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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.
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