Lecture notes for medical students

1. Tips on using my ppt.
1. You can freely download, edit, modify and put your
name etc.
2. Don’t be concerned about number of slides. Half the
slides are blanks except for the title.
3. First show the blank slides (eg. Aetiology ) > Ask
students what they already know about ethology of
today's topic. > Then show next slide which enumerates
aetiologies.
4. At the end rerun the show – show blank> ask questions >
show next slide.
5. This will be an ACTIVE LEARNING SESSION x
three revisions.
6. Good for self study also.
7. See notes for bibliography.

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

4. Definition

5. 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

6. PHYSIOLOGY(SECREATION&
ABSORBTION)

7. 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

8. PHYSIOLOGY(MOTILITY)

9. 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

10. INTESTINAL MOTILITY

11. 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

12. 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

13. Intestinal obstruction can be
classified(according to pathophysiological
events into):

14.  Dynamic
(Mechanical)
 Failure of forward
intestinal progression
due to organic
occlusion:
I. Intraluminal:
gallstone,FB,Bezoar
s,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):

15. 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

16. Intestinal obstruction could be:

17. Intestinal obstruction could be:
I. Simple:Luminal Obstruction with NO
interference of mesenteric blood supply
II.Strangulated:There is interference
of mesenteric blood supply

18. Strangulated intestinal
obstruction:

19. 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

20. Closed loop
obstruction

21. 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)

22. Closed Loop
Obstruction:

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

25. Pathophysiology

26. 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

27. 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

28. 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

29. 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

30. 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)

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

32. Pathophysiology:(strangulated
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

33. 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.

34. Pathophysiology:(syste
mic 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)

35. 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.

36. 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

37. etiology

38. 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

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

40. 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)

41. ADHESIVE INTESTINAL
OBSTRUCTION

42. ADHESIVE INTESTINAL
OBSTRUCTION

43. 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)

44. 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

45. Strangulated small bowel
loop(strangulated ing.h.)

46. 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

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

48. 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.

49. • 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.
Malrotation & neonatal volvulus

50. 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

52. Intussusception

53. INTUSSESCEPTION(IN
ADULT)

54. 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

56. 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

57. 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


58. Sigmoid volvulus

59. 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

60. III. Strictures(benign):
I. Diverticular
II. Inflammatory(IBD)
III.Ischemic
IV.Intussussception:Due to colonic polyps
V. External Hernia
VI.Faecal impaction

61. 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

62. 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

63. 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

64. 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

65. 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

66.  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%)

68. diagnosis
history
clinical examination
plain abdominal X-RAY

69. 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

70. 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

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

72. 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

73. 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)

74. 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

75. 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

76. 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)

77. 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
.

78. 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

79. 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

80. 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)

81. 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

82. The Difference between small
and large bowel obstruction
Small Bowel
Large bowel
•Central ( diameter 2.5cm+ vulvulae
connventines)
•Ileum: may appear tubeless
•Peripheral ( diameter 5cm+)
•Presence of haustration
•Presence of solid faeces

95. Diagnosis
objectives

96. 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

97. 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

98.  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

99.  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

100. 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)

101. 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

102. 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)

103. 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)

104. V. The likely cause of
obstruction
This Depends Upon :
 Clinical Course Of Obstruction
 Anatomical Level Of Obstruction
 Age Of The Patient

105.  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

106.  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

107. 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

108. treatment

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

110. 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

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

112. 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

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

114. 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

115. 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

119. 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

125. 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

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

130. IV. Definitive surgical
intervention
PRINCIPLES:
 Decompress The Bowel
 Resect Obstructing Lesion / Ischemic
Bowel
 Restore Intestinal Continuity

131. 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

132. 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

133.  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

134.  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)

135. 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

136. 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

137. Thank you

138. Get this ppt in mobile
1. Download Microsoft
PowerPoint from play
store.
2. Open Google assistant
3. Open Google lens.
4. Scan qr code from
next slide.

139. Get this ppt in mobile

140. Get my ppt collection
• https://www.slideshare.net/drpradeeppande/
edit_my_uploads
• https://www.dropbox.com/sh/x600md3cvj8
5woy/AACVMHuQtvHvl_K8ehc3ltkEa?dl
=0
• https://www.facebook.com/doctorpradeeppa
nde/?ref=pages_you_manage