DIAGNOSIS AND MANGMENT OF BOWEL OBSTRUCTION

1. Intestinal Obstruction
Assessment And Management
DR.
Moh.Hazem El-Foll
FRCS ED.UK.
Consultant General Surgeon
KJO Hospital KSA

3. Definition
 Failure of forward progression of
intestinal contents
 Intestinal obstruction may be:-
I. complete :No passage of fluid and air past the
obstruction.
II. Incomplete : passage of some air and fluid
past the obstruction.
 Intestinal Obstruction accounts for approx.20%
of acute surgical admission and about 5-10% of
Acute Abdomen Patients

4. PHYSIOLOGY(SECREATION&
ABSORBTION)
 Approximately; 9.0 liters of fluid enters the small
bowel/day
 2.0 liters ingested fluid
 1.0 liters saliva
 2.0 liters gastric juice
 4.0 liters biliary;pancreatic and succus entericus
 4.0-5.0 liters absorbed in jejunum
 3.0-4.0 liters absorbed in ileum
 1.0 liters enters Rt.colon/day
 800ml. Reabsorbed in the colon
 200ml.excreated in faeces

5. PHYSIOLOGY(MOTILITY)
 Autonomic control:
 Parasympathetic: stim.intestinal motility
and inhibitory to sphincters
 Sympathetic: inhibit intestinal motility
Types of intestinal motility:
1) Peristaltic contractions: in small
bowel;these are strong coordinated propulsive
contractions moving forward at distance of 1-
2cm/sec.These are initiated by pacemaker
potential originating in duodenum

6. INTESTINAL MOTILITY
2) Mass contractions: in colon.these
are strong propagating contractions
occure 2-3 times/day;initiated by
gastrocolic reflex sweeping across
distal colon to deliver faecal matter
into the rectum

7. PHYSIOLOGY(MOTILITY)
3. Segmental contractions:in both small&large
bowel
 These are segmental annular contractions moving
contents for short distance in both directions
 They are involved in mixing&absorbtion
4. Migrating Myoelectrical
Complex(MMC):These are waves of contractions
start in duodenum and sweep down the small bowel
and colon.These are called hous-keeper potential
as they cleared bowel from its contents
Motiline (enteric neurohormone) is associated with
MMC

8.  Dynamic
(Mechanical)
 Failure of forward
intestinal
progression due to
organic occlusion:
I. Intraluminal:
gallstone,FB,Bezoa
rs,parasitic worms
as ascaris,polypoid
tumer,impacted
faeces
 Adynamic
(Functional)
 Failure of forward
intestinal
progression due to
failure of propulsive
peristaltic movement
with no mechanical
occlusion
 It covers a variety of
syndromes:
• .
• :
INTESTINAL OBSTRUCTION CAN BE
CLASSIFIED(ACCORDING TO
PATHOPHYSIOLOGICAL EVENTS INTO):

9. II. Intramural:
 IBD
 Diverticulitis
 Neoplastic
III. Extraluminal:
 Intraperit.Bands
 Hernial Sacs&
Rings
 Intussessception
 volvulus
1. Paralytic Ileus
2. Acute Colonic
Pseudo-
obstruction
3. Acute Mesentric
Ischemia
MECHANICAL FUNCTIONAL

10. INTESTINAL OBSTRUCTION
COULD BE:
I.Simple:Luminal Obstruction with NO
interference of mesenteric blood supply
II.Strangulated:There is interference
of mesenteric blood supply

11. STRANGULATED INTESTINAL
OBSTRUCTION:
1. Direct External compression causing local
pressure necrosis as in :tight hernial sacs and
rings ,intraperitoneal bands and adhesions
2. Interruption of mesent.blood flow as
in:volvulus and intusseception
3. Primary occlusion of mesentric blood vessles
:acute mesentric ischemia
4. Closed Loop Obstruction

12. CLOSED LOOP OBSTRUCTION
 This occures when loop of bowel is occluded at
both proximal and distal ends by constricting
lesion ;causing rise in intraluminal pressure&bowel
wall tension; leading to ischemic necrosis
I. When bowel loop is trapped in hernial sac
II. When bowel loop is twisted around unyielding
band( volvulus)
III. Commonest in obst.lt.colonic ca. with competent
ileocaecal valve;causing creation of closed loop
between the obst.ca and the valve;leading to
ischemic necrosis(common in caecum as it has
thinner wall and wide diameter)

13. Closed Loop
Obstruction:
Bowel loop trapped
in hernial sac or
twisted around
unyieldind band
with increase in
intraluminal
pressure

15. PATHOPHYSIOLOGY

16. PATHOPHYSIOLOGY:
IN BOTH MECH. AND FUNCTIONAL
OBSTRUCTION
 Dist.Obst.:Early bowel exhibt normal perisalisis
and absorption untile it becomes empty and
peristalsis diminished.Eventually it becomes
empty,pale and flacid.
 Proximal to obstruction.:
The bowel distends with fluid and gas
 Fluid persistently augmented by continous
intestinal secreation
 Gas derived initially from swallowed air ;later from
profilerating enteric flora(amonia;H2sulfid)This is
the cause of faeculenet odour and nature of
vomiting

17. PROXIMALTO OBSTRUCTION:
(EARLY)
 The bowel exhibtes strong peristaltic
contractions(due to distention and stim.of
local stretch receptores)to overcome the
obstruction These accounts for
colicky abd.pain;audibule peristaltic rushes
;and high pitched bowel sounds
 Continuous accumulation of fluid and gas
There rise in intraluminal pressure which
result in increase in bowel wall tension
 The rise in bowel wall tension causing
compression and occlusion of lymph.;then
veins ;and finally the arteries

18. PROXIMAL TO
OBSTRUCTION:(EARLY)
 Impairement of the venous return from bowel wall
increase in capp.pressure Fluid transudation
and RBCdiapedesis into the bowel wall
 So;bowel wall oedematous and haemorrhagic
further increase in bowel wall tension and further
impairment of blood supply
 Fluid transudation and RBCs diapedesis into bowel
lumen and into perit.surface
 Haemorrhagic exudate

19. PROXIMAL TO
OBSTRUCTION:(_LATE AFTER
FEW HOURS)
 There is cessation of peristaltic activity(due to
increased local injury of bowel wall and
systemic electrolyte disturbance) This is
protective function preventing further increase
in intraluminal pressure and bowel wall
tension so prevent excessive vascular
occlusion
 Except in closed loop obstruction:where the
rise in luminal pressure and wall tension is
sufficent to compromise blood supply and
cause ischemic necrosis

20. PATHOPHYSIOLOGY:(COLONIC
OBSTRUCTION)
 IN 20%of patients ileocaecal valve becomes
incomptent;there are anteperistaltic activity and
reflux of colonic contents into small bowel and
colonic pressure relieved so there is distention of
both small and large bowel
 If ileocaecal valve is comptent;closed loop is
created between the obst.lesion and the valve with
progressive rise in colonic pressure and wall
tension to degree to comprise blood supply and
infarction and perforation occure.According to
Laplace Law this is commonest in caecum(caecm
has thin wall&wide diameter)

21. Colonic
obstruction
Type1A:comptent
valve
Progress to Type
1B with some SB
dilatation
Type2:incomp.valv
e and colonic &SB
dilatation

22. PATHOPHYSIOLOGY:(STRANGULA
TED OBSTRUCTION)
Early:There is ischemia of bowel wall and
loss of intestinal mucosal barrier there is
translocation of enteric flora across serosal
surface into peritoneal cavity . So
haemorrhagic peritoneal exudate is
contaminated So there is a risk of gm-ve
septicaemia even before gross perforation
 With perforation there is Faecal
Peritonitis; Septic Shock and circulatory
failure
IN Neglected cases ;MOF occure

23. PATHOPHYSIOLOGY:(SYSTEMIC
EFFECTS)
 There is decrease in ECF volume due to:
 Sequestration of large volume of isotonic fluid in bowel
lumen augmented by continuous CIT secretion at higher
rate
 Decrease oral intake and vomiting
 Initially BP is maintained due compensatory changes:
 Decrease urinary excretion of water and Na
 Shift of fluid from interstial comp.intoECF comp.

24. PATHOPHYSIOLOGY:(SYSTEMIC
EFFECTS)
So;EARLY:BP is maintained but there
signs of EC .Dehydration:dry tongue;sunken
eyes;loss of skin texture ;oligourea
LATER:there is HYPOVOLAEMIC SHOCK
and prerenal uraemia
IN STRANG.ther is SETICAEMIC SHOCK;
global damage to capp.Endoth.with
compartmental fluid shift accentuating
hypovol, and eventually MOF.(due to toxic and
ischemic damage to renal and pulmonary
cappillaries)

25. PATHOPHYSIOLOGY:(SYSTEMIC
EFFECTS)ELECROLYTES:
 Plasma electrolytes conc.(Na,K)are not
accurate for the present depletion and so for
Replacment:
 Plasma Na is normal or even high as H2O loss
is more than Na loss
 Plasma K is normal until late as K is mainly IC
and there is diffusion from IC to EC
compartment
 There is marked deficit in total body K due to:
loss of K in the sequestered GIT fluid and
renal absorp. Of Na at expense of K secretion.

26. PATHOPHYSIOLOGY:(ACID-BASE
DISTURBANCE)
 In high jujenal obst.excessive vomiting and
loss of HCl with Hco3 retention(alk.tide)
leading to Metabolic Alkalosis which is
worsened by renal reabsorp.of Na at the
expence of H secreation
 In distal obstruction the sequestered intestinal
fluid is highly alkaline and Metabolic Acidosis
develop

27. ETIOLOGY

28. ETIOLOGY:(SMALL BOWEL)
I. Adhesions(80%of causes)
A. Postoperative:
 Commonest after lower abdominal and
gynaecological surgery
 Patients can present as early as 4 weeks
postop.but often 1-5 years postoperative.
 70% of patients have single band
 Patients with complex bands are likely for
recurrent symptomatic adhesions

29. I. ADHESIONS
B.Inflamatory:
 Cholecystitis
 Appendicitis
 PID
 T.B
 Peritonitis
C. Radiation
D. F.B and Drugs

30. I. ADHESIONS
E. Congenital:
 Ladds Band associated with midgut
malrotation
 Band arise from Meckles diverticulum
 Bands can cause obstruction by:
 Kinking or snaring of bowel loop
 Twisting of loop(volvulus)

31. ADHESIVE INTESTINAL
OBSTRUCTION

32. ADHESIVE INTESTINAL
OBSTRUCTION

33. ETIOLOGY(SMALL BOWEL)
II. Hernia(10% of causes)
A. External:
 Inguinal ; Femoral; Umbilical
B. Internal:
 Anatomical defects(Foramen of Winslow;
paraduod fossa; cong.mesen.defects)
 Iatrogenic defects(mesentric defects;
lateral space in stoma)

34. II. HERNIA(10% OF CAUSES)
 Femoral hernia commonly present by
obstruction or srang.for first time
 We should differentiate between obstructed hernia
and increase size of pre-existing hernia due to
bowel obstruction due to any other cause
 Richter,s hernia present with functional obst,
with evidences of srangulation
 Evidence of strang.will appear in hernia without
obstruction;if the omentum is strangulated
content
 The term incarcerated is inaccurate; better to use
Irreducable ; Obstructed; or Strangulated

35. STRANGULATED SMALL BOWEL
LOOP(STRANGULATED ING.H.)

36. III.NEOPLASMS(5% OF CAUSES)
1. Primary Tumers:
 Benign: Adenoma;lipoma;Fibroma;Liomyoma
 Malignant:Lymphoma;Adenoca.;Carcinoid
2. Metastatic: ca.ovary;colon;stomach
 Metastatic involvement is much more likely to
cause small bowel obstruction than the rare
Pr.tumers
 Primary T.cause obstruction by luminal obstruction
OR Intusseception
 Caecal ca.near ileocaecal valve present by small
bowel obstruction

37. IV. STRICTURES
A.Congenital: Intestinal Atresia
B. Inflammatory:
 Crohns Disease
 Tuberculosis
 Drugs :enteric-coated KCLtab. ;NSAIS drugs
C. Neoplastic:
 Lymphoma
 Carcinoid

38. V. VOLVULUS
 Small Bowel volvulus ;when loop of small
bowel is twisted around unyielding band.360
degree rotation cause closed-loop obstruction:
A. congenital bands:
 Volvulus neonatorum; occure around narrow
mesenyric vas.pedicle or Ladds band
 Volvulus of terminal ileum around band remanant
of vitillo-intestinal duct
B. Acquired bands: postoperative. Inflammatory.

39. • Treatment:
• The volvulus is reduced, the transduodenal band(Ladd’s
band) divided, the duodenum mobilised & the mesentry
freed.
• Appendicectomy is routinely performed to avoid
diagnostic difficulty with appendicitis in the future.
• Infarcted bowel necessitates resection.
MALROTATION & NEONATAL VOLVULUS

40. V.INTUSSUSCEPTION:
 Invagination of segment of bowel(intussusceptum)
into another(intussuscepien).it is often antegrade
 Most common:It is ileocolic(ileocaecal)
Ileo-ileal; ileo-ileo-colic; colo-colic (less common)
 It causes strangulated bowel obstruction
A. Primary: infants&young children
 Due to lymphoid hypertrophy of terminal ileum
B. Secondary: older children&adult
 Due pathological lead point :
 Meckles diverticulum ;polyp ;submucous lipoma ;
haemangiomas ;Lymphoproliferative disease

42. INTUSSUSCEPTION

43. JEJUNO-JEJUNAL
INTUSSESCEPTION(IN ADULT)

44. V.BOLUS OBSTRUCTION
1. F.B. usually impacted in esophagus or
duodenum;but can progress to obstruct small
bowel
2. Bezoars:
 Trichobezoars:(human hair) in neurotics
 Phytobezoars:(ingested fruits&vegetables) after
partial or tootal gastrectomy
3. Parasitic worms; AS ascaris worms
4. Gall stone :(Gall stone ileus) It is mechanical
obstruction where stone passes via
cholycystoduodenal fistula and becomes impacted
in ileum

46. ETIOLOGY(COLONIC)
I. Colorectal carcinoma:
 Commonest cause in western
countries&North america
 75% occure in Rectosigmoid colon
 15-20% of colorectal cancer present with
obstruction
 LT.colon commonest site of obstruction
due to constricting lesion&solid faeces

47. II. COLONIC VOLVULUS
A. Sigmoid volvulus:
 Commonest cause of colonic obstruction in
Eastern&Africa&Middle EAST. Commonest
site(80%)due to long redundant colon with freely
mobile mesocolon and narrow mesosigmoid pedicle
attached to post.parietal perit.
 Strangulation is early due to 360D.anteclockwise
rotation and interruption of mesentric B.supply
 There are 2 types of presentation:
1. Acute: mostly in young&middle age
2. Intermittent subacute: mostly in old age


48. SIGMOID VOLVULUS

49. B. CAECAL VOLVULUS :
 Less common;account for 1% of intestinal obst.
 The caecum(and asc.colon) are mobile and have
mesocolon(not attached to post.abd.wall
 The caecum(and asc.colon) rotate 360 D.in
clockwise direction with occlusion of mesentrin
B.supply and early strangulation
 The patient presents with picture of low small
bowel obstruction
C. In Hirschsprungs disease &Chagas
disease: megacolon affecting lower sig.&upper
rectum predispose to volvulus

50. III. STRICTURES(BENIGN):
I. Diverticular
II. Inflammatory(IBD)
III.Ischemic
IV.Intussussception:Due to colonic polyps
V. External Hernia
VI.Faecal impaction

51. ADYNAMIC OBSTRUCTION
I. Paralytic Ileus:
 There is Reflex Inhibition of Peristaltaic
Activity of SB. Due to increase
sympathetic Drive to SB. Leading to
hyperpolarisation of smooth muscle which
become unresponsive to neural and
hormonal stimuli
 Causes:
1) Postlaparotomy: after Abd.Pelvic surgery

52. I. PARALYTIC ILEUS( CAUSES)
2) Intra-abdominal Sepsis
3) Abdomino-pelvic Trauma (Retroperitoneal
Haematoma)
 Other Contributing Factors:
 Electrolytes Imbalance
 Uraemia
 Diabetic Ketoacidosis
 Drugs: Narcotics ; Antichlonergices;
phenothiazines

53. II. ACUTE COLONIC PSEUDO-
OBSTRUCTION
 It is massive colonic dilatation affecting caecum
and Rt.colon (occasionally extend to the rectum)
with presentation of colonic obstruction without
mechanical blockage
 It is likely results from imbalance of autonomic
regulation of colonic motility with excessive
parasympathetic suppression causing atony to
distal colon and functional obstruction
 The vast majority of patients are Elderly
hospitalised patients with major TRAUMA;
ILLENESS; MAJOR NON-INTESTINAL SURGERY

54. ETIOLOGICAL FACTORES
 Major non-operative TRAUMA
 SEPSIS
 Myocardial infarction ; Heart Failure
 Major Abdomino-pelvic Surgery
 Orthopedic Surgery
 Gynecological ; Neurosurgical Procedures
 Cerebrovasular accident ; Spinal cord Injury
 Advanced Malignancy
 Respiratory ; Renal Failure
 Drugs: Opiates; phenothiazines ;Chanel blockers

55. III.ACUTE MESENTERIC
ISCHEMIA( AMI)
1. Embolic: (50%) due to detached thrombi from
mural thrombi in MI; atrial thrombus in AF;
vegetative endocarditis; and athr.plaques in Ao.
2. Trombotic(20%) due to acute thrombosis on top
of pre-existing athr. of visc.A
3. Venous Thrombosis: Sec.to
Hypercoagulopathy
4. Non-occlusive:( 20-30%) Sec.to sever reduction
of mesentric blood flow with sec.mesen. VC. In:
 SHOCK: hypovolemic& septic
 Acute heart failure and cadiogenic Shock

56.  Cancer (75%)
 Diverticulos.(10%)
 Volvulus(10%)
 Miscellan.(10%)
 In Eastern Countries&
Middle East volvulus
accounts for > 50% of
causes of colon
obstruction
 Adhesions(80%)
 Hernia(10%)
 Tumors(5%)
 Miscellan.(5%)
INCIDENCE
Small Bowel
(85%)
COLON
(15%)

58. DIAGNOSIS
HISTORY
CLINICAL EXAMINATION
PLAIN ABDOMINAL X-RAY

59. I. HISTORY
 The four cardinal symptoms are:
1. PAIN
2. VOMITING
3. ABDOMINAL DISTENSION
4. ABSOLUTE CONSTIPATION
 These clinical features and also the clinical
course vary according to the LEVEL &CAUSE
of obstruction

60. INTESTINAL OBSTRUCTION CAN
BE CLASSIFIED ACC. TO CLINICAL
PRESENTATION INTO 4 TYPES:
A. Acute: Rapid clinical course with acute
complete obstruction
 This is typically seen in small bowel obstruction
B. Chronic: Slow clinical course with progressive
constipation ; vague lower abdominal pain with
late vomiting and abdominal distension
 This is typically seen in colonic obstruction
C. Subacute: Mild symptoms with passage of gas
and liquid stool
 This is seen in partial bowel obstruction either
small bowel or colon

61. D.INTERMITTENT :
 These are recurrent acute attacks of
acute small bowel obstruction which are
relieved spontaneously
 This is almost invariably due to adhesions

62. 1) ABDOMINAL PAIN
 Sever colicky abdominal pain Not localized
 In SBO periumbilical occure in waves/ 2-5 minutes
 In colonic obst. Less sever lower abdominal pain-
free period up to 20-30 minutes
 Persistent sharp localized pain
 It is accompained by localised tenderness(Late)
 Due to cessation of peristaltic contractions and
distension of bowel loop with inflammation of the
overlying serosa
 It signifies the onset of strangulation

63. 2) VOMITING
 Faeculent vomiting accompany all forms of bowel
obstruction at some stage The more distal the
obstruction ;The late onset of vomiting
 In high SB obst. Vomting is EARLY and initially it is
bilious
 In low SB. Obst.vomiting is LATE after onset of pain
and usually faeculent
 In colonic Obst. Vomiting is LATE MANY DAYS after
onset of even complete obstruction if ileo-caecal
valve is incomptenet.Vomiting may never occure in
complete colonic obst.if valve is competent(closed-
loop obstruction)

64. 3) CONSTIPATION
 EARLY: The patient may have normal
bowel motion which persist for sometime
especially in high jejunal obstruction
 Later: in complete bowel
obstruction(especially low ileal&colonic)
there is ABSOLUTE CONSTIPATION TO
FAECES AND FLATUS
 Occasionally: in subacute partial
obstruction There is DIARRHEA due to
fermentation of faecal matter by enteric
flora

65. 4) ABDOMINAL DISTENTION
 It varies according to level of obstruction:
 In HIGH SB.Obst.and EARLY mesenteric
ischemia;There is minimal distention
 In LOW SB.Obstruction.(and caecal
obstruction.) there is PROMINENT CENTRAL
DISTENSION
 In colonic obstruction:LATE DISTENSION mainly
in flanks and upper abdomen
 However; MARKED ABDOMINAL DISTENSION IN:
 Obstructing lt colonic ca.(comp. ileocaecal valve)
 Sigmoid volvulus
 Hirschprung disease

66. II. EXAMINATION
GENERAL
 EARLY: Signs of EC Dehydration:
 Dry Tongue ;Loss of tissue texture;Thirst;
 Oliguria Foeter Smel ;Mild pyrexia. BP is initially
maintained
 LATE: Hypovolaemic shock: tachycardia; cold
extremities; low BP
 High pyrexia; signifies onset of :
STRANGULATION OR PERFORATION
 Inflammatory phlegmon(Diverticular abscess or
pericolic abscess with IBD)

67. II. EXAMINATION
LOCAL
1) Inspection:
Scares; Distension; Hernial orifices
2) Palpation:
Localized tenderness; and rebound tenderness in
impending strangulation
Localized guarding; in perforation and peritonitis
Localized tender Mass; in Neoplasm and Inflamm.
Phlegmon
.

68. II. EXAMINATION
LOCAL
3) Percussion: Tympantic Abdomen(gas filled
loops)
4) Auscultation: EARLY; Frequent; high pitched
bowel sounds. LATER; OR STRANGULATION; silent
abdomen
5) Careful Exam. Of HERNIAL ORIFICES
6) PR: IMPORTANT IN ALL CASES
 Low rectal cancer(blood in exam.figer)
 Hard stool; in faecal impaction
 Soft stool; in simple constipation
 Rectal ballooning below obstructed colonic cancer

69. II. EXAMINATION
LOCAL
7) Rigid Sigmoidoscopy:
 This will complete examination of the
rectosigmoid colon:
 It can detect low sigmoid neoplasm
 It can detect rectal ballooning below
obstructing colonic carcinoma
 Insertion of rectal tube via sigmoidoscope
can be diagnostic and therapeutic for
sigmoid volvulus

70. III. INVESTIGATIONS (BASIC)
LABORATORY
 CBC
 BUN
 SERUM ELECTROLYTES
 PT;PTT
 SERUM CREATININ
 LIVER FUNCTION TESTS
 EARLY: lab.Results may be normal
 LATE: Rise inPCV and blood urea(dehydration)
 High leucocytosis(Strang.or Peritonitis)
 Hypokalaemia(depletion of K BODY STORES)

71. III. INVESTIGATION(BASIC)
PLAIN ABDOMINAL X- RAY
 Confirm presence of intestinal obstruction
 Suspect level of obstruction
A. Supine Film: Gas distended Bowel Loops
B. Erect Film: Multiple Fluid Levels
 Gas-Distended CAECUM :indicate colonic
obstruction
 Collapsed CAECUM(and large bowel): indicate
small bowel obstruction
 CAECAL OBSTRUCTION(near ileocaecal valve):
present as small bowel obstruction

72. THE DIFFERENCE BETWEEN
SMALL AND LARGE BOWEL
OBSTRUCTION
Small BowelLarge bowel
•Central ( diameter 2.5cm+ vulvulae
connventines)
•Ileum: may appear tubeless
•Peripheral ( diameter 5cm+)
•Presence of haustration
•Presence of solid faeces

85. DIAGNOSIS
OBJECTIVES

86. DIAGNOSIS
OBJECTIVES
Five Questions Should Be Answered:
I. Is The Diagnosis INTESTINAL
OBSTRUCTION
II.Mechanical Vs Adynamic
III.Simple Vs Strangulated
IV.Proximal SB / Distal SB / Colonic
V. The Likely ETIOLOGY

87. I. IS THE DIAGNOSIS
INTESTINAL OBSTRUCTION
 The diagnosis of intestinal obstruction depend on:
A. The standard clinical presentation: PAIN;
VOMITING; ABD.DISTENSION; CONSTIPATION
 These cardinal features predominate according to
LEVEL OF OBSTRUCTION& STAGE OF
PRESENTATION
B. ABDOMINAL X-RAY:Revealing gas-distended bowel
loops
 However gas-distended bowel loops(SEC.ILEUS)
occure in other acute intra-abdominal pathology:
 Peritonitis.Localised intra-abdominal abscess
 Acute pancreatitis ;Perforation hollow viscus
 Primary Mesentric Occlusion

88.  NO
 Early episodes of
sever colic.Later
sharp constant
pain(due distension
and sec.perist.Failure
 Distention; less
 NO air or faeces
 History of major
surgery/
Trauma/Sepsis
 Usually NO PAIN(or
mild abdominal
discomfort)
 Diffuse marked
abd.distention
 Continue to pass air
and diarrheaa
II. IS MECHANICAL VS ADYNAMIC
Adynamic(Ileus) Mechanical

89.  Bowel sounds:
Hypoactive
 Abd.X-Ray:diffuse
distended SB
loops colon also
distended with
GAS in RECTUM
 Gastrograffine SB
follow-through:
confirmatory
 Early:Hyperactive
bowel sounds
Late: silent
abdomen
 SB loops distended
colon collapsed NO
GAS in RECTUM
 Gastrograffine SB
follow-through:
detect the presence
of mechanical
occlusion
ADYNAMIC MECHANICL

90. III. SIMPLE VS STRANGULATED
Strangulated bowel obstruction:
 Prolonged History
 Sever constant sharp abdominal Pain
 High Fever;Tachycardia (Toxaemia)
 Localised Tenderness&Rebound Tenderness
 Muscle Gaurding ( Peritonitis)
 High Leucocytosis>18000/ml
 Abd.X-RAY: pnemoperitonium
;Pnemointestinalis (late signs of perforation
and peritonitis)

91. IV. LEVEL OF OBSTRUCTION
Proximal Small Bowel:
 Early colic
 Early Vomiting;Bilious then Faeculent
 Mild or NO Distention
 Early Marked Hypovolaemia(profuse
vomiting)
 ABD.X-RAY:Gas-Distended Bowel Loops in
upper lt.Q

92. IV. LEVEL OF OBSTRUCTION
Distal Small Bowel:
 Early Abdominal Colic
 Early Marked Central Distention
 Late Vomiting Less in Amount
 Marked Hypovolaemia(Sequestered Fluid)
 Abd.x-Ray: Centrally Distended SB
loops(Ladder Pattern)

93. IV. LEVEL OF OBSTRUCTION
Colonic Obstruction:
 Progressive Constipation With LATE
Distention Mainly in Flanks& Upper Abd.
 Late Vomiting (may be absent in closed
loop)
 Vague lower Abdominal Pain
 Abd.X-RAY: Distended Caecum ;NO Gas in
Rectum; small bowel dilatation
(incompetent ileocaecal valve)

94. V. THE LIKELY CAUSE OF
OBSTRUCTION
This Depends Upon :
 Clinical Course Of Obstruction
 Anatomical Level Of Obstruction
 Age Of The Patient

95.  Ileocaecal
Intussessception
 Ing.Hernia
 Meckles Diverticulum
 Adhesions
 Hirschsprungs
Disease
 Foreign Bodies
 Meconium Ileus
 Cong.Intes.Atresia
 Volv.Neonatorum
 Hirschsprung Dis.
 Cong.Anorectal
Anomalies
 Neonatal Necrotising
Enterocolitis
AGE-RELATED COMMON
OBSTRUCTING LESIONS
Neonates
Infants&
Children

96.  Adhesions
 Hernia
 Strictures (Crohns)
 Intussessception
 Colonic (common):
 Volvulous
 Carcinoma
 Diverticulitis
 Adhesions
 Hernia
 Meckeles
Diverticulum
 Strictures (Crohns D.)
 Intussessc.(Polyp)
 Colonic Rare (volv. Or
Carcinoma)
AGE-RELATED COMMON
OBSTRUCTING LESIONS
Young Adult Middle Age

97. AGE-RELATED COMMON
OBSTRUCTING LESIONS
 OLD –AGE (>65 Y.):
 SMALL BOWEL OBSTRUCTION:
 Adhesions ;Hernia ;Gall Stone Ileus
 Small Bowel Tumers
 Colonic Obstruction:
 Obstructing carcinoma
 Sigmoid volvulus
 Diverticulitis
 Faecal Impaction
 Acute Colonic Psedoobstruction
 Acute Mesentric Vascular Occlusion

98. TREATMENT

99. TREATMENT
I. URGENT RESUSCITATION
II. CLOSE PATIENT MOINTORING
III.THE NEED&TIMING OF SURGERY
IV.PRINCIPLES OF DEFINITIVE
SURGICAL INTERVENTION

100. I. RESUSCITATION&MOITORING
 NPO
 NG TUBE (BOWEL DECOMPRESSION)
 IV FLUIDS(CORRECT
FLUID&ELECTROLYTES DISTURBANCES)
 START IV ANTIBIOTICES(IF INDICATED)
 OPTIMISE CARDIO-RESPIRATORY STATE
 CLOSE CLINICAL&RADIOLGICAL
MOINTORING OF THE PATIENT

101. II. INDICATIONS OF SURGICAL
INTERVENTION
1.URGENT:
Strangulation / Suspected
Strangulation
Closed-Loop Obstruction
Complete Obstruction
Pnumoperitonium/ Peritonitis

102. 2. LESS URGENT
Adhesive SB. Obstruction NO
Strang.
Observe&Mointoring For 48-Hours
Incomplete SB or Colonic
Obstruction:
Investigate With Contrast Studies To
Detect Level & Cause Of Obstruction

103. 3. NOT TO OPERATE
PARALYTIC ILEUS
ACUTE COLONIC PSEUDO-
OBSTRUCTION

104. A. CONTINUE CONSERVATIVE
 Adhesive SB. Obstruction Provided: Pain Is
Settled& Radiological Improvement
 Immediate Postop.Periode: Where P. Ileus Is
Likely
 Disseminated Malignancy OR Extensive
Radiation Enteritis Where Prognosis Is Bad
 Patients With History Of IBD: When
Preservation Of Bowel Length Is Major Concern

105. B. INVESTIGATE WITH
CONTRAST STUDIES
1)SB. Gastrograffine Follow-
through/Enema:
 It can detect SB. Strictures(Crohns)
 It can detect rare small bowel tumers
 Differentiate between mechanical
Obstruction&P.Ileus( in postop. Period)
 Mointoring The Saftey of continuing
Conservative Treatment

109. 2) INSTANT GASTROGRAFFINE
ENEMA
 Slow installation of the contrast under
Fluoroscopic Screening:
 Indicated in all cases of suspected colonic
obstruction:
a) Differentiate between mechanical& colonic Pseudo-
obstruction
b) Detect site and cause of obstruction:
 Shouldered Cut-Off in MALIGNANT OBSTRUCTION
 Long tapperd in Diverticular stricture
 Coiled-spring in Intussessception
 Bird-beak sign in volvulus

115. 3) CT-SCAN WITH CONTRAST:
 Highly Sensitive&Better than contrast Radiology in
High-grade obstruction to detect Level of Obst.;
closed-loop obstruction And Strangulation
 Highly Accurate in detecting intra-abdominal
NEOPLASTIC OR INFLAMMATORY MASSES (That
may present as small bowel obstruction)
 It can detect small amount of intra-peritoneal AIR

119. 4) FIBRE-OPTIC COLONOSCOPY
 In colonic Obstruction:
 Differentiate Mechanical From Pseudo-obstruction
 Confirm Mechanical Cause& Biopsy From LESION
 Colonoscopic Decompression In Pseudo-
obstruction

120. IV. DEFINITIVE SURGICAL
INTERVENTION
PRINCIPLES:
 Decompress The Bowel
 Resect Obstructing Lesion /
Ischemic Bowel
 Restore Intestinal Continuity

121. IN SMALL BOWEL:
 Adhesiolysis For Intraperitoneal Adhesions
 Division Of Tight Hernial Sacs and Rings&
Herniotomy
 In idiopathic Intussessception: Gentle backward
Milking & Application of Warm Packs
 In Adult type: Resection & PR. Anastomosis of
involved bowel segment
 Stricturoplasty For Short SB.Strictures
 Mini-resection For Long Strictures> 5cm or Multiple
adjacent Strictures

122.  IN SMALL BOWEL:
 Assessment of Small Bowel Viability ;Primary
Resection& Anastomosis If Gangrenous OR
Doubtful Viability
 In Disseminated Intra-abdominal Carinomatosis
With SB. Involvement:
 BY-PASS : Anastomosis of Proximal Distended
Loop With Collapsed Distal Loop OR
 Defunctionning Ileostomy Using Proximal
Distended Loop

123.  IN SIGMOID VOLVULUS:
 Hartmanns procedure : If Ischemic or Gangrenous
Colon
 Sigmoidopexy : High Reccurance Rate 40%
 Sigmoid Colectomy With PR. Anastomosis Is The
Best Option (On-Table Colonic Lavage)
IN CAECAL VOLVULUS:
 Caecopexy Or Tube-Caecostomy: High Reccurance
Rate
 Rt. Hemicolectomy: Is The Best Option

124.  IN OBSTRUCTED COLONIC
CARCINOMA
Rt. Colonic:
 Rt. Hemicolectomy OR Extended Rt.
Hemicolectomy Can be done safely
Lt. Colonic: Options:
1) Two-Staged Procedure; Hartmanns OR Paul-
Mickulicz Procedure With Delayed
Anastomosis(After 8-12 Weeks)
2) One-Stage Procedure ; Primary Resection-
Anastomosis ( On-Table Colonic Lavage)

125. SURGICAL OPTIONS :
OBSTRUCTED LT.COLONIC CA.
3) Total Colectomy With Ileo-Rectal
Anastomosis
4) Subtotal Colectomy With Ileo-
Sigmoid Anastomosis
 In Closed-Loop Or Ischemic / Gangrenous
Caecum
 They Have Low Morbidity& Mortality And
Remove synchronous colonic Lesions And
Avoid Metachronous Lesions

126. LT.COLONIC CARCINOMA
SURGICAL OPTIONS
5. Self-Expanding Metallic Stent
(SEMS)
 SEMS; Has been used Recently To
Decompress The Colon (placed
Endoscopically To By-Pass The Tumer)
 Interval Period : for Optimising Patient
General Condition And Recovery Of The
Bowel
 On Stage Elective Resection & Primary
Anastomosis

127. THANK YOU