limited surgery is justify only
in high risk patients, otherwise D2 resection.
FINE
Role of CT in staging of gastric
carcinoma
Helical CT is able to identify:
1% of LN < 5mm
45% of LN of 5-9 mm
70% of LN > 9mm
Over 80% of lymph nodes > than 14 mm
contains metastasis
Role of CT in staging and gastric
carcinoma
Evaluation of:
- extension of the tumor along the wall and
adjacent areas.
- lymph node metastasis.
- distant metastasis.
Endoscopic Ultrasound
Lymph Nodes EUS features
Bhutani et al.
Am J Gastroenterology 1995
Role of laparoscopy in staging of gastric
cancer
In 16/32 (50%) of pts. with T3 and T4 gastric cancer,
laparoscopy changed the staging of the disease
in 5 pts (15.6%) - down staging
in 11 pts.(34.4%) – up staging
After laparoscopy 15/32 (46.9%) were diagnosed as
candidates for curative resection.
13 (86.7%) - R0 and R1 resection
2 (13.3%) – palliative resection –undetected
peritoneal metastasis by laparoscopy
Patients judged non curable (11) received neoadjuvant
therapy and 7/11 underwent salvage surgery (1-R0)
Yano M, World J Surg 2000 Sep,24
Role of laparoscopy in staging of
gastric cancer
Pretherapeutic staging system for the selection of the
best therapeutic option ( nonoperative or
neoadjuvant treatments).
Stage I non serosal involvement
Stage II serosal involvement
Stage III adjacent organ invasion
Stage IV distant disease found at laparoscopy
Excellent agreement with surgical pathologic
findings (98.4%) and prognosis.
Luis F Onate-Oncana
Ann Surg Oncol 2001 Sept; 8 (8)
Role of peritoneal cytology in staging of
gastric cancer
- 5 year survival of pts.with serosa exposed
gastric cancer is 30%.
- etiology peritoneal seeding is yet to be fully
understood
- peritoneal seeding is the main factor in
development of recurrence
Role of peritoneal cytology in
staging of gastric cancer
In a large retrospective study (1297 pts.) multivariate
analysis found that cytological findings was:
- independent prognostic factor for survival
- the most important factor for predicting
peritoneal recurrence
5- year survival rate with positive cytology was
only 2% ( even pts. with macroscopic dissemination had better survival)
CEA and CA-19-9 was higher in cytology positive
patients.
Bando E, Am J Surg – 1999 Sep;178
Role of peritoneal cytology in staging of
gastric cancer
The future
The use of molecular biology in diagnosis and
prognosis of gastric cancer.
- telomerase activation
- genetic instability
- abnormalities in oncogens, tumor suppressor genes,
cell cycle regulators, cell adhesion molecules DNA
repair genes.
Role of peritoneal cytology in staging of
gastric cancer
Conclusions:
- should be employed for all advance cancers
undergoing potentially curative resection.
- pts. with positive cytology must enter in the
future clinical trials involving perioperative
and intraperitoneal chemotherapy
The incidence of metastasis at each lymph
node station in antrum and fundus carcinoma
Node station
Antrum
Right cardiac
7
Lt cardiac
0
Lesser curve
38
Greater curve
35
Supra-pyloric
12
Sub-pyloric
49
Lt. Gastric artery
23
Common hepatic
25
Fundus
31
13
39
11
2
3
19
7
The incidence of metastasis at each lymph
node station in antrum and fundus
Node station
Coeliac artery
Splenic hilum
Splenic artery
Porta hepatis
Antrum
carcinoma
13
0
4
8
Fundus
13
10
12
1
Pattern in 1931 patients
Muryama Ann Surg 1989
D-2 gastrectomy
R0 resection: resection of all primary tumor
such that there is no macroscopic or
microscopic remaining.
The extend of lymphadenectomy is N1 and
N2 lymph nodes, but will vary according to
the position of primary tumor
Pre-operative assessment and
preparation
This procedure should be considered only
in patients with resectable tu and
reasonable chance of long term survival.
- Staging of the tumor
- Assessment of general status of the patient:
* pulmonary & cardiovascular
* nutritional status
Procedure
Roof top incision (Omnitracrt or Balfour
retractor) allowing good exposure of stomach,
duodenum, lesser and greater omentum
Procedure
Initial assessment – than deciding on operative strategy
* Detection for distant metastasis (liver, peritoneum) –
precede radical surgery
* Assessment of the tumor itself:
- position of the carcinoma
- extent ( linitis, localized )
- the depth of invasion (serosa, adjacent structure)
* Inspection and palpation of regional lymph nodes
(enlarge lymph nodes at the root of mesentery or
along the aorta – systemic dissemination? or
reactive enlargement ?  histology )
Procedure
1. Mobilization of hepatic flexure of the colon
and Kocherisation of the duodenum
Procedure
2. Detachment of the greater omentum from
the colon trough the avascular plain.
Procedure
Procedure
Posterior layer of
greater omentum
Anterior layer of
transverse mesocolon
Posterior layer
transverse mesocolon
Procedure
3. Removal of sub-pyloric LN and ligation of rt.
gastro-epiploic artery.(and surrounding lymphatics)
Ligation of rt.
gastro-epiploic artery
Procedure
4. Exposure and removal of supra-pyloric LN
5.Dissection of lesser
omentum and
hepato-duodenal
ligament.
Division of the reflection of the lesser
omentumon the live
( starting at the hiatus
and working to the right)
Procedure
Dissection of lesser omentum
Procedure
6. Ligation of rt. gastric artery and division of
the duodenum (GIA)
Procedure
7. Dissection the area of celiac axis and its
tributaries.
separation of pancreatic capsule
Procedure
7 . Dissection the area of celiac axis and its
tributaries (cont.)
identification of common hepatic artery
Procedure
7. Dissection in area of celiac axis and its
tributaries (cont.)
removing the tissue inferior to common hepatic
artery and approaching celiac axis , lt. gastric
vein is identified and ligated along superior border
of the pancreas
What are the results of D-2
lymphadenectomy in Japan and USA?
Center Operat. n Morbidity Mortality
Yokohama Distal 377 87(23%) 2(0.5%)
MSKCC
241 56(23%) 3(1.2%)
Yokohama Total 192 72(37%) 4(2.1%)
MSKCC
414 149(36%) 19
(4.6%)
Noguchi Y et al. Cancer 2000