This document discusses intestinal obstruction, including its definition, types, causes, classification, pathophysiology, clinical features, investigations, and treatment. Intestinal obstruction can be dynamic, caused by mechanical blockage, or adynamic, where peristalsis is absent. Common causes include adhesions, tumors, hernias, and fecal impaction. Clinical exam and imaging help evaluate for mechanical obstruction or paralytic ileus. Treatment involves relieving the obstruction through surgery if needed, along with supportive measures like IV fluids and nasogastric decompression.

1. INTESTINAL OBSTRUCTION
LT COL SM SHAHADAT HOSSAIN
MCPS,FCPS(surgery)FCPS(Thoracic Surgery)
Adv Trg on Thoracoscopy CNU, South Korea

2. Definition
When the normal propulsion and passage of
intestinal contents does not occur.
Dynamic Adynamic
Types

3. CLASSIFICATION
Dynamic:
 Peristalsis is working against a mechanical
obstruction.
 It may be acute or chronic.
Adynamic:
 There is no mechanical obstruction.
 Peristalsis is absent or inadequate (e.g.
paralytic ileus or pseudo-obstruction).

4. CLASSIFICATION
A. Simple obstruction (no vascularimpairment)
B. Closed loop ( both ends are obstructed e.g.
volvulus)
C. Strangulation obstruction

5. Causes of intestinal obstruction
Dynamic
Intraluminal
• Faecal impaction
• Foreign bodies
• Bezoars
• Gallstones
Intramural
• Stricture
• Malignancy
• Intussusception
• Volvulus

6. Causes
Extramural
• Bands/adhesions
• Hernia
Adynamic
• Paralytic ileus
• Pseudo-obstruction

7. Causes of intestinal obstruction
1. Adhesions- 40%
2. Tumors -15%
3. Inflammatory- 15%
4. Obstructed hernia-12%
5. Intraluminal-10%
6. Fecal impaction-8%
7. Pseudo-obstruction-5%
8. Miscellaneous -5%

8. Pie chart

9. Adhesion

10. Tumour

11. Duodenal atresia

12. Stricture

13. PATHOPHYSIOLOGY
In dynamic obstruction :
1. Above the obstruction:
Peristalsis increases Intestine dilate
Reduction in peristaltic strength Flaccidity and
paralysis
2. Below the obstruction:
Normal peristalsis & absorption Until it
becomes empty It contracts & becomes
immobile.

14. Distension due to
Gas: Mainly nitrogen (90%) and hydrogen
sulphide.
Fluid:
 Saliva 500 ml.
 Bile 500 ml.
 Pancreatic secretions 500 ml.
 Gastric secretions 1 litre – all per 24 hours.

15. Dehydration and electrolytes loss are due
to
 Reduced oral intake.
 Defective intestinal absorption.
 Vomiting.
 Sequestration in the bowel lumen.
 Transudation of fluid into the peritoneal cavity.

16. Pathogenesis
Increased peristalsis
↓
Becomes vigorous, if not relieved
↓
Peristalsis ceases
↓
Flaccid, paralysed
↓
Dilated bowel.

17. Pathogenesis
Venous return is impaired and congested bowel
↓
Jeopardizes the arterial supply.
↓
Gangrene.
↓
Perforation.
↓
Peritonitis.

18. STRANGULATION
Causes:
Direct pressure on the bowel wall
• Hernial orifices
• Adhesions/bands
Interrupted mesenteric blood flow
• Volvulus
• Intussusception
Increased intraluminal pressure
• Closed-loop obstruction

19. Gangrene

20. CLOSED-LOOP OBSTRUCTION
When the bowel is obstructed at proximal and
distal points.

21. SPECIAL TYPES OF
MECHANICAL INTESTINAL
OBSTRUCTION

22. INTERNAL HERNIA
1. Framen of Winslow
2. Defect in the mesentery
3. Defect in the transverse mesocolon
4. Defects in the broad ligament
5. Diaphragmatic hernia
6. Duodenal retroperitoneal fossae
7. Caecal/appendiceal retroperitoneal
8. Intersigmoid fossa.

23. OBSTRUCTION FROM ENTERIC
STRICTURES
 Small bowel strictures usually due to
tuberculosis or Crohn’s disease.
 Malignant strictures: lymphoma are
uncommon, whereas carcinoma and
sarcoma are rare.

24. Stricture

25. BOLUS OBSTRUCTION
i. Gallstones
ii. Trichobezoars
iii. Phytobezoars
iv. Foreign body
v. Food bolus
vi. Stercoliths
vii. Worms

26. Gall stone

27. CLINICAL FEATURES
Vary according to:
● Location of the obstruction;
● Duration of the obstruction;
● Underlying pathology;
● Presence or absence of intestinal
ischaemia.

28. Pain
 Pain is the first symptom.
 Occurs suddenly and is usually severe.
 Colicky in nature.
 Usually centred on the umbilicus (small
bowel).
 Lower abdomen (large bowel).

29. Vomiting
More distal the obstruction, longer the
interval between the onset of symptoms and
appearance of nausea and vomiting.

30. Distension
 In small bowel degree of distension is
dependent on the site of obstruction and
more distal the lesion.
 Distention is much less in high small bowel
obstruction.
 Visible peristalsis may be present

31. Constipation
This may be
• Absolute (i.e. neither faeces nor flatus is
passed) or
• Relative (where only flatus is passed).

32. Other manifestations
 Dehydration
 Hypokalaemia
 Pyrexia
 Hypothermia
 Abdominal tenderness
 Bowel sounds:

33. Dehydration
Most commonly in small bowel obstruction.
It results in
 dry skin and tongue
 poor venous filling
 sunken eyes with oliguria.

34. PHYSICAL EXAMINATION
 Inspection
 Palpation
 Percussion
 Auscultation
 Rectal examination

35. Inspection
 Shape of the abdomen
 Movement of the abdomen wall
 Umbilicus
 Visible peristalsis
 Scar
 Prominent veins
 Hernial orifices

36. PALPATION
 Muscle guarding.
 Tenderness and rigidity.
 Hernial orifices.

37. Percussion
 Dullness
 Tympanic
 Tenderness on light percussion suggest
strangulation.

38. Auscultation
 High-pitched bowel sounds.
 Scanty or absent: longstanding and Paralytic
ileus.

39. RECTAL EXAMINATION
• Presence of mass.e.g.cancer,
Intussuception.
• Feces.

40. Clinical features of strangulation
 Constant pain
 Severe pain
 Tenderness with rigidity
 Peritonism
 Shock

41. Band adhesion causing closed-loop
obstruction

42. INVESTIGATIONS
LABORATORY
• CBC, blood grouping
• RBS/LFT
• Urea & electrolytes
• Serum amylase level

43. Radiology
Small Bowel Obstruction
 Central distention (GAS)
 Valvulae conniventes
 “Ladder-like dilatation”
 Small diameter
Large Bowel Obstruction
 Peripheral distention “Picture frame”
 More gross distention
 Haustral indentation & large diameter

44. Plain x-ray abdomen

45. Plain x-ray abdomen

46. Ultrasound

47. CT scan

48. Barium studies

49. TREATMENT
1. Gastrointestinal drainage via a nasogastric
tube
2. Fluid and electrolyte replacement
3. Relief of obstruction
4. Surgical treatment

50. TREATMENT
Supportive:
 Nasogastric aspiration by ryles tube.
 IV fluids- hartmnn’s solution or normal
saline.
 Urinary catheter.
 Check temp. And pulse 2 hourly.
 Abdominal examination 8 hourly.
 Broad spectrum antibiotics.

51. Indications for surgery:
a. Obstructed external hernia.
b. Intestinal strangulation.
c. Obstruction in a ‘virgin’ abdomen
Surgery depends on cause:
 Division of bands.
 Adhesiolysis.
 Excision and exteriorization.
 Bypass.

52. Difference between viable and non-viable
intestine

53. ACUTE INTUSSUSCEPTION
When one portion of the gut invaginates into
an immediately adjacent segment; the
proximal into the distal.

54. CAUSES
 Most common: children.
 Peak incidence: 5 and 10 months.
Infant:
 90%-idiopathic.
 Upper respiratory tract infection.
 Gastroenteritis.
 Hyperplasia of peyer’s patches.

55. CAUSES
Children:
 Meckel’s diverticulum
 Polyp, duplication
 Henoch–Schönlein purpura or appendix.
Adult:
 Polyp (e.g. Peutz–jeghers syndrome)
 Submucosal lipoma
 Tumour.

56. Mechanism of intussusception

57. Types

58. Clinical features of intussusception
 Screaming and drawing up of the legs in a
previously well male infant.
 During attacks the child appears pale;
between episodes he may be listless.
 Vomiting may or may not occur but bile-
stained.

59. Clinical features
 Initially, the passage of stool may be
normal, later, blood and mucus are
evacuated – the ‘redcurrant jelly’ stool.
 A lump that hardens on palpation
associated feeling of emptiness in the right
iliac fossa (the sign of Dance).

60. Clinical features
On rectal examination:
 Blood-stained mucus
 The apex of intussusception may be
palpable.

61. DIFFERENTIAL DIAGNOSIS
1. Acute gastroenteritis
Abdominal pain, vomiting with occasional
blood and mucus in the stool.
2. Henoch–schönlein purpura
Characteristic rash and abdominal pain.
3. Rectal prolapse
The projecting mucosa can be felt in
continuity with the perianal skin whereas in
intussusception the finger may pass
indefinitely into the depths of a sulcus.

62. INVESTIGATIONS

63. Imaging
Jejunum shows concertina effect due to valvulae
conniventes (Herring bone pattern)

64. Imaging

65. Imaging

66. Triad of small bowel obstruction in plain
x-ray
1. Dilated small bowel loops > 3 cm.
2. Multiple air fluid levels in erect x-ray.
3. Paucity of air in the colon.

67. Treatment of intussusception
1. Intravenous fluids
2. Broad-spectrum antibiotics
3. Nasogastric drainage
4. Non-operative reduction using an air or
barium enema

68. SURGERY
 Transverse right sided abdominal incision
 Reduction is achieved by gently
compressing the most distal part of the
intussusception toward its origin not to
pull.

69. Treatment of sigmoid volvulus
 NG suction
 IV fluids
 Antibiotics
 Catheterisation
 Sigmoidoscopy and insertion of a flatus
tube to allow deflation of the gut.

70. VOLVULUS
 A volvulus is a twisting or axial rotation of a
portion of bowel about its mesentery.
 The rotation causes obstruction to the
lumen (>180° torsion) and if tight enough
also causes vascular occlusion in the
mesentery (>360° torsion).

71. Types of Volvulus
Primary:
 Volvulus neonatorum
 Caecal volvulus
 Sigmoid volvulus
Secondary: Common and is due to rotation of
a segment of bowel around an acquired
adhesion or stoma.

72. SIGMOID VOLVULUS
 Rotation nearly always occurs in the
anticlockwise direction.
Predisposing factors:
 Elderly patient
 High-residue diet
 Constipation

73. Causes

74. PRESENTATION
Fulminant:
 Sudden onset
 Severe pain
 Early vomiting, rapidly deteriorating clinical
course.
Indolent:
 Insidious onset,
 Slow progressive course
 Less pain, late vomiting.

75. Treatment of sigmoid volvulus
 NG suction
 IV fluids
 Antibiotics
 Catheterisation
 Sigmoidoscopy and insertion of a flatus
tube to allow deflation of the gut.

76. Treatment
Failure to derotates need in an early
laparotomy, with untwisting of the loop.

77. pic

78. Surgical options
1. Fixation of sigmoid colon to the posterior
abdominal wall.
2. Paul–mikulicz procedure.
3. Hartmann’s procedure.

79. Surgical options
A flatus tube or Sigmoidoscope is passed in
operation theatre.
If derotation does not occur, laparotomy
If viable, it can be fixed to the lateral wall of
abdomen or pelvis—sigmoidopexy.

80. Surgical options
If gangrene, it is resected and proximal cut end
brought out as colostomy and distal end brought
out as mucous fistula, (Paul-Mikulicz Operation).
Resection of the gangrenous sigmoid done;
proximal cut is brought out as end colostomy:
distal end closed—Hartmann’s operation.
Primary resection and anastomosis.

81. ADYNAMIC OBSTRUCTION
Failure of transmission of peristaltic waves
secondary to neuromuscular failure in the
myenteric (Auerbach’s) and submucous
(Meissner’s) plexuses).

82. CAUSES
 Postoperative: hypoproteinaemia or
metabolic abnormality
 Infection: intra-abdominal sepsis
 Reflex ileus: fractures of the spine or ribs,
retroperitoneal haemorrhage.
 Metabolic: uraemia and hypokalaemia

83. CLINICAL FEATURES
1. No passage of flatus.
2. No bowel sounds.
3. Marked abdominal distension.
4. Vomiting of large volume of fluid.
5. Tachycardia.
6. Respiratory distress
7. High-pitched tinkling note ‘like bells at
evening pealing’.
8. Dull abdominal pain (not colicky).

84. INVESTIGATIONS
 Serum electrolytes
 X-ray abdomen.
 Ultrasound abdomen e.g. sepsis

85. TREATMENT
a. Nasogastric aspiration.
b. IV fluids.
c. Electrolyte management.
d. Catheterisation and urine output measurement.
e. The primary cause is treated.