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I.

4a Small Intestine (Lecture-based)


Dr. Bibera July 6, 2013
ANATOMY Small Intestine is the longest organ extending from the duodenal cap to the ileocecal valve Longest organ and 80% of the GIT Measures 4 to 6 m Historically, believed to have 2 key functions: Absorption of nutrients Maintain balance between absorption and secretion of H2O and electrolytes Serves as the largest and most complex endocrine gland Important immunologic defense barrier DUODENUM Duodenal cap/bulb Invested by mesentery Measures 5cm and closely related to the pancreas Site of over 90% of ulcer usually penetrating and eroding the gastroduodenal artery Posteriorly related are pancreas, portal vein and common bile duct Descending portion Measures 10cm coursing posteriorly and caudally at L1 and L2 Closely attached to the pancreas Overlying the Gerotas fascia and medial to IVC Midpoint of the 2nd portion enters papilla Transverse portion Entirely retroperitoneal in location Attached to the uncinate process of the pancreas Wedged between the SMA and aorta Fourth portion Turns superiorly & obliquely from the SMA along the border of the pancreas Bends sharply Passes superiorly and obliquely from the SMA along the border of the pancreas to reach the ligament of Trietz JEJANUM & ILEUM Extends from the ligament of Trietz to the ileocecal valve (valve of Gaerlach) Measuring about 250 cm to 270 cm JEJUNUM Widest portion of SI in volume Measures 100-110cm in length (40%) Diameter progressively decreases with distance ILEUM Distal 3/5 which is about 150-160cm in length (60%) Thin-walled with abundant lymphoid tissues (Peyers patches) Table 1. Comparison between Jejunum and Ileum JEJENUM ILEUM Length 100-110 cm 150-160 cm Walls Thicker Thinner Plica Circularis More prominent Less prominent Diameter Wider Narrow Mesenteric fat Thinner Thicker Vasa Recta Longer Shorter Arcades Few Numerous ARTERIAL BLOOD SUPPLY Duodenum Hepatic artery o Gastroduodenal artery o Pancreatico-duodenal artery Superior Mesenteric artery
Pat, Suzie, Dale, Lenard, Morrice, Charlie, Gemmy

Jejenum and Ileum Superior Mesenteric artery BLOOD SUPPLY FROM SUPERIOR MESENTERIC ARTERY Jejenum Vasa recta long and end arteries from short arcades Vessels not obscured by fatty tissues Mucosa smooth interrupted by valvulae circulares Ileum Shorter and less frequent vasa recta Numerous arcade Obscured by fatty tissues VENOUS AND LYMPHATIC DRAINAGE Venous drainage follows the arteries Dwell in the distal portion of the Peyers patches Drains from the mucosa wall regional lymph nodes Proceeds to the cisterna chili to the thoracic duct Provides transport of lipids, immune system and spread of malignancy EXTRINSIC NERVOUS SYSTEM Parasympathetic fibers from the vagus provides efferent fibers mediating peristalsis, feeling of nausea, vomiting and distention Sympathetic fibers travel in the splanchnic area and synapse with the superior ganglia Inhibits motility and secretion Mediates pain sensation HISTOLOGY Table 2. Layers of the Small Intestine SEROSA visceral peritoneum single layer of mesothelium MUSCULARIS Thin, outer longitudinal muscle and thicker circular muscle between layers are the Ganglion of Auerbach SUBMUCOSA strongest layer with fibroelastic tissue contains networks of lymphatics, blood vessels and Meissners ganglion MUCUS consisting of: MEMBRANE muscularis mucosa lamina propria epithelium PHYSIOLOGY DIGESTION AND ABSORPTION main role Epithelium responsible for the absorption and secretion Mechanism is either by: Active transport- transfer of solutes in the absence of electrochemical gradients Passive transport- diffusion or convection with existing gradient WATER AND ELECTROLYTE ABSORPTION AND SECRETION Fluid going in: 8-10 liters per day Absorption by SI: 7500ml Diffusion, Osmosis, Active Transport Absorption by Colon: 1500 ml Most are absorbed by the small bowel by simple diffusion, osmosis and active transport
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500ml to 1500ml Electrolytes absorbed and water-soluble vitamins by active transport Fat-soluble vitamins absorbed with the micelle

Digestion continue in the SI and split further the dipeptides, tripeptides and longer proteins These pass the cellular membrane and goes to portal circulation 80-90% complete in the jejunum

Figure 2. Water and Electrolyte Absorption and Secretion Table 3. Regulation of Intestinal Absorption and Secretion Agents that Agents that STIMULATE STIMULATE ABSORPTION SECRETION (or inhibit secretion of (or inhibit absorption water) of water) Aldosterone Secretin Glucocorticoids Bradykinin Angiotensin Prostaglandins Norepinephrine Acetylcholine Epinephrine Atrial natriuretic factor Dopamine Vasopressin Somatostatin Vasoactive intestinal Neuropeptide Y peptide Peptide YY Bombesin Enkephalin Substance P Serotonin Neurotensin Histamine

Figure 4. Protein Digestion FAT ABSORPTION Adult consumes 60g to 100g/d (40%) Triglycerides (glycerol, FFA and phospholipids cholesterol and lecithin) Digestion occurs in the small bowel Broken down into free fatty acids and 2 monoglycerides Emulsification facilitated by bile making it soluble to water Micelles formation with hydrophilic outer portion make absorption easily by diffusion

ELECTROLYTE ABSORPTION Nutrient-coupled Na Na/H+ exchange Na channels on the basolateral membrane mediated by Na/K+ ATPase CARBOHYDRATE ABSORPTION Adult consumes about 400 gm 60% starch, 30% sucrose, 10% lactose 20% of starch is amylose broken down to maltotriose and maltose Brush borders of SI contain enzymes Absorption of monosaccharides by active transport Figure 5. Fat Digestion VITAMIN AND MINERAL ABSORPTION Vitamin B12 (cobalamin) malabsorption can result from a variety of surgical manipulations. water-soluble vitamins for which specific carriermediated transport processes have been characterized include : ascorbic acid, folate, thiamine, riboflavin, pantothenic acid, and biotin Fat-soluble vitamins A, D, and E appear to be absorbed through passive diffusion. Vitamin K appears to be absorbed through both passive diffusion and carrier-mediated uptake. BARRIER AND IMMUNE FUNCTION Epithelium limits penetration of harmful substances: zonula occludens, zonula adherens and desmosomes Immune system of mucosa Bacteria ingested with the nutrients Presented to APC by M cells, IgA, IgM Production of defenses by GALT, IgA, mucins and defensins MOTILITY Contractions of the muscularis mucosa contribute to mucosal or villus motility, but not to peristalsis. Propulsion of food
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Figure 3. Carbohydrate Digestion PROTEIN ABSORPTION Protein breakdown initiated in the stomach (15%) by trypsin into simple amino acids

1.4a Small Intestine (Lecture)

Mediated by pacesetter in the muscularis mucosa known as interstitial cells of Cajal and external neurohormonal signals PATTERNS OF MUSCULARIS PROPRIA ascending excitation descending inhibition DIFFERENT TYPES OF CONTRACTION Fed or postprandial pattern begins within 10 to 20 minutes of meal ingestion and abates 4 to 6 hours afterward Rhythmic segmentations pressure waves traveling only short distances also are observed The FASTING PATTHER Or interdigestive motor cycle (IDMC) consists of three phases: Phase I motor quiescence Phase II seemingly disorganized pressure waves occurring at submaximal rates Phase III sustained pressure waves occurring at maximal rates This pattern is hypothesized to expel residual debris and bacteria from the small intestine. The median duration of theIDMC ranges from 90 to 120 minutes ENDOCRINE FUNCTION Rich source of regulatory peptides Released as response to stimuli Exerts action locally as paracrine or distally as hormone Peptides used in practice (Secretin, Ocreotide, Cholecystokinin) Table 4. Representative Regulatory Peptides HORMONE SOURCE ACTIONS SomatoD cell inhibits gastrointestinal statin secretion, motility and splanchnic perfusion Secretin S cell Stimulate exocrine pancreatic secretion; stimulate intestinal secretion CholeI cell Stimulate exocrine cystokinin pancreatic secretion; stimulate gallbladder emptying; inhibit sphincter of Oddi contraction Motilin M cell Stimulates intestinal motility Peptide YY L Cell Inhibits intestinal motility and secretion GlucagonL cell Stimulate intestinal like epithelium proliferation peptide 2 NeuroN cell Stimulate pancreatic and tensin biliary secretion; inhibits small bowel motility; stimulate intestinal mucosal growth SMALL BOWEL OBSTRUCTION Approach to intestinal obstruction parallel to the development of safe surgery Frederick Treves in 1884, laid the foundation of recognition and management of SBO In 1912, recognized the value of IV fluid resuscitation In 1920, radiograph used for diagnosis In 1925, decompression recognized to provide relief Principles of management established i.e. rapid IVF and electrolyte resuscitation, decompression and early operation, before antibiotic, TPN and monitoring Definition: When there is failure of contents to pass distally.

TERMINOLOGY AND CLASSIFICATION Mechanical obstruction Inability of the luminal contents to pass thorough due to blockade Neurogenic or Functional obstruction Passage is prevented due to disturbance of gut motility Ileus- if it involves the small intestine Pseudo-obstruction- if it involves the large intestine PRESENCE OR ABSENCE OF VASCULAR INVOLVEMENT Simple obstruction- there is no compromise of blood flow Partial or incomplete o Narrowed lumen but permits passage of contents o Dx: radiographic exam o Tx: not necessarily operative Complete o Lumen totally occluded and prevents passage of contents distally Strangulated obstruction- there is compromise of blood flow, necrosis and gangrene imminent even if obstruction is partial or complete INTRALUMINAL Foreign bodies Barium inspissations (colon) Bezoar Inspissated feces Gallstone Parasites Other (swallowed objects, enterocolitis) Intussuception Polypoidexophytic lesion INTRAMURAL Congenital Atresia, stricture or stenosis Web Intestinal duplication Meckels Diverticulum Neoplasms Inflammatory process Crohns disease Diverticulitis Chronic intestinal ischemia Postischemic stricture Radiation enteritis Medication induced (NSAIDS, KCl tablets) EXTRINSIC Adhesions Congenital Laddormeckels bands Postoperative Postinflammatory Hernias External (inguinal, femoral) Internal Volvulus External mass effect Abscess Annular pancreas Carcinomatosis Endometriosis Pregnancy Pancreatic pseudocyst SITE OR SEGMENT INVOLVED Proximal or high obstruction includes the pylorus, duodenum and proximal jejunum Intermediate from the mid-jejunum to mid-ileum Distal obstruction from distal ileum to proximal colon Low obstruction beyond the transverse colon Open obstruction

1.4a Small Intestine (Lecture)

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flow of contents blocked but proximal decompression possible loss of gastric, pancreatic and biliary secretions metabolic alkalosis develops Closed-loop obstruction both the inflow and outflow are blocked, e.g. torsion, volvulus, hernia Rapid increased pressure, hasten infection, gangrene and perforation. SYMPTOMS AND SIGNS OF BOWEL OBSTRUCTION Symptom or sign PAIN Proximal Small Bowel Intermittent, intense, colicky, often relieved by vomiting Large volumes, billous and frequent Distal Bowel Intermittent to constant Low volume and frequency, progressively feculent with time Diffuse and progressive

Figure 6.Common causes of small bowel obstruction in industrialized countries. PATHOPHYSIOLOGY Motility Fluid and gas accumulation elicit myoelectric proximal and distal functions Intense period of peristalsis, above and below Protective mechanism receptive relaxation Diminution of activity and ineffective contraction due to fatigue causing distension Mediated by neurohormones, toxins, luminal and conditions Intestinal Gas Mostly from swallowed air in 80% Consisting mostly of nitrogen and small amounts of other gasesas oxygen, carbon dioxide, etc Fluid/Electrolytes Non-obstructed: Mostly from swallowed air from 80% Consisting mostly of nitrogen and small amounts of other gases as oxygen, carbon dioxide, etc Absorption of fluid not impaired In SBO: Increasing pressure and distention>20cm H2O inhibits absorption and stimulates secretion of salts and water into the lumen Release of pro-secretory and anti-anbsorptive hormones as vasoactive inhibitory peptide and prostaglandins Flora Non-obstructed: Chyme entering the duodenum nearly sterile Small number of aerobic gram +/- and anaerobes in the distal portion Normal flora responsible for the secretions and motility of the bowel, short chain FA, bile acid metabolism, fat-soluble vitamins and gas formations In SBO: Stasis favors change of flora and overgrowth Alters motility, transport properties, perfusion, and lymph flow Endotoxin production stimulates secretions and altered response to inflammation and nitric oxide Intestinal Blood Flow Increased flow as initial response Hydrostatic and osmotic pressure favor flow of ECF to lumen Perfusion is compromised Bacterial invasion causes edema of fluid Wall ischemia and necrosis Partial bowel obstruction Part of the lumen is obstructed Allows passage of gas and fluid Less likely to develop strangulation Closed-loop obstruction Dangerous form Proximal and distal obstruction of a segment Rapid rise of luminal pressure and gangrene CLINICAL MANIFESTATIONS Colicky abdominal pain Nausea and vomiting Abdominal distension Failure to pass flatus and feces Fever Tachycardia and hypotension Distended peristaltic waves Hyperactive bowel sounds
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VOMITING

TENDERNES S

Epigastric, or periumbilical; quite mild unless strangulation is present DISTENTION Absent OBSTIPATIO N Symptom or sign PAIN May not be present

Moderate to marked present

Small Bowel Colon and (Closed Loop) Rectum Progressive, Continuous intermittent to constant, rapidly worsens VOMITING May be Intermittent, not prominent prominent, (reflex) feculent when present TENDERNES Diffuse, Diffuse S progressive DISTENTION Often absent Marked OBSTIPATIO N May not be present Present

COMMON ETIOLOGIES Adhesions- most common Neoplasms Primary small bowel neoplasms Secondary small bowel cancer (melanoma-derived metastasis) Local invasion by intra-abdominal malignancy (desmoids tumors) Carcinomatosis Hernia External (inguinal and femoral) Internal (following Roux-en-Y gastric bypass surgery) Chrons disease Volvulus Intussusceptions

1.4a Small Intestine (Lecture)

Mild tenderness with or without mass Examination to include groin and rectal DIAGNOSIS Focused on the following: Mechanical vs ileus What is the etiology Partial vs complete obstruction Simple or strangulated COMPLICATIONS AND SYSTEMIC EFFECTS Rapid onset of manifestations due to obstruction Gangrene and necrosis occurs Toxins from bacterial overgrowth released to systemic circulation Septicemia and shock IMAGING STUDIES Radiograph Imaging sensitivity of 70-80% To confirm the presence of obstruction To determine the site of obstruction To determine the etiology

Collapsed distal ileum Doppler ultrasound (Ogata, et al) Akinetic bowel Presence of peritoneal fluid Bulls eye sign

Doughnut Sign

MANAGEMENT PLAIN FILM OF THE ABDOMEN TRIAD of findings: Dilated Bowel Loops o >3cm if the small intestine involved o >8-10cm of the cecal diameter and 4-5cm o If the colon is obstructed Step-ladder Sign or Air Fluid levels Paucity of air in the colon Pneumoperitoneum (not sure kung under itong above. Labong numbering ni Doc) A. Contrast Studies With the use of barium, gastrografin or hypaque Specific site of obstruction Usually unnecessary in SBO Helpful in colonic obstruction Recurrent obstruction Low grade mechanical SBO Birds Beak or Ace of Spade in Volvulus NON-OPERATIVE TREATMENT For non-complicated SBO CONTRAST STUDIES IN PARTIAL SBO Passage of contrast medium into the colon after 8 hours Resolution in 19% Landescasper in 4 yr study Non-operative recurrence 53% Operative recurrence 29% CONTRAST STUDIES IN COMPLETE SBO Fleshner Study found 45% success rate OPERATIVE MANAGEMENT Lysis of adhesions By-pass procedure Decompression ileostomy or colostomy Bowel resection Reduction and hernia repair Drainage of abscess Questions regarding viability 1. Color 2. Peristalsis 3. Pulsations 4. Doppler studies 5. Fluorescein dyes 6. Second look MANAGEMENT Objective: To correct the existing fluid/electrolyte imbalance To treat the underlying cause of obstruction Questions to be asked: 1. Severity of the pain 2. Rapidity of onset and development 3. Fluid and electrolyte imbalance 4. Determine if complete or partial obstruction 5. Determine presence of strangulation TREATMENT Restriction of oral feedings Correction of fluid/electrolyte imbalance Decompression Antibiotics

Apple-core appearance in Colon CA

B.

CT Scan SB distended > 25 mm, detects transition zone Ability to distinguish complete or partial obstruction Nature of cause of obstruction or location Determine additional pathologic conditions e.g. tumors, abscess, IBD Strangulation late stage, intestinal wall Limited use in partial SBO

C. Ultrasound Detects bowel diameter >25mm


1.4a Small Intestine (Lecture)

SURGICAL Determine if surgical intervention is necessary like: Rapid progression of symptoms Peritoneal manifestations Failure to resolve in 24 to 48 hours Complete obstruction
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SPECIFIC TYPES OF SMALL BOWEL OBSTRUCTION ADHESIONS Comprises about 50% of all SBO Occurs about 5% of all patients who had history of laparotomy esp. pelvic operations Spontaneously resolves in 80% of cases if obstruction is partial Foreign body reaction found in pathologic studies of fibrous adhesions Prevention includes: Removal of foreign body as: sponge, starch or debris Good surgical technique: gentle tissue handling, unnecessary dissection and serosal trauma Choice of suture material Application of tissue plasminogen activator Use of omentum around site of surgery HERNIA Ranks 2nd cause of SBO Femoral hernia Internal herniation Rrichters hernia Special type GALLSTONE ILEUS Escape of gallstone >2.5cm from fistulous tract between GB and duodenum Occurs in 6/1000 cases SBO radiologic appearance: Stone lodge in the area of RLQ, ileocecal region Aerobilia- air in the biliary tree Recurrence rate of 5-10% Elective biliary surgery

1. Bent inner tube sign 2. Ace of spade 3. Birds beak Management: Endoscopic decompression - 85% to 90% effective with 60% recurrence Planned resection Colostomy Fixation INFLAMMATION OF THE SMALL INTESTINE CROHNS DISEASE 1932:CrohnGinzburg and Oppenheimer reported on regional ileitis First termed as terminal Ileitis Cure comes with complete resection Recurrence - due to incomplete resection INCIDENCE : Young adults (2nd to 3rd decade of life) CLASSIFICATION (AS TO LOCATION) Ileum: 75% Small intestine ONLY: 15 -30% Ileum and colon: 40 -60% Colon ONLY: 5 -30% Anorectal: 5-10%

ETIOLOGY Remains a mystery \m/ Environmental Genetic first degree relatives high risk of Crohns Findings of IBD 1 chr 16 Microbial M. paratuberculosis, Chlamydia, Reovirus, Pseudomonas Immunologic defective immune regulatory mechanism or protracted response to flora derived antigens PATHOLOGY A. GROSS APPEARANCE Thickened wall with violaceous appearance of the serosa Messenteric fat encroaches with anti-messenteric portion usually thickened, edematous and with enlarged nodes fattening of the bowels and pathognomonic Apthous ulcers, 3mm Transmural inflammation causing stricture, abscess, fistula and perforation Skip areas of normal bowel Narrowing of the lumen with mucosal ulceration, rake ulcer with intervening raised mucosa (cobblestone appearance) B. MICROSCOPIC Ulcerations Marked fibrosis Lymphangiectasia Nodular hyperplasia Non-caseating necrosis in 70% of cases in any layer and LN CLINICAL MANIFESTATIONS Abdominal Pain or mimics appendicitis Loss of appetite Weight loss Diarrhea, malabsorption and anemia Specific manifestations: Genitourinary due to endovesical fistula or hydronephrosis Fistula formation Perianal disease or fistula-in-ano Gynecologic as rectovaginal fistula Gallbladder disease Extraintestinal Manifestations Dermatologic
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Figure 7. Aerobilia INTUSSUSCEPTION Occurs in about 5% among adults Associated with other conditions as tumors, diverticulum, adenitis Occurs post-operatively: Suture lines 20% Adhesions 30% Internal tubes 50% Types: Enteric Ileocolic Ileocecal Colonic Diagnosis Currant jelly stool Dance sign Sausage shaped soft tissue Coil-spring sign on barium enema Bulls eye or dough nut sign on ultrasound VOLVULUS loop of bowel twists 180 degrees around its axis involves the sigmoid (65%), cecum, transverse colon Chilaiditi syndrome redundant between the liver and the diaphragm form of a closed loop type of obstruction Diagnosis Xray findings of:
1.4a Small Intestine (Lecture)

o Erythema nodosum o Pyoderma gangrenosum Rheumatologic o Peripheral arthritis o Ankylosing spondylitis DIAGNOSIS Based on history and physical exam e.g. unusual fistula-in-ano Intra op findings Small bowel series: Thickened mucosal folds Thumb printing Cobblestone appearance of the mucosa String sign Fistulous tract with other organs or small intestine pANCA determination TREATMENT Medical palliation than cure is the objective Control of diarrhea with cholysteramin Care of the perianal disease Antibiotic coverage: Sulfasalazine Corticosteroids Immunosuppressive agents Anti TNF (Infliximab) for resistant causes Surgical Intervention Acute onset of severe disease: Colitis -/+ Toxic megacolon Failure of medical therapy Recurrence of symptoms with tapering of steroids Drug induced complications Complications of Crohns Disease 1. Bowel obstruction-most common 2. Perforation with abscess formation - rare 3. Fistula formation 4. Hemorrhage 5. Malignancy PROCEDURES 1. Resection as ileoascending colostomy or segmental resection with primary anastomoses 2. Stricturoplasty 3. Others as bY-pass operation RESULTS OR OUTCOME Overall complications 15-30% as abscess, leakage and wound infection Recurrence: Endoscopy: 79% after 1yr and 85% after 3 years Clinical recurrence about 33% after 5 years from operation Reoperation after 5 years common DIVERTICULAR DISEASE OF THE SMALL BOWEL Uncommon clinical entity and usually discovered when looking for other diseases Varies with anatomic location Autopsy series have the highest incidence 9-20% ERCP findings about 2-5% Classifications Congenital true diverticulum with protrusion of full thickness of the wall of SI Acquired mucosa, submucosa with lack of muscle DUODENAL DIVERTICULUM Vast majority are congenital If acquired it is located at the mesenteric side 2nd portion of the duodenum near the exit of the biliary and pancreatic ducts Incidental findings on EGD or barium swallow with small bowel follow through
1.4a Small Intestine (Lecture)

Difficult to treat due to its relationship with other organs and vascular areas MANIFESTATIONS Biliary in nature as gallstones, cholangitis, and jaundice Pancreatitis Diverticulitis and perforation which maybe secondary to instrumentation DIAGNOSIS EGD, ERCP UGI series with small bowel follow through Contrast CT scan in cases of perforation TREATMENT Usually no treatment necessary in asymptomatic cases Prophylactic removal is not indicated due to high mortality Surgical intervention necessary in the presence of perforation, diverticulitis and hemorrhage Primary excision if the biliary and pancreatic ducts not involved Closure if the defect is small invert, tie, excise then close Serosal patch Roux-en-Y duodenojejunostomy In the presence of perforation extensive edema: Duodenal diverticulization i.e. gastrojejunostomy, closure of the pylorus, repair of the perforation and tube duodenostomy If there is hemorrhage (erosion of the arcade) Angiographic embolization Surgical suture and repair Endoscopic management destined to fail JEJUNAL DYSKINESIA A specific intestinal pseudoobstruction characterized by intermittent partial bowel obstruction Have significant relationship to complications of cholangitis, pancreatic and stone disease JEJUNAL DIVERTICULA Symptoms secondary to: Myenteric dysfunction: o Chronic abdominal pain o Early satiety o Diarrhea o Malabsorption with development of vitB12 deficiency and anemia Perforation, hemorrhage and obstruction Both types are asymptomatic Symptomatic in infection, perforation, hemorrhage, and obstruction. TWO TYPES Congenital Acquired usually increasing incidence with age; false diverticula where part of the mucosa or submucosa protrude thru the muscular wall DIAGNOSIS UGI series with small bowel follow through Enteroclysis Capsule with wireless endoscopy CTscan in cases of diverticulitis and perforation Angiography Technetium 99 scan

TREATMENT None is asymptomatic Resection: Multiple diverticulae Perforation


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Diverticulitis Bleeding MECKELS DIVERTICULUM 17th century- diverticula was observed as content of a hernia 1672 - Lavater 1701 - Mercy 1770 - Littres Hernia 1808 -Johann Friend Meckel discovered that it is a remnant or duct between the intestinal tract and yolk sac 1898 - Kulter described as a case of intusseption involving Meckel diverticulum 1904 - Salzer noted gastric mucosa and ulcer of the ulcer of the adjacent ileum INCIDENCE In autopsy series the incidence is 0.3-2.5% Soderlund noted 3.2% of patients who had appendectomy Common among children 2 years old M:F 2:1 Incidental findings in adults RULE OF TWO: 2% of general population 2 years old 2 feet from ileocecal valve 2:1 M:F ratio 2 of the most common ectopic tissues 2most common complications: Bleeding and ulceration ETIOLOGY Partial or complete failure of the omphalomesentericduct to obliterate giving rise to the ff: Meckels Diverticulum Mesodiverticulum band Opthalomesenteric fistula Enterocyst PATHOLOGY Length varies from 1-26 cm (2-5cm) Location 10-150cm from the ileocecal valve Soderlund, 1959: Children 40 cm, adult 50 cm Associated with congenital anomalies as exomphalos, atresias, anomalies of the CNS and CVS

Incisional 10% 6. Neoplasm Weinstein, 1963 in 106 cases Benign 26% Malignant 80% o Sarcoma 35% o AdenoCA 16% o Carcinoid 29% DIAGNOSIS CT Scan: not clinically useful Use of contrast studies as fistulogram Technetium scan- (Jewett, 1970) if the diverticulum contains gastric mucosa the accuracy is 90% in younger but <50% in adults Angiogram if actively bleeding TREATMENT Symptomatic Diverticulum Resection of the diverticulum Segmental Ileal resection - Bleeding due to present nearby ileal ulceration - Presence of inflammation and perforation Asymptomatic Diverticulum Infants, children, and young adult resection of the diverticulum Adult NOT advisable since overall complication is 2- 4%; 30 year, 2%; 75 years , 1 % Selective adult management is: palpable ectopic tissue, tumor, enterocolitis and wide based >2 cm and attached by bands NEOPLASMS OF THE SMALL BOWEL Rare e through the GIT comprise 40% of all neoplasms Incidence is 1-3% Reasons why it is rarely involved: 1. Rapid transit of contents -2 hrs 2. Local immune system IgA 3. Alkalinity prevents mucosal injury 4. Absence of bacteria prevents genetic alterations 5. Presence of mucosal enzymes benzyopyrene hydroxylase detoxifying the effects of benzopyrenes 6. Rapid replication BENIGN Adenoma Lipoma Leiomyoma Hemartroma Hemagioma PREV. 15% 15% 18% 15% 13% MALIGNANT Adenocarcinoma Sarcoma* Lyphoma Carcinoid Malignant Carcinoid PREV. 35-50% 15-20% 10-15% 20-40%

MICROSCOPIC Heterotropic mucosa in 60%: gastric 60%, pancreaticacini second, colonic, endometriosis and hepatobiliary CLINICAL MANIFESTATIONS Complications in 4% of patients, 50% asymptomatic diverticulamoccu in 10 yr old or younger Certainty of diagnosis is made during the operation 1. Hemorrhage 40-50% due to peptic ulceration described as bright red or maroon red in 47-57%, tarry stool 7% 2. Obstruction, volvulus, intussusceptions, entrapment 3. Inflammation or Diverticulitis in 20% Mimics acute appendicitis Reason to look for if the appendix is normal Perforate and causes peritonitis 4. Umbilical fistula Ileal contents ooze thru the umbilicus 5. Littres hernia Inguinal hernia 50% Umbilical 20% Femoral 20%
1.4a Small Intestine (Lecture)

Heterotropic Tissue *GIST- GI Stromal Tumor from interstitial cells of Cajal as leiomyoma or leiomyosarcoma RISK FACTORS Pre-existing condition Adenomatous polyp FAP PeutzJeghers Syndrome Crohns Disease Leiomyoma Celiac Sprue HIV; H. Pylori; EBV Potential CA Adenocarcinoma Leiomyosarcoma (GIST) Adeno CA/Lymphoma Lyphoma CLINICAL PRESENTATION MALIGNANT Absence of pathognomonic signs/symptoms
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Usually they are non-specific Vague complaints lead to errors and delay of diagnosis Symptomatic usually the ileum is involved Diagnosis expedited by onset of complications S/Sx Asymptomatic Abdominal Pain Weight Loss Nausea and Vomiting Bleeding Anemia Abdominal Mass BENIGN S/Sx Asymptomatic Abdominal Pain Bleeding Anemia Intermittent Obstruction Frequency 47-60% 24-50% 29-44% 28-58% 12-28% Frequency 6-12% 62-83% 38-55% 23-64% 6-31% 12-38% 5-32%

Arise from interstitial ells of Cajal which over 90% of GIST express CD117 ckit protooncogenes and 70-80% express CD34 (progenitor antigen) Involving the jejunum and usually solitary Bleeding results due to outgrowing the vascular supply causing necrosis and ulceration Presence of 2 mitotic figures/ 50 HPF have a higher risk of local recurrence LIPOMA More in males than females Involving the ileum and duodenum Arise from the adipose tissue of the submucosa and mesenteric fat at the base No malignant potential Can be diagnosed by CT scan PEUTZ-JEGHERS SYNDROME Inherited disorder Mucocutaneous melanotic pigmentation circum-orally, palms and soles of feet and GIT polyps and other parts of the body Polyps are hamartomatous in the jejunum and ileum, colon 50% and stomach in 25% Few reports of malignant degeneration Obstruction secondary to intussusceptions HEMANGIOMA Vascular neoplasm Related to Osler-Weber-Rendu disease Bleeding of the lower GIT MALIGNANT NEOPLASMS Primary malignant tumors: Adenocarcinoma Leiomyosarcoma (GIST) Lymphoma Carcinoid ADENOCARCINOMA Most common occurring 30-50% of cases Involves duodenum and proximal small bowel 35% Patients usually in their 6th-7th decade Male predominance Origin Epithelial cells of the intestinal mucosa Polyp-to-cancer sequence Peutz Jeghers syndrome Crohns disease

DIAGNOSIS Duration varies from weeks to months Infrequency of incidence Omission of diagnosis Limited imaging techniques: Plain X-ray Rarely helpful unless obstruction is present Useless if presentation is bleeding IMAGING DIAGNOSIS

CT scan Identify presence of tumor Presence of obstruction Other pathologic conditions UGIS with small bowel series Failure of CT to identify tumor Identify tumor of duodenum 85-90% Decrease accuracy with length 53-87% Enteroclysis Using Ba and methycellulose distending the bowel will compromise peristalsis Able to identify luminal tumor -90% Small bowel enteroscopy Push enteroscopy with pediatric colonoscopy Intraoperative colonoscopy Video capsule endoscopy 11x26 mm camera w/ battery, light source and transmitter Angiography and technetium scan BENIGN TUMORS Accounts for 30-51% of primary tumor Half of these are asymptomatic Symptoms consists of: Obstruction, Bleeding, Perforation Reason enough to have further evaluation ADENOMA Tubular adenoma Mostly asymptomatic involving the duodenum Low malignant potential Hemorrhage and obstruction if symptomatic Amendable to polypectomy Villous adenoma Distinct malignant potential Peri-ampullary, bleeding, obstruction and over 3cm size requires removal Brunner gland adenoma Hyperplasia of the exocrine gland Polypoid lesion involving the duodenum LEIOMYOMA Most common symptomatic tumor

DIAGNOSIS Endoscopic examination Incidental findings on surgery PRESENTATION Depend on location of tumor Weight loss Abdominal pain Obstructive jaundice in peri-ampullary lesion Obstruction if the ileum is involved Occult blood loss TREATMENT Surgical Management Resection of the small bowel Small lesions involving the duodenum Laparoscopic assisted mid-jejunoileal segment Right hemicolectomy in terminal ileum Whipples operation 2nd portion of the duodenum Medical Management Role of chemotherapy and RT is unclear Response rate using 5 FU is less than 20% RT no recommended since mucin producing tumor is radio resistant PROGNOSIS AND SURVIVAL Diagnosed late and nodes are involved

1.4a Small Intestine (Lecture)

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Overall 5 yr survival is 5-30% [ (-) nodes 50-70%, (+) nodes 15%] LEIOMYOSARCOMA Should be reclassified as gastrointestinal stromal tumor or GIST Arises from connective tissues from muscle blood vessels deep skin and nerve Origin: Mesodermal component usually the tunica mucosa or muscularis mucosa INCIDENCE nerve Sporadic occurrence Involving 10-20 cases per 1 million population One of 3-4 cases is malignant PRESENTATION Tendency to grow extra-luminal Obstruction is late manifestation Abdominal pain and weight loss GIT bleeding in 60% Perforation in 10% PATHOGENESIS In the GIT it arises from the interstitial cells of Cajal (ICC) Part of the ANS with pacemaker function Responsible in controlling the motility of GIT Due to gene mutation known as c-kit (CD117 or CD 34) which is a tyrosine kinase DIAGNOSIS Barium filled cavity on contrast study CT scan will show bulky extra luminal mass TREATMENT Surgical: wide en-bloc resection Extended lymphactenectomy not indicated Palliative by-pass operating Chemotherapy and RI Adriamycin and cyclophosphamide Radio-resistant PROGNOSIS Depends on the grade of the tumor which determines prognosis Presence of mitotic figures/HPF: Low grade < 10/HPF 60% to 80% High grade> 10/HPF - <20% LYMPHOMA/NON HODGKINS Occurs in about 10% - 15% of SB neoplasm Part of the GIT most involved include mostly the stomach followed by small bowel (25%-35%), ileocecal region and colon ORIGIN From the lymphoid tissue within the wall of the ileum Virtually a Non-Hodgkins lymphoma, B-cell lymphoma Usually intermediate to high grade tumor with immunoblastic feature and diffuse INCIDENCE Younger population related to Burkitts lymphoma involving the ileocecal area Older age group 5th to 6th decades with male predominance PRESENTATION Non-specific, fatigue, malaise, weight loss and abdominal pain In 25% of cases it presents as acute abdomen Perforation with peritonitis Obstruction secondary to intussusception Hemorrhage Palpable mass
1.4a Small Intestine (Lecture)

Malabsorption STAGE I II II II II III IV SURVIVAL 40-60% 20% EXTENT Tumor confined to GIT single or multiple Extends from the primary site to lymph node but confined below the diaphragm Tumor penetrated the serosa and adjacent structures Local Nodal Involvement Distal Nodal Involvement Supradiagphragmatic involvement Disseminated both sides of the diaphragm

Negligible

DIAGNOSIS Contrast study coarse mucosal folds and sub-mucosal nodules CT scan diffuse bowel wall thickening and nodal enlargement TREATMENT Surgical Resection due to obstruction or hemorrhage Debulking procedure Staging of the disease Chemotherapy and RT Controversial in curative resection in Stage IE and IIE For advance cases adjuvant therapy indicated CARCINOID TUMOR Most complex malignancy of the GIT Indolent with variable malignant potential Secretes endocrine and vasoactive substances or serotonin and tachykinins In US occur 600 new cases per year Occurs patients in their 6th decade of life ORIGIN Arise from Kulchitsky cells (enterochromaffin or argentaffin cells) in the crypts of Lieberkuhn Similar to islet cell tumor or carcinoma Innocuous appearance of cells with uniform nucleoli and cytoplasm Oberndorfer called this tumorkarzioide or cancer-like PRESENTATION Mostly asymptomatic Incidental findings in other surgical procedure Metastatic or manifest as carcinoid syndrome Occasionally presents as bleeding and obstruction DIAGNOSIS Tumor mass on CT scan Urinary determination of 5-HIAA usually normal TREATMENT Appendectomy if the size is <2cm en bloc dissection dissection or right hemicolectomy if >2cm segmental resection small bowel movement w/ regional lymphadenectomy METASTATIC NEOPLASM The most common malignant neoplasm of the small intestine Two sources Intra-abdominal Extra-abdominal: Melanoma is the most common source Treatment usually palliative, limited resection or bypass operation

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CARCINOID SYNDROME spectrum of vasomotor, GIT, , respiratory and cardiac manifestations flushing of face, neck, and upper trunk and extremities in 86% of cases diarrhea 75% bronchospasm telangiectasia of face and neck pellagra-like appearance cardiac 60-70% as endocardial fibrosis of tricuspid and pulmonary valves and CHF MEDIATORS serotonin tachynins (substance P and neuromedin) bradykinin dopamine histamine prostaglandin E and F PATHOPHYSIOLOGY Normally monoamine oxidase deactivates the mediators Action impaired or absent in the ff: Bronchial carcinoids Retroperitoneal carcinoid Extensive liver metastasis DIAGNOSIS elevated urine 5-HIAA (N: 9mg /24 h) >25mg/24hr Indium 111 Octreotide tag scan TREATMENT palliation of symptoms Cyproheptadine, Methylsergide, histamine antagonist and ocreotide an analogue of somatostatin hepatic ligation or embolization which is good up to 4 months hepatic transplant debulking procedure CHEMOTHERAPY AND RT Modest response with the use of doxorubicin, 5FU, and streptozocin, 20-30% No benefit with RT PROGNOSIS Five year survival of 60% Patients with carcinoid syndrome is 38 months -END-

- Gary Provost, quoted in Roy Peter Clarks (terrific) Writing Tools

~o~

An Amazing Article on Procrastination by David McRaney: Capable psychonauts who think about thinking, about states of mind, about set and setting, can get things done not because they have more willpower or drive, but because they know productivity is a game played against a childish primal human predilection for pleasure and novelty that can never be excised from the soul. Your effort is better spent outsmarting yourself than making empty promises through plugging dates into a calendar or setting deadlines for push-ups.

~o~

This sentence has five words. Here are five more words. Five-word sentences are fine. But several together become monotonous. Listen to what is happening. The writing is getting boring. The sound of it drones. Its like a stuck record. The ear demands some variety. Now listen. I vary the sentence length, and I create music. Music. The writing sings. It has a pleasant rhythm, a lilt, a harmony. I use short sentences. And I use sentences of medium length. And sometimes, when I am certain the reader is rested, I will engage him with a sentence of considerable length, a sentence that burns with energy and builds with all the impetus of a crescendo, the roll of the drums, the crash of the cymbalssounds that say listen to this, it is important. 1.4a Small Intestine (Lecture) Page 11 of 11

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