THE SMALL BOWEL AND

APPENDIX
 ANATOMY SMALL BOWEL
Three regions: duodenum, jejunum and ileum
Duodenum- deeply placed ,C-shaped,
receives bile and pancreatic juice through
Vater ampulla- D2
Jejunum- upper left part of the abdo. cavity
Ileum- lower right part of the abdominal and
pelvic cavity
 6 m small bowel
2/5 jejunum, 3/5 ileum
 ANATOMY SMALL BOWEL
Jejunum is larger in diameter, thicker
walled, more prominent mucosal folds
Arterial supply – branches of the SMA
Absorbtion area of the nutrients- 500 m2
Submucosa is the strongest layer,
provides strength to an intestinal
anastomosis
PHYSIOLOGY SMALL BOWEL
The primary functions: digestion and
absorbtion

All ingested food and fluid and secretions

from the stomach, liver, pancreas reach
the small bowel- total volume- 9 l /day and
all but 1-2l will be absorbed
PHYSIOLOGY SMALL BOWEL
Motility- two types of contractions
To-and-fro motion mixes chyme with
digestive juices for prolonged exposure to
the absorbative mucosa
Peristaltic contractions move food distally
PNS- contractions, SNS- relaxation
Absorbtion: vit., proteins, carbohydrates,
water, electrolytes are all absorbed
 INVESTIGATIONS
SMALL BOWEL DISORDERS
Radiology- plain erect film- obstruction and
perforation
Small bowel follow-through- the established
investigation to outline the small bowel-
tumors, Crohn’s disease, fistulas, polyps.
Enteroclysis
Radiological criteria for malabsorbtion:
flocculation of barium, thickening of the
mucosal folds, loop dilatation
 SBFT
(small bowel follow through)
The esophagus, stomach, and duodenum are easily
evaluated in detail.
The small bowel is then radiographed at periodic
intervals and fluoroscopically spotted by the attending
Radiologist.
This type of SBFT can take hours to complete and detail
of the lumen cannot be assessed as the loops of small
intestine overlap as the barium progresses.
A better diagnostic tool would be an enteroclysis small
bowel exam. "Entero" is Greek for intestine.
"Clysis" is Greek for washing out.
Thus, enteroclysis is washing out of the intestine.
 Enteroclysis

It is a minimally invasive radiographic procedure of the small

intestine, which requires the introduction of a catheter into the
small intestine followed by the injection of barium and
methylcellulose.

The barium coats the intestine and the methylcellulose

distends the lumen to give a double contrast exam that allows
for fluoroscopic visualization of the entire small bowel.
The enteroclysis study may be helpful in diagnosing almost
all diseases that affect the small bowel.
It may also be helpful in ruling out diseases in patients with
unexplained abdominal complaints.
Indications:
Suspected or known small bowel obstruction
Neoplasms (cancers)
Inflammatory bowel disease
Unexplained gastrointestinal bleeding
Malabsorption
Polyps
Adhesive bands
Post surgical changes
 Disadvantages

There are two drawbacks:

The placement of the enteroclysis catheter is the largest

disadvantage. It can be uncomfortable for the patient, even
with the use of anesthetic spray and Xylocaine jelly or a
similar lidocaine product.

The patient will receive higher doses of radiation in

comparison to the traditional small bowel follow through exam
during this exam.
 Advantages

This examination is much quicker than a routine single

contrast Small Bowel Follow Through exam.
There is an increase in the distention of the lumen, which is
very important; the distention straightens the circular folds
and will help to determine: fold thickness, ulceration, polyps,
constrictions, and adhesive bands are more readily
identified.
Distention of the small bowel makes it possible to display all
dilated bowel loops simultaneously at the end of the exam.
 The catheter is being held up at the pylorus.
When this occurs, rolling the patient to the left will
widen the bulb, allowing the catheter to advance
into the duodenum.
Jejunum
 Methylcellulose
Methylcellulose has a natural tendency to retain water in the lumen,
which promotes peristalsis and prevents lumen collapse. When used in
an Enteroclysis study, this product mixes with the barium and produces
the desired air contrast effect.
 Enteroclysis parameters

Fold shape Fold thickness

 Enteroclysis parameters

Fold height Number of folders/inch

 Enteroclysis parameters

Wall thickness Lumen diameter

 INVESTIGATIONS
SMALL BOWEL

Selective splanhnic angiography- reliable

method for detection of angioplastic
lesions

The bleeding site can be located if the

patient is bleeding actively at the time of
investigation
 INVESTIGATIONS
SMALL BOWEL
USS of the abdomen
Can differentiate fluid-filled dilated small
bowel loop from abdominal cystic
structures
Can assess free fluid within peritoneal
cavity
Can assess a solid mass belonging to the
small bowel if large enough
 INVESTIGATIONS
SMALL BOWEL
Isotope scintigraphy
Isotope-labelled red cells- occult GI
bleeding
Isotope-labelled white cells- suspected
intraabdominal inflammation/abscess
formation, inflammed bowel (Crohn’s
disease)
Isotope labelled meal- intestinal transit
time
 INVESTIGATIONS
SMALL BOWEL

Estimation of fecal fat- the quantitative

estimation of fecal fat remains the most
sensitive test of disorders of digestion and
absorbtion
On a standard diet of 100g. of fat, the
fecal fat output normally is less than
6g./day
 INVESTIGATIONS
SMALL BOWEL

Jejunal mucosal biopsy

Celiac disease- subtotal villous atrophy

Whipple’s- abnormal mucosal pathogens

 INVESTIGATIONS
SMALL BOWEL
Breath Tests- detection of bacterial
overgrowth, carbohydrate malabsorbtion
and small bowel transit
Hydrogen Breath Test- small bowel transit
time and bacterial overgrowth
Consists of repeated measurements of the
H2 in the end-expiratory air taken every
few minutes after ingestion of a meal
HYDROGEN BREATH TEST
When the radiolabelled meal reaches the
cecum, the resulting bacterial fermentation
induces a sustained rise in the breath H2
concentration
The test measures the oral- cecal transit
time which includes gastric emptying time
In pts. with bacterial overgrowth, the
fasting H2 level in the expired breath is
elevated
BACTERIAL OVERGROWTH
The small bowel becomes colonized by
bacteria
There is an increase in the concentration
organisms which are normally confined to
the lower small bowel and colon
The affected intestine becomes inflammed
and dilated
Symptoms and signs- colicky pain,
meteorism, diarrhea, anemia
BACTERIAL OVERGROWTH
Causes of bacterial overgrowth:

1. Excessive entry of bacteria into the

small bowel

2. Intestinal stasis
BACTERIAL OVERGROWTH
1. Excessive entry of bacteria
– Achlorhydria
– Gastro-jejunostomy
– Gastrectomy
– Enterocolic fistulas
– Cholangitis
– Loss of ileocecal valve following RHC
BACTERIAL OVERGROWTH
2. Intestinal stasis:
– Stenotic Crohn’s disease
– Stenotic intestinal stasis
– Small bowel diverticulosis
– Afferent loop stasis
– Entero- enteric anastomosis
– Diabetis mellitus- autonomic neuropathy
– Radiation enteritis- stenosis
– Scleroderma- impaired intestinal motility
BACTERIAL OVERGROWTH
Clinical features:
– Abdominal colicky pain
– Asthenia, nausea, vomiting
– Weight loss, excessive bowel sounds
– Diarrhea
– Anemia, hypoproteinemia
– Paresthesia, peripheral neuropathy- B12
deficiency
BACTERIAL OVERGROWTH

Treatment
– Surgical treatment of the underlying condition
whenever possible

– Jejunal diverticulosis, scleroderma-

tetracycline and metronidazol for 10-14 days
 SHORT-GUT SYNDROME
Encountered after massive resection of
the small bowel

Encountered in pts. with jejuno-ileal by-

pass for morbid obesity
 SHORT-GUT SYNDROME

Conditions necessitating extensive

resection of the small bowel:
– Crohn’s disease
– Mesenteric infarction
– Radiation enteritis
– Multiple fistulas
– Small bowel tumors
 SHORT GUT SYNDROME
Resections of more than half of the small
bowel length- serious malabsorbtion
Pts.with residual small bowel length of
less 2m.- diminished work capacity
Pts. with residual small bowel length of
less 1m. require home parenteral nutrition
on an indefinite basis
Ileal resections are less well tolerated than
jejunal resections
 SHORT-GUT SYNDROME

Clinical outcome following small bowel

resection depending on:

– Extent and site of resection

– Age of the patient
– Physical and mental condition
 SHORT-GUT SYNDROME
Treatment:
– Massive small bowel resection- TPN
– The regimen must provide 40 Kcal/Kg. body weight
– Pts. with about 1m. of small bowel, TPN
discontinued with time- small bowel will
hypertrophy
– Oral nutrition is based on an elemental diet
– antiperistaltic agents should be given, vitamins,
B12 parenteral
 PROTEIN-LOSING
ENTEROPATHY
Loss of plasma proteins- low plasma
proteins- secondary hyperaldosteronism
with water and salt retention- edema
Causes:- mucasal disease- Whipple’s,
- ulcerating lesions- villous tumors
- lymphatic obstruction- lymphoma
Treat the underlying disease
 SMALL BOWEL TUMORS
10% of all GI tumors (benign or malignant)

Benign small bowel tumors:

– Adenomatous polyps
– Hamartomatous polyps- Peutz-Jagers sdr.
– Leiomyomas, lipomas, fibromas
– Hemangiomas, neurofibromas
 BENIGN SMALL BOWEL
TUMORS
Clinical presentations:
– Bowel obstruction due to intussusception
– Chronic blood loss- chronic anemia- fecal ocult blood
test+
– Melena- acute anemia
DIAGNOSIS- barium follow-through
- abdominal CT
- endoscopic videocapsule for
nonobstructing lesions
TREATMENT- bowel resection with end to end
anastomosis
 MALIGNANT SMALL BOWEL
TUMORS

ADENOCARCINOMAS

MALIGNANT CARCINOID

LYMPHOMA

METASTASES FROM DISTANT TU.

 MALIGNANT SMALL BOWEL
TUMORS
Clinical presentations:
– Lower GI bleeding- ocult or melena
– Diarrhea
– Perforation- peritonitis
– Bowel obstruction
DIAGNOSIS- contrast follow-through, CT for
elective cases, plain abdo X ray- acute
cases
TREATMENT- segmental bowel resection
 SMALL BOWEL
ADENOCARCINOMA
Commonly- well-differentiated mucus-
secreting tumors
Usually located in the proximal intestine
Spreading to lymph nodes, liver,
peritoneal serosa
Pts. with resectable tumors, 25%- 5 year-
survival rate
 CARCINOID TUMORS
Derived from enterochromaffin cells
Apudomas
Common places: appendix, ileum, rectum
Clinical features: flushing, diarrhea,
bronchoconstriction caused by serotonin
and other vasoactive substances secreted
by the tumor
 CARCINOID TUMOR

Diagnosis- elevated levels of 5 HIAA-

5 hydroxyindolacetic acid- the breakdown
product of serotonin in the urine
TREATMENT- resection of the primary
tumor and resection of the metastases
 GIST- GI STROMAL TUMORS
• M o s t c o m m o n g a s tr o in t e s tin a l ( G I) s a r c o m a
– A t u m o r o f m e s e n c h y m a l (c o n n e c t iv e t is s u e ) o r ig in
– 0 . 2 % o f a ll G I t u m o rs , b u t 8 0 % o f G I s a rc o m a s
• H ig h e s t in c id e n c e in-6 0th yee 4a 0r a g e g r o u p
– S im ila r m a le / fe m a le in c id e n c e , a lt h o u g h s o m e r e p o r ts s u g g e s t
s lig h t ly h ig h e r in c id e n c e in m e n
• R e c e n tl y id e n tifie d a s a d is tin c t c lin ic a l a n dn tith isy to p a t h o lo g ic e
– P r e v io u s ly m is c la s s ifie d a s le io m y o s a rc o m a /no ct he ersr s p in d le c e ll c
• G IS T h a v e a n in c id e n c e o f 1 4 .5 p e r m illio n a n n u a ll y ( c o m p a
w ith c h r o n ic m y e lo id le u k e m ia ) a n d a p r e v a leonnc e o f 1 2 9 p e r
 GIST-CLINICAL PRESENTATION
• Often asymptomatic, especially when small
– May be symptomatic if large
• Symptomatic: signs/symptoms related to
location and size of tumor
– Vague GI pain or discomfort
– GI hemorrhage
– Anemia
– Anorexia, weight loss, nausea, fatigue, and additional
GI complaints
– Acute intraperitoneal bleeding or perforation
GIST- SITES OF GROWTH
Colon Other (rectum, esophagus,
mesentery, retroperitoneum)
10%
15%
25%
Small
50%
intestine
Stomach
 GIST
• GIST have 2 major histologic patterns, which overlap
with many non-GIST sarcomas and other malignancies
– Spindle cell
– Epithelioid
• In the past, GIST were usually classified as
– Leiomyoma
– Leiomyoblastoma
– Leiomyosarcoma
• Many patients previously diagnosed with one of these
tumors actually had a GIST
GIST-IMMUNOPHENOTYPE
• ~95% of reported cases of GIST
are positive for KIT (CD117)
• Other markers often positive in
GIST
– CD34 (mesenchymal/hematopoietic
precursor cell marker)
• Positive in 60%-70%
– Smooth-muscle actin
• Positive in 15%-60%
– S-100
• Positive in 10%
• GIST rarely express desmin
 GIST-ASSESSMENT MALIGNANT
POTENTIAL
Risk Size Mitotic Rate
High Any size >10/50 HPF
>10 cm Any rate
>5 cm >5/50 HPF
Intermediate 5-10 cm <5/50 HPF
<5 cm 6-10/50 HPF
Low 2-5 cm <5/50 HPF
Very low <2 cm <5/50 HPF
 GIST OVERVIEW
• GIST is the most common sarcoma of the GI tract
– May arise from the same stem cells as ICC of the myenteric
plexus
• Pathologic characteristics of GIST are now well defined,
but diagnosis remains challenging in some cases
• Clinical presentation is variable
– Tumors are often asymptomatic
– Patients may have common, nonspecific symptoms, resulting in
underdiagnosis or misdiagnosis
• All GIST have the potential to become malignant
– Risk is based on size and mitotic index at presentation
NORMAL BIOLOGIC FUNCTION OF
KIT RECEPTOR TYROZINE KINASE
• KIT is ess ential for
– H em atopoiesis
– S k in pigm ent
– F ertility
– G ut m otility (pac em ak er c ells)
• KIT plays a role in different cell functions
– Proliferation
– D ifferentiation
– A poptosis/s urvival
– A dhes ion/c hem otaxis
• F am ilial gain
-of-function KIT m utations result in high
incidence of G IST, m elan oc ytic dysfunction, and
cutaneous m astoc ytos is
 GIST DIAGNOSIS
• Initial GIST patient workup should include imaging
– CT of abdomen and pelvis with oral/IV contrast
– Consider 18FDG-PET
– Endoscopic ultrasound
• Liver function tests
• Complete blood counts
• Surgical assessment
– Resectable vs nonresectable
– Primary tumor only vs metastatic
 GIST METHODS OF DETECTION
• Endoscopic ultrasound (EUS)
• MRI
• CT
• 18FDG-PET
ENDOSCOPY AND EUS
ULCERATED GASTRIC GIST
EUS- Homogenous submucosal
mass
CT- Massive stromal gastric tumor
Endobiopsy negative
 Positron Emission Tomography
• Diagnosis
– 18FDG-PET is highly sensitive, but not
specific, for metabolically active GIST
• Staging workup
– Evaluate the extent of the disease
– Assess for metastatic disease
 FDG - PET
Fluorodeoxyglucose- positron emission
tomography:

– Provides the status of glucose metabolism in

tumors
– GIST are highly metabolically active
– Easily detected with FDG-PET
 GIST FDG-PET Imaging
Hepatic, abdominal and pelvic
metastases
 CT AND FGD-PET
• Patients with suspected GIST should be
evaluated using CT and possibly 18FDG-PET
• CT provides anatomic detail of tumor(s) for
possible surgical resection and may suggest
diagnosis
• 18FDG-PET may detect small tumors and can be
used as an indicator of early response to
treatment
 GIST- TREATMENT
• Standard sarcoma chemotherapy is ineffective
– Limited response rate ~5%
– Median time to progression 3-4 months
– No impact on survival
• Comorbidity due to tumor localization limits
effectiveness of radiation therapy
– Possible role in treatment of rectal tumors
• Surgery remains the principal treatment for
resectable primary GIST
 GIST- SURGERY FOR PRIMARY
TUMORS
• Complete gross resection of tumor with
pseudocapsule
• Fragility of tumor risks rupture
– Bleeding
– Dissemination
• Abdomen should be examined for metastases
– Peritoneal surfaces
– Liver
• GIST can often be lifted off surrounding organs
 SURGICAL
CONSIDERATIONS
• Complete gross resection with the intact
pseudocapsule is the goal of resection
– Careful tumor handling is critical
– Rupturing of the pseudocapsule can cause tumor
bleeding and/or dissemination
• Unlike adenocarcinomas, GIST tend to displace,
not invade, surrounding organs
• Negative microscopic margins are desirable
• Lymphadenectomy is unnecessary, as GIST
rarely metastasize to the regional lymph nodes
RECURRENCE AFTER SURGERY
• After surgery, recurrence is common
– Majority of high-risk patients have recurrence of GIST
following surgery
– Median time to recurrence is 7 months to 2 years
– Only 10% of patients remain disease-free after
extended follow-up
– Investigational protocols are indicated to reduce the
rate of recurrence after resection
– Recurrent disease should be treated as metastatic
disease
 NEOADJUVANT IMATINIB
MESYLATE THERAPY FOR GIST
• Few complete responses with imatinib
mesylate therapy
– Most responding lesions have viable cells
• Cytoreduction may improve surgical
outcomes
• Potential to increase resectability or
reduce the extent of surgery
 GIST TREATMENT OPTIONS
• Intermediate and high-risk GIST have a high
rate of recurrence
– Recurrent disease should be treated as metastatic
disease
• Traditional chemotherapy and radiation therapy
are ineffective for GIST
• Patient follow-up is necessary
• Neoadjuvant therapy may enhance resectability
• Adjuvant therapy may reduce recurrence
 MECHANISM OF ACTION
• Ima tin ibm e sy la te
occ u p iesth eA T P
bind in gp oc ke to f
theK ITk ina s e
dom a in
• Thisp re v e
n ts
sub s tra te
pho sp h ory la tion a
n d
sign a lin g
• Ala c ko fsig n alin g
inhib itsp ro life ra tion
ands u rviva l
 TYROSINE KINASE INHIBITORS
MOLECULARLY TARGETED
THERAPY
• ~ 9 0 % o f G IS T h a v e a n o n c o g e n ic m u ta tio n o f K IT o r
PDGFRA
• M u ta tio n s o c c u r e a rly in G IS T d e v e lo p m e n t
– K IT m utatio ns a re d ete cta b le in inc id e≤n1tac m
l tu m o rs
– P a tie n ts w ith g e rm lin e K IT m utatio ns de v e lo p m u ltip le G IS T
– K IT m utatio ns p rec e d e c yto g e ne tic c ha n g es in G IS T d e v e lo p m e nt
• Im a tin ib m e s y la t e is a s p e c ific in h ib it o r o f K IT tyr o s in e
k in a s e a c tivit y a n d b lo c-m
k se Kd ia
I Tte d d o w n s tre a m
s ig n a lin g
 SCIENTIFIC RATIONALE FOR
IMATINIB MESYLATE IN THE
TREATMENT OF GIST
• Im a tinib m es yla te is an-mA im
TPe tic TK I
of the K IT, B-Ac rbl, a n d P D G F R A /B
re c ep to rs
• In ce ll c u ltu re e xp e rim e nts , im a tin ib
m es yla te effe ctiv ely inh ibits ac tiv a te d K IT ,
re s ultin g in d e a th of G IS T c ells in c ultu re
 JEJUNAL STROMAL TUMOR
WITH MUCOSAL ULCERATION
 INTRAOPERATIVE VIEW-
JEJUNAL STROMAL TUMOR
 RESECTED SPECIMEN
TUMOR WITH A SEGMENT OF JEJUNUM
RESECTED SPECIMEN
MACROSCOPIC TUMORAL
ASPECT
ENDOSCOPIC VIEW TAKEN BY
SWOLLEN VIDEOCAPSULE
PROTRUSIVE ENDOLUMINAL TUMOR OF THE
JEJUNAL WALL
SMALL MUCOSAL LACERATION RESPONSIBLE
FOR HDI
DOUBLE CONTRAST
FOLLOW-THROUGH
DOUBLE CONTRAST
FOLLOW- THROUGH
USS of the UPPER ABDOMEN
SMALL BOWEL DIVERTICULOSIS
Duodenal diverticula- 90% are asymptomatic
70% -periampullary region- cholangitis,
pancreatitis, CBD stones
Jejunal diverticula-rare, may cause obstruction,
bleeding, perforation, bacterial overgrowth within
the diverticulum
Meckel’s diverticulum- within 40 cm. of the
ileocecal valve
Meckel’s diverticulum may cause bleeding,
obstruction, acute inflammation
TREATMENT- resection with enteroraphy
 ACUTE APPENCITIS
Commonest condition requiring acute
abdominal surgery
The peak incidence in the 2nd-3rd decades
Etiology:
– Obstruction of the lumen (fecaliths, worms,
cecal cancer)
– Persistent appendiceal secretions, distention
with inflammation, bacterial overgrowth,
ischemia, gangrene, perforation
 ACUTE APPENDICITIS
DIAGNOSIS
History 1-12 h. of digestive symptoms
Symptoms: RIF pain, anorexia, nausea,
vomiting
Physical signs: fever, tachycardia, RIF
guarding, rebound tenderness, Rowsig’s
sign, psoas sign
Lab.tests: WBC elevated, predominance
of neutrophils
 ACUTE APPENDICITIS
COMPLICATIONS IF LEFT UNTREATED

Perforation with localized peritonitis

Appendiceal inflammatory mass
Appendiceal abscess +/- diffuse peritonitis
Septicemia
Multiple Systemic Organ Failure
 ACUTE APPENDICITIS
DIFFERENTIAL DIAGNOSIS

Mesenteric lymphadenitis
Chrohn’s disease- flare up
Pelvic inflammatory disease
Ruptures ovarian cyst
Ureteric calculi, UTI
Sigmoid diverticulitis
 ACUTE APPENDICITIS
TREATMENT

Broad-spectrum antibiotics
Iv. fluids, nil by mouth more than 6 h.
preoperatively.
Laparoscopic / open appendicectomy
Drainage depending on the severity of the
lesion