Small Intestine

James Taclin C. Banez, MD

Small Intestine
one of the most important organs for
immune defense
largest endocrine organ of the body
Starts from the pylorus and ends at the
cecum
3 parts:
1. Duodenum (20cm)
2. Jejunum (100 to 110cm)
3. Ileum (150 to 160 cm)

Anatomy
A.

Has plicae circulares or valves of

Kerkring
Duodenum:

B.

Jejunum:

C.

Retro-peritoneal
Supplied by the celiac artery
Occupies upper left of the abdomen
Thicker wall and wider lumen than the
ileum
Mesentery has less fat and forms only
1-2 arcades

Ileum:

Occupies the lower right; has more fat

and forms more arcades
Contains Payers patches
Ileum & jejunum is supplied by the SMA

Function
A. Digestion & Absorption:
B. Endocrine Function:
Secretes numerous hormones involved in GIT
function.
1.
2.
3.
4.
5.
6.
7.
8.
9.

Secretin
Cholecystokenin
Gastric inhibitory peptide
Enteroglucagon
Vasoactive intestinal peptide
Motilin
Bombesin
Somatostatin
Neurotensin

Function
C. Immune function:
1. Major source of IgA
2. Integrity of the GUT wall prevents bacterial
translocation into the wall of the intestine
and abdominal cavity which can lead to
sepsis
3. Gut associated lymphoid tissue part of the
immune defense system which clears the
abdominal cavity of pathogenic bacteria
found in Peyers patches

Small Bowel Surgical Lesions

1. Small bowel obstruction:
a. Mechanical
b. Ileus
2. Small bowel infection
3. Chronic inflammation
4. Neoplasm
5. Diverticula
6. Short bowel syndrome

Small Bowel Obstruction

Causes of Mechanical Obstruction:
1.
2.
3.
4.

Post-operative adhesion (75%)

Hernias
Crohns disease
Neoplasm (primary or extrinsic compression
or invasion)
5. Superior mesenteric artery syndrome
(compression of transverse duodenum)

Pathophysiology:
Accdg. to its anatomical relationship to
the intestinal wall:
1. Intraluminal ( foreign bodies, gallstone, and
meconium)
2. Intramural (neoplasm, Crohns,
hematomas)
3. Extrinsic (adhesion, hernias &
carcinomatosis)

Pathophysiology:
Air-fluid level:
Gas due to swallowed air
Fluid a) swallowed fluid
b) gastrointestinal
secretion
(increase epithelial water
secretion).

Bowel distention /
elevated intramural
pressure ---> ischemia
------> necrosis.
(strangulated bowel
obstruction)

Pathophysiology:
Partial small-bowel obstruction
passage of gas and fluid.
Complete small-bowel obstruction
(obstipation)
Closed loop obstruction (obstructed
proximal and distal) ex. volvulus

Manifestation:
colicky abdominal pain
nausea / vomiting
obstipation
abdominal distention
hyperactive bowel sound
signs of dehydration (sequestration of fluid in
bowel wall and lumen as well as poor oral
intake)
7. lab. findings:
1.
2.
3.
4.
5.
6.

a.
b.
c.

hemoconcentration
fluid & electrolyte imbalance
leucocytosis

Manifestation:
Features of Strangulated obstruction:
1.
2.
3.
4.
5.
6.

tachycardia
localized abd. tenderness
fever
marked leucocytosis
acidosis
lab result:
- elevated serum amyase, lipase, LDH,
phosphate and potassium

Diagnosis:
Focus on the following goals:
1. distinguish between mechanical obstruction
from ileus
2. determine the etiology
3. whether it is partial or complete obstruction
4. differentiate between simple and
strangulating obstruction

Diagnosis:
1. Clinical history & PE
2. Radiological examination:
a. FPA (supine and upright)
Triad:

1. dilated small bowel (>3cm )

2. air-fluid levels seen in upright
3. paucity of air in the colon
Sensitivity of 70-80% but with low specificity for
ileus and colonic obstruction mimics
False (-): - proximal small bowel obstruction
- bowel lumen filled with fluid (cant see
air-fluid level)

Diagnosis:
b. CT scan (90% sensitive / 90% specific)
Findings of small bowel obstruction:
a.
b.
c.

Strangulation is suggested:
a.
b.
c.
d.
e.

Discrete transition zone

Intra-luminal contrast unable to passed beyond the
transition zone
Colon containing little gas or fluid
Thickening of the bowel wall
Pneumatosis intestinalis
Portal venous gas
Mesentery haziness
Poor uptake of intravenous contrast into the wall of the
affected bowel

Limitation: unable to detect partial intestina

obstruction (<50% sensitivity)

Diagnosis:
c. Small bowel series (barium / gastrografin)
d. Enteroclysis
200 to 250 ml of barium followed by 1 to 2 L of
methylcellulose in water is instilled into the
proximal jejunum via a long naso-enteric tube

Treatment:
1.

Correct fluid & electrolyte imbalance:

Isotonic fluid
Monitor resuscitation (foley catheter/CVP)

NPO / TPN
Broad spectrum antibiotic (due to bacterial
translocation)
4. Placed NGT to decompress the stomach and
decrease nausea, distention and risk of
aspiration
5. Expeditious celiotomy (to minimize risk of
strangulation).
2.
3.

Type of operation based on operative finding

causing intestinal obstruction

Ileus / Pseudo-Obstruction
Impaired intestinal motility
Most common cause of delayed discharge
following abdominal operations
Temporary and reversible

Ileus / Pseudo-Obstruction
Etiologies:
1.
2.
3.
4.
5.
6.

Abdominal surgery
Infection & inflammation (sepsis/peritonitis)
Electrolyte imbalance (Hypo K, Mg & Na)
Drugs (anticholinergic, opiates)
Visceral myopathies (degeneration/fibrosis of
smooth muscle)
Visceral neuropathies (degenerative disorders of
myenteric & submucosal plexuses)

Symptoms:
1. Inability to tolerate solid & liquid by
2.
3.
4.
5.

mouth
Nausea/vomiting
Lack of flatus & bowel movements
Diminished or absent bowel sound
Abdominal pain and distention

Diagnosis:
1. History of recent abdominal surgery
2. Discontinue opiates
3. Serum electrolyte determination
4. CT scan better than FPA in postoperative

setting to exclude presence of abscess or

mechanical obstruction

Therapy:
1. NPO, if prolong TPN is required
2. NGT to decompress the stomach
3. Correct fluid & electrolyte imbalance
4. Give ketorolac and reduce the dose of

opioids

CROHNS DISEASE
Regional, transmural, granulomatous
enteritis).
Chronic, idiopathic inflammatory dse
Ethnic groups ---> East Europe
(Ashkenazi Jewish)
Female predominance, 2x higher smokers
Familial association (30x in siblings / 13 x
in 1st degree relatives).
Higher socioeconomic status
Breast feeding is protective

Etiology:
Unknown
Hypothesis:
1. Infectious: - Chlamydia / Pseudomonas /
Mycobacterium paratuberculosis / Listeria
monocytogenesis / Measles / Yersinia
enterocolitica
2. Immunologic abnormalities:

Humeral & cell-mediated immune reactions against

gut cells.

3. Genetic factors:

Chromosome 16 (IBD1 --> NOD2)

Pathology:
Affect any portion of GIT:

Small bowel alone (30%)

Ileocolitis (55%)
Colon alone (15%)

Hallmark focal,
transmural inflammation of
the intestine
Earliest sign --> aphthous
ulcers surrounded by halo
erythema over a noncaseating granuloma.

Pathology:
As the aphthous ulcer enlarge
and coalesce transversely
forming cobblestone
appearance.
Advanced dse ---> transmural
inflammation. This results to:
1.
2.
3.
4.

adhesions to adjacent bowel,

stricture formation (fibrosis),
intra-abdominal abscesses,
fistula or free perforation
(peritonitis)

Skip lesions and w/ fat

wrapping (encroachment of
mesenteric fat onto the serosal
surface) --> pathognomonic
for Crohns.

Clinical Manifestation:
Most common symptom:
1. Abdominal pain
2. Diarrhea
3. Weight loss

Other symptoms depends on type of

complications:
1.
2.
3.

obstruction (fibrosis)
perforation (peritonitis, fistula, intraabdominal abscess)
toxic megacolon (marked colonic dilatation, adb.
tenderness, fever & leukocytosis)
4. cancer (6x greater/more advanced---> poor prognosis)
5. perianal dse (fissure, fistula, stricture or abscess)

Extra-intestinal manifestation:

erythema nodosum & peripheral arthritis are correlated

w/ severity of intestinal inflammation.

Diagnosis:
1. Endoscopy

2.
3.
4.

(esophagogastroduodenoscopy (EGD)
/colonoscopy) w/ biopsy.
Barium enema / intestinal series
Enteroclysis (small bowel) more accurate
CT scan to reveal intra-abd. abscesses

Treatment:
Medical:

I.

Intravenous fluids
NGT to rest GIT (elemental diet/TPN)
Medications:
1.
2.
3.
4.

5.

to relieve diarrhea
relieve pain
control infection (antibiotic)
Anti-inflammatory ( aminosalicylates, corticosteroid,
immunomodulators azathioprime 6mercaptopurine and cyclosporine
Infliximab chimeric monoclonal anti-tumornecrosis-factor antibody inducing remission and in
promoting closure of enterocutaneous fistulas

Surgical:

II.

Indicated if:
with complications
Medication-induced complications arise

Cushingoid features, cataract, glaucoma, systemic

hypertension, compression fracture or aseptic
necrosis

Types:
Segmental resection w/ primary anastomosis:

Microscopic evidence of the dse at the resection

margin does not compromise a safe anastomosis,
hence, a frozen section is unnecessary.

Stricturoplasty
Bypass procedures (gastrojejunostomy)

Prognosis:
High recurrence rate (most common
proximal to the site of previous
resection).
70% recur w/in 1 yr and 85% w/in 3 yrs.
Most common complication:
1. Wound infection
2. Postoperative intra-abdominal abscess
3. Anastomotic leaks

60-300 x more frequent to develop CA

Tuberculous Enteritis:
In developing and under develop countries
Resurgence in develop countries due to:
1.
2.
3.

AIDS epidemic
Influx of Asian migrants
Use of immunosuppressive agents

Forms:
1. Primary infection (caused by M. tuberculosis
bovine from ingested milk)
2. Secondary infection (swallowing bacilli from
active pulmonary) TB

Tuberculous Enteritis:
Patterns:
1.
2.
3.

Hypertrophic causes stenosis or obstruction

Ulcerative diarrhea and bleeding
Ulcero-hypertrophic

Treatment:
Chemotherapy (given 2 wks prior to surgery up
to 1 yr).
Rifampicin
Isoniazid
Ethambutol

Surgery (perforation, obstruction, hemorrhage).

Typhoid enteritis:
Caused by Salmonella typhi
Diagnosis:
Culture from blood or feces
Agglutinins against O and H antigen

Treatment:
Medical:
Chloramphenicol / trimethropin-sulfamethoxazole /
amoxycillin / quinolones

Surgical:
perforations / hemorrhage
Segmental resection (w/ primary anastomosis or
ileostomy)

Neoplasm
Rare:
1. Rapid transit time
2. Local immune system of the small bowel mucosa
(IgA)
3. Alkaline pH
4. Relatively low concentration of bacteria; low
concentration of carcinogenic products of bacterial
metabolism.
5. Presence of mucosal enzymes (hydrolases) that
destroy certain carcinogens
6. Efficient epithelial cellular apoptotic mechanisms
that serve to eliminate clones harboring genetic
mutation

Neoplasm
50 60 y/o
Risk factors:
1.
2.
3.
4.
5.

Red meat
Ingestion of smoked or cured foods
Crohns dse
Celiac sprue
Hereditary nonpolyposis colorectal cancer
(HNPCC)
6. Familial adenomatous polyposis (FAD) 100% to
develop duodenal CA
7. Peutz-Jeghers syndrome

Neoplasm
Symptoms:

Most are asymptomatic

Symptoms:
1. Vague abdominal pain (epigastric discomfort, N/V,
abd. pain, diarrhea).
2. Bleeding (hematochezia or hematemesis)
3. Obstruction (intussuception, circumferencial growth,
kinking of the bowel, intramural growth).

Most common mode of presentation is --->

crampy abd. pain, distention, nausea /

vomiting
Hemorrhage usually indolent 2nd common
mode of presentation

Neoplasm
Diagnosis:
For most are asymptomatic it is rarely
diagnosed preoperatively
Serological examination
Serum 5-hydroxyindole acetic acid (HIAA) for
carcinoid.
CEA associated w/ small intestinal
adenocarcinoma but only if w/ liver metastasis.

Neoplasm
Diagnosis:
Radiological examination:
1. Enteroclysis (test of choice 90% sensitivity)
2. UGIS w/ intestinal follow through
3. CT scan
4. Angiography / RBC scan --> bleeding lesions

Endoscopy:
EGD (esophagus, gastric, and duodenum)
Colonoscopy

I.

Benign tumors:

A. Adenomas: (most common benign neoplasm

duodenum):
1. True adenomas:
Associated w/ bleeding and obstruction
Usually seen in the ileum
Majority are asymptomatic

2. Villous adenoma:
Most common in the duodenum
soap bubble appearance on contrast radiography
No report of secretory diarrhea

3. Brunners gland adenoma

In the duodenum
No malignant potential
Mimic PUD

Benign tumors:
B. Leiomyoma:
Most common symptomatic benign lesion
Associated w/ bleeding
Diagnosed by angiography and commonly
located in the jejunum
2 growth pattern:
1. Intramurally ----> obstruction
2. Both intramural and extramural (Dumbbell

shaped)

Benign tumors:
C. Lipoma:
Most common in the ileum
Causes obstruction (lead point of an
intussusception)
Bleeding due to ulcer formation
No malignant degeneration

Benign tumors:
D. Peutz-Jeghers Syndrome:
Inherited syndrome of:
1.
2.

Symptoms:
1.
2.

Mucocutaneous melatonic pigmentation (face, buccal

mucosa, palm, sole, peri-anal area)
Gastrointestinal polyp (enteric jejunum and ileum are
most frequent part of GIT followed by colon, rectum and
stomach).
colicky abd. pain (due to intermittent intussuception)
Hemorrhage

Treatment:
Segmental resection of the bowel causing obstruction or
bleeding.
Cure impossible due to widespread intestinal involvement

II.

Malignant neoplasm:

Histologic types:
Tumor type

Cell of origin Frequency Predominant

Site

adenocarcinoma

Epithelial cell

35 50%

Duodenum

carcinoid

Enterochromaffin
cell

20 40%

Ileum

lymphoma

lymphocyte

10 15%

Ileum

GIST

? Interstitial cell
of Cajal

10 15%

(gastrointestinal
stromal tumors)

Malignant neoplasm:
1. Adenocarcinoma:
Most common CA of small bowel
Most common in duodenum and proximal
jejunum
Half involve the ampulla of Vater.

Malignant neoplasm:
2. Carcinoid:
From enterochromaffin cells or
Kultchitsky cells
Arise from foregut, midgut & hindgut
Appendix (46%) > Ileum (28%) >
Rectum (17%)

Malignant neoplasm:
2. Carcinoid:
Aggressive behavior than the appendiceal
carcinoid.
appendix 3% metastasize; Ileum 35% metastasize
Appendix solitary; Ileum 30% multiple

25-50% w/ carcinoid tumor with liver

metastasis develops carcinoid syndrome.
Secretes serotonin, bradykinin and substance P
1.
2.
3.
4.
5.

Diarrhea
Flushing
Hypotension
tachycardia
fibrosis of endocardium and valves of the right heart.

Malignant neoplasm:
3. Lymphomas:
Most common intestinal neoplasm in
children under 10y/o.
In adult = 10-15% of small bowel malignant
tumors
Most common presentation
1. intestinal obstruction
2. Perforation (10%)

Malignant neoplasm:
3. Lymphomas:
Criteria of primary lymphomas of the small
bowel:
1. Absence of peripheral lymphadenopathy
2. Normal chest x-ray w/o evidence of
mediastinal LN enlargement.
3. Normal WBC count and differential
4. At operation, the bowel lesion must
predominate and the only nodes are
associated w/ the bowel lesion
5. Absence of disease in the liver and spleen

Malignant neoplasm:
4.

GISTs: (gastrointestinal stromal tumors)

Most common mesenchymal tumors arising in the
small bowel
70% arises from the stomach followed by the small
bowel
15% of small bowel malignancies
Formerly classified as:
1.
2.
3.

Leiomyomas
Leiomyosarcomas
Smooth muscle tumors of small bowel

Associated w/ overt hemorrhage

Has its expression of the receptor tyrosine kinase
KIT (CD117). There is pathological KIT signal
transduction

Treatment:
For Benign lesions:

I.

All symptomatic benign tumors should be

surgically resected or removed
endoscopically (EGD / colonoscopy).
Duodenal tumors:
1 cm. ----> endoscopic polypectomy
2cm. ----> surgically resected (Whipples
located near the ampulla of Vater).
Duodenal adenomas w/ FAP shd undergo
Whipples for it is usually multiple and sessile
and has 100% degenerate to CA.

Treatment:
Malignant lesions:

II.
1.

Adenocarcinoma:
Wide local resection w/ its mesentery to
achieve regional lymphadenectomy
Chemotherapy has no proven efficacy in the
adjuvant or palliative treatment of smallintestinal adenoCA.

2.

Small intestinal lymphoma:

For localized: segmental resection w/ adjacent
mesentery
If w/ diffused involvement: -->chemotherapy
rather than surgery, is primary therapy

Treatment:
3. Carcinoid:
Segmental intestinal resection & regional
lymphadenectomy.
< 1cm rarely has LN metastases
> 3cm 75 to 90% LN metastases

30% are multiple, hence entire small

bowel shd be examined prior to surgery.

Treatment:
3. Carcinoid:
Is w/ metastatic lesions---> debulking,
associated w/ long-term survival &
amelioration of symptoms of carcinoid
syndrome
Chemotherapy: ---> 30 -50% response
1. Doxorubicin
2. 5-fluorouracil
3. Streptozocin

Octreotide: - most effective for

management of symptoms of carcinoid
syndrome

Treatment:
4.

Small-intestine GISTs:
Segmental resection
If was preoperatively diagnosed, lymphadenectomy
shd not be done, for rarely associated w/ LN
metastases.
Resistant to conventional chemotherapy
IMATINIB (Gleevec):

Formerly known as ST1571

80% of pt w/ unresectable lesions showed clinical
benefits
50 60% showed evidence of reduction in tumor
volume
Role as neoadjuvant and adjuvant tx under investigation

Treatment:
5. Metastatic cancers:
Melanoma associated w/ propensity for
metastasis to the small bowel.
Palliative resection / bypass procedure
Systemic therapy depends on the responds
of the primary site.

Meckels Diverticulum
Most prevalent congenital anomaly of GIT
3:2 (male:female)
True diverticula
60% contains heterotopic mucosa:
1.
2.
3.
4.
5.
6.
7.

Gastric mucosa (60%)

Pancreatic acini
Brunners gland
Pancreatic islets
Colonic mucosa
Endometriosis
Hepatobiliary tissues

Meckels Diverticulum
Rules of Twos:
1.
2.
3.

2% prevalence
2:1 female predominance
Location 2 feet proximal to the ileocecal valve in
adults.
4. Half of those are asymptomatic are younger than 2
years of age.

Complications:
1. Bleeding (most common) due to ileal mucosal
ulceration.
2. Obstruction:
a.
b.
c.
d.
e.

Volvulus of the intestine

Entrapment of intestine by the mesodiverticular band
Intussuception
Stricture due to diverticulitis
As Littres hernia found in inguinal or femoral hernia sac.

Meckels Diverticulum
Clinical manifestation:
1. Asymptomatic
2. 4% symptomatic due to complication
50% are younger than 10y/o
Symptomatic (Bleeding > obstruction > diverticulitis)
bleeding is 50% in children and pt younger 18y/o
bleeding is rare in pt older than 30y/o
intestinal obstruction most common in adult
diverticulitis is indistinguishable to appendicitis

Neoplasm seen: ---> Carcinoid

Meckels Diverticulum
Diagnosis:

1.
2.

3.

For asymptomatic usually discovered as an

incidental findings in radiographic imaging,
endoscopy, or intraoperatively.
Enteroclysis has 75% accuracy but not
applicable during acute cases.
Radionuclide scans (99m Tc-pertechnate)
for ectopic gastric mucosa or in active
bleeding
Angiography to localize site of bleeder

Meckels Diverticulum
Management:
Diverticulectomy:
diverticulitis
obstruction (w/ removal of associated band)

Segmental resection for:

Bleeding
If with tumor

Acquired Small Bowel Diverticula

Epidemiology:
False diverticula
Increases w/ age; seldom seen < 40y/o (5070y/o)
1. Duodenum:
1. Most common; usually adjacent to ampulla
2. Called periampullary, juxtapapillary, or peri-

Vaterian diverticula
3. 75% arise in the medial wall

2. Jejunoileal:
80% - jejunum (tends to be large and multiple)
15% - ileum (tends to be small and solitary)
5% - both ileum and jejunum

Acquired Small Bowel Diverticula

Pathophysiology:
Abnormalities of intestinal smooth muscle
or dysregulated motility leading to herniation.
Associated w/:
1. Bacterial overgrowth vit B12 deficiency,

megalobalstic anemia, malabsorption &

steatorrhea
2. Periampullary duodenal diverticula:
1. Obstructive jaundice
2. Pancreatitis

3. Intestinal obstruction due to compression of

adjacent bowel

Acquired Small Bowel Diverticula

Diagnosis:
Best diagnosed w/ enteroclysis

Treatment:
Asymptomatic ---> left alone
Bacterial overgrowth --> antibiotics
Bleeding and obstruction ---> segmental
resection for jejunoileal diverticula.

Acquired Small Bowel Diverticula

Treatment:
Diverticulectomy if located in the duodenum
1. For medial duodenal diverticula ---> do lateral
duodenotomy and oversewing of the bleeder
2. May invaginate the diverticula into the
duodenal lumen then excised
3. If related to the ampulla ---> extended
sphincterotoplasty
4. If perforated ----> excised and closed w/
omental patch; if to inflammed ---> placed
gastrojejunostomy

Mesenteric Ischemia
Clinical Syndrome:
1. Acute mesenteric ischemia
Pathophysiology
1. Arterial embolus: (most common-50%; heart;
2.
3.

4.

usually lodge distal to origin of the middle colic

Arterial thrombosis: occlusion occurs at proximal
near its origin.
Vasospasm (nonocclusive mesenteric ischemia
NOMI): usually in critically-ill pt. receiving
vasopressors.
Venous thrombosis: (5-15%) and 95% SMA
a. Primary no etiologic factor identified
b. Secondary heritable or acquired coagulation disorder

Mesenteric Ischemia
Clinical Syndrome:
2. Chronic Mesenteric Ischemia:
Develops insidiously allows for collateral
circulation to develop
Rarely leads to infarction.
Usually due to arteriosclerosis
Usually two mesenteric arteries are involved
Chronic mesenteric venous thrombosis can
lead to portal hypertension

Mesenteric Ischemia
Manifestation:
A. Acute mesenteric ischemia:
Severe abdominal pain out of proportion to the
degree of abd. tenderness (hallmark)
Colicky at the mid-abdomen.

Nausea / vomiting, diarrhea

On PE, early ischemia char. Absent
onset of bowel necrosis abd. distention,
peritonitis, passage bloody stool

B. Chronic mesenteric ischemia:

Postprandial abd. pain food-fear, (most common)

Mesenteric Ischemia
No laboratory test sensitive for
the detection of acute mesenteric
ischemia prior to the onset of
intestinal infarction.
The presence of its hallmark
sign, is an indication for
immediate celiotomy.

Mesenteric Ischemia
Angiography most reliable; 74 100%
sensitivity and 100% specificity;

It is gold standard for the diagnosis of Chronic

arterial mesenteric ischemia.

CT scanning is used to:

1. Disorder other abd. condition causing abd.
pain
2. Evidence of occlusion or stenosis of
mesenteric vasculature.
3. Evidence of ischemia in the intestine &
mesentery
4. Test of choice for acute mesenteric venous
thrombosis

Mesenteric Ischemia
Treatment:
Therapeutic option for acute mesenteric
ischemia is based on:
1.
2.
3.
4.

Presence or absence of signs of peritonitis

Presence or absence of ischemic but viable intestine
General condition of the patient
Specific vascular lesion causing mesenteric
ischemia

w/ signs of peritonitis --> celiotomy check for

viability of the bowel:
Necrotic ----> segmental resection
Questionable viability ----> second look laparotomies

Mesenteric Ischemia
Surgical revascularization (embolectomy /
thrombectomy / mesenteric bypass).
Not done if:
segment is necrotic
is too unstable patient

Done pt diagnosed w/ emboli or thrombus-induced

acute mesenteric ischemia w/o signs of peritonitis.

May give thrombolysis (streptokinase, urokinase,
recombinant tissue plasminogen activator).
Useful only in partially occluded vessels and has
given w/in 12 hrs. after onset of symptoms.

Mesenteric Ischemia
NOMI std tx. Is infusion of vasodilator
(papavarine hydrochloride) into the SMA. If
w/ signs of peritonitis --> immediate celiotomy
and resect necrotic segment.
Acute mesenteric venous thrombosis
Std tx. anticoagulant (heparin / warfarin).
Signs of peritonitis --> explore and resects if needed

For chronic arterial mesenteric ischemia:

Surgical revascularization
Aortomesenteric bypass grafting
Mesenteric endarterectomy
Percutaneous transluminal mesenteric angioplasty alone
or w/ stent.

Short Bowel Syndrome

Presence of less than 200cm of residual
small bowel in adult pts.
Functional definition: - insufficient
intestinal absorptive capacity results in
the clinical manifestations of:
1.
2.
3.

Diarrhea
Dehydration
malnutrition

Short Bowel Syndrome

Etiologies (adult):
1. Acute mesenteric ischemia
2. Malignancy
3. Crohns disease
Etiologies (pediatric):
1. Intestinal atresias
2. Volvulus
3. Necrotizing enterocolitis

Short Bowel Syndrome

Factors predictive of achieving
independence from TPN:
1. Presence or absence of an intact colon
(capacity to absorb fluid & electrolytes and
absorb short-chain FA).
2. Intact ileocecal valve
3. A healthy, rather disease, residual small
intestine is associated w/ decreased severity of
malabsorption
4. Resection of jejunum is better tolerated than
the ileum, due to bile salt and vit B12
absorption capacity of the ileum.

Short Bowel Syndrome

Medical therapy:
Mx of primary condition causing
intestinal resection
Correct fluid & electrolyte imbalance
due to severe diarrhea
TPN, enteral nutrition is gradually
introduced, once ileus is resolved

Short Bowel Syndrome

Medical therapy:
H2 receptor antagonist --> to reduce
gastric acid secretion
Antimotility agents (loperamide HCL or
diphenoxylate)
Octreotide to reduce volume of
gastrointestinal secretion
TPN complication:
1. Catheter sepsis
2. Venous thrombosis
3. Liver and kidney failure
4. osteoporosis

Short Bowel Syndrome

Surgical Therapy:
Non-transplant:
Goal is to increase nutrient and fluid absorption
by either slowing intestinal transit or increasing
intestinal length
Slow intestinal transit:
1.
2.
3.
4.

Segmental reversal of the small bowel

Interposition of a segment of colon
Construction of small intestinal valves
Electrical pacing of the small bowel
Limited case report
Frequently associated w/ intestinal obstruction

Short Bowel Syndrome

Surgical Therapy:
Non-transplant:
Intestinal lengthening operation:
1. Longitudinal Intestinal lengthening and tailoring (LILT)
2. Serial transverse enteroplasty procedure (STEP)

Intestinal transplant

THANK YOU