Seminar presentation by 5th-year medical students under the supervision of in house lecturer. He was previously working as a consultant surgeon in Syria. Reference as mentioned in the slides.

1. P R E S E N T E D B Y
N U R U L H I D A Y U
A U D I R A H M A N
A F F A N S Y A F I Q I
M A N A G E M E N T O F I N T E S T I N A L
O B S T R U C T I O N

2. 1 . I n t r o d u c t i o n
2 . C l a s s i f i c a t i o n o f I n t e s t i n a l O b s t r u c t i o n
3 . P a t h o p h y s i o l o g y
4 . C l i n i c a l P r e s e n t a t i o n
5 . I n v e s t i g a t i o n – I m a g i n g S t u d y
6 . M a n a g e m e n t
O U T L I N E
 L o c a t i o n
 D e g r e e o f o b s t r u c t i o n
 C a u s e s
 V a s c u l a r C o m p r o m i s e

3. INTRODUCTION
 Bowel obstruction occur when there is any form of
impedance of the normal flow of material through a
hollow viscous
(Garden, 6th edition)
 Lead to dilatation of bowel proximally and disrupts
peristalsis
 Obstruction can be functional (due to abnormal
intestinal physiology) or due to a mechanical
obstruction, which can be acute or chronic.

4. INTRODUCTION

5. RISK FACTOR
Factors that may lead to increase risk developing IO :
 Abdominal or pelvic surgery which may cause adhesion
 Previous history of obstruction
 Crohn’s disease – cause intestinal walls to be thicken, narrowing the
passageway
 Cancer within abdomen especially history of removal abdominal
tumor
 History of constipation – impacted faeces
 Malrotation – congenital

6. INTRODUCTION

7. P R E S E N T E D B Y
N U R U L H I D A Y U
C L A S S I F I C AT I O N O F I N T E S T I N A L
O B S T R U C T I O N

8. A. LOCATION
SMALL BOWEL LARGE BOWEL
PROXIMAL DISTAL
 Bilious
vomiting
 Shorter onset
 Abdominal
distension
 Fecaloid
vomitus
 Longer onset
Common Causes :

9. A. LOCATION

10. A. LOCATION
Prognosis
 GOOD PROGNOSIS (proper diagnosis and treatment of the obstruction)
 Complete obstructions treated successfully non-operatively have a higher incidence
of recurrence than do those treated surgically.
Morbidity/mortality
 Morbidity and mortality are dependent on the early recognition and correct
diagnosis of obstruction.
 If untreated, strangulated obstructions cause death in 100% of patients.
 If surgery is performed within 36 hours, the mortality rate decreases to 8%.
 The mortality rate is 25% if the surgery is postponed beyond 36 hours in these
patients.
 Some factors associated with death and postoperative complications include age,
comorbidity, and treatment delay.
Small Bowel Obstruction

11. A. LOCATION
Mortality & Prognosis
 Mortality is determined by the patient's overall medical condition and the presence of
any comorbidities that may influence the patient's surgical risk.
 If large bowel obstruction is treated early, the outcome is generally good.
Mortality is higher in patients who have developed bowel ischemia or perforation.
 After surgical decompression, the prognosis is determined by the underlying disease.
 In general, overall mortality for large-bowel obstruction is 20%, which increases to
40% if there is colonic perforation.
 Mortality for acute colonic pseudo-obstruction (ACPO; Ogilvie syndrome) is 15% with
early care; it increases to 36% if colonic ischemia or perforation develops.
Large Bowel Obstruction

12. B. DEGREE OF OBSTRUCTION
DEGREE OF
OBSTRUCTION
PARTIAL COMPLETE
 Lumen narrowed but allow
transit some content
 Abdominal distension
 Presence of flatus
 Presence of bowel
movement
 Lumen totally
obstructed
 Complete obstipation
Closed loop
(both ends are obstructed)
Simple obstruction
(no vascular impairment)
Strangulation

13. B. DEGREE OF OBSTRUCTION
Degree of obstruction is
based on degree of
collapse and amount of
residual contents distal
to obstruction.
OGILVIE SYNDROME

14. C. CAUSES
EXTRAMURAL
MECHANICAL /
DYNAMIC
FUNCTIONAL /
ADYNAMIC
CAUSES
INTRAMURAL INTRALUMINAL
 Adhesions
 Hernias
 Congenital
bands
 Tumors
 volvulus
 Strictures :
inflammatory
(Crohn , TB )
 Tumors
 Intussusception
 Lymphomas
 Impacted
faeces
 Gallstones
 Bezoar
 Foreign
bodies
 Paralytic ileus
- Post op : 24-72 hour
- Infection
- Metabolic – uremic /
hypokalemia
 Pseudo-obstruction
Peristalsis against a
mechanical obstruction
Absent peristalsis due to
intestinal atony in absence
of mechanical cause

15. INTESTINAL OBSTRUCTION

16. CAUSES
INTUSSUSCEPTION

17. INTESTINAL OBSTRUCTION
TRICHOBEZOARS AND PHYTOBEZOARS
 Trichobezoars (Undigested hair ball):
Due to persistent hair chewing or
sucking, and may be associated with
underlying psychiatric abnormality.
 Phytobezoars (Fruit/vegetable fibre):
Due to high fibre intake, inadequate
chewing, previous gastric surgery and
loss of the gastric pump mechanism.
Preoperative diagnosis is difficult
even with high resolution CT
scanning.
WORMS
 Ascaris lumbricoides may cause low
small bowel obstruction, particularly
in children.
 Diagnosis by: Worms in the stool or
vomitus, eosinophilia or the sight of
worms within gas-filled small bowel
loops on a plain radiograph.
 Occasionally, worms may cause a
perforation and peritonitis,
especially if the enteric wall is
weakened by such conditions as
ameobiasis.

18. ADHESION
 Most commonly occurs due to previous abdominal
surgery.
 Risk of acquiring adhesion subsequent to abdominal
surgery is 4% and that after laparotomy is 2%
 Adhesions start to form within hours of abdominal
surgery.
 Classified into 2 types: early (fibrinous) and late
(fibrous)

19. BAND
Usually only one band is culpable.
This maybe:
 Congenital, eg. Obliterated vitellointestinal duct
 A string band following previous bacterial peritonitis
 A portion of greater omentum usually adherent to the parietals

20. OBLITERATED VITELLOINTESTINAL
DUCT
 Embryologically vitellointestinal tract comprises of
three structures: the vitelline duct, artery, and vein.
 During early phases of development, the yolk sac acts
as a prime source of nutrition for the quickly growing
fetus.
 The vitellointestinal duct is the developing structure
joining the primary yolk sac to the developing midgut
during fetal enlargement.
 Typically, at the 5th-10th week of gestation, it turns
out to be a thin fibrous band that spontaneously
obliterates and separates from the intestine.
Source : NCBI

21. OBLITERATED VITELLOINTESTINAL
DUCT
 Partial or complete failure of abolition of vitellointestinal duct may lead to
diverse type of congenital intestinal malformations comprising; Meckel's
diverticulum, vitelline cord, umbilical sinus, enteric fistula and haemorrhagic
umbilical granuloma.
 Though rare, intestinal obstruction is one of the complications of
vitellointestinal duct, occurs due to numerous mechanisms including
intussusceptions of the diverticulum, internal herniation or volvulus from a
patent band.
 It is very challenging to know the reasons of the intestinal obstruction
without diagnostic laparotomy or laparoscopy.
Source : NCBI

22. HERNIA
 Most common cause of small bowel obstruction in patients
with no prior history of surgery is hernia.
 Careful search for inguinal, femoral and umbilical hernia must
be made. Consider internal hernia too.
 Internal herniation occurs when a portion of the small
intestine becomes trapped in one of the retroperitoneal
fossae or in a congenital mesenteric defect

23. HERNIA

24. HERNIA

25. D. VASCULAR COMPROMISE
STRANGULATED NON-STRANGULATED
Absence of signs and symptoms
strangulation
 Life threatening condition
 “Hemodynamic instability”
 Peritoneal signs
Direct pressure
on the bowel wall
Interrupted
mesenteric blood
flow
Increased
intraluminal
pressure
 Hernial orifices
 Adhesion/bands
 Volvulus
 Intussusception
 Closed – loop
obstruction

26. CLOSED LOOP IO
 This occur when the bowel is obstructed at both the proximal and distal points
 Its is present in many cases of intestinal strangulation
 When gangrene of the strangulated segment is imminent, retrograde thrombosis of
the mesenteric vein result in distension of both sides of the strangulated segment

27. STRANGULATED IO
 Strangulation occurs in nearly 25% of people with small bowel obstruction.
 Usually, strangulation results when part of the intestinal becomes trapped in an
abnormal opening such in diagram above.
 Gangrene can develop in as few as 6 hours.
 Mortality rate : 10-35%
Gangrene  the intestinal wall dies  usually causing rupture  peritonitis, shock
and if untreated, death

28. P R E S E N T E D B Y
A F F A N S Y A F I Q I
P AT H O P H Y S I O L O G Y A N D C L I N I C A L
F E AT U R E S

29.  Irrespective of aetiology or acuteness of onset, in dynamic (mechanical)
obstruction the bowel proximal to the obstruction dilates and the bowel
below the obstruction exhibits normal peristalsis and absorption until it
becomes empty and collapse.
 Initially, proximal peristalsis is increased in an attempt to overcome the
obstruction. If the obstruction is not relieved, the bowel continue to
dilate, ultimately there is a reduction in peristaltic strength, resulting in
flaccidity and paralysis.
PATHOPHYSIOLOGY

30. The distension of proximal to an obstruction is caused by two factors:
 Gas : there is significant overgrowth of both aerobic and anerobic
organism, resulting in considerable gas production. Following the
reabsorption of oxygen and carbon dioxide, the majority is made up of
nitrogen (90%) and hydrogen sulphide.
 Fluid : this is made up of the various digestive juice (Saliva 500mL, bile
500mL, pancreatic secretion 500mL, gastric secretion 1Litre- in all per
24 hours.) this accumulate in the guts lumen as absorption by the
obstructed gut is retarded. Dehydration and electrolyte loss are
therefore due to:
- reduced oral intake
- defective intestinal absorption
- sequestration in the bowel lumen
- transudation of fluid into the peritoneal cavity
PATHOPHYSIOLOGY

31. Cardinal features
1. Colicky pain
2. Vomiting
3. Abdominal
distension
4. Constipation
Other features
1. Dehydration
2. Hypokalemia
3. Pyrexia
4. Abdominal tenderness
CLINICAL FEATURES

32. P R E S E N T E D B Y
A F F A N S Y A F I Q I
I N V E S T I G AT I O N S

33.  ABDOMINAL X-RAY ( SUPINE )
 CONTRAST ABDOMINAL X-RAY
 CT SCAN
TYPES

34.  Supine (Most of diagnosis made by this
position)
 Erect (May be requested when in doubt)
 (3/6/9 rule) : 3cm for the small bowel, 6cm for
the colon and 9cm for the caecum
ABDOMINAL X-RAY

35. OBSTRUCTED SMALL BOWEL
 Characterized by straight segments that are generally
central and lie transversely
 No/minimal gas is seen in the colon
JEJUNUM
Characterized by its valvulae conniventes, which
completely pass across the width of the bowel and are
regularly spaced, giving a ‘concertina’ or ladder effect
RADIOLOGICAL FEATURES OF
IO

36. ILEUM
The distal ileum has been described by
wangensteen as featureless
CAECUM
A distended caecum is shown by a rounded gas
shadow in the right iliac fossa
LARGE BOWEL
Except for the caecum, shows haustral folds, which
are spaced irregularly & do not cross the whole
diameter of the bowel.
RADIOLOGICAL FEATURES OF
IO

37. RADIOLOGICAL FEATURES OF
IO

38. LARGE BOWEL OBS. SMALL BOWEL OBS.

39.  In intestinal obstruction, fluid levels appear later
than gas shadows as it takes time for gas and fluid
to separate. (Most prominent on an erect film)
 When fluid levels are pronounced, the obstruction
is advanced.
 In the small bowel, the number of fluid levels is
directly proportional to the degree of obstruction
and to its site, the number increasing the more
distal the lesion.

40. BARIUM STUDIES
 Done in patients without evidence of strngulation
 Adhesive small bowel obstruction
 Predicts resolution of small bowel obstruction
 Contraindicated in acute obstruction
CONTRAST ABD X-RAY

42.  Widely used nowadays
 Highly accurate
 Limitation : cannot
diagnose ischemia
CT SCAN

43. 1. Plain X-ray : evidence of small or large bowel obstruction
with an absent caecal shadow in ileocecal cases
2. Barium enema : shows claw sign in ileocolic
intussusception
3. CT scan : shows a target or sausage-shaped soft tissue
mass with a layering effect ( mesenteric vessels within bowel
lumen )
4. Ultrasound : shows a doughnut appearance of concentric
rings in transverse section
IMAGING IN
INTUSSUSCEPTION

45. CAECAL VOLVOLUS
Characterised with
 Caecal dilatation (98-100%),
 Single air-fluid level (72–88 %),
 Small bowel dilatation (42–55 %)
 Absence of gas in distal colon (82
%)
IMAGING IN VOLVULUS

46. SIGMOID VOLVULUS
 Shows massive colonic
distension.
 The classic appearance: two
twisted loops with a central
doubled wall component. (
On plain xray)
 Coffee bean sign
IMAGING IN VOLVULUS

47.  Rigler’s triad
1. Pneumobilia
2. Small bowel obstruction
3. Atypical mineral shadow
 2 of these 3 signs are
pathognomic of gallstone ileus.
GALLSTONES ILEUS

48. P R E S E N T E D B Y
A U D I R A H M A N
M A N A G E M E N T

49. DANGEROUS SIGNS
 Constant pain
 Absent bowel sounds
 Tenderness with rigidity
 Leukocytosis
 Fever and tachycardia
 Shock

50. ACUTE INTESTINAL
OBSTRUCTION
It involves:
i. Conservative management
ii. Surgical management
 Some cases will settle by using conservative regimen, other
need surgical intervention
 Surgery should be delayed till resuscitation is complete unless
signs of strangulation and evidence of closed-loop obstruction
 Cases that show reason for delay should be monitored
continuously for 72 hours in hope of spontaneous resolution

51. ACUTE INTESTINAL
OBSTRUCTION
SUPPORTIVE MANAGEMENT
 Nasogastric aspiration by Ryle's tube
 IV fluid
 NPO
 Urinary catheter
 Check temperature and pulse 2 hourly
 Abdominal temperature 8 hourly
 Broad spectrum antibiotics initiated early

52. ACUTE INTESTINAL
OBSTRUCTION
SURGICAL MANAGEMENT
Principles:
 Management of segment at site of obstruction
 Management of distended proximal bowel
 Management of underlying cause of obstruction

53. ACUTE INTESTINAL
OBSTRUCTION
INDICATION FOR SURGERY
 Failure of conservative management
 Tender and irreducible hernia
 Strangulation
 Virgin abdomen
If the site of obstruction is unknown, laparotomy assessment is directed to:
i. The site of obstruction
ii. The nature of obstruction
iii. The viability of gut

54. The type of surgical procedure depend upon the cause of
obstruction via division of bands, adhesiolysis, excision, or bypass
Once obstruction relieved, the bowel is inspected for viability, and
if non-viable, resection is required
SURGICAL TREATMENT
 Absent peristalsis
 Loss of normal shine
 Loss of pulsation in mesentery
 Green or black color of bowel
 Absent mesenteric pulsations
INDICATION FOR NON-VIABILITY

55. SURGICAL TREATMENT
VIABLE NON-VIABLE
CIRCULATION
Dark color becomes lighter Dark color remain
Visible pulsation in mesenteric
arteries
No detectable pulsation
GENERAL
APPEARANCE
Shiny Dull and lusterless
INTESTINAL
MUSCULATURE
Firm Flabby, thin and friable
Peristalsis may be observed No peristalsis

56. IN CASE OF SMALL BOWEL OBSTRUCTION
SURGICAL TREATMENT
 The first maneuver is to deliver the distended small bowel into the wound
 The small bowel should be covered with moist swabs and the weight of the
fluid filled bowel supported so that the blood supply to the mesentery is not
impaired
 Operative decompression should be performed whenever possible. This
reduces pressure on the abdominal wound, reducing pain and improving
diaphragmatic movement
 This is done via large bore orogastric tube and milking the bowel content in
retrograde manner to the stomach for aspiration
 All volumes of fluid removed should be accurately measured and
appropriately replaced
 Following relief of obstruction, the viability of the involved bowel should be
carefully assessed

57. PLAN
 IV fluids and electrolytes resuscitation for all
 NG tube if repeated vomiting
 Antibiotics for all
 Hernia –> Operation
 Adhesions –> Conservative first
 Obstruction –> Remove
 Volvulus –> Derotate and/or operate
 Mesenteric ischemia –> Operate
 Abscess or peritonitis –> Drain and treat
 Intussusception –> Pneumatic or barium reduction
or operate

58. IN CASE OF ACUTE LARGE BOWEL OBSTRUCTION
SURGICAL TREATMENT
 After full resuscitation the abdomen should be opened
through a midline incision
 Distension of caecum will confirm large bowel involvement.
Identification of a collapsed distal segment of large bowel and
its sequential proximal assessment will readily lead to
identification of the cause
 When a removable lesion is found in the caecum, ascending
colon, hepatic flexure or proximal transverse colon, an
emergency right hemicolectomy should be performed
 If the lesion is irremovable, a proximal stoma or
ileotransverse bypass should be considered

59. IN CASE OF ACUTE LARGE BOWEL OBSTRUCTION
SURGICAL TREATMENT
 Obstructing lesions at the splenic flexure should be
treated by an extended right hemicolectomy with
ileodescending colonic anastomosis
 For obstructing lesions of left colon or rectosigmoid
junction, immediate resection should be considered
unless there are clear contraindications
CONTRAINDICATIONS TO IMMEDIATE RESECTION INCLUDE:
i. Inexperienced surgeon
ii. Moribund patient
iii. Advanced disease

60. IN CASE OF CHRONIC LARGE BOWEL OBSTRUCTION
SURGICAL TREATMENT
 Arise from 2 sources – the cause and the subsequent
obstruction
 The cause can be organic or functional
 Organic disease requires decompression
 Stomal stenosis can be managed at abdominal level
 Functional disease requires colonoscopic
decompression and conservative management

61. MANAGEMENT
DYNAMIC VS ADYNAMIC
SMALL INTESTINE VS LARGE INTESTINE
SIMPLE VS COMPLICATED

62. DYNAMIC VS ADYNAMIC
DYNAMIC ADYNAMIC
 Peristalsis is working against a
mechanical obstruction
 May be in acute and chronic form
 Peristalsis is absent or inadequate
where there is no obstruction
Causes:
 Intraluminal
 Intramural
 Extramural
Causes:
 Paralytic ileus
 Pseudo-obstruction
 Abdominal pain
 Abdominal distension
 Vomiting
 Absolute constipation
Paralytic ileus:
 Clinical significance after 72 hours
 Absence of bowel sound and no
passing out flatus
 Abdominal distension becomes
more marked and tympanic
 Effortless vomiting

63. DYNAMIC OBSTRUCTION
ADHESIVE OBSTRUCTION
CONSERVATIVE MANAGEMENT
 NG decompression and rehydration
 Not prolonged beyond 72 hours
SURGICAL MANAGEMENT
 Divide the causative adhesion(s) and limit the dissection
 Repair serosal tears, resect areas of doubtful viability
 Laparoscopic adhesiolysis in expert surgeon’s hands

64. DYNAMIC OBSTRUCTION
INTUSSUSCEPTION
CONSERVATIVE MANAGEMENT
NG drainage, resuscitation with IV fluids, antibiotics
NON OPERATIVE MANAGEMENT
Air OR barium enema performed if there are no signs of
peritonitis, perforation
OPERATIVE MANAGEMENT
 Reducible intussusception
 Irreducible intussusception – resection with primary
anastomosis

65. DYNAMIC OBSTRUCTION
VOLVULUS
CAECAL VOLVULUS
 If viable, volvulus should be reduced
achieved after decompression of caecum using needle
 Further management consists of fixation of caecum to right iliac
fossa (caecopexy) or caecostomy

66. DYNAMIC OBSTRUCTION
VOLVULUS
SIGMOID VOLVULUS
 Flexible sigmoidoscopy or rigid sigmoidoscopy & insertion of a
flatus tube should be carried out to allow deflation of gut
 The tube should be secured in place with tape for 24 hours and
a repeat X-Ray taken to ensure that decompression has
occurred
 This will resolve the acute problem

67. DYNAMIC OBSTRUCTION
VOLVULUS
SIGMOID VOLVULUS
FURTHER TREATMENT
 YOUNG: Elective sigmoid colectomy is required
 ELDERLY: If endoscopic decompression is successful, it is
reasonable to not offer further treatment as 80% death rate
If it’s recurrent, the options available are:
i. Resection
ii. Two point fixation with combine endoscopic /
percutaneous tube insertion
 Failure results in an early laparotomy with untwisting of the
loop and per anum decompression

68. ADYNAMIC OBSTRUCTION
Failure of transmission of peristaltic waves secondary to
neuromuscular failure
PARALYTIC ILEUS
CAUSES
Post operative, infection, reflex ileus, metabolic
MANAGEMENT
 NG suction, fluid replacement
 Use prokinetics (domperidone/erythromycin) in resistant case
 Laparotomy – if inactivity persists > 7 days, only after
confirmation of abdominal sepsis / mechanical obstruction

69. ADYNAMIC OBSTRUCTION
Obstruction in absence of mechanical cause or acute intra-abdominal disease
PSEUDO-OBSTRUCTION
ASSOCIATIONS
Metabolic, severe trauma, shock, retroperitoneal irritation
 Radiographs show colon obstruction and distension
 If no obstruction, confirm by colonoscopy & barium enema
MANAGEMENT
 Treat the identifiable cause
 IV Neostigmine 1mg
 Repeat with second dose after few minutes if first dose is ineffective
 Colonoscopic decompression
 Surgery is associated with high mortality and morbidity

70. SBO VS LBO
HIGH SMALL BOWEL LOW SMALL BOWEL LARGE BOWEL
 Vomiting occurs early and
profuse
 Vomitus contain
undigested food
 Rapid dehydration
 Minimal distension
 Upper abdominal
discomfort
 Little evidence of dilated
small bowel loops
 Pain is predominant with
central distension
 Vomiting is delayed
 Vomitus may contain
feaculant material
 Multiple small bowel
loops is dilated
 Distension is early and
pronounced
 Less severe pain
 Vomiting and dehydration
present later
 Obstipation indicates
complete obstruction
 History of constipation
 The proximal colon and
caecum are distended on
abdominal radiography
 Presence of haustral folds
 The small bowel is dilated
if ileocecal valve is
incompetant

71. SIMPLE VS COMPLICATED OBSTRUCTION
SIMPLE OBSTRUCTION COMPLICATED OBSTRUCTION
 Blood supply is intact
 The obstruction occludes the lumen
only
 Strangulation occurs when there is
interference with the blood flow
 Obstruction with strangulation impairs
the blood flow leading to necrosis to
intestinal wall
CLINICAL FEATURES
 Vomiting
 Abdominal distension
 Abdominal pain
 Constipation
CLINICAL FEATURES
 Fever
 Constant severe pain
 Generalized tenderness with rigidity
 Shock
PLAIN X RAY
 Dilated small bowel loops with air fluid
levels
CT SCAN
 Shows a discrepancy in the caliber
between distended proximal bowel
and collapsed distal intestine
CT SCAN
 Thickening of bowel wall
 Air in the bowel wall / portovenous
system
 Absence of mesenteric fluid
 Intrapertoneal free air indicated
perforation

72.  Bailey and Love 26th Edition
 UpToDate
 MedTube.Net
 MSDManuals
REFERENCE

73. THANK YOU