Predisposing Factors

Postoperative adhesions occur

after almost every abdominal
surgery and are the leading
cause of intestinal obstruction,
accounting for more than 40%
of all cases and 60% to 70% of
those involving the small
bowel. Adhesion formation
after abdominal and pelvic
operations remains extremely
common and is a source of
considerable morbidity.

Mechanical damage of
the peritoneal and
intestinal serosa
following abdominal
surgery

Damaged mesothelial
cells cause flow of
proinflammatory
mediators (cytokines)
towards area

Proinflammatory
cytokines increases
blood vessel
permeability

Extravasation of
serosanguine liquid in
abdominal cavity

Extravasated fibrogen
escapes blood vessels

Fibrin develops as
influenced by
thrombokinase
 Fibrin forms loose
three- dimensional
networks. Fibrinous
exudate causes
adjacent surface to
stick together
(premature adhesions)

Constant presence of
trauma or ischemia in
the intestine prevent
fibrinolysis
(degradation of fibrin)

Decrease in
plasminogen activity

Fibrinous adhesion are

not lysed

Macrophages form the

foundation of
fibrinous bands that
bridge tissue surface
and the adhesion
continue to mature

Tighter fibrin network

forms. Increase in
proliferation of
fibroblast

Mucoploysaccaride,
collagen and
tropocollagen from
fibroblasts strengthens
the existing adhesions

Adhesions are now fibrous

and permanent,
increasingly becoming
vascular and organized in
structure, incudling
distinct collagen fibers
 No new adhesion formation. Existing
adhesion continue to mature into
dense fibrous bands

Adhesion cause abdominal organs to

stick to one another or stick to
abdominal wall

Adhesion cause extrinsic

compression on the bowels leading
to intestinal obstruction

Mechanical obstruction of the

intestines partially/completely
blocks movement of stool and food

Food stuck in the Small Fecal matter stuck in

intestine is metabolized amounts of the intestines produces
by intestinal bacteria air we nitrogenous gas
breathe
enters the
Bacteria produce bowels
Nitrogenous gas and
nitrogenous gas as a by- ammonia toxins build
product of up
metabolization

Abdominal
distention & Build up of gas and
Obstipation obstructed food causes
bowel distention

Distended bowels cause venous Nausea Distended bowels Distended bowels

compression on surrounding and result to vagal nerve compress other organs
blood vessels Vomiting
stimulation

Compressed veins leak Compression of liver or

Decrease Venous compression
fluid into the bowels Biliary duct causes
Peristalsis decrease oxygenation on
obstruction/inflammation
affected area
Abdominal Incr Loss of H2O
Obstruction/inflammation
pain Ischemia of intestinal ease and electrolytes
thirs increases formation of
tissues and cells
unconjugated bilirubin

Excess in unconjugated
Jaundice bilirubin leaks out and
enters systemic circulation
 LABORATORY WORK-UPS

Physical exam X-ray CT scan CBC Air/Barium enema Ultrasound

Doctor will ask To confirm a CT scan may show if An air or barium When an intestinal
for medical diagnosis of combines a you have an enema is basically obstruction occurs in
history. Doctor intestinal series of X- infection, or enhanced imaging of children, ultrasound
will also obstruction, ray images if you are the colon that may be is often the preferred
perform your doctor taken from dehydrated. done for certain type of imaging
physical exam may different Dehydration suspected causes of
by observing recommend angles to can develop obstruction.
the abdomen an abdominal produce when your
or listening for X-ray. cross- intestines
bowel sounds However, sectional cannot
some images. absorb liquid
intestinal properly.
obstructions

Intestinal
Obstruction

If Treated
If Untreated

Medical Management Nursing Bowel distention

Management persist
MEDICATION SPECIAL
Antibiotic PROCEDURES 1. Take a careful medical
- Antibiotics are used to cover gram- history of patient about Rise in
Leaking of
negative and anaerobic organisms. -IV Therapy current symptoms and venous fluids bacteria.
can protect against bacterial -Nasogastric previous disease
translocation and subsequent continue. Ischemia
Intubation manifestation
bacteremia in patients with intestinal -Urinary Vomiting leads to
2. Assess level of pain,
obstruction catheterization location, intensity, also persists necrosis
duration
IV fluids SURGICAL 3. Provide comfortable
- Fluid replacement with aggressive -Surgical position and promote
intravenous (IV) resuscitation using resection restful environment Steady loss Intestinal
isotonic saline or lactated Ringer -Laparotomy 4. Administer analgesics of fluids and cells die
solution is indicated. IV fluid to -Laparoscopy as prescribed electrolytes from lack
correct electrolyte imbalances, -Stent placement 5. Monitor for signs of of O2
dehydration, and for nutritional - dehydration and
replacements Colostomy/Ileosto electrolyte imbalance
my 6. Monitor IV fluids and Dehydration
Oxygen - administer as ordered
- Given to relieve anxiety and Revascularization 7. Maintain strict intake Prolifer
prevent further ischemia and output record ation of
8. Monitor proper bacteria
Analgesics placement and patency of Fluid and
- Analgesics ensure patient comfort, nasogastric tube electrolyte
promote pulmonary toilet, and have 9. Encourage patient and imbalance
sedating properties, which are assist in doing oral care are apparent Bacteria
beneficial for patients who 10. Explain about the in blood
experience pain. disease condition at the stream
level of patient
Antiemetics understanding
- These agents should be Hypovolemia
administered for symptomatic relief, Sepsi
usually in conjunction with GI s
decompression via placement of an
NG tube for suction.

Decreasing GFR
 SHOCK
Hypovolemic/Septic

Prognosis:
GOOD
Symptoms of shock leads to a
systemic damage throughout the
body

Cardiovascular Renal Pulmonary Circulatory Neurologic

system system system system system

Left ventricular juxtaglomerular cells Due to chronic Bacteria Cerebral

hypertrophy in release renin as a pyelonephritis, begins to vessel
response to response to decreased metabolic acidosis spread constricts due
increase cardiac bp. renin converts become through out to elevation of
work load due to angiotensinogen to proliferate as the blood bicarbonate
hemodynamic angiotensin i. HCO3 levels stream which can
overload. In LV angiotensin i circulates decrease while causing severely
Hypertrophy, it through blood vessels there is an septicemia. compromise
increases the and is converted to increase of plasma Septicemia cerebral O2
stiffness in the left angiotensin ii by K level. affects other supply
ventricle and endothelial cells. Metabolic organs
increases left angiotensin ii acidosis prompt
atrial pressure stimulates contraction stimulation of
which causes smooth muscles which respiratory rate
atrial fibrillation increases peripheral Septicemia Brain
and a decrease in
and decreased resistance. angiotensin ischemia,
PCO2. Increase
cardiac output ii acts on the kidneys stroke,
rate and depth of
cells to hold on to cognitive
respiration
more water. dysfunction
angiotensin ii also
Myocardial
stimulates the
hypoxia, impaired Respiratory
production of
cardiac function failure
antidiuretic hormone
from the pituitary
gland. angiotensin ii
also stimulates the
adrenal gland to
secrete aldosterone.
aldosterone acts on
kidney cells to retain
water.

Renal failure

DEATH