Surgery 3A – Finals2014 - Santos

Diseases of the Stomach

Peptic Ulcer Disease
• One of the most prevalent and costly GIT diseases
• Chronic and recurrent Duodenal Ulcer
• Estimated 3-4 M are seen by a physician/yr for dx and tx Disease of multiple etiologies
• 3-4 M patients self medicate – problematic Absolute Requirements
1. Acid and pepsin secretions
• Hospitalization rate for duodenal ulcer has decreased but
a. Bad combination à ulceration
has remained stable for gastric ulcer
b. pH ≤3.5
• 2 types : duodenal & gastric. Can’t differentiate clinically 2. H. pylori infection
• Complications: usually very low ∴ hosp rate decreased a. Untreated à recurrent ulceration
• Pyloric sphincter as landmark between duo & gastric 3. NSAIDS infection
• Erosion – superficial to the muscularis mucosa a. –profens
o Mucosa + submucosa + muscularis b. Take this drug with meals
• Ulcer – extends through the muscularis mucosa c. Take with antacids

Duodenal Gastric
Location Duodenal pyloric junction Oxyntic antral junction
Antral pyloric junction
Esophago-gastric junction
Clinical On and off epigastric pain Recurrent episodes of quiescence and
Manifestations Mid-epigastric that is well-localized relapse
Usually tolerable and relieved by food intake Need to differentiate from carcinoma
Pain is relieved by food – Follows a pain-food-relief pattern
• Only seen in early part of dse
May be episodic, recurrent, or seasonal
If constant suggest deep penetration
Radiation to the back
Nocturnal pain – wakens at night of epigastric pain bc of the double
peaking of hypersecretion of acid in morning and night
• Give tx 30 min after meals so acid is present
• Give tx before bedtime to relieve nocturnal pains
Complications Bleeding (25%) Bleeding (35-40 %)
• MC complication of duodenal ulcer Common in types 2, 3, and 4
Perforation (5%) Perforation - MC complication & occurs
• Spillage into peritoneal cavity at the anterior aspect of the lesser
• Golden period for immd operation is 4-6 hours curvature
o Any more than is secondary bacterial infection Obstruction – common in types 2 and 3
Gastrocolic fistula – communication
• Localized pancreatitis - penetration between stomach and colon
Obstruction
• Inflammation from ulcer à healing à Fibrosis à gastric
outlet obstruction à distended stomach à vomiting
Intractable Pain
• Pain in the back
• Localized pancreatitis (retroperitoneal) – penetration
• Not responsive to conventional ulcer tx
Gastric Incompitence of pyloric sphincter will let duodenal contents into gastric
• Rarely develop below 40; usually 55-65 yo space and vice versa (bile acids + gastric acids)
• Likely occur in lower social class
• Most common among female (2:1) • Chronic alcohol intake
Predisposing factors: • Smoking
• NSAIDS • Long term corticosteroid therapy
• Abnormalities in acid and pepsin secretions • *The presence of acid - essential for gastric ulcer
• Gastric stasis through delayed gastric emptying production but the total secretory output appears to be
less important
• Coexisting duodenal ulcer
• *In the presence of gastric mucosal damage, acid is
• Bile reflux
ulcerogenic even when present in normal or less than
• Gastritis normal amount
• H. pylori infection

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Types of Gatric Ulcer
Assoc w excessive
acid secretion?
Type I 60- • Located at lesser curvature near incisura angularis
70% • Have low to normal acid output
NO o Purely gastric. Doesn’t need to have high acid
• Assoc with diffuse antral gastritis or multifocal atrophic
gastritis
Type 15% • Located in body of stomach in combination with active
II or chronic duodenal ulcer
YES
• Usually assoc with excess acid secretion
• Duo+Gastric ulcer ∴ needs presence of high amounts of acid
Type 20% • Found before pylorus
III • Prepyloric ulcer (within 2 cm of pylorus) pyloric channel
YES ulcer
• Behave like duodenal ulcers with hypersecretion of acid
• Acid secretion is elevated
Type <10% • Rarest
IV • Occur high on lesser curvature near the
NO
gastroesophageal junction

Diagnosis H. pylori Testing

Upper Gastrointestinal Radiography • Invasive vs Noninvasive
• Barium contrast • Non-invasive tests
• Ulcer “crater” o Serology (90% sensitivity and specificity)
• Cauliflower-like c/b fibrosis – may indicate obstruction § Test of choice when endoscopy is not
• Demonstrate an ulcer crater indicated
• Determine location, depth of penetration, and extent of § Not a good measure to determine if patient
deformation is not responsive to treatment
§ Cannot be used to determine
• Single contrast – 50% miss rate
eradication because titers remain high
• Double contrast – 80-90% accuracy o Urea breath test (>95% sensitivity and
• Larger lesions likely to be malignant specificity)
• Presence of mass or irregular filling defects suggest § Based on ability to hydrolyze urea
malignancy § A carbon labeled urea breath test, urea
Fiberoptic Endoscopy metabolized to ammonia and
• Allows you to treat when there is bleeding bicarbonate which is secreted in the
• Can cauterize bleeding, rubber band, and other therapeutic breathe as labeled CO2; method to test
interventions eradication
• Most reliable, 97% accuracy § Urease breaks urea to ammonia and
• Multiple biopsies or brushings for cytology is done carbon dioxide (which is inhaled out).
• Ability to sample tissues for H. pylori • Invasive
o Rapid urease Assay (90% sensitive and 98%
• May be used for therapeutic interventions
specificity)
• Conditions that need endoscopy (help differentiate from § Results available in hours
carcinoma) W.O.M.A.G. o Histology (gold standard with 95% sensitivity
o Major weight loss and 99% specificity)
o Gastric outlet obstruction o Culture (80% sensitivity and 100% specificity)
o Palpable abdominal mass § Expensive and required expertise
o Blood loss anemia
o Guiac positive stool - (+) fecal occult blood

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Treatment
• Medical management
• Lifestyle modifications – reduce stress
• Stop smoking and alcohol
• Stop NSAIDs
• Antacids – neutralize existing acid
• H2 receptor antagonists – give before meals, to stop
formation of acid
• Proton Pump inhibitors – give after meals, when there
is acid to activate it (PPI is a prodrug, needs to be
activated by acid)
o DO NOT give PPI + antacid. PPI effectivity
dec. Na-K exchange will not occur.
• Sulcralfate – coating and strengthening the mucosal
wall - Give in diffuse gastritis
• Treat helicobacter pylori (+)
o Amoxicillin, Clarithromycin, Metronidazole
Goals of treatment:
• Relief of symptoms
• Heal ulcer
• Prevent recurrence
o 72 % if no other tx
o 25% if with H2 receptor maintenance
o 2% if H pylori treated
Helicobacter pylori Treatment
• Chloromycetin, Metronidazole and amoxicillin -1 wk
• PPI - 2 weeks
• H2RA – 4-6 weeks
Surgical Management (NTK)
• No need for this now bc of the good response to drugs
• Truncal Vagotomy and Pyloroplasty
o Cut Vagus N to cut communication
between brain and parietal cells
• Highly Selective Vagotomy
• Antrectomy and BTV
• Substotal gastrectomy
o Purpose is to remove the parietal cell
containing part of stomach
o Resect fundus (parietal cells)
o Resect antrum (G cells that secrete gastrin)
Metabolic Distrubances
• Anemia – (Iron and B12 deficiency)
o B12 def: Dec intrinsic factor formerly
secreted by parietal cells à megaloblastic
anemia or pernicious anemia
• Steatorrhea (impaired absorption of fat)
• Osteoporosis and osteomalacia
Afferent Loop Syndrome – caused by:
• Kinging and angulation
• Internal herniation behind efferent limb
• Stenosis of GI anastomosis
• Volvulus of afferent limb
• Adhesions involving afferent limb
Efferent Loop Syndrome
• Caused commonly by herniation of the limb behind
in a RàL fashion occurring in both antecolic and
retrocolic gastrojejunostomies
• Occurs within the first month
• LUQ pain colicky with bilious vomiting and
abdominal distention
• Diagnosed by UGI series
Alkaline Reflux Gastritis
• Associated with severe epigastric pain, bilious
vomitting and weight loss
• Not relieved by food or antacids
• Iron deficiency anemia common
• HIDA scan diagnostic
• Treat symptoms
• Convert to roux en Y gastrojejunostomy
Retained Antrum Syndrome
• Highly ulcerogenic syndrome responsible for 80% of
recurrent ulceration
• A technetium scan helps in diagnosis of retained
antrum
• Treat with proton pump; if not responsive
reconstruct or excise the retained antrum

Postgastrectomy syndromes Postvagotomy diarrhea

Dumping syndrome • 30% incidence
• Symptom complex that occurs following ingestion of • Not usually severe and disappears within 3 to 4
a meal when a portion of the stomach has been months. Self limiting
removed or the normal pyloric sphincter mechanism
• Explosive Diarrhea occurs 2-3x weekly or once to
has been disrupted.
2x a month
• Symptom complex:
• Treated with cholestyramine which absorbs bile
o N/V
salts
o Epigastric fullness
o Crampy abdl pain
Postvagotomy gastric atony
o Explosive diarrhea
o Palpitations • Gastric emptying is delayed, because of loss of antral
o Tachycardia pump function
o Diaphoresis • Diagnosis by scintographic assessment of gastric
o Fainting emptying
o Dizziness • Patient presents with abdominal pain and fullness
o Flushing
o Blurred vision
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Stress Gastritis
Stress Ulcerations Predisposing Clinical Conditions
Stress erosive gastritis ARDS
Hemorrhagic gastritis Multiple trauma
Major burn (35%)
Usually occurs after Oliguric renal failure
o Physical trauma Large transfusion requirements
o Shock Hepatic dysfunction
o Sepsis Hypotension
o Hemorrhage Prolonged surgical procedures
o Respiratory failure Sepsis
o Severe burns (more than 30%) – Curling
ulcers Presentation and Diagnosis
o CNS disease – Cushing’s ulcers • Painless UGI bleeding that may be delayed at onset
• The common denominator here is stress • 50% develop bleeding w/in 1-2 days after trauma
• Characterized by multiple superficial non-ulceration • Bleeding is usually slow and intermittent and seen
erosions that begin in the proximal or acid secreting as flecks of blood in that NGT or anemia
portion of the stomach and progress distally • On occasion may present as massive UGI bleed with
hypotension and hematemesis
CLASSIFICATION
• Melena and hematochezia is not common
Early
• ENDOSCOPY is the diagnostic procedure of choice
• Appears within 24 hours after injury
• Typically multiple shallow and discrete areas of Therapy
erythema along with focal hemorrhage or adherent • Address the precipitating cause
clot
• Medical Management includes:
• Almost always seen in the fundus of the stomach and
o NPO – put stomach to rest
rarely in the distal stomach o NGT insertion with lavage
o Correct fluid and clotting abnormalities
Late
o Blood transfusion as needed
• Appear after 24 to 72 hours after injury o Proton pump inhibitors/ H2 antagonists
• There is tissue reaction, organization around a clot o Vasopressin max of 48-72 hours
or an inflammatory exudate o Embolization
• Appear identical to a regenerating mucosa around a
healing gastric ulcer Surgical Management
o When bleed is recurrent or needs ≥6units (3000 L)
Pathophysiology of blood transfusion
• Multifactorial o Suture ligation when BTV pyloroplasty
• Require presence of acid o BTV with partial gastrectomy
o Total gastrectomy
• Stress as a triggering facto is considered present
when hypoxia, sepsis or organ failure occur
Prophylaxis
Predisposing factors • Treat 1º cause
• Impaired mucosal defense mechanisms • Optimize patient care
• Reduction in blood flow, mucus, bicarb secretion, • Administer prophylactic drugs for bleeding:
endogenous prostaglandins o Antacids – hourly through NGT and
o PG – responsible for stimulation sec of mucus maintain pH above 3.5 (97% accuracy)
from goblet cells. No mucus à vulnerable o H2RA given by continuous infusions 97%
gastric wall accuracy
o Sucralfate (efficacious in 90-97%)
o PPI

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GASTRIC NEOPLASIA
Benign Tumors
Usually incidental findings on endoscopy
Detected in 2-3% of gastroscopic endoscopy
Gastric polyps and Ectopic Pancreas
Gastric polyps
• Fundic gland polyps – most common
o 47% of all gastric polyps
o no malignant potential
o Multiple 2-3mm sessile lesions in the body
and fundus
o Most cases sporadic but can occur in 53% of
patients with familial polyposis or
Gardner’s Syndrome
• Hyperplastic polyps
o 28% of all gastric polyps
o Typically <1.5 cm and arise in a setting of
chronic atrophic gastritis in 40-70% and
most commonly to H.pylori infection
o Although non-neoplastic, dysplastic
changes may occur
• Adenomatous polyps – main concern
o 10% of all gastric polyps
o Most commonly antral, sessile and eroded
o Can present as tubular, tubulovillous, or
villous
o Distinct risk for malignancy
§ Gastric adenocarcinoma in 21% of
cases
§ Polyps >4cm have 40% risk of
developing malignancy
§ Endocscopic polypectomy for
small lesions
§ Operative excision for >2cm
polyps with invasive carcinoma
and symptomatic polyps with pain
or bleeding
§ Villous most likely to develop
carcinoma

Malignant tumors –
Adenocarcinoma Pathology:
Epidemiology 95% are adenocarcinomas
• The incidence increases with age, peaking in the 7th Other histologic types:
decade • Squamous cell carcinoma
• Higher rates in japan and some parts of South • Adenoacanthoma
America and lower rates in Western Europe and the • Carcinoid tumors
USA • GIST – gastrointestinal stromal tumors
• Twice as common in men than women (5:1) • Lymphoma
• Noticeable shift of gastric cancer from the distal to
the proximal stomach BORMANN’S CLASSIFICATION.
• Most common are adenocarcinomas; M>F. Type 4 is worst types of cancers of stomach.
• Trends show increasing incidence in proximal Type I – Polypoid or fungating lesions
area/fundus Type II - Ulcerating lesions surrounded by
Nutritional elevated borders
• Low fat or protein consumption Type III – Ulcerating lesions with infiltration
• Salted meat or fish through the gastric wall
Type IV – Diffusely infiltrating lesions
• High nitrate consumption
(linitis plastica)
• High complex carbohydrate consumption Type V – Lesions not fitting in other
Environmental categories
o Poor food prep (smoked, salted)
o Lack of refrigeration
o Poor drinking water (well water)
o Smoking – common to all cancers
Social – low social class LAUREN CLASSIFICATION:
Medical Intestinal Diffuse
o Prior gastric surgery
Environmental Familial
o Helicobacter pylori infection
Gastric atrophy, Blood type A
o Gastric atrophy and gastritis
Intestinal metaplasia
o Adenomatous polyps
Men>women Women>men
o Male gender
o Pernicious anemia Inc incidence w age Younger age group
Gland formation Poorly diff’d signet ring cells
Hematogenous spread Transmural/lymphatic
Microsatellite instability Decreased E-cadherin
APC gene mutations
P53, P16 inactivation P53, P16 inactivation

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Preoperative Evaluation
• Hx and PE
• Flexible upper endoscopy – modality of choice (98%
accuracy)
• Double contrast UGI series (90% accuracy)
• CT scan
o See relationship of CA with adjacent organs
o Limitation in small gastric primaries and
small (<5mm) metastasis in liver and
peritoneum
• Endoscopic US (EUS) (75% accuracy)
o Not as accurate at CT scan
o Tells you depth of induration but not as well as
CT
o Not good to monitor response to therapy
• Laparoscopy
o To see if you need to open this patient up or not.
Metastasis everywhere à open-close procedure
wait for patient to eventually die.
o With or without ultrasound
Surgical Treatment
• The optimal surgical management of gastric cancer
must be tailored to the extent and location of the
disease
• In the absence of distant metastasis aggressive
surgical resection is determined by the need to
obtain a resection margin free of microscopic disease
(RO resection)
• Appropriate surgical procedure determined by the
location of the tumor and the known pattern of
spread.
• Maintain at least 6cm margin of resection because of
intramural spread
• Role of extended lymphadenectomy is controversial
(D1 vs D2 vs D3 dissection)
• Di dissection – removal of group 1 nodes
• D2 dissection – removal of group 1 and 2 nodes
• D3 dissection – D2 dissection plus removal of para
aortic nodes
RO resection – curative. Remove everything and nothing left
R1 resection – palliative. Resect tumor but there’s still mets
elsewhere
Palliative Tx
• Goal is relief of symptoms with minimal morbidity
• Surgical palliation may include resection or bypass
alone or in conjunction with percutaneous,
endoscopic or radiotherapeutic techniques
• Improvement of the quality of life
• Resect tumor, do anastomosis. Patient can eat
comfortably. Resect bc of bleeding, but patient will still
eventually die
• Lessen pain, so patient is able to eat.
• We cannot do anything about patient’s length of survivial
Adjuvant Therapy
Treatment given after surgery
Chemotherapy
Radiotherapy
Outcomes
• Overall, 5 yr survival after diagnosis is 10-21%
• After curative resection survival is 24-57%
• Recurrence rate after gastrectomy is high at 40-80%,
occurring within the first 3 years
Surveillance
• History and PE every 4 months for 1 year then
every 6 months for 2 years then annually thereafter
Gastric Lymphoma
• Most common site for lymphomas in the GIT
• Less than 15% of gastric malignancies and 2% of
lymphoma
• Occur in older patients with peak in the 6th and 7th
decades
• Patients present as epigastric pain, early satiety, and
fatigue
• 50% of patients with anemia
• Commonly occur in the antrum
• Considered if the stomach is the exclusive or
predominant site of disease
• The most ccommon type is diffuse large B cell
lymphoma (55%), followed by extranodal marginal
cell lymphoma (MALT)
• Evaluation by endoscopy . Staging by CT and EUS
• Multimodality treatment consisting of surgery,
chemotherapy and radiotherapy.
Good response after resection for chemo and radiotherapy
Gastric Sarcoma
• 3% of all gastric malignancies
• Arise from mesenchymal components of the gastric
wall
• GISTs are the most common mesenchymal tumor of
the GIT and located in the stomach in 60-70%
• Patient commonly present in the 4th decade with
mean age of 60 years
• Most GIST express the kit (CD117) and CD34
• Most common presentation is GI bleeding, pain and
dyspepsia
• Evaluated by endoscopy, UGI series and Ct scan
• Goal of surgery is a margin negative resection to
include en-bloc resection of adjacent organs if
involved by direct extension
• Since lymph node metastases is rare, no benefit for
extended lymphadenectomy
• Chemotherapy and radiation not so effective
• Imatinib mesylate is promising treatment
Rare – involves muscle layer
CD117 determination is important
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Menetrierʼs Disease
• Hypoproteinemic hypertrophic gastritis
• A rare acquired premalignant disease characterized
by massive gastric folds in the fundus and corpus of
the stomach, giving the mucosa a cobblestone or
cribriform appearance
• Associated with protein loss from the stomach,
excessive mucus production as well as
hypochlorhydia or achlorhydia
• Associated with cytomegalovirus in children and H.
pylori infection in adults
• Patients present with epigastric pain, vomiting,
weight loss, anorexia and peripheral edema.
• Medical treatment includes: anticholinergic drugs,
acid suppression, octretide and H pylori eradication
• Total gastrectomy for continuing massive protein
loss or if dysplasia or carcinoma develops
Protein loss ∴ edema
Assoc with CMV in children and H.pylori in adults
Mallory-Weiss Tear
• Related to forceful vomiting, retching, coughing or
straining that results in disruption of the gastric
mucosa high on the lesser curve at the GE junction.
• Account for 15% of UGIB, and rarely associated
with massive bleeding
• Overall mortality is 3-4%
• Most managed by endoscopic methods such as
multipolar electric coagulation, epinephrine
injection, endoscopic band ligation, or endoscopic
hemoclipping
• Angiographic intra arterial infusion of vasopresssin
or transcatheter embolization may be used in
selective high risk cases
• Surgery required for massive bleeding not
controlled by conservative means
Alcoholics
Forceful vomiting, retching, …
Retching is violent vomiting, may not have vomitus
Dieulafoyʼs Gastric lesion
• Caused by an abnormally large tortuous artery
coursing through the submucosa eroded by
pulsation of such vessels and action of gastric
contents leading to bleeding
• Generally occur 6-10 cm from the GE junction,
generally in the fundus near the cardia
• More common in men (2:1) with a peak incidence in
the 5th decade.
• Presentation is sudden onset of massive, painless,
recurrent hematemesis with hypotension
• Esophagogastroduodenoscopy is the diagnostic
modality of choice (80% accuracy)
• Angiography , done if unable to diagnose
endoscopically, reveals a tortuous ectatic artery in
the distribution of the left gastric artery with
accompanying contrast extravasations in the setting
of acute bleeding
• Treatment endoscopically by mutipolar
electrococagulation, injection sclerotherapy, band
ligation, hemoclipping, heater probe, or noncontact
laser photocoagulation
• Surgery (wedge resection) for those not controlled
by conventional treatment.
Fundus near GE jnc
à Resect
Gastric Varices
• Usually develop secondary to portal hypertension in
conjunction with esophageal varices or secondary to
sinistral from splenic vein thrombosis.
• Incidence of bleeding is 3-30%
• 78% bleeding in splenic vein thrombosis and fundic
varices
• Two types: gastroesophageal varices and isolated
gastric varices (subclassified as Type 1 – located in
fundus and Type 2 – isolated ectopic varices located
anywhere in the stomach)
• Increasing size of varices and child’s classification
increases the risk of bleeding
• Varices due to splenic vein thrombosis, documented
by ultrasound is treated by splenectomy
• Varices in the setting of portal hypertension should
be treated like esophageal varices with conventional
management as: Tamponade by Sengstake-
Blakemore tube, endoscopic banding (89% success)
or sclerotherapy
• Major problem is rebleeding , of which 50% are
secondary to ulcers
• Transjugular Intrahepatic Portosystemic Shunting
(TIPS) with 30% rebleeding rate
Related to portal hpn
Treat portal hpn
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Gastric Volvulus
• Torsion occurs along the stomach’s longitudinal
axis(organo-axial in2/3 cases), and along the
vertical axis (mesenteroaxial in 1/3)
• Organoaxial occurs acutely asssociated with a
diaphragmatic defect
• Mesenteroaxial is partial and recurrent and not
associated with diaphragmatic defect
• In adults diaphragmatic defect due to trauma or
paraesophageal hernia
• In children diaphragmatic defect due to congenital
defects like foramen of Bochdalek or eventration
• Manifests as sudden onset of constant and severe
upper abdominal pain, recurrent retching with
production of little vomitus and inability to pass
NGT (Borchardt’s Triad)
• Diagnosis confirmed y UGI endoscopy or barium
contrast.
• Plain film of abdomen reveals a gas filled viscus in
the chest or upper abdomen
• Acute volvulus is a surgical emergency. Stangulation
can occur in 5-28% of cases and may need resection
• Spontaneous volvulus treated by detorsion and
fixation of stomach by gastropexy or tube
gastrostomy
Adults: MC cause: trauma
Children: MC cause: congenital like foramen of bochdalek or
eventation
Borchard’s triad
Gastric Bezoars
• Collections of nondigestible materials, usually but
not of vegetable origin (phytobezoar) but also of
hair (trichobezoar)
• Phytobezoars found in patients who have undergone
gastric surgery and have impaired gastric emptying.
Symptoms include early satiety, nausea, pain,
vomiting, weight loss and a large abdominal mass
• Diagnosis confirmed by contrast studies or
endoscopy
• Treated by enzyme dissolution, tube lavage or
endoscopic fragmentation, and surgery
• Trichobezoars present as pain from gastric
ulceration, fullness from gastric outlet obstruction
with occasional gastric perforation and small bowel
obstruction
• Small trichobezoars treated by endoscopic
fragmentation,vigorous lavage or enzymatic
therapy.
• Large trichobezoars are treated surgically
•
Undigested food
Common among psych px: HAIR
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