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					Gastric Carcinoma

Vic Vernenkar, D.O.
St. Barnabas Hospital
Department of Surgery
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 after
  resection for cure.
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.
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.
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 part
 Recently the # of lesions proximally has
  increased.
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.
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
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.
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.
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 II
  and III disease have better outcomes than similar
  stages in the west.
 Some believe this reflects a biologic difference
  between diseases in Asia and west.
 Black race, low socioeconomic class.
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
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.
History
 Late complications include: pleural
  effusions, peritoneal effusions, GOO, GE
  obstruction, SBO, bleeding, jaundice,
  cachexia.
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.
Etiology
 Diet
 H. Pylori
 Previous stomach surgery
 Pernicious anemia
 Polyps(rarely a precursor)
 Atrophic gastritis
 Radiation, genetics
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.
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.
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.
Genetic Factors
 Poorly understood
 Some familial aggregation exists
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.
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.
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.
Endoscopic Ultrasound
 Endoscopic ultrasound: becoming extremely
  useful 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 and
  fibrosis.
 Overall staging accuracy of 75%
 Poor for T2 lesions (38%)
 Better for T1(80%), T3 (90%)
Histology
 Adenocarcinoma 95%
 Lymphomas 2%
 Carcinoids 1%
 Adenocathomas 1%
 Squamous cell 1%
Histology
 Adenocarcinoma is classified according to
  the most unfavorable microscopic element
  present: tubular, papillary, mucinous,
  signet-ring cells.
 Also identified by gross appearance:
  ulcerative, polypoid, scirrous, superficial
  spreading, multicentric, or Barrett ectopic.
 Variety of other schemes: Borrmann,
  Lauren.
Borrmann Classification
 5 categories
 Type I: polypoid or fungating
 Type II: ulcerating lesions with elevated
  borders
 Type III: ulceration with invasion of wall
 Type IV: diffuse infiltration
 Type V: cannot be classified
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.
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.
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
Regional Lymph Nodes
NX- cannot be assessed
N0- no nodes
N1- mets in 1-6 regional nodes
N2- mets in 7-15 regional nodes
N3- mets in more than 15 regional nodes
Distant Metastases
 MX- cannot be assessed
 M0- no distant metastases
 M1-distant metastases
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
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.
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.
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.
Lymph Node Dissection
 AJCC: number rather than location of LN is
  prognostic.
 Extent of dissection controversial.
 Nodal involvement indicates poor prognosis, and
  more aggressive approaches to remove them are
  taking favor.
 Ongoing trials regarding this in Europe.
 Critics argue that the apparent benefit associated
  with extended LND reflects stage migration (each
  LN is reviewed more carefully).
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.
“D” Nomenclature
 Describes extent of resection and
  lymphadenectomy.
 D1- removes all nodes within 3cm of tumor.
 D2- D1 plus hepatic, splenic, celiac, and left
  gastric nodes.
 D3- D2 plus omentectomy, splenectomy, distal
  pancreatectomy, clearance of porta hepatis nodes.
 Current standards include a D1 dissection only.
Type of Surgery
 In general most surgeons perform total
  gastrectomy ( if required for negative
  margins), esophagogastrectomy for tumors
  of the cardia and GE junction, and a
  subtotal gastrectomy for tumors of the distal
  stomach.
 Similar 5 year rates for subtotal vs. total in
  tumors of distal stomach.
 Extensive lymphatics require 5cm margin.
Outcome
 5-year survival for a curative resection is
  30-50% for stage II disease, 10-25% for
  stage III disease.
 Adjuvant therapy because of high incidence
  of local and systemic failure.
 A recent Intergroup 0116 randomized study
  offers evidence of a survival benefit
  associated with postoperative
  chemoradiotherapy
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, reflux
  esophagitis, osteoporosis.
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 comparison
  to chemo alone.
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 response
  rates.
Advanced Unresectable Disease
 Surgery is for palliation, pain, allowing oral
  intake
 Radiation provides relief from bleeding,
  obstruction and pain in 50-75%. Median
  duration of palliation is 4-18 months

				
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