Transcript Surgery of Cancer Stomach

Stomach
Blood supply
Lymphatic D1
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Lymphatic D2
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Peptic ulcer
Peptic ulcer
Helicobacter pylori
H. Pylori is gram-negative spiral flagellated bacterium
Important in the etiology of peptic ulcers and gastric
cancer
Found in:
– 90% patients with duodenal ulceration
– 70% patients with gastric ulceration
– 60% patients with gastric cancer
H pylori Is located beneath the mucus layer, and
produce various enzymes and toxins
– Endo-peptidase that causes mucolysis
– Large amounts of NH3, from urea, that changes the surface pH,
and cellular permeability leading to back diffusion of HCL, and
also increasing serum gastrin production
– Vacuolizing toxin, and less importantly hemolysin toxin
Peptic ulcer
Helicobacter pylori (Investigation)
The organism can be detected by
– Microscopy – silver or Giemsa staining of antral
biopsies
– Culture – difficult and requires special culture
techniques
– Rapid urease test – color changes due to change in
pH
– 13C or 14C breath test – Ingested radioactive urea is
broken down to carbon dioxide
– Serology – detected immunologically using an ELISA
Peptic ulcer
Aspirin and NSAIDS.
– NSAIDs are pathogenic through their inhibition of the
cyclooxygenase-1 (COX-1) pathway, which normally
produces protective prostaglandins.
– Recently, the potential for decreased GI mucosal
injury with newer cyclooxygenase-2 (COX-2) selective
inhibitors, celecoxib and rofecoxib, has been
emphasized.
– These newer NSAIDs do not inhibit COX-1 and,
therefore, do not have the disadvantage of reducing
the synthesis of protective prostaglandins.
Lifestyle factors influencing development of DU.
Increased consumption of alcohol, smoking,
coffee and cola
Duodenal ulcer
Hyperacidity
Defective mucosal barrier
Predisposing factors
Helicobacter pylori
Clinical picture
Age incidence 25- 50
Remitting disease with seasonal exacerbations
Typically epigastric pain when the stomach is
empty, and awaken the patient from sleep
Back radiation indicates pancreatic penetration
Vomiting without obstruction is rare and due to
exacerbation
Bleeding is either minor, and intermittent (pallor)
or severe (hematemesis and melena)
Gastric ulcer
Defective mucosal barrier dt decrease
• secretion
• Pg
• BS
• Pyloric function
Gastric ulcer
Healing ulcer
Pre pyloric gastric ulcer
Clinical picture
Less common
Two types,
– type I (at incisura angularis)
– type II pyloric channel ulcer (NB prepyloric ulcer is like DU in all
aspects)
Type I affects middle aged and elderly patients
It is associated with hypo acidity and may come on top of
atrophic gastritis
Pain is induced by meals (more as discomfort)
Vomiting and nausea are common
May present also with complications (perforation,
obstruction or bleeding)
Investigations
Endoscopy
– To see the ulcer,
– to take biopsy (gastric ulcers) to test for H pylori, and
– to follow up treatment and healing
Double contrast or simple barium meal
– To delineate anatomy, the most important signs of
duodenal ulcerations are deformities (linear or
trifoliate) and ulcer niche or craters
– To detect lesions that may make endoscopy
dangerous
Medical treatment
PPI (proton pump inhibitors) are the most useful
drugs
H2 blockers comes as number two with less cost
in long term treatment, but higher recurrence
rate
Sucralfate, and bismuth are locally acting drugs
used as adjuvant to previous medications (not
with PPI since it needs to react with HCL to form
the coating membrane)
For H.pylori eradication
– three drug regimen can be used (bismuth,
metronidazole, and amoxycillin) or
– two drug regimen (PPI &clarithromycin).
– H pylori eradication can prevent recurrence
Surgery for peptic ulcer
Indications for surgery
Non compliance to medical treatment
Resistant DU
GU persistent >3 months despite medical
treatment irrespective of complications
Onset of complications
Options of surgical treatment for
DU
Truncal vagotomy and drainage (either
pyloroplasty or gastrojujenostomy)
– Very commonly used operation,
– although the side effects are numerous,and
the recurrence rate is high.
– Used commonly for its simplicity, and less
surgical complications.
Options of surgical treatment for
DU
Truncal vagotomy and anterectomy
– Is the operation with the least recurrence rate,
and best option for pyloric channel ulcers
– Is used as the ultimate goal for all recurrent
ulcers after surgery
– Unfortunately associated with the side effects
of both vagotomy and resection surgery
Options of surgical treatment for
DU
Highly selective vagotomy
– Is the most physiologic and least side effects.
– High recurrence rate is due to surgeon’s abilities, and
is proportional to the completeness of the technique.
– Not used with the presence of obstruction, and
prepyloric ulcers.
– Two modifications described
where the posterior vagus is cut at the trunk with anterior
seromyotomy (Taylor) or
anterior HSV (Hill)
Super selective vagotomy
Surgical options for GU
Standard treatment for GU is partial gastrectomy
with Billroth I operation (resection includes the
lesser curve, the ulcer and antrum with
gastroduodenal ananstomosis).
Sometimes BII (gatrojujenostomy is used to
reestablish the anastomosis.
HSV +excision of the ulcer is an alternative with
less side effects but high recurrence rate .It is
the best for the rare high GU located just
beneath the cardia
Gastric ulcer excision
Side effects of gastric surgery
and vagotomy
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Early dumping
Late dumping (reactive hypoglycemia)
Bile vomiting
Diarrhea
Recurrence
Enterogastric reflux
Gastroesophageal reflux
Mechanical loops obstruction & intussusception
Nutritional complications
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Weight loss
Anemia
Bone disease
Small stomach syndrome
Dumping due to hypovolemia
due to rapid gastric emptying
This will include vasomotor systemic
manifestations and gastrointestinal
manifestations (after 30 -60 minutes)
The vasomotor manifestations are partially due
to hypo-volemia initiated by
– the rapid gastric emptying of hypertonic food into the
small bowel where much fluids are poured on it to
create isotonicity,
– partially to the release of various vasomotor
mediators initiated by the sudden confrontation of the
small bowel with hypertonic food stuff.
Late Dumping (Reactive
hypoglycemia)
2-3 hours after meals due to increased
release of insulin, which is again due to
rapid gastric evacuation of hypertonic
foodstuff into the small bowel
This causing too much insulin, release
which lag behind causing hypoglycemia.
This is usually associated with dumping
and diarrhea
Bile vomiting
Occurs early in the morning
It is usually associated with severe
nausea and also after meals and
It is due to low reflux or due to
intermittent afferent loop obstruction.
Diarrhea
Usually accompanied by dumping, and initiated
by food
It can be in the form of
– Frequent loose stools
– Intermittent episodes of short-lived diarrhea
– Explosive diarrhea with disability
May be due to
– Rapid gastric emptying
– Fat malabosrption
– Bacterial overgrowth due to decreased HCL and
presence of blind loop
– Denervation of the gut (accelerated small bowel
transit time
Reflux
Enterogastric reflux (low reflux)
– Causes severe erosive gastritis
– Pain, nausea, vomiting, bile vomiting early in the
morning and early postprandial
– Pallor is due to chronic blood loss
– Prolonged gastritis will lead to atrophic gastritis,
intestinal metaplasia with predisposition to cancer
GERD (high reflux)
– Vagotomy per se does not initiate GERD
– Destruction of the phrenoesophageal ligaments may
initiate GERD
– If there is bile gastritis, the refluxate will be extremely
injurious to the esophagus (BE)
Nutritional side effects
Weight loss
– Diminished food intake (small stomach syndrome)
– Fat malabsorption
– Dumping and diarrhea
Anemia
– Iron deficiency due malabsorption of iron due to lack of HCL and
pepsin
– Chronic blood loss in biliray gastritis
– Macrocytic anemia due to B12 deficiency due to loss of intrinsic
factor and loss of HCL, also bacterial overgrowth can induce B12
D
Bone disease
– The exclusion of the duodenum, which is the main site of Ca
absorption, is the cause
– Also loss of HCL that helps Ca absorption
– It occurs many years after operation
Mechanical side effects
Afferent loop obstruction
– Predisposed to by long loops and antecolic
anastomosis
– Kinking and adhesions
– Volvulus
– Internal herniation
– Jejunogastric intussusceptions
Other side effects
Gall stones due to vagotomy
Cancer in gastric remnant due to
decreased HCL, bacterial overgrowth, and
biliary gastritis that lead to intestinal
metaplasia
Bezoars, of vegetable and fruit remnants
due to loss of HCL and pyloric mill function
Recurrence rates after different
operations
Causes of recurrent ulceration
Incomplete vagotomy
G cell hyperplasia
Antral exclusion
Inadequate subtotal gastrectomy
Hypercalcemia
Zollinger Ellison syndrome (gastrinoma)
Steps of management
Start with endoscopy and barium studies
Since there is no superior method of vagal integrity
testing attempt accurate measurement of gastric acid
secretion in both basal and stimulated status
– BAO>2 mEq/h indicates inadequate vagotomy
– BAO>4 mEq/h indicates recurrent ulceration
– MAO>15 mEq/h strongly supports the diagnosis of recurrent
ulcer
– BAO=MAO indicates Zollinger Ellison or other hypersecretory
conditions like retained antrum
Serum gastrin is characteristically responsive by
increase in ZE after secretin or calcium infusion
Upper GIT bleeding
Causes
Esophageal or gastric varices (almost 80% in
our country)
Gastric erosions
Peptic ulcer
Gastric neoplasia
Mallory-Weiss tear
Reflux esophagitis
Dieulafoy malformation
Upper GIT bleeding
(Management)
Start with resuscitation
– I.V. lines to get blood sample for cross
matching and install replenishment fluids
(colloids and crystalloids)
– Monitor pulse and blood pressure, a central
venous line for CVP is optional
– Best bedside monitor for tissue perfusion is
urinary output (insert a catheter)
Upper GIT bleeding
(Management)
Synchronously start to lavage the stomach to
prepare for
Diagnostic endoscopy (corner stone of
management). Endoscopy can correctly
determine the site and cause of bleeding in over 90%
of patients.
An ulcer should be accepted as the bleeding source
only if it has one of the stigmata of active or recent
hemorrhage.
The signs of recent hemorrhage include an
adherent clot without oozing,
an adherent slough within the ulcer base, or
a visible vessel within the ulcer.
Upper GIT bleeding
(Management)
The nasogastric tube is a good bleeding
monitor until endoscopy is done
Endoscopic therapy
– Laser photocoagulation using the Nd-YAG
laser
– Bipolar diathermy
– Heat probes
– Adrenaline or sclerosant injection
– No technique is superior
Upper GIT bleeding
(Management)
Management specific for ulcers
Drugs used
– Sucralfate given via the nasogastric tube is for
stress acute ulcerations only
– H2 blockers and omeprazole are used to
prevent rebleeding with doubtful efficiency
– Somatostatin infusions are of little help except
if used with HCL supressor drugs
– Tranexamic acid (antifibrinolytic agent) is
proved to be efficient in reducing the rate of
rebleeding and need for surgery
Upper GIT bleeding
(Management)
Indications of surgery
Endoscopic findings
– Arterial spurter &visible vessel
– The presence of a clot attached is equivocal
sign
Bleeding criteria
– Continued bleeding
– Recurrent bleeding
– 4 units after the initial resuscitation especially
in an elderly patient
Upper GIT bleeding
(Management)
For DU
the pylorus and duodenum are incised
longitudinally and
the vessel is undermined or the ulcer
excised and
the closure is transverse as in pyloroplasty,
usually with addition of TV specially if the
general condition permits.
Upper GIT bleeding
(Management)
For GU: partial gastrectomy.
A bleeding gastric ulcer is most commonly
managed by a distal gastrectomy that
includes the ulcer
with a gastro-duoden-ostomy or
a gastro-jejun-ostomy reconstruction.
Gastric outlet obstruction
Gastric outlet obstruction
The most important causes of gastric outlet obstruction are
1. the stricture caused by scatrized duodenal ulcer, and
2. malignancy of the stomach involving the pyloric antrum.
3. The third common cause is congenital hypertrophic
pyloric stenosis.
4. A very common malignant cause is pancreatic cancer
which in fact obstructs the duodenum.
5. Less important cuases are:
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Adult pyloric hypertrophy
Mucosal diaphragm
Megaduodenum
Annular pancreas
Duodenal hematoma
Arteriomesenteric compression (Wilkie’s disease
Clinical picture
Ulcer pain becomes constant, generalized
and lose periodicity
Vomiting is prominent, bile free, retained
foul odoured food residue
Constipation
Dehydration, loss of weight
+Succusion splash, and upper left
abdominal fullness, with possible visible
peristalsis (left to right)
Management
Correct dehydration and electrolyte imbalance
– Use saline infusions with K supplements
– Monitor by frequent Na &K
– Success is indicated by increase in urinary output and
secreting alkaline urine
Gastric lavage
– Wide bored tube,
– Use saline irrigation
Surgery
– Gastrojujenostomy is ideal for bypassing the
obstruction, TV should be added
– For gastric ulcers partial gastrectomy is again the
solution
Perforated peptic ulcer
Clinical picture
The moment of perforation is often
identified by the patient as an excruciating
epigastric pain
Early there is no manifestations of shock
(no hypovoleamia, no septicemia),
However, late variable degrees of
circulatory collapse may be present
Respiration is shallow and grunting due to
severe abdominal rigidity
Clinical picture
The abdomen is usually
– First, showing board like rigidity, tenderness and
rebound, with dead silent abdomen (chemical
peritonitis
– however, this ameliorates in the lucid phase by
dilution, and then the
– third stage of septic peritonitis starts with toxemia and
fever
Two common variations are causing conflict
– Early sealing with less symptoms and signs
– Leakage towards the right paracolic gutter causing
signs and symptoms of appendicitis
Diagnosis
Plain standing abdomen
– Free air under the copula
– (right side is more informative)
– (higher and liver with no gastric air bubble)
CT scans of the abdomen:
– This modality can be a valuable investigative tool,
providing differential morphologic information not
obtainable with plain radiography or ultrasonography.
Gastrographin meal and follow through
– In sealed perforations, or in minor gastric perforations
to differentiate from pancreatitis
Serum amylase should be done
– It is a bit high in perforations, yet it is very high
(around 1000 units) in pancreatitis
Endoscopy is controversial
Management
Resuscitation
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Nasogastric tube,
I.V. fluids,
antibiotics,
PPI or H2 blockers and analgesics,
estimation of urinary output
Operative interference
– Closure of the perforation (use of omental patch)
– Peritoneal toilet (warm saline irrigation)
– Addition of a definitive operation (HSV for DU or PG
for GU) only if
There is a long history of ulcer (chronic ulcers
Early perforation (6 to 8 hours)
No much sepsis
Previous or synchronous second ulcer complication
Penetration
Penetrated ulcer is that one that erodes
the wall of the stomach or duodenum with
sealing from surrounding visceral
structures with no loss of luminal contents
Sites of penetration:
– For DU: pancreas, biliary tree, colon
– For GU, gastrohepatic ligament,
mesocolon, liver, pancreas
Clinical picture &Management
Clinical picture
Loss of periodicity
A new radiation of pain (to the back if pancreas is
affected)
Manifestations of gastrocolic fistula
Diarrhea with severe weight loss
Passage of undigested food
Foul odoured breath and eructations and feculent vomiting
Diagnosis is by barium enema due to pressure
difference
Treatment is by the usual ways of treatment of
non-complicated ulcers, with leaving the base of
the ulcer in the penetrated organ untouched
Cancer stomach
Cancer stomach (Etiology)
Dietary nitrates: Bacteria in the stomach break down
nitrites to compounds (eg, N-nitroso compounds) that
are carcinogenic in animals.
Hypochlorhydria: This condition occurs in gastric atrophy
and promotes bacterial colonization of the stomach. It
leads to increased nitrite formation, which may have a
mutagenic effect on the atrophic gastric mucosa.
Helicobacter pylori: Antral gastritis caused by H pylori
has been lined to the development of gastric cancer.
Patients with H pylori gastritis are 3-6 times more likely
to develop gastric cancer than individuals without the
infection.
Certain foods: Starch, pickled vegetables, salted fish and
meat, smoked foods, and salt have all been implicated.
Cancer stomach (Etiology)
Cigarette smoking: Those who smoke more than 30
cigarettes per day have a 5-fold increased risk of gastric
carcinoma.
Several precancerous conditions are recognized:
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Chronic atrophic gastritis
Pernicious anemia
Previous partial gastrectomy
Ménétrier disease
Gastric dysplasia
Adenomatous polyps (20% of all gastric polyps)
Hereditary factors
Approximately 95% of all malignant gastric neoplasms
are adenocarcinomas. The remaining tumors are
lymphomas, leiomyosarcomas, carcinoids, or sarcomas.
Etiology (Lauren DIO
classification)
Diffuse gastric cancer (D)
– Hereditary factors
– Proximal locatio
– Younger, more females
– No relation to intestinal metaplasia or
dysplasia
– Associated with pernicious anemia
Etiology (Lauren DIO
classification)
Intestinal type GC (I)
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Distally located
Older patients, more males
Frequently endemic
Associated with inflammatory changes
Associated with H pylori infection
On top of dysplasia or intestinal metaplasia
On top of adenomatous polyps not hyperplastic
polyps (75%)
– On top of chronic gastritis (atrophic)
There is a mixed type (O type only 10%)
Morphologic types of GC
Morphologic types of early cancer
(Japanese endoscopic society JES)
– (by definition the penetration of the tumor
does not exceed the submucosa even if LN
are positive )
Morphological classification of
advanced cancer stomach Borrmann
– ( by definition , the penetration of the tumor
exceeds the submucosa even if LN are
negative )
Spread of cancer stomach
Direct extension
– Ulcerative and polypoid type penetrates
through the wall
– The scirrhous type spreads through the
submucosa and musculosa to encase the
stomac
– Direct extension into the omenta, pancreas,
diaphragm, transverse colon or mesocolon,
and duodenum is common.
Spread of cancer stomach
Lymphatics
– To perigastric LN
– To regional LN (along splenic, common hepatic left
gastric and celiac arteries)
– Virschow (supraclavicular) or left axillary LN (Irish’s
node)
– Umbilical nodule (Sister Joseph nodule)
Blood borne
– Liver (40%), lung (40%)sclerotic bone metastasis
Transcelomic
– Krukenberg (ovaries),
– rectal wall (Blummer shelf) or peritoneum
Clinical picture
At the fundus and near the cardia (
Esophegeal obstruction) The triad of
dysphagia,
regurgitation, and
chest infections
At the pyloric antrum and sphincter
(gastric outlet obstruction) The triad of
early satiety,
vomiting of retained food, and
constipation and dehydration
Clinical picture
At the midzone away from sphincters
– Recent dyspepsia in an old male (anorexia
&early satiety &distaste for meat)
– Dyspepsia above 40
– Change nature of dyspepsia
3 A syndrome
– Unexplained anemia
– Anorexia
– Athena
Pain (60%), weight loss (50%) vomiting
(40%) and mass (30%)
Diagnostic studies
Endoscopy
– With biopsy or exfoliative cytology or brush
biopsy to detect >95% of lesions (biopsy
alone is valid in 80% only)
Barium meal
– The barium meal findings in case of gastric
cancer depends on
the location of the tumor, and also
on the Bormmann type of gross pathology
Diagnostic studies
A filling defect in case of the presence of
nodular, polypoidal or cauliflower mass located
in the stomach away from the inlet or outlet
Pyloric obstruction with the presence of an antral
filling defect and mild gastric dilatation, or if
associated with linitis plastic (Borrmann IV) it will
show a very small no dilated stomach
Pseudoachalasia of the cardia if the tumor is
located just below the cardia with submucous
infiltration upwards in the esophagus
An ulcer niche on top of a filling defect (inside
the boundaries of the stomach) usually due to
exophytic ulcer (Bormmann II) on he lesser
curve side
Diagnostic studies
CT abdomen
– To assess the extent of the disease,
– depth of infiltration, LN, and
– omental cakes and ascites
Laparoscopy
– New method to assess more accurately the
advancement of the disease specially concerning the
peritoneal deposits and mild ascites
EUS
– 6 times more accurate than CT in assessing the stage
of the disease especially for cardiac lesions
Staging of cancer stomach
According to TNM
Tumor
T1 tumor limited to the mucosa and submucosa
T2 tumor involves the muscularis properia
or subserosa
T3 tumor penetrates the serosa
T4 tumor involves contiguous structures
Staging of cancer stomach
Node
N0 no metastases to the regional lymph nodes
N1 involvement of the perigastric lymph nodes
– within 3 cm of the primary tumor or
– from 1 to 6 LN
N2 involvement of the regional lymph nodes
– more than 3 cm from the primary including those located along
the left gastric , common hepatic , splenic and celiac arteries or
– from 7 to 15 LN
N3 more than 15 LN
Metastases
M0 no evidence of distant metastases
M1 evidence of distant metastases
Staging of cancer stomach
Stage1
– T1 N0 M0,
– T1 N1 M0,
– T2 N0 M0
Stage 2
– T1 N2 M0,
– T2 N1 M0,
– T3 N0 M0
Stage 3a
– T2 N2 M0,
– T3 N1 M0,
– T4 N0 M0
Stage 3b
– T3 N2 M0
Stage 4
– T4 N1-3 M0,
– Tx N3 M0
– Tx Nx M1
Prognostic factors
The three grave signs are
– Serosal involvement
– Nodal involvement
– Tumor at the line of resection
Stage
– The most important determinant is the No of LN involved (up to 3
is like non)
Grade
Nature and extent of resection
– Curative R>palliative
– Distal R>proximal R
– Subtotal R> total R
Surgery of Cancer Stomach
Gastrectomy
– An appropriate resection with adequate
tumor free margins, this margin is
proximal in distal tumors and should
never be less than 5 cm.
– However, in proximal tumors total
gastrectomy is done, and no part of the
antrum is left behind since it will be
denervated and will perform no function.
Greater and lesser omenta with excised
stomach (most commonly used type
Surgery of Cancer Stomach
A regional LN clearance corresponding to
location of primary tumor
– R1 (removal of N1 lymph nodes) in
practice is achieved by removal of
– R2 (removal of N2 lymph nodes)
Necessitates removal of LN around
main arteries (left gastric, common
hepatic, celiac and splenic arteries)
In addition, splenectomy and distal
pancreatectomy may be added to
achieve LN clearance
Surgery of Cancer Stomach
Safe and well functioning reconstruction
– In potentially curable resections try to
restore duodenal continuity by using
jujenal interposition with or without a
pouch or
colon interposition in case of total
gastrectomy, or
BII in case there is subtotal gastrectomy.
Surgery of Cancer Stomach
Safe and well functioning reconstruction
–In potentially incurable resection a
duodenal bypass procedure as
Hunt Lawrance
jujenal Roux en Y loop with or
without a pouch is used in case of
total gastrectomy or
BII in case of subtotal gastrectomy
potentially incurable resection a duodenal
bypass procedure
Surgery of Cancer Stomach
Potentially curable resection
Proceed with R1 or R2 and
reconstruct with
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jujenal interpostion with or without a pouch or
with colon interposition .
All should be isoperistaltic.
Duodenal continuity is preferred
Much controversy exists as regards R2 types of
resection, because it adds little to the curability rate if
compared with R1 and at the same time has got much
side effects due to denervation of the celiac axis and
other arteries leading to intolerable diarrhea.
Surgery of Cancer Stomach
Potentially incurable
Three main grave signs
(a) serosal or extraserosal involvement,
(b) extensive nodal involvement
(c) suspected safety margin,
proceed with R1 and
reconstruct with either
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BII in subtotal gastrectomy or
with Hunt Lawrence roux en Y jujenal loop with
esophagojujenostomy in total gastrectomy.
Duodenal continuity is not preferred as after potentially
curable resection due to early obstruction in these type
of reconstruction if local recurrence occurs.
Surgery of Cancer Stomach
Un-resectable cancer
A bypass operation (gastrojujenostomy) is done
if there is obstruction of the pylorus, or
metal prosthesis is endoscopically inserted as in
esophageal cancer if the cardia is obstructed.
A terminal patient with extensive peritoneal
seedlings and ascites with liver deposits are
better to be left without any surgery if they are
not obstructed or bleeding
Un-resectable cancer
A bypass operation
(gastrojujenostomy)
Surgery of Cancer Stomach
The best palliation is resection, and this is
helpful in patients beyond any cure like
those with liver or peritoneal seedlings but
is bleeding or obstructed with a
respectable tumor.
It is done to rid the patient of infected,
bleeding, obstructed, or ulcerated gastric
lesions.
Limited gastric resection may suffice.