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BOWEL OBSTRUCTION

Abdominal Operations

Maingots Edisi 11
McGraw-Hills Srgery
By:
Resti Fratiwi Fitri

DEFINITION
WHAT IS BOWEL OBSTRUCTION??
The

normal propulsion and passage of intestinal contents does not

occur.

WHERE?
the small intestine (small bowel obstruction), the large intestine (large
bowel obstruction), or via systemic alterations (generalized ileus)

DEFINITION
Mech
anical
Bowel
Obstr
c.
Intestinal obstruction
caused by either
paralysis or
dysmotility of
intestinal peristalsis

intestinal obstruction
caused by a physical

blockage of the
intestinal lumen

Functi
onal
Bowel
Obstr
c.

MECHANICAL BOWEL OBSTRUCTION

DEFINITION

LESIONS EXTRINSIC

LESIONS INTRINSIC

TO THE INTESTINAL WALL

TO THE INTESTINAL WALL

ADHESIONS:
Post-operative, Congenital, Post-inflammatory

CONGENITAL:
Intestinal atresia, Meckels diverticulum, duplications

HERNIA:
H. External abdominal wall, H. Internal, H. Incisional

INFLAMMATORY:
Chrons disease, eosinophilic granuloma

CONGENITAL:
Annular pancreas, malrotation, Omphalomesenteric duct
remnant

INFECTIONS:
Tuberculosis, actinomycosis, complicated diverticulitis

NEOPLASTIC:
Carcinomatosis, Extraintestinal neoplasm

NEOPLASTIC:
Primary or metastatic neoplasms, appendicitis

INFLAMMATORY:
Intra-abdominal abscess, Starch peritonitis

MISCELLANEOUS:
Intussusception, endometriosis, radiation stricture,
intramural hematoma, ischemic stricture

MISCELLANEOUS:
Volvulus, Gossypiboma, Superior mesentric artery
syndrome

INTRALUMINAL/OBTURATOR OBSTRUCTION:
Gallstone, enterolith, phytobezoar, parasite infestaion,
swallowed foreign body

MECHANICAL BOWEL OBSTRUCTION

DEFINITION

OBSTRUCTION

PARTIAL
OBSTR.

SIMPLE
OBSTR.

an obstruction without any


vascular compromise
possible to decompress the
intestine proximally

COMPLETE
OBSTR.

CLOSEDLOOP OBSTR.

STRANGULATION OBSTR.

occurs when both ends of


the involved intestinal
segment are obstructed

occurs when the blood


supply to the affected
segment is compromised

increase in intraluminal
pressure secondary

will progress to transmural


necrosis

DEFINITION

FUNCTIONAL BOWEL OBSTRUCTION


INTRA-ABDOMINAL

EXTRA-ABDOMINAL

CAUSES

CAUSES

INTRAPERITONEAL PROBLEMS:
peritonitis, intra-abdominal abscess, post-operative
, chemical (gastric juice, bile, blood), Autoimmune
(Serositis, vasculitis) & Intestinal ischemia (arterial
or venous, sickle
disease)
Thecell
most
common cause is

METABOLIC ABNORMALITIES:
Electrolyte imbalance, sepsis, lead poisoning,
porphyria, hyperglicemia, hypothiroidsm, uremia

RETROPERITONEAL
PROBLEMS: ILEUS
THORACIC PROBLEMS:
POST-OPERATIVE
Urolithiasis,
pyelonefphritis,
metastasis,
Myocardial
It is correlate
with
the degree of
surgical trauma as well
as the infarction, congestive heart failure,
pancreatitis, retroperitoneal
pneumonia, thoracic trauma
type of trauma
operation.
MEDICINES:
opiates,
Different anatomic segments of the gastrointestinal
tractanti-cholinergic, alpha-adrenergik
agonists,
also recover at different rates after manipulation
and antihistamines

trauma.

MISCELLANEOUS:
Spinal cord injury, pelvic fracture, head trauma,
radiation therapy, renal
The small bowel recovers within several hourschemotherapy,
posttransplantation

operatively. Stomach within one day later. Colon about 3-5


days later.

EPIDEMIOLOGY
frequency in

>

Occur in Small intestinal > Colon


Both the etiology and frequency of bowel obstruction changed
dramatically during the 1900s.
1/3 of the 20th century incarcerated hernia.
of the 20th century postoperative adhesive obstruction.
In the future? It may decrease the frequency of bowel obstr. secondary to post operative
adhesions cause minimal access laparoscopic approaches.

Mortality & morbidity of bowel obstruction is substansial.


Mortality rates 3% - 30%, when there is vascular compromie or perforation of the
obstructed bowel. Morbidity it is reccurent problem, 12% of patients after primary
conservative treatment.

PHATOPHYSIOLOGY
the pathophysiology of bowel obstruction remains

incompletely understood.

Bowel distension, decreased absorption, intraluminal hypersecretion, and


alterations in motility are found universally, yet the mechanisms responsible for these
pathophysiologic derangements are not clear.
DISTENTION, ABSORPTION & SECRETION
INTESTINAL MOTILITY
CIRCULATORY CHANGES
MICROBIOLOGY & BACTERIAL
TRANSLOCATION

PATOPHYSIOLOGY

DISTENTION,
ABSORPTION & SECRETION

Mechanical bowel obstruct BOWEL DISTENTION

BOWEL DISTENTION ??
Early phases of obstruct, accumulates gas from

swallowed air (75%

nitrogen).
The next phases, gas arise from the

fermentation of sugars ,

production of carbon dioxide by interaction of gastric acid and


bicarbonates in pancreatic and biliary secretions, and diffusion of oxygen
and carbon dioxide from the blood.

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PATOPHYSIOLOGY

DISTENTION,
ABSORPTION & SECRETION
Dilatation &
inflammation bowel

The amount and activity of nitric oxide


synthase, correlates with the severity of
intestinal dilatation.

Activated
Activated
neutrophils &
macrophages
macrophages

Inflammatory cause Inflammatory response increase


dilatation
dilatation &
&
inhibition of nitric oxyde potent inhibitor of
contractilite
contractilite activitiy
activitiysmooth-muscle tone dilatation

Accumulate
Accumulate within
within
muscular layer of
the
the bowel
bowel wall
wall

Damage
By release of reactive proteolytic enzymes,
Damage to
to secretory
secretory
&
& motor
motor processess
processesscytokines & other locally substances

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PATOPHYSIOLOGY

DISTENTION,
ABSORPTION & SECRETION
12 hours of
obstruct.

Water
Water &
&
electrolytes
electrolytes
accumulate
accumulate
secondary
secondary

Decrease
Decrease
absorption
absorption

24 hours of
obstruct.

water
water &
&
electrolytes
electrolytes
accumulate
accumulate
more
more rapidly
rapidly

Decrease
Decrease in
in
absorption
flux
absorption flux

Mucosal injury

Increase
Increase
intestinal
intestinal
secretion
secretion (flux)
(flux)

Increased
Increased
permeability
permeability
Intraluminar leakage plasma,

electrolytes & extracellular


fluid occurs

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PATOPHYSIOLOGY

DISTENTION,
ABSORPTION & SECRETION

Decrease in absorptive capacity


Increase in secretion leads to
important fluid loses

DEHYDRATION
OBSTRUCTED BOWEL
WITH SECRETORY FLUX

Bile

vasoavasoac
tive intestinal
polypeptide

prostaglandins

Intraluminar
bacteria toxins

Oxygen
Free
radical

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PATOPHYSIOLOGY

INTESTINAL MOTILITY
Early phase of bowel obstruction,
Intestinal contractile activity increases propel intraluminal contents past
the obstruction
Later phase of bowel obstruction,
The contractile activity diminishes intestinal wall hypoxia

exaggerated intramural inflammation


Intestinal motility are disruption of the normal

autonomic
parasympathetic (vagal) and sympathetic splanchnic
innervation.

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PATOPHYSIOLOGY

CIRCULATORY CHANGES
Distention of the bowel lumen with a concomitant results in
increased transmural pressure on capillary blood flow
within the wall of the bowel risk

of ischemic.

Intestinal wall ischemia is real concern in Large Bowel


Obstruction. The Ascending Colon luminal diameter is the
greatest and (by Laplace's law) the wall tension (and ischemia) is also
the greatest high risk to ischemia.

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PATOPHYSIOLOGY

MICROBIOLOGY &
BACTERIAL TRANSLOCATION
Upper small intestine gram-positive
concentrations, <10 6 colonies/mL.

facultative organisms in small

More distally, in the distal ileum the bacterial count increases in


concentration to about 10 8 colonies/mL, the flora primarily coliforms

and

anaerobic organisms
in the presence of obstruction, a rapid proliferation of bacterial
organisms occurs consisting predominantly of fecal-type organisms.
reaching a plateau of 10 91010 colonies/mL after 1248 hours of an
established obstruction.
Bacterial toxins have an important role in the mucosal response to bowel
obstruction.

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ETIOLOGY
ADHESIONS
HERNIA
MALIGNANT BOWEL OBSTRUCTION
GRANULOMATOUS DISEASE AND CHROHNS
DISEASE
INTUSSUSCEPTION
VOLVULUS
OTHER CAUSE

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DIAGNOSIS
The diagnosis of bowel obstruction is suspected clinically
based on the presence of classic signs and symptoms and then

confirmed by some form of imaging test, such as


abdominal radiography or more recently by computed tomography.
The etiology can often be pinpointed by careful history-taking
complemented with imaging studies.

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HISTORY &

DIAGNOSIS

PHYSICAL EXAMINATION
Abdominal pain & distention precede the appearance
of NAUSEA & VOMITING by several hours
The more Proximal the obstruction,
the earlier and more prominent are the
nausea & vomiting, distention usually less.
DISTENTI
DISTENTI
ON
ON

The location

CRAMPY
CRAMPY
ABDOMINAL
ABDOMINAL PAIN
PAIN

and
character of pain may be
helpful in differentiating
mechanical bowel obstruction and
ileus.

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HISTORY &

DIAGNOSIS

PHYSICAL EXAMINATION
MECHANICAL SMALL BOWEL
OBSTRUCTION

MECHANICAL LARGE BOWEL


OBSTRUCTION

VISCERAL PAIN
POORLY LOCALIZED
CRAMPY WITH RECCURENT
PAROXYSMS occuring short (30
seconds to 2 minutes)

THE EPISODES ARE USUALLY SPACED


FARTHER APART IN TIME and tend to last
longer (mintes rather than seconds)

the presence of constant or a localized pain has been


regarded as a sign of strangulation

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HISTORY &

DIAGNOSIS

PHYSICAL EXAMINATION
FEVER??
infectious cause or strangulations

VITAL
VITAL SIGNS
SIGNS
POTENSIAL
ABD.
HYDRATION
ABD.
RECTAL
AUSCULTA-TION
PALPATION
INSPECION
HERNIA
EXAMS
STATUS
DEFECT
POTENSIAL
ABD.
HYDRATION
ABD.
RECTAL
AUSCULTA-TION
PALPATION
INSPECION
HERNIA
EXAMS
STATUS
DEFECT

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HISTORY &

DIAGNOSIS

PHYSICAL EXAMINATION

VITAL
VITAL SIGNS
SIGNS
POTENSIAL
ABD.
HYDRATION
ABD.
RECTAL
AUSCULTA-TION
PALPATION
INSPECION
HERNIA
EXAMS
STATUS
DEFECT
POTENSIAL
ABD.
HYDRATION
ABD.
RECTAL
AUSCULTA-TION
PALPATION
INSPECION
HERNIA
EXAMS
STATUS
DEFECT

DEHYDRATION??
Tachycardia +
Hypotension + Oligouria

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HISTORY &

DIAGNOSIS

PHYSICAL EXAMINATION

VITAL
VITAL SIGNS
SIGNS
POTENSIAL
ABD.
HYDRATION
ABD.
RECTAL
AUSCULTA-TION
PALPATION
INSPECION
HERNIA
EXAMS
STATUS
DEFECT
POTENSIAL
ABD.
HYDRATION
ABD.
RECTAL
AUSCULTA-TION
PALPATION
INSPECION
HERNIA
EXAMS
STATUS
DEFECT

Functional Bow. Obst.


absence of sounds
Mechanical Bow. Obst. metalic
sounds
Determine the presence, frequency of
bowel sound & quality of the obstructed
bowel sounds

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HISTORY &

DIAGNOSIS

PHYSICAL EXAMINATION

VITAL
VITAL SIGNS
SIGNS
POTENSIAL
ABD.
HYDRATION
ABD.
RECTAL
AUSCULTA-TION
PALPATION
INSPECION
HERNIA
EXAMS
STATUS
DEFECT
POTENSIAL
ABD.
HYDRATION
ABD.
RECTAL
AUSCULTA-TION
PALPATION
INSPECION
HERNIA
EXAMS
STATUS
DEFECT

PERITONITIS??
Rebound, localized tenderness,
involuntary guarding that herald
vascular or perforations

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DIAGNOSIS

LABORATORY
Completed
Completed blood
blood cell
cell count
count &
& diff
diff

Electrolyte
Electrolyte panel
panel

Blood
Blood urea
urea nitrogen
nitrogen

Creatine
Creatine serum
serum

This laboratory data


should be obtained to

evaluate fluid and


electrolyte
imbalance and to

rule out sepsis

Urinalysis
Urinalysis

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DIAGNOSIS

RADIOLOGIC FINDINGS
Flat & upright (supine)
abdominal radiographs
Contrast studies
Computed tomography
ultrasonography

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DIAGNOSIS

RADIOLOGIC FINDINGS
Flat & upright (supine)
abdominal radiographs
Contrast studies
Computed tomography
ultrasonography

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DIAGNOSIS

RADIOLOGIC FINDINGS
Flat & upright (supine)
abdominal radiographs
Contrast studies
valuable tool in the diagnosis of bowel

Computed tomography
ultrasonography

obstruction, especially when abdominal

films are nonspecific and fail to


provide an accurate diagnosis or
when strangulation is suspected

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DIAGNOSIS

RADIOLOGIC FINDINGS
Flat & upright (supine)
abdominal radiographs
Contrast studies
Computed tomography
ultrasonography

Diagnosis intestinal loops measure


more that 25 mm in diameter and the distal
ileum is found to be collapsed.
USG sensitive and specific than plain
abdominal films for the diagnosis of bowel
obstruction.

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MANAGEMENT
SMALL BOWEL OBSTRUCTION
Focus on aggressive fluid

resuscitation & on prevention of

aspiration.
Resuscitation

Aspiration

Guided by urine
output,hemodyna
mically stable
and normal renal
function.

Use functioning
NGT for
nasogastric
decompression to
prevent swallowed
air.

Use Crystalloid.

LARGE BOWEL
OBSTRUCTION

SURGICAL Intervention!!!
surgical exploration should be
undertaken as soon as possible after
appropriate resuscitation.

Prior to exploration, it has same


principles with non-operative small
bowel obstruction.
Resuscitation with crystalloid, NGT for
nasogatric decomprossion , Bladder
chateter & antibiotics pre operation

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MANAGEMENT

SMALL BOWEL OBSTR.


NON-OPERATIVE MANAGEMENT
ONLY UNCOMPLICATED small bowel obstruction

Treatment Principles for Managed Non-Operatively


Adequate proximal
decompression

Aggresive
resuscitatio
n

Electrolyte
replacement

Contraindications to nonoperative management include: Suspected


Ischemia, Large Bowel Obstruction, Closed-loop Obstruction,
Strangulated Hernia, And Perforation.
Relative Contraindications COMPLETE small bowel obstruction.

MANAGEMENT

SMALL BOWEL OBSTR.


CONVERT TO OPERATIVE MANAGEMENT?
UNCOMPLICATED OBSTRUCTION develops evidence of a
COMPLICATED OBSTRUCTION
Vital Sign
Fever
Tachycardia

Physic
Exam.
Localized
tenderness
Continous
abdominal
pain
Peritonitis

Lab.
leukocytosis

Minimal 3
sign & symptomp

EVIDENCE OF COMPLICATED OBSTRUCTION

WHEN?
Non-operative management
can be continued longer
than 48 hours with the
understanding that delaying
invitable
operative
treatment.

MANAGEMENT

SMALL BOWEL OBSTR.


OPERATIVE MANAGEMENT

prevent peri- and postoperative complications.

beta-blockers
to patient with
cardiovascular
cormorbidities

Antibiotic preoperatif

Correction
electrolyte
abnormalities

Use
nasogastric
tube

MANAGEMENT

SMALL BOWEL OBSTR.


OPERATIVE MANAGEMENT

Identify the site & cause of obstruction


Do incision
Manual retrograde decompression
Patients with malignant small bowel obstruction or if the offending obstruction is
unable to be released, intestinal bypass can be performed .it is preventing
a closed-loop obstruction.
Patients with certain chronic inflammatory diseases will remain at risk for
ongoing problems related to the inflammation and may be served better by
resection than simple bypass.

MANAGEMENT

LARGE BOWEL OBSTRUCTION


Exploration in patients with large bowel obstructions is best performed
through a low midline incision. Open exploration is best.
Obstructing lesions of the cecum and ascending colon should be resected via
right hemicolectomy.
Lesions in the transverse colon should be managed with an extended right
hemicolectomy and again, with a primary anastomosis
Lesions in the transverse colon should be managed with an extended right
hemicolectomy and again, with a primary anastomosis
The management of obstructing lesions in the descending and sigmoid colon
is Intraoperative bowel preparation allows for segmental resection and
primary anastomosis of the involved colon provided the remnant bowel to be
reanastomosed is healthy and neither too edematous nor too dilated

TERIMAKASIH

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