Carcinoma stomach - its etiology classification investigations, staging and management

1. Dr. kundan
Junior Resident , Department of surgery
Patna medical college

2. Anatomy
The stomach J-shaped. The stomach
has two surfaces (the anterior &
posterior), two curvatures (the greater
& lesser), two orifices (the cardia &
pylorus). It has fundus, body and
pyloric antrum.

3. a. The left gastric artery
b. Right gastric artery
c. Right gastro-epiploic artery
d. Left gastro-epiploic artery
e. Short gastric arteries
The corresponding veins drain
into portal system. The lymphatic
drainage of the stomach
corresponding its blood supply.

4. Histology
Consist of four layers
serous layer
muscular layer
submucous layer
mucous layer

5. PHYSIOLOGY
Function:
1. Digestion of food, reduce the size of food
2. Acts as reservoir
3. Absorption of Vit. 12, iron and calcium
Stimulant of Gastric secretion:
1. Gastrin -----> (+) parietal cell
2. Acetylcholine (vagus) ---> (+) gastric cells
3. Histamine (mast cells) ---> parietal & chief cells

6. Carcinoma stomach
Clinical Presentation
Diagnosis
Staging
Treatment
Screening

8. Spectrum of gastric cancer
Proposed progression:
chronic gastritis -->
chronic atrophic gastritis -->
 intestinal metaplasia -->
dysplasia -->
adenocarcinoma

10. Risk Factors for gastric cancer
Diet
 nitroso compounds
 low fruit/vegetable, high fried foods/processed meat
 High salt intake
Obesity
Smoking (HR 2-3)
? Alcohol
H. Pylori
Low socioeconomic status
Hereditary diffuse gastric cancer
 40-67% lifetime risk for men, 60-83% for women
Immigrants from endemic areas
 maintain native country risk, risk to offspring similar to new homeland

15. Precursors of Gastric Cancer
Adenomatous polyps
Chronic atrophic gastritis
Pernicious gastritis
Menetries’s disease
Previous gastric surgery for non- cancerous
conditions

16. Symptoms at presentation

17. Symptoms (cont’d)
Dysphagia: more common with proximal gastric
tumors
Occult GI bleeding very common, overt bleeding
<20%.

18. Signs
Palpable abdominal mass: most common physical
finding
If cancer spreads via lymphatics…
Left supraclavicular node (Virchow’s)
Periumbilical node (Sister Mary Joseph)
Left axillary node (Irish)
Enlarged ovary (Krukenberg's tumor)
Ascites

19. Investigations
Routine blood examination
low hemoglobin , high ESR
 stool examination for occult blood
 gastric function test - will reveal gross hypo / achlorhydria
 Endoscopy – helpful in diagnosing early cases and taking biopsy
 Ultrasonography - helps in assesing thickening of agstric wall, local
invasion, peritoneal involvement , ascitis
 CT scan - extent of the disease , lymph node involvement , liver metastasis
 Barium studies
 Staging laproscopy

20. Diagnosis
Endoscopy
Gold standard
Single biopsy from ulcer -> sensitivity ~ 70%
Seven biopsies from ulcer -> sensitivity >98%
Brush cytology increases sensitivity of single biopsies,
aid in multiple biopsies unclear

21. Preoperative Staging
Abdominal / pelvic CT scanning
Endoscopic ultrasound (EUS)
Depth of the tumour
Enlarged perigastric/coeliac lymph nodes

22. Endoscopic ultrasound
A small, high frequency ultrasound
transducer incorporated into the distal end
of the endoscope.
Advantages:
- superior resolution.
- image not compromised by intervening
gases.
- lesion as small as 2-3 mm in diameter can
be imaged.

24. Barium studies
False negative in as many as 50% of cases
Sensitivity as low as 14% in early cases
May be superior to EGD for linitis plastica
EGD may be normal while “leather-bottle” will be
apparent on radiograph

25. Staging Laparoscopy

27. Malignant Neoplasms of the Stomach
Primary
Adenocarcinoma (94%)
Lymphoma (4%)
Malignant GIST (1%)
Haematogenous spread
Breast
Malignant melanoma
Direct invasion
Pancreas; Liver; colon; ovary

28. Staging of Gastric Cancer
Two systems:
Japanese classification (more elaborate and anatomic
based)
Western: developed by American Joint Committee on
Cancer (AJCC) and International Union Against
Cancer (UICC) -- more widely used
Tumors at GE junction of in cardia of stomach
within 5cm of GE junction
Classified using esophageal staging

29. Gastric carcinoma
CLASSIFICATION
Depth of invasion
EARLY GASTRIC CA - mucosa & submucosa
ADVANCED GASTRIC CA - into or through
muscularis propria
Macroscopic growth pattern – Ming classification
Expanding
Infiltrative - "linitis plastica"
Histologic subtype
Intestinal
Diffuse (gastric); poorly differentiated; "signet ring"
cells

30. Gastric carcinoma
CLASSIFICATION
WHO Classification:
1. Adenocarcinoma:
a. Papillary adenocarcinoma
b. Tubular adenocarcinoma
c. Mucinous adenocarcinoma
d. Signet-ring cell carcinoma
2. Adenosquamous carcinoma
3. Squamous cell CA
4. Small cell CA
5. Undifferentiated CA
6. Others
Lauren Classification:
1. Intestinal type (53%)
2. Diffuse type (33%)
3. Unclassified (14%)
Ming Classification:
1. Expanding type (67%)
2. Infiltrative type (33%)

32. Histologic type:
1. Papillary
2. Tubular
3. Mucinous
4. Signet ring
Mode of spread:
1. Direct
2. Lymphatic
3. Hematologic
4. Transcoelomic route

35. Linitis Plastica
Diffuse-type gastric cancer
Tumor often infiltrates the submucosa and
muscularis propria
Superficial biopsies may be falsely negative
Combination of strip and bite biopsy needed if
suspicious for linitis plastica

36. Linitis Plastica, “leather bottle stomach”

37. Staging workup
Biopsy
Imaging
CT: evaluates for metastases (M stage)
 20-30% with negative CT have intraperitoneal disease at
laparatomy
 Accuracy of 50-70% for T stage
 Slightly worse accuracy for N stage compared to EUS
EUS: most reliable nonsurgical method to evaluate
depth of invasion
 More accurate than CT for T stage
 65-90% accurate for N stage

38. Staging workup
PET
More sensitive than CT for detection of distant
metastases.
Also useful for detecting LNs
Negative PET not helpful- even large tumors can be
falsely negative if metabolic activity low.
 Most diffuse gastric cancers (signet ring) are not FDG avid

39. Staging workup
Serologic markers
CEA, CA-125, CA 19-9, CA 72-4 may be elevated but
have low sensitivity/specificity
None are diagnostic
Preoperative elevation in markers usually pretends high
risk of adverse outcome
No serologic finding should exclude surgical
consideration

40. AJCC Staging System

42. AJCC Staging System

43. Treatment
Locoregional (stage I-III) disease
Potentially curable
multidisciplinary evaluation and consideration of
surgery
Advanced (stage IV) disease
Palliative therapy
Studies indicate longer survival and better quality of life
with systemic treatment

44. Surgery
The extent of gastric resection depends on:
- tumor size
- location
- depth of invasion
- histological type

45. Treatment
Complete surgical resection with removal of LNs
(only chance of cure)
Possible in < 1/3 of cases
Subtotal gastrectomy for distal carcinomas, total or
near-total for proximal masses
Reduction of tumor bulk (palliative)
Chemotherapy (cisplatin + 5-FU or irinotecan)
 Partial response in 30-50% of patients
Radiation (for pain control, no mortality benefit with
XRT alone)

47. The Japanese Research Society for Gastric Cancer
The 16 lymph node locations were classified into 4
concentric groups: N1, N2, N3, N4
Periepigastric Extraepigastric

48. 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

49. 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)

50. Prognosis
Stage TNM Features
% of
Cases*
% 5-year
survival*
0 TisN0M0 Node negative; limited to mucosa 1 90
IA T1N0M0
Node negative; invasion of lamina propria or
submucosa 7 59
IB T2N0M0 Node negative; invasion of muscularis propria 10 44
II
T1N2M0 Node positive; invasion beyond mucosa but
within wall 17 29T2N1M0
T3N0M0 Node negative; extension through wall
IIIA
T2N2M0
Node positive; invasion of muscularis propria
or through wall
21 15
T3N1-2M0
IIIB T4N0-1M0
Node negative; adherence to surrounding
tissue 14 9
IV T4N2M0
Node negative; adherence to surrounding
tissue 30 3
Any M1 Distant Metastases
** Data from American Cancer Society

51. Pharmacologic Therapy
 Cisplatin + epirubicin & infusional 5-FU or + irinotecan
 Complete remissions are uncommon.
 Partial responses in 30-50% of cases are transient.
 Overall influence on survival has been unclear.
 Adjuvant chemotherapy alone following complete
resection has only minimally improved survival.
 Perioperative treatment and postoperative chemotherapy
+ radiation therapy reduce the recurrence rate and
prolongs survival.

52. Treatment: Supportive:
Nutrition (jejunal enteral feedings or total parenteral
nutrition),
Correction of metabolic abnormalities that arise from
vomiting or diarrhea
Treatment of infection from aspiration or spontaneous
bacterial peritonitis.
To maintain lumen patency, endoscopic laser
treatment or stenting for palliation.

53. Screening
Mostly barium studies, EGD is concerning findings
Some use serum pepsinogen testing for high risk with EGD
confirmation
H. pylori: sensitivity 88%, specificity 41% (Japan)
 5-year survival 74-80 in screened group, 46-56% for non-
screened group.