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Intestinlobstruction.pptx
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5. Definition
īą Failure of forward progression of
intestinal contents
īą 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.
īą Intestinal Obstruction accounts for approx.20%
of acute surgical admission and about 5-10% of
Acute Abdomen Patients
9. PHYSIOLOGY(MOTILITY)
īą Autonomic control:
ī§ Parasympathetic: stim.intestinal motility
and inhibitory to sphincters
ī§ Sympathetic: inhibit intestinal motility
īąTypes 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
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
ī§ These are segmental annular contractions moving
contents for short distance in both directions
ī§ 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
14. ī§ Dynamic
(Mechanical)
ī§ Failure of forward
intestinal progression
due to organic
occlusion:
I. Intraluminal:
gallstone,FB,Bezoar
s,parasitic worms as
ascaris,polypoid
tumer,impacted
faeces
ī§ Adynamic
(Functional)
ī§ Failure of forward
intestinal progression
due to failure of
propulsive peristaltic
movement with no
mechanical occlusion
īą It covers a variety of
syndromes:
âĸ .
âĸ :
Intestinal obstruction can be
classified(according to pathophysiological
events into):
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
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
21. Closed loop
obstruction
ī§ 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)
26. functional
obstruction
ī§ Dist.Obst.:Early bowel exhibt normal perisalisis and
absorption untile it becomes empty and peristalsis
diminished.Eventually it becomes empty,pale and
flacid.
ī§ Proximal to obstruction.:
The bowel distends with fluid and gas
īą Fluid persistently augmented by continous intestinal
secreation
īą 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)
īą 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
īą Continuous accumulation of fluid and gas
There rise in intraluminal pressure which result
in increase in bowel wall tension
īą The rise in bowel wall tension causing
compression and occlusion of lymph.;then veins
;and finally the arteries
28. Proximal to obstruction:(early)
īą Impairement of the venous return from bowel wall
increase in capp.pressure Fluid transudation
and RBCdiapedesis into the bowel wall
ī§ So;bowel wall oedematous and haemorrhagic
further increase in bowel wall tension and further
impairment of blood supply
ī§ Fluid transudation and RBCs diapedesis into bowel
lumen and into perit.surface
ī Haemorrhagic exudate
29. Proximal to obsTruction:(_late
after few hours)
ī§ 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
ī§ 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)
ī§ 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
ī§ 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)
32. Pathophysiology:(strangulated
obstruction)
īąEarly: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
īą With perforation there is Faecal Peritonitis;
Septic Shock and circulatory failure
īąIN Neglected cases ;MOF occure
33. pathophysiology:(systemic
effects)
ī§ There is decrease in ECF volume due to:
ī Sequestration of large volume of isotonic fluid in bowel
lumen augmented by continuous CIT secretion at higher
rate
ī Decrease oral intake and vomiting
ī§ Initially BP is maintained due compensatory changes:
īŧ Decrease urinary excretion of water and Na
īŧ Shift of fluid from interstial comp.intoECF comp.
34. Pathophysiology:(syste
mic effects)
īąSo;EARLY:BP is maintained but there signs
of EC .Dehydration:dry tongue;sunken eyes;loss
of skin texture ;oligourea
īąLATER:there is HYPOVOLAEMIC SHOCK
and prerenal uraemia
īąIN 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:
īą Plasma electrolytes conc.(Na,K)are not
accurate for the present depletion and so for
Replacment:
ī§ Plasma Na is normal or even high as H2O loss is
more than Na loss
ī§ Plasma K is normal until late as K is mainly IC
and there is diffusion from IC to EC
compartment
īą 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)
īą 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
īą In distal obstruction the sequestered intestinal
fluid is highly alkaline and Metabolic Acidosis
develop
38. etiology:(small bowel)
I. Adhesions(80%of causes)
A. Postoperative:
īą Commonest after lower abdominal and
gynaecological surgery
īą Patients can present as early as 4 weeks postop.but
often 1-5 years postoperative.
īą 70% of patients have single band
īą Patients with complex bands are likely for recurrent
symptomatic adhesions
40. I. adhesions
E. Congenital:
īą Ladds Band associated with midgut malrotation
īą Band arise from Meckles diverticulum
ī Bands can cause obstruction by:
ī§ Kinking or snaring of bowel loop
ī§ Twisting of loop(volvulus)
43. Etiology(small bowel)
II. Hernia(10% of causes)
A. External:
ī§ Inguinal ; Femoral; Umbilical
B. Internal:
ī§ Anatomical defects(Foramen of Winslow;
paraduod fossa; cong.mesen.defects)
ī§ Iatrogenic defects(mesentric defects;
lateral space in stoma)
44. II. Hernia(10% of causes)
īą Femoral hernia commonly present by obstruction
or srang.for first time
īą We should differentiate between obstructed hernia
and increase size of pre-existing hernia due to bowel
obstruction due to any other cause
īą Richter,s hernia present with functional obst,
with evidences of srangulation
īą Evidence of strang.will appear in hernia without
obstruction;if the omentum is strangulated
content
īą The term incarcerated is inaccurate; better to use
Irreducable ; Obstructed; or Strangulated
46. III.Neoplasms(5% of causes)
1. Primary Tumers:
īą Benign: Adenoma;lipoma;Fibroma;Liomyoma
īą Malignant:Lymphoma;Adenoca.;Carcinoid
2. Metastatic: ca.ovary;colon;stomach
ī§ Metastatic involvement is much more likely to cause
small bowel obstruction than the rare Pr.tumers
ī§ Primary T.cause obstruction by luminal obstruction
OR Intusseception
ī§ Caecal ca.near ileocaecal valve present by small
bowel obstruction
47. IV. strictures
A.Congenital: Intestinal Atresia
B. Inflammatory:
īą Crohns Disease
īą Tuberculosis
īą Drugs :enteric-coated KCLtab. ;NSAIS drugs
C. Neoplastic:
īą Lymphoma
īą Carcinoid
48. V. volvulus
īą Small Bowel volvulus ;when loop of small bowel
is twisted around unyielding band.360 degree
rotation cause closed-loop obstruction:
A. congenital bands:
ī§ Volvulus neonatorum; occure around narrow
mesenyric vas.pedicle or Ladds band
ī§ Volvulus of terminal ileum around band remanant of
vitillo-intestinal duct
B. Acquired bands: postoperative. Inflammatory.
49. âĸ Treatment:
âĸ The volvulus is reduced, the
transduodenal band(Laddâs
band) divided, the
duodenum mobilised & the
mesentry freed.
âĸ Appendicectomy is
routinely performed to
avoid diagnostic difficulty
with appendicitis in the
future.
Malrotation & neonatal volvulus
50. V.Intussusception:
īą Invagination of segment of bowel(intussusceptum)
into another(intussuscepien).it is often antegrade
īą Most common:It is ileocolic(ileocaecal)
Ileo-ileal; ileo-ileo-colic; colo-colic (less common)
īą It causes strangulated bowel obstruction
A. Primary: infants&young children
īą Due to lymphoid hypertrophy of terminal ileum
B. Secondary: older children&adult
īą Due pathological lead point :
ī Meckles diverticulum ;polyp ;submucous lipoma ;
haemangiomas ;Lymphoproliferative disease
54. V.Bolus obstruction
1. F.B. usually impacted in esophagus or
duodenum;but can progress to obstruct small bowel
2. Bezoars:
ī§ Trichobezoars:(human hair) in neurotics
ī§ 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
55.
56. Etiology(colonic)
I. Colorectal carcinoma:
īą Commonest cause in western
countries&North america
īą 75% occure in Rectosigmoid colon
īą 15-20% of colorectal cancer present with
obstruction
īą LT.colon commonest site of obstruction due
to constricting lesion&solid faeces
57. II. Colonic volvulus
A. Sigmoid volvulus:
īą 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.
īą Strangulation is early due to 360D.anteclockwise
rotation and interruption of mesentric B.supply
īą There are 2 types of presentation:
1. Acute: mostly in young&middle age
2. Intermittent subacute: mostly in old age
īą
59. B. Caecal volvulus :
īą Less common;account for 1% of intestinal obst.
īą The caecum(and asc.colon) are mobile and have
mesocolon(not attached to post.abd.wall
īą The caecum(and asc.colon) rotate 360 D.in
clockwise direction with occlusion of mesentrin
B.supply and early strangulation
īą 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
61. Adynamic obstruction
I. Paralytic Ileus:
ī§ 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
ī§ Causes:
1) Postlaparotomy: after Abd.Pelvic surgery
63. II. Acute colonic pseudo-
obstruction
īĸ It is massive colonic dilatation affecting caecum and
Rt.colon (occasionally extend to the rectum) with
presentation of colonic obstruction without
mechanical blockage
īĸ It is likely results from imbalance of autonomic
regulation of colonic motility with excessive
parasympathetic suppression causing atony to distal
colon and functional obstruction
īĸ The vast majority of patients are Elderly hospitalised
patients with major TRAUMA; ILLENESS; MAJOR
NON-INTESTINAL SURGERY
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:
ī§ SHOCK: hypovolemic& septic
ī§ Acute heart failure and cadiogenic Shock
66. ī§ Cancer (75%)
ī§ Diverticulos.(10%)
ī§ Volvulus(10%)
ī§ Miscellan.(10%)
īą In Eastern Countries&
Middle East volvulus
accounts for > 50% of
causes of colon
obstruction
ī§ Adhesions(80%)
ī§ Hernia(10%)
ī§ Tumors(5%)
ī§ Miscellan.(5%)
incidence
Small Bowel
(85%)
COLON
(15%)
69. I. history
ī§ The four cardinal symptoms are:
1. PAIN
2. VOMITING
3. ABDOMINAL DISTENSION
4. ABSOLUTE CONSTIPATION
ī§ 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
īą 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
īą This is typically seen in colonic obstruction
C. Subacute: Mild symptoms with passage of gas
and liquid stool
īą This is seen in partial bowel obstruction either small
bowel or colon
71. D.Intermittent :
īą These are recurrent acute attacks of acute
small bowel obstruction which are relieved
spontaneously
īą This is almost invariably due to adhesions
72. 1) Abdominal pain
īą Sever colicky abdominal pain Not localized
ī§ In SBO periumbilical occure in waves/ 2-5 minutes
ī§ In colonic obst. Less sever lower abdominal pain-
free period up to 20-30 minutes
īą Persistent sharp localized pain
ī§ It is accompained by localised tenderness(Late)
ī§ Due to cessation of peristaltic contractions and
distension of bowel loop with inflammation of the
overlying serosa
ī§ It signifies the onset of strangulation
73. 2) vomiting
īą Faeculent vomiting accompany all forms of bowel
obstruction at some stage The more distal the
obstruction ;The late onset of vomiting
īą In high SB obst. Vomting is EARLY and initially it is
bilious
īą In low SB. Obst.vomiting is LATE after onset of pain
and usually faeculent
īą 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
īą EARLY: The patient may have normal bowel
motion which persist for sometime
especially in high jejunal obstruction
īą Later: in complete bowel
obstruction(especially low ileal&colonic)
there is ABSOLUTE CONSTIPATION TO
FAECES AND FLATUS
īą Occasionally: in subacute partial
obstruction There is DIARRHEA due to
fermentation of faecal matter by enteric
flora
75. 4) Abdominal distention
īą It varies according to level of obstruction:
ī§ In HIGH SB.Obst.and EARLY mesenteric
ischemia;There is minimal distention
ī§ In LOW SB.Obstruction.(and caecal obstruction.)
there is PROMINENT CENTRAL DISTENSION
ī§ In colonic obstruction:LATE DISTENSION mainly
in flanks and upper abdomen
ī§ However; MARKED ABDOMINAL DISTENSION IN:
ī Obstructing lt colonic ca.(comp. ileocaecal valve)
ī Sigmoid volvulus
ī Hirschprung disease
76. II. examination
general
īą EARLY: Signs of EC Dehydration:
ī§ Dry Tongue ;Loss of tissue texture;Thirst;
ī§ Oliguria Foeter Smel ;Mild pyrexia. BP is initially
maintained
īą LATE: Hypovolaemic shock: tachycardia; cold
extremities; low BP
īą High pyrexia; signifies onset of :
STRANGULATION OR PERFORATION
ī§ 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
ī§ Low rectal cancer(blood in exam.figer)
ī§ Hard stool; in faecal impaction
ī§ Soft stool; in simple constipation
ī§ Rectal ballooning below obstructed colonic cancer
79. II. examination
local
7) Rigid Sigmoidoscopy:
ī§ This will complete examination of the
rectosigmoid colon:
ī§ It can detect low sigmoid neoplasm
ī§ It can detect rectal ballooning below
obstructing colonic carcinoma
ī§ Insertion of rectal tube via sigmoidoscope
can be diagnostic and therapeutic for
sigmoid volvulus
80. III. Investigations (BASIC)
LABORATORY
īą CBC
īą BUN
īą SERUM ELECTROLYTES
īą PT;PTT
īą SERUM CREATININ
īą LIVER FUNCTION TESTS
ī§ EARLY: lab.Results may be normal
ī§ LATE: Rise inPCV and blood urea(dehydration)
ī§ High leucocytosis(Strang.or Peritonitis)
ī§ Hypokalaemia(depletion of K BODY STORES)
81. III. INVESTIGATION(BASIC)
PLAIN ABDOMINAL X- RAY
īą Confirm presence of intestinal obstruction
īą Suspect level of obstruction
A. Supine Film: Gas distended Bowel Loops
B. Erect Film: Multiple Fluid Levels
ī§ Gas-Distended CAECUM :indicate colonic
obstruction
ī§ Collapsed CAECUM(and large bowel): indicate small
bowel obstruction
ī§ CAECAL OBSTRUCTION(near ileocaecal valve):
present as small bowel obstruction
82. The Difference between small
and large bowel obstruction
Small Bowel
Large bowel
âĸCentral ( diameter 2.5cm+ vulvulae
connventines)
âĸIleum: may appear tubeless
âĸPeripheral ( diameter 5cm+)
âĸPresence of haustration
âĸPresence of solid faeces
96. Diagnosis
objectives
īąFive 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
īą The diagnosis of intestinal obstruction depend on:
A. The standard clinical presentation: PAIN;
VOMITING; ABD.DISTENSION; CONSTIPATION
ī§ These cardinal features predominate according to
LEVEL OF OBSTRUCTION& STAGE OF
PRESENTATION
B. ABDOMINAL X-RAY:Revealing gas-distended bowel
loops
ī§ However gas-distended bowel loops(SEC.ILEUS)
occure in other acute intra-abdominal pathology:
ī Peritonitis.Localised intra-abdominal abscess
ī Acute pancreatitis ;Perforation hollow viscus
ī Primary Mesentric Occlusion
98. ī§ NO
ī§ Early episodes of
sever colic.Later sharp
constant pain(due
distension and
sec.perist.Failure
ī§ Distention; less
ī§ NO air or faeces
ī§ History of major
surgery/
Trauma/Sepsis
ī§ Usually NO PAIN(or
mild abdominal
discomfort)
ī§ Diffuse marked
abd.distention
ī§ Continue to pass air
and diarrheaa
II. Is mechanical vs adynamic
Adynamic(Ileus) Mechanical
99. ī§ Bowel sounds:
Hypoactive
ī§ Abd.X-Ray:diffuse
distended SB loops
colon also
distended with
GAS in RECTUM
ī§ Gastrograffine SB
follow-through:
confirmatory
ī§ Early:Hyperactive
bowel sounds
Late: silent
abdomen
ī§ SB loops distended
colon collapsed NO
GAS in RECTUM
ī§ Gastrograffine SB
follow-through:
detect the presence
of mechanical
occlusion
adynamic
mechanicl
100. III. Simple vs
strangulated
īąStrangulated bowel obstruction:
ī§ Prolonged History
ī§ Sever constant sharp abdominal Pain
ī§ High Fever;Tachycardia (Toxaemia)
ī§ Localised Tenderness&Rebound Tenderness
ī§ Muscle Gaurding ( Peritonitis)
ī§ High Leucocytosis>18000/ml
ī§ Abd.X-RAY: pnemoperitonium
;Pnemointestinalis (late signs of perforation and
peritonitis)
101. IV. Level of obstruction
īąProximal Small Bowel:
ī§ Early colic
ī§ Early Vomiting;Bilious then Faeculent
ī§ Mild or NO Distention
ī§ Early Marked Hypovolaemia(profuse
vomiting)
ī§ ABD.X-RAY:Gas-Distended Bowel Loops in
upper lt.Q
102. IV. Level of obstruction
īąDistal Small Bowel:
ī§ Early Abdominal Colic
ī§ Early Marked Central Distention
ī§ Late Vomiting Less in Amount
ī§ Marked Hypovolaemia(Sequestered Fluid)
ī§ Abd.x-Ray: Centrally Distended SB
loops(Ladder Pattern)
103. IV. level of obstruction
īąColonic Obstruction:
ī§ Progressive Constipation With LATE
Distention Mainly in Flanks& Upper Abd.
ī§ Late Vomiting (may be absent in closed
loop)
ī§ Vague lower Abdominal Pain
ī§ Abd.X-RAY: Distended Caecum ;NO Gas in
Rectum; small bowel dilatation
(incompetent ileocaecal valve)
104. V. The likely cause of
obstruction
īąThis Depends Upon :
ī§ Clinical Course Of Obstruction
ī§ Anatomical Level Of Obstruction
ī§ Age Of The Patient
110. I. RESUSCITATION&MOITORING
īą NPO
īą NG TUBE (BOWEL DECOMPRESSION)
īą IV FLUIDS(CORRECT
FLUID&ELECTROLYTES DISTURBANCES)
īą START IV ANTIBIOTICES(IF INDICATED)
īą OPTIMISE CARDIO-RESPIRATORY STATE
īą CLOSE CLINICAL&RADIOLGICAL
MOINTORING OF THE PATIENT
111. II. INDICATIONS OF SURGICAL
INTERVENTION
1.URGENT:
īąStrangulation / Suspected
Strangulation
īąClosed-Loop Obstruction
īąComplete Obstruction
īąPnumoperitonium/ Peritonitis
112. 2. LESS URGENT
īąAdhesive SB. Obstruction NO
Strang.
Observe&Mointoring For 48-Hours
īąIncomplete SB or Colonic
Obstruction:
Investigate With Contrast Studies To
Detect Level & Cause Of Obstruction
113. 3. NOT TO OPERATE
īąPARALYTIC ILEUS
īąACUTE COLONIC PSEUDO-
OBSTRUCTION
114. A. CONTINUE CONSERVATIVE
īą Adhesive SB. Obstruction Provided: Pain Is
Settled& Radiological Improvement
īą Immediate Postop.Periode: Where P. Ileus Is
Likely
īą Disseminated Malignancy OR Extensive
Radiation Enteritis Where Prognosis Is Bad
īą 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:
ī§ It can detect SB. Strictures(Crohns)
ī§ It can detect rare small bowel tumers
ī§ Differentiate between mechanical
Obstruction&P.Ileus( in postop. Period)
ī§ Mointoring The Saftey of continuing
Conservative Treatment
116.
117.
118.
119. 2) Instant gastrograffine
enema
īą Slow installation of the contrast under
Fluoroscopic Screening:
ī§ Indicated in all cases of suspected colonic
obstruction:
a) Differentiate between mechanical& colonic Pseudo-
obstruction
b) Detect site and cause of obstruction:
ī Shouldered Cut-Off in MALIGNANT OBSTRUCTION
ī Long tapperd in Diverticular stricture
ī Coiled-spring in Intussessception
ī Bird-beak sign in volvulus
120.
121.
122.
123.
124.
125. 3) Ct-scan with contrast:
īą Highly Sensitive&Better than contrast Radiology in
High-grade obstruction to detect Level of Obst.;
closed-loop obstruction And Strangulation
īą Highly Accurate in detecting intra-abdominal
NEOPLASTIC OR INFLAMMATORY MASSES (That
may present as small bowel obstruction)
īą It can detect small amount of intra-peritoneal AIR
126.
127.
128.
129. 4) FIBRE-OPTIC COLONOSCOPY
īą In colonic Obstruction:
ī§ Differentiate Mechanical From Pseudo-obstruction
ī§ Confirm Mechanical Cause& Biopsy From LESION
ī§ Colonoscopic Decompression In Pseudo-obstruction
131. īąIn small bowel:
ī§ Adhesiolysis For Intraperitoneal Adhesions
ī§ Division Of Tight Hernial Sacs and Rings&
Herniotomy
ī§ In idiopathic Intussessception: Gentle backward
Milking & Application of Warm Packs
ī§ In Adult type: Resection & PR. Anastomosis of
involved bowel segment
ī§ Stricturoplasty For Short SB.Strictures
ī§ Mini-resection For Long Strictures> 5cm or Multiple
adjacent Strictures
132. īąIn small bowel:
ī§ Assessment of Small Bowel Viability ;Primary
Resection& Anastomosis If Gangrenous OR Doubtful
Viability
ī§ In Disseminated Intra-abdominal Carinomatosis With
SB. Involvement:
ī BY-PASS : Anastomosis of Proximal Distended Loop
With Collapsed Distal Loop OR
ī Defunctionning Ileostomy Using Proximal Distended
Loop
133. īą In sigmoid volvulus:
īą Hartmanns procedure : If Ischemic or Gangrenous
Colon
īą Sigmoidopexy : High Reccurance Rate 40%
īą Sigmoid Colectomy With PR. Anastomosis Is The
Best Option (On-Table Colonic Lavage)
īąIN CAECAL VOLVULUS:
īą Caecopexy Or Tube-Caecostomy: High Reccurance
Rate
īą Rt. Hemicolectomy: Is The Best Option
134. īą In obstructed colonic
carcinoma
īąRt. Colonic:
ī§ Rt. Hemicolectomy OR Extended Rt. Hemicolectomy
Can be done safely
īąLt. 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
ī§ In Closed-Loop Or Ischemic / Gangrenous
Caecum
ī§ 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)
ī§ SEMS; Has been used Recently To
Decompress The Colon (placed
Endoscopically To By-Pass The Tumer)
ī§ Interval Period : for Optimising Patient
General Condition And Recovery Of The
Bowel
ī§ On Stage Elective Resection & Primary
Anastomosis
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