Download Small Intestine Surgery

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 Payer’s 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 Peyer’s patches
Small Bowel Surgical Lesions
1. Small bowel obstruction:
a. Mechanical
b. Ileus
2.
3.
4.
5.
6.
Small bowel infection
Chronic inflammation
Neoplasm
Diverticula
Short bowel syndrome
Small Bowel Obstruction
Causes of Mechanical Obstruction:
1.
2.
3.
4.
Post-operative adhesion (75%)
Hernias
Crohn’s disease
Neoplasm (primary or extrinsic compression
or invasion)
5. Superior mesenteric artery syndrome
(compression of transverse duodenum)
Pathophysiology:
Accdg. to it’s anatomical relationship to
the intestinal wall:
1. Intraluminal ( foreign bodies, gallstone, and
meconium)
2. Intramural (neoplasm, Crohn’s,
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. hemoconcentration
b. fluid & electrolyte imbalance
c. 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 (can’t 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
CROHN’S 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 Crohn’s.
Clinical Manifestation:
Most common symptom:
1. Abdominal pain
2. Diarrhea
3. Weight loss
Other symptoms depends on type of
complications:
1. obstruction (fibrosis)
2. perforation (peritonitis, fistula, intraabdominal abscess)
3. 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
(esophagogastroduodenoscopy (EGD)
/colonoscopy) w/ biopsy.
2. Barium enema / intestinal series
3. Enteroclysis (small bowel) more accurate
4. 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. AIDS epidemic
2. Influx of Asian migrants
3. 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. Hypertrophic – causes stenosis or obstruction
2. Ulcerative – diarrhea and bleeding
3. 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
Crohn’s 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. Brunner’s 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/ it’s 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
Brunner’s gland
Pancreatic islets
Colonic mucosa
Endometriosis
Hepatobiliary tissues
Meckels Diverticulum
Rules of Twos:
1. 2% prevalence
2. 2:1 female predominance
3. 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 Littre’s 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:
For asymptomatic usually discovered as an
incidental findings in radiographic imaging,
endoscopy, or intraoperatively.
1. Enteroclysis has 75% accuracy but not
applicable during acute cases.
2. Radionuclide scans (99m Tc-pertechnate)
for ectopic gastric mucosa or in active
bleeding
3. 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;
usually lodge distal to origin of the middle colic
2. Arterial thrombosis: occlusion occurs at proximal
near it’s origin.
3. Vasospasm (nonocclusive mesenteric ischemia –
NOMI): usually in critically-ill pt. receiving
vasopressors.
4. 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 it’s 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. Diarrhea
2. Dehydration
3. malnutrition
Short Bowel Syndrome
Etiologies (adult):
1. Acute mesenteric ischemia
2. Malignancy
3. Crohn’s 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