SlideShare a Scribd company logo
Tumors of Small Bowel
Presenter-
Dr. Akshay Sarraf
2nd Year Resident
Dept. of General Surgery
1
Introduction
• Small intestine contains over 90% of the mucosal surface area of the GI
tract but only 1.1% to 2.4% of all GI malignancies.
• The incidence of small bowel cancer has increased an average of
approximately 2% each year during the past 15 years.
• The 5-year survival for localized small bowel cancer is approximately
85%(vs. 42% in distant disease).
• Mean age at presentation- 62 years for benign tumors and approximately
57 years for malignant tumors.
2
• The incidence of small bowel cancer is particularly low in India,
Romania, and other parts of Eastern Europe.
• Most benign neoplasms are asymptomatic and often identified as an
incidental finding.
• Malignant neoplasms account for 75% of symptomatic lesions that
lead to surgery.
3
• Stromal tumors and adenomas are the most frequent of the benign
tumors and appear to be more common in the distal small bowel.
• Adenocarcinoma is the most common malignant neoplasm.
• Neuroendocrine tumors (NETs) account for 25% to 30% of small
intestine malignant neoplasms.
4
• Risk factors-
1. Familial Adenomatous Polyposis (FAP) 6. Prior peptic ulcer disease
2. Hereditary Nonpolyposis Colorectal Cancer 7. Cystic fibrosis
3. Peutz-Jeghers syndrome 8. Biliary diversion (i.e., previous cholecystectomy)
4. Crohn disease 9. Smoking, heavy alcohol consumption
(>80 g/day of ethanol),
5. Gluten-sensitive enteropathy (i.e., celiac sprue) 10. Consumption of red meat or salt cured
foods.
5
• Genetics
• KRAS gene mutation.
• Deletion of 5q (APC gene), 17q (p53 gene), and 18q (DCC [deleted in colon
cancer] and DPC4 [SMAD4] genes).
• DNA mismatch gene repair is inactivated.
• Microsatellite instability (MSI-H)- typical of small bowel carcinomas
associated with celiac disease.
• Epidermal growth factor receptor and vascular endothelial growth factor
(VEGF) expression.
6
• Presentation
• Most patients with benign neoplasms remain asymptomatic.
• Often vague and nonspecific and may include dyspepsia, anorexia, malaise,
and dull abdominal pain, often intermittent and colicky.
• Pain, most often related to obstruction, is the most frequent complaint.
• Bleeding is usually occult; hematochezia or hematemesis may occur.
7
• Diagnosis
• High index of suspicion must be present for these neoplasms to be diagnosed.
• Correct preoperative diagnosis is made in only 50% of symptomatic patients.
• Plain X-Ray- just for confirming obstruction.
• Small bowel follow-through yields an accurate diagnosis in 53% to 83% of
patients with malignant neoplasms
8
• CT of the abdomen can prove particularly useful in detecting extraluminal
tumors, such as GISTs.
• Ultrasonography has not proved effective for preoperative diagnosis of small
bowel neoplasms.
• CT enteroclysis appears to be a more sensitive technique, with a diagnostic
accuracy of approximately 95%.
• MRI enteroclysis has a sensitivity and specificity of 98% and 97%,
respectively.
9
• Flexible endoscopy- duodenal lesions; the colonoscope can be advanced into
the terminal ileum for visualization and biopsy.
• Capsule endoscopy in the setting of obscure bleeding is highly sensitive and
specific.
• CT Angiography is of value in diagnosing and localizing tumors of vascular
origin.
• Diagnosis of a small bowel tumor is often achieved only at the time of surgical
exploration.
10
Benign Tumors
• The most common benign neoplasms include benign stromal tumors,
adenomas, and lipomas.
• Adenomas are the most common benign tumors reported in autopsy
series.
• Stromal tumors are the most common benign small bowel lesions that
produce symptoms.
• At operation, a thorough search of the remainder of the small bowel is
warranted because multiple tumors are not uncommon.
11
• Stromal Tumors-
• GIST make up 20% of all soft tissue sarcomas occurring throughout the
gastrointestinal tract
• Most prevalent in the stomach (60%) and jejunum and ileum (30%), and rarely
in duodenum (5%).
• Arise from the interstitial cell of Cajal, an intestinal pacemaker cell of
mesodermal descent.
• GISTs can be malignant tumors and nearly 20% of patients are found to have
metastatic disease, most commonly in the liver.
12
• Median age of diagnosis is 65 years of age, no sex predilection.
• A median size of 6 cm at diagnosis; some GISTs can even be larger than 20
cm.
• Symptoms include abdominal pain, fullness, bowel obstruction, or tumor
hemorrhage resulting in anemia, melena, or hematemesis.
• The workup of GIST is often initiated with a CT scan.
13
• An endoscopic core biopsy with immunohistochemical staining for KIT (95%)
and anoctamin-1 (98%) confirms the diagnosis.
• More than 95% of stromal tumors express CD117, and 70% to 90% express
CD34.
• Stromal tumors are firm, gray-white lesions with a whorled appearance noted
on cut surface.
• Microscopic examination demonstrates well-differentiated smooth muscle
cells.
14
• May grow intramurally and cause obstruction.
• Sometimes achieve considerable size and eventually outgrow their blood
supply, resulting in bleeding manifestations.
• The mitotic index is classified as low (<5 mitoses/50 hpf ) or high (>5
mitoses/50 hpf ).
• Tumors larger than 5 cm, regardless of mitotic index, have higher rates of
metastasis and recurrence
• Surgical resection is necessary for appropriate treatment.
• Higher-risk GIST lesions may require adjuvant therapy after resection.
15
• Adenomas:
• Account for approximately 15% of all benign small bowel tumors.
• Three primary types: true adenomas, villous adenomas, and Brunner gland
adenomas.
• 20% in the duodenum, 30% are found in the jejunum, and 50% are found in
the ileum.
• Are asymptomatic; most occur singly and are found incidentally at autopsy.
• most common presenting symptoms are pain, bleeding and obstruction.
16
• Villous adenomas: rare, premalignant; are most commonly found in the
duodenum
• May be associated with the familial polyposis syndrome.
• malignant potential is reportedly between 35% and 55%.
• Endoscopic ultrasound is a useful modality in the preintervention evaluation
and may help guide management planning.
17
• The options for treatment are endoscopic and surgical.
• In the jejunum and ileum, the treatment of choice is segmental resection.
• Surgical management has potential morbidity (20%–30%) associated with
duodenal resection by pancreaticoduodenectomy or pancreas-preserving
duodenectomy.
• Endoscopic resection (i.e., snare excision, thermal ablation, argon plasma
coagulation, or photodynamic therapy) is a safe alternative.
18
• Lifelong risk of recurrence is approximately 50% after endoscopic treatment
• Endoscopic mucosal resection(EMR) for the treatment of duodenal adenomas
and Brunner gland tumors has a high success rate for complete removal.
• The risk of delayed bleeding a/w EMR is significant
• Invasive changes or a recurrence after polypectomy necessitates a more
definitive approach (e.g., pancreaticoduodenectomy).
19
• Adenomas a/w FAP
• Adenomas in the duodenum can be found in 50% to 90% of cases.
• Increasing age is an independent risk factor for adenoma development.
• 5% lifetime risk for development of duodenal adenocarcinoma.
• For direct surveillance and treatment, patients are classified by the Spigelman
classification.
• Screening endoscopy is performed at regular intervals with biopsy of all
suspicious, villous, or large (>3 cm) adenomas.
20
21
• Peutz-Jeghers Syndrome:
• Inherited syndrome of mucocutaneous melanotic pigmentation and
gastrointestinal hamartomatous polyps.
• Autosomal dominant, with a high degree of penetrance.
• Brown or black spots located in the circumoral region of the face, buccal
mucosa, forearms, palms, soles, digits, and perianal area.
• Hamartomas are most commonly found in the jejunum and ileum
22
• The most common symptom is recurrent colicky abdominal pain, a palpable
mass in 1/3 patients.
• Hemorrhage as a result of autoamputation of the polyps may occurs.
• Adenomatous changes have been reported in 3% to 6% of hamartomas.
• Extracolonic cancers are common, occurring in 50% to 90% of patients (small
intestine-m/c, stomach, pancreas, ovary, lung, uterus, and breast).
23
• Treatment is directed at bowel obstruction or persistent gastrointestinal
bleeding
• Resection should be limited to the segment of bowel that is producing
complications
• Because of the widespread nature of intestinal involvement, cure is not
possible; therefore, extensive resection is not indicated.
24
• Hemangiomas-
• Developmental malformations consisting of submucosal proliferation of blood
vessels.
• Can occur at any level of the gastrointestinal tract; jejunum is the most
commonly affected small bowel segment.
• 3% to 4% of all benign tumors of the small bowel and are multifocal in 60% of
patients.
• A/w Osler-Weber-Rendu disease and Turner syndrome.
25
• The most common symptom of small bowel hemangiomas is intestinal
bleeding.
• Angiography and technetium Tc-99m red blood cell scanning are the most
useful diagnostic studies.
• If a hemangioma is localized preoperatively, resection of the involved
intestinal segment is warranted.
• Intraoperative transillumination and palpation may help to identify a
nonlocalized hemangioma.
26
Malignant Neoplasms
• Incidence of malignant neoplasms of the small intestine has increased
steadily during the past three decades.
• Neuroendocrine neoplasms (NENs) increased more than fourfold.
• 5-year survival rate is 34.9% compared to 51.5% survival rate for
colorectal cancer
27
• Almost always produce symptoms, the most common of which are
pain and weight loss.
• Obstruction develops in 15% to 35% of patients as a result of tumor
infiltration and adhesions
• Gastrointestinal bleeding, manifested by anemia and occult blood-
positive stools or occasionally by melena or hematochezia.
• A palpable mass may be felt in 10% to 20% of patients, and
perforations develop in approximately 10%.
28
• Neuroendocrine Neoplasms:
• Arise from enterochromaffin cells (Kulchitsky cells).
• “carcinoid” has become a misnomer, as all NENs have
malignant potential.
• Reported in a number of organs, including lungs, bronchi,
and the gastrointestinal tract.
• Median age for gastroenteric NEN of 63 years.
29
• Divided into NETs and neuroendocrine carcinomas.
• The distinction between a G3 well-differentiated NET and a G3 poorly
differentiated NEC can be difficult and may require additional pathologic
confirmation or immunohistochemical staining. 30
• Midgut NETs are characterized by having high serotonin production.
• The most prominent neuropeptide- serotonin and substance P
• Almost always occur within the last 2 feet of the ileum.
• Carcinoid syndrome- cutaneous flushing (80%); diarrhea (76%);
hepatomegaly (71%); cardiac lesions, most commonly right-sided heart
valvular disease (41%–70%); and asthma (25%) and are present mostly in
those patients with hepatic metastases.
31
• Found in five typical sites: small intestine (38%), rectum (34%), colon (16%),
stomach (11%), and unknown sites (1%).
• Are multicentric in 20% to 30% of patients.
• The malignant potential is related to location, size, depth of invasion, and
growth pattern.
• 3% of appendiceal NETs, 35% of ileal NETs are associated with metastasis.
• GI NETs of <1 cm in diameter(75%) have 2% chance of metastasis, NETs 1 to
2 cm -50% and larger than 2 cm are associated with metastasis 80% to 90% of
cases.
32
33
• After invasion of the serosa, the intense desmoplastic reaction produces
mesenteric fibrosis, intestinal kinking, and intermittent obstruction.
• Larger mesenteric mass caused by nodal disease and desmoplastic invasion of
the mesentery, which is often mistaken for the primary tumor.
• Frequent coexistence of a second primary malignant neoplasm of a different
histologic type, usually a synchronous adenocarcinoma.
• As mesenteric and nodal extension progresses, local venous engorgement and,
ultimately, ischemia of the affected segment of intestine.
34
• Rarely diagnosed preoperatively.
• Elevated urinary levels of 5-HIAA measured during 24
hours are highly specific although not sensitive.
• Chromogranin A (CgA) is elevated in more than 80% of
patients with NETs. (specificity of 95%, sensitivity 55%)
35
• Radiologically a solid mass with spiculated borders and radiating surrounding
strands that is associated with linear strands within the mesenteric fat and
kinking of the bowel, a diagnosis of gastrointestinal NET can be made fairly
confidently.
• Scintigraphic(indium(111In)-labeled pentetreotide) localization has a higher
sensitivity than CT for delineating and localizing NETs.
• MRI can be helpful in diagnosing metastatic disease, especially in the liver.
• FDG is taken up only in highgrade NETs (e.g., high Ki-67 expression),
whereas most NETs have low Ki-67 expression
36
• Treatment small bowel NETs is based on tumor size, location, and presence of
metastatic disease.
• primary tumors smaller than 1 cm in diameter without evidence of regional
lymph node metastasis, a segmental intestinal resection is adequate
• wide excision of bowel and mesentery- lesions >1 cm, multiple tumors, or
with regional lymph node metastasis.
• Lesions of the terminal ileum are best treated by right hemicolectomy.
37
• Small duodenal tumors can be excised locally; however, more extensive
lesions may require pancreaticoduodenectomy.
• In cases of mesenteric disease aggressive surgical resection and debulking
achieve relief of 93% of obstruction and 83% of mesenteric vessel
encasement.
• In contrast to metastases from other tumors, there is a definite role for surgical
debulking, which often provides beneficial symptomatic relief.
• Metastasectomy (Liver) provides the most durable survival benefit compared
with other treatment modalities.
38
39
• NETs have the best prognosis of all small bowel tumors.
• Resection of a NET localized to its primary site approaches a 100% survival
rate.
• Five-year survival rates are approximately 65% in patients with regional
disease and 25% to 35% in those with distant metastasis
• Tumors recur in 40% to 60% of patients.
• An elevated level of CgA is an independent predictor of an adverse prognosis.
40
• Adenocarcinoma-
• Constitute ~40% of the malignant tumors of the small bowel.
• Median age at diagnosis is in the sixth decade of life, M>F.
• Most of these tumors are located in the duodenum and proximal jejunum.
• Those associated with Crohn disease tend to occur at a somewhat younger age,
and more than 70% arise in the ileum.
41
• May have important gene mutations- APC, β-CATENIN, EGFR, VEGF-A,
KRAS, HER2, TP53.
• m/c familial causes include FAP, Lynch syndrome, and Peutz Jeghers
syndrome.
• Tumors of the duodenum manifest early because of the earlier presentation of
symptoms, which are usually jaundice and chronic bleeding.
• Jejunum and ileum- nonspecific symptoms like vague abdominal pain and
weight loss, Intestinal obstruction and chronic bleeding; Perforation is
uncommon.
42
43
• Treatment
• Is determined by location and stage.
• An R0 resection of the primary tumor with locoregional lymph node resection
is the only curative treatment.
• Regional lymphadenectomy of the periduodenal, peripancreatic, and hepatic
lymph nodes as well as involved vascular structures is necessary.
• Neoadjuvant chemotherapy- if there is tumor invasion into adjacent structures.
44
• Jejunal and ileal adenocarcinomas require surgical resection with regional
lymphadenectomy and jejunojejunal or ileoileal anastomosis.
• Ileocecectomy with right hemicolectomy with ligation of the ileocolic artery
and subsequent regional lymphadenectomy for terminal ileum lesion.
45
• Poorly differentiated cancers or those who had incomplete lymph node
resections (<10 nodes identified) should at least be considered for adjuvant
chemotherapy.
• Adjuvant fluoropyrimidine and oxaliplatin may increase overall survival in
patients with advanced disease.
• BALLAD trial- proposes adjuvant chemotherapy will result in an
improvement in disease-free survival and overall survival compared with
observation alone after potentially curative surgery for patients with stage I, II,
and III small bowel adenocarcinoma.
46
• Metastatic disease- studies have determined that using FOLFOX (oxaliplatin,
5-FU, and leucovorin) and FOLFIRI (irinotecan, 5-FU, and leucovorin) as
first-line therapy.
• Unresectable metastatic disease may require surgical intervention for
uncontrolled bleeding, bowel obstruction, or perforation.
• Prognosis of small bowel adenocarcinoma is poor.
• Five-year survival rates are typically in the 14% to 33% range.
• Duodenal adenocarcinoma has a 5-year survival rate of 50%.
47
• Stage III- >3 positive lymph nodes 5-year disease-free survival rate was 37%; 1 or 2
positive lymph nodes was 57%.
• Advanced age, advanced stage, ileal location, recovery of fewer than 10 lymph nodes,
and number of positive nodes are significant predictors of poor overall survival.
• Any attempts at curative resection should always include an extensive regional
lymphadenectomy.
48
• Lymphoma-
• Primary or as a manifestation of systemic disease.
• One-third of gastrointestinal lymphomas occur in the small bowel, accounts
for 5% of all lymphomas.
• 25% of small bowel malignant tumors in the adult; most common intestinal
neoplasm in children younger than 10 years.
• Most commonly found in the ileum, d/t greatest concentration of gut-
associated lymphoid tissue.
• Primary small bowel lymphomas was associated with celiac disease and
immunodeficient states (e.g., AIDS).
49
• Usually large, with most greater than 5 cm and may extend beneath the
mucosa.
• There is often diffuse infiltration of the intestinal wall.
• Symptoms include pain, weight loss, nausea, vomiting, and change in bowel
habits.
• Perforation may occur in up to 25% of patients.
• Fever is uncommon and suggests systemic involvement.
50
51
• Treatment
• A combination of surgery, chemotherapy, and radiation therapy is used for all
small bowel tumors.
• In the absence of symptoms, small bowel lymphomas are often chemo
responsive and do not require surgery.
• B-cell lymphomas are more chemosensitive have high remission rates with or
without surgery.
• T-cell lymphomas are traditionally more resistant to therapy and will progress
to symptoms of obstruction or perforation if not resected.
• Five-year survival of 50% to 60% can be expected and is dictated by response
to systemic therapy.
52
• GIST-
• Constitute about 20% of malignant neoplasms of the small bowel.
• More common in the jejunum and ileum.
• Typically are diagnosed in the fifth and sixth decades of life with slight male
predilection.
• Larger than 5 cm at the time of diagnosis in 80% of patients.
• Mostly arise from the muscularis propria and generally grow extramurally.
• Most common indications for surgery include bleeding and obstruction, free
perforation as a result of hemorrhagic necrosis in large tumor masses.
53
• Invade locally or spread by direct extension into adjacent tissues and
hematogenously to the liver, lungs, and bone; lymphatic metastases are
unusual
• The treatment regimen is based on localized versus metastatic disease.
• Surgical management includes complete resection of localized GISTs
• If capsule rupture occurs, patients should receive adjuvant therapy
• A laparoscopic approach in patients with large tumors is strongly discouraged.
• Radiologic criteria for unresectability include infiltration of the celiac trunk,
superior mesenteric artery, or portal vein.
54
• Current guidelines suggest that patients with high-risk disease should receive 3
years of adjuvant treatment with imatinib.
• Imatinib- Tyrosine kinase inhibitor that blocks the unregulated mutant c-kit
tyrosine kinase and inhibits the BCR-ABL and PDGF tyrosine kinases.
• Not recommended for low-risk patients after an R0 resection.
• Neoadjuvant imatinib should be considered for patients requiring extensive
surgery to allow for tumor shrinkage prior to resection.
• Deletions affecting exon 11, codon 557/558 of the c-kit gene, and D842V
PDGFRα mutations have a higher risk of recurrence within the first 3 to 4
years after surgery.
55
56
• Nilotinib is a second-generation tyrosine kinase inhibitor active in chronic
myeloid leukemia and has an inhibitory effect on ckit and PDGF
• Phase 3 trials have shown minimal differences between this drug and imatinib
or sunitinib.
• Sorafenib is a VEGF, c-kit, PDGFR, and BRAF inhibitor and has been
effective in imatinib- and sunitinib-resistant tumors.
• The combination of imatinib and doxorubicin has shown some benefit in
patients with wild-type GISTs.
57
Metastatic Neoplasm
• Much more common than primary neoplasms.
• usually arise from other intraabdominal organs, including the uterus
cervix, ovaries, kidneys, stomach, colon, and pancreas.
• By direct extension or implantation of tumor cells.
• May be found in patients with adenocarcinoma of the breast and
carcinoma of the lung.
• Cutaneous melanoma is the most common extraabdominal source
58
• Common symptoms of metastatic disease include anorexia, weight
loss, anemia, bleeding, and partial bowel obstruction.
• Palliation to relieve symptoms or, occasionally, a bypass if the
metastatic tumor is extensive and not amenable to resection.
• Nonoperative palliation includes endoscopic or radiologic placement
of self-expandable metal stents.
• Gastrostomy and jejunostomy tubes also may be placed to provide
decompression when other palliative methods are not possible.
59
References
1. Bailey & Love’s Short Practice of Surgery, 28th Edition.
2. Sabiston Textbook of Surgery, 21st Edition.
3. Schwartz’s Principles of Surgery, 11th Edition.
60
THANK YOU
61

More Related Content

What's hot

Crohns disease
Crohns diseaseCrohns disease
Crohns disease
Dr. Naveed Quetta
 
Small bowel neoplasms
Small bowel neoplasmsSmall bowel neoplasms
Small bowel neoplasms
Anushuya Gunaseelan
 
Retroperitoneal mass
Retroperitoneal massRetroperitoneal mass
Retroperitoneal mass
Kundan Singh
 
Abdominal tuberculosis
Abdominal tuberculosisAbdominal tuberculosis
Abdominal tuberculosis
Shilpa Bhaskar
 
recurrent pyogenic cholangitis
recurrent pyogenic cholangitisrecurrent pyogenic cholangitis
recurrent pyogenic cholangitis
Shankar Zanwar
 
Peritoneal carcinomatosis
Peritoneal carcinomatosisPeritoneal carcinomatosis
Peritoneal carcinomatosis
Dr Dharma ram Poonia
 
Cholangiocarcinoma
CholangiocarcinomaCholangiocarcinoma
Cholangiocarcinoma
Dr. Thakur Prashant Singh
 
Management of presarcral tumors
Management of presarcral tumorsManagement of presarcral tumors
Management of presarcral tumors
Jawad Ahmad
 
radiological imaging of pancreatic malignancy - solid neoplasms radiological ...
radiological imaging of pancreatic malignancy - solid neoplasms radiological ...radiological imaging of pancreatic malignancy - solid neoplasms radiological ...
radiological imaging of pancreatic malignancy - solid neoplasms radiological ...
RagubharathiRavi
 
Bile duct injuries.slideshare
Bile duct injuries.slideshareBile duct injuries.slideshare
Bile duct injuries.slideshare
drksreenath
 
Choledocholithiasis- Management
Choledocholithiasis- ManagementCholedocholithiasis- Management
Choledocholithiasis- Management
Lilamani Rajthala
 
Benign liver lesions
Benign liver lesionsBenign liver lesions
Benign liver lesions
airwave12
 
Management of duodenal trauma
Management of duodenal traumaManagement of duodenal trauma
Management of duodenal trauma
Uday Sankar Reddy
 
gallbladder polyp.pptx
gallbladder polyp.pptxgallbladder polyp.pptx
gallbladder polyp.pptx
RahulRamesh370792
 
Rif mass
Rif massRif mass
Rif mass
drvijayabhasker
 
Component seperation technique for the repair of very large ventral hernias
Component seperation technique for the repair of very large ventral hernias Component seperation technique for the repair of very large ventral hernias
Component seperation technique for the repair of very large ventral hernias
nikhilameerchetty
 
Staging and Diagnostic approach of rectal cancer
 Staging and Diagnostic approach  of rectal cancer Staging and Diagnostic approach  of rectal cancer
Staging and Diagnostic approach of rectal cancer
Dr.Bhavin Vadodariya
 
Management of Rectal Cancer
Management of Rectal CancerManagement of Rectal Cancer
Management of Rectal Cancer
Subhash Thakur
 
Duodenal injuries
Duodenal injuriesDuodenal injuries
Duodenal injuries
joemdas
 
Tumors of appendix
Tumors of appendixTumors of appendix
Tumors of appendix
Dr.Waqar Hussain
 

What's hot (20)

Crohns disease
Crohns diseaseCrohns disease
Crohns disease
 
Small bowel neoplasms
Small bowel neoplasmsSmall bowel neoplasms
Small bowel neoplasms
 
Retroperitoneal mass
Retroperitoneal massRetroperitoneal mass
Retroperitoneal mass
 
Abdominal tuberculosis
Abdominal tuberculosisAbdominal tuberculosis
Abdominal tuberculosis
 
recurrent pyogenic cholangitis
recurrent pyogenic cholangitisrecurrent pyogenic cholangitis
recurrent pyogenic cholangitis
 
Peritoneal carcinomatosis
Peritoneal carcinomatosisPeritoneal carcinomatosis
Peritoneal carcinomatosis
 
Cholangiocarcinoma
CholangiocarcinomaCholangiocarcinoma
Cholangiocarcinoma
 
Management of presarcral tumors
Management of presarcral tumorsManagement of presarcral tumors
Management of presarcral tumors
 
radiological imaging of pancreatic malignancy - solid neoplasms radiological ...
radiological imaging of pancreatic malignancy - solid neoplasms radiological ...radiological imaging of pancreatic malignancy - solid neoplasms radiological ...
radiological imaging of pancreatic malignancy - solid neoplasms radiological ...
 
Bile duct injuries.slideshare
Bile duct injuries.slideshareBile duct injuries.slideshare
Bile duct injuries.slideshare
 
Choledocholithiasis- Management
Choledocholithiasis- ManagementCholedocholithiasis- Management
Choledocholithiasis- Management
 
Benign liver lesions
Benign liver lesionsBenign liver lesions
Benign liver lesions
 
Management of duodenal trauma
Management of duodenal traumaManagement of duodenal trauma
Management of duodenal trauma
 
gallbladder polyp.pptx
gallbladder polyp.pptxgallbladder polyp.pptx
gallbladder polyp.pptx
 
Rif mass
Rif massRif mass
Rif mass
 
Component seperation technique for the repair of very large ventral hernias
Component seperation technique for the repair of very large ventral hernias Component seperation technique for the repair of very large ventral hernias
Component seperation technique for the repair of very large ventral hernias
 
Staging and Diagnostic approach of rectal cancer
 Staging and Diagnostic approach  of rectal cancer Staging and Diagnostic approach  of rectal cancer
Staging and Diagnostic approach of rectal cancer
 
Management of Rectal Cancer
Management of Rectal CancerManagement of Rectal Cancer
Management of Rectal Cancer
 
Duodenal injuries
Duodenal injuriesDuodenal injuries
Duodenal injuries
 
Tumors of appendix
Tumors of appendixTumors of appendix
Tumors of appendix
 

Similar to Tumors of small bowel.pptx

Tumor small intestine
Tumor small intestineTumor small intestine
Tumor small intestine
kansal007
 
Duodenal neoplasms.pdf
Duodenal neoplasms.pdfDuodenal neoplasms.pdf
Duodenal neoplasms.pdf
TimWiyuleMutafyaMD
 
Management of Neoplasms of Small Intestine.pptx
Management of Neoplasms of Small Intestine.pptxManagement of Neoplasms of Small Intestine.pptx
Management of Neoplasms of Small Intestine.pptx
Nabin Paudyal
 
GALLBLADDER CANCER.pptx
GALLBLADDER CANCER.pptxGALLBLADDER CANCER.pptx
GALLBLADDER CANCER.pptx
SujanPandey11
 
Kidney and ureteric tumors
Kidney and ureteric tumorsKidney and ureteric tumors
Kidney and ureteric tumors
Dr./ Ihab Samy
 
Gastric carcinoma
Gastric carcinoma Gastric carcinoma
Gastric carcinoma
Dr.Saadvik Raghuram
 
Appendicular neoplasm.pptx
Appendicular neoplasm.pptxAppendicular neoplasm.pptx
Appendicular neoplasm.pptx
Abd266
 
Biliary Tumors.pptx
Biliary Tumors.pptxBiliary Tumors.pptx
Biliary Tumors.pptx
HarmonyOyiko
 
Git j club secondaries.
Git j club secondaries.Git j club secondaries.
Git j club secondaries.
Shaikhani.
 
Carcinoma colon-and-management
Carcinoma colon-and-managementCarcinoma colon-and-management
Carcinoma colon-and-management
shiv kishor
 
Carcinoma anal canal.pptx
Carcinoma anal canal.pptxCarcinoma anal canal.pptx
Carcinoma anal canal.pptx
Pradeep Pande
 
Colon cancer.ppt.pptx
Colon cancer.ppt.pptxColon cancer.ppt.pptx
Colon cancer.ppt.pptx
Bijo10
 
Colon cancer.ppt.pptx
Colon cancer.ppt.pptxColon cancer.ppt.pptx
Colon cancer.ppt.pptx
anamikaberidze2
 
RENAL CELL CARCINOMA, Urothelial (Transitional Cell) Bladder Tumours
RENAL CELL CARCINOMA, Urothelial (Transitional Cell) Bladder TumoursRENAL CELL CARCINOMA, Urothelial (Transitional Cell) Bladder Tumours
RENAL CELL CARCINOMA, Urothelial (Transitional Cell) Bladder Tumours
Dr. Roopam Jain
 
Germ cell tumor ovary.pptx
Germ cell tumor ovary.pptxGerm cell tumor ovary.pptx
Germ cell tumor ovary.pptx
Dr. Abani Kanta Nanda
 
TUMORS OF LOWER URINARY TRACT
TUMORS OF LOWER URINARY TRACT TUMORS OF LOWER URINARY TRACT
TUMORS OF LOWER URINARY TRACT
Dr. Roopam Jain
 
Pathology ca bladder
Pathology   ca bladderPathology   ca bladder
Pathology ca bladder
dr vipin Drvipinsharma3
 
Carcinoma Colon (large intestine ).pptx
Carcinoma Colon (large intestine  ).pptxCarcinoma Colon (large intestine  ).pptx
Carcinoma Colon (large intestine ).pptx
Dr Ashwini kumar
 
Colon cancer lecture
Colon cancer lectureColon cancer lecture
Colon cancer lecture
Abdulgadir Almograby
 
Malignancy of the stomach and other stomach dysplasia.pptx
Malignancy of the stomach and other stomach dysplasia.pptxMalignancy of the stomach and other stomach dysplasia.pptx
Malignancy of the stomach and other stomach dysplasia.pptx
BarikielMassamu
 

Similar to Tumors of small bowel.pptx (20)

Tumor small intestine
Tumor small intestineTumor small intestine
Tumor small intestine
 
Duodenal neoplasms.pdf
Duodenal neoplasms.pdfDuodenal neoplasms.pdf
Duodenal neoplasms.pdf
 
Management of Neoplasms of Small Intestine.pptx
Management of Neoplasms of Small Intestine.pptxManagement of Neoplasms of Small Intestine.pptx
Management of Neoplasms of Small Intestine.pptx
 
GALLBLADDER CANCER.pptx
GALLBLADDER CANCER.pptxGALLBLADDER CANCER.pptx
GALLBLADDER CANCER.pptx
 
Kidney and ureteric tumors
Kidney and ureteric tumorsKidney and ureteric tumors
Kidney and ureteric tumors
 
Gastric carcinoma
Gastric carcinoma Gastric carcinoma
Gastric carcinoma
 
Appendicular neoplasm.pptx
Appendicular neoplasm.pptxAppendicular neoplasm.pptx
Appendicular neoplasm.pptx
 
Biliary Tumors.pptx
Biliary Tumors.pptxBiliary Tumors.pptx
Biliary Tumors.pptx
 
Git j club secondaries.
Git j club secondaries.Git j club secondaries.
Git j club secondaries.
 
Carcinoma colon-and-management
Carcinoma colon-and-managementCarcinoma colon-and-management
Carcinoma colon-and-management
 
Carcinoma anal canal.pptx
Carcinoma anal canal.pptxCarcinoma anal canal.pptx
Carcinoma anal canal.pptx
 
Colon cancer.ppt.pptx
Colon cancer.ppt.pptxColon cancer.ppt.pptx
Colon cancer.ppt.pptx
 
Colon cancer.ppt.pptx
Colon cancer.ppt.pptxColon cancer.ppt.pptx
Colon cancer.ppt.pptx
 
RENAL CELL CARCINOMA, Urothelial (Transitional Cell) Bladder Tumours
RENAL CELL CARCINOMA, Urothelial (Transitional Cell) Bladder TumoursRENAL CELL CARCINOMA, Urothelial (Transitional Cell) Bladder Tumours
RENAL CELL CARCINOMA, Urothelial (Transitional Cell) Bladder Tumours
 
Germ cell tumor ovary.pptx
Germ cell tumor ovary.pptxGerm cell tumor ovary.pptx
Germ cell tumor ovary.pptx
 
TUMORS OF LOWER URINARY TRACT
TUMORS OF LOWER URINARY TRACT TUMORS OF LOWER URINARY TRACT
TUMORS OF LOWER URINARY TRACT
 
Pathology ca bladder
Pathology   ca bladderPathology   ca bladder
Pathology ca bladder
 
Carcinoma Colon (large intestine ).pptx
Carcinoma Colon (large intestine  ).pptxCarcinoma Colon (large intestine  ).pptx
Carcinoma Colon (large intestine ).pptx
 
Colon cancer lecture
Colon cancer lectureColon cancer lecture
Colon cancer lecture
 
Malignancy of the stomach and other stomach dysplasia.pptx
Malignancy of the stomach and other stomach dysplasia.pptxMalignancy of the stomach and other stomach dysplasia.pptx
Malignancy of the stomach and other stomach dysplasia.pptx
 

More from AkshaySarraf1

Management of Traumatic Splenic injury.pptx
Management of Traumatic Splenic injury.pptxManagement of Traumatic Splenic injury.pptx
Management of Traumatic Splenic injury.pptx
AkshaySarraf1
 
Approach to Upper Urinary Tract Tumors.pptx
Approach to Upper Urinary Tract Tumors.pptxApproach to Upper Urinary Tract Tumors.pptx
Approach to Upper Urinary Tract Tumors.pptx
AkshaySarraf1
 
Treatment of Advanced Renal Cell Carcinoma.pptx
Treatment of Advanced Renal Cell Carcinoma.pptxTreatment of Advanced Renal Cell Carcinoma.pptx
Treatment of Advanced Renal Cell Carcinoma.pptx
AkshaySarraf1
 
Approach to Upper GI Tract Bleed (UGI Bleed).pptx
Approach to Upper GI Tract Bleed (UGI Bleed).pptxApproach to Upper GI Tract Bleed (UGI Bleed).pptx
Approach to Upper GI Tract Bleed (UGI Bleed).pptx
AkshaySarraf1
 
Principles of Laparoscopic Surgery and SAFE Cholecystectomy.pptx
Principles of Laparoscopic Surgery and SAFE Cholecystectomy.pptxPrinciples of Laparoscopic Surgery and SAFE Cholecystectomy.pptx
Principles of Laparoscopic Surgery and SAFE Cholecystectomy.pptx
AkshaySarraf1
 
Neurofibromatosis.pptx
Neurofibromatosis.pptxNeurofibromatosis.pptx
Neurofibromatosis.pptx
AkshaySarraf1
 
Septic Shock.pptx
Septic Shock.pptxSeptic Shock.pptx
Septic Shock.pptx
AkshaySarraf1
 
Etiopathogenesis and Risk factors of Ca Breast.pptx
Etiopathogenesis and Risk factors of Ca Breast.pptxEtiopathogenesis and Risk factors of Ca Breast.pptx
Etiopathogenesis and Risk factors of Ca Breast.pptx
AkshaySarraf1
 
Anatomy of Anterior Abdominal wall.pptx
Anatomy of Anterior Abdominal wall.pptxAnatomy of Anterior Abdominal wall.pptx
Anatomy of Anterior Abdominal wall.pptx
AkshaySarraf1
 
Classification and staging of Lung Cancer.pptx
Classification and staging of Lung Cancer.pptxClassification and staging of Lung Cancer.pptx
Classification and staging of Lung Cancer.pptx
AkshaySarraf1
 

More from AkshaySarraf1 (10)

Management of Traumatic Splenic injury.pptx
Management of Traumatic Splenic injury.pptxManagement of Traumatic Splenic injury.pptx
Management of Traumatic Splenic injury.pptx
 
Approach to Upper Urinary Tract Tumors.pptx
Approach to Upper Urinary Tract Tumors.pptxApproach to Upper Urinary Tract Tumors.pptx
Approach to Upper Urinary Tract Tumors.pptx
 
Treatment of Advanced Renal Cell Carcinoma.pptx
Treatment of Advanced Renal Cell Carcinoma.pptxTreatment of Advanced Renal Cell Carcinoma.pptx
Treatment of Advanced Renal Cell Carcinoma.pptx
 
Approach to Upper GI Tract Bleed (UGI Bleed).pptx
Approach to Upper GI Tract Bleed (UGI Bleed).pptxApproach to Upper GI Tract Bleed (UGI Bleed).pptx
Approach to Upper GI Tract Bleed (UGI Bleed).pptx
 
Principles of Laparoscopic Surgery and SAFE Cholecystectomy.pptx
Principles of Laparoscopic Surgery and SAFE Cholecystectomy.pptxPrinciples of Laparoscopic Surgery and SAFE Cholecystectomy.pptx
Principles of Laparoscopic Surgery and SAFE Cholecystectomy.pptx
 
Neurofibromatosis.pptx
Neurofibromatosis.pptxNeurofibromatosis.pptx
Neurofibromatosis.pptx
 
Septic Shock.pptx
Septic Shock.pptxSeptic Shock.pptx
Septic Shock.pptx
 
Etiopathogenesis and Risk factors of Ca Breast.pptx
Etiopathogenesis and Risk factors of Ca Breast.pptxEtiopathogenesis and Risk factors of Ca Breast.pptx
Etiopathogenesis and Risk factors of Ca Breast.pptx
 
Anatomy of Anterior Abdominal wall.pptx
Anatomy of Anterior Abdominal wall.pptxAnatomy of Anterior Abdominal wall.pptx
Anatomy of Anterior Abdominal wall.pptx
 
Classification and staging of Lung Cancer.pptx
Classification and staging of Lung Cancer.pptxClassification and staging of Lung Cancer.pptx
Classification and staging of Lung Cancer.pptx
 

Recently uploaded

Integrating Ayurveda into Parkinson’s Management: A Holistic Approach
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachIntegrating Ayurveda into Parkinson’s Management: A Holistic Approach
Integrating Ayurveda into Parkinson’s Management: A Holistic Approach
Ayurveda ForAll
 
Adhd Medication Shortage Uk - trinexpharmacy.com
Adhd Medication Shortage Uk - trinexpharmacy.comAdhd Medication Shortage Uk - trinexpharmacy.com
Adhd Medication Shortage Uk - trinexpharmacy.com
reignlana06
 
THERAPEUTIC ANTISENSE MOLECULES .pptx
THERAPEUTIC ANTISENSE MOLECULES    .pptxTHERAPEUTIC ANTISENSE MOLECULES    .pptx
THERAPEUTIC ANTISENSE MOLECULES .pptx
70KRISHPATEL
 
OCT Training Course for clinical practice Part 1
OCT Training Course for clinical practice Part 1OCT Training Course for clinical practice Part 1
OCT Training Course for clinical practice Part 1
KafrELShiekh University
 
A Classical Text Review on Basavarajeeyam
A Classical Text Review on BasavarajeeyamA Classical Text Review on Basavarajeeyam
A Classical Text Review on Basavarajeeyam
Dr. Jyothirmai Paindla
 
NVBDCP.pptx Nation vector borne disease control program
NVBDCP.pptx Nation vector borne disease control programNVBDCP.pptx Nation vector borne disease control program
NVBDCP.pptx Nation vector borne disease control program
Sapna Thakur
 
Cardiac Assessment for B.sc Nursing Student.pdf
Cardiac Assessment for B.sc Nursing Student.pdfCardiac Assessment for B.sc Nursing Student.pdf
Cardiac Assessment for B.sc Nursing Student.pdf
shivalingatalekar1
 
Phone Us ❤8107221448❤ #ℂall #gIRLS In Dehradun By Dehradun @ℂall @Girls Hotel...
Phone Us ❤8107221448❤ #ℂall #gIRLS In Dehradun By Dehradun @ℂall @Girls Hotel...Phone Us ❤8107221448❤ #ℂall #gIRLS In Dehradun By Dehradun @ℂall @Girls Hotel...
Phone Us ❤8107221448❤ #ℂall #gIRLS In Dehradun By Dehradun @ℂall @Girls Hotel...
chandankumarsmartiso
 
Light House Retreats: Plant Medicine Retreat Europe
Light House Retreats: Plant Medicine Retreat EuropeLight House Retreats: Plant Medicine Retreat Europe
Light House Retreats: Plant Medicine Retreat Europe
Lighthouse Retreat
 
Cell Therapy Expansion and Challenges in Autoimmune Disease
Cell Therapy Expansion and Challenges in Autoimmune DiseaseCell Therapy Expansion and Challenges in Autoimmune Disease
Cell Therapy Expansion and Challenges in Autoimmune Disease
Health Advances
 
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...
Donc Test
 
Chapter 11 Nutrition and Chronic Diseases.pptx
Chapter 11 Nutrition and Chronic Diseases.pptxChapter 11 Nutrition and Chronic Diseases.pptx
Chapter 11 Nutrition and Chronic Diseases.pptx
Earlene McNair
 
Netter's Atlas of Human Anatomy 7.ed.pdf
Netter's Atlas of Human Anatomy 7.ed.pdfNetter's Atlas of Human Anatomy 7.ed.pdf
Netter's Atlas of Human Anatomy 7.ed.pdf
BrissaOrtiz3
 
Identification and nursing management of congenital malformations .pptx
Identification and nursing management of congenital malformations .pptxIdentification and nursing management of congenital malformations .pptx
Identification and nursing management of congenital malformations .pptx
MGM SCHOOL/COLLEGE OF NURSING
 
REGULATION FOR COMBINATION PRODUCTS AND MEDICAL DEVICES.pptx
REGULATION FOR COMBINATION PRODUCTS AND MEDICAL DEVICES.pptxREGULATION FOR COMBINATION PRODUCTS AND MEDICAL DEVICES.pptx
REGULATION FOR COMBINATION PRODUCTS AND MEDICAL DEVICES.pptx
LaniyaNasrink
 
Journal Article Review on Rasamanikya
Journal Article Review on RasamanikyaJournal Article Review on Rasamanikya
Journal Article Review on Rasamanikya
Dr. Jyothirmai Paindla
 
CHEMOTHERAPY_RDP_CHAPTER 2 _LEPROSY.pdf1
CHEMOTHERAPY_RDP_CHAPTER 2 _LEPROSY.pdf1CHEMOTHERAPY_RDP_CHAPTER 2 _LEPROSY.pdf1
CHEMOTHERAPY_RDP_CHAPTER 2 _LEPROSY.pdf1
rishi2789
 
CHEMOTHERAPY_RDP_CHAPTER 4_ANTI VIRAL DRUGS.pdf
CHEMOTHERAPY_RDP_CHAPTER 4_ANTI VIRAL DRUGS.pdfCHEMOTHERAPY_RDP_CHAPTER 4_ANTI VIRAL DRUGS.pdf
CHEMOTHERAPY_RDP_CHAPTER 4_ANTI VIRAL DRUGS.pdf
rishi2789
 
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...
Oleg Kshivets
 
#cALL# #gIRLS# In Dehradun ꧁❤8107221448❤꧂#cALL# #gIRLS# Service In Dehradun W...
#cALL# #gIRLS# In Dehradun ꧁❤8107221448❤꧂#cALL# #gIRLS# Service In Dehradun W...#cALL# #gIRLS# In Dehradun ꧁❤8107221448❤꧂#cALL# #gIRLS# Service In Dehradun W...
#cALL# #gIRLS# In Dehradun ꧁❤8107221448❤꧂#cALL# #gIRLS# Service In Dehradun W...
chandankumarsmartiso
 

Recently uploaded (20)

Integrating Ayurveda into Parkinson’s Management: A Holistic Approach
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachIntegrating Ayurveda into Parkinson’s Management: A Holistic Approach
Integrating Ayurveda into Parkinson’s Management: A Holistic Approach
 
Adhd Medication Shortage Uk - trinexpharmacy.com
Adhd Medication Shortage Uk - trinexpharmacy.comAdhd Medication Shortage Uk - trinexpharmacy.com
Adhd Medication Shortage Uk - trinexpharmacy.com
 
THERAPEUTIC ANTISENSE MOLECULES .pptx
THERAPEUTIC ANTISENSE MOLECULES    .pptxTHERAPEUTIC ANTISENSE MOLECULES    .pptx
THERAPEUTIC ANTISENSE MOLECULES .pptx
 
OCT Training Course for clinical practice Part 1
OCT Training Course for clinical practice Part 1OCT Training Course for clinical practice Part 1
OCT Training Course for clinical practice Part 1
 
A Classical Text Review on Basavarajeeyam
A Classical Text Review on BasavarajeeyamA Classical Text Review on Basavarajeeyam
A Classical Text Review on Basavarajeeyam
 
NVBDCP.pptx Nation vector borne disease control program
NVBDCP.pptx Nation vector borne disease control programNVBDCP.pptx Nation vector borne disease control program
NVBDCP.pptx Nation vector borne disease control program
 
Cardiac Assessment for B.sc Nursing Student.pdf
Cardiac Assessment for B.sc Nursing Student.pdfCardiac Assessment for B.sc Nursing Student.pdf
Cardiac Assessment for B.sc Nursing Student.pdf
 
Phone Us ❤8107221448❤ #ℂall #gIRLS In Dehradun By Dehradun @ℂall @Girls Hotel...
Phone Us ❤8107221448❤ #ℂall #gIRLS In Dehradun By Dehradun @ℂall @Girls Hotel...Phone Us ❤8107221448❤ #ℂall #gIRLS In Dehradun By Dehradun @ℂall @Girls Hotel...
Phone Us ❤8107221448❤ #ℂall #gIRLS In Dehradun By Dehradun @ℂall @Girls Hotel...
 
Light House Retreats: Plant Medicine Retreat Europe
Light House Retreats: Plant Medicine Retreat EuropeLight House Retreats: Plant Medicine Retreat Europe
Light House Retreats: Plant Medicine Retreat Europe
 
Cell Therapy Expansion and Challenges in Autoimmune Disease
Cell Therapy Expansion and Challenges in Autoimmune DiseaseCell Therapy Expansion and Challenges in Autoimmune Disease
Cell Therapy Expansion and Challenges in Autoimmune Disease
 
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...
 
Chapter 11 Nutrition and Chronic Diseases.pptx
Chapter 11 Nutrition and Chronic Diseases.pptxChapter 11 Nutrition and Chronic Diseases.pptx
Chapter 11 Nutrition and Chronic Diseases.pptx
 
Netter's Atlas of Human Anatomy 7.ed.pdf
Netter's Atlas of Human Anatomy 7.ed.pdfNetter's Atlas of Human Anatomy 7.ed.pdf
Netter's Atlas of Human Anatomy 7.ed.pdf
 
Identification and nursing management of congenital malformations .pptx
Identification and nursing management of congenital malformations .pptxIdentification and nursing management of congenital malformations .pptx
Identification and nursing management of congenital malformations .pptx
 
REGULATION FOR COMBINATION PRODUCTS AND MEDICAL DEVICES.pptx
REGULATION FOR COMBINATION PRODUCTS AND MEDICAL DEVICES.pptxREGULATION FOR COMBINATION PRODUCTS AND MEDICAL DEVICES.pptx
REGULATION FOR COMBINATION PRODUCTS AND MEDICAL DEVICES.pptx
 
Journal Article Review on Rasamanikya
Journal Article Review on RasamanikyaJournal Article Review on Rasamanikya
Journal Article Review on Rasamanikya
 
CHEMOTHERAPY_RDP_CHAPTER 2 _LEPROSY.pdf1
CHEMOTHERAPY_RDP_CHAPTER 2 _LEPROSY.pdf1CHEMOTHERAPY_RDP_CHAPTER 2 _LEPROSY.pdf1
CHEMOTHERAPY_RDP_CHAPTER 2 _LEPROSY.pdf1
 
CHEMOTHERAPY_RDP_CHAPTER 4_ANTI VIRAL DRUGS.pdf
CHEMOTHERAPY_RDP_CHAPTER 4_ANTI VIRAL DRUGS.pdfCHEMOTHERAPY_RDP_CHAPTER 4_ANTI VIRAL DRUGS.pdf
CHEMOTHERAPY_RDP_CHAPTER 4_ANTI VIRAL DRUGS.pdf
 
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...
 
#cALL# #gIRLS# In Dehradun ꧁❤8107221448❤꧂#cALL# #gIRLS# Service In Dehradun W...
#cALL# #gIRLS# In Dehradun ꧁❤8107221448❤꧂#cALL# #gIRLS# Service In Dehradun W...#cALL# #gIRLS# In Dehradun ꧁❤8107221448❤꧂#cALL# #gIRLS# Service In Dehradun W...
#cALL# #gIRLS# In Dehradun ꧁❤8107221448❤꧂#cALL# #gIRLS# Service In Dehradun W...
 

Tumors of small bowel.pptx

  • 1. Tumors of Small Bowel Presenter- Dr. Akshay Sarraf 2nd Year Resident Dept. of General Surgery 1
  • 2. Introduction • Small intestine contains over 90% of the mucosal surface area of the GI tract but only 1.1% to 2.4% of all GI malignancies. • The incidence of small bowel cancer has increased an average of approximately 2% each year during the past 15 years. • The 5-year survival for localized small bowel cancer is approximately 85%(vs. 42% in distant disease). • Mean age at presentation- 62 years for benign tumors and approximately 57 years for malignant tumors. 2
  • 3. • The incidence of small bowel cancer is particularly low in India, Romania, and other parts of Eastern Europe. • Most benign neoplasms are asymptomatic and often identified as an incidental finding. • Malignant neoplasms account for 75% of symptomatic lesions that lead to surgery. 3
  • 4. • Stromal tumors and adenomas are the most frequent of the benign tumors and appear to be more common in the distal small bowel. • Adenocarcinoma is the most common malignant neoplasm. • Neuroendocrine tumors (NETs) account for 25% to 30% of small intestine malignant neoplasms. 4
  • 5. • Risk factors- 1. Familial Adenomatous Polyposis (FAP) 6. Prior peptic ulcer disease 2. Hereditary Nonpolyposis Colorectal Cancer 7. Cystic fibrosis 3. Peutz-Jeghers syndrome 8. Biliary diversion (i.e., previous cholecystectomy) 4. Crohn disease 9. Smoking, heavy alcohol consumption (>80 g/day of ethanol), 5. Gluten-sensitive enteropathy (i.e., celiac sprue) 10. Consumption of red meat or salt cured foods. 5
  • 6. • Genetics • KRAS gene mutation. • Deletion of 5q (APC gene), 17q (p53 gene), and 18q (DCC [deleted in colon cancer] and DPC4 [SMAD4] genes). • DNA mismatch gene repair is inactivated. • Microsatellite instability (MSI-H)- typical of small bowel carcinomas associated with celiac disease. • Epidermal growth factor receptor and vascular endothelial growth factor (VEGF) expression. 6
  • 7. • Presentation • Most patients with benign neoplasms remain asymptomatic. • Often vague and nonspecific and may include dyspepsia, anorexia, malaise, and dull abdominal pain, often intermittent and colicky. • Pain, most often related to obstruction, is the most frequent complaint. • Bleeding is usually occult; hematochezia or hematemesis may occur. 7
  • 8. • Diagnosis • High index of suspicion must be present for these neoplasms to be diagnosed. • Correct preoperative diagnosis is made in only 50% of symptomatic patients. • Plain X-Ray- just for confirming obstruction. • Small bowel follow-through yields an accurate diagnosis in 53% to 83% of patients with malignant neoplasms 8
  • 9. • CT of the abdomen can prove particularly useful in detecting extraluminal tumors, such as GISTs. • Ultrasonography has not proved effective for preoperative diagnosis of small bowel neoplasms. • CT enteroclysis appears to be a more sensitive technique, with a diagnostic accuracy of approximately 95%. • MRI enteroclysis has a sensitivity and specificity of 98% and 97%, respectively. 9
  • 10. • Flexible endoscopy- duodenal lesions; the colonoscope can be advanced into the terminal ileum for visualization and biopsy. • Capsule endoscopy in the setting of obscure bleeding is highly sensitive and specific. • CT Angiography is of value in diagnosing and localizing tumors of vascular origin. • Diagnosis of a small bowel tumor is often achieved only at the time of surgical exploration. 10
  • 11. Benign Tumors • The most common benign neoplasms include benign stromal tumors, adenomas, and lipomas. • Adenomas are the most common benign tumors reported in autopsy series. • Stromal tumors are the most common benign small bowel lesions that produce symptoms. • At operation, a thorough search of the remainder of the small bowel is warranted because multiple tumors are not uncommon. 11
  • 12. • Stromal Tumors- • GIST make up 20% of all soft tissue sarcomas occurring throughout the gastrointestinal tract • Most prevalent in the stomach (60%) and jejunum and ileum (30%), and rarely in duodenum (5%). • Arise from the interstitial cell of Cajal, an intestinal pacemaker cell of mesodermal descent. • GISTs can be malignant tumors and nearly 20% of patients are found to have metastatic disease, most commonly in the liver. 12
  • 13. • Median age of diagnosis is 65 years of age, no sex predilection. • A median size of 6 cm at diagnosis; some GISTs can even be larger than 20 cm. • Symptoms include abdominal pain, fullness, bowel obstruction, or tumor hemorrhage resulting in anemia, melena, or hematemesis. • The workup of GIST is often initiated with a CT scan. 13
  • 14. • An endoscopic core biopsy with immunohistochemical staining for KIT (95%) and anoctamin-1 (98%) confirms the diagnosis. • More than 95% of stromal tumors express CD117, and 70% to 90% express CD34. • Stromal tumors are firm, gray-white lesions with a whorled appearance noted on cut surface. • Microscopic examination demonstrates well-differentiated smooth muscle cells. 14
  • 15. • May grow intramurally and cause obstruction. • Sometimes achieve considerable size and eventually outgrow their blood supply, resulting in bleeding manifestations. • The mitotic index is classified as low (<5 mitoses/50 hpf ) or high (>5 mitoses/50 hpf ). • Tumors larger than 5 cm, regardless of mitotic index, have higher rates of metastasis and recurrence • Surgical resection is necessary for appropriate treatment. • Higher-risk GIST lesions may require adjuvant therapy after resection. 15
  • 16. • Adenomas: • Account for approximately 15% of all benign small bowel tumors. • Three primary types: true adenomas, villous adenomas, and Brunner gland adenomas. • 20% in the duodenum, 30% are found in the jejunum, and 50% are found in the ileum. • Are asymptomatic; most occur singly and are found incidentally at autopsy. • most common presenting symptoms are pain, bleeding and obstruction. 16
  • 17. • Villous adenomas: rare, premalignant; are most commonly found in the duodenum • May be associated with the familial polyposis syndrome. • malignant potential is reportedly between 35% and 55%. • Endoscopic ultrasound is a useful modality in the preintervention evaluation and may help guide management planning. 17
  • 18. • The options for treatment are endoscopic and surgical. • In the jejunum and ileum, the treatment of choice is segmental resection. • Surgical management has potential morbidity (20%–30%) associated with duodenal resection by pancreaticoduodenectomy or pancreas-preserving duodenectomy. • Endoscopic resection (i.e., snare excision, thermal ablation, argon plasma coagulation, or photodynamic therapy) is a safe alternative. 18
  • 19. • Lifelong risk of recurrence is approximately 50% after endoscopic treatment • Endoscopic mucosal resection(EMR) for the treatment of duodenal adenomas and Brunner gland tumors has a high success rate for complete removal. • The risk of delayed bleeding a/w EMR is significant • Invasive changes or a recurrence after polypectomy necessitates a more definitive approach (e.g., pancreaticoduodenectomy). 19
  • 20. • Adenomas a/w FAP • Adenomas in the duodenum can be found in 50% to 90% of cases. • Increasing age is an independent risk factor for adenoma development. • 5% lifetime risk for development of duodenal adenocarcinoma. • For direct surveillance and treatment, patients are classified by the Spigelman classification. • Screening endoscopy is performed at regular intervals with biopsy of all suspicious, villous, or large (>3 cm) adenomas. 20
  • 21. 21
  • 22. • Peutz-Jeghers Syndrome: • Inherited syndrome of mucocutaneous melanotic pigmentation and gastrointestinal hamartomatous polyps. • Autosomal dominant, with a high degree of penetrance. • Brown or black spots located in the circumoral region of the face, buccal mucosa, forearms, palms, soles, digits, and perianal area. • Hamartomas are most commonly found in the jejunum and ileum 22
  • 23. • The most common symptom is recurrent colicky abdominal pain, a palpable mass in 1/3 patients. • Hemorrhage as a result of autoamputation of the polyps may occurs. • Adenomatous changes have been reported in 3% to 6% of hamartomas. • Extracolonic cancers are common, occurring in 50% to 90% of patients (small intestine-m/c, stomach, pancreas, ovary, lung, uterus, and breast). 23
  • 24. • Treatment is directed at bowel obstruction or persistent gastrointestinal bleeding • Resection should be limited to the segment of bowel that is producing complications • Because of the widespread nature of intestinal involvement, cure is not possible; therefore, extensive resection is not indicated. 24
  • 25. • Hemangiomas- • Developmental malformations consisting of submucosal proliferation of blood vessels. • Can occur at any level of the gastrointestinal tract; jejunum is the most commonly affected small bowel segment. • 3% to 4% of all benign tumors of the small bowel and are multifocal in 60% of patients. • A/w Osler-Weber-Rendu disease and Turner syndrome. 25
  • 26. • The most common symptom of small bowel hemangiomas is intestinal bleeding. • Angiography and technetium Tc-99m red blood cell scanning are the most useful diagnostic studies. • If a hemangioma is localized preoperatively, resection of the involved intestinal segment is warranted. • Intraoperative transillumination and palpation may help to identify a nonlocalized hemangioma. 26
  • 27. Malignant Neoplasms • Incidence of malignant neoplasms of the small intestine has increased steadily during the past three decades. • Neuroendocrine neoplasms (NENs) increased more than fourfold. • 5-year survival rate is 34.9% compared to 51.5% survival rate for colorectal cancer 27
  • 28. • Almost always produce symptoms, the most common of which are pain and weight loss. • Obstruction develops in 15% to 35% of patients as a result of tumor infiltration and adhesions • Gastrointestinal bleeding, manifested by anemia and occult blood- positive stools or occasionally by melena or hematochezia. • A palpable mass may be felt in 10% to 20% of patients, and perforations develop in approximately 10%. 28
  • 29. • Neuroendocrine Neoplasms: • Arise from enterochromaffin cells (Kulchitsky cells). • “carcinoid” has become a misnomer, as all NENs have malignant potential. • Reported in a number of organs, including lungs, bronchi, and the gastrointestinal tract. • Median age for gastroenteric NEN of 63 years. 29
  • 30. • Divided into NETs and neuroendocrine carcinomas. • The distinction between a G3 well-differentiated NET and a G3 poorly differentiated NEC can be difficult and may require additional pathologic confirmation or immunohistochemical staining. 30
  • 31. • Midgut NETs are characterized by having high serotonin production. • The most prominent neuropeptide- serotonin and substance P • Almost always occur within the last 2 feet of the ileum. • Carcinoid syndrome- cutaneous flushing (80%); diarrhea (76%); hepatomegaly (71%); cardiac lesions, most commonly right-sided heart valvular disease (41%–70%); and asthma (25%) and are present mostly in those patients with hepatic metastases. 31
  • 32. • Found in five typical sites: small intestine (38%), rectum (34%), colon (16%), stomach (11%), and unknown sites (1%). • Are multicentric in 20% to 30% of patients. • The malignant potential is related to location, size, depth of invasion, and growth pattern. • 3% of appendiceal NETs, 35% of ileal NETs are associated with metastasis. • GI NETs of <1 cm in diameter(75%) have 2% chance of metastasis, NETs 1 to 2 cm -50% and larger than 2 cm are associated with metastasis 80% to 90% of cases. 32
  • 33. 33
  • 34. • After invasion of the serosa, the intense desmoplastic reaction produces mesenteric fibrosis, intestinal kinking, and intermittent obstruction. • Larger mesenteric mass caused by nodal disease and desmoplastic invasion of the mesentery, which is often mistaken for the primary tumor. • Frequent coexistence of a second primary malignant neoplasm of a different histologic type, usually a synchronous adenocarcinoma. • As mesenteric and nodal extension progresses, local venous engorgement and, ultimately, ischemia of the affected segment of intestine. 34
  • 35. • Rarely diagnosed preoperatively. • Elevated urinary levels of 5-HIAA measured during 24 hours are highly specific although not sensitive. • Chromogranin A (CgA) is elevated in more than 80% of patients with NETs. (specificity of 95%, sensitivity 55%) 35
  • 36. • Radiologically a solid mass with spiculated borders and radiating surrounding strands that is associated with linear strands within the mesenteric fat and kinking of the bowel, a diagnosis of gastrointestinal NET can be made fairly confidently. • Scintigraphic(indium(111In)-labeled pentetreotide) localization has a higher sensitivity than CT for delineating and localizing NETs. • MRI can be helpful in diagnosing metastatic disease, especially in the liver. • FDG is taken up only in highgrade NETs (e.g., high Ki-67 expression), whereas most NETs have low Ki-67 expression 36
  • 37. • Treatment small bowel NETs is based on tumor size, location, and presence of metastatic disease. • primary tumors smaller than 1 cm in diameter without evidence of regional lymph node metastasis, a segmental intestinal resection is adequate • wide excision of bowel and mesentery- lesions >1 cm, multiple tumors, or with regional lymph node metastasis. • Lesions of the terminal ileum are best treated by right hemicolectomy. 37
  • 38. • Small duodenal tumors can be excised locally; however, more extensive lesions may require pancreaticoduodenectomy. • In cases of mesenteric disease aggressive surgical resection and debulking achieve relief of 93% of obstruction and 83% of mesenteric vessel encasement. • In contrast to metastases from other tumors, there is a definite role for surgical debulking, which often provides beneficial symptomatic relief. • Metastasectomy (Liver) provides the most durable survival benefit compared with other treatment modalities. 38
  • 39. 39
  • 40. • NETs have the best prognosis of all small bowel tumors. • Resection of a NET localized to its primary site approaches a 100% survival rate. • Five-year survival rates are approximately 65% in patients with regional disease and 25% to 35% in those with distant metastasis • Tumors recur in 40% to 60% of patients. • An elevated level of CgA is an independent predictor of an adverse prognosis. 40
  • 41. • Adenocarcinoma- • Constitute ~40% of the malignant tumors of the small bowel. • Median age at diagnosis is in the sixth decade of life, M>F. • Most of these tumors are located in the duodenum and proximal jejunum. • Those associated with Crohn disease tend to occur at a somewhat younger age, and more than 70% arise in the ileum. 41
  • 42. • May have important gene mutations- APC, β-CATENIN, EGFR, VEGF-A, KRAS, HER2, TP53. • m/c familial causes include FAP, Lynch syndrome, and Peutz Jeghers syndrome. • Tumors of the duodenum manifest early because of the earlier presentation of symptoms, which are usually jaundice and chronic bleeding. • Jejunum and ileum- nonspecific symptoms like vague abdominal pain and weight loss, Intestinal obstruction and chronic bleeding; Perforation is uncommon. 42
  • 43. 43
  • 44. • Treatment • Is determined by location and stage. • An R0 resection of the primary tumor with locoregional lymph node resection is the only curative treatment. • Regional lymphadenectomy of the periduodenal, peripancreatic, and hepatic lymph nodes as well as involved vascular structures is necessary. • Neoadjuvant chemotherapy- if there is tumor invasion into adjacent structures. 44
  • 45. • Jejunal and ileal adenocarcinomas require surgical resection with regional lymphadenectomy and jejunojejunal or ileoileal anastomosis. • Ileocecectomy with right hemicolectomy with ligation of the ileocolic artery and subsequent regional lymphadenectomy for terminal ileum lesion. 45
  • 46. • Poorly differentiated cancers or those who had incomplete lymph node resections (<10 nodes identified) should at least be considered for adjuvant chemotherapy. • Adjuvant fluoropyrimidine and oxaliplatin may increase overall survival in patients with advanced disease. • BALLAD trial- proposes adjuvant chemotherapy will result in an improvement in disease-free survival and overall survival compared with observation alone after potentially curative surgery for patients with stage I, II, and III small bowel adenocarcinoma. 46
  • 47. • Metastatic disease- studies have determined that using FOLFOX (oxaliplatin, 5-FU, and leucovorin) and FOLFIRI (irinotecan, 5-FU, and leucovorin) as first-line therapy. • Unresectable metastatic disease may require surgical intervention for uncontrolled bleeding, bowel obstruction, or perforation. • Prognosis of small bowel adenocarcinoma is poor. • Five-year survival rates are typically in the 14% to 33% range. • Duodenal adenocarcinoma has a 5-year survival rate of 50%. 47
  • 48. • Stage III- >3 positive lymph nodes 5-year disease-free survival rate was 37%; 1 or 2 positive lymph nodes was 57%. • Advanced age, advanced stage, ileal location, recovery of fewer than 10 lymph nodes, and number of positive nodes are significant predictors of poor overall survival. • Any attempts at curative resection should always include an extensive regional lymphadenectomy. 48
  • 49. • Lymphoma- • Primary or as a manifestation of systemic disease. • One-third of gastrointestinal lymphomas occur in the small bowel, accounts for 5% of all lymphomas. • 25% of small bowel malignant tumors in the adult; most common intestinal neoplasm in children younger than 10 years. • Most commonly found in the ileum, d/t greatest concentration of gut- associated lymphoid tissue. • Primary small bowel lymphomas was associated with celiac disease and immunodeficient states (e.g., AIDS). 49
  • 50. • Usually large, with most greater than 5 cm and may extend beneath the mucosa. • There is often diffuse infiltration of the intestinal wall. • Symptoms include pain, weight loss, nausea, vomiting, and change in bowel habits. • Perforation may occur in up to 25% of patients. • Fever is uncommon and suggests systemic involvement. 50
  • 51. 51
  • 52. • Treatment • A combination of surgery, chemotherapy, and radiation therapy is used for all small bowel tumors. • In the absence of symptoms, small bowel lymphomas are often chemo responsive and do not require surgery. • B-cell lymphomas are more chemosensitive have high remission rates with or without surgery. • T-cell lymphomas are traditionally more resistant to therapy and will progress to symptoms of obstruction or perforation if not resected. • Five-year survival of 50% to 60% can be expected and is dictated by response to systemic therapy. 52
  • 53. • GIST- • Constitute about 20% of malignant neoplasms of the small bowel. • More common in the jejunum and ileum. • Typically are diagnosed in the fifth and sixth decades of life with slight male predilection. • Larger than 5 cm at the time of diagnosis in 80% of patients. • Mostly arise from the muscularis propria and generally grow extramurally. • Most common indications for surgery include bleeding and obstruction, free perforation as a result of hemorrhagic necrosis in large tumor masses. 53
  • 54. • Invade locally or spread by direct extension into adjacent tissues and hematogenously to the liver, lungs, and bone; lymphatic metastases are unusual • The treatment regimen is based on localized versus metastatic disease. • Surgical management includes complete resection of localized GISTs • If capsule rupture occurs, patients should receive adjuvant therapy • A laparoscopic approach in patients with large tumors is strongly discouraged. • Radiologic criteria for unresectability include infiltration of the celiac trunk, superior mesenteric artery, or portal vein. 54
  • 55. • Current guidelines suggest that patients with high-risk disease should receive 3 years of adjuvant treatment with imatinib. • Imatinib- Tyrosine kinase inhibitor that blocks the unregulated mutant c-kit tyrosine kinase and inhibits the BCR-ABL and PDGF tyrosine kinases. • Not recommended for low-risk patients after an R0 resection. • Neoadjuvant imatinib should be considered for patients requiring extensive surgery to allow for tumor shrinkage prior to resection. • Deletions affecting exon 11, codon 557/558 of the c-kit gene, and D842V PDGFRα mutations have a higher risk of recurrence within the first 3 to 4 years after surgery. 55
  • 56. 56
  • 57. • Nilotinib is a second-generation tyrosine kinase inhibitor active in chronic myeloid leukemia and has an inhibitory effect on ckit and PDGF • Phase 3 trials have shown minimal differences between this drug and imatinib or sunitinib. • Sorafenib is a VEGF, c-kit, PDGFR, and BRAF inhibitor and has been effective in imatinib- and sunitinib-resistant tumors. • The combination of imatinib and doxorubicin has shown some benefit in patients with wild-type GISTs. 57
  • 58. Metastatic Neoplasm • Much more common than primary neoplasms. • usually arise from other intraabdominal organs, including the uterus cervix, ovaries, kidneys, stomach, colon, and pancreas. • By direct extension or implantation of tumor cells. • May be found in patients with adenocarcinoma of the breast and carcinoma of the lung. • Cutaneous melanoma is the most common extraabdominal source 58
  • 59. • Common symptoms of metastatic disease include anorexia, weight loss, anemia, bleeding, and partial bowel obstruction. • Palliation to relieve symptoms or, occasionally, a bypass if the metastatic tumor is extensive and not amenable to resection. • Nonoperative palliation includes endoscopic or radiologic placement of self-expandable metal stents. • Gastrostomy and jejunostomy tubes also may be placed to provide decompression when other palliative methods are not possible. 59
  • 60. References 1. Bailey & Love’s Short Practice of Surgery, 28th Edition. 2. Sabiston Textbook of Surgery, 21st Edition. 3. Schwartz’s Principles of Surgery, 11th Edition. 60

Editor's Notes

  1. with the highest cancer rates found among the Maori of New Zealand and ethnic Hawaiians.
  2. , accounting for 30% to50% of malignant neoplasms of the small intestine
  3. may be present for months or years before diagnosis. , although life-threatening hemorrhage is uncommon
  4. can provide helpful information about the staging of malignant cancers
  5. between 89% and 95% and between 75% and 95%, respectively. Despite these sophisticated imaging and diagnostic modalities,
  6. c-kit proto-oncogene, which cause KIT to become constitutively activated, presumably leading to persistence of cellular growth or survival signals. Because the interstitial cells of Cajal normally express KIT
  7. GISTs are often large, with
  8. KIT proto-oncogene protein that is a transmembrane receptor for the stem cell growth factor, the human progenitor cell antigen. GIST with spindle-cell features
  9. however, some series showed that the
  10. however, the risk of delayed bleeding is significant. 17% risk of other complications, including perforation, hemorrhage, and pancreatitis.
  11. therefore,routine lifelong surveillance is a priority.
  12. The presence of high-grade dysplasia, carcinoma in situ, or a Spigelman stage IV classification necessitates pancreaticoduodenectomy or pancreas-preserving duodenectomy.
  13. usually the result of intermittent intussusception. Lower abdominal pain associated with but infrequently, and is most commonly manifested by anemia.
  14. whereas changes in the frequency of adenocarcinomas, stromal tumors, and lymphomas are less pronounced.
  15. is more common with GISTs. %, usually secondary to lymphomas and sarcomas.
  16. neural crest cells situated at the base of the crypts of Lieberkühn. term Karzinoide to indicate the carcinoma-like appearance and the presumed lack of malignant potential.
  17. may be benign or of the well-differentiated malignant type and are further subdivided into three groups, low grade (grade 1, G1), intermediate-grade (grade 2, G2), or highgrade (grade 3, G3) tumors, based on the appearance, mitotic rates, behavior (invasion of other organs, angioinvasion), and Ki- 67 proliferative index. On the other hand, neuroendocrine carcinomas are all G3, poorly differentiated malignant tumors Nuclear non histone protein present in all proliferating cells as a proliferation marker
  18. These tumors may derive from the foregut (respiratory tract, thymus), midgut (jejunum, ileum and right colon, stomach, proximal duodenum), and hindgut (distal colon, rectum). 5-Hydroxy indoleacetic acid (5-HIAA) is the primary metabolite of serotonin. Serotonin is broken down into 5-hydroxy indoleacetic acid within the liver , secondary to serotonin or tachykinin production-
  19. these tumors are small, firm, submucosal nodules that are usually yellow on the cut surface They may be as subtle as a small whitish plaque seen on the antimesenteric border of the small intestine
  20. tend to grow very slowly, but
  21. Barium radiographic studies of the small bowel may exhibit multiple filling defects as a result of kinking and fibrosis of the bowel 5-Hydroxy indoleacetic acid (5-HIAA) is the primary metabolite of serotoni
  22. F-fluorodeoxyglucos
  23. Jejunal adenocarcinoma. Large circumferential mucinous adenocarcinoma of the jejunum. (
  24. (A) Malignant tumors should be resected with a wide margin of normal bowel and a wedge of mesentery to remove the immediate draining lymph nodes. (B) End-to-end anastomosis of the small bowel and repair of the mesentery.
  25. A prospective international phase 3 trial
  26. Probably because of the delayed presentation and presence of advanced disease at diagnosis. probably because of the earlier symptom presentation and diagnosis.