Sabiston Stomach Flashcards
The embryonic stomach
-two mesenteries:
dorsal (which becomes the gastrosplenic, gastrocolic, and gastrophrenic ligaments)
ventral (which becomes the hepatoduodenal and gastrohepatic ligaments of the lesser omentum and the falciform ligament).
Blood Supply
-The celiac artery
-four main arteries :
the left and right gastric arteries along the lesser curvature
the left and right gastroepiploic arteries along the greater curvature
the left gastric artery being the largest.
proximal stomach > inferior phrenic arteries and short gastric arteries from the spleen.
15% to 20% of patients > aberrant left hepatic artery originating from the left gastric artery.
-proximal ligation of the left gastric artery can result in acute left-sided hepatic ischemia.
-The right gastric artery from the hepatic artery or the gastroduodenal artery
-The left gastroepiploic artery from the splenic artery
-the right gastroepiploic artery from the gastroduodenal artery.
Venous Supply
the veins of the stomach parallel the arteries.
-The left gastric (coronary) and right gastric veins usually drain into the portal vein.
-The right gastroepiploic vein drains into the superior mesenteric vein
-the left gastroepiploic vein drains into the splenic vein
Gastric LN
-The superior gastric group : drains lymph from the upper lesser curvature into the left gastric and paracardial nodes.
-The suprapyloric group of nodes drains the antral segment on the lesser curvature of the stomach into the right suprapancreatic nodes.
-The pancreaticolienal group of nodes drains lymph high on the greater curvature into the left gastroepiploic and splenic nodes.
-The inferior gastric and subpyloric group of nodes drains lymph along the right gastroepiploic vascular pedicle.
All four zones of lymph nodes drain into the celiac nodes and eventually into the thoracic duct.
Vagus Nerve
LARP
Left : Anterior
Right : Posterior
Vagus Nerve Again
-The left vagus > hepatic branch to the liver and continues along the lesser curvature as the nerve of Latarjet.
-criminal nerve of Grassi > first branch of the right posterior vagus nerve;
it is recognized as a potential cause of recurrent ulcers when left undivided.
The right vagus nerve > branch off to the celiac plexus and continues posteriorly along the lesser curvature.
Vagotomies
A truncal vagotomy > above the celiac and hepatic branches of the vagi
selective vagotomy > below.
A highly selective vagotomy > dividing the crow’s feet to the proximal stomach while preserving the innervation of the antral and pyloric parts of the stomach.
Morphology
-muscularis propria or externa > three layers of smooth muscles.
-The middle layer > circular and is the only complete muscle layer of the stomach wall.
The outer muscle layer > Longitudinal and predominates in the distal two thirds of the stomach.
Within the muscularis externa > Auerbach myenteric plexus.
The submucosa > strongest layer of the gastric wall contains network of blood vessels and lymphatics + Meissner plexus of autonomic nerves.
Gastric acid secretion by the parietal cell is regulated mainly by three stimuli
acetylcholine, gastrin, and histamine
Helicobacter pylori
secretes various proteases and lipases that break down mucin and impair the protective function of the mucous layer.
Vagotomy and gastric emptying
results in loss of receptive relaxation and gastric accommodation in response to meal ingestion
with resultant early satiety, postprandial bloating, accelerated emptying of liquids, and delay in emptying of solids.
hyperglycemia on gastric motility
decrease in contractility of the gastric antrum
increase in pyloric contractility
relax the proximal stomach
suppress the migrating myoelectric complexes
How to assess gastric emptying
The most common is a radionucleotide scan
meal of radiolabeled food.
Scans are obtained immediately after ingestion of the meal and at 1, 2, and 4 hours after the meal.
Measurement of residual gastric contents at 4 hours
> At 4 hours, retention of 10% to 15% signifies mild gastroparesis, 15% to 35% is moderate, and greater than 35% is severe.
Other Diagnostic Studies
-upper abdominal x-ray series after barium swallow > mechanical causes
-electrogastrogram or antroduodenal motility study assesses for nerve and muscle abnormalities
-Wireless motility capsules > alternative to scintigraphy
Tx of Gastroparesis
first-line for mild gastroparesis
> dietary modification > multiple, small meals with little fat or insoluble fiber, Acidic and spicy foods avoided.
opioids, calcium channel blockers, tricyclic antidepressants, and dopamine agonists, should be stopped
Glycemic control
Pharmacologic therapy for persistent symptoms despite nonpharmacologic modifications.
First-line therapy > metoclopramide a dopamine 2 receptor antagonist stimulates antral contractions and decreases postprandial relaxation of the fundus.
domperidone, dopamine 2 antagonist, patients who do not respond to metoclopramide
Macrolide antibiotics (erythromycin and azithromycin) are motilin agonists that act by stimulating fundal contraction (second-line therapy)
H. pylori
-spiral-shaped, flagellate, gram-negative bacteria
-potent producer of urease, which is capable of splitting urea into ammonia and bicarbonate
H. pylori can also be found in heterotopic gastric mucosa
-proximal esophagus
-in Barrett esophagus
-in gastric metaplasia in the duodenum
-within a Meckel diverticulum
-in heterotopic gastric mucosa in the rectum
Mechanism of H. pylori–induced GI injury
1- Production of toxic products > breakdown products from urease activity (e.g., ammonia), cytotoxins, mucinase
2-Induction of a local mucosal immune response > proinflammatory cytokines and reactive oxygen metabolites
3- Increased gastrin levels and changes in acid secretion
4- Gastric metaplasia occurring in the duodenum.
Invasive Tests for H.Pylori
Endoscopic biopsy > gastric body and the antrum > tested for urease.
Endoscopy > biopsy gastric mucosa, > histologic visualization of H. pylori
Culturing of gastric mucosa obtained at endoscopy
Noninvasive Tests
Urea breath test :
ability of H. pylori to hydrolyze urea
discontinue antibiotics for 4 weeks and PPIs for 2 weeks
Stool Antigen :
monoclonal antibodies to H. pylori antigens to test fecal specimens
the most cost-effective method for assessing treatment efficacy.
Serology :
presence of IgG antibodies to H. pylori.
Antibody titers can remain high for 1 year or longer after eradication > not used to check Tx Efficacy
Gastric Perforation Site
Most perforations occur along the anterior aspect of the lesser curvature.
gastric outlet obstruction can also occur in which type of ulcer
in patients with type II or III gastric ulcers
Gastric Ulcer Pain Description
pain > becomes constant > deeper penetration of the ulcer.
Referral of pain to the back > penetration into the pancreas
diffuse peritoneal irritation > free perforation.
PPIs have a healing rate of
85% at 4 weeks
96% at 8 weeks
Maintenance PPI therapy is considered in
-patients with large (>2 cm) ulcers
-refractory or frequent PUD
-those with failed H. pylori eradication
-or patients requiring continued NSAID use
Forrest classification of stigmata of recent hemorrhage
Active spurting IA Risk of reBleed > 90%
Active oozing IB Risk of reBleed > 10%–20%
Nonbleeding, visible vessel IIA Risk of rebleed > 50%
acute upper GI bleed should undergo endoscopy
within 24 hours.
All patients undergoing endoscopic examination for UGB should be tested for
H. pylori status.
embolization compared to surgery for UGIB
higher rates of rebleeding with Embolization
useful, especially for patients who are poor surgical candidates based on other medical comorbidities
Indications for surgical intervention in UGIB
failed endoscopic treatment (or recurrent hemorrhage after multiple endoscopic treatments),
hemodynamic instability
continued slow bleeding with transfusion requirement
How The gastroduodenal artery is oversewn
three-point U stitch technique
effectively ligates the main vessel
(superior and inferior stitches) and prevents back-bleeding from any smaller branches (medial stitch),
such as the transverse pancreatic artery, that head to the patient’s left toward the body of the pancreas
When Oversew the Gastrodudenal Be Careful
careful to avoid incorporating the common bile duct into the stitch.
The course of the common bile duct > identified by inserting a probe through the ampulla of Vater transduodenally or performing an intraoperative cholangiogram
For very large perforations (>3 cm)
omentum or jejunal serosa from a Roux-en-Y type limb.
a pyloric exclusion is typically performed by oversewing the pylorus using absorbable suture or stapling across it using a noncutting linear stapler.
A gastrojejunostomy is created to bypass the duodenum in a Billroth II or Roux-en-Y fashion.
An alternative in this difficult situation is antrectomy and a Billroth II or Roux-en-Y reconstruction.
After Surgery for perforation when to do upper scope
elective upper endoscopy should be performed 6 to 8 weeks after surgery to
assess for evidence of malignancy, ulcer healing, and to test for H. pylori if that diagnosis has not yet been established
Gastric outlet obstruction
- develop a hypochloremic, hypokalemic metabolic alkalosis
-NG tube placement
-correction of fluid and electrolyte abnormalities.
-Nutritional status
-Gastric outlet obstruction from PUD is not a surgical emergency
-gastric cancer is the most common cause of this disorder. -Upper endoscopy should be performed for malignancy and H. pylori assesment
-Endoscopic dilation (with or without stenting) and H. pylori eradication are the mainstays of initial therapy.
Patients with refractory obstruction are best managed with
primary antrectomy and reconstruction along with vagotomy.
Intractable peptic ulcer disease
failure of an ulcer to heal after an initial trial of 8 to 12 weeks of therapy
or if patients relapse after therapy has been discontinued
For any intractable ulcer
adequate duration of therapy
H. pylori eradication
and elimination of NSAID must be confirmed.
A fasting serum gastrin level should be obtained
truly intractable ulcer disease that fails medical management should be treated with
a vagotomy, with or without an antrectomy
Truncal vagotomy
division of the left and right vagus nerves above the hepatic and celiac branches, just above the GE junction.
vagotomy without a drainage procedure can cause delayed gastric emptying.
Truncal vagotomy in combination with a Heineke-Mikulicz pyloroplasty
Selective vagotomy
divides the main right and left vagus nerves just distal to the celiac and hepatic branches, and a pyloric drainage procedure is also performed.
However, selective vagotomy results in higher ulcer recurrence rates than truncal vagotomy,
Highly selective vagotomy
AKA parietal cell vagotomy or proximal gastric vagotomy.
divides only the vagus nerves supplying the acid-producing portion of the stomach within the corpus and fundus.
preserves the vagal innervation of the gastric antrum and pylorus,
no need for routine drainage procedures.
Highly selective vagotomy Exactly Where
These nerves are divided up until a point approximately 7 cm proximal to the pylorus
Superiorly, division of these nerves is carried to a point at least 5 cm proximal to the GE junction on the esophagus
Ideally, two or three branches to the antrum and pylorus should be preserved.
The criminal nerve of Grassi represents a very proximal branch of the posterior trunk of the vagus, and great attention is needed to avoid missing this branch in the division process because it is frequently cited as a ‘‘predisposition for ulcer recurrence if left intact’’
highly selective vagotomy has lower rates of
postvagotomy dumping syndrome and diarrhea.
But higher Recurrence than Truncal
For benign disease, gastroduodenostomy is generally favored because it avoids the problem of
retained antrum syndrome
duodenal stump leak
and afferent loop obstruction associated with gastrojejunostomy after resection
The retrocolic anastomosis minimizes the length of the afferent limb and decreases the likelihood
of twisting or kinking that could lead to afferent loop obstruction and predispose patients to the devastating complication of a duodenal stump leak
Endoscopy frequently demonstrates prominent gastric rugal folds
reflecting the trophic effect of hypergastrinemia on the gastric fundus. > Zollinger
best initial imaging study to localize the gastrin-secreting tumor
triple-phase CT or MR imaging (MRI) of the abdomen.
these imaging modalities have a relatively low sensitivity in detecting tumors that are less than 1 cm in diameter as well as small liver metastases.
If initial imaging is nondiagnostic, localization can sometimes be achieved using somatostatin receptor scintigraphy or endoscopic ultrasound (EUS)
For Zollinger Resection
a resection according to oncologic principles should be performed (rather than a tumor enucleation) with at least 10 lymph nodes removed.
The two strongest risk factors for developing clinically significant bleeding from gastric stress ulcers are
coagulopathy
respiratory failure requiring prolonged mechanical ventilation (>48 hours)
what reduces the risk of stress ulcer formation
Enteral nutrition > initiated as soon as possible.
PPI
Prophylaxis should be limited only to high-risk patients
bleeding from stress ulcers
In experienced centers, vasopressin can be administered into the left gastric artery and can be embolized as well to help control bleeding
Bleeding that results in hemodynamic instability or requires persistent transfusions is an indication for surgery
-lesions are in the proximal stomach or fundus, a long anterior gastrotomy should be made in this area.
-The gastric lumen is cleared of blood, and the mucosal surface is inspected for bleeding points.
-All bleeding areas are oversewn with figure-of-eight stitches taken deep within the gastric wall.
In stable patients, the operation is completed by closing the anterior gastrotomy and performing a truncal vagotomy and pyloroplasty to reduce acid secretion.
Dumping Syndrome Tx
-Dietary measures > avoiding large amounts of sugar, frequent feeding of small meals rich in protein, fats, and fiber, and separating liquids from solids during a meal.
-imodium for diarrhea and meclizine for nausea.
-Anticholinergics can slow gastric emptying and treat spasms.
-Octreotide is the best studied medication for dumping syndrome and can be very effective.
-Patients with severe symptoms may require a reoperation
-Pyloric reconstruction
-Patients with a gastrojejunostomy without a gastrectomy, takedown of the gastrojejunostomy
-patients with a prior distal gastrectomy, converting a loop gastrojejunostomy to a Roux-en-Y reconstruction
The most common metabolic defect appearing after gastrectomy is
anemia > Iron ( more common )
Or
Vit b12
Osteoporosis and osteomalacia
If fat malabsorption is also present, the calcium malabsorption is aggravated further because fatty acids bind calcium.
usually associated with a Billroth II gastrectomy.
Patients with Billroth II or Roux-en-Y reconstruction that bypasses the duodenum should also receive supplementation of the fat-soluble vitamins (vitamins A, D, E, and K).
Afferent Loop Syndrome
-Is the duodenojejunal loop proximal to the gastrojejunal anastomosis
-After obstruction pancreatic and hepatobiliary secretions accumulate
-empty the contents forcefully into the stomach, resulting in projectile bilious vomiting that offers immediate relief of symptoms.
blind loop syndrome.
If the obstruction has been present for a long time
bacterial overgrowth occurs in the static loop,
bind with vitamin B12 and deconjugated bile acids;
results in a systemic deficiency of vitamin B12 (with the development of megaloblastic anemia), fat malabsorption, and deficiency in fat-soluble vitamins.
How to Diagnose Diagnose ?
Failure to visualize the afferent limb on upper endoscopy is suggestive of the diagnosis.
Radionuclide studies imaging the hepatobiliary tree
Normally, the radionuclides should pass into the stomach or distal small bowel after being excreted into the afferent limb. If this does not occur, the possibility of an afferent loop obstruction should be considered.
Tx
-Surgical correction is indicated for this mechanical problem to prevent bowel necrosis or duodenal stump blowout.
-A long afferent limb is usually the underlying problem, so treatment involves the elimination of this loop.
-conversion of the Billroth II construction into a Billroth I anastomosis,
enteroenterostomy below the afferent and efferent loops, and conversion to a Roux-en-Y reconstruction.
Efferent Loop Obstruction
diagnosis > upper GI series or CT with oral contrast, with failure of contrast to enter the efferent limb.
Operative intervention > reducing the retroanastomotic hernia if this is the cause of the obstruction and closing the retroanastomotic space to prevent recurrence
Alkaline Reflux Gastritis
MC with Billroth II anastomosis.
The diagnosis > careful history.
A technetium biliary scan
Upper endoscopy demonstrates friable, beefy red mucosa.
Tx
For patients with intractable symptoms, the surgical procedure of choice is conversion of the Billroth II anastomosis into a Roux-en-Y gastrojejunostomy, in which the Roux limb has been lengthened to more than 40 cm
Gastric Atony
Gastric emptying is delayed after truncal and selective vagotomies but not after a highly selective vagotomy
reduction in the ability to empty solids
increases risk of gastric cancer development.
Increase levels of interleukin-1β and tumor necrosis factor-α expression
at what age PTG for hereditary diffuse gastric cancer
Prophylactic total gastrectomy should be considered for patients with this mutation prior to age 30
Polyps
isolated polyp greater than 1 cm in size should have a complete polypectomy.
For those with multiple polyps, the largest should be removed endoscopically
remaining polyps should be biopsied.
Biopsies of normal mucosa should be performed as well to assess for underlying dysplasia and H. pylori infection.
Polyp that needs operative excision
If the polyp is larger than 2 cm
is sessile
proven focus of invasive carcinoma
Fundic gland polyps
benign lesions , strongly associated with PPI
Hyperplastic polyps
associated with H. pylori infection and chronic gastritis,
PPI , Gastritis and Cancer
patients with H. pylori taking long-term PPIs, the low-acid environment allows the bacteria to colonize the gastric body, leading to corpus gastritis. One third of these patients develop atrophic gastritis, which is significantly more common in patients with H. pylori who are taking PPIs.
atrophic gastritis is considered a major risk factor for the development of gastric cancer.
pernicious anemia
increased risk for developing gastric cancer.
Achlorhydria is the defining feature of this condition; it occurs when chief and parietal cells are destroyed by an autoimmune reaction
Diffuse Vs Intestinal
see
if a suspicious mass or ulcer is encountered in the stomach, how many Bx to take
harvesting six to eight biopsy specimens from different areas of the lesion in order to maximize the diagnostic yield
endoscopic mucosal resection (EMR) or endoscopic submucosal dissection can be used for what size lesion
Small lesions (≤2 cm in diameter) can be resected at the time of initial diagnostic endoscopy
repeat staging laparoscopy after neoadjuvant therapy ??
detects a nontrivial amount of occult metastatic disease and should be strongly considered prior to undergoing a laparotomy for curative intent.
cancers of the distal stomach, including the body and antrum
distal gastrectomy
the proximal stomach > at the level of the incisura at a margin of at least 2 to 3 cm for early cancers and at least 4 to 6 cm for advanced cancers.
The distal margin is the proximal duodenum just distal to the pylorus.
Frozen section analysis should be performed before reconstruction
proximal lesions of the fundus or cardia that do not invade the GE junction
total gastrectomy with a Roux-en-Y esophagojejunostomy and proximal gastrectomy are equivalent from an oncologic perspective.
However, rates of anastomotic stenosis and reflux esophagitis are much higher after proximal gastrectomy and the lymph node harvest may be inadequate.
Standard criteria for endoscopic resection of gastric adenocarcinoma
- Intestinal-type adenocarcinoma
- Tumor confined to the mucosa
- Absence of lymphovascular invasion
- Nonulcerated tumor
- Less than 2 cm in diameter
Who should be referred for gastrectomy with lymphadenectomy
Patients with positive vertical margins
lymphovascular invasion
submucosal invasion
Gastric Lymphoma
usually occur in the gastric antrum
associated with gastric lymphoma > H. pylori infection, certain autoimmune diseases (i.e., rheumatoid arthritis, systemic lupus erythematous), immunosuppression, and celiac disease
The most common gastric lymphoma
diffuse large B cell lymphoma
followed by gastric MALT lymphoma
risk factors for the development of primary DLBCL
Immunodeficiency and H. pylori infection
Work Up
Endoscopy with biopsy > submucosal growth nondiagnostic.
EUS
Evidence of distant disease > upper airway examination to evaluate Waldeyer tonsillar ring, bone marrow biopsy, and CT of the chest and abdomen to detect lymphadenopathy.
A PET/CT is often performed for patients with DLBCL as part of their initial assessment.
Biopsies should be performed of enlarged lymph nodes.
Histologic H. pylori testing should be performed and, if negative, confirmed by serology
Gastric MALT lymphoma
lower grade than DLBCL
preceded by H. pylori–induced gastritis
four chromosomic translocations t(1;14), t(3;14), t(11;18), and t(14;18).
Patients with early-stage MALT lymphomas and active H. pylori infection
treated by H. pylori eradication alone.
careful follow-up is necessary, with repeat endoscopy in 2 months to document clearance of the infection and biannual endoscopy for 3 years to document regression
predict failure after H. pylori eradication alone
The presence of transmural tumor extension
nodal involvement,
transformation into a large cell phenotype
and nuclear BCL-10 expression
MALT lymphoma with H. pylori–negative
radiation therapy (if all the involved sites can be encompassed in a single field) and chemotherapy
MALT lymphoma prognostic index
-age of 70 or above
-stage IV disease
-elevated lactate dehydrogenase (LDH) level.
Immunohistochemical staining for GIST
CD117, CD34, and PDGFRA
PDGFRA mutations are restricted to the stomach.
Recurrence in GIST
Most patients who experience recurrence demonstrate metastasis to the liver, with one-third having only isolated local recurrence.
Recurrence can occur over 20 years after resection; thus, long-term follow-up is warranted.
Gastric carcinoid types.
see
Type I gastric NETs
most common
associated with chronic achlorhydria from atrophic gastritis, pernicious anemia, or possibly prolonged PPI use
biomarker for these tumors.
Chromogranin A is often elevated
reatment for localized NETs
complete removal.
For small pedunculated lesions that do not invade beyond the submucosa, complete removal can be accomplished endoscopically.
Larger (>1 cm) lesions may require wedge resection or partial gastrectomy
localized type III NETs
oncologic resection with lymphadenectomy.
For patients with recurrent or metastatic disease, somatostatin analogues or chemotherapy
Ménétrier disease (hypoproteinemic hypertrophic gastropathy)
-massive gastric folds in the fundus and body of the stomach, giving the mucosa a cobblestone or cerebriform appearance
-associated with cytomegalovirus infection in children and H. pylori infection in adults.
Dieulafoy Gastric Lesion
-abnormally large (1–3 mm), tortuous artery coursing through the submucosa without a primary ulcer
-The lesions generally occur near the GE junction along the lesser curvature.
Gastric varices in the setting of splenic vein thrombosis
are readily treated by splenectomy
organoaxial gastric volvulus
occurs acutely and is associated with a diaphragmatic defect
whereas mesenteroaxial volvulus is partial (<180 degrees), recurrent, and not associated with a diaphragmatic defect
Borchardt triad
severe upper abdominal pain, recurrent retching with production of little vomitus, and the inability to pass an NG tube
in GIST, Resistance to TKIs is most often due to acquired mutations in the driver mutation
For KIT-mutated GISTs, these secondary mutations occur in exons 13, 14, and 17.
For PDGFRA-mutated GIST, secondary mutations occur in exons 13, 14, and 15.
