Transcript Stomach Surgery

STOMACH
James Taclin C. Banez, MD, FPSGS, FPCS
Anatomy
 Arterial blood supply
 Lymphatic drainage
 Nerve supply
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
PHYSIOLOGY
BAO: 2 – 5 meq of acid/hr. (vagal tone and basal
histamine secretion)
MAO:
1. Cephalic (vagus) ---> (+) parietal & G cell
 10 meq acid/hr.
2. Gastric: ---> (+) vagus & G cell
 15 – 25 meq of acid/hr pH = < 2.0
3. Intestinal:
 Chyme enters the duodenum
 (-) gastric release
 Secretin, gastric inhibitory peptide, peptide YY

ACID condition sterilized the area, except for
HELICOBACTER PYLORI
GASTRIC DISEASES:
 Acid peptic Disease
 Neoplasm
Acid peptic Disease:


Due to imbalance in the normal interplay
between acid-pepsin and mucosal
defense mechanism
Types:
1. Acute Gastritis (erosive):

Inflammation confined in the mucosa
2. True Ulcers:

Extends through the mucosa
Peptic ulcer
A. Duodenal Ulcer
B. Gastric Ulcer
Duodenal ulcer
>
gastric ulcer
Female
>
Male
Duodenal ulcer is younger by 10 yrs
Location:
1. Duodenal:
 duodenal bulb
 Hyper-secretion of acid
Peptic ulcer
Location:
2. Gastric
Type I - proximal antrum and body
(disturbance in mucosal defense)
Type II - arises secondary to duodenal
ulcer w/ pyloric stenosis
Type III - Prepyloric and pyloric channel
- (hyper-secretion of acid)
Peptic ulcer
Pathogenesis:
1. For both Duodenal & Gastric Ulcers:
a. Infection w/ H. pylori:

Decreases resistance of mucus layer from acid
permeation (hydrophobicity)

Increase acid secretion

Slow duodenal emptying

Reduced both duodenal and gastric bicarbonate
secretion
Peptic ulcer
Pathogenesis:
b. Effects of NSAIDs
 Decreases Prostagladin
Prostaglandin – inhibits acid secretion, stimulates
mucus and HCO3 secretion and mucosal blood
flow
c. Zollinger-Ellison Syndrome (1%):





Massive secretion of HCL due to ectopic gastrin
production from non-beta islet cell tumor
(gastrinoma)
Associated w/ type I (MEN) PPP
20% multiple, 2/3 malignant, w/ slow growing
Parietal cell mass is increased
> gastrin 3-6 x the normal
Peptic ulcer
2. For Duodenal
a. Acid Hypersecretion:
a) More parietal and chief cells
 Genetic
 Due to release of tophic factors - gastrin
b) Increase capacity of individual cell to secret
b. Gastric Motility abnormality
c. Impaired duodenal acid disposal

Reduced basal and peak duodenal bicarbonate
secretion and defect in mucus
Peptic ulcer
3. For Gastric Ulcer:
a. Reflux of Duodenal contents (pancreas and
biliary)
 Gastritis -----> Ulceration
 Pyloric sphincter dysfunction
 Cigarette smoking:
a. Increases duodeno-gastric reflux
b. Decrease prostaglandin synthesis
c. Decreases duodenal, gastric and pancreatic
bicarbonate secretion
 Bile acids, lysolecithin and pancreatic
secretions – disturb surface mucus layer
Clinical Manifestation
1. Abdominal pain:

Due to irritation of afferent nerves w/in the ulcer by
the acid or due to peristaltic waves passing through
the ulcer
 Duodenal: colicky or burning pain relieved w/ food
intake
 Gastric: gnawing or burning usually during or after
eating.
2. N/V
3. Weight loss
4. Epigastric tenderness
Diagnosis:
1. UGIS (double contrast)
2. Endoscopy
Treatment:
A. Medical:
Avoid the following:
1.
2.
3.
4.
Smoking
Aspirin / NSAIDs
Coffee (acid secretion)
Alcohol (damage the mucosa)
Mechanism of Pharmacologic Therapy:
1. Neutralize gastric secretion (HCL): ANTACID
2. Inhibits Secretion of Acid:
a. H2 receptor antagonist – CIMETIDINE,
RANITIDINE, FAMOTIDINE
Treatment:
Mechanism of Pharmacologic Therapy:
2. Inhibits Secretion of Acid:
b. Anticholinergic:
 Inhibits acetylcholine
Pirenzepine HCL
c. H+ / K+ - ATPase inhibitor proton pump
 Benzimidazole selectively inhibits parietal cells
Omeprazole, Lanzoprazole, Pantoprazole
3. Protection of Gastric Mucosa:
a. Prostaglandin:
Methylated E2 analog inhibits gastric secretion,
increases mucosal bld flow & HCO3 & mucosa
secretion
Treatment:
Mechanism of Pharmacologic Therapy:
3. Protection of Gastric Mucosa:
b. Sulfated disaccharide (sucralfate)
 Binds to protein in the ulcer as protective
coat
 It can inhibits peptic activity
c. Colloid bismuth
 Binds w/ protein & against H. pylori
Treatment:
Mechanism of Pharmacologic Therapy:
4. For eradication of H. pylori:
a. Bismuth based triple therapy
 Bismuth + Tetracycline + Metronidazole
b. Proton pump inhibitor
 Omeprazole + Amoxicillin/Clarithromycin
+ metronidazole
Treatment:
Surgical Treatment:
Indication:
1. Intractability:

Highly selective vagotomy


Low septic complication, (-) dumping and
diarrhea
For gastric ulcer:

Total or subtotal gastrectomy w/ or w/o vagotomy
Treatment:
Surgical Treatment:
Indication:
2. Hemorrhage: s/sx



Critically ill
Endoscopy
Surgery:
a. continue bleeding for more
than 6 units
b. recurrent bleeding after
endoscopically controlled
- pyloroduodenostomy + HSV
- pyloroduodenostomy + vagotomy + pyloroplasty
Treatment:
Surgical Treatment:
Indication:
3. Perforation: S/Sx



Graham omental patch only for shock, perforation
> 48 hrs or other medical problem
Vagotomy + pyloroplasty; HSV
Vagotomy + Gastrojejunostomy
4. Obstruction: S/Sx; Saline loading test


Vagotomy + Antrectomy
Vagotomy + Gastroenterostomy
Acute Gastritis (erosive)

Stress erosions are usually multiple, small
punctuate lesion in the proximal acid secreting
portion of the stomach
Clinical Settings:
1. Severe illness, trauma, burns (Cushing ulcer) or
sepsis
 Due to (-) mucosal defense (ischemia)
2. Drug and Chemical ingestion
 Aspirin / NSAIDs
3. CNS trauma:
 Increase gastrin ---> elevated acid secretion
 Curling ulcer
Acute Gastritis
Pathogenesis:
1. Aspirin, bile salts (backflow), alcohol
2. Mucosal ischemia
Clinical manifestations:
1. Gastrointestinal bleeding
2. Abdominal pain
Diagnosis:

Endoscopy / radionuclide scanning / visceral
angiography
Acute Gastritis
Treatment:





NPO
NGT / Saline lavage
Antacids / omeprazole / sucralfate
Intra-arterial infusion of vasopressin
Surgery --> if 6-8 units over 24 hrs

1.
2.
3.
Mortality ---> 40%
Near total gastrectomy
Vagotomy + pyloroplasty + over sewing of bleeder
Partial gastrectomy + vagotomy
Zollinger-Ellison Syndrome

(Gastrinoma)
Symptoms tends to be more severe, unrelenting and less
responsive to therapy.
Clinical Manifestation:
1. Pain
2. Diarrhea
3. Steatorrhea
Diagnosis:
1. Acid secreting studies (50meq/hr)
2. UGIS
3. Radio-immuno assay for serum Gastrin level

Diff:
a) Pernicious anemia
b) Renal insufficiency
c) Antral gastrin hyperplasia or hyperfunction
4. CT scan and angiography to localize gastrinoma
5. Venous sampling
Gastric Neoplasm:

90% malignant
1. 95% adenocarcinoma
2. 4% lymphoma
3. 1% leiomyosarcoma (GIST-malignant gastrointestinal
stromal tumors)
4. Rare – carcinoid, angiosarcoma, squamous cell CA.
5. As metastatic lesion of -->
- colon/pancreas
- melanoma/breast
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
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Malaysia, Chile, Iceland and JAPAN
Male:Female (2:1); more common twice in
black than white
6 -7 decade of life: if it occurs in young(30-40y/o)
becomes more aggressive (linitis plastica or signet ring
histology)
Low socioeconomic
Adenocarcinoma:
Etiology:
1. Diet - high in nitrates----->nitrites (bacteria & bile salts)
- pickled, salted or smoked food
- fresh fruit & vegetable and vit C & E ---> lowers
2. H. pylori infection
 3 fold increase risk
3. Ebstein Barr virus
4. Genetic factor:


Suppression of p53 (tumor suppression gene);
over expression of COX-2
Adenocarcinoma:
Etiology:
5. Cigarette smoking (alcohol (-) effect)
6. Gastric polyp: (epithelial, inflammatory,
hamatomatous, heterotopic, hyperplastic &
adenoma) – adenoma & hyperplastic polyps can
lead to CA.
7. Chronic atrophic gastritis (CAG):


Most common precursor of CA (intestinal type)
H. pylori causes CAG
Adenocarcinoma:
Etiology:
8. Intestinal metaplasia: (H. pylori)
9. Benign gastric ulcer:

It is now generally recognized that all gastric ulcers
are cancer until proven otherwise
10. Previous Gastric resection:

10 yrs later near the stoma
11. Others:
- Radiation exposure
- Pernicious anemia
- Family hx
- Bld type A
(1.2 risk)
Gastric Neoplasm:
Pathology:
Gastric dysplasia --->
precursor of gastric CA
Early gastric cancer:



Limited to the mucosa
and submucosa,
regardless of LN status
70% are well
differentiated
Cure rate is 90%
Pathology:
Macroscopic Subtypes:
1.
2.
3.
4.
5.
Superficial spreading
Polypoid (well differentiated)
Fungating
Ulceration
Scirrhous (linitis plastica): infiltrates the entire
thickness of the wall
 Leather bottle stomach
 Poor prognosis
 Usually undifferentiated
Location of primary tumor:

40% distal / 30% middle / 30% distal
HISTOLOGY:
WHO Classification:
Lauren Classification:
1.
1. Intestinal type (53%)
2. Diffuse type (33%)
3. Unclassified (14%)
Adenocarcinoma:
a.
b.
c.
d.
2.
3.
4.
5.
6.
Papillary adenocarcinoma
Tubular adenocarcinoma
Mucinous adenocarcinoma
Signet-ring cell carcinoma
Adenosquamous
carcinoma
Squamous cell CA
Small cell CA
Undifferentiated CA
Others
Ming Classification:
1. Expanding type (67%)
2. Infiltrative type (33%)
Pathologic Staging: (TNM)
Microscopic Subtypes:
1. Intestinal Type
2. Diffuse Type:
Histologic type:
1.
2.
3.
4.
Papillary
Tubular
Mucinous
Signet ring
Mode of spread:
1.
2.
3.
4.
Direct
Lymphatic
Hematologic
Transcoelomic route
Clinical Manifestation:
1. Weight loss due to anorexia and early
satiety is the most common symptoms
2. Abdominal pain (not severe) common
3. Nausea / vomiting
4. Chronic occult blood loss is common;
GIT bleeding (5%)
5. Dysphagia (cardia involvement)
Clinical Manifestation:
6. Paraneoplastic syndromes ( Trousseau’s
syndrome – thrombophlebitis; acanthosis
nigricans – hyperpigmentation of axilla and
groin; peripheral neuropathy)
7. Signs of distant metastasis:
a.
b.
c.
d.
e.
Hepatomegally / ascites
Krukenbergs tumor
Blummers shelf (drop metastasis)
Virchow’s node
Sister Joseph node (pathognomonic of
advances dse)
Diagnosis:
1. UGIS (double contrast)
2. Endoscopy (Biopsy / Ultrasound)




GOLD STANDARD
Best pre-operative staging
Needle aspiration of LN w/ ultrasound guidance
Can even give preop neoadjuvant tx
3. CT scan (intravenous and oral contrast):

For pre-operative staging
4. Whole body Positron Emission
Tomography scanning (PET):

Tumor cell preferentially accumulate positronemitting 18F fluorodeoxyglucose.
TREATMENT:
SURGERY:
 The only curative tx for gastric cancer
 Except:
1. Can’t tolerate abdominal surgery
2. Overwhelming metastasis



Palliation is poor w/ non-resective
operations
GOAL: resect all tumors, w/ negative
margins (5cm) and adequate
lymphadenectomy (need for RFS)
Enbloc resection of adjacent organ is done
if needed.
TREATMENT:
SURGERY:
Radical subtotal
gastrectomy

Standard operation for
gastric cancer
Organs resected:
1. Distal 75% of stomach
2. 2 cm of duodenum
3. Greater & lesser omentum
4. Ligation of R & L gastric
artery and gastroepiploic
vesels
5. Billroth II
gastojejunostomy
TREATMENT:
SURGERY:
Radical subtotal
gastrectomy

Standard operation for
gastric cancer
If gastric remnant left is small
(<20%) do Roux-en-Y
reconstruction
Extent of lymphadenectomy:
N1 – 3 to 6 N2 – 1, 2, 7, 8 & 11
N3 – 9, 10 & 12
 N1 nodes are w/in 3cm of the tumor
 N2 along hepatic & splenic arteries
 N3 more distant nodes
 Agreed upon: to avoid under staging of gastric CA,
a minimum of 15 nodes should be resected w/ the
gastrectomy specimen.
Adjuvant Treatment for
Gastric Carcinoma:
1. Chemotherapy:


5-fluorouracil, leucovorin, cisplatin,
doxorubicin and methotrexate
Can not prolong survival in unresectable,
metastatic or recurrent diseases
2. Radiation (4500cGy):


Effective in palliation for pain and bleeding
For stages II and III adenocarcinoma
Radical subtotal gastrectomy:
1. D1 resection (standard in USA):

Removes tumor and N1
2. D2 resection(standard in Asia):




Gastrectomy and N1 and N2 removal
Removes the peritoneal layer over the
pancreas and anterior mesocolon
Removes LN along hepatic & splenic
Splenectomy and distal pancreatectromy
not routinely removed due to higher
morbidity postop.
Endoscopic Resection of
Gastric Carcinoma
Criteria:
1. Tumor < 2cm in size
2. Node negative
3. Tumor confined on the mucosa
Nodes metastasis is < 1%:
1. No mucosal ulceration
2. No lymphatic invasions
3. <3cm tumor
Screening of Gastric
Cancer

Patients at risk for gastric CA should
undergo yearly endoscopy and biopsy:
1.
2.
3.
4.
5.
6.
Familial adenomatous polyposis
Hereditary nonpolyposis colorectal cancer
Gastric adenomas
Menetrier’s disease
Intestinal metaplasia or dysplasia
Remote gastrectomy or gastrojejunostomy