surgerystomachduodenumtg 090527001223-phpapp021

بسم الله الرحمن الرحيم

SurgerySurgeryStomach and duodenumStomach and duodenum

Prof. Ismail Kotb

SURGERY OF STOMACH AND DUODENUM

Surgical AnatomyArterial blood supply 1—left gastric artery 2—right gastric artery

3—gastroduodenal artery ( from hepatic artery) divide a –superior pancreatico –duodenal artery, b- right gastroepiploic artery

4-inferior pancreatico-duodenal artey artery abranch of superior mesenteric artery

5-left gastroepiploic artery a branch of splenic artery..

6-short gastric arteries from splenic artery

Venous drainage 1—right & left gastric veins draine into

portal vein2-left gastro epiploic vein & vasa

brevia join splenic vein3-right gastro epiploic vein join

superior mesenteric vein4- vein of mayo

Stomach anatomyStomach anatomy

Nerve supply1-intrinsic, a- myenteric plexus of Auerbach, , b- submucosal plexus of Meissner2-Extrensic, a ant. Vagus, b- post vagus3-sympathetic

PEPTIC ULCERCommon sites;1-first part duodenum. 2-lesser curve

stomach. 3- oesophagus. 4- stoma following gastric surgery. 5- Meckls diverticulum.

1-Acute peptic ( gastric & duodenal ) ulcer.& acute stress ulcer.causes are major illness,uraemia,,food poisoning,,bacteraemia ,,burn,,aspirin,,steroid & NSAID.

PathologySome times it is single & some times are multiple as

diagnosed by OGD.it involve the mucous membrane & does not penetrate the muscles,,some times it bleed,,or perforate..

DUODENAL ULCERIncidenceThere have been marked changes in the

last 2 decades in the domography of patients presenting with duodenal ulcer first by the use of OGD second the introduction of H2 receptor antagonists (wide spread use of anti ulcer drugs & eradication therapy as proton pump ) ,

PathologyOccur in first part duodenum it involve the

mucosa,,muscle coat,leading to fibrosis and pyloric stenosis,,it may penetrate post. to pancreas & invade gastro duodenal artery,

Some times there is multiple ulcers,,or ANT,& POST.ulcer called kissing ulcers,,

ANT.ulcer tend to perforate while POST.ulcer tend to bleed.

Big ulcer called GIANT ulcer.(more than 2 cm.)Chronic duodenal ulcer never become malignant.Chronic gastric & chronic duodenal ulcer may co

exist at same time.

GASTRIC ULCERIncidenceSame etiological factors Gastric ulcer is less common than

D.U.sex are equal male to female,population is older than d.u. patient,,it is more prevalent in low socioeconomic patients,,.

PathologyUsually on the lesser curve

stomach,,but it is larger than du.,also invade mucosa & muscle coat & fibrosis,may cause stomach deformity hour glass stomach or tea pot deformity,,may penetrate to pancreas or blood vessel or invade transverse colon ..

Malignancy in gastric ulcer1-On the long run ch. G.U.might become

malignant so on OGD. To take multiple biopsies2-other type of g.u is malignant g.u from the

start. Other types of peptic ulcer 1-stomal ulcer at jujunal site of

gastrojejunostomy.2-Billroth 2 (polya) gastrectomy.3- prepyloric gastric ulcer it carry risk of cancer

so it need biopsy.

The clinical features of gastric & duodenal ulcers

PAIN;;in the epigastric region ,,may radiate

to the back,it is intermittent ;may last weeks or monthes with interval of pain free,,.some time patient do not eat cause of pain & some time patient eat to relieve pain .

PERIODICITY; attack of pain last from 2—6 weeks, attack is more in spring & autum

VOMITING ;;absent unless there is pyloric stenosis .

ALTERATION IN WEIGHT ;;BLEEDING;;either chronic presented as

anaemia;;or fresh as haematemasis & melaena.

CLINICAL EXAMINATIONTenderness at epigastric region,,stomach

splash in case of pyloric stenosis.

INVESTIGATIONS OF PEPTIC ULCER 1--OGD with or without multiple biopsy

(CHECK ESOPHAGUS ,,, STOMACH,,DUODENUM),,& STOMA OF GASTROJEJUNOSTOMY to exclude stomal ulcer.

2—BARIUM MEAL

TREATMENT OF CHRONIC PEPTIC ULCERThe vast majority of uncomplicated peptic

ulcer are treated medically ,,surgical treatment of uncomplicated peptic ulcer has decreased markedly since 1990.due to the use of H2 recepter antagonist or proton pump inhibitor &eradication therapy.

The aim of surgical treatment is to reduce gastric acid secretion,(now it is reserved for the complicated P.U.)

MEDICAL TREATMENT1-cessation of cigarette smoking ,,NSAIDs &

Cortisone.2-H2 receptor antagonist a-cemetidine

(tagamet)---b—ranetidine ( zantac ).—c sucralphate (ulcar).

3-Proton pump inhibiter (omeprazole )4-Eradication therapy.either give flagyl

3times aday plus amoxil 500mg cap,3 times aday for 2 weeks or to give flagyl plus erthromycin 500mg twice a day for 2 weeks.

SURGICAL TREATMENT OF UNCOMPLICATED PEPTIC ULCER

Although it is rare now ,but some time it need to be performed if there is failer of medical treatment.

Operations for D. U. aim is excluding the damage effect of acid to the duodenum by diversion of the acid away from duodenum,

HISTORICAL SURGICAL PROCEDURES 1-BILLROTH I & BILLROTH II ( or called polya)

GASTRECTOMY,by billroth in 1881. 2-OR TO DO ONLY GASTRO JEJUNOSTOMY (by wolfler

in 1881)will end with high rate of stomal ulcer.

At present time the operation of choice in cases of D.U.are the followings:

1—Truncal vagotomy(first introduced1943 by

Dragstedt) plus drainage procedureTypes of drainage procedure:A—PYLOROPLSTY types :1—finnys pyloroplasty. 2—

Heineke-Mikulicz pyloroplasty.B—GASTROJEJUNOSTOMY post.,,isoperistaltic.at

antrum post.2- OR –Selective vagotomy plus drainage procedure.3-or highly selective vagotomy only ( with

preservation to the nerve of latarjet that supply the pylorus ).no need to do drainage procedure.

4—OR Truncal vagotomy and antrectomy.(billroth I)

Operations for gastric ulcer 1—BILLROTH I OR BILLROTH II OPERATION

PLUS EXCISION TO GASTRIC ULCER FOR HISTOPATHOLOGY TO EXCLUDE MALIGNANCY

2—Or to do vagotomy plus drainage procedure plus excision biopsy to the ulcer..

Comparing Duodenal and Gastric Comparing Duodenal and Gastric UlcersUlcers

DUODENAL ULCER Incidence

Age 30–60Male: female 2–

3:180% of peptic

ulcers are duodenal

GASTRIC ULCER

Usually 50 and over

Male: female 1:115% of peptic

ulcers are gastric

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Signs, Symptoms, and Clinical Signs, Symptoms, and Clinical Findings Findings

DUODENAL ULCER Hypersecretion of

stomach acid (HCl) May have weight

gain Pain occurs 2–3 hours

after a meal; often awakened between 1–2 AM;

ingestion of food relieves pain

Vomiting uncommon

GASTRIC ULCER Normal—hyposecretion

of stomach acid (HCl) Weight loss may occur Pain occurs 1⁄2 to 1

hour after a meal; rarely occurs at night; may be relieved by vomiting;

ingestion of food does not

help, sometimes increases

pain Vomiting common

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DUODENAL ULCER

Malignancy Possibility

RareRisk FactorsH. pylori, alcohol,

smoking, cirrhosis, stress

GASTRIC ULCER

OccasionallyH. pylori,

gastritis, alcohol, smoking, use of NSAIDs, stress

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DUODENAL ULCER

Hemorrhage less likely than with gastric ulcer, but if present melena more common than Hematemesis More likely to perforate than

gastric ulcers

GASTRIC ULCER

Hemorrhage more likely to occur than with duodenal

ulcer; hematemesis more common than melena

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Surgical TreatmentSurgical TreatmentTruncal Vagotomy -- Antrectomy & Truncal Vagotomy -- Antrectomy & Roux-en-Y AnastomosisRoux-en-Y Anastomosis

Surgical TreatmentSurgical TreatmentTruncal Vagotomy -- Heineke-Truncal Vagotomy -- Heineke-Mikulicz PyloroplastyMikulicz Pyloroplasty

Proximal Gastric Proximal Gastric VagotomyVagotomy

Dumping syndromeDumping syndrome

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Bleeding UlcersBleeding UlcersCommon; seen in 10-20%

patients with active PUD; 6-10% mortality; 50% of UGI bleeding is from ulcers.

May be first sign/symptom vs antecedant ulcer symptoms.

Hematemesis and/or melena vs hematochezia dependent on amount.

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Treatment: Bleeding UlcerTreatment: Bleeding UlcerVolume expansion (isotonic fluids);

transfuse when needed.Bleeding stops spontaneously in 80%.Endoscopy identifies site, stability of

bleeding site; also used to stop bleeding when necessary (theromocoag, vasoconstricters, clips/staples, etc.).

IV PPI or high dose oral PPI- decrease re-bleeding, need for transfusion or repeat interventions, including surgery.

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Ulcer Perforation Ulcer Perforation 5% incidence in ulcer patients.Anterior wall of stomach or

duodenum.Results in chemical peritonitis- severe,

generalized abdominal pain, rigid abd, rebound, WBC, free air on KUB/upright.

Laparoscopic perforation closure carries morbidity compared to laparotomy with vagotomy, antrectomy.

Intensive medical Rx also required.

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Other Complications (IO) Other Complications (IO) Ulcer Penetration of posterior wall of

stomach/duodenum into pancreas, liver or biliary tract.

Symptoms: increase in pain, radiates to back, unresponsive to antacids and other meds; amylase may be elevated. Rx is intensive PPI regimen or IV H2 blocker.

IO- interest only

StomachStomachMallory- Weiss syndromeMallory- Weiss syndrome

Upper GI hemorrhage due to tearing of GEJ.

Repeated retching or vomiting may be responsible for the tears in the mucosa

Significant hemorrhage can occur results from prolonged and forceful

vomiting, coughing or convulsions. It may occur as a result of

excessive alcohol ingestion. This is an acute condition which

usually resolves within 10 days without special treatment.

Mallory-Weiss TearMallory-Weiss Tear

Mallory –Weiss TearMallory –Weiss Tear

StomachStomachMallory-Weiss syndromeMallory-Weiss syndrome Tx:

ConservativeDue to hypovolemia (bleeding) fluid resuscitation

Acid suppressionH2, PPI’sSurgery is last resort

StomachStomachZollinger- Ellison SyndromeZollinger- Ellison SyndromeGastrinomas can be part of an

inherited familial disorder.60 % of gastrinomas are malignant.Hypergastrinemia --- stimulate parietal

cells --- HCL acid is constantly secreted.

50% of pts with malignant variant die within 5 years of Dx.

Due to slow growth long term survival up to 15 years has been seen.

StomachStomachZollinger- Ellison SyndromeZollinger- Ellison Syndrome

multiple duodenal ulcers in atypical places (jejunun or ileum)

Family or personal Hx of refractory PUD or endocrine disease (MEN-1)

Dx: hypergastrinemia (fasting serum gastrin

levels over 1000 pg/ml is a comfirmatory testing + hypersecretion of acid

tumor localization Clinical staging CT scan, MRI and U/S screening for MEN-1

INTRODUCTION - INTRODUCTION - STOMACHSTOMACH

Benign Polyps

◦ Hyperplastic◦ Fundic gland◦ Neoplastic◦ Multiple

Tumors◦ Leiomyomas◦ Lipomas◦ Heterotopic pancreas

Malignant Tumors

◦ Carcinoma◦ Lymphoma◦ Sarcoma◦ Carcinoid

Others Menetriers Disease Bezoar Volvulus

GASTRIC POLYPSGASTRIC POLYPSHyperplastic polyps

◦Most common type of polyp (65 – 90%)◦Inflammatory or regenerative polyps

In reaction to chronic inflammation or regenerative hyperplasia

Often found in HP infections◦Sessile and seldom pedunculated

Mostly in the antrum Multiple in 50% of cases Varying in size but seldom < 2cm

◦Rate of malignant transformation 1 – 3% Usually larger than 2 cm

GASTRIC POLYPSGASTRIC POLYPSFundic Gland

◦Small elisions in the fundus Hyperplasia of the normal fundic glands

◦Often associated with FAP Therefore important as a marker for

disease elsewhere in the GIT tract

GASTRIC POLYPSGASTRIC POLYPSNeoplastic polyps

◦Types Tubular Villous (often larger - > 2cm - and malignant)

◦Macroscopically More often in antrum Pedunculated with malignant potential Solitary, large and ulcerated

◦Treatment Endoscopic removal if no malignancy

identified with surveillance Excision with malignant focus or where

endoscopic removal failed

GASTRIC POLYPSGASTRIC POLYPSMultiple gastric polyps

◦Rare condition Adenomatous and hyperplastic polyps 20% incidence f adenocarcinoma

◦Treatment If confined to corpus and antrum – distal

gastrectomy Otherwise total gastrectomy

◦Sometimes associated with Polyposis syndromes FAP Gardner Peutz-Jeghers

GASTRIC LEIOMYOMAGASTRIC LEIOMYOMAIncidence of 16% at autopsyPathology

◦Arise from smooth muscle of the GIT tract Difficult to distinguish from GIST

◦75% benign Differentiation only on mitotic index

◦Large protruding elisions with central ulcer

Usually presents with bleeding if at all

Treatment is local excision with 2 – 3cm margin

HETEROTOPIC HETEROTOPIC PANCREASPANCREAS

Ectopic pancreas◦Most common found in stomach

Within 6 cm from the pylorus

◦Also in Meckl’s diverticulumRarely larger than 4 cm

◦Sessile and rubbery◦Submucosal in location◦Histological identical to normal

pancreas

ADENOCARCINOMAADENOCARCINOMAOF THE STOMACHOF THE STOMACH

Declining incidence in western world◦HP associated due to chronic atrophic

gastritis◦Also related to

Low dietary intake vegetables and fruit High dietary intake of starches More common in males ( 3 : 1 )

Histology◦ Invariably adeno-carcinoma◦Squamous cell carcinoma from oesophagus

Involves fundus and cardia


Histological typing◦Ulcerated carcinoma (25%)

Deep penetrated ulcer with shallow edges Usually through all layers of the stomach

◦Polipoid carcinoma (25%) Intraluminal tumors, large in size Late metastasis

◦Superficial spreading carcinomas (15%) Confinement to mucosa and sub-mucosa Metastasis 30% at time of diagnosis Better prognosis stage for stage


Histological typing◦Linitis plastica (10%)

Varity of SS but involves all layers of the stomach

Early spread with poor prognosis

◦Advanced carcinoma (35%) Partly within and outside the stomach Represents advanced stage of most of

the fore mentioned carcinomas


Symptoms and signs◦Vague discomfort difficult to distinguish

from dyspepsia◦Anorexia

Meat aversion Pronounced weight loss

◦At late stage Epigastric mass Haematemesis usually coffee ground seldom

severe◦Metastasis

Vircho node in neck


Surgical resection only cure◦Late presentation makes surgary often

futile◦Palliation controversial for

Haemorrhage Gastric outlet

◦Simple gastrectomy as effective as abdominal block Splenectomy often added due to direct

involvement Only for the very distal partial gestrectomy Rest total gastrectomy

Prognosis overall 12% 5 year survival◦90% for stage I disease

GASTRIC LYMPHOMAGASTRIC LYMPHOMA5% of all primary gastric neoplasm's2 different types of lymphoma

◦Part of systemic lymphoma with gastric involvement (32%)

◦Part of primary involvement of the GIT (MALT Tumors) 10 – 20% of all lymphomas occur in the abdomen 50% of those are gastric in nature

Risk factors◦HP due to chronic stimulation of the MALT ◦ In early stages of disease Rx of HP leads to

regression of the disease

GASTRIC LYMPHOMAGASTRIC LYMPHOMAPrimary MALTPrimary MALT

Early stages also referred to as pseudo-lymphoma◦ Indolent for long periods◦Low incidence of

Spread to lymph nodes Involvement of bone marrow

◦Therefore much better prognosisMostly involves the antrum5 different types according to

appearance◦ Infiltrative - Ulcerative◦Nodular - Polypoid◦Combination

GASTRIC LYMPHOMAGASTRIC LYMPHOMAPrimary MALTPrimary MALT

At time of presentation◦Larger than 10 cm (50%)◦More than 1 focus (25%)◦Ulcerated (30 – 50%)

Pattern of metastasis similar to gastric carcinoma

Signs and symptoms◦Occur late and are vague◦Relieved by anti-secretory drugs◦Diagnosis based on histology

Gastric lymphomaGastric lymphoma

Malignant neoplasm of mucosa associated lymphoid tissue (MALT)

A (usually) low grade B-cell (marginal cell) lymphoma

Gastric lymphoma Gastric lymphoma (maltoma)(maltoma)

Neoplastic cells infiltrate the epithelium (lymphoepithelial lesions)

Strongly associated with H. pylori

Gastrointestinal stromal Gastrointestinal stromal tumours (GIST)tumours (GIST)Mesenchymal neoplasmsDerived from interstitial cells of

Cajal (pacemaker cells controlling peristalsis)

Overexpress c-kit oncogene◦Used as diagnostic aid on tissue◦A target for therapy with tyrosine

kinase inhibitor imatinib (also used in CML)

GIST-spindle cell GIST-spindle cell neoplasm of GI tractneoplasm of GI tract

GISTGIST

Larger tumours with high mitotic rate tend to behave malignantly

Stomach is commonest site

Neuroendocrine tumoursNeuroendocrine tumoursCarcinoids are tumours of

resident neuroendocrine cells in gastric glands

Usually seen in context of chronic atrophic gastritis (driven by gastrin)

Clinical behaviour variable

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