BENIGN GASTRIC DISEASES -SURGICAL ASPECTS

Dr Paszt Attila

DEPARTMENT OF SURGERY,

UNIVERSITY OF SZEGED

• Peptic ulcer diseases

• Dyspepsia

• Helicobacter pylori infection

• Gastritis (acute, erosive, chronic atrophic)

• NSAID gastropathy

• Motility disorders

• Hypertensive gastropathy, Crohn’s disease

• Benign tumors of the stomach

• -leiomyomas

• -hyperplastic polyps

• -adenomatous polyps

• -GIST

Benign diseases of the stomach

Gastric surgery

History

• 1879 Pean

• 1881 Billroth I

• 1883 Billroth II ( Wölfler )

• 1920 Petz

• 1943 Dragstedt - vagotomy

• 1963 Helicobacter pylori

• 1960 -76 H2(Histamin) receptor ant.

Non-specific gastritis

Gastritis acuta (spirit, allergy, digitalis)

Gastritis corrosiva (acids)

Gastritis phlegmonosa ( streptococcus haemolyticus)

Gastritis necrotisans (spirocheta + fusiformis bacillus)

Gastritis chronica superficialis (antrum gastritis)

Gastritis chronica atrophicans – praecancerosis (Cc 20x .)

A tip: achlorhydria, hypergastrinaemia, anaemia perniciosa

causa: autoimmun - Biermer gastritis

B tip: irritatio (spicy foods) + Helicobacter pylori

Gastritis chronica hypetrophicans (Menetrier sy) -

diarrhoea, protein loss, oedema,

Crohn disease – antral localisation- rare

The proven etiologic factors

of the peptic ulcer disease

Helicobacter pylori infection

Non steroid anti-inflammatory drugs

(NSAID)

Smoking

Hypotethic but not proven factors

Diet

Coffee

Alcohol consumption

The rare causes of ulcer

diseaseStress ulcer

Different pills (steroid, potassium,iron, 5-FU)

Crohn’s d.

Dieulafoy ulcer

GIST

The diagnosis of the peptic

ulcer disease

History

Physical examination

Helicobacter pylori

Endoscopy

Radiology

The characteristics of the

abdominal pain caused by peptic

ulcerEpigastrial or right upper abdominal

localized, not irradiating, can be

shown by pointing the finger at the

site

Diminishing after meal

Lasting for a several days or weeks

period

Accompanied by nausea

The diagnosis of the peptic ulcer

is based on the history, on the

characteristic pattern of pain

In case of a long lasting peptic ulcer the complaints arenot tipical

Using an anacid or antisecretory therapy the complaintsare not typical

In case of complications the complaints are not typical

In a quarter of the peptic ulcer cases there is no pain.

but

The „characteristic” complaints

Lord Moynihan stated in the early years of the XX.century, the 90 % of the cases can be diagnosedsolely by the characteristic complaints.

It was recommended to call the peptic ulcer diseasehaving the characteristic complaints Moynihan’sdisease.

The „silent” ulcer Among 857 peptic ulcer 86 % had pain

before treatment (i. e. 14 %had no pain –

„silent” ulcer )

The frequency of the different

complaints:

% pain bleeding bloating vomiting

ulcus duodeni 79,3 33 30,6 14,5

ulcus ventriculi 43,2 45 12,8 7,1

Porro et al. 1994

Mungan et al. 1994

The pain as a marker of the

peptic ulcer disease

Sensitivity (complaint positive - ulcer is

present) 60 %Specificity (complaint negative – ulcer is

absent) 70 %

Petersen et al. 1988

The „silent” ulcer

10 % of the peptic ulcer cases treatedbecause of complications, had no painearlier.

In 2 % of the duodenal ulcer patients theperforation is the first symptome

The majority of the complication of theNSAID treatment are without any earliersymptoms.

The physical examination

Epigastric tenderness

Differentiation from other diseases

Complication(perforation,stenosis?)

The treatment of peptic ulcer

disease I.

Diet

Helicobacter pylori eradication

Antacid treatment

Antisecretory drugs

H2 receptor blockers

Proton pump inhibitors

Only in case of complication - surgery

TREATMENT OF GASTRIC ULCER

1., AVOID ULCER-PROMOTING FACTORS2., USE ANTACIDS3., REASSESS FOR HEALING AT 6 TO 8 WEEKS

WHY?70% OF GASTRIC ULCERS HEALBUT RECURRANCE RATE 40% WITHIN 2 YEARS

4., REPEAT GASTROSCOPY AND BIOPSY5., PROCEED gastroTOMY AND GASTRIC RESECTION

TO REMOVE ULCER OR CARCINOMA

CHRONIC DUODENAL ULCER DISEASE

IT PRODUCES SYMPTOMES THAT MAY BE INDISTINGUISHABLE FROM THOSE PRODUCE BYGASTRIC ULCER.THE FIRST SYMPTOMES OF DUODENAL ULCER OCCUR

AT YOUNGER AGE THAN THOSE OF GASTRIC ULCER.MEN ARE MORE OFTEN AFFECTED THAN WOMAN.SYMPTOMES OCCUR RHYTHMICALLY,PERIODICALLY, AND FREQUENTLY AT CERTAIN TIMES OF THE YEAR.

ETIOLOGYMUCOSAL INJURY BY GASTRIC ACID, PEPSIN, EXACERBATED BY NICOTINE, CAFFEINE, ALCOHOL, SALICYLATES

„TYPE IV” OR ACUTE GASTRIC ULCER

ASSOCIATED WITH THE USE OF DRUGS, SEPSIS, BURNS, OR HEAD INJURIES BECOMES MANIFEST BY UPPER GI BLEEDING.

THESE PATIENTS ARE BEST TREATED BY REMOVING THE OFFENDING DRUGS AND TREATING THEIR TRAUMA AND SEPSIS APPROPRIATELY.

ADDITIONAL THERAPY INCLUDES IV. NUTRITIONAL SUPPLEMENTATION, ANTACID THERAPY, H2-BLOCKERS.

BLEEDING FROM A STRESS ULCER MAY STOP SPONTANEOUSLY.

COMMONLY PERFORMED OPERATION FOR DUODENAL ULCER

TWO-THIRDS TO THREE-FOURTHS DISTAL GASTRECTOMYMORTALITY RATE 2-4%, RECURRENCE RATE 1-5%

VAGOTOMY AND DRAINAGEMORTALITY RATE <1%, RECURRENCE RATE 5-10%

VAGOTOMY AND DISTAL GASTRECTOMYMORTALITY RATE 1%, RECURRANCE RATE 2-3%

PARIETAL CELL VAGOTOMYMORTALITY RATE <1%, RECURRENCE RATE 5-25%

SOME COMPLICATIONS THAT OCCUR AFTER GASTRIC SURGERY

SMALL POUCH SYNDROME

REFLUX GASTRITIS

EFFERENT LOOP OBSTRUCTION

MARGINAL ULCER

AFFERENT LOOP SYNDROME

EARLY DUMPING SYNDROME

POST VAGOTOMY DIARRHEA

GASTRODUDENAL ULCER COMPLICATIONS: PERFORATION

ETIOLOGY: INTRAPERITONEAL LEAKAGE OFDUODENAL FLUID FROM TRANSMURAL DUODENAL ULCERDIAGNOSIS : ACUTE ONSET OF SEVERE ABDOMINAL PAIN, HYPOTENSION, TACHYCARDIA, RIGID ”BOARDLIKE” ABDOMEN, ABSENT OF BOWEL SOUNDS, PNEUMOPERITONEUM IN MORE THAN HALF THE PATIENTS, LEUKOCYTOSIS AND HYPERAMYLASAEMIA

TREATMENT IV. HYDRATION, ANTIBIOTICS, ELECTROLYTE CORRECTION, NASOGASTRIC DECOMPRESSION,AND PROMPT CLOSURE OF PERFORATED ULCER WITH OR WITHOUT DEFINITIVE ULCER OPERATION PREFERRED IN MOST PATIENTS

GASTRODUODENAL ULCER COMPLICATIONS: OBSTRUCTION

ETIOLOGY PYLORIC CHANNEL NARROWING

FROM ULCER-ASSOCIATED EDEMA AND FIBROSIS

DIAGNOSIS HISTORY OF ULCER SYMPTOMS, VOMITING, WEIGHT LOSS, HYPOKALEMIC ALKALOSIS

UPPER GI SERIES SHOWS BARIUM RETENTION,GASTRIC DILATATION

TREATMENTIV. HYDRATION, ELECTROLYTE

AND ACID-BASE CORRECTIONNASOGASTRIC TUBE DECOMPRESSION

NUTRITIONAL ASSESSMENT AND THERAPY

GASTRODUODENAL ULCER COMPLICATIONS: HEMORRHAGEETIOLOGY

ULCER EROSION INTO ADJACENT ARTERY (FREQUENTLY GASTRODUODENAL ARTERY)

DIAGNOSIS HEMATEMESIS, MELENA, SHOCK,

HYPOTENSION, ANEMIA, ENDOSCOPY, CELIAC ARTERIOGRAPHY

TREATMENT IV. HYDRATION, TRANSFUSION, NASOGASTRIC

TUBE DECOMPRESSION, AND LAVAGE CIMETIDINE AND ANTACIDS

SURGERY:OVERSEWING ULCER AND DEFINITIVE

ULCER OPERATION FOR MASSIVE HEMORRHAGE OR MEDICAL FAILURE TO CONTROL HEMORRHAGE

GASTRO-JEJUNO-COLIC FISTULA

IT OCCURS AFTER A GASTRECTOMY AND

BILLROTH II ANASTOMOSIS.

THE RECURRENT ULCER AT THE GASTROJEJUNOSTOMY LIES

IN CLOSE PROXIMITY TO THE TRANSVERSE COLON,

WHICH IS ULTIMATELY ERODES RESULTING

A FISTULA BETWEEN THE COLON, JEJUNUM AND ILEUM.

DIAGNOSIS BARIUM ENEMA

TREATMENT

RESECTION OF THOSE SEGMENTS

OF TRANSVERSE COLON, JEJUNUM AND STOMACH

AND BILLROTH I OR II ANASTOMOSIS

MALLORY-WEISS SYNDROME

IT IS UPPER GI BLEEDING FOLLOWING VOMITING AND FORCEFUL RETCHING.

ENDOSCOPY SHOWS A LINEAR TEAR THROUGH THE MUCOSA AND SUBMUCOSA

IN THE AREA OF ESOPHAGOGASTRIC JUNCTION.

THERAPY

CONSERVATIVE TREATMENT OR EXPOSUREOF THE LESION SO THAT IT MAY BE OVERSEWN.

GASTRINOMA(ZOLLINGER-ELLISON SYNDROME)

SEVERE - ATIPICALLY LOCATED, - MULTIPLE, AND UNRELENTING DUODENAL OR JEJUNAL PEPTIC ULCERTHAT OFTEN RETURN PROMPTLY AFTER MEDICAL OR

SURGICAL TREATMENT:SUCH ULCERATIONS ARE CAUSED BY MARKED GASTRIC ACID HYPERSECRETION INDUCED BY GASTRIN-SECRETING TUMORS. APPROXIMATELY 60% TO 75% OF GASTRINOMAS ARE MALIGNANT AND MULTIFOCAL WITHIN THE PANCREAS.

DIAGNOSIS IS BASED ON THE DEMONSTRATION OF HYPERGASTRINEMIA UNDER FASTING CONDITION (>200 PG/ML)ULTRASOUNDCOMPUTED TOMOGRAPHYANGIOGRAPHY ARE OFTEN UNSUCCESFUL.

Gastric neuroendocrine tumors (carcinoids)

Gastric neuroendocrine tumors are derived from enterochromaffin-like (ECL) cells.

Etiology — Gastric neuroendocrine tumors are subdivided into types 1 to 3 as they

have different etiologies, biologic behavior, and prognoses

- Type 1 tumors represent 70 to 80 percent of all gastric neuroendocrine tumors.

They are associated with prolonged hypergastrinemia typically resulting from

autoimmune (corpus-restricted) atrophic gastritis.

- Type 2 gastric neuroendocrine tumors account for 5 to 8 percent of gastric

neuroendocrine tumors and result from prolonged hypergastrinemia from a gastrin-

secreting tumor.

- Type 3 neuroendocrine tumors are sporadic and account for 20 percent of gastric

neuroendocrine tumors.

Clinical manifestations – Type 1 gastric neuroendocrine tumors are found more

commonly in older adults, particularly women, with atrophic gastritis and often are

associated with pernicious anemia.

Type 2 gastric neuroendocrine tumors are frequently detected as part of the work-up

for MEN-1 syndrome or for Zollinger–Ellison syndrome in patients who present with

peptic ulcer disease, abdominal pain, diarrhea, or bleeding.

Type 3 tumors can be associated with atypical carcinoid syndrome.

TYPES OF GASTRIC POLYPS AND SPECIFIC MANAGEMENT — The

management of gastric polyps and surveillance are specific to the underlying

presentation, pathology, and malignant potential.

Hyperplastic polyps — Hyperplastic polyps account for approximately 75 percent of

gastric polyps in geographic areas where H. pylori is common.

Etiology — Hyperplastic polyps result from hyper-regenerative epithelium in

response to an underlying chronic inflammatory stimulus.

Clinical and pathologic features — Men and women are equally affected.

Hyperplastic polyps typically appear in mid to late adult life.

●Clinical manifestations – Hyperplastic polyps are usually asymptomatic and are

discovered incidentally on upper endoscopy. Over time, polyps may remain stable,

increase in size, or regress following H. pylori eradication

●Endoscopic features and pathology – On upper endoscopy, hyperplastic polyps

are smooth, dome-shaped, or stalked with an average size ranging from 0.5 to 1.5

cm.

●Malignant potential – Malignancy develops in hyperplastic polyps through

a dysplasia/carcinoma sequence . Between 1 and 20 percent of hyperplastic polyps

have been reported to harbor foci of dysplasia. The risk of malignancy in hyperplastic

polyps is increased in polyps >1 cm and pedunculated in shape.

Management — Hyperplastic polyps measuring >0.5 cm should be resected

completely. All patients with H. pylori should be treated with eradication therapy.In

patients with dysplasia or carcinoma beyond the confines of the polyp, a subtotal

gastrectomy or endoscopic mucosal resection should be performed.

Fundic gland polyps — In Western countries, where H. pylori infection has a low

prevalence and proton pump inhibitor (PPI) use is common, fundic gland polyps are the

most commonly encountered polyps.

Etiology — Most fundic gland polyps are sporadic. Fundic gland polyps may also occur

in association with polyposis syndromes, familial adenomatous polyposis (FAP),

MUTYH-associated polyposis (MAP), and gastric adenocarcinoma and proximal

polyposis of the stomach.

Clinical and pathologic features — Sporadic fundic gland polyps occur in females

more often than in males and usually occur in middle age. Up to 40 percent of patients

have multiple polyps.

●Clinical manifestations – Fundic gland polyps are usually asymptomatic and

discovered incidentally at endoscopy. Only in rare cases can they reach a size large

enough to cause obstruction or symptoms of abdominal pain or vomiting.

●Malignant potential – Somatic APC gene mutations have been detected in over 70

percent of syndromic fundic gland polyps without dysplasia, but in less than 10 percent

of sporadic lesions.

Management — Fundic gland polyps are frequently multiple and biopsies of one or

more representative polyps is sufficient. The remaining polyps should be carefully

inspected on endoscopy and any lesion that appears significantly different should be

biopsied and, if possible, resected.

●Surveillance – Regular surveillance by upper endoscopy is not routinely

recommended for sporadic fundic gland polyps without dysplasia as progression to

gastric cancer is rare.

Gastric adenomas — Gastric adenomas, or raised intraepithelial neoplasia, are the

most common gastric neoplastic polyp

Etiology — Gastric adenomas typically occur in a background of chronic atrophic

gastritis.

Clinical and pathologic features — Sporadic gastric adenomas occur equally in

men and women and are most commonly seen in the sixth or seventh decade.

●Clinical manifestations – Most gastric adenomas are asymptomatic.

●Endoscopic features and pathology – Adenomas may be flat or polypoid, and are

usually <2 cm in size .

The narrow band imaging features of gastric adenomas have not been well defined.

●Malignant potential – It is estimated that 8 to 59 percent of adenomas are

associated with synchronous gastric carcinomas. The presence of invasive carcinoma

in an adenoma correlates with increasing size, villous contour, and the degree of

dysplasia.

Dysplasia is a precursor of invasive adenocarcinoma.

Management — Given the increased risk of gastric cancer, all gastric adenomas

should be resected. This can usually be accomplished endoscopically, but on

occasion surgery may be required for lesions that contain invasive carcinoma or in

patients with multiple adenomas.

Because of the association of gastric dysplasia with synchronous gastric carcinomas,

the remainder of the stomach must be examined carefully.

●Surveillance – We perform an upper endoscopy for surveillance one year after

initial resection.

GIST-Epidemiology

• The most common mesenchymal tumors in the digestive tract.

• Incidence, prevalence:

– Incidence 14,5 new cases /year/1 million (Sweden)

– Hungary 5-8 new cases /year/1 million

– Most common between ages 40-70 y

– Gender ratio is 1:1Thomas RM, Sobin LH. Gastrointestinal cancer. Cancer. 1995 Jan 1;75(1 Suppl):154-70.

Nilsson B és mtsai. Gastrointestinal stromal tumors: the incidence, prevalence, clinical course, and prognostication in the preimatinib mesylate era--a population-based study in western Sweden. Cancer. 2005 Feb 15;103(4):821-9. Eckhardt S és mtsai: Az Imatinib kezelés hatása gastrointestinalis stroma eredetű daganatokban. Orv. Hetil., 2003, 144, 2207-12.

Genetical variability of GIST

• GIST : tumors of mesenchymal origin presenting with c-KIT

(CD 117) positivity in 95 %

– In a smaller portion of GIST thrombocyte derived growth

factor receptor alpha (PDGFRalpha) mutation is present

• Normally c-KIT protein is present in Cajal cells (regulating

the motility of the GI tract)

• Cajal cells and GIST-cells might have common precursors.

Hirota S, Isozaki K, Moriyama Y, Hashimoto K, Nishida T, Ishiguro S et al. Gain-of-function mutations of c-kit in human gastrointestinal stromal tumors. Science 1998; 279: 577-580.

Joensuu H et al. Management of malignant gastrointestinal stromal tumours. Lancet Oncol. 2002 Nov;3(11):655-64. Review.

Sihto H et al. Platelet-derived growth factor receptor family mutations in gastrointestinal stromal tumours. Scand J Gastroenterol. 2006 Jul;41(7):805-11.

A B

C D

Various histological structures on haematoxylin – eosin stained slides, and IH slides

Courtesy of Institute of Pathology University of Szeged

spindle cell epitheloid light cell palissade

mucoid C-kit + PDGFR α

+

CD 34+

Localization of GIST

- stomach (60 %)

- small intestine (25 %)

- colon and rectum (10 %)

- esophagus (5 %)

Diagnosis of GIST

• Based on histopathology

• Imaging might raise suspicion of GIST

• Praeoperative histological diagnosis is rare – inadeqate sample

• Intraoperative histology – suspicion of GIST, benign lesion

Characteristic cross-section of a specimen

GIST – therapeutic consideration

• 50-60 % of tumors are localized at the time of

diagnosis.

• Disease metastases commonly develop in the liver

and peritoneum, but are extremely rare in

locoregional lymphnodes.

• Aim of surgery must be the achievement of

complete gross resection with negative

histological margins; lymphadenectomy is

unnecessary.

Complaints and Symptoms

Main symptom

Nº percent

Massive bleeding(melena, haemascos)

8 18.56 %

Occult (anaemia) 16 37.1 %

Pain, nausea, weight loss

9 20.88 %

Palpable mass 2 4.6 %

None (accidental ) 8 18.56%

Diagnosis, Investigation

• CT/MRI and endoscopy performed in every

elective case

• Informative praeoperative biopsy

• Endoscopic US

Atypical laparoscopic resection

• 3 or 4 operating ports

• for preparation, dissection and a ligation of blood vessels we used „LigaSure” systems- „cut and sew” or using endoscopic staplers

• - the GIST was removed by the „Endobag”system

• dual laparoscopic-endoscopic approach - double visual control

Exploration and mobilisation

Endoscopic control of the cardia

Resected specimen

Fletcher’s classification

Tumor Size (cm) Mitotic count

Very low risk < 2 cm < 5/50 HPF

Low risk 2–5 cm < 5/50 HPF

Intermediate risk < 5 cm 6–10/50 HPF

5–10 cm < 5/50 HPF

High risk > 5 cm > 5/50 HPF

> 10 cm any mitotic rate

any size > 10/50 HPF

Proposed approach for defining risk of aggressive behavior in GIST, by Fletcher [2]World J Surg Oncol. 2005; 3: 78.

Thank

You !