gastric carcinoma (no videos)د.ياسر عبدالمغني

8/3/2019 Gastric Carcinoma (No videos).

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Gastric Carcinoma

YASSIR AHMED ABDULMUGHNI, FRCSIDEPUTY DEAN FACULTY OF MEDICINE


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Background

Second most common cancer-related death.

Korea, Japan, China, Taiwan high rates.

22,000 diagnosed annually in US. 14th most common cancer.

Difficult to cure, as advanced disease.

Most die of recurrent disease even afterresection for cure.


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Anatomy

Stomach begins at GE junction, ends at

duodenum.

3 parts- uppermost is cardia, largest part in

middle is body, the last part is pylorus.

Cardia contains mucin producing cells.

Fundus or body mucoid cells, chief cells,parietal cells.

Pylorus has mucin producing cells.


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Anatomy

Five layers: Mucosa, submucosa, muscular

layer, subserosal layer, serosal layer.

Peritoneum of greater sac covers anterior

surface

A portion of lesser sac drapes posteriorly

over stomach.

The GE junction has limited serosal

covering.


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Anatomy

The site of the lesion is classified on basis

of relationship to long axis of stomach.

40% lower part

40% middle part

15% upper part

10% more than one partRecently the # of lesions proximally has

increased.


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Pathophysiology

Understand vascular supply, allows for

understanding of routes of spread.

Derived from celiac artery.

Left gastric supplies upper right stomach.

Right gastric off common hepatic- lower

portion.Right gastroepiploic -lower portion of

greater curve.


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Pathophysiology

Understanding lymphatic drainage can

clarify nodal involvement.

Complex drainage

Primarily along celiac axis.

Minor drainage along splenic hilum,

suprapancreatic nodal groups, porta hepatis,and gastroduodenal areas


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Frequency

US: seventh leading cause of cancer deaths,

with 22,000 diagnosed yearly, and 14,000

deaths.

Internationally: second most common

cancer. Tremendous geographic variation,

with highest death rates in Chile, Japan, and

former USSR.


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Mortality and Morbidity

5-year survival for curative resections

ranges from 30-50% for stage II disease and

10-25% in stage III.

High likelihood of systemic and local

relapse.

Adjuvant therapy is offered .

Operative mortality is less than 3% for

curative resections.


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Race

Higher in Asian countries.

Japanese detect patients at very early stage,

patients appear to do quite well.

In Asian studies, patients with resected stage IIand III disease have better outcomes than similar

stages in the west.

Some believe this reflects a biologic differencebetween diseases in Asia and west.

Black race, low socioeconomic class.


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Sex, Age

Men>women

Most are elderly at diagnosis. Median age

65 years. The ones that present in younger

patients may represent a more aggressive

variant.

Cigarettes


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History

Early disease has no symptoms, some

patients with incidental complaints get an

early diagnosis.

If symptoms, it reflects advanced disease;

These may include indigestion, nausea,

dysphagia, early satiety, anorexia, weight

loss.


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History

Late complications include: pleural

effusions, peritoneal effusions, GOO, GE

obstruction, bleeding, jaundice, cachexia.


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Physical

All physical signs are late events.

Too late for curative procedures.

Palpable stomach with succussion splash,hepatomegaly, Virchow nodes, sister MJ

nodes, Blumer shelf, weight loss, pallor

from bleeding and anemia.


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Etiology

Diet

H. Pylori

Previous stomach surgeryPernicious anemia

Polyps(rarely a precursor)

Atrophic gastritisRadiation, genetics


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Diet

Certain diets are implicated.

Rich in pickled vegetables, salted fish,

excessive dietary salt, smoked meats.

A diet that includes fruits and vegetables

rich in vitamin C may have a protective

effect.


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Helicobacter

Implicated as precursor of gastric cancer.

H. Pylori associated with atrophic gastritis,

and patients with a history of prolonged

gastritis have a 6-fold increase in risk.

Particularly true of tumors of antrum, body,

and fundus of stomach, but not in cardia.


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Previous Surgery

Implicated as risk factor, the rational being

that previous gastric surgery alters normal

pH of stomach.

Retrospective studies show that a small

percentage of patients who have a gastric

polyp removed have evidence of invasive

carcinoma in the polyp.

Polyps may therefore be premalignant.


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Genetic Factors

Poorly understood

Some familial aggregation exists


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Laboratory

Assists in determining optimal therapy.

CBC identifies anemia, with may be caused

by bleeding, liver dysfunction, or poor

nutrition.

30% have anemia.

Electrolyte panels and LFTs are also

essential to better characterize patients

clinical state.


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Imaging Studies

EGD: safe, simple, providing a permanent

color photographic record.

Obtains tissue for diagnosis.

UGI: detects large tumors, but only

occasionally detects extension into

esophagus or duodenum, especially if small

or submucosal.


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Imaging Studies

CXR: done to evaluate for metastases.

CT scan or MRI of chest, abdomen, pelvis:

evaluate local disease process, and areas of

spread. Some tumors are deemed

unresectable based on the testing.

Accurately predicts stage 66-77%.

Poor nodal status prediction.


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Endoscopic Ultrasound

Endoscopic ultrasound: becoming extremelyuseful as a staging tool, when CT fails to show T3,T4, or metastatic disease.

Used with neoadjuvant chemo to stratify pts

Can achieve resolution of 0.1 mm.

Cannot reliably distinguish between tumor andfibrosis.

Overall staging accuracy of 75% Poor for T2 lesions (38%)

Better for T1(80%), T3 (90%)


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Histology

Adenocarcinoma 95%

Lymphomas 2%

Carcinoids 1%Adenocathomas 1%

Squamous cell 1%


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Histology

Adenocarcinoma is classified according tothe most unfavorable microscopic elementpresent: tubular, papillary, mucinous,

signet-ring cells.Also identified by gross appearance:

ulcerative, polypoid, scirrous, superficialspreading, multicentric, or Barrett ectopic.

Variety of other schemes: Borrmann,Lauren.


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Borrmann Classification

5 categories

Type I: polypoid or fungating

Type II: ulcerating lesions with elevatedborders

Type III: ulceration with invasion of wall

Type IV: diffuse infiltrationType V: cannot be classified


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Lauren System

Epidemic or endemic

The intestinal, expansive epidemic type

gastric cancer is associated with atrophic

gastritis, retained glandular structure, little

invasiveness, sharp margins. It would be a

Borrmann I or II.


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Lauren System

The epidemic or Borrmann I or II carries

better prognosis, shows no family history.

The diffuse, infiltrative, endemic, is poorly

differentiated, with dangerously deceptive

margins, invades large areas of stomach.

Younger patients, genetic factors, blood

groups, and family history.


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Staging

Primary tumor

Tx- cannot be assessed

T0- no evidence

Tis- carcinoma in situ, no invasion of lamina

T1- invades lamina propria or submucosa

T2- invades muscularis or subserosa

T3- penetrates serosa, no adjacent structure

T4- invades adjacent structures


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Regional Lymph Nodes

NX- cannot be assessed

N0- no nodes

N1- mets in 1-6 regional nodesN2- mets in 7-15 regional nodes

N3- mets in more than 15 regional nodes


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Distant Metastases

MX- cannot be assessed

M0- no distant metastases

M1-distant metastases


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LN group

1 R cardiac2 L cardiac

3 Lesser curvature

4 Greater curvature

5 Suprapyloric

6 Infrapyloric

7 L gastric artery

8 Common hepatic artery

9 Celiac artery

10 Splenic hilar

11 Splenic artery

12 Hepatic pedicle13 Retropancreatic

14 Mesenteric root

15 Middle colic artery

16 Paraaortic

N1

N2


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Prognostic Features

Depth of invasion through gastric wall,

presence or absence of regional lymph node

involvement

The greater number of positive nodes, the

greater the likelihood of local or systemic

failure postoperatively


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Spread Patterns

Directly, via lymphatics, or hematogenously

Direct extension into omentum, pancreas,

diaphragm, transverse colon, and

duodenum.

If lesion extends beyond wall to a free

peritoneal surface, peritoneal involvement is

frequent.


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Spread Patterns

The visible gross lesion frequently underestimates

true extent.

Abundant lymphatic channels in submucosal and

subserosal layers allow for easy spread. The submucosal plexus is prominent in esophagus,

the subserosal plexus prominent in duodenum,

which allows for proximal and distal spread.

Liver mets common, from hematogenous spread.


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Laparoscopy

Inspect peritoneal surfaces, liver surface.

Identification of advanced disease avoids

non-therapeutic laparotomy in 25%.

Patients with small volume metastases in

peritoneum or liver have a life expectancy

of 3-9 months, thus rarely benefit from

palliative resection.


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Lymph Node Dissection

AJCC: number rather than location of LN isprognostic.

Extent of dissection controversial.

Nodal involvement indicates poor prognosis, andmore aggressive approaches to remove them aretaking favor.

Ongoing trials regarding this in Europe.

Critics argue that the apparent benefit associatedwith extended LND reflects stage migration (eachLN is reviewed more carefully).


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Residual Disease R Status

Tumor status following resection.

Assigned based on pathology of margins.

R0- no residual gross or microscopic

disease.

R1- microscopic disease only.

R2- gross residual disease.Long term survival only in R0 resection.


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D Nomenclature

Describes extent of resection and

lymphadenectomy.

D1- removes all nodes within 3cm of tumor.

D2- D1 plus hepatic, splenic, celiac, and leftgastric nodes.

D3- D2 plus omentectomy, splenectomy, distal

pancreatectomy, clearance of porta hepatis nodes.

Current standards include a D1 dissection only.


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Type of Surgery

In general most surgeons perform totalgastrectomy ( if required for negativemargins), esophagogastrectomy for tumors

of the cardia and GE junction, and asubtotal gastrectomy for tumors of the distalstomach.

Similar 5 year rates for subtotal vs. total in

tumors of distal stomach.

Extensive lymphatics require 5cm margin.

Distal Tumors


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35%-Subtotal gastrectomy

Midbody Tumors15-30%-Total gastrectomy

Proximal Tumors35-50%

Siewert ClasssificationType I: Barretts esophagusIvor-LewisType II: GE junction tumor (2 cmsquamocolumnar junction) Roux-en-Ytotal gastrectomy

Type III: Subcardial region tumor Roux-en-Y total gastrectomy


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Outcome

5-year survival for a curative resection is30-50% for stage II disease, 10-25% forstage III disease.

Adjuvant therapy because of high incidenceof local and systemic failure.

A recent Intergroup 0116 randomized studyoffers evidence of a survival benefitassociated with postoperativechemoradiotherapy


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Complications

Mortality 1-2%

Anastamotic leak, bleeding, ileus, transit

failure, cholecystitis, pancreatitis,

pulmonary infections, and

thromboembolism.

Late complications include dumping

syndrome, vitamin B-12 deficiency, refluxesophagitis, osteoporosis.


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Adjuvant Therapy

Rationale is to provide additional loco-

regional control.

Radiotherapy- studies show improved

survival, lower rates of local recurrence

when compared to surgery alone.

In unresectable patients, higher 4 year

survival with mutimodal tx, in comparisonto chemo alone.


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Chemotherapy

Numerous randomized clinical trials

comparing combination chemotherapy in

the adjuvant setting to surgery alone did not

demonstrate a consistent survival benefit.The most widely used regimen is 5-FU,

doxorubicin, and mitomycin-c. The addition

of leukovorin did not increase responserates.


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Advanced Unresectable Disease

Surgery is for palliation, pain, allowing oral

intake

Radiation provides relief from bleeding,

obstruction and pain in 50-75%. Medianduration of palliation is 4-18 months


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GASTRIC POLOYP

*SINGLE OR MULTIPLE(BENIGN).

*HYPERPLASTIC

*ADENOMATOUS

*INFLAMMATORY

ANAEMIA

EXFOLIATIVE CYTOLOGY & BRUSHBIOPSY

EXSCION BY ENDOSCOPE ORLAPAROTOMY

GASTRIC LYMPHOMA & PSEUDO


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LYMPHOMA

Lymphoma is the second most common primary cancer of the stomach (2%)

Non Hodgkin lymphoma (MALT)

*SYMPTOMS:

Epigastric pain &weight loss

Palpable mass (50%)

*RADIOLOGY

*ENDOSCOPY& BIOPSY

*PREOPERATIVE STAGING

*TREATMENT:

Low grade cyclophosphmide

High grade excision +total abdominal radiotherapy

Intra-operative staging

splenectomy?Extension to the esophagus &duodenum?

GASTRIC LEIOMYMA & LEIOMYOSARCOMA


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