SEQUELAE OF GASTRIC SURGERY

Minor postprandial complaints are commonly expierenced by patients after

gastric operations. These usually improve with time and dietary adjustments.
In 5-20% of gastric surgery patients, the symptoms are severe, persistent and
cause considerable disability and malnutrition.
The various postgastric surgery syndromes arise on a background of altered
anatomy and physiology of the upper gastrointestinal tract although the exact
mechanisms responsible for some of the severe symptoms remain unclear.

Sequelae of gastric surgery

1. Recurrence of the disease-recurrent ulcer
2. Nutritional consequences-weight loss, milk intolerance
3. Dumping symptoms
4. Reactive hypoglycemia
5. Bile vomiting
6. Diarrhea
7. Small stomach syndrome
8. Mechanical complications- afferent/efferent loop obstruction
- jejunogastric intussusception
- gastro-esophageal reflux
9. Other-cholelithiasis, bezoar formation, gastric stump carcinoma

A bezoar is a tightly packed collection of partially digested or undigested

material that is unable to exit the stomach. It often occurs in patients with
abnormal gastric emptying, especially those that have diabetic gastroparesis, as
well as after gastric surgery. Many bezoars are asymptomatic, but some produce
symptoms of gastric outlet obstruction. Some can be dissolved enzymatically,
others removed endoscopically, and some require surgery.

Disabling symptoms after gastric surgery are more often encountered in the
following:- female sex
- operation for peptic ulceration in the young (below 30 years of age)
- extensive gastrectomy with duodenal diversion .
Dumping
The syndrome which is one of the commonest sequelae of gastric surgery
consists of postprandial vasomotor (systemic) and gastrointestinal symptoms.
Manifestations of the dumping syndrome
Vasomotor (systemic) symptoms
- weakness, tiredness, dizziness
- headache, fainting, warmth, palpitations
- dyspnea, sweating
2.

Gastrointestinal symptoms
- fullness, epigastric discomfort, heaviness
- nausea, vomiting
- excessive distension, diarrhea
The dumping syndrome is associated with rapid gastric emptying although some
have postulated that enterogastric reflux of bile is responsible for some of the
symptoms.

The vasomotor symptoms occur within minutes of eating and are due to
hypovolemia which is accompanied by diminished cardiac output and peripheral
resistance.
The attacks are typically precipitated by high carbohydrate meals.
The hypovolemia is secondary to a massive outpouring of fluid from the vascular
compartment into the bowel lumen as a consequence of the hyperosmolar nature
of the intestinal contents resulting from the precipitous gastric emptying.
Several vasoactive peptides have been held responsible for the vascular and
gastrointestinal manifestations of the dumping syndrome. These include kinins,
enteroglucagon, etc.
The gastrointestinal symptoms occur later during the course of a dumping attack.
Treatment
- small dry meals rich in protein and fat but low in carbohydrate.
- additive which slow gastric emptying such as methoxy-pectin or bran, are
beneficial.
- remedial gastric surgery is required for patients with severe and persistent
dumping symptoms.

Reactive Hypoglycemia
This complication is rare and has an incidence of 1-6% of patients after gastric
surgery.
The symptoms which occur 2-3 hours after a meal are due to hypoglycemia and
include sweating, tremor, difficulty in concentration .Reactive hypoglycemia
often coexists with other symptoms including vasomotor dumping and diarrhea.
The diagnosis is best confirmed by an extended oral glucose tolerance test which
demonstrates an initial hyperglycemia. This is accompanied by an exagerated
insulin release with elevated plasma insulin and enteroglucagon which are
followed by hypoglycemia.
Reactive hypoglycemia usually responds to dietary measures including low-
carbohydrate, high protein meals.

Bile Vomiting
Vomiting of bile or bile-stained fluid before or after meals is a common
complaint after gastric surgery.
It may be a manifestation of the following disorders:
- recurrent ulceration
- enterogastric reflux
3.

- intermittent obstruction of the afferent or efferent loop of a gastroenterostomy

- cardioesophageal incompetence
Enterogastric reflux causes a reflux erosive gastritis and bile vomiting.
The symptoms include epigastric pain, nausea and vomiting in the early
postprandial period.
The pain is usually of a burning nature, is aggravated by food and not relieved by
antacids.
The attack usually culminates in the vomiting of bile-stained fluid 1-2 hours after
a meal.
The erosive gastritis leads to chronic blood loss with the development of an iron-
deficiency anemia.
The diagnosis is established by upper GI endoscopy which shows a diffuse
gastritis with an edematous friable mucosa in addition to pooling of bile-stained
fluid.
Treatment
- bile salt-binding agents-cholestiramine
- remedial surgical intervention
Prolonged enterogastric reflux can result in atrophic gastritis and intestinal
metaplasia. It has been incriminated as a factor in the development of carcinoma
of the stomach after gastric surgery.

Extrinsic Loop Obstruction

The causes of extrinsic loop obstruction are:
- internal herniation
- kinking of the anastomosis
- adhesions
- volvulus, stenosis, intussusception
- development of carcinoma of the gastric remnant.

Diarrhea
Three patterns of diarrhea are encountered after gastric surgery: frequent loose
motions, intermittent episodes of short-lived diarrhea and severe intractable
explosive diarrhea.
The latter is a serious but rare disability, being encountered in 2% of patients
after truncal vagotomy.
Severe intractable diarrhea is characterized by extreme urgency and often causes
incontinence during an acute attack.
Malabsorbtion of bile salts and fatty acids consequent on the intestinal
denervation has been implicated. The small bowel transit is markedly
accelerated.
Treatment
- low animal fat diet
- codeine phosphate, lomotil, imodium and bile-salt binding agents such as
cholestyramine.
4.

Small Stomach Syndrome

This term is sometimes used for the early satiety complained of by some patients
after vagotomy which causes motolity disfunction of the gastrointestinal tract.
Also it appears after extensive gastrectomy.
The condition leads to gross malnutrition.
In severe cases, surgical intervention is designed to reconstruct a gastric
reservoir and restore duodenal continuity.

Other Complications
These include the formation of gallstones and bezoars and the development of
gastric carcinoma.
Vagotomy and partial gastrectomy may induce cholelithiasis. The factors
implicated in the formation of bezoars after gastric surgery include hypoacidity,
impaired proteolytic activity,inadequate mastication and loss of the antral pump.
There is now good evidence that previous gastric surgery predisposes to the
development of gastric carcinoma in the stomach remnant.
It is said that reflux gastritis with the development of intestinal metaplasia,
particularly of the type III variety, bacterial overgrowth with formation of
nitrosamines in the hypochlorhydric gastric stump have been implicated.
There is a long latent period of 15-20 years between gastric surgery and
carcinoma of the gastric stump.

Gastric Tumours
Gastric tumours may be benign or malignant.
Gastric Polyps
Gastric polyps are usually small benign adenomas of the gastric mucosa. Various
types of gastric polyps are recognized, the commonest being the regenerative
(hyperplastic) variety.
1. Regenerative polyps often occur in association with gastritis and peptic
ulceration form smooth nodules and consist of proliferating glands with no
cellular atypia.
2. The inflammatory fibroid polyps; are rare lesions which are most commonly
found in the gastric antrum and can be sessile or pedunculated.
3. Myoepithelial hamartomas are composed of glands surrounded by smooth
muscle and arise from the submucosal layer of the antrum and pylorus where
they form smooth sessile masses.
Polyps may be solitary or multiple and sessile or pedunculated in form. They
rarely grow to more than a few cm. in diameter and are usually asymptomatic.
Most are found only incidentally on radiological or endoscopic examination.
Up to 20% of gastric polyps show histological features of dysplasia.
Treatment is by endoscopic excision biopsy. Regular endoscopy is usually
arranged to monitor recurrence or the appearance of new lesions.
5.

Leyomyomas
Leyomyomas are benign tumours of smooth muscle and may arise anywhere in
the muscular wall of the GI tract. They are especially common in the stomach
and small bowel.
These lesions are usually discovered incidentally on endoscopy or barium
examinations.
Occasionally, large lesions are found to be the cause of chronic GI blood loss or
intermittent gastric outlet obstruction.
Leiomyomas are sessile or pedunculated lesions covered by normal mucosa.
This may ulcerate, causing insidious blood loss and anemia. Major hemorrhage
is rare.
Leiomyosarcomas, the malignant counterpart of leiomyomas are rare and present
with similar symptoms or as an abdominal mass.
Leiomyosarcomas spread locally and tend to metastasise early via the blood
stream. Treatment involves resection of the primary lesion plus palliative
chemotherapy if metastasis has occurred.

Lymphomas
Primary lymphomas may arise in the stomach or small bowel. In the stomach,
they constitute about 10% of malignancies.
Gastric lymphomas become extensive, either projecting into the lumen as a
bulky ulcerating mass of diffusely infiltrating the stomach wall. They closely
resemble gastric carcinomas in symptoms and endoscopic appearance but it is
particularly important to make the distinction because the prognosis of treated
lymphomas is much better than adenocarcinomas.
Biopsy is the only reliable means of diagnosis.
Diagnosis: - barium studies
- endoscopic biopsies
But only laparotomy can usually distinguish primary lymphomas from secondary
lesions.
Treatment
Primary lymphomas are often discrete and amenable to surgical excision.
Subsequent radiotherapy or chemotherapy or both may be necessary.

Malignant Gastric Tumours

Approximately 90-95% of gastric tumours are malignant and of the malignancies
95% are adenocarcinomas.
This disease continues to carry a dismal prognosis. A better outcome is obtained
in Japan which has the highest incidence in the world. The improved survival in
Japan is due to an active screening programme resulting in early diagnosis and
an aggressive surgical approach designed to reduce loco-regional recurrence in
the gastric bed.
Etiology
Although the results of several epidemiological studies have failed to
demonstrate specific causative factors, the following have been implicated:
6.

- highly spiced salted foods

- high consumption of animal fat
- excess alcohol consumption
- tabacco smoking
- diatary nitrates
- refluxed bile acids

The recognized risk factors in the development of gastric carcinoma are:

- atrophic gastritis and pernicious anemia
- previous partial gastrectomy
- adenomatous polyps
- bood group A
- hypogammaglobulinemia

There are three morphological forms:

- fungating tumours- these tend to be polypoid and may grow to a huge size.
- malignant ulcers- these lesions probably result from necrosis at the centre of
broad-based solid tumours. Malignant ulcers are often larger than peptic ulcers
with a heaped-up indurated margin. There is no surrounding mucosal puckering
typical of inflammatory scarring.
- infiltrating carcinoma- this form of gastric cancer spreads widely beneath the
mucosa and diffusely invades the muscular wall. This causes considerable wall
thickening and rigidity and the whole stomach contracts to a very small capacity.
This is known as linitis plastica and its appearance is likened to a “leather
bottle”. Linitis plastica affects a slightly younger age group and has a very poor
prognosis.

Early Gastric Cancer

This is defined as cancer limited to the mucosa and submucosa and is rarely
encountered in the West but accounts for up to 30% of newly diagnosed tumours
in Japan as a result of screening for the disease.
The prognosis with adequate resection is excellent with 5-year survival rates
which exceed 80%.
Early gastric cancer assumes different endoscopic appearance which have been
classified as follows:
- protruding
- superficial- this may be elevated, flat or depressed
- excavated.
Some 10-15% of gastric carcinomas confined histologically to the mucosal and
submucosal layers have metastasized to the regional lymph nodes and have a
poor prognosis.
This subgroup is sometimes referred to as early-simulating advanced gastric
carcinoma.
7.

Advanced Gastric Carcinoma

This is defined as a tumour which has involved the muscularis propria of the
stomach wall. In the vast majority of cases spread to the regional lymph nodes is
present alone or in association with peritoneal and hepatic deposits.

Staging of Gastric Cancer

The important prognostic factors in patients without detectable distant
metastases are depth of invasion of the stomach wall by the tumour and lymph
node spread.

TNM Staging System for the Gastric Cancer

T- primary tumour
T1- tumour limited to the mucosa and submucosa
T2- tumour involves the muscularis propria
T3- tumour penetrates the serosa
T4- tumour involves contiguous structures
N- regional lymph nodes
N0- no metastases to the regional lymph nodes
N1- involvement of the perigastric lymph nodes within 3 cm.of the primary
tumour.
N2- involvement of the regional lymph nodes more than 3 cm. from the primary
tumour including those located along the left gastric, common hepatic, splenic
and celiac arteries.
M- distant metastases
M0- no evidence of distant metastases
M1- evidence of distant metastases.

Spread of Gastric Cancer

The diffuse type of gastric cancer spreads rapidly through the submucosal and
subserosal lymphatic plexuses and penetrates the gastric wall at an early stage.
Spread to the lymph nodes along the greater and lesser curvatures tends to occur
once the muscular coat of the stomach is invaded by the neoplasm. Thereafter,
spread occurs to the nodes along the celiac axis and its trifurcation (left gastric,
splenic, common hepatic arteries) to the nodes in the splenic hilum, the root of
the mesentery, the retropancreatic nodes and the hepatoduodenal nodes.
Involvement of the para-aortic nodes above and below the transverse colon then
ensues.
The exact nodal groups are involved depend on the anatomical site of the
primary tumour (upper, middle, lower third)
Metastatic spread is usually to the peritoneal cavity and the liver. The most
common organs involved by the direct extension are the omentum, transverse
colon and mesocolon and the left lobe of the liver.
Blummer tumour= pelvic peritoneal metastasis
Krukenberg tumour= ovarian metastases.
8.

Clinical features
Early gastric cancer may be asymptomatic or may present with dyspepsia
simulating peptic ulceration.
The early symptoms are often vague and include indigestion, malaise, early
satiety, postprandial fullness and loss of appetite.
Weight loss is a significant feature of the disease but usually signifies an
advanced lesion which has involved the muscular coat of the stomach or beyond.
Lesions of the cardia may present with dysphagia and circumferential growth of
the middle third and the pyloric antrum cause obstructive symptoms with
vomiting after meals.
Acute presentation with hematemesis or melena is encountered more often with
advanced than early lesions.
The most common presentation is that of recent dyspepsia in a patient above the
age of 50 years.
The most frequent reason for the delay in the diagnosis of cancer of the stomach
is a period of symptomatic therapy with antacids or H2-receptor blockers often
lasting several months before referral for endoscopy is undertaken.

The diagnosis must be established in all patients with indigestion before

treatment of any sort is initiated.
Anemia which is often present at the time of diagnosis is usually of the iron-
deficiency type due to chronic blood loss.

Evidence of weight loss is usually present on examination and hypoalbuminemia

is frequent.
Enlarged left supraclavicular lymph nodes are a rare physical finding in a gastric
cancer- Virchow Troisier sign.
A palpable mass usually signifies incurable, though not necessarily a non-
resectable tumour.
Jaundice, hepatomegaly or ascites indicate advanced incurable disease and
limited survival.

The key investigations are upper GI endoscopy with multiple biopsy and brush
cytology and air contrast barium meal.
Other tests are used to detect extragastric disease. These include chest X ray,
liver function tests, CT or ultrasound examination of the stomach to determine
the depth of involvement of the gastric wall by the neoplasm.
Laparoscopy has also been found valuable in the asessment of the stage and
curability of the disease.
9.

Treatment of Gastric Carcinoma

An adequate surgical resection remains the only effective treatment which offers
a chance of cure or long-term survival.
Furthermore, a palliative resection whenever feasible is more effective in
relieving symptoms than bypass or intubation procedures.
With the currently available drugs, chemotherapy is ineffective as is
radiotherapy.
The principles underlying a potentially curative resection of a gastric
carcinoma are:
- an appropriate resection with adequate tumour-free margins
- a regional lymph node clearance corresponding to the location of the primary
tumour in the stomach
- safe and well functioning reconstruction
There is a clasification of gastric resections for cancer based on the radicality
of the procedure: R0, R1, R2.
R0= complete resection, no microscopic tumour left
R1= residual microscopic tumour
R2= residual macroscopic tumour

Extent of Gastric Resection

A total gastrectomy is necessary for the following:
- to achieve a safe tumour free margin
- when the neoplasm involves 2 or 3 sectors of the stomach
- diffuse carcinoma irrespective of size
Omentectomy
The lesser omentum should be detached from the liver. The removal of the
greater omentum must include the anterior leaf of the transverse mesocolon to
ensure the removal of the lymph nodes accompanying the colic arteries and
veins.
Lymph Node Clearance
This must be adequate and appropriate to the site of the primary neoplasm. The
principle of an adequate node clearance is that this should encompass the tier of
lymph nodes beyond those which are macroscopicaly involved. Thus for a
tumour which is accompanied by involvement of N1 nodes an D2 type of
resection is necessary.
Extent of lymph node clearance in D1 resection: 1 and 2- right and left cardiac
lymph nodes, 3 and 4- lymph nodes along greater and lesser curvature, 5 and 6-
supra and infrapyloric lymph nodes.
Extent of lymph node clearance in D 2 resection: 7-lymph nodes along left
gastric artery, 8-lymph nodes along common hepatic artery, 9-lymph nodes
around celiac artery, 10-lymph nodes at splenic hilum, 11-lymph nodes along
splenic artery.
10.

Extent of lymph node clearance in D3 resection: 12- lymph nodes in

hepatoduodenal ligament, 13- retropancreaticoduodenal lymph nodes, 14- lymph
nodes at the root of mesenterium, 15- lymph nodes around middle colic artery,
16-lymph nodes around abdominal aorta.

Definition of a Curative Resection

An absolute curative resection for gastric cancer may be deemed to have been
performed when:
- there is no peritoneal or hepatic metastases
- the serosa is not involved by the tumour
- the resection level exceeds the level of nodal involvement.

Reconstruction
When a subtotal gastrectomy has been performed then the reconstruction might
be a gastro-jejunal anastomosis or a Roux-en Y procedure.
When a total gastrectomy has been performed then a esophago-jejunostomy
restores the digestive continuity.

Palliative Surgical Treatment

The symptoms which require palliation.
Other procedures- gastroenterostomy (by pass procedure for stenotic antral
carcinoma).
Intubation for cardia carcinoma (Celestin tube or Atkinson tube)

Adjuvant Treatment
The cytotoxic agents which have some activity against gastric cancer are 5FU,
mitomycin C, Doxorubicine.
Adjuvant radiotherapy is also used in some centres.
There is no evidence that the adjuvant treatment improves survival.

Study questions
1. A patient 23 years old underwent a partial gastric resection Reichel-Polya
type for pyloric stenosis. 2 weeks after discharge he has been complaining
of weakness, sweating, epigastric heaviness and diarrhea following eating
sweets. What do you think it is wrong with this patient ?
2. What are the premalignant conditions in gastric tumors ?
3. What are the ways of spread of tumor cell in gastric cancer ?
4. What is role of laparoscopy in the management of gastric cancer ?
5. What is meant by R2 resection ?