surgery_1.4 small intestine (lecture).docx

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Pat, Suzie, Dale, Lenard, Morrice, Charlie, Gemmy Page 1of 11

I.4aSmall Intestine (Lecture-based)Dr. Bibera

July 6, 2013

ANATOMY

Small Intestine is the longest organ extending fromthe 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 caudallyat 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 ofTrietz

JEJANUM & ILEUM Extends from the ligament of Trietz to the ileocecal

valve (valve of Gaerlach)

Measuring about 250 cm to 270 cmJEJUNUM

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 prominentDiameter Wider Narrow

Mesenteric fat Thinner Thicker

Vasa Recta Longer Shorter

Arcades Few Numerous

ARTERIAL BLOOD SUPPLY Duodenum

Hepatic arteryoGastroduodenal arteryoPancreatico-duodenal artery

Superior Mesenteric artery

Jejenum and Ileum Superior Mesenteric arteryBLOOD SUPPLY FROM SUPERIOR MESENTERIC

ARTERY Jejenum

Vasa recta long and end arteries from shortarcades

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 distalportion of the Peyers patches Drains from the mucosa wall regional lymph

nodes Proceeds to the cisterna chilito the thoracic duct Provides transportof 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 andsynapse with the superior ganglia

Inhibits motility and secretion Mediates pain sensation

HISTOLOGYTable 2.Layers of the Small Intestine

SEROSA visceral peritoneum singlelayer of mesothelium

MUSCULARIS Thin, outer longitudinal muscle andthicker circular muscle

between layers are the Ganglion ofAuerbach

SUBMUCOSA strongest layerwith fibroelastictissue

contains networks of lymphatics,blood vessels and Meissnersganglion

MUCUSMEMBRANE

consisting of: muscularis mucosa lamina propria epitheliumPHYSIOLOGY

DIGESTION AND ABSORPTION main role Epithelium responsible for the absorption and

secretion Mechanism is either by:

Active transport- transfer of solutes in theabsence of electrochemical gradients

Passive transport- diffusion or convection withexisting gradient

WATER AND ELECTROLYTE ABSORPTION ANDSECRETION

Fluid going in: 8-10 liters per dayAbsorption by SI: 7500ml Diffusion, Osmosis, Active TransportAbsorption by Colon: 1500 ml Most are absorbed by the small bowel by simple

diffusion, osmosis and active transport


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1.4a Small Intestine (Lecture)Page 2of 11

500ml to 1500ml Electrolytes absorbed and water-soluble vitamins by

active transport Fat-soluble vitamins absorbed with the micelle

Figure 2.Water and Electrolyte Absorption andSecretion

Table 3.Regulation of Intestinal Absorption andSecretion

Agents thatSTIMULATE

ABSORPTION(or inhibit secretion of

water)

Agents thatSTIMULATESECRETION

(or inhibit absorptionof water)

Aldosterone Glucocorticoids Angiotensin Norepinephrine Epinephrine Dopamine Somatostatin Neuropeptide Y Peptide YY Enkephalin

Secretin Bradykinin Prostaglandins Acetylcholine Atrial natriuretic factor Vasopressin Vasoactive intestinal

peptide Bombesin Substance P Serotonin Neurotensin Histamine

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 3. Carbohydrate Digestion

PROTEIN ABSORPTION

Protein breakdown initiated in the stomach (15%) bytrypsin into simple amino acids

Digestion continue in the SI and split further thedipeptides, tripeptides and longer proteins

These pass the cellular membrane and goes to portalcirculation

80-90% complete in the jejunum

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

Figure5. Fat Digestion

VITAMIN AND MINERAL ABSORPTION Vitamin B12 (cobalamin) malabsorption can result

from a variety of surgical manipulations. water-soluble vitamins for which specific carrier-

mediated transport processes have been characterizedinclude : 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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Mediated by pacesetter in the muscularis mucosaknown as interstitial cells of Cajal and externalneurohormonal 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 alsoare observed

The FASTING PATTHER Or interdigestive motor cycle (IDMC) consists of three phases:

Phase I motor quiescence

Phase II seemingly disorganized pressurewaves occurring at submaximal rates

Phase III sustained pressure waves occurring atmaximal rates

This pattern is hypothesized to expel residualdebris and bacteria from the small intestine.

The median duration of theIDMC ranges from 90to 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 ACTIONSSomato-

statinD cell inhibits gastrointestinal

secretion, motility andsplanchnic perfusion

Secretin S cell Stimulate exocrinepancreatic secretion;stimulate intestinalsecretion

Chole-cystokinin

I cell Stimulate exocrinepancreatic secretion;stimulate gallbladderemptying; inhibit sphincterof Oddi contraction

Motilin M cell Stimulates intestinalmotility

Peptide YY L Cell Inhibits intestinal motilityand secretion

Glucagon-like

peptide 2

L cell Stimulate intestinalepithelium proliferation

Neuro-tensin

N cell Stimulate pancreatic andbiliary secretion; inhibitssmall bowel motility;stimulate intestinalmucosal 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 earlyoperation, before antibiotic, TPN and monitoring

Definition: When there is failure of contents to passdistally.

TERMINOLOGY AND CLASSIFICATION Mechanical obstruction

Inability of the luminal contents to pass thoroughdue 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 VASCULARINVOLVEMENT

Simple obstruction- there is no compromise ofblood flow Partial or incompleteoNarrowed lumen but permits passage of contentsoDx: radiographic examoTx: not necessarily operative

CompleteoLumen 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 completeINTRALUMINAL 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 DiverticulumNeoplasmsInflammatory process Crohns disease Diverticulitis Chronic intestinal ischemia Postischemic stricture Radiation enteritis Medication induced (NSAIDS, KCl

tablets)

EXTRINSIC AdhesionsCongenital Laddormeckels bands Postoperative PostinflammatoryHernias External (inguinal, femoral) InternalVolvulusExternal mass effect Abscess Annular pancreas Carcinomatosis Endometriosis Pregnancy Pancreatic pseudocyst

SITE OR SEGMENT INVOLVED Proximal or high obstruction

includes the pylorus, duodenum and proximaljejunum

Intermediate from the mid-jejunum to mid-ileum

Distal obstruction from distal ileum to proximal colon

Low obstruction beyond the transverse colon

Open obstruction


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flow of contents blocked but proximaldecompression 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 orsign

Proximal SmallBowel

Distal Bowel

PAIN Intermittent,intense, colicky,often relieved byvomiting

Intermittent toconstant

VOMITING Large volumes,billous andfrequent

Low volume andfrequency,progressively

feculent withtime

TENDERNES

S

Epigastric, orperiumbilical;quite mild unless

strangulation ispresent

Diffuse andprogressive

DISTENTION Absent Moderate tomarked

OBSTIPATIO

NMay not be

presentpresent

Symptom orsign

Small Bowel(Closed Loop)

Colon andRectum

PAIN Progressive,intermittent toconstant, rapidlyworsens

Continuous

VOMITING May beprominent(reflex)

Intermittent, notprominent,feculent whenpresent

TENDERNESS

Diffuse,progressive

DiffuseDISTENTION Often absent MarkedOBSTIPATION

May not bepresent

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

Figure 6.Common causes of small bowel obstruction inindustrialized 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/ElectrolytesNon-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 impairedIn SBO: Increasing pressure and distention>20cm H2O

inhibits absorption and stimulates secretion of saltsand water into the lumen

Release of pro-secretory and anti-anbsorptivehormones as vasoactive inhibitory peptide andprostaglandins

FloraNon-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 acidmetabolism, fat-soluble vitamins and gasformations

In SBO: Stasis favors change of flora and overgrowthAlters 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 obstructedAllows 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 vomitingAbdominal distension Failure to pass flatus and feces Fever Tachycardia and hypotension Distended peristaltic waves Hyperactive bowel sounds


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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 STUDIESRadiograph Imaging sensitivity of 70-80% To confirm the presence of obstruction To determine the site of obstruction To determine the etiology

PLAIN FILM OF THE ABDOMEN TRIAD of findings:

Dilated Bowel Loopso>3cm if the small intestine involvedo>8-10cm of the cecal diameter and 4-5cmoIf 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

Apple-coreappearance 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

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

Bulls eye sign

Doughnut Sign

MANAGEMENT

NON-OPERATIVE TREATMENTFor 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 rateOPERATIVE MANAGEMENT

Lysis of adhesions By-pass procedure Decompression ileostomy or colostomy Bowel resection Reduction and hernia repair Drainage of abscess Questions regarding viability1. Color2. Peristalsis3. Pulsations4. Doppler studies5. Fluorescein dyes6. Second look

MANAGEMENTObjective: To correct the existing fluid/electrolyte imbalance To treat the underlying cause of obstructionQuestions to be asked:

1. Severity of the pain2. Rapidity of onset and development3. Fluid and electrolyte imbalance4. Determine if complete or partial obstruction5. Determine presence of strangulation

TREATMENT Restriction of oral feedings Correction of fluid/electrolyte imbalance Decompression Antibiotics

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 typeGALLSTONE 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

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 ofobstruction

Diagnosis Xray findings of:

1. Bent inner tube sign2. Ace of spade3. Birds beak

Management: Endoscopic decompression - 85% to 90% effective

with 60% recurrence Planned resection Colostomy Fixation

INFLAMMATION OF THE SMALL INTESTINECROHNS DISEASE

1932:CrohnGinzburg and Oppenheimer reported onregional 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 orprotracted 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 withenlarged nodes fattening of the bowels andpathognomonic

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 orhydronephrosis

Fistula formation Perianal disease or fistula-in-ano Gynecologic as rectovaginal fistula Gallbladder disease

Extraintestinal Manifestations Dermatologic


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oErythema nodosumoPyoderma gangrenosum

RheumatologicoPeripheral arthritisoAnkylosing spondylitis

DIAGNOSIS

Based on history and physical exam e.g. unusualfistula-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 common2. Perforation with abscess formation - rare3. Fistula formation4. Hemorrhage5. Malignancy

PROCEDURES1. Resection as ileoascending colostomy or

segmental resection with primary anastomoses2. Stricturoplasty3. Others as bY-pass operation

RESULTS OR OUTCOME

Overall complications 15-30% as abscess, leakageand 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 muscleDUODENAL DIVERTICULUM

Vast majority are congenital If acquired it is located at the mesenteric side 2nd

portion of the duodenum near the exit of the biliaryand pancreatic ducts

Incidental findings on EGD or barium swallow withsmall bowel follow through

Difficult to treat due to its relationship with otherorgans and vascular areas

MANIFESTATIONS

Biliary in nature as gallstones, cholangitis, andjaundice

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 asymptomaticcases

Prophylactic removal is not indicated due to highmortality

Surgical intervention necessary in the presence ofperforation, diverticulitis and hemorrhage

Primary excision if the biliary and pancreatic ducts notinvolved 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 andtube 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:

oChronic abdominal painoEarly satietyoDiarrheaoMalabsorption 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; falsediverticula where part of the mucosa or submucosaprotrude 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 aremnant or duct between the intestinal tract and yolk

sac

1898 - Kulter described as a case of intusseptioninvolving Meckel diverticulum

1904 - Salzer noted gastric mucosa and ulcer of theulcer 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 adultsRULE OF TWO:

2% of general population 2years old 2feet from ileocecal valve 2:1 M:F ratio 2of the most common ectopic tissues 2most common complications: Bleeding and

ulceration

ETIOLOGY

Partial or complete failure of theomphalomesentericduct to obliterate giving rise to theff: 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

MICROSCOPIC

Heterotropic mucosa in 60%: gastric 60%,pancreaticacini second, colonic, endometriosis andhepatobiliary

CLINICAL MANIFESTATIONS

Complications in 4% of patients, 50% asymptomaticdiverticulamoccu in 10 yr old or younger

Certainty of diagnosis is made during the operation1. Hemorrhage

40-50% due to peptic ulceration described asbright 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%

Incisional 10%6. Neoplasm

Weinstein, 1963 in 106 cases Benign 26% Malignant 80%

oSarcoma 35%oAdenoCA 16%oCarcinoid 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% inyounger but 2 cmand 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 hrs2. Local immune system IgA3. Alkalinity prevents mucosal injury4. Absence of bacteria prevents genetic alterations5. Presence of mucosal enzymes benzyopyrenehydroxylase detoxifying the effects of benzopyrenes6. Rapid replication

BENIGN PREV. MALIGNANT PREV.

Adenoma 15% Adenocarcinoma 35-50%

Lipoma 15% Sarcoma* 15-20%

Leiomyoma 18% Lyphoma 10-15%

Hemartroma 15% Carcinoid 20-40%

Hemagioma 13% MalignantCarcinoid

HeterotropicTissue

*GIST- GI Stromal Tumor from interstitial cells of Cajalas leiomyoma or leiomyosarcoma

RISK FACTORSPre-existing condition Adenomatous polyp FAP PeutzJeghers Syndrome Crohns Disease Leiomyoma Celiac Sprue HIV; H. Pylori; EBVPotential 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 complicationsS/Sx Frequency

Asymptomatic 6-12%

Abdominal Pain 62-83%

Weight Loss 38-55%

Nausea and Vomiting 23-64%Bleeding 6-31%

Anemia 12-38%

Abdominal Mass 5-32%

BENIGN

S/Sx Frequency

Asymptomatic 47-60%

Abdominal Pain 24-50%

Bleeding 29-44%

Anemia 28-58%

Intermittent Obstruction 12-28%

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 enteroscopyPush 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 evaluationADENOMA

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

Arise from interstitial ells of Cajal which over 90% ofGIST 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 otherparts 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 Endoscopic examination Incidental findings on surgeryPRESENTATION

Depend on location of tumor Weight loss Abdominal pain Obstructive jaundice in peri-ampullary lesion Obstruction if the ileum is involved Occult blood lossTREATMENTSurgical 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


10/11


Overall 5 yr survival is 5-30% [ (-) nodes 50-70%,(+) nodes 15%]

LEIOMYOSARCOMA

Should be reclassified as gastrointestinal stromaltumor or GIST

Arises from connective tissues from muscle bloodvessels deep skin and nerve

Origin:Mesodermal component usually the tunicamucosa or muscularis mucosa

INCIDENCE nerve Sporadic occurrence Involving 10-20 cases per 1 million population One of 3-4 cases is malignantPRESENTATION 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 massTREATMENT 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 -


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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 FPATHOPHYSIOLOGY 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 scanTREATMENT palliation of symptoms

Cyproheptadine, Methylsergide, histamineantagonist and ocreotide an analogue ofsomatostatin

hepatic ligation or embolization which is good up to 4months

hepatic transplant debulking procedureCHEMOTHERAPY AND RT Modest response with the use of doxorubicin, 5FU,

and streptozocin, 20-30% No benefit with RTPROGNOSIS Five year survival of 60% Patients with carcinoid syndrome is 38 months

-END-

This sentence has five words. Here are five more words. Five-wordsentences 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 shortsentences. 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, thecrash of the cymbalssounds that say listen to this, it is important.

- 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 gameplayed against a childish primal human predilection for pleasure andnovelty 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~

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