Stomach Flashcards
A 68-year-old male with a history of hypertension and hypercholesterolemia presents to his primary care physician’s office with a chief complaint of worsening epigastric pain and weakness. The pain is improved with oral intake, especially milk-based products. The patient has been treating his pain with naproxen.
In the office, the patient is non-toxic with normal vital signs. His physical examination reveals mild epigastric tenderness with deep palpation. Serum hemoglobin was 8.3 g/dL. Fecal occult blood testing was positive. The patient underwent colonoscopy, which was normal.
Esophagogastroduodenoscopy (EGD) revealed a 2.5 cm ulcerated lesion with elevated, irregular borders 5 cm distal to thegastroesophageal junction.
Appropriate management of the ulcer includes?
A. Observation
B. Cessation of naproxen and begin sucralfate and a proton-pump inhibitor with repeat EGD in 3 months
C. Biopsy the ulcer
D. Proximal gastrectomy
E. Total gastrectomy
C.
Historically, biopsy of gastric ulcers was uniform practice throughout medical and surgical disciplines since there was a 5% to 11% attendant risk of malignancy. However, data now suggest that the incidence of gastric cancer is decreasing, thereby rendering mandatory biopsy of all gastric ulcers unnecessary.
When gastric ulcers have features suggestive of malignancy such as elevated irregular folds, association with a polypoid or fungated mass, and abnormal adjacent mucosal folds, then biopsy is warranted. Several biopsies, typically 6 or more, are necessary to minimize the false negative risk. If benign ulcers are diagnosed, then EGD is repeated in 6 weeks to ensure resolution. All ulcers should be followed and biopsied until complete resolution occurs.
If malignancy is detected, then further work-up with potential operative intervention is pursued.
Ulcers with a diameter of 3 cm or greater are termed giant gastric ulcers (Fig. 23-2). These large ulcers harbor an underlying malignancy in 30% of lesions.
Given the higher incidence of malignancy, perforation, and bleeding, surgical treatment is warranted.
A 68-year-old male with a history of hypertension and hypercholesterolemia presents to his primary care physician’s office with a chief complaint of worsening epigastric pain and weakness. The pain is improved with oral intake, especially milk-based products. The patient has been treating his pain with naproxen. In the office, the patient is non-toxic with normal vital signs. His physical examination reveals mild epigastric tenderness with deep palpation. Serum hemoglobin was 8.3 g/dL. Fecal occult blood testing was positive. The patient
underwent colonoscopy, which was normal. Esophagogastroduodenoscopy (EGD) revealed a 2.5 cm ulcerated lesion with elevated, irregular borders 5 cm distal to the gastroesophageal junction.
Final pathology reveals a poorly differentiated adenocarcinoma. The most sensitive preoperative examination to determine and N stage is:
A. Positron emission tomography (PE) scan
B. Endoscopic ultrasound (EUS)
C. Magnetic resonance imaging (MRI) with gadolinium
D. Diagnostic laparoscopy
E. Triple-phase helical computed tomography (CT) scan
B.
EUS is important in preoperative locorégional staging for gastric cancer. It is currently the best imaging modality for assessing both tumor depth and nodal invasion. Spatial resolution of 0.1 mm can be achieved with EUS. T staging accuracy ranges from 60% to 90%, whereas N staging accuracy ranges from 50% to 80% EUS is better at identifying T1 (80%) and T3 (90%) lesions as opposed to T2 (38.5%).
EUS is not reliable at delineating between individual benign and malignant lymph nodes. Increasing T stage directly correlates with increased risk of nodal and distant metastasis (> 80% likelihood of nodal metastasis in T3 disease versus < 5% in stage T1 m).
CT remains an important preoperative tool to evaluate for metastatic disease. If metastatic disease is present, an unnecessary operation can be avoided.
T staging accuracy with CT approaches 80% (66% to 77%). N stage determination is variable with a wide range of 25% to 86%.
Small gastric tumors and metastases less than 5 mm can be missed on CT.
CT, MRI, and PET scanning show promise for preoperative staging, but have yet to become standard of care.
Routine diagnostic laparoscopy to minimize unnecessary operations has become a less popular pre-resection strategy.
However, diagnostic laparoscopy still has a role in advanced gastric cancer. Power et al., in 2009, evaluated patients with known gastric cancer without obvious metastatic disease and stratified them into low-risk (Tl-2, NO) and high-risk (T3-4, N+ , or both) groups based on EUS. Both
groups underwent diagnostic laparoscopy, which identified Ml disease in 20.5% of the high-risk patients and 4% of the low-risk patients.
The study concluded that laparoscopy can be avoided in patients with EUS early stage cancer, whereas more advanced
gastric cancers would benefit from diagnostic laparoscopy to rule out occult metastatic disease.
When diagnostic laparoscopy is performed, peritoneal lavage cytology should be obtained as positive results
can alter further therapy. Diagnostic laparoscopy, however, does not address the N stage.
A 68-year-old male with a history of hypertension and hypercholesterolemia presents to his primary care physician’s office with a chief complaint of worsening epigastric pain and weakness. The pain is improved with oral intake, especially milk-based products.
The patient has been treating his pain with naproxen. In the office, the patient is non-toxic with normal vital signs. His physical examination reveals mild epigastric tenderness with deep palpation. Serum hemoglobin was 8.3 g/dL. Fecal occult blood testing was positive. The patient underwent colonoscopy, which was normal.
Esophagogastroduodenoscopy (EGD) revealed a 2.5 cm ulcerated lesion with elevated, irregular borders 5 cm distal to the gastroesophageal junction.
The EUS suggests a T3N0 lesion. The most appropriate next step would be:
A. Neoadjuvant therapy
B. Proximal gastrectomy with negative margins (RO) only
C. Total gastrectomy
D. Total gastrectomy with splenectomy and distal pancreatectomy
E. Esophagogastrectomy with colonic interposition graft
A.
Although the patient will ultimately need an operation, the MAGIC trail demonstrates that the patient will benefit from neoadjuvant therapy instead of proceeding straight to the operating room, unless the patient is hemorrhaging from the mass resulting in hemodynamic instability.
Neoadjuvant therapy consisting of epirubicin, cisplatin, and fluorouracil is recommended for patients with T2 lesions or higher.
The benefits from the preoperative therapy are to reduce tumor size and stage, eliminate micrometastases, improve tumor-related symptoms, and determine whether tumors are sensitive to chemotherapy.
Gastric adenocarcinoma exists as two distinct entities: diffuse and intestinal type:
INTESTINAL Age: Older Gender: M>F Mets: Hematologic Site of mets: Liver Risk factors: Atrophic gastritis, intestinal metaplasia, H. pylori, diet high in salt, smoked and preserved food Cellular etiology: Glandular gastric mucosa Prognosis: Better
DIFFUSE Age: Younger Gender: M=F Mets: Lymphatic, submucosal spread which can result in a thickened, non-distensible stomach (linitis plastica) Site of mets: Peritoneum Risk factors: CHD-1 mutation, obesity Cellular etiology: Lamina propria Prognosis: Poor
Controversies surrounding the surgical management of gastric adenocarcinoma include: adequacy of surgical margins, need for resection of adjacent structures (i.e. spleen and distal pancreas), and extent of lymphadenectomy.
Diffuse type gastric adenocarcinoma spreads in the submucosa, thereby increasing the risk of microscopic residual positive margin (R1 resection).
In order to minimize the risk of leaving microscopic disease or recurrence, a 5 to 6 cm margin is considered acceptable for an R0 resection.
Newer studies emerging from Japan suggest that smaller proximal resection margins of 2 to 3 cm are adequate for T1 lesions.
If the patient went straight to surgery, total gastrectomy is preferred as the tumor is within 5 cm of the gastroesophageal junction.
Esophagogastrectomy is unnecessary when the gastroesophageal junction has no direct tumor involvement and surgical margins exceed 5 cm.
Assessing nodal disease at the time of operation can be difficult. A minimum of 15 lymph nodes is recommended for staging. Most surgeons tend to remove the perigastric lymph nodes (DI resection).
In countries like Japan where gastric cancer has a higher prevalence, a more aggressive D2 lymphadenectomy is frequently employed harvesting lymph nodes along the celiac trunk and its named branches, the middle colic artery, the superior mesenteric artery, and the periaortic area.
Several studies have demonstrated prolonged survival with the more aggressive (D2) lymphadenectomy. This is thought to be related to better locorégional disease control.
A recent randomized trial comparing DI versus D2 lymphadenectomy did not reveal a significant difference in long-term survival. Accordingly, more studies regarding the extent of lymphadenectomy
are required before a long-term endorsement of this more aggressive strategy can be made.
Removal of adjacent structures (ie., distal pancreas and spleen) confer no survival benefit and actually increase morbidity and mortality. Resection of these adjacent structures should be reserved for primary tumor invasion.
A 68-year-old male with a history of hypertension and hypercholesterolemia presents to his primary care physician’s office with a chief complaint of worsening epigastric pain and weakness. The pain is improved with oral intake, especially milk-based products.
The patient has been treating his pain with naproxen. In the office, the patient is non-toxic with normal vital signs. His physical examination reveals mild epigastric tenderness with deep palpation. Serum hemoglobin was 8.3 g/dL. Fecal occult blood testing was positive. The patient underwent colonoscopy, which was normal.
Esophagogastroduodenoscopy (EGD) revealed a 2.5 cm ulcerated lesion with elevated, irregular borders 5 cm distal to the
gastroesophageal junction.
The final pathology revealed a T4N1 lesion with negative margins. The patient should next receive:
A. No additional therapy
B. Imatinib
C. External-beam radiation only
D. Fluorouracil-based chemotherapy only
E. External-beam radiation and fluorouracil-based chemotherapy
E.
The final pathology revealed Stage III gastric cancer. Given the high rate of locorégional failure (40% to 70%) and a 5-year survival rate of 20% to 28%, adjuvant therapy is recommended. This recommendation originates from the Intergroup Trial 0116, which demonstrated a benefit for those patients with advanced
gastric cancer undergoing curative resection combined with postoperative fluorouracil-based chemotherapy and radiation.
The CLASSIC trial demonstrated survival advantages using an adjuvant chemotherapy therapy regimen of capecitabine and oxaliplatin.
Resection without adjuvant therapy resulted in decreased survival when compared with those who received postoperative chemoradiation.
Palliation can be achieved with either external-beam radiation or chemotherapy, but local control and long-term survival are poor. Imatinib is a tyrosine-kinase
inhibitor currently used for gastrointestinal stromal tumors and other malignancies.
Which of the following describes the association between Irish’s node and gastric cancer?
A. An anterior mass palpable on digital rectal examination
B. A metastatic left supraclavicular lymph node
C. An ovarian mass from metastatic tumor
D. Metastatic left axillary lymph node
E. Umbilical mass suggestive of metastatic gastric cancer
D.
In general, physical findings portend advanced disease. Patients are typically cachectic and jaundiced when nodal metastatic disease obstructs the common bile duct.
Irish’s node is an enlarged lymph node within the left axilla.
A prerectal mass palpable on digital rectal examination is a Blumer shelf suggestive of a drop metastasis.
Virchow’s node, also known as Troisier’s sign, refers to carcinomatous involvement of the left supraclavicular lymph nodes at the junction of the thoracic duct with the subclavian vein.
Krukenberg tumors are ovarian masses from metastatic gastric cancer.
The Sister Mary Joseph node is a periumbilical nodule suggestive of carcinomatosis. It reflects tumor extension from the falciform ligament.
A 62-year-old man with hypertension was referred to the general surgery clinic for further evaluation of chronic abdominal pain, bloating, and early satiety, which had been worsening over several months. He was previously healthy except for hypertension controlled with metoprolol and a history of inguinal hernia repair.
His last screening colonoscopy performed 2 years ago was negative. On review of systems, he endorses significant fatigue. Laboratory results are consistent with mild anemia. An abdominal CT scan was obtained for
further evaluation and revealed a large tumor of gastric origin (pictured below).
The best next step to definitively diagnose this lesion is:
A. Abdominal MRI
B. Endoscopic ultrasound with FNA
C. Percutaneous image-guided biopsy
D. Diagnostic laparoscopy with biopsy and peritoneal washings
B.
The CT slice shown demonstrates a large, well-demarcated, heterogeneously enhancing mass that appears to grow outward from the wall of the stomach.
These findings are characteristic of gastric GIST, although the differential diagnosis includes gastric adenocarcinoma, carcinoid, lymphoma,or leiomyosarcoma, as well as tumors of pancreatic, renal, or adrenal
origin.
GIST is a relatively uncommon neoplasm, with an incidence of about 7 per million population in the United States and Europe. The benefits of EUS include defining the layer of stomach wall from which the tumor originates, delineating its relationship to surrounding structures, and obtaining a tissue diagnosis transluminally, which avoids the risk of seeding a percutaneous biopsy tract.
Percutaneous image-guided biopsy may result in intraperitoneal tumor spillage or
hemorrhage as a result of the friable, vascular nature of these tumors and is therefore less desirable.
MRI offers no additional benefit over CT diagnostically, though it may provide more information regarding the tumors relationship to surrounding tissues. Diagnostic laparoscopy with peritoneal washings for cytology has a prognostic role in gastric adenocarcinoma, but a similar role has not been established in GIST.
Laparoscopic excision of the lesion may be performed without a tissue diagnosis for a small tumor, but the goal in this case is resection to clear margins, rather than simply to obtain tissue for diagnostic purposes and therefore, endoscopic ultrasound is the best choice.
Biopsied tissue is positive for KIT (CD 117) upon immunochemical staining. Which of the following is true of this type of tumor?
A. Gastrointestinal stromal tumor (GIST) most commonly arises from the stomach.
B. The most common subtype is epithelioid.
C. A positive stain tor KIT (CD 117) is required to make the diagnosis of GIST.
D. The most common site of metastatic spread is the peritoneum.
E. All tumors >1 cm should be considered potentially malignant.
A.
The presence of the c-kit receptor tyrosine kinase on tumor cells, as in this case, is diagnostic of GIST.
However, it is noteworthy that about 5% of gastrointestinal stromal cells tumors are KIT-negative and only about 80% have a KIT mutation.
Other useful histologic markers include CD34 and smooth-muscle actin, if KIT negative GIST is suspected. The most common histologic subtype is the spindle-cell variety (70%), followed by epithelioid (20%) and mixed subtypes (10%).
All tumors greater than 2 cm in size should be considered malignant, even in the absence of metastases on initial work-up. The most common site of metastatic spread of GIST is the liver, followed by the omentum
and peritoneum. If present, these metastases are often identified by contrast enhanced CT scanning.
Metastasis to the lymph nodes, lung, or other distant sites may occur, but this is quite rare. Thus, extended surgical lymphadenectomy is not indicated for these tumors.
Over half of all GISTs arise from the stomach, making it the most common primary site.
Further review of the CT scan raises concerns that this 6-cm tumor may involve the neck of the pancreas. There is no evidence of distant metastatic disease. Further therapy in this case should include:
A. Surgical resection with en-bloc removal of the involved pancreas to achieve 1 cm negative margins.
B. Neoadjuvant imatinib prior to surgical therapy.
C. Avoidance of pancreatectomy by enucleation of the tumor.
D. An open rather than laparoscopic approach should be used.
E. An extended lymphadenectomy should be performed.
B.
When surgical morbidity can be reduced by its use, preoperative therapy with imatinib, a receptor tyrosine kinase inhibitor, should be strongly considered.
In this case, tumor down-staging could potentially eliminate involvement with the pancreas and obviate the need for pancreatectomy.
For localized GIST, surgical resection is indicated and is curative for low risk lesions. If necessary to achieve an R0 resection, en-bloc removal of involved organs outside the primary site is indicated. However, there is no additional survival benefit to resection beyond microscopically negative margins.
An extended lymphadenectomy also offers no benefit to the patient, as nodal metastasizes are uncommon with GIST occurring about 1% of the time.
Enucleation of the tumor risks violating its pseudocapsule which may result in intraoperative tumor spillage, resulting in recurrence rates approaching 100%. Though laparoscopic surgery for GIST has not been prospectively evaluated, there is good retrospective evidence to show adequate oncologic outcomes with this approach.
Rates of R0 resection between 97% and 100% and disease free survival and overall survival rates of over 90%.
In the past, an open approach for tumors larger than 5 cm has been recommended.
Current guidelines indicate that laparoscopy is appropriate for larger tumors, providing
sound oncologic principles are maintained.
Af er appropriate therapy, final pathology returns with a GIST of gastric origin, 6 cm in greatest dimension with 15 mitoses per high-power field.
Which of the following is true regarding this patient?
A. Adjuvant therapy with imatinib will increase his chance of recurrence-free and overall survival at 5 years.
B. If this lesion were in the small bowel, the prognosis would be better.
C. This patient is at low risk of tumor recurrence.
D. Five year overall survival for all GIST patients is about 50%.
A.
Tumor size, mitotic rate, and location are important prognostic factors in GIST. Tumors with a size < 5 cm have a 5-year overall survival of about 70%.
This drops to about 45% when tumor size is > 10 cm.
Similarly, about 75% of patients with < 5 per
high-power field will survive 5 years, only 20% of those with more than 5 per high-powered field are alive at 5 years. Tumors of gastric origin are more favorable than those originating in the small bowel, with survival rates of approximately 75% and 50%, respectively, after 5 years.
Tumor rupture before or during surgery also portends a poor prognosis, as discussed above. Given the mitotic rate of the tumor in
this case, the patient has a relatively poor prognosis.
Adjuvant therapy with imatinib for 1 year has been shown to increase recurrence free survival by 15% and, if continued for 3 years, improve 5-year overall survival by 10%. However, about half of all patients will develop resistance to the drug within 2 years of its initiation. For these patients, other tyrosine kinase inhibitors (i.e. sunitinib) remain effective second line therapy.
Historically, the overall survival for all patients with GIST at 5 years has been about 50%. However, in the era of imatinib, the 5-year OS has improved to 84%, though survival varies markedly between patients with Stage 1 tumors (nearly 100%) versus more Stage 3 and higher tumors (22%).
Which of the following is true of gastrointestinal stromal tumors?
A. Because they arise from the mucosa, GISTs are easily identified at endoscopy.
B. Surgical resection is often appropriate for patients with recurrent or metastatic GIST.
C. These tumors arise from the smooth-muscle cells of the intestinal wall.
D. GIST tends to arise as a solitary lesion.
E. Abdominal pain is the most common clinical manifestation of GIST.
D.
Gastrointestinal stromal tumors are more likely to be solitary than multiple. This stands in contrast to carcinoid tumors, which often occur multiply. They arise from the muscular layer of the intestinal wall, but
from the interstitial cells of Cajal, not the smooth muscle cells.
Their location in the muscular layer can make small GISTs somewhat difficult to detect and lead to underestimation of tumor extent by endoscopy.
At presentation, GIST is frequently found to be metastatic, most commonly to the liver or peritoneum. Presenting symptoms may include abdominal pain, dyspepsia, or early satiety, but gastrointestinal bleeding is the most common occurrence, leading to the eventual diagnosis of a GIST. Life-threatening hemorrhage from intraperitoneal rupture of these highly vascular tumors may also occur.
Generally speaking, imatinib chemotherapy is considered first line therapy for metastatic or recurrent GIST and surgical resection is often inappropriate due to high rates of recurrence.
However, some patients with tumors response to imatinib and lesions that are felt
to be completely resectable may benefit. I
A 56-year-old man with a 4-month history of vague epigastric abdominal pain, decreased appetite and weight loss presents to his local gastroenterologist for evaluation. An esophagogastroduodenoscopy (EGD) reveals
non-specific gastritis and a polypoid lesion in the region of the antrum. Laboratory findings note mild anemia, elevated LDH, and H. pylori positive samples from the EGD.
Follow-up endoscopic ultrasound (EUS) notes a thickened antral wall, and multiple biopsies obtained reveal an extra-nodal marginal zone B cell lymphoma of mucosa (gut)-associated lymphoid tissue (MALT) type (MALT lymphoma). Computed tomography of the
chest, abdomen, and pelvis reveals thickening of the distal half of the stomach with no evidence of adenopathy. Bone marrow biopsy reveals no evidence of disease dissemination.
After the patient has undergone a complete staging work-up as noted above, what stage low-grade gastric MALT lymphoma does this patient have?
A. Stage I
B. Stage II
C. Stage III
D. Stage IV
E. Unknown
A.
The staging of gastric lymphoma is paramount in the proper management of the disease. Although often indolent, approximately 10% of patients with gastric lymphoma will present with advanced disease.
EGD allows for visualization of the lesion and often tissue sampling as well as H. pylori diagnosis. Endoscopic ultrasound is also an important diagnostic procedure that can determine extent of disease, depth of invasion, and often allows more complete tissue sampling.
EUS also allows for accurate estimates of
depth of invasion, which is an important prognostic marker for disease recurrence. CT of the chest, abdomen, and pelvis is important to assess for disseminated disease while a bone marrow biopsy will detect evidence of distant disease in up to 15% of patients.
Standard laboratory testing includes complete blood count and LDH, as well as other standard chemistries.
Based on the National Comprehensive Cancer Network (NCCN) Clinical Practice Guidelines, the Lugano Staging System for Gastrointestinal Lymphoma is adequate. This modification of the Ann
Arbor Staging System is noted below, directly compared with the Ann Arbor Staging System.
Utilizing either staging system is appropriate. Based these staging systems, the above patient has Stage I disease.
Lugano Staging System
Stage I - The tumor is confined to the gastrointestinal tract. It can be a single primary lesion or multiple, noncontiguous lesions.
Stage II - The tumor extends into the abdomen. This is further subdivided based upon the location of nodal involvement:
• Stage II1 - Involvement of local nodes (paragastric nodes for gastric lymphoma or para-intestinal nodes for intestinal lymphoma)
• Stage II2: Involvement of distant nodes (paraaortic, para-caval, pelvic, or inguinal nodes for most tumors; mesenteric nodes in the case of
intestinal lymphoma)
• Stage IIE: The tumor penetrates the serosa to involve adjacent organs or tissues
Stage III - There is no stage III disease in this system.
Stage IV - There is disseminated extranodal involvement or concomitant supra-diaphragmatic nodal involvement.
Ann Arbor Staging System
Stage I - Involvement of a single lymph node region (I) or of a single extralymphatic organ or site (IE)*
Stage II - Involvement of two or more lymph node regions or lymphatic structures on the same side of the diaphragm alone (II) or with involvement of limited, contiguous extralymphatic
organ or tissue (IIE)
Stage III - Involvement of lymph node regions on both sides of the diaphragm (ID), which may include the spleen (HIS) or limited, contiguous extralymphatic organ or site (HIE) or both (IIIES)
Stage IV - Diffuse or disseminated foci of involvement of one or more extralymphatic organs or tissues, with or without associated lymphatic involvement
A 56-year-old man with a 4-month history of vague epigastric abdominal pain, decreased appetite and weight loss presents to his local gastroenterologist for evaluation. An esophagogastroduodenoscopy (EGD) reveals
non-specific gastritis and a polypoid lesion in the region of the antrum. Laboratory findings note mild anemia, elevated LDH, and H. pylori positive samples from the EGD.
Follow-up endoscopic ultrasound (EUS) notes a thickened antral wall, and multiple biopsies obtained reveal an extra-nodal marginal zone B cell lymphoma of mucosa (gut)-associated lymphoid tissue (MALT) type (MALT lymphoma). Computed tomography of the
chest, abdomen, and pelvis reveals thickening of the distal half of the stomach with no evidence of adenopathy. Bone marrow biopsy reveals no evidence of disease dissemination.
The proper surgical management of this patient with gastric lymphoma is:
A. Total gastrectomy with D2 lymph node dissection
B. Total gastrectomy with D1 lymph node dissection
C. Partial gastrectomy with D1 lymph node dissection
D. Partial/total gastrectomy with no lymph node dissection
E. Surgical resection is not warranted in most cases
E. Gastric lymphoma is the second most common gastric malignancy (behind gastric adenocarcinoma) and the most frequent cite of extra-nodal non-Hodgkin’s Lymphoma. For decades, surgical resection was considered appropriate therapy for all stages of “resectable” gastric lymphomas.
Although surgical resection has provided outstanding results and excellent long-term survival, stomach preserving methods have provided equivalent results without the morbidity associated with gastrectomy (partial or total) for both low-grade and high-grade B-cell lymphomas.
A prospective trial by the German Multicenter Trial group in 2005 examined 185 patients with Stage I and II low-grade gastric lymphoma and noted no difference in survival between those patients treated surgically and those receiving no surgical intervention.
A follow-up study by the same group examined an additional 393 patients and provided similar results. The results are similar for high-grade gastric lymphomas, where survival rates between primary
surgery and primary chemotherapy and radiation therapy groups is equivalent.
Surgical intervention for gastric lymphoma is largely reserved for rare cases of perforation, or hemorrhage that cannot be
controlled endoscopically.
Stomach preserving treatment strategies are now the standard of care in the management of gastric lymphoma.
A 56-year-old man with a 4-month history of vague epigastric abdominal pain, decreased appetite and weight loss presents to his local gastroenterologist for evaluation. An esophagogastroduodenoscopy (EGD) reveals non-specific gastritis and a polypoid lesion in the region of the antrum. Laboratory findings note mild anemia, elevated LDH, and H. pylori positive samples from the EGD.
Follow-up endoscopic ultrasound (EUS) notes a thickened antral wall, and multiple biopsies obtained reveal an extra-nodal marginal zone B cell lymphoma of mucosa (gut)-associated lymphoid tissue (MALT) type (MALT lymphoma).
Computed tomography of the chest, abdomen, and pelvis reveals thickening of the distal half of the stomach with no evidence of adenopathy. Bone marrow biopsy reveals no evidence of disease dissemination.
First line therapy for a MALT lymphoma as noted in the patient above would consist of which of the following?
A. Surgical resection
B. Radiation therapy
C. Chemotherapy
D. H. pylori eradication
E. Watchful waiting
D.
Gastric MALT lymphomas arise from B-cells and constitute approximately 50% of gastric lymphomas, with the diffuse large B-cell lymphoma making up the other large proportion of gastric lymphomas.
Although surgical therapy was considered the mainstay of therapy for decades, in the late 1980s, a connection between Campylobacter (later Helicobacter) pylori, chronic gastritis and mucosal associated lymphoid tissue (MALT) was suspected.
By the early 1990s, the connection between the two was firmly established and the treatment of gastric MALT lymphoma with H. pylori eradication was
instituted. A meta-analysis of 34 studies with 1271 patients noted an overall H. pylori eradication rate of 98.3%, associated with a complete remission of
gastric lymphoma in 77.8% of patients.
The relapse rate for patients was 2.2% per year, and only 0.05% of patients had transformation of low-grade lymphoma into an aggressive, high-grade lymphoma.
Frequent endoscopic monitoring (3 month intervals initially) is paramount to assess for treatment response. Patients with pathology revealing clearance of H. pylori and resolution of lymphoma will require continued surveillance. Those patients with persistent H. pylori should receive additional eradication therapy. If gastric lymphoma persists despite multiple rounds of anti-H. pylori therapy, the
addition of external beam radiation and/or chemotherapy is warranted.
Patients with H. pylori negative gastric MALT lymphoma often have a documented translocation t(ll;18), and thus eradication therapy is often not effective. These patients are treated with radiation
therapy as first-line therapy. Rituximab has shown some effectiveness in these patients as well, and is currently considered in those patients with persistent localized disease and a contraindication to radiotherapy.
What is the management for persistent, localized, MALT lymphoma following repeatedly failed efforts at H. pylori eradication therapy?
A. Radiation therapy
B. Surgical resection
C. Chemotherapy
D. Rituximab
E. Bevacicumab
A.
The management of persistent, localized, early stage gastric MALT lymphoma is radiation therapy. Although there are various approaches taken in the management of these patients, radiation therapy (external beam, 30-40 cGy) has shown excellent
results and is the recommended treatment by NCCN guidelines.
In general, first-line salvage therapy provides remission rates of 90.1%. Radiation therapy was superior to chemotherapy or surgery, with a 97.3% remission rate versus 92.5% for surgery, and 85.3% for chemotherapy.
In fact, radiation therapy as a sole therapy was found to be superior to even combined
modality approaches.
Further support for radiation therapy is provided by Goda, et al. who noted an overall remission rate of 92% with excellent long-term (10-year) survival data.
Additional studies show long-term remission rates of 88% to 97% (5 to 7.8 years).
For some patients with Stage I disease, chemotherapy may be added to radiotherapy, but this is not considered the standard approach.
Chemotherapy for low-grade gastric MALT lymphoma is typically reserved for persistent Stage II disease or patient presenting with more advanced disease (Stage IIE or IV).
The exact chemotherapeutic regimen for advanced stage gastric MALT lymphoma is not well established, but is often treated with agents utilized against follicular lymphomas.
How does the treatment strategy change in patients with high-grade gastric lymphoma (advanced MALT lymphoma or diffuse large B-cell lymphoma)?
A. Surgical resection
B. Radiation therapy alone
C. Chemotherapy alone
D. H. pylori eradication
E. Combined chemotherapy with or without radiation therapy
E.
As addressed earlier, surgical therapy has been largely abandoned as the primary treatment of gastric lymphoma, including patients with advanced gastric MALT lymphoma and gastric diffuse large B-cell lymphoma (DLBCL).
A study examining the long-term outcomes in patients treated with surgery alone, surgery followed by radiation therapy, surgery followed by chemotherapy and chemotherapy alone noted that complete response rates were similar in
the 4 arms.
But, survival was significantly improved in patients receiving chemotherapy, with no clear benefit to combined modality therapy with surgery and chemotherapy.
In fact, late toxicity was more frequent and severe in patients who had surgery.
In terms of H. pylori eradication, studies are ongoing. It was once thought that there was little benefit in treating H. pylori in these patients, since there was no MALT component in most patients.
Although there are cases exhibiting both gastric MALT lymphoma and DLBCL, first-line therapy was typically targeted at the more aggressive entity.
Recently, there has been some success noted with H. pylori eradication in early stage DLBCL patients that are H. pylori positive.
In comparing patients with pure gastric DLBCL and mixed (MALT and DLBCL), H. pylori eradication rates were 100% and 94.1%, respectively.
Remission rates were 68.8% for pure DLBCL and 56.3% for the mixed gastric DLBCL. Prospective studies are ongoing.
Currently, chemotherapy, with or without biologic therapy, is considered first-line therapy for gastric DLBCL, which is considered the more aggressive of the two most common gastric lymphomas.
NCCN clinical practice guidelines note that Stage I and II disease are treated with chemotherapy with localized radiation therapy added in certain cases.
The chemotherapeutic regimens utilized vary, but the most common regimen combines cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) and often the addition of a biologic agent (riuximab) (R-CHOP).
The CHOP regimen shows complete remission (CR) rates of 87% to 100% with good long-term survival.
An examination of the R-CHOP regimen reveals similar statistics with a CR rate of 87%, with the remaining 13%exhibiting a partial remission.
The addition of radiation therapy for early stage disease has been examined and there was a notable decrease in local recurrences in those patients treated with radiation therapy.
But, radiation therapy did not add to overall survival when compared with chemotherapy alone. Overall, radiation therapy is selectively added to chemotherapy in patients with gastric DLBCL, specifically for local control.
For patients with more advanced disease (specifically Lugano Stage IV), chemotherapy alone is utilized with radiation therapy reserved as needed for local control of symptoms.
A 58-year-old male presents to your clinic with upper abdominal pain and heartburn alter meals. He occasionally relieves symptoms with chewable antacids (calcium carbonate). He denies other problems except for gaining 5 lbs over the last year with decreased exercise. He has no surgical history, takes no medications, and has no significant family history. He used to smoke, but quit 15 years ago and drinks 2 glasses of red wine each night.
Other than improving his diet and decreasing his alcohol intake, what medication would you prescribe to best limit his esophageal acid exposure?
A. Proton pump inhibitor (PPI)
B. H2 receptor antagonist (H2RA)
C. Calcium carbonate
D. Sucralfate as needed
A.
The mainstay of medical treatment of GERD is acid suppression. Patients with persistent symptoms should be given PPIs, such as omeprazole. In doses as high as 40 mg/d, they can effect an 80% to 90% reduction in gastric acidity.
In patients with reflux disease, esophageal acid exposure is reduced by up to 80% with H,RAs and up to 95% with PPIs. Despite the superiority of the latter class of drug over the former, periods of acid breakthrough still occur.
A 58-year-old male presents to your clinic with upper abdominal pain and heartburn alter meals. He occasionally relieves symptoms with chewable antacids (calcium carbonate). He denies other problems except for gaining 5 lbs over the last year with decreased exercise. He has no surgical history, takes no medications, and has no significant family history. He used to smoke, but quit 15 years ago and drinks 2 glasses of red wine each night.
He is started on the medication and experiences relief. He returns to your clinic 1 year later, but now the medication is no longer relieving his symptoms. He also reports occasional cough and the sensation that he has to clear his throat. What should be your next step?
A. Esophagogastroduodenoscopy (EGD)
B. Perform barium swallow
C. Perform 24 hr ambulatory pH monitoring
D. Perform pulmonary function tests
A.
If after a year of successful symptom relief, the symptoms are no longer controlled by a single medication and he has developed extraesophageal symptoms (cough and sensation of postnasal drip) of GERD, then consideration should be given to prescribing another PPI.
It is important, though, to rule out ulcers, malignancy, a hiatal hernia, esophagitis or other esophageal, gastric, or duodenal erosive pathology. Therefore, EGD is the best option for direct mucosal visualization.
If no other pathology can account for the symptoms, a 24-hour pH monitoring would be the next step in diagnosis. This would determine if acid reflux is the cause of the patient’s symptoms.
A barium swallow could add some more information but is not diagnostic.
Halitosis would be an indicator of a diverticulum (Zenker’s) or possibly achalasia in which food is retained within the esophagus.
A better study to evaluate these pathologies is barium swallow esophagram. Pulmonary function tests are not indicated for evaluation of the patients cough.
A 58-year-old male presents to your clinic with upper abdominal pain and heartburn after meals. He occasionally relieves symptoms with chewable antacids (calcium carbonate). He denies other problems except for gaining 5 lbs over the last year with decreased exercise. He has no surgical history, takes no medications, and has no significant family history. He used to smoke, but quit 15 years ago and drinks 2 glasses of red wine each night.
He follows up in 3 weeks with a barium swallow, pH monitoring, and an EGD from an outside provider. He provides a copy of the 24 hr ambulatory pH monitoring report to you, which can be viewed below. He has a sliding (Type I) hiatal hernia, and
no evidence of intestinal metaplasia or ulcers.
ACID REFLUX COMPOSITE SCORE ANALYSIS (JOHNSON/DEMEESTER) (pH)
Upright time in reflux: 10.4% (5.1) (NV: <6.3)
Recumbent time in reflux: 10.0% (21.9) (NV: <1.2)
Total time in reflux: 10.2% (7.3) (NV: <4.2)
Episodes over 5 min: 5.4 (4.9) (NV: <3.1)
Longest episode: 41.7min (15.1) (NV: <9.2)
Total episodes: 48.6 (2.9) (NV: <50.1)
Composite score: 57.1 (NV: <22)
What is the intervention would you offer him at this time?
A. Esophagectomy
B. Nissen fundoplication
C. Heller myotomy with Dor fundoplication
D. Botulinum toxin injection
B.
The acid reflux composite score analysis shown is consistent with the diagnosis of GERD. Therefore, a Nissen fundoplication is an appropriate surgical choice for this patient with refractory GERD and a sliding hiatal hernia.
Since the patient does not have high-grade dysplasia or evidence of esophageal cancer, esophagectomy would not be the correct choice.
The patient has a type I sliding hiatal hernia, not a paraesophageal hernia (Types II, III, and IV), therefore answer C would not be correct (see diagram).
Botulinum toxin and Heller myotomy with Dor fundoplication are used in the treatment of achalasia, but would not be indicated in a patient with GERD.
What is the most common long-term complication of a Nissen fundoplication?
A. Stricture
B. Gastroesophageal leak
C. Gas bloat syndrome
D. Dysphagia
E. Slipped Nissen
D. Early complications of Nissen fundoplication: gastroesophageal leak, pneumothorax, abscess, and hematoma.
Of these, the most common is dysphagia.
Late complications of Nissan fundoplication: stricture, gas bloat syndrome, wrap disruption, wrap herniation, and dysphagia.
A 58-year-old male presents to your clinic with upper abdominal pain and heartburn alter meals. He occasionally relieves symptoms with chewable antacids (calcium carbonate). He denies other problems except for gaining 5 lbs over the last year with decreased exercise. He has no surgical history, takes no medications, and has no significant family history. He used to smoke, but quit 15 years ago and drinks 2 glasses of red wine each night.
He undergoes a Nissen fundoplication without complication and is discharged the following day. Five days after surgery, he returns for follow up appointment reporting left upper quadrant pain. He is hemodynamically normal and has a hemoglobin one point lower than his preoperative values. CT scan of the chest, abdomen, and pelvis shows a heterogeneous left upper quadrant fluid collection without rim enhancement and an associated small left pleural effusion.
What is the most appropriate initial management for this patient?
A. Admit for fluids and observation
B. Admit for antibiotics and total parenteral nutrition
C. Return to the operating room
D. Percutaneous drainage
A.
Development of fluid collection postoperatively without instability in vital signs, fever, WBC or other evidence of infection is most suspicious for hematoma.
The development of the collection of five days postoperatively would indicate a slow bleed, not requiring urgent reoperation.
Percutaneous drainage would increase the risk of introducing bacteria and infecting the fluid collection. Conservative management including hydration and observation is recommended for a small, stable hematoma. Antibiotics are not indicated without evidence of infection.
A 63-year-old female with a long history of gastroesophageal reflux disease presents to your clinic after a gastroenterologist performs an EGD. She is diagnosed with Barretts esophagus without evidence of dysplasia based upon the results of several biopsies.
When should her next EGD with biopsy be performed for appropriate surveillance?
A. 3 months
B. 6 months
C. 1 year
D. 3 years
C. Barrett’s esophagus without dysplasia has a risk of 0.1% to l%rate of progression to adenocarcinoma and initial surveillance should be with annual EGD with biopsy. Low grade dysplasia requires surveillance every 6 months until no dysplasia is found.
If no more dysplasia is found, surveillance can be extended to once every 3 years. High-grade dysplasia has a 5-year risk of adenocarcinoma of 30% and must be intervened upon with excision or ablation or
undergo endoscopic surveillance every 3 months.
A 63-year-old female with a long history of gastroesophageal reflux disease presents to your clinic after a gastroenterologist performs an EGD. She is diagnosed with Barretts esophagus without evidence of dysplasia based upon the results of several biopsies.
Her follow-up EGD demonstrates Barrett esophagus with low-grade dysplasia on multiple biopsies, so she is scheduled for follow up EGD in 6 months. She presents to the ER 12 hours later with rapid respirations, tachycardia, fever, and elevated WBC. Based upon your clinical suspicions, what is the best initial diagnostic test?
A. Gastrografin esophagography
B. Thin barium esophagography
C. CT with IV contrast for PE/DVT protocol
D. EGD
A. The patient has suffered an iatrogenic esophageal perforation.
The best initial test for diagnosis of this is esophagram with water-soluble contrast such as gastrografin.
If this does not demonstrate leak, thin barium should be used next.
The WBC elevation and acute nature of the presentation in relationship to the EGD procedure makes PE less likely than esophageal perforation.
EGD would not be recommended in this scenario as it could enlarge the perforation.
A 63-year-old female with a long history of gastroesophageal reflux disease presents to your clinic after a gastroenterologist performs an EGD. She is diagnosed with Barretts esophagus without evidence of dysplasia based upon the results of several biopsies.
A small intrathoracic perforation is confirmed. In your determination of a management plan, which of the following is an absolute contraindication to non-operative management?
A. Time of perforation >72 hrs
B. A history of Barrett’s esophagus with low grade dysplasia
C. Perforation contained in the mediastinum
D. Evidence of SIRS (systemic inflammatory response syndrome)
D.
Operative management is imperative in the
patient who is becoming unstable (developing a SIRS response) as it may become life-threatening. It should be considered if the perforation is not well-contained, in the acute time period after the procedure, or there is associated malignancy. In contrast, non-operative
management should be considered if the time of perforation > 72 hrs, there is no evidence of associated malignancy, or the perforation is well-contained.
A 63-year-old female with a long history of gastroesophageal reflux disease presents to your clinic after a gastroenterologist performs an EGD. She is diagnosed with Barretts esophagus without evidence of dysplasia based upon the results of several biopsies.
The patient has a small thoracic esophageal perforation with a left sided effusion and is
developing low blood pressure. After beginning resuscitation, you determine she needs to go to surgery for repair of the leak. Based upon the most likely location of these types of injuries, which incision would you use to expose the esophagus for repair?
A. Right postcriolatcral thoracotomy
B. Left postcriolatcral thoracotomy
C. Median sternotomy
D. Laparotomy
B. The surgical approach to the distal esophagus is a left posteriolateral thoracotomy. Any esophageal injury should be buttressed with other tissue like nearby pleura, a pericardial at pad, pedicled intercostal muscle, or the diaphragm.
A 78-year-old female with arthritis and asthma presents to the emergency room with an acute onset of epigastric pain a couple of hours ago. Her pulse is 104, her blood pressure is unchanged trom her baseline of 110/74 mmHg, and her temperature is 98.2 Fahrenheit. Her medications include occasional naproxen and prednisone for occasional exacerbations of her asthma. On physical exam, her abdomen demonstrates significant epigastric tenderness with rebound. She has a mild leukocytosis of 12.5 cells/mcL. Her acute abdominal series demonstrates a small amount of free air.
1What is the most reasonable current treatment option for this patient as the next step?
A. Laparoscopic highly selective vagotomy without resuscitation
B. Nasogastric tube insertion, cessation of all oral feeds, & intravenous fluid initiation for the next 24 hours
C. Open truncal vagotomy with pyloroplasty
D. Open Graham patch with parietal cell vagotomy despite laparoscopic experience and resources
E. Emergent anterior seromyotomy
B. Of all the listed options, nasogastric tube insertion with NPO status and initiation of IV fluid is a very reasonable first step in the modern era of H. pylori detection and treatment, especially in a stable patient.
Graham patch with parietal cell vagotomy is also a very reasonable option but an
open approach is more problematic if laparoscopic experience and resources are available.
The verification of resuscitation is required prior to going to the operating room for patients. The verification in this patient can simply be assessing volume status (e.g.,
urine output of 0.5 cc/kg/hour or normal heart rate for a patient not on a beta-blocker.
Truncal vagotomy with pyloroplasty is not a first-line treatment in the modern era of H. Pylori. Anterior seromyotomy, division of the seromuscular layer of the lesser curvature in order to achieve a highly selective vagotomy effect, is a reasonable approach but not as a first option.
A 78-year-old female with arthritis and asthma presents to the emergency room with an acute onset of epigastric pain a couple of hours ago. Her pulse is 104, her blood pressure is unchanged trom her baseline of 110/74 mmHg, and her temperature is 98.2 Fahrenheit. Her medi¬
cations include occasional naproxen and prednisone for occasional exacerbations of her asthma. On physical exam, her abdomen demonstrates significant epigastric
tenderness with rebound. She has a mild leukocytosis of 12.5 cells/mcL. Her acute abdominal series demonstrates a small amount of free air.
If she does not demonstrate improvement during the 12 hours after onset of symptoms, what is the most reasonable and expedient next step?
A. Truncal vagotomy with antrectomy and a Billroth II reconstruction
B. Continued observation
C. Selective angioembolization
D. Laparoscopic Graham patch only and H. Pylori testing with possible treatment
E. Laparoscopic Graham patch with parietal cell vagotomy
D. Laparoscopic Graham patch with H. Pylori testing and subsequent testing is the best choice of those presented.
Truncal vagotomy with antrectomy is no longer a first- line option in the modern era of H. Pylori detection and treatment.
Observation is not reasonable if the patient is not improving and a more aggressive management choice is most likely necessary.
Angioembolization maybe considered for
bleeding peptic ulcer disease in selective cases but not for perforation of an ulcer. Parietal cell vagotomy is no longer considered one of the early line treatments but to be reserved as a treatment option for
refractory peptic ulcer disease.
A 78-year-old female with arthritis and asthma presents to the emergency room with an acute onset of epigastric pain a couple of hours ago. Her pulse is 104, her blood pressure is unchanged trom her baseline of 110/74 mmHg, and her temperature is 98.2 Fahrenheit. Her medications include occasional naproxen and prednisone for occasional exacerbations of her asthma. On physical exam, her abdomen demonstrates significant epigastric tenderness with rebound. She has a mild leukocytosis of 12.5 cells/mcL. Her acute abdominal series demonstrates a small amount of free air.
What testing should be done for follow-up?
A. Secretin stimulation test
B. H. pylori stool antigen testing
C. Emergent urea breath testing
D. Colonoscopy
E. Both A and C
B.
H. Pylori stool antigen testing is a very reasonable approach and can even be ordered semi emergently in the emergency room at some institutions to help in decisions with early treatment options.
Secretin stimulation test is utilized for gastrinoma work-up, which is not yet necessary during this part of the work-up for this patient since recalcitrant peptic ulcer disease is not yet identified.
Urea breath testing for H. pylori is reasonable but is not an emergent process as obtaining this test requires a clinical lab.
Colonoscopy is reasonable in a patient over the age of 50 who has not had a screening process done but is not required to address the follow-up for peptic ulcer disease perforation.
A 78-year-old female with arthritis and asthma presents to the emergency room with an acute onset of epigastric pain a couple of hours ago. Her pulse is 104, her blood pressure is unchanged trom her baseline of 110/74 mmHg, and her temperature is 98.2 Fahrenheit. Her medications include occasional naproxen and prednisone for occasional exacerbations of her asthma. On physical exam, her abdomen demonstrates significant epigastric tenderness with rebound. She has a mild leukocytosis of 12.5 cells/mcL. Her acute abdominal series demonstrates a small amount of free air.
What further follow-up is necessary if she has no further symptoms?
A. Long-term intravenous pantoprazole
B. Nothing
C. Chronic suppressive antibiotics
D. Serum gastrin level
E. Esophagogastroduodenoscopy with biopsy of ulcer if still present
E.
Esophagogastroduodenoscopy (EGD) is necessary to rule out a gastric carcinoma that caused the perforation, especially in older patients. Pantoprazole, another proton-pump inhibitor, or H2 blockers
are reasonable to start on admission for perforated peptic ulcer disease but long-term treatment is not absolutely necessary, especially after treatment for H. Pylori.
Treatment of H. Pylori with a course of
antibiotics but chronic suppression should not be necessary. Serum gastrin level can be checked for a patient who is suspected of gastrinoma but is not necessary if the patient’s peptic ulcer is healed.
A 51-year-old female presents to the emergency department. She complains of abdominal pain that has gotten worse over the last several days. The pain is sharp and
located right under her “breast bone.” It seems to happen right after she eats or drinks and this morning it doubled her over.
She relates that she has had this feeling
before, but it was never this bad. She has some nausea but no vomiting.
Past medical history is significant for hypertension, obstructive sleep apnea on CPAP, hypercholesteremia, and type 2 diabetes (which she states has been normal since her one month post op visit).
Her surgical history is significant for one C-section about 15 years ago and a laparoscopic gastric bypass 9 months ago. She denies any drug use. She drinks a glass of red wine most evenings to “help her heart.”
After much probing she relates that even though she quit smoking 6 months prior to surgery, she resumed smoking about 6 months ago and is back up to one pack per day. She relates that at the time of her surgery she weighed 345 lbs with a BMI of 59 kg/m2 and now has lost 120 lbs with a BMI of 38.6 kg/m2. She hasn’t seen a bariatric surgeon since her 3 month postoperative visit, mostly because she is embarrassed that she started smoking
again. She stopped taking her omeprazole 4 months ago when her prescription ran out. She also started taking 81mg aspirin after watching a documentary on heart disease and obesity.
Vital signs are: HR 115, BP 97/62, RR 18, Pulse Ox 98% on RA. Her exam is noted to have diffuse abdominal tenderness, significant tenderness in the epigastrium, with voluntary guarding. Bowel sounds are absent. Hemo-occult testing is positive.
Which of the following is a factor that is potentially contributing to this patient’s current problem?
A. Hypercholesterolemia
B. Active smoking
C. Obstructive sleep apnea
D. Increase in carbohydrate intake
E. Age >50
B.
This patient most likely has a marginal ulcer,
which, at a rate of about 5% after Roux-en-Y gastric bypass, is one of the more common complications.
Risk factors associated with the development of marginal (gastrojejunal/anastomotic) ulcers include environmental (smoking and alcohol), medication (NSAIDs), anatomical (gastro-gastric fistula or an enlarged gastric pouch), and technique (use of nonabsorbable sutures).
There is no link associated with specific food types and ulcer formation. Other risk factors that are associated with marginal ulcer (MU)
are increased acid exposure via a gastro-gastric fistula (not confirmed in this patient but more commonly seen with patients that have had an open gastric bypass versus laparoscopic), hypertension, and use of non-absorbable suture in the anastomosis and recent surgery.
Which of the following is the most common
complication (early or late) following laparoscopic gastric bypass?
A. Internal hernias
B. Small bowel obstruction
C. Marginal ulceration (anastomotic/gastro-jejunal ulcer)
D. Gastrojejunal leak
C.
Marginal ulcers are a late complication of gastric bypass surgery. Along with gastrojejunostomy (GJ) stricture they are one of the most common complications (early or late) of gastric bypass surgery.
Reported rates of MU range from 1% to 25%, with most series indicating 5% incidence. GJ stricture rates are reported between 3% to 27%. The incidence of internal hernia after gastric bypass is nearly non-existent in the open gastric bypass, but after laparoscopic gastric bypass occurs in approximately 2.5% of patients.
Small bowel obstruction is linked to internal hernia formation and the rates are equivalent. GJ leaks are an early complication after gastric bypass.
In the laparoscopic approach, rates are reported at about 1% to 1.8%.
Which of the following statements is true with regards to marginal ulcer following gastric bypass?
A. Most marginal ulcers are asymptomatic.
B. Over one-third of patients with marginal ulcer formation smoke.
C. Active H. pylori infection is an independent risk factor for ulcer perforation.
D. Use of proton pump inhibitors is not protective of ulcer formation in the setting of nonsteroidal anti-inflammatory drugs (NSAID) use.
E. Suture material or type of anastomosis performed does not relate to ulcer formation.
B.
Of patients presenting with MU, over 30% are found to be smoking at the time of diagnosis. Most MU are symptomatic (72%).
Those symptoms that are most common after surgery that lead to the diagnosis of MU are: pain (34%), dysphagia (17%), weight gain (13%), nausea and vomiting (8%), and GI bleed (3%).
Active H. pylori infection has not been determined to be an independent risk factor in the development of perforated MU. There is data that suggests that in the setting of patients that must use NSAIDs following gastric bypass that proton pump inhibitors (PPIs) are protective of MU formation.
While there is still debate as to whether hand-sewn gastrojejunostomy (GJ) versus stapled anastomosis is better with relationship to post operative outcomes, the data clearly relates that non-absorbable suture material at the anastomosis has a high association with MU formation. Because of this fact, the use of non-absorbable suture at the GJ anastomosis has essentially ceased.
Regarding treatment of marginal ulcers (MU) following gastric bypass:
A. The majority can be successfully managed medically.
B. Nearly half of patients will require revision of the gastrojejunostomy for persistent and/or recurrent ulcers.
C. Late MU are self-limiting and rarely require treatment.
D. H. pylori infection pre-operatively or persistence postoperatively increases perforation rates.
E. Endoscopy is of limited value in the treatment of marginal ulcer.
A. The Ireatment of MU is largely medical. The standard of treatment is PPI therapy initiation/continuation and cytoprotective agents (i.e., sucralfate or carafate).
Additionally cessation of smoking and/or NSAID use is critical, as recurrence is high
in patients that continue with these high level risk factors.
Studies report the incidence of surgical intervention for MU to be 4% to 10%. This usually occurs in this subset of MU for recalcitrant and/or recurrent ulcers. Continued smoking and NSAID use were found to be independent risk factors for
continued non-healing ulcers. Late ulcers (those that occur after 30 days) are rarely self-limiting. In a study by Csendes they did a prospective evaluation of patients and performed endoscopy at 1 month and at 1 to 2 years. They found a 12% rate of MU at 1 month. Many authors believe this to be part of the natural progression and healing process of the anastomosis within such a short time frame. Most clinicians advocate for PPI use in the immediate postoperative period because of this. Clinically apparent MU is unlikely to heal without intervention (as mentioned above).
While the data is not completely clear about the role of II. pylori infection and ulcer formation, the risk of perforation of MU is not increased by the presence of H. pylori. One study found that in patients that were H. pylori positive and eradicated prior to surgery, the rate of MU after surgery with short term PPI use was significantly reduced.
Endoscopy should be part of the armamentarium of diagnosing and treating MU. Most ulcers become apparent within the first 12 months following surgery. While they can develop beyond 18 months following surgery this is not the most common time frame that they are seen.
The incidence of perforation in all patients undergoing laparoscopic gastric bypass is approximately 1% and the incidence of MU on average is 5% (range l%to 16%), therefore the rate of perforation of MU is 20%.
Felix et al. in 2008 found that many cases could be managed laparoscopically. In their series, over 30% were managed by oversewing of the ulcer and utilizing an
omental patch. Other series have confirmed similar treatment strategies for MU perforation utilizing the omental patch.
Times when it may be necessary or more appropriate to consider revising the G-J may
include MU with bleeding, with or without perforation; recurrent ulceration, when a gastro-gastric fistula is present; or when the pouch is greatly enlarged.
A 41-year-old female has a history of a Billroth II gastric bypass. Since the operation, the patient has had frequent nausea and vomiting and experiences palpitations dizziness, and flushing after meals. All of the following are management options for this patient except:
A. High protein diet
B. Octreotide
C. Conversion to Roux-en-Y bypass
D. Shortening of the afferent limb
E. Creation of a jejunal pouch
D. Shortening of the afferent limb
A 62-year-old male comes to the emergency room complaining of abdominal pain and bilious vomiting. He had a Billroth II procedure performed two weeks ago for intractable ulcer disease. A contrast barium study shows an obstructed loop of bowel. Which of the following is true regarding limb obstruction after a Billroth II?
A. An efferent loop obstruction is treated with a Roux-en-Y gastrojejunostomy
B. Chronic afferent loop obstruction may lead to megaloblastic anemia
C. Afferent loop obstructions often occur due to a retrocolic position of the anastomosis
D. Obstruction of the efferent limb can lead to accumulation of hepatobiliary secretions in a blind loop
E. Complete obstructions of the afferent loop often resolve with conservative management
B. Chronic afferent loop obstruction may lead to megaloblastic anemia
A 52-year-old male with a past medical history of peptic ulcer disease presents to the emergency department with burning abdominal pain and dark, tarry stools. An EGD is performed to evaluate a possible bleeding ulcer. Which of the following findings has the highest risk of rebleeding?
A. Ulcer with a central black spot
B. Nonbleeding visible vessel
C. Diffuse gastritis
D. An adherent clot
E. Ulcer with a clean base
B. Nonbleeding visible vessel
Which of the following is associated with large sliding hiatal hernias?
A. Curling’s ulcer
B. Cushing’s ulcer
C. Cameron’s ulcer
D. Marjolin’s ulcer
E. Marginal ulcer
C. Cameron’s ulcer
A 52-year-old male presents to the emergency room with hematemesis. He undergoes an EGD which shows active bleeding from a duodenal ulcer. There is a visible vessel at the base of the ulcer which is clipped, and epinephrine is injected. The bleeding is controlled, and the patient is transferred to the ICU for further management. Twelve hours later, he develops recurrent hematemesis. He is hemodynamically stable. What is the next best course of action?
A. Antrectomy and Billroth II reconstruction
B. Duodenotomy and oversewing of the gastroduodenal artery (GDA) with sutures placed superiorly, inferiorly, medially to the ulcer
C. Duodenotomy and oversewing of the GDA with sutures placed superiorly, inferiorly and laterally to the ulcer
D. Repeat endoscopy
E. Angiogram with attempted embolization
D. Repeat endoscopy
A 55-year-old female presents to the ER complaining of substernal chest pain and blood stools. She has a history of poorly controlled peptic ulcer disease. An NG lavage is performed, which is positive for bright red blood. The patient is taken to the OR for repair of a bleeding ulcer. The surgeon decides to proceed with a truncal vagotomy once the bleeding is controlled. Which of the following is TRUE regarding a truncal vagotomy?
A. Shown to benefit Type I and Type IV ulcers
B. Complications include a slowed emptying of liquids due to a loss of receptive relaxation
C. Majority of patients will have post-operative chronic diarrhea
D. A truncal vagotomy decreases acidic output by 50%
E. Incomplete transection of the left vagus is more common than the right
D. A truncal vagotomy decreases acidic output by 50%
Review Modified Johnson Classification
A 45-year-old female with a history of Crohn’s disease presents to the ER with abdominal pain, vomiting, and distension. A CT scan shows inflammatory changes and a stricture located at the proximal duodenum causing an obstruction. After one week of conservative management, the patient has no improvement in symptoms. What is the BEST surgical option for the patient?
A. No surgery unless complicated by perforation, fistula or abscess to avoid bowel shortening
B. Heineke-Mikulicz stricturoplasty
C. Finney stricturoplasty
D. Gastrojejunostomy
E. Whipple procedure
D. Gastrojejunostomy
The consistently largest artery to the stomach is the
A. Right gastric
B. Left gastric
C. Right gastroepiploic
D. Left gastroepiploic
B
The consistently largest artery to the stomach is the left gastric artery, which usually arises directly from the celiac trunk and divides into an ascending and descending branch along the lesser gastric curvature. Approximately 20% of the time, the left gastric artery supplies an aberrant vessel that travels in the gastrohepatic ligament (lesser omentum) to the left side of the liver.
Rarely, this is the only arterial blood supply to this part of the liver, and inadvertent ligation may lead to clinically significant hepatic ischemia in this unusual circumstance.
Which of the following inhibits gastrin secretion?
A. Histamine
B. Acetylcholine
C. Amino acids
D. Acid
D
Luminal peptides and amino acids are the most potent stimulants of gastrin release, and luminal acid is the most potent inhibitor of gastrin secretion.
The latter effect is predominantly mediated in a paracrine fashion by somatostatin released from antral D cells.
Gastrin-stimulated acid secretion is significantly blocked by H2 antagonists, suggesting that the principal mediator of gastrin-stimulated acid production is histamine from mucosal enterochromaffin-like (ECL) cells.
Acetylcholine released by the vagus nerve leads to stimulation of ECL cells, which in turn produce histamine.
Helicobacter pylori infection primarily mediates duodenal ulcer pathogenesis via
A. Antral alkalinization leading to inhibition of somatostatin release
B. Direct stimulation of gastrin release
C. Local inflammation with autoimmune response
D. Upregulation of parietal cell acid production
A
Helicobacter pylori possess that enzyme urease, which converts urea into ammonia and bicarbonate, thus creating an environment around the bacteria that buffers the acid secreted by the stomach.
H. pylori infection is associated with decreased levels of somatostatin, decreased somatostatin messenger RNA production, and fewer somatostatin-producing D cells.
These effects are probably mediated by H. pylori-induced local alkalinization of the antrum (antral acidification is the most potent antagonist to antral gastrin secretion), and H. pylori-mediated increases in other local mediators and cytokines.
The result is hypergastrinemia and acid hypersecretion, presumably leading to the parietal cell hyperplasia seen in many patients with duodenal ulcer.
Other mechanisms whereby H. pylori can induce gastrointestinal mucosal injury include the production of toxins (vacA and cagA), local elaboration of cytokines (particularly interleukin-8) by infected mucosa, recruitment of inflammatory cells and release of inflammatory mediators, recruitment and activation of local immune factors, and increased apoptosis.
The effect of erythromycin on gastric emptying is through its function as a
A. Dopamine antagonist
B. Cholinergic agonist
C. Motilin agonist
D. Cholinergic antagonist
C
Erythromycin is a common prokinetic agent used to treat delayed gastric emptying, and works as a motilin agonist.
Domperidone and metoclopramide, two other commonly used medications, function as dopamine antagonists.
Metoclopramide 10mg PO QID (Dopamine antagonist)
Erythromycin 250mg PO QID (Motilin agonist)
Domperidone 10mg PO QID (Dopamine antagonist)
Which if the following is secreted by gastric parietal cells?
A. Pepsinogen
B. Intrinsic factor
C. Gastrin-releasing peptide
D. Ghrelin
E. Histamine
B
Activated parietal cells secrete intrinsic factor in addition to hydrochloric acid. Presumably the stimulants are similar, but acid secretion and intrinsic factor secretion may not be linked.
Intrinsic factor binds to luminal vitamin B12, and the complex is absorbed in the terminal ileum via mucosal receptors.
Vitamin B12 deficiency can be life-threatening, and patients with total gastrectomy or pernicious anemia require B12 supplementation by a non-enteric route.
The most accurate diagnostic test or Zollinger-Ellison Syndrome (ZES) is
A. Fasting serum gastrin
B. Computed tomography (CT) scan
C. Endoscopy
D. Secretin stimulation test
D
All patients with gastrinoma have an elevated gastrin level, and hypergastrinemia in the presence of elevated basal acid output (BAO) strongly suggests gastrinoma.
Patients with gastrinoma usually have a BAO >15mEq/h or >5 mEq/h if they have had a previous procedure or peptic ulcer.
Acid secretory medications should be held for several days before gastrin measurement, because acid suppression may falsely elevate gastrin levels.
Causes of hypergastrinemia can be divided into those associated with hyperacidity and those associated with hypoacidity.
The diagnosis of Zollinger-Ellison syndrome (ZES) is confirmed by the secretin stimulation test.
An intravenous (IV) bolus of secretin (2 U/kg) is given and gastrin levels are checked before and after injection. An increase in serum gastrin of 200 pg/mL or greater suggests the presence of gastrinoma.
Patients with gastrinoma should have serum calcium and parathyroid hormone levels determined to rule out multiple endocrine neoplasia type 1 (MEN1) and, if present, parathyroidectomy should be considered before resection of gastrinoma.
See figure 26-1 (p.205, Schwartz ABSITE 10th Ed)
Which of the following is the preoperative imaging study of choice for gastrinoma?
A. CT scan
B. Magnetic resonance imaging (MRI)
C. Endoscopic ultrasound (EUS)
D. Angiographic localization
E. Somatostatin receptor scintigraphy
E
CT will detect most lesions >1cm in size and magnetic resonance imaging (MRI) is comparable.
Endoscopic ultrasound (EUS) is more sensitive than these other noninvasive imaging tests, but it still misses many of the smaller lesions, and may confuse normal lymph nodes for gastrinomas.
Currently, the preoperative imaging study of choice for gastrinoma is somatostatin-receptor scintigraphy (the octreotide scan).
When the pretest probability of gastrinoma is high, the sensitivity and specificity of this modality approach 100%.
Gastrinoma cells contain type II somatostatin receptors that bind the indium-labeled somatostatin analogue (octreotide) with high affinity, making imaging with a gamma camera possible.
Currently, angiographic localization studies are infrequently performed for gastrinoma. (See Schwartz 10th ed., pp.1072–1073.)
Patients taking nonsteroidal anti-inflammatory drugs (NSAIDs) or aspirin need concomitant acid suppressing medication if which of the following is present?
A. Age over 50
B. Heavy smoking history
C. Concurrent steroid intake
D. Heavy alcohol consumption
C
The overall risk of significant serious adverse gastrointestinal (GI) events in patients taking nonsteroidal anti-inflammatory drugs (NSAIDs) is more than three times that of controls.
This risk increases to five times in patients older than 60 years.
Factors that clearly put patients at increased risk for NSAID-induced GI complications include age >60, prior GI event, high NSAID dose, concurrent steroid intake, and concurrent anticoagulant intake.
Alcohol is commonly mentioned as a risk factor for peptic ulcer disease (PUD), but confirmatory data are lacking.
High doses of H2 blockers have been shown to be less effective than proton pump inhibitors (PPIs) in preventing GI complications in these high risk patients on antiplatelet therapy, but clearly they are better than no acid suppression.
(See Schwartz 10th ed., table26-6,p.1058.)
The optimal initial management of a patient hospitalized for a bleeding peptic ulcer is
A. Ulcer oversew
B. Vagotomy and pyloroplasty
C. Distal gastrectomy
D. Intravenous PPIs
Answer: D
The management of bleeding peptic ulcer is summarized in the algorithm in Fig. 26-2.
All patients admitted to hospital with bleeding peptic ulcer should be adequately resuscitated and started on continuous IV PPI.
Seventy-five percent of patients will stop bleeding with these measures alone, but 25% will continue to bleed or will rebleed in hospital.
Among the high risk group, endoscopic hemostatic therapy is indicated and usually successful. Only then should surgical intervention be considered, with indications including massive hemorrhage unresponsive to endoscopic control and transfusion requirement of more than four to six units of blood, despite attempts at endoscopic control.
Long-term maintenance PPI therapy should be considered in all patients admitted to hospital with ulcer complications.
(See Schwartz 10th ed., Figure 26-42, pp. 1061, 1064–1065, and 1069.)
Which of the following options is the least preferable reconstruction for patients undergoing antrectomy for PUD?
A. Billroth I.
B. Billroth II.
C. Roux-en-Y gastrojejunostomy.
D. All are equally preferable.
C
Following antrectomy, GI continuity may be reestablished with a Billroth I gastroduodenostomy or a Billroth II loop gastrojejunostomy.
Since antrectomy routinely leaves a 60 to 70% gastric remnant, routine reconstruction as a Roux-en-Y gastrojejunostomy should be avoided.
Although the Roux-en-Y operation is an excellent procedure for keeping duodenal contents out of the stomach and esophagus, in the presence of a large gastric remnant, this reconstruction will predispose to marginal ulceration and/or gastric stasis.
(See Schwartz 10th ed., p. 1063.)
A 55-year-old executive who is seen because of severe epigastric pain is found on esophagogastroduodenoscopy to have a large ulcer in the duodenal bulb and tests positive for H. pylori.
He is treated for H. pylori and instructed to quit smoking, but his symptoms persist and he is referred to you for further management. At this time, it would be most appropriate to recommend
A. NSAID cessation and urea breath test
B. Highly selective vagotomy
C. Truncal vagotomy and antrectomy
D. Truncal vagotomy and pyloroplasty
A
The indications for surgery in PUD are bleeding, perforation, obstruction, and intractability or nonhealing.
Intractability should be an unusual indication for peptic ulcer operation nowadays. The patient referred for surgical evaluation because of intractable PUD should raise red flags for the surgeon: maybe the patient has a missed cancer, is noncompliant, or has Helicobacter despite the presence of a negative test or pre- vious treatment (differential for intractability, Table 26-3).
In this setting, the patient with persistent symptoms despite appropriate treatment requires further evaluation before any consideration of operative treatment.
If surgery is necessary, a lesser operation may be preferable.
(See Schwartz 10th ed., Table 26-13, pp. 1059 and 1069–1071.)
Which blood group is associated with an increased risk of gastric cancer?
A. A
B. B
C. AB
D. O
Answer: A
Gastric cancer is more common in patients with pernicious anemia, blood group A, or a family history of gastric cancer.
When patients migrate from a high-incidence region to a low-incidence region, the risk of gastric cancer decreases in the subsequent generations born in the new region.
This strongly suggests an environmental influence on the development of gastric cancer.
Environmental factors appear to be more related etiologically to the intestinal form of gastric cancer than the more aggressive diffuse form.
The commonly accepted risk factors for gastric cancer are listed in Table 26-4.
(See Schwartz 10th ed., Table 26-15, pp. 1074–1075.)
A subtotal gastrectomy with D2 dissection performed for Stage 3 gastric adenocarcinoma in the antrum includes
A. Grossly negative margins of 2cm
B. More than 15 lymph nodes removed
C. Billroth II reconstruction
D. Splenectomy
Answer: B
Surgical resection is the only curative treatment or gastric cancer and most patients with clinically resectable locoregional disease should have gastric resection.
The standard operation or gastric cancer is radical subtotal gastrectomy, which entails ligation of the left and right gastric and gastroepiploic arteries at the origin, as well as the en bloc removal of the distal 75% of the stomach, including the pylorus and 2cm of duodenum, the greater and lesser omentum, and all associated lymphatic tissue.
Generally, the surgeon strives for a grossly negative margin of at least 5cm.
More than 15 resected lymph nodes are required or adequate staging, even in the low-risk patient. The operation is deemed an adequate cancer operation provided that tumor-free margins are obtained, >15 lymph nodes are removed, and all gross tumor is resected.
In the absence of involvement by direct extension, the spleen and pancreatic tail are not removed.
Reconstruction is usually by Billroth I gastrojejunostomy or Roux-en-Y reconstruction.
(See Schwartz 10th ed., p. 1081.)
The standard treatment for an isolated 3cm gastrointestinal stromal tumor (GIST) in the body of the stomach is
A. Imatinib
B. Endoscopic ablation
C. Wedge resection
D. Subtotal gastrectomy
Answer: C
Gastrointestinal stromal tumors (GISTs) are submucosal tumors that are slow growing, and arise from interstitial cells of Cajal (ICC).
Prognosis in patients with GISTs depends mostly on tumor size and mitotic count, and metastasis, when it occurs, is typically by the hematogenous route.
Any lesion >1cm can behave in a malignant fashion and may recur. Thus, all GISTs are best resected along with a margin of normal tissue—wedge resection with clear margins is adequate surgical treatment.
True invasion of adjacent structures by the primary tumor is evidence of malignancy.
If safe, en bloc resection of involved surrounding organs is appropriate to remove all tumor when the primary is large and invasive.
Five-year survival following resection for GIST is about 50%. Most patients with low-grade lesions are cured (80% 5-year survival), but most patients with high-grade lesions are not (30% 5-year survival).
Imatinib, a chemotherapeutic agent that blocks the activity of the tyrosine kinase product of c-kit, yields excellent results in many patients with metastatic or unresectable GIS, and is also recommended in high risk groups as an adjuvant therapy.
Fig. 26-3 shows an algorithm
for treatment of patients with GIST.
(See Schwartz 10th ed., Figure 26-59, pp. 1085–1086.)
Which of the following options is the best management of a low-grade gastric lymphoma of the gastric antrum?
A. H. pylori eradication
B. Chemotherapy ± radiationtherapy
C. Wedge resection
D. Antrectomy
Answer:A
Low-grade mucosa-associated lymphoid tissue (MALT) lymphoma, essentially a monoclonal proliferation of B cells, presumably arises from a background of chronic gastritis associated with H. pylori.
These relatively innocuous tumors then undergo degeneration to high-grade lymphoma, which is the usual variety seen by the surgeon.
Remarkably, when the H. pylori are eradicated and the gastritis improves, the low- grade MALT lymphoma often disappears.
Thus, low-grade MALT lymphoma is NOT a surgical lesion.
An algorithm or gastric lymphoma treatment is found in Fig. 26-4.
(See Schwartz 10th ed., Figure 26-58, pp. 1084–1085.)
Type III gastric carcinoid tumors
A. Often do not require resection
B. Are associated with hypergastrinemia
C. Are sporadic lesions
D. Have better outcomes than typeI and II tumors
Answer: C
Type III gastric carcinoids are sporadic tumors, most often solitary (usually>2cm), occur more commonly in men, and behave more aggressively than types I and II.
Unlike types 1 and II, they are not associated with hypergastrinemia.
Type I gastric carcinoids are the most common type of gastric carcinoid, and occur in patients with chronic hypergastrinemia secondary to pernicious anemia or chronic atrophic gastritis.
Type II is rare, and is associated with MEN1 and ZES.
Gastric carcinoids should all be resected,
and small lesions (<2cm) conjoined to the mucosa may be treated endoscopically with endoscopic mucosal resection (EMR) if there are only a few lesions (<5) and if margins are histologically negative.
Locally invasive lesions, or those >2 cm, should be removed by radical gastric resection and lymphadenectomy.
Survival is excellent for node-negative patients (>90% 5-year survival); node-positive patients have a 50% 5-year survival.
The 5-year survival or patients with type I gastric carcinoid is close to 100%; for patients with type III lesions, the 5-year survival is less than 50%.
Most type III patients have nodal or distant metastases at the time of diagnosis, and some present with symptoms of carcinoid syndrome.
(See Schwartz 10th ed., p. 1086.)
Watermelon stomach is best treated by
A. Acid-reducing agents
B. Beta-blockers
C. Antrectomy
D. Total gastrectomy
Answer: C
The parallel red stripes atop the mucosal folds of the distal stomach give this rare entity its name.
Histologically, gastric antral vascular ectasia (GAVE) is characterized by dilated mucosal blood vessels that often contain thrombi, in the lamina propria.
Mucosal fibromuscular hyperplasia and hyalinization often are present (Fig. 26-5). The histologic appearance can resemble portal hypertensive gastropathy, but the latter usually affects the proximal stomach, whereas watermelon stomach predominantly affects the distal stomach.
Beta blockers and nitrates, useful in the treatment of portal hypertensive gastropathy, are ineffective in patients with gastric antral vascular ectasia.
Patients with GAVE are usually elderly women with chronic GI blood loss requiring transfusion.
Most have an associated autoimmune connective tissue disorder, and at least 25% have chronic liver disease.
Nonsurgical treatment options include estrogen and progesterone, and endoscopic treatment with the neodymium yttrium- aluminum garnet (Nd:YAG) laser or argon plasma coagulator.
Antrectomy may be required to control blood loss, and this operation is quite effective but carries increased morbidity in this elderly patient group.
Patients with portal hypertension and antral vascular ectasia should be considered for transjugular intrahepatic portosystemic shunt (TIPSS).
(See Schwartz 10th ed., Figure 26-61, pp. 1088–1089.)
Treatment for severe early dumping after gastrectomy that is persistent despite an antidumping diet and fiber is
A. Expectant management
B. Oral glucose for symptoms
C. Octreotide
D. Surgical conversion to a Roux-en-Y drainage
Dumping is a phenomenon consisting of a constellation of postprandial symptoms thought to be the result o the abrupt delivery of a hyperosmolar load into the small bowel due to ablation of the pylorus or decreased gastric compliance.
Early dumping occurs 15 to 30 minutes after a meal, with patients becoming diaphoretic, weak, light-headed, and tachycardic.
Late dumping occurs hours later, and is due to a reactive hypoglycemia. Late dumping is relieved by the administration of sugar.
The medical therapy for the dumping syndrome consists of dietary management and somatostatin analogue (octreotide). Often, symptoms improve if the patient avoids liquids during meals.
Hyperosmolar liquids (eg, milk shakes) may be particularly troublesome. There is some evidence that adding dietary fiber compounds at mealtime may improve the syndrome.
If dietary manipulation fails, the patient is started on octreotide, 100 μg subcutaneously twice daily. This can be increased up to 500 μg twice daily if necessary. The long-acting depot octreotide preparation is useful. Octreotide not only ameliorates the abnormal hormonal pattern seen in patients with dumping symptoms, but also promotes restoration of a fasting motility pattern in the small intestine (ie, restoration o the migrating motor complex [MMC]).
Only a very small percentage of patients with dumping symptoms ultimately require surgery. Therefore, the surgeon should not rush to re-operate on the patient with dumping syndromes.
(See Schwartz 10th ed., p. 1091.)
Ménétrier disease is characterized by
A. Hypertrophic gastric folds and hypoproteinemia
B. A tortuous submucosal congenital arteriovenous malformation
C. Gastric antral vascular ectasia
D. Epithelial hyperplasia and hypergastrinemia
Answer: A
There are two clinical syndromes characterized by epithelial hyperplasia and giant gastric folds: ZES and Ménétrier disease.
The latter is characteristically associated with protein-losing gastropathy and hypochlorhydria.
A few patients with these unusual diseases have been successfully treated with the epidermal growth factor receptor blocking monoclonal antibody cetuximab.
There may be an increased risk of gastric cancer with this disease, and gastric resection may be indicated for bleeding, severe hypoproteinemia, or cancer.
The other options describe Dieulafoy lesions, watermelon stomach, and ZES, respectively.
(See Schwartz 10th ed., p. 1088.)
A 52-year-old male presents to the emergency department with hematemesis. He undergoes an EGD which shows active bleeding from a duodenal ulcer. There is a visible vessel at the base of the ulcer which is clipped, and epinephrine is injected. The bleeding is controlled, and the patient is transferred to the ICU for further management. Twelve hours later, he develops recurrent hematemesis. He is hemodynamically stable. What is the next BEST course of action?
a. Antrectomy and Billroth II reconstruction
b. Duodenotomy and oversewing of the gastroduodenal artery
c. Repeat endoscopy
d. Angiogram with attempted embolization
c. Repeat endoscopy
A 66-year-old female presents to your office with severe epigastric abdominal pain, bilious vomiting, and weight loss. The vomiting sometimes awakens her from sleep. It is not projectile in nature. She does not get any relief with over the counter antacids or omeprazole. There is no relief with food. She has a history of a stomach surgery 25 years ago for “ulcer disease”.What is the BEST treatment option for this patient?
a. Cholecystectomy
b. Nissen fundoplication
c. Conversion of previous gastric surgery to Roux-en-Y reconstruction
d. Shortening the afferent limb
c. Conversion of previous gastric surgery to Roux-en-Y reconstruction
A 44-year-old female presents to the emergency department with severe epigastric pain and nausea. She has recently been taking Ibuprofen for headaches daily. A chest x-ray shows air under the diaphragm. She is hemodynamically stable. She is brought to the operating room and is found to have a duodenal ulcer. What is the MOST appropriate surgical management?
a. Omental patch repair
b. Primary suture repair of perforation
c. Omental patch repair with highly selective vagotomy
d. Antrectomy, truncal vagotomy, and Billroth II reconstruction
a. Omental patch repair
Endoscopic evaluation of a 32/F with UGIB shows a 1 cm ulcer at the pre-pyloric area with adherent black slough at the ulcer base. Vital signs are stable. Hb is 9.9 gm%. The abdomen is unremarkable. The most logical treatment of the case is:
a. Emergency surgery
b. Transfusion and treatment with H2 receptor antagonist
c. Selective arteriography with embolization
d. Sclerotherapy followed by elective surgery
b. Transfusion and treatment with H2 receptor antagonist
Where does the lesser curvature abruptly angle to the right and the body of the stomach ends and the antrum begins?
Angularis incisura
Term for where the fundus forms with the left margin of the esophagus:
Angle of His
What is the arterial blood supply to the stomach?
4 main arteries: left gastric and right gastric arteries along the lesser curvature and left and right gastroepiploic arteries along the greater curvature; blood is also supplied to the proximal stomach by the inferior phrenic arteries and short gastric arteries and to the pylorus by the gastroduodenal artery
Approximate percentage that an aberrant left hepatic artery originates from the left gastric artery:
15% to 20%.
What is the largest artery to the stomach?
Left gastric artery
In general, what is the maximal number of arteries that can be ligated, provided that the arcades along the greater and lesser curvatures are intact, that will still supply enough blood flow for the stomach to survive?
3 of 4 arteries can be ligated
Describe the venous drainage of the stomach:
Left gastric (coronary) and right gastric veins usually drain into the portal vein; left gastroepiploic vein drains into the splenic vein; right vein drains into the superior mesenteric vein
What happens to the left vagus and right vagus at the gastroesophageal (GE) junction?
Left vagus becomes anterior and the right vagus becomes posterior (LARP mnemonic)
Where does the stomach receive its extrinsic parasympathetic and sympathetic innervation?
Parasympathetic via the vagus and sympathetic via the celiac plexus
Where does the sympathetic nerve supply to the stomach originate from?
From T5 to T10 (travels in splanchnic nerve to celiac ganglion)
Sensation of gastroduodenal pain via afferent sympathetic fibers
Which vagus gives off a hepatic branch to the liver and continues along the lesser curvature as the anterior nerve of Latarjet?
The left vagus
Which nerve gives off a branch to the celiac plexus and continues posteriorly along the lesser curvature?
The right vagus
Which nerve is the first branch of the risbt or posterior vagus nerve and can lead to recurrent ulcers if left undivided?
The criminal nerve of Grassi
Where along the vagus is a truncal vagotomy performed?
Above the celiac and hepatic branches of the vagi
Where along the vagus nerve is a selective truncal -vagotomy performed?
Below the celiac and hepatic branches of the vagi
Where along the vagus nerve is a highly selective vagotomy performed?
At the crows feet to the proximal stomach while preserving the portion innervating the antrum and pylorus
The intrinsic or enteric nervous system of the stomach consists of which autonomic plexuses?
Auerbach and Meissner autonomic plexuses
What layer of the stomach lies between the mucosa and the muscularis propria that is the strongest layer of the gastric wall?
Submucosa
How many layers of smooth muscle make up the muscularis propria (muscularis externa) of the stomach?
3 layers of smooth muscle
Which layer of the muscularls propria (muscularis externa) is the only complete muscle layer of the stomach wall, is circular, and becomes progressively thicker and functions as a true anatomic sphincter at the pylorus?
The middle layer of smooth muscle
Gastric mucosa consists of what kind of epithelium?
Columnar glandular epithelium
Where are parietal cells in the stomach mainly found? What do parietal cells secrete?
Body; secretion of intrinsic factor and acid
Intrinsic factor binds to B12 and is taken up in the terminal ileum
Pernicious anemia etiology is frequently an autoimmune process that destroys parietal cells, leading to a deficiency in intrinsic factor;
low B12 levels lead to a macrocytic anemia
Parietal cells are inhibited by somatostatin, PGEl, secretin, and CCK
Where in the stomach will there be a complete absence of parietal cells?
The cardia and prepyloric antrum
Where are chief cells in the stomach mainly found? What do chief cells secrete?
Body; pepsinogen
Converted to pepsin by gastric acid and is first enzyme of proteolysis
Where are G cells in the stomach mainly found? What do G cells secrete?
Antrum; gastrin
Release stimulated by amino acids and acetylcholine; inhibited by acidification of the duodenum
Why antrectomy can decrease acid secretion
Where are D cells in the stomach mainly found? What do D cells secrete?
Body and antrum; somatostatin Release stimulated by acidification of antrum and duodenum; inhibits gastrin and acid release
Where are gastric mucosal interneurons mainly found? What peptide is released by gastric mucosal interneurons?
Body and antrum; gastrin-releasing peptide
Where are endocrine cells in the stomach mainly found? What hormone do endocrine cells in the stomach release?
Body; ghrelin Stimulates appetite, increases food intake, promotes fat storage; released when stomach is empty and inhibited by stomach stretch; acts on hypothalamic brain cells Stomach
Process by which the proximal portion of the stomach relaxes in anticipation of food intake:
Receptive relaxation and gastric accommodation
Name ulcerogenic (excess add secretion) causes of hypergastrinemia:
Antral G-cell hyperplasia or hyperfunction, gastric outlet obstruction, retained excluded antrum, short-gut syndrome, Zollinger-Ellison syndrome
Name nonulcerogenic (normal or low add secretion) causes of hypergastrinemia:
Acid-reducing procedure (vagotomy), antisecretory agents (proton pump inhibitors [PPis] ), atrophic gastritis, chronic renal failure, Helicobacter pylori infection, pernicious anemia
What are the 3 local stimuli that regulate gastric add secretion by the parietal cell?
Acetylcholine,
gastrin, and
histamine
The basal level of acid secretion accounts for roughly what percentage of maximal add output?
10%
What is the approximate rate of hydrochloric add production during basal add secretion?
1 to 5 mmol/h
What are the 3 phases of add secretory response to a meal?
Cephalic, gastric, and intestinal
Histamine utilizes which second messenger to stimulate add secretion by parietal cells?
Intracellular cyclic AMP
Acetylcholine and gastrin utilize which second messenger to stimulate add secretion by parietal cells?
Calcium (phospholipase C converts membrane-bound phospholipids into inositol triphosphate [IP3], which mobilizes calcium from intracellular stores)
Mechanism by which PPis inhibit add secretion:
A covalent disulfate bond forms between the drug and the cysteine residues on the subunit of the H/K-ATPase leading to irreversible inhibition of the proton pump
Why do PPls have a longer duration of action than their plasma half-life?
The drug is covalently bonded to the H/K-ATPase leading to irreversible inhibition, so new proton pumps need to be synthesized before the recovery of acid secretion occurs
What converts pepsinogen into pepsin?
Gastric acid
How is the maximal acid output (MAO) determined after gastric analysis?
By averaging the output of the last two 15-minute periods after secretagogue administration
What is the usual range for MAO?
10 to 15 mEq/h 190
How is the peak acid output obtained after gastric analysis?
It is the highest rate of secretion obtained during a 15-minute period following secretagogue administration
Gastric motility begins with the depolarization of which cells?
Gastric pacemaker cells of Cajal located in the midbody of the stomach along the greater curvature
How many phases are in the myoelectric migrating complex (MMC)?
4 phases
How long does each cycle of the MMC last?
90 to 120 minutes
What happens in phase I of the MMC?
Also known as the quiescent phase; slow waves are present without action potentials; increase in gastric tone but no gastric contraction
What happens in phase II of the MMC?
Motor spikes are associated with slow waves and occasional gastric contractions; gallbladder contraction
What happens in phase III of the MMC?
Motor spike activity is associated with each slow wave; forceful gastric contractions happen every 15 to 20 seconds; the stomach is cleared oflarge indigestible food substances
What happens in phase IV of the MMC?
A brief recovery period before the next MMC cycle
List protective factors to gastric barrier function:
Blood flow, bicarbonate secretion, cell renewal, endogenous prostaglandins, growth factors, mucus production
List damaging factors to gastric barrier function:
Duodenal reflux of bile, ethanol ingestion, H. pylori, hydrochloric acid secretion, hypoxia, ischemia, nonsteroidal antiinflammatory drugs (NSAIDs}, pepsins, smoking
Approximate percentage of gastric ulcers associated with H. pylori:
75%
Approximate percentage of duodenal ulcers associated with H. pylori:
90%
Most common cause of peptic ulcer disease:
H. pylori infection; eradication is imperative-treated with a combination of PPI and antibiotics
What is the second most common cause of peptic ulcer disease?
NSAID ingestion; blocks COX-1 enzyme, disrupts prostaglandin production leading to less protective mucus
Where do gastric ulcers usually occur?
On the lesser curve near the incisura (60%; type I)
What is a type I gastric ulcer?
Gastric ulcer occurring on the lesser curvature near the incisura
What is a type II gastric ulcer?
Gastric ulcer located in the body of the stomach in combination with a duodenal ulcer
What is a type III gastric ulcer?
Prepyloric gastric ulcer
What is a type IV gastric ulcer?
Gastric ulcer that occurs high on the lesser curve near the GE junction
What is a type V gastric ulcer?
Drug-induced (NSAIDs) gastric ulcer that may occur anywhere in the stomach
Which types of gastric ulcer are not associated with excess acid secretion?
Type I and IV
Which types of gastric ulcer are associated with excess acid secretion?
Type II and III
Name the ulcer: multiple, superficial erosions that begin in the proximal stomach and progress distally in a patient with central nervous system disease:
Cushing ulcer
Name the ulcer: multiple, superficial erosions that begin in the proximal stomach and progress distally in a patient with >30% body surface area burn:
Curling ulcer
Where in the stomach is stress gastritis usually seen?
Fundus
Initial management for a patient with stress gastritis with UGI bleeding:
ABCs; fluid resuscitation with correction of any platelet/coagulation abnormalities; blood transfusion if needed; administration of broad-spectrum IV antibiotics in patients with sepsis, saline lavage of the stomach through a nasogastric (NG) tube; administration of antisecretory agents after the NGT aspirate runs clear
Dose of vasopressin for the control of acute GI bleeding:
0.2 to 0.4 IU/min as a continuous infusion for a maximum of 48 to 72 hours
Indications for operation with stress gastritis:
Recurrent or persistent bleeding requiring >6 units of blood (3000 mL)
After taking the patient to the operating room, how would you control the bleeding associated with stress gastritis in a hemodynamically stable patient?
Make a long anterior gastrotomy along the proximal stomach/fundus; clear the gastric lumen of blood; inspect the mucosa! surface for bleeding points; oversew all bleeding areas with figure-of-eight stitches taken deep within the gastric wall; close the anterior gastrotomy; perform a truncal vagotomy and pyloroplasty (less commonly, a partial gastrectomy with vagotomy can be performed)
After taking a patient with life-threatening hemorrhage refractory to other forms of therapy to the operating room, what procedure would you perform to control the bleeding?
Gastric devascularization procedure (faster) versus total gastrectomy
Term for a disruption of the gastric mucosa (high on lesser curve at GE junction) that results from forceful vomiting, retching, coughing, or straining:
Mallory-Weiss tear
What percentage of acute UGI bleeds are accounted for by Mallory-Weiss tears?
15%
What is the overall mortality rate from a Mallory-Weiss tear?
3% to 4%
Treatment for active bleeding from a Mallory-Weiss tear that continues after initial resuscitation?
Esophagogastroduodenoscopy (EGD) {band ligation, epinephrine injection, hemoclipping, multipolar electric coagulation) versus angiographic intraarterial infusion of vasopressin or transcatheter embolization (in patients with severe comorbidities)
Indications for surgery in a patient with an acute bleed from a Mallory-Weiss tear?
> 6u packed red blood cells (PRBCs) transfused;
failure of EGD to stop bleeding;
failure of angiographic embolization (in patients with severe comorbidities)
If surgery for active bleeding from a Mallory-Weiss tear is indicated, what procedure would you perform?
Anterior gastrotomy and oversewing ofthe bleeding site with deep 2-0 silk ligatures with reapproximation ofthe gastric mucosa
If surgery for active bleeding from a Mallory-Weiss tear in the distal esophagus is indicated, how might your operative approach change?
Rather than laparotomy and anterior gastrotomy, you may need a left thoracotomy and esophagotomy followed by suture ligation
What disease process is characterized by erosion of the superficial mucosa overlying an abnormally large (1-3 mm) tortuous vessel resulting in bleeding?
Dieulafoy lesion
Are Dieulafoy lesions more common in men or in women?
Men (M:F= 2:1)
Peak incidence for Dieulafoy lesion:
Fifth decade
Diagnostic modality of choice for Dieulafoy lesion:
EGD
Where do Dieulafoy lesions usually occur in the stomach?
6 to 10 cm from the GE junction, generally in the fundus near the cardia
What is the classic presentation of a patient with a Dieulafoy lesion?
Sudden onset of massive, painless, recurrent hematemesis with hypotension
After resuscitation, what initial attempts should be made to stop acute bleeding from a Dieulafoy lesion?
Endoscopic modalities (band ligation, heater probe, hemoclipping, injection sclerotherapy, multipolar electrocoagulation, noncontact laser photocoagulation) or angiography if endoscopy cannot identify the bleeding source
