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 Gerota’s 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 (Peyer’s 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
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 Peyer’s 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 Meissner’s ganglion
MUCUS
MEMBRANE consisting of: 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
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 and
Secretion
Table 3. Regulation of Intestinal Absorption and
Secretion
Agents that STIMULATE ABSORPTION (or inhibit secretion of
water)
Agents that STIMULATE SECRETION (or inhibit absorption
of 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%) by trypsin into simple amino acids
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 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
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 carrier-mediated 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.
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
Somato-statin
D cell inhibits gastrointestinal secretion, motility and splanchnic perfusion
Secretin S cell Stimulate exocrine pancreatic secretion; stimulate intestinal secretion Chole-cystokinin I cell Stimulate exocrine 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
Glucagon-like peptide 2
L cell Stimulate intestinal epithelium proliferation
Neuro-tensin N cell
Stimulate pancreatic and 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 Meckel’s Diverticulum Neoplasms Inflammatory process Crohn’s disease’ Diverticulitis
Chronic intestinal ischemia
Postischemic stricture
Radiation enteritis
Medication induced (NSAIDS, KCl tablets) EXTRINSIC Adhesions Congenital Laddormeckel’s 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
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 Proximal Small Bowel Distal Bowel PAIN Intermittent, intense, colicky, often relieved by vomiting Intermittent to constant
VOMITING Large volumes, billous and frequent
Low volume and frequency, progressively feculent with time TENDERNES S Epigastric, or periumbilical; quite mild unless strangulation is present
Diffuse and progressive
DISTENTION Absent Moderate to marked
OBSTIPATIO
N May not be present present
Symptom or
sign (Closed Loop) Small Bowel Colon and Rectum PAIN Progressive, intermittent to constant, rapidly worsens Continuous VOMITING May be prominent (reflex) Intermittent, not prominent, feculent when present TENDERNES
S Diffuse, progressive Diffuse
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)
Chron’s disease
Volvulus
Intussusceptions
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
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
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
Bird’s Beak or Ace of Spade in Volvulus
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
Collapsed distal ileum
Doppler ultrasound (Ogata, et al) Akinetic bowel
Presence of peritoneal fluid
Bull’s eye sign
Doughnut Sign
MANAGEMENT
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
SURGICAL
Determine if surgical intervention is necessary like: Rapid progression of symptoms
Peritoneal manifestations
Failure to resolve in 24 to 48 hours Complete obstruction
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 Rrichter’s 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
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
Bull’s 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. Bent inner tube sign 2. Ace of spade
3. Bird’s beak
Management:
Endoscopic decompression - 85% to 90% effective with 60% recurrence
Planned resection Colostomy Fixation
INFLAMMATION OF THE SMALL INTESTINE
CROHN’S 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 Crohn’s 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
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 Crohn’s 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
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
Diverticulitis Bleeding
MECKEL’S DIVERTICULUM
17th century- diverticula was observed as content of a hernia
1672 - Lavater
1701 - Mercy
1770 - Littre’s 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: Meckel’s 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 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. Littre’s hernia Inguinal hernia 50% Umbilical 20% Femoral 20% 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 ½-2 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 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% Malignant Carcinoid Heterotropic Tissue
*GIST- GI Stromal Tumor from interstitial cells of Cajal as leiomyoma or leiomyosarcoma RISK FACTORS Pre-existing condition Adenomatous polyp FAP PeutzJegher’s Syndrome Crohn’s Disease Leiomyoma Celiac Sprue
HIV; H. Pylori; EBV
Potential CA Adenocarcinoma Leiomyosarcoma (GIST) Adeno CA/Lymphoma Lyphoma CLINICAL PRESENTATION MALIGNANT
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 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 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
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-JEGHER’S 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 Jegher’s syndrome Crohn’s disease
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
Whipple’s 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
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 HODGKIN’S
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-Hodgkin’s lymphoma, B-cell lymphoma
Usually intermediate to high grade tumor with immunoblastic feature and diffuse
INCIDENCE
Younger population related to Burkitt’s 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
Malabsorption
STAGE SURVIVAL EXTENT
I 40-60% Tumor confined to GIT single or multiple
II 20% Extends from the primary site to lymph node but confined below the diaphragm
II Tumor penetrated the serosa and adjacent structures II Local Nodal Involvement II Distal Nodal Involvement III Negligible Supradiagphragmatic
involvement
IV Disseminated both sides of the diaphragm
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
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-
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. It’s 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 cymbals–sounds that say listen to this, it is important.
- Gary Provost, quoted in Roy Peter Clark’s (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.”
