gastric cancer surgery”b” department “meir” hospital kfar-saba

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?


Displasia/ MetaplasiaCarcinoma


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 assessedN0- no regional lymph node metastasisN1- metastasis in 1-6 regional LNN2- metastasis in 7-15 regional LNN3- metastasis in more than15 regional LN

Distant metastasis(M)MX – cannot be assessedM0 – no distant metastasis

M1- distant metastasis

Histopathologic Grade

G1 Well differentiated

G2 Moderately differentiated

G3 Poorly differentiated

G4 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.


Image / Drawing


T1 lesion


T2 lesion


T3 lesion


T4 lesion


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)


N stage

Low accuracy of EUS in assessment of LN invasion ( correct in 50-80% of the cases).

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


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


carcinoma Accuracy of CT in diagnosis of:

-Hepatic metastasis is 79% -96% (will miss the majority of meta <1cm)

-Peritoneal metastasis is 73 -80%

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%)


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

Lt. and Rt. cardiac

Lesser curvature

Greater curvature

Sub-pyloric

Supra-pyloric

N-1 perigastric LN - closest to the tumor

N-2 lymph nodes- located along the course of feeding arteries

Lt gastric artery LN

Common hepatic artery LN

Coeliac 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

- rout of mesentery

- LN along meddle colic artery

- para-aortic LNN4

N3

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 pyloricD2- 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


Morbidity Mortality

Authors n DST TG DST TG

Gouzi 169 34% 32% 3.2% 1.3%

1989

Bozzetti 624 9% 13% 1% 2%

1999


5% -Year Survival

Authors n DST TG

Gouzi 169 48% 48%

1989

Bozzetti 648 64% 62%

1999

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


Conclusion:Total gastrectomy offered no benefit over sub-total 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 TrailBenenkamp 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 TrialCuschieri 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 PDent D-1 n = 35 68% NS

D-2 n = 31 67% Robertson D-1 n = 25 45% NS

D-2 n = 30 35% Benenkamp D-1 n = 380 45% NS

D-2 n = 331 47%Cuschieri D-1 n = 200 35% NS

D-2 n = 200 45%

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


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


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 proportionof 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 CancerSurvival

With appropriate resection

< 90% - 5year survival

< 80% - 10 year survival

Early Gastric CancerMacroscopic 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 CancerPrognostic 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


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 CancerPrognostic Factors

Sub-mucosal (SM) tumors

- LN metastasis (19.8%) including to N2 nodes(3.7%)

-the size and histological type correlates with LN involvement ( Tu > 2cm , undifferentiated)

Early Gastric CancerPrognostic factors

The overall 5-years survival

without LN meta - 96.7%

with LN meta - 75.9%


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 CancerLess invasive treatment?

The trends in the management of EGC are different between Japan and the West.

Aggressive Conservative

Early Gastric cancerLess invasive treatment?

Trends in treatment for EGC at National Cancer Hospital - Tokyo

Early Gastric CancerLess 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%


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 .


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 .


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.


Lymph Nodes EUS features

Bhutani et al.

Am J Gastroenterology 1995


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 (9)


gastric cancer Pretherapeutic staging system for the selection of the best therapeutic option ( nonoperative or neoadjuvant treatments).Stage I non serosal involvementStage II serosal involvement Stage III adjacent organ invasionStage 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 instaging 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 andprognosis 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 Fundus

Right cardiac 7 31

Lt cardiac 0 13

Lesser curve 38 39

Greater curve 35 11

Supra-pyloric 12 2

Sub-pyloric 49 3

Lt. Gastric artery 23 19

Common hepatic 25 7

The incidence of metastasis at each lymph node station in antrum and

fundus carcinoma Node station Antrum Fundus

Coeliac artery 13 13

Splenic hilum 0 10

Splenic artery 4 12

Porta hepatis 8 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

ProcedureInitial 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 transverse mesocolon

Anterior layer of transverse mesocolon

Posterior layer of greater omentum

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 refle-

ction 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)

Procedure7 .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 MortalityYokohama 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

gastric cancer surgery”b” department “meir” hospital kfar-saba

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