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Small Bowel

Dr. Imad Al-Fahad M.B.Ch.B, F.I.B.M.S Associate Professor, General Surgery Dept. Baghdad Medical College Consultant Surgeon, Baghdad Teaching Hospital
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References :

Short practice of surgery. By Bailey and Love. Clinical surgery. By Harold Allis.
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Structural and Functional Anatomy

280cm long Jejunum begins at LOT, no clear demarcation to ileum Jejunum has long vas recta, large plicae, thick walls, transparent mesentery Ileum has short vasa, small plicae, thin walls, fat in the mesentery.
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Structural and Functional Anatomy

Mesentery attaches the small intestine to the posterior abdominal wall. Contains nerves, blood vessels, lymphatics, lymph nodes, and fat.
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Structural and Functional Anatomy
Lymph tissues known as Peyer’s patches are abundant.SMA supplies the midgut structures (duodenum distal to the ampulla, pancreas, small intestine, ascending and transverse colon.) Al-Madena copy
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Histology

Four layersMucosa turns over every 3-7 daysSubmucosa contains vessels, nerves, lymph, Meissner’s plexus. This layer provides the major strength when suturingMuscularis outer long layer, inner circ layerAdventitia is a layer of visceral peritoneum Al-Madena copy
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Physiology (CHO)

Daily CHO load is 350g of starch, lactose, sucrose Initial enzyme digestion is by pancreatic and salivary amylase CHO broken down to monosaccharides by microvilli
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Physiology (Protein)

The jejunum is responsible for 80-90% of protein absorption Proteins are converted by acid and pepsin from stomach to polypeptides Acid is neutralized and pepsin is inactivated as chyme enters the duodenum
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Physiology (Protein)

Trypsinogen is activated from pancreas to trypsin by enterokinase in the duodenum Trypsin activates chymotrypsin and elastase, further digesting polypeps Amino acids and dipeptides are absorbed
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Physiology (Fats)
Emulsification begins in the stomach Fat enters the duodenum, where pancreatic and biliary secretions mix Lipase breaks down fats in to monoglycerides, which are absorbed by diffusion
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Physiology (Fats)

In epithelial cells, triglycerides are resynthesized, chylomicrons are formed and enter the lymphatic system thru small lacteals Bile salts are reabsorbed in the ileum Most of the excreted fat comes from desquamated cells and bacteria
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Physiology (H2O, Lytes, Minerals, Vitamins)

Iron is absorbed mainly in the duodenum Most minerals and water soluble vitamins absorbed in jejunum B12 is absorbed only in terminal ileum Of the 5-10 liters entering the small bowel, only 500cc enter the colon.
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The Job of the Bowel

To digest food (involves a corrosive solution and potentially pathogenic bacteria) To absorb the food into the blood while keeping the corrosive substances and the bacteria inside the gut To keep the solution moving down the bowel at the right rate for digestion and absorption
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Problems that Affect Bowel Functions

Inflammation and damage to the bowel wallHemorrhage  anemiaPerforation  peritonitisDecreased mucosal function  malabsorptionDecreased bacterial containment  sepsisMalabsorption Malnutrition, dehydration, electrolyte imbalancesObstructionMalabsorptionCompartment syndrome  ischemia Al-Madena copy
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Bowel Problems: Interrelationships
Inflammation
Obstruction
Malabsorption
Reflex paralysis
Distension, ischemia
Decreased mucosal function
Food does not pass through bowel at correct rate
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Short Bowel Syndrome

Inadequate length of intestine Generally occurs when more than 50% of the small intestine is resected or if less than 100cm remains. Leads to diarrhea, steatorrhea, weight loss, nutritional deficiencies, hypergastrinemia If the terminal ileum and valve are retained, 70% can be resected.
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Motility

The order of recovery of bowel function after surgery is Small bowel Colon Stomach
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DIVERTICULAR DISEASE
TypesDiverticula can occur in a wide number of positions in the gut,from the oesophagus to the rectosigmoid. There are two varieties:1. Congenital. All three coats of the bowel are present in the wallof the diverticulum, e.g. Meckel’s diverticulum.2. Acquired. The wall of the diverticulum lacks a propermuscular coat. Most alimentary diverticula are thought tobe acquired. Al-Madena copy
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Duodenal diverticula

There are two types: 1. Primary. In older patients on the inner wall of the second and third parts, these diverticula are found incidentally on barium meal and are usually asymptomatic. They can cause problems locating the ampulla during endoscopic retrograde cholangiopancreatography (ERCP). 2. Secondary. Diverticula of the duodenal cap result from longstanding duodenal ulceration.
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Jejunal diverticula

These are usually of variable size and multiple. Clinically, they may (1) be symptomless, (2) give rise to abdominal pain, (3) produce a malabsorption syndrome or (4) present as an acute abdomen with acute inflammation and occasionally perforation. They are more common in patients with connective tissue disorders. In patients with major malabsorption problems giving rise to anaemia, steatorrhoea, hypoproteinaemia or vitamin B12 deficiency, resection of the affected segment with end-to-end anastomosis can be effective.
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Meckel’s diverticulum In 2% of the population; it is situated on the anti-mesenteric border of the small intestine,commonly 60 cm from the ileocaecal valve, and is usually 3–5 cm long. Many variations occur (2% – 2 feet – 2 inches is a useful aide-mйmoire).possesses all three coats of the intestinal wall and has its own blood supply. It is therefore vulnerable to infection and obstruction in the same way as the appendix. If a silent Meckel’s is found incidentally during the course of an operation, it can be left alone provided it is wide mouthed and not thickened. In 20% of cases, the mucosa contains heterotopic epithelium, namely gastric, colonic or sometimes pancreatic tissue,If ectopic gastric epithelium is present within the diverticulum, it may be the source of gastrointestinal bleeding. Al-Madena copy
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Signs and Symptoms

In order of frequency, these symptoms are as follows:1 Severe haemorrhage, caused by peptic ulceration. Painless bleeding occurs per rectum and is maroon in colour. 2 Intussusception. In most cases, the apex of the intussusception is the swollen, inflamed, heterotopic epithelium at the mouth of the diverticulum.3 Meckel’s diverticulitis. may be difficult to distinguish from the symptoms of acute appendicitis. When a diverticulum perforates, the symptoms may simulate those of a perforated duodenal ulcer. 4 Chronic peptic ulceration. As the diverticulum is part of the mid-gut, the pain, although related to meals, is felt around the umbilicus.5 Intestinal obstruction. The presence of a band between the apex of the diverticulum and the umbilicus may cause obstruction either by the band itself or by a volvulus around it. Al-Madena copy
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‘Silent’ Meckel’s diverticulum An aphorism attributed to Dr Charles Mayo is: ‘a Meckel’s diverticulum is frequently suspected, often sought and seldom found’.A Meckel’s diverticulum usually remains symptomless throughou life and is found only at necropsy. When a silent Meckel’s diverticulum is encountered in the course of an abdominal operation, it can be left provided it is wide mouthed and the wall of the diverticulum does not feel thickened. Where there is doubt and it can be removed without appreciable additional risk, it should be resected.Exceptionally, a Meckel’s diverticulum is found in an inguinal or a femoral hernia sac – Littre’s hernia.can be very difficult to demonstrate by contrast radiology; small bowel enema would be the most accurate investigation. Technetium-99m scanning may be useful in identifying Meckel’s diverticulum as a source of gastrointestinal bleeding. Al-Madena copy
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Meckel’s diverticulectomy A Meckel’s diverticulum that is broad based should not be amputated at its base and invaginated in the same way as a vermiform appendix, because of the risk of stricture. Furthermore, this does not remove heterotrophic epithelium when it is present. Alternatively, a linear stapler device may be used. Where there is indurations of the base of the diverticulum extending into the adjacent ileum, it is advisable to resect a short segment of ileum containing the diverticulum, restoring continuity with an end-to-end anastomosis. Al-Madena copy
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Crohn’s Disease Chronic, transmural, inflammatory process primarily affecting young individuals Also known as regional enteritis, terminal ileitis, and granulomatous ileocolitis Incurable condition requiring ongoing medical management and frequent surgical interventions Long term pain and disability
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Frequency

5.3 cases per 100,000, incidence increasing in adults and children Males and females equally affected Peak age of onset is between 2nd and fourth decades, but 5% of cases under 5y
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Frequency

More common in Ashkenazi Jews, white populations Positive family history in 10-15%, suggesting a genetic predisposition Relative risk of first degree relatives of these patients developing the disease is 10-21 times greater than general population
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Etiology
Unknown, but many hypotheses Likely multifactorial, involving an infectious agent, environmental exposure activating an immune response in a genetically susceptible host
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Etiology

The first gene locus linked to Crohn’s was the IBD1 gene on Chr 16Bacterial agents have long been thought to be involved in the pathogenesis of the disease although none identified as of yet. Al-Madena copy
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Etiology

Environmental factors such as smoking, second hand smoke have been linked to the development of Crohn’sHLA-DR2 and DRB1 associated with UC not Crohn’s Al-Madena copy
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Pathology

Characteristically progresses in a discontinuous manner with affected bowel interspersed with normal bowel Mouth to anus
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Pathology

Most common site terminal ileum (40%), colon only (35%), small bowel only (20%), perianal (5%). Appendix often involved. Rectum frequently spared Anal involvement may be characterized by fissures (most common), abscesses,or fistulae. Most are off midline, not the usual posterior midline.
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Pathology
Endoscopically appears as patchy areas of inflammation separated by uninvolved bowel “Skip”. The earliest lesions are apthous ulcers, tiny erosions that typically occur over lymphoid folliclesProgress to lineal ulcers, which cross over transverse folds causing the “cobblestone appearance” Al-Madena copy
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Ulcers

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Ulcers

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Cobblestone

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Pathology

Grossly, surgical specimens are rigid, thickened as a result of chronic inflammation and fibrosis during healing periodsMesentery is thickened and shortened, may surround the bowel “creeping fat” Al-Madena copy
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Pathology
Because of the transmural nature of the disease, fistulous connections can occur to other bowel or organs. Non-caseating granulomas are found in lamina propria or submucosa in 50% of patients Fibrosis may lead to strictures
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Clinical Features

Intestinal manifestations Diarrhea Pain Anorexia Nausea, weight loss Perirectal disease Bleeding is uncommon in comparison to UC
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Clinical Features

Extraintestinal manifestations Arthritis Erythema nodosum, multiforme Pyoderma gangrenosum Sclerosing cholangitis, cholelithiasis Renal calculi Endocrine disorders (growth, amenorrhea), ocular disease
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Diagnosis

Combination of laboratory, radiological, pathologic examinations Differential includes bacterial enteritis, viral enteritis, ulcerative colitis, among others. Labs may show anemia, malnutrition, increased ESR B12 anemia, iron deficiency, folic acid deficiency Deficiencies in copper, selenium, zinc common
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Work-up

ColonoscopyUGI series with small bowel follow thruCT scanBarium enemaFistulogramDespite work-up, 10% will have indeterminate colitis, with features of both Crohn’s and UC Al-Madena copy
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Complications of Crohn’s Fistula (29%) Pelvic abscess (20%) Obstruction (30-50%) Hemorrhage (2%) Cancer (1%) Perforation (1%) Ureteral obstruction (1%)
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Medical Management

Aminosalicylates often 1st line, include sulfasalazine(old), mesalamine(Asacol, Pentasa), olsalazine, balsalazide The newer meds lack the sulfapyridine carrier, so better tolerated. Also come in enema form for colon symptoms 5-ASA blocks prostaglandin release, decreases inflammation
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Medical Management

Corticosteroids for treating acuter disease, not long term or for achieving remission. Topical steroids used in colitis, as enema, without the side effects of systemic.
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Medical Management

Flagyl most commonly used antibioticCan heal perianal fistulas caused by Crohn’s to completionCipro is the most common alternative Al-Madena copy
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Medical Management

Immunosupressants such as Azathioprine and 6-mercaptopurine used, especially to reduce time on steroids, effective in maintenance therapy Cyclosporine, oral treats active disease, used as bridge therapy until the above two start working, effects go on after stopping drugs for months
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Medical Management
Biologic therapies against TNF-alpha (inflammatory cytokine) FDA approved infliximab (Remicade), an antibody that targets TNF-alpha Used for active disease, fistula
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Surgical Therapy

Reserved for complications of the disease, and failure of medical management Most patients will require surgery during their lifetime Within 20y of the onset of their symptoms, 75% require surgery, many multiple resections, so attempts to conserve bowel are a must to avoid SBS No surgical cure
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Surgical Therapy

An alternative to bowel resection is stricuroplasty In cases of long strictures (>12cm), or multiple strictures in close proximity, resection with primary anastamosis is required. Anastomotic leak around 9% Recurrence is 2%
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Tumors of the Small Bowel

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Tumors of the Small Bowel

Rare disorder: ~6000 new cases, ~1000 deaths in 2006 from small bowel malignanciesComprise ~2% of GI malignancies, <0.4% of all cancersIncidence ~1 per 100,000Slight male predominanceMedian age of presentation = 57Known disease associations: Peutz-Jeghers, Crohn’s disease, FAP, Gardner’s syndrome, autoimmune diseases, immune deficiency states, immune suppresion Al-Madena copy
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Tumors of the Small Bowel
Histologies: Adenocarcinoma ~45% Carcinoid ~30% Lymphoma ~15% Sarcoma ~10%
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Tumors of the Small Bowel

Why are they so rare?Putative factors:Rapid transit of intestinal contents – less carcinogen exposureLiquid bowel contents – less mucosal irritationLower bacterial load than colon – less conversion of bile acids into carcinogens by organismsIncreased lymphoid tissue/IgA may be protective Al-Madena copy
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Tumors of the Small Bowel

Risk factors:Diet (i.e. red meat, salt-cured foods)Tobacco (cigarette smoking)Alcohol useImpaired GI motilityOther disease states: Peutz-Jeghers, Crohn’s disease, Gardner’s syndrome, FAP, celiac sprue, immune deficiency states (AIDS, post-transplant), autoimmune diseases Al-Madena copy
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Tumors of the Small Bowel

Clinical Presentation: Non-specific symptoms including abdominal pain (dull, cramping), weight loss/anorexia, anemia/occult bleeding, palpable mass, small bowel obstruction, rare bowel perforation Often advanced disease by the time patients present with symptoms
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Tumors of the Small Bowel

Diagnosis:H&P, CBC, CMP; urine 5-HIAA if carcinoid suspectedNo clear role for CEA or other tumor markersImaging: No single standard preferred method Choices include CT, MRI, upper GI with SBFT, and enteroclysis (double contrast study), octreotide or MIBG scan (carcinoid sx)Diagnostic procedures:GI procedures include capsule endoscopy, upper endoscopy (standard – to duodenum), upper endoscopy with push enteroscopy (visualize most of small bowel) Exploratory laparotomy – particularly if indicated for complete SBO, bowel perforation, bleeding, etc. Al-Madena copy
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Tumors of the Small Bowel
AdenocarcinomaMost common histology (up to ~50%)Most common in 50s-60s, M>FHighest incidence in duodenum, except in Crohn’s disease (ileum)~2/3 are resectable at time of diagnosisStage at presentation predicts prognosis Al-Madena copy
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Tumors of the Small Bowel

Adenocarcinoma: 5 year survival by stage: Stage I: 100% Stage II: 52% Stage III: 45% Stage IV: 0% 5 year survival by resectability: 54% in resected, 0% in unresected Curative-intent resection performed in 61% (Barnes et al., Ann Surg Oncol 1994; 1:73; retrospective analysis of 67 pts, MD Anderson)
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Adenocarcinoma of Small Bowel

Retrospective review of 217 patients: Median age 55, male predominant (61%) Stage: I (4%), II (20%), III (39%), IV (35%) Site of origin: Duodenum 52%, jejunum 25%, ileum 13% Curative-intent surgery in 67% (Whipple done in 17%) Mode of Dx: <1998: Surgery 39%, Upper GI 36%, EGD 14% >1998: EGD 28%, Surgery 26%, Upper GI 22%, CT 18% Mode of Dx (by location): Duodenum: EGD 42%, Upper GI 24%, CT 16%, Surgery 15% Ileum: Surgery 57%, Upper GI 21%, CT 7%, Phys exam 7% (MD Anderson, Dabaja et al., Cancer 2004; 101:518)
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Adenocarcinoma of Small Bowel

(217 pts @ MD Anderson; Dabaja et al., Cancer 2004; 101:518)
Overall Survival
Overall Survival by Stage
** Median OS: 20 months ** 5-yr OS rate: 26% **
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Adenocarcinoma of Small Bowel
(217 pts @ MD Anderson; Dabaja et al., Cancer 2004; 101:518)
Overall survival by node status
Overall survival by treatment
** Only lymph node involvement and curative-intent surgery were independent predictors of overall survival in multivariate analysis **
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Adenocarcinoma of Small Bowel

So what about adjuvant therapy? (217 pts @ MD Anderson; Dabaja et al., Cancer 2004; 101:518)
“Adjuvant chemotherapy after a Whipple procedure or resection did not appear to significantly affect the survival curve (P = 0.49) (Table 7)” Al-Madena copy
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Adenocarcinoma of Small Bowel

So, what about adjuvant therapy? Halfdanarson et al., ASCO 2006 Abstract #4127 - Retrospective review of 491 pts with adenocarcinoma of SB @ Mayo - Stage distribution: I (7%), II (27%), III (28%), IV (33%) - Median OS 20.7 months, 5-yr OS 26% - OS not better with adjuvant chemoRT or 5-FU based chemo - RR 1.17, p=0.45 (n=40 for CRT, n=33 for 5-FU) - Adjusted for age, sex, LN, grade, tumor location
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Adenocarcinoma of Small Bowel

Role of adjuvant therapy? Limited data, no prospective trials No proven benefit in retrospective trials Adjuvant regimens used in colon cancer are often employed in clinical practice Role of adjuvant therapy remains undefined, as benefits remain unknown
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Adenocarcinoma of Small Bowel
Adenocarcinoma: Chemo in advanced disease No standard chemotherapy regimen Regimens used include: 5-FU, doxorubicin, mitomycin C (FAM) RR 18%, OS 8 months (39 pts; Gibson et al., Oncologist 2005; 10:132) 5-FU + cisplatin or carboplatin or oxaliplatin RR 21%, OS 14 months (20 pts; Locher et al., Oncology 2005; 69:290) Gemcitabine and irinotecan, 5-FU based regimens RR 36%; palliative chemo predicts OS: HR 0.47, p = 0.035 (113 pts reviewed, 44 pts received chemo; Fishman et al., Am J Clin Oncol 2006; 29:225) 5-FU based chemotherapy Median OS 15.3 mos v. 3.1 mos (BSC) (491 pts reviewed, ? received chemo; Halfdanarson et al., ASCO 2006 Abstract #4127) Chemo appears active; prospective trials lacking
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Tumors of the Small Bowel

Carcinoid: Roughly 30% of small bowel tumors Originate from Kulchitsky cell, an enterochromaffin cell in crypts of Lieberkuhn Most commonly found in ileum Often secrete serotonin and other bioactive products including histamine, prostaglandins, polypeptides such as VIP, gastrin, glucagon, etc. In addition to abdominal symptoms, may present with symptoms related to secretory products (carcinoid syndrome): watery diarrhea, flushing, sweating, dyspnea, facial edema, tachycardia, hypotension, etc. Metastatic disease present in 90% of symptomatic pts
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Tumors of the Small Bowel

Carcinoid:If suspected, diagnostic tests include:24 hr urine for 5-HIAA (serotonin by-product)Also consider other biochemical tests (urine 5-HT, serum 5-HT, serum chromogranin A, etc.)Octreotide scan - 90% sensitivity if carcinoid sxMIBG scan (radiolabeled iodine, taken up by tumor and stored in granules) – 50-60% sensitive Al-Madena copy
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Carcinoid Tumors

Management:Surgery is treatment of choice if localizedAppendiceal carcinoids – appendectomySecond GI malignancies common:Endoscopy recommended prior to surgeryRx for advanced disease/carcinoid syndrome:Octreotide (somatostatin analogue)Hepatic regional therapy (RFA, cryotherapy, chemoembolization, etc.)InterferonChemotherapy/clinical trial Al-Madena copy
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Tumors of the Small Bowel

Lymphoma of the small bowel:15% of small bowel tumorsSmall percentage of GI lymphomas:Stomach 75%, small bowel 9%, ileocecal 7%Most common in ileumRisk factors: autoimmune diseases, immune deficiency or immune suppression, Crohn’s dz Al-Madena copy
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Tumors of the Small Bowel
Lymphoma of the small bowel:Histologies include:Extranodal marginal zone B-cell lymphoma of MALT type (MALToma)Marginal zone lymphomaBurkitt’s lymphomaImmunoproliferative small intestinal disease (IPSID) – common in Middle East Al-Madena copy
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Lymphoma of the Small Bowel

Treatment:Surgical ResectionLocoregional Radiation TherapyChemotherapy for advanced diseaseTreatment per histologic subtype of NHLMALToma – follicular lymphoma-like regimensMCL, Burkitt’s – more aggressive regimens Al-Madena copy
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Tumors of the Small Bowel

Sarcoma:Account for 10% of small bowel tumorsMost in jejunum or ileumMajority are leiomyosarcoma (75%)Then fibrosarcoma, liposarcoma, angiosarcomaEnlarge extraluminally – may grow extensively without causing obstructionSimilar histologically to benign counterparts:Leiomyosarcoma: leiomyoma; liposarcoma: lipomaCriteria for malignancy: number of mitoses, nuclear atypia, cellularity, presence of necrosis Al-Madena copy
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Tumors of the Small Bowel

Small bowel sarcoma: Treatment: Surgical resection is mainstay of therapy Incomplete resection may still palliate symptoms Chemotherapy may be considered Limited data for sarcoma regimens for SB sarcoma
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THANK YOU

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