Small Intestine

Earle J. Niervo
Medical Clerk
 INTRODUCTION
• Raison d’être of the gastrointestinal tract as it
is the principle site of nutrient digestion and
absorption.
• Largest reservoir of immunologically active
and hormone-producing cells.
• Diseases are infrequent.
 GROSS ANATOMY
• Tubular structure that extends from the
pylorus to the cecum.
• Measures about 4 to 6 m.
• Consists of three segments
– the duodenum, the jejunum, and the ileum.
• Duodenum
• Proximal segment
– lies in the retroperitoneum
– Adjacent to the head and inferior border of the
body of the pancreas.
• Demarcated from the stomach by the pylorus
and from the jejunum by the ligament of
Treitz.
• Jejunum and Ileum
– Lie within the peritoneal cavity and are tethered
to the retroperitoneum by a broad-based
mesentery.
• Jejunoileal segment ( no distinct demarcation)
– 40% - jejunum
– 60% - ileum
• Plicae circulares or valvulae conniventes
– Visible upon gross inspection and radiographically.
– Prominent in the proximal intestine.
• Characteristic of the proximal than distal small
intestine
– larger circumference, thicker wall, less fatty
mesentery, and longer vasa recta.
• Gross examination of the small-intestinal
mucosa also reveals aggregates of lymphoid
follicles. ( Ileum – Peyers patches)
 Blood Supply
• Duodenum
– Celiac and the superior mesenteric arteries.
• Distal duodenum, the jejunum, and the ileum
– Superior mesenteric artery.
• Venous drainage - Superior mesenteric vein.
• Lymph drainage - lymphatic vessels coursing
parallel to corresponding arteries.
• This lymph drains -> mesenteric lymph ->
nodes to the cisterna chyli -> thoracic duct ->
left subclavian vein.
• The parasympathetic and sympathetic
innervation - Vagus and splanchnic nerves
 Histology
• Four distinct layers:
– Mucosa, submucosa, muscularis propria, and serosa
• Mucosa is the innermost layer, and it consists of
three layers: epithelium, lamina propria, and
muscularis mucosae.
• Lamina propria is located immediately external to
the epithelium and consists of connective tissue
and a heterogeneous population of cells.
• Mucosa is organized into villi and crypts
(crypts of Lieberkuhn).
• Villi are finger-like projections of epithelium
and underlying lamina propria that contain
blood and lymphatic (lacteals) vessels that
extend into the intestinal lumen.
• Crypts - epithelial cellular proliferation (250 –
300 cells)
• Enterocytes - predominant absorptive cell.
• Submucosa - dense connective tissue and a
heterogeneous population of cells, including
leukocytes and fibroblasts.
• Muscularis propria - outer, longitudinally oriented
layer and an inner, circularly oriented layer of
smooth muscle fibers.
– Located at the interface between these two layersare
ganglion cells of the myenteric (Auerbach’s) plexus.
• Serosa consists of a single layer of mesothelial
cells and is a component of the visceral
peritoneum.
• Function: Digestion and absorption
– Secrete hormones
SMALL BOWEL OBSTRUCTION
• Most frequent surgical disorder.
• Etiologies
1. Intraluminal (e.g., foreign bodies, gallstones,
or meconium)
2. Intramural (e.g., tumors, Crohn’s disease–
associated inflammatory strictures)
3. Extrinsic (e.g., adhesions, hernias, or
carcinomatosis)
• Intra-abdominal adhesions related to prior
abdominal surgery – 75% of the cases.
 Pathophysiology
• Obstruction ->
• Gas and fluid accumulation proximal to the site of
obstruction ->
• intestinal activity increases (colicky pain and the
diarrhea) ->
• ongoing gas and fluid accumulation ->
• bowel distends ->
• intraluminal and intramural pressures rise->
• intestinal motility is eventually reduced ->
 Pathophysiology
• With obstruction, the luminal flora of the
small bowel (usually sterile, changes, and a
variety of organisms have been cultured from
the contents “translocation”) ->
• intraluminal pressure increase ->
• impaired perfusion ->
• ischemia ->
• necrosis “strangulated bowel obstruction”.
• Type of obstruction
– Partial small bowel obstruction, only a portion of
the intestinal lumen is occluded, allowing passage
of some gas and fluid.
– Complete small bowel obstruction – entire lumen
is occluded.
• Closed-loop obstruction in which a segment of
intestine is obstructed both proximally and
distally (e.g., with volvulus).
 Clinical Presentation
– Colicky abdominal pain
– Nausea
– Vomiting
– Obstipation
• Strangulated obstruction
– Abdominal pain often disproportionate to the degree of abdominal
findings suggestive of intestinal ischemia.
– Tachycardia
– Localized abdominal tenderness
– Fever
– Marked leukocytosis
– Acidosis
 Diagnosis
• Diagnostic evaluation should focus on the
following goals:
• (a) distinguish mechanical obstruction from ileus
• (b) determine the etiology of the obstruction
• (c) discriminate partial from
• complete obstruction
• (d) discriminate simple from strangulating
obstruction.
 Diagnosis
• Abdominal series
• (a) a radiograph of the abdomen with the
patient in a supine position
• (b) a radiograph of the abdomen with the
patient in an upright position
• (c) a radiograph of the chest with the patient
in an upright position.
• Findings
– Dilated small bowel loops (>3 cm in diameter)
– Air-fluid levels seen on upright films
– Paucity of air in the colon
• Sensitivity:70 – 80%
• Specificity: Low
• Computed tomography
– 80% to 90% sensitive
– 70% to 90% specific
• Findings
– Discrete transition zone with dilation of bowel proximally
– Decompression of bowel distally
– Intraluminal contrast that does not pass beyond the
transition zone
– Colon containing little gas or fluid
• Closed-loop obstruction
– U-shaped or C-shaped dilated bowel loop
associated
– radial distribution of mesenteric vessels
converging toward a torsion point.
• Strangulation
• Thickening of the bowel wall
• Pneumatosis intestinalis (air in the bowel
• wall)
• Portal venous gas
• Pesenteric haziness
• Poor uptake of intravenous contrast into the
wall of the affected bowel
 Management
• Fluid resuscitation
– Isotonic fluid and indwelling bladder catheter.
• Nasogastric (NG) tube
– Effective gastric decompression decreases nausea, distention,
and the risk of vomiting and aspiration.
• Nothing per orem (NPO)
• Broad-spectrum antibiotics
– bacterial translocation may occur in the setting of small bowel
obstruction
• Expeditious surgery,
– standard therapy for complete small bowel obstruction
• Operative procedure performed for small
bowel obstruction varies according to the
etiology
– Adhesions are lysed
– Tumors are resected
– Hernias are reduced and repaired
• Criteria suggesting viability:
– Normal color
– Peristalsis
– Marginal arterial pulsations
 Outcome
• Prognosis is related to the etiology of
obstruction
– Adhesive small bowel obstruction less than 20%
admission over 5 years.
• Mortality
– <5% nonstrangulating small bowel obstruction
– Strangulating obstruction range from 8% to 25%
 Prevention
• Good surgical technique
• Careful handling of tissue
• Minimal use and exposure of peritoneum to
foreign bodies
ILEUS AND OTHER DISORDERS OF INTESTINAL
MOTILITY
• Impaired intestinal motility
– Intestinal obstruction in the absence of a lesion-
causing mechanical obstruction.
• Ileus
– Temporary motility disorder that is reversed with
time as the inciting factor is corrected.
 Pathophysiology
• Surgical stress-induced sympathetic reflexes,
inflammatory response mediator release, and
anesthetic/analgesic side effects ->
• Inhibit intestinal motility ->
• Returning to normal within the first 24 hours
after laparotomy and gastric and colonic
motility returning to normal by 48 hours and 3
to 5 days
• Small bowel motility is returned before colonic
and gastric motility
 Clinical Presentation
• Resembles that of small bowel obstruction
• Inability to tolerate liquids and solids by
mouth
• Nausea
• Lack of flatus or bowel movements
 Diagnosis
• Routine postoperative ileus should be
expected and requires no diagnostic
evaluation.
• Persists beyond 3 to 5 days postoperatively or
occurs in the absence of abdominal surgery
– Review medications
– Serum electrolytes
– Abdominal radiographs
• CT scanning is the test of choice
– Intra-abdominal abscess or other evidence of
peritoneal sepsis that may be causing ileus and can
exclude the presence of complete mechanical
obstruction.
• Chronic pseudo-obstruction
– Clinical features and confirmed by radiographic and
manometric studies.
– Diagnostic laparotomy or laparoscopy with full-
thickness biopsy
 Management
• Limiting oral intake
• Correcting the underlying inciting factor
• Decompression and hydration – presence of
distention and vomiting
• TPN if duration is prolonged
CROHN’S DISEASE
• Chronic, idiopathic transmural inflammatory
disease with a propensity to affect the distal
ileum. (Any of the alimentary tract can be
affected)
• United States - 3.6 to 8.8 per 100,000
• Ashkenazi Jewish: two- to four-fold higher risk
• Females>males
• Peak 3rd decade of life, 2nd peak: 6th decade of life
(bimodal distribution)
 Risk
• Genetic and environmental
• First-degree relatives of patients with Crohn’s
disease 14 to 15 times higher
• Monozygotic twins is as high as 67%
• Higher socioeconomic status - increased risk
of Crohn’s disease
• Crohn’s disease is more prevalent among
smokers.
 Pathophysiology
• Candidate organisms have included chlamydia,
Listeria monocytogenes, Pseudomonas species,
reovirus, Mycobacterium paratuberculosis->
• Sustained intestinal inflammation is the result of
either abnormalepithelial barrier function or
immune dysregulation->
• Poor barrier function is hypothesized to permit
inappropriate exposure of lamina propria
lymphocytes to antigenic stimuli derived from the
intestinal lumen ->
• Overresponsiveness of mucosal T cells to
enteric flora-derived antigens ->
• Immune tolerance and sustained
inflammation
• Locus on chromosome 16 (the so-called IBD1
locus) identified as NOD2 gene
• Earliest lesion is the aphthous ulcer(arise over
lymphoid aggregates, granulomas are
noncaseating) ->
• Stellate- shaped ulcers (Linear or serpiginous
ulcers may form when multiple ulcers or fuse
transverse coalescence of ulcers “cobble stone
appearance”) ->
• Chronic inflammation lead to transmural with
presence fat wrapping around the intestine
 Clinical Presentation
• Abdominal pain
• Diarrhea
• Weight loss.
• The onset of symptoms is insidious, and once
present, their severity follows a waxing and
waning course
• Small bowel – 80%, Colon – 20%
 Diagnosis
• Endoscopic findings that is compatible clinical history.
• presenting with acute or chronic
• Abdominal pain - right lower quadrant
• chronic diarrhea
• Evidence of intestinal inflammation on radiography or
endoscopy
• Discovery of a bowel stricture or fistula arising from
the bowel, and evidence of inflammation or
granulomas on intestinal histology.
• No single symptom, sign, or diagnostic test
establishes the diagnosis of Crohn’s disease
• Diagnosis is based:
– Complete assessment of the clinical presentation
– Confirmatory findings derived from radiographic,
endoscopic, and
– Colonoscopy with intubation of terminal ileum is the
main diagnostic tool (focal ulcerations adjacent to
areas of normal-appearing mucosa “cobble stone
appearance)
 Therapy
• No curative therapies
• Medical Therapy:
• Antibiotics
– adjunctive role in the treatment of infectious complications
associated with Crohn’s disease.
• Aminosalicylates
– Induces disease remission (unknown)
• Corticosteroids
– Mildly to moderately severe disease that does not respond
to aminosalicylates.
• Immunomodulators.
– thiopurine antimetabolites azathioprine and its
active metabolite, 6-mercaptopurine
– 3 to 6 months response
– Alternative : methothrexate
– Infliximab (anti tumor necrosis factor alpha) :
Closure of fistulae
• Surgery
– 50 – 70% will require at least one surgery
– Unresponsive to aggressive medical therapy or who
develop complications of their disease
– Abscess – Percutaneuos drainage
– Segmental resection with anastomosis
– Stricturoplasty – fig 28-19
• Preservation of intestinal surface area and is especially
well suited to patients with extensive disease and fibrotic
strictures
 Outcomes
• Overall complication rates following surgery for Crohn’s
disease range from 15% to 30%.
• 70% recur within 1 year of a bowel resection and 85% by 3
years
• Clinical recurrence, defined as the return of symptoms
confirmed as being due to Crohn’s disease, affects 60% of
patients by 5 years and 94% by 15 years after intestinal
resection.
• Reoperation becomes necessary in approximately one third
of patients by 5 years after the initial operation, with a
median time to reoperation of 7 to 10 years.
INTESTINAL FISTULAS
• Abnormal communication between two
epithelialized surfaces.
• Internal fistula
– Communication occurs between two parts of the
GI tract or adjacent organs
• External fistula
– Involves the skin or another external surface
epithelium.
• Enterocutaneous fistula
– Drains less than 200ml/day – low output fistula
– Drains more than 500ml/day – high output fistula
Pathophysiology
 Clinical Presentation
• Evident between the fifth and tenth
postoperative days.
• Fever, leukocytosis, prolonged ileus,
abdominal tenderness, and wound infection
are the initial signs.
• Obvious when drainage of enteric material
through abdominal wound
 Diagnosis
• CT scan with contrast
– Leakage of contrast material from the intestinal
lumen can be observed
• Small bowel series or enteroclysis examination
– R/O distal obstruction
• Fistulogram
– in which contrast is injected under pressure
through a catheter placed percutaneously into the
fistula tract
 Therapy
• 1. Stabilization
– Fluid and electrolyte
– Nutrition
– Sepsis is controlled
– Ostomy appliances or fistula drains.
• 2. Investigation
• 3. Decision.
– The available treatment options
• 4. Definitive management
– surgical procedure
– preoperative planning and surgical experience.
• 5. Rehabilitation.
• Somatostatin analogue octreotide
– Patients with high-output fistulas
– reduces the volume of fistula output
– facilitating fluid and electrolyte management.
• Timing of Surgical Intervention
– 2-3 months conservative management
– 90% of fistulas usually within 5 weeks
 Outcomes
• 50% of intestinal fistulas close spontaneously
• “FRIEND”
– Foreign body within the fistula tract
– Radiation enteritis
– Infection/Inflammation at the fistula origin
– Epithelialization of the fistula tract
– Neoplasm at the fistula origin
– Distal obstruction of the intestine)
SMALL BOWEL NEOPLASMS
• Adenomas are the most common benign
neoplasm of the small intestine.
• Other benign tumors include fibromas,
lipomas, hemangiomas, lymphangiomas, and
neurofibromas.
• Frequently encountered in the duodenum.
• Benign neoplasm: 30 – 50% (adenomas,
lipomas, hamartomas, and hemangiomas.)
• Primary small bowel cancers: Rare
– 5300 cases per year in the United States
– Adenocarcinomas: 35% - 50%
– Carcinoid tumors: 20% to 40%
– lymphomas comprise 10% to 15%.
– Metastatic: Melanoma
• Risk factors
– Consumption of red meat
– Ingestion of smoked or cured foods
– Crohn’s disease
– Celiac sprue
– Hereditary nonpolyposis colorectal cancer
(HNPCC)
– Familial adenomatous polyposis (FAP)
– Peutz-Jeghers syndrome
 Pathophysiology
• Low frequency of smallintestinal neoplasms
– dilution of environmental carcinogens in the liquid chyme present
in the small-intestinal lumen
– rapid transit of chyme limiting the contact time between
carcinogens and the intestinal mucosa
– low concentration of bacteria in small-intestinal chyme and low
concentration of carcinogenic products of bacterial metabolism
– Mucosal protection by secretory IgA and hydrolases such as
benzpyrene hydroxylase that may render carcinogens less active
– efficient epithelial cellular apoptotic mechanisms that serve to
eliminate clones harboring genetic mutations.
 Clinical Presentation
• Partial small bowel obstruction
– Crampy abdominal pain and distention
– Nausea and vomiting (most common)
– Palpable abdominal mass
– Jaundice secondary to biliary obstruction or
hepatic metastasis may be present.
– Cachexia, hepatomegaly, and ascites may be
present with advanced disease.
 Diagnosis
• Rarely diagnosed preoperatively
• Carcinoid syndrome
– elevated serum 5-hydroxyindole acetic acid (5-HIAA)
• Small-intestinal adenocarcinomas
– Elevated carcinoembryonic antigen (CEA)
– Metastasis
• Enteroclysis –
– Sensitivity of over 90%
– Test of choice
• Upper GI with small bowel followthrough
examinations - only 30% to 44%
• CT scanning
– low sensitivity for detecting mucosal or intramural
lesions but can demonstrate large tumors and is
useful in the staging of intestinal malignancies
• Angiography or radioisotope-tagged red blood
cell (RBC) scans
– Tumors associated with significant bleeding
• Esophagogastroduodenoscopy
– Duodenal tumor
• Endoscopic ultrasonography (EUS)
– Additional information such as the layers of the
intestinal wall involved by the lesion
• Colonoscopy
– Distal ileum
 Therapy
• TF
 Outcomes
• Complete resection of duodenal
adenocarcinomas
– 5-year survival rates ranging from 50% to 60%.
• Complete resection of adenocarcinomas
jejunum or ileum
– 5-year survival rates of 20% to 30%
• Small-intestinal carcinoid tumors
– Five-year survival rates of 75% to 95%
• Carcinoid tumor–derived liver metastases
– 5-year survival rates of 19% to 54%
• Intestinal lymphoma
– 5 year survival 20% to 40%
• GISTs
– 35% to 60% 5 year survival
– Recurrence rate 35%
RADIATION ENTERITIS
• Radiation therapy is a component of
multimodality therapy for:
– intra-abdominal and pelvic cancers: cervix,
endometrium, ovary, bladder, prostate, and rectum
• Acute radiation enteritis
– Transient condition (75%)
• Chronic radiation is enteritis
– Inexorable and develops in approximately 5%
to15% of these patients.
 Pathophysiology
• Radiation therapy
– cellular injury directly
– Generation of free radicals
– Receiving at least 4500 cGy
• Free radicals -> breaks double stranded DNA
-> Apoptosis -> Cell Death
 Diagnosis
• Review of the records of their radiation
treatments
• Enteroclysis is the most accurate imaging test
for diagnosing chronic radiation enteritis
• CT scanning
– Rule out the presence of recurrent cancer
– Manifestation will overlap chronic radiation
enteritis.
 Therapy
• Acute radiation enteritis are self-limited
– Supportive therapy
• Antiemetics
• diarrhea-induced dehydration – Hospitalization and parenteral
fluid administration
• Chronic radiation enteritis
– Surgery: highgrade obstruction, perforation, hemorrhage,
intra-abdominal abscesses, and fistulas
– High mortality rate
– Resection of diseased intestine with primary anastomosis
between healthy bowel segment
 Outcomes
• Acute radiation injury to the intestine is self-
limited
• Surgery for chronic radiation enteritis
– high morbidity rates and reported mortality rates
averaging 10%.
 Prevention
• Radiation exposure below 5000 cGy
• Multi-beam radiation techniques to minimize
the area of maximal radiation exposure and
tilt tables to move the bowel out of the pelvis
during radiation
• Oral sulfasalazine
– Reduce incidence of Acute radiation-induced
enteritis
MECKEL’S DIVERTICULUM
• 2% of the general population
• true diverticula because their walls contain all
of the layers found in normal small intestine
• ileum within 100 cm of the ileocecal valve
• Meckel’s diverticula contain heterotopic
mucosa
– Gastric mucosa 60%
– Pancreatic acini next most common
– Brunner’s glands, pancreatic islets, colonic
mucosa, endometriosis, and hepatobiliary tissues.
• Rule of two’s”:
– 2% prevalence
– 2:1 male predominance
– location 2 feet proximal to the ileocecal valve in
adults, and half of those who are symptomatic are
under 2 years of age
 Pathophysiology
• 8th week of gestation -> omphalomesenteric
(vitelline) duct normally undergoes obliteration.
• Failure or incomplete vitelline duct obliteration
-> abnormalities
• Most common: Meckel’s diverticulum
• Omphalomesenteric fistula, enterocyst, and a
fibrous band connecting the intestine to the
umbilicus
• Intestinal obstruction associated with Meckel’s
diverticulum:
– Volvulus of the intestine around the fibrous band
attaching the diverticulum to the umbilicus
– Entrapment of intestine by a mesodiverticular
band
– Intussusception with the diverticulum acting as a
lead point
– Stricture secondary to chronic diverticulitis
• Littre’s hernia
– Meckel’s diverticula in inguinal or femoral hernia
sacs
 Clinical Presentation
• Asymptomatic unless associated complications
arise (4% to 6%)
• Bleeding – Common presentation in children
(50%)
• Intestinal obstruction – common presentation
in adult
• Diverticulitis
 Diagnosis
• Incedental finding on:
– Radiographic imaging, during endoscopy, or at the time of
surgery
• CT scanning – low sensitivity
• Enteroclysis
– Accuracy of 75%
– Not applicable during acute presentations
• Radionuclide scans (99mTc-pertechnetate)
– positive only (ectopic gastric mucosa)
• Angiography – localize site of bleeding
 Therapy
• Symptomatic Meckel’s diverticulum
– Diverticulectomy with removal of associated
bands connecting the diverticulum
– If bleeding: segmental resection of ileum that
includes the diverticulum and ulcer
• Asymptomatic Meckel’s diverticula
– Prophylactic removal of asymptomatic Meckel’s
diverticula
ACQUIRED DIVERTICULA
• false diverticula
– walls consist of mucosa and submucosa but lack a complete
muscularis
– more common in the duodenum and tend to be located near
the ampulla
• Periampullary
• Juxtapapillary 75% medial wall of duodenum
• Perivaterian
– jejunoileal diverticula –
• jenunum 80%
• Ileum 15%
• Both 5%
• Incidince increase with age
• Rare in less than 40 yo
• The mean age of diagnosis ranges from 56 to
76 years.
 Pathophysiology
• Related:
– Acquired abnormalities of intestinal smooth
muscle or dysregulated motility -> herniation of
mucosa and submucosa through weakened areas
of muscularis
– Associated with bacterial overgrowth, leading to
vitamin B deficiency, megaloblastic anemia,
12

malabsorption, and steatorrhea.

 Clinical Presentation
• Acquired diverticula are asymptomatic unless associated
complications arise:
– Intestinal obstruction, diverticulitis, hemorrhage, perforation,
and malabsorption.
• Periampullary duodenal diverticula:
– Choledocholithiasis, cholangitis, recurrent pancreatitis, and
sphincter of Oddi dysfunction
• 10% to 30% jejunoileal diverticula:
– Intermittent abdominal pain
– Flatulence
– Diarrhea, and constipation
 Diagnosis
• Incedental finding:
– Radiographic imaging, during endoscopy, or at the
time of surgery
 Therapy
• Asymptomatic acquired diverticula should be left
alone
• Bacterial overgrowth (acquired diverticula):
antibiotics
• Bleeding and diverticulitis
– segmental intestinal resection for diverticula located in the
jejunum or ileum.
• Bleeding and obstruction related to lateral duodenal
diverticula
– Diverticulectomy alone
MESENTERIC ISCHEMIA
• Acute mesenteric ischemia and chronic
mesenteric ischemia.
• Four distinct pathophysiologic mechanisms can
lead to acute mesenteric ischemia:
– Arterial embolus
– Arterial thrombosis
– Vasospasm (also known as nonocclusive
mesenteric ischemia[NOMI])
– Venous thrombosis
• Embolus
– most common cause of acute mesenteric ischemia
and is responsible for over 50% of cases
– Embolic source: heart
• left atrial or ventricular thrombi or valvular lesions
• Embolism of SMA (50%) –
– wedged and cause occlusion at branch points in the
mid to distal superior mesenteric artery, usually
distal to the origin of the middle colic artery
• acute occlusions due to thrombosis
– proximal mesenteric arteries, near their origins
• Regardless of the pathophysiologic mechanis:
– Acute mesenteric ischemia can lead to intestinal
mucosal sloughing within 3 hours of onset and
full-thickness intestinal infarction by 6 hours
• Chronic mesenteric ischemia
– Atherosclerotic (celiac, superior mesenteric, and inferior
mesenteric arteries).
– develops insidiously, allowing for development of collateral
circulation
– rarely leads to intestinal infarction.
• A chronic form of mesenteric venous thrombosis can
involve the portal or splenic -> portal hypertension ->
– esophagogastric varices
– Splenomegaly
– hypersplenism.
 Clinical manifestation
• Acute mesenteric ischemia
– Severe abdominal pain, out of proportion to the
degree of tenderness on examination
– Colicky and most severe in the midabdomen.
– Associated symptoms: nausea, vomiting, and
diarrhea
• Chronic mesenteric ischemia
– Presents insidiously
– Postprandial abdominal pain is the most prevalent
symptom
– Producing a characteristic aversion to food (“food
fear”) and weight loss
 Therapy
• TF
• mesenteric artery occlusive disease in the
chapter on arterial
• disease.
MISCELLANEOUS CONDITIONS
Obscure Gastrointestinal Bleeding
• Obscure GI bleeding
– GI bleeding for which no source has been identified by
routine endoscopic studies (EGD and colonoscopy)
• Overt GI
– presence of hematemesis, melena, or hematochezia
• occult GI bleeding
– occurs in the absence of overt bleeding and is identified
on laboratory tests (e.g., iron-deficiency anemia) or
examination of the stool (e.g., positive guaiac test).
 Etiology
• Small-intestinal angiodysplasias
– 75% of cases in adults
• Neoplasms
– Approximately 10%.
• Meckel’s diverticulum
– most common etiology of obscure GI bleeding in
children
 Etiology
• Other etiologies
– Crohn’s disease
– Infectious enteritides
– nonsteroidal anti-inflammatory drug (NSAID)-
– induced ulcers and erosions
– Vasculitis
– Ischemia
– Varices
– Diverticula
– Intussusception.
 Diagnostics
• Push enteroscopy
– advancing a long endoscope (such as a pediatric or
adult colonoscope or a specialized instrument)
beyond the ligament of Treitz into the proximal
jejunum.
– 60 cm of the proximal jejunum.
– Diagnostic yield - 3% to 65%.
– allows for cauterization of bleeding sites
• Sonde enteroscopy
– a long, thin fiberoptic instrument is propelled
through the intestine by peristalsis following
inflation of a balloon at the instrument’s tip.
– Visualization is done during instrument
withdrawal; approximately 50% to 75% of the
small-intestinal mucosa can be examined.
– Instrument lacks biopsy or therapeutic capability
• Wireless capsule enteroscopy
– Radiotelemetry capsule enteroscope that is small
enough to swallow and has no external wires,
fiberoptic bundles, or cables
– Capsule is being propelled through the intestine
by peristalsis, video images are transmitted using
radiotelemetry to an array of detectors attached
to the patient’s body
• Angiography
– to help localize the bleeding source.
• Exploratory laparoscopy or laparotomy with
intraoperative enteroscopy
– If above management fails
Small Bowel Perforation
 Etiology

• Duodenal perforation due to peptic ulcer

disease most common perforation of small
bowel (1980s)
• Iatrogenic injury (GI endoscopy)
– Most common cause of small bowel
perforation(today)
– Duodenal perforation during ERCP with
endoscopic sphincterotomy (ES)
 Etiology

• Other etiologies
– Infection(especially tuberculosis, typhoid, and CMV)
– Crohn’s disease
– Ischemia
– Drugs (e.g., potassium- and NSAID-induced ulcers)
– Radiation-induced injury
– Meckel’s and acquired diverticula
– Neoplasms (especially lymphoma, adenocarcinoma, and
melanoma)
– Foreign bodies
 Manifestation
• Resemble those of ERCP-induced pancreatitis
(hyperamylasemia)
 Diagnostics
• CT scanning
– Most sensitive test
• Pneumoperitoneum for free perforations
(retroperitoneal air)
• contrast extravasation
• paraduodenal fluid collections
 Management
• True cases of retroperitoneal perforations of the
duodenum can be managed nonoperatively, in the
absence of progression and sepsis
• Intraperitoneal duodenal perforations require
surgical repair with pyloric exclusion and
gastrojejunostomy or tube duodenostomy.
• Iatrogenic small bowel perforation incurred during
endoscopy, if immediately recognized, can
sometimes be repaired using endoscopic techniques
• Perforation of the jejunum and ileum occurs
into the peritoneal cavity and usually causes
overt symptoms and signs:
– abdominal pain, tenderness, and distention
accompanied by fever and tachycardia
• Jejunal and ileal perforations
– Surgical repair or segmental resection.
Chylous Ascites
• Accumulation of triglyceride-rich peritoneal
fluid with a milky or creamy appearance,
caused by the presence of intestinal lymph in
the peritoneal cavity
 Etiology
• Abdominal malignancies and cirrhosis in
western countries
• Infectious etiologies, such as tuberculosis and
filariasis, account for most cases in eastern
and developing countries
• abdominal and thoracic operations and
trauma
 Etiology
• Operations associated Chylos ascites
– Abdominal aortic aneurysm repair
– Retroperitoneal lymph node dissection
– Inferior vena cava resection
– Liver transplantation
• Other etiologies
– Congenital lymphatic abnormalities (e.g., primary
– Lymphatic hypoplasia)
– Radiation
– Pancreatitis
– Right-sided heart failure.
• Three mechanisms have been postulated to
cause chylous ascites:
– exudation of chyle from dilated lymphatics on the
wall of the bowel and in the mesentery caused by
obstruction of lymphatic vessels at the base of the
mesentery or the cisterna chili (e.g., by
malignancies)
– Direct leakage of chyle through a
lymphoperitoneal fistula (e.g., those that develop
as a result of trauma or surgery)
– exudation of chyle through the wall of dilated
retroperitoneal lymphatic vessels (e.g., in
congenital lymphangiectasia or thoracic duct
obstruction).
 Manifestation
• Distention
• Dyspnea due to distention
 Diagnostic
• Paracentesis
– cloudy and turbid appearance
– clear in fasting patients
– Fluid triglyceride concentrations above 110 mg/dL
are diagnostic
• CT scan
– Identifying pathologic intra-abdominal lymph
nodes and masses and in identifying extent and
localization of fluid.
• Lymphangiography and lymphoscintigraphy
– localize lymph leaks and obstruction (surgical
planning)
 Management
• Evaluating and treating the underlying causes
– infectious, inflammatory, or hemodynamic
• High-protein and low-fat diet supplemented with
medium-chain triglycerides (Intestine->portal vein)
• Fasted and placed on TPN (Not Responding)
• Octreotide
– Decrease lymph flow
• Paracentesis
– indicated for respiratory difficulties related to abdominal
distention.
 Management
• Surgical repair
– postoperative and trauma-related cases that fail to
respond to initial nonoperative therapy
– Lymphatic leaks are localized and repaired with
fine nonabsorbable sutures
• Extravasation of chyle is localized to the
periphery of the small bowel mesentery
– limited small bowel resection can be performed
 Management
• Poor surgical candidates and do not respond
to prolonged conservative therapy
– peritoneovenous shunting
– high rates of complications, including sepsis and
disseminated intravascular coagulation
– high occlusion rate (viscous)
Intussusception
• Condition where one segment of the intestine
becomes drawn in to the lumen of the
proximal segment of the bowel
• Seen in the pediatric population
• Cecum intussuscepts into the ileum (ileocolic
intussusception)
• Idiopathic condition
– Treated nonsurgically by radiologic reduction.
• Adult intussusceptions
– less common
– distinct pathologic lead point, which can be
malignant in up to one half of case
– History of intermittent abdominal pain and signs
and symptoms of bowel obstruction.
• CT scan
– investigation of choice
– “target sign”
 Treatment
• Surgical resection of the involved segment and
the lead point,
• Pathologic evaluation to rule out an
underlying malignancy
Pneumatosis Intestinalis
• Indicates the presence of gas within the bowel
wall
• Commonly seen in the jejunum
• Pneumatosis intestinalis is not a disease
– sign that can be idiopathic
– associated with many intestinal
– nonintestinal disorders such as obstructive
pulmonary disease and asthma
– Are idiopathic
• Pathogenesis of pneumatosis intestinalis is not
fully understood
• Surgical interest in this finding is the
association of it with bowel ischemia and
infarction
– Necessitate emergent surgical intervention
– With this radiologic finding need to be fully
evaluated and monitored closely to rule out such
intra-abdominal catastrophes
SHORT BOWEL SYNDROME
• Presence of less than 200 cm of residual small
bowel in adult patients
• Insufficient intestinal absorptive capacity
results in the clinical manifestations of
diarrhea, dehydration, and malnutrition, is
more broadly applicable.
 Etiology
• Adults
• Acute mesenteric ischemia
• Malignancy
• Crohn’s disease
• Pediatric
• Intestinal atresias
• Volvulus
• Necrotizing enterocolitis
 Pathophysiology
• Resection <50% - Well Tolerated
• Resection of 50 – 80%: Significant
malabsorption
• Lack a functional colon
– TPN dependence is likely to persist if there is less
than 100 cm of residual small intestine.
• Intact and functional colon
– TPN dependence is likely to persist if there is less
than 60 cm of residual small intestine.
• Infants with short bowel syndrome
– Weaning from TPN dependence has been
achieved with as little as 10 cm of residual small
intestine.
• Residual bowel length is not the only factor
predictive of achieving independence from
TPN (enteral autonomy)
• Intact ileocecal valve is believed to be associated
with decreased malabsorption
• Ileocecal valve delays transit of chyme from the
small intestine into the colon
• Prolonging the contact time between nutrients
and the small-intestinal absorptive mucosa
• Healthy, rather than diseased, residual small
intestine is associated with decreased severity of
malabsorption.
• Resection of jejunum is better tolerated than
resection of ileum, as the capacity for bile salt
and vitamin B12 absorption is specific to the
ileum
 Therapy
• Medical Therapy
• Management of the primary condition
precipitating the intestinal resection
• Repletion of fluid and electrolytes lost
• TPN
• Enteral nutrition - ileus has resolved
• High-dose histamine- 2 receptor antagonists
or proton pump inhibitors
• Antimotility agents,
– loperamide hydrochloride or diphenoxylate
• Octreotide
– Reduce the volume of GI secretions
 Nontransplant Surgical Therapy
• Patients with stomas - Restoration of intestinal
continuity
• Longitudinal intestinal lengthening and
tailoring (LILT) procedure
– Separation of the dual vasculature of the small
intestine, followed by longitudinal division of the
bowel with subsequent isoperistaltic end-to-end
anastomosis
• Small bowel is the serial transverse
enteroplasty procedure (STEP)
– accomplish lengthening of dilated small intestine
without the need for separating its dual
vasculature
• Intestinal Transplantation
– Indication - life-threatening complications
attributable to intestinal failure and/or long-term
TPN therapy
• Specific complications
– (a) impending or overt liver failure
– (b) thrombosis of major central veins
– (c) frequent episodes of catheter-related sepsis
– (d) frequent episodes of severe dehydration.