Intestinal Obstruction Assessment And Management

DR. Moh.Hazem El-Foll FRCS ED.UK. Consultant General Surgeon KJO Hospital KSA

Definition

Failure of forward progression of intestinal contents Intestinal obstruction may be:complete :No passage of fluid and air past the
obstruction.

I.

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

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

PHYSIOLOGY(MOTILITY)
Autonomic

Parasympathetic: stim.intestinal motility and inhibitory to sphincters Sympathetic: inhibit intestinal motility

control:

Types of intestinal motility: 1) Peristaltic contractions: in small

bowel;these are strong coordinated propulsive contractions moving forward at distance of 12cm/sec.These are initiated by pacemaker potential originating in duodenum

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

PHYSIOLOGY(MOTILITY)
3. Segmental

bowel

contractions:in both small&large

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

INTESTINAL OBSTRUCTION CAN BE CLASSIFIED(ACCORDING TO PATHOPHYSIOLOGICAL EVENTS INTO):

Dynamic (Mechanical)

Adynamic (Functional)

Failure of forward intestinal progression due to organic occlusion: I. Intraluminal: gallstone,FB,Bezoa rs,parasitic worms as ascaris,polypoid tumer,impacted faeces

Failure of forward intestinal progression due to failure of propulsive peristaltic movement with no mechanical occlusion It covers a variety of syndromes:

.
:

MECHANICAL
II. Intramural: IBD Diverticulitis Neoplastic

FUNCTIONAL
1. Paralytic Ileus

2. Acute Colonic Pseudoobstruction 3. Acute Mesentric Ischemia

III. Extraluminal:
Intraperit.Bands Hernial Sacs& Rings Intussessception volvulus

INTESTINAL OBSTRUCTION COULD BE:

I. Simple:Luminal Obstruction with NO

interference of mesenteric blood supply

II.Strangulated:There is interference
of mesenteric blood supply

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

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)

Closed Loop Obstruction:

Bowel loop trapped
in hernial sac or twisted around

unyieldind band
with increase in intraluminal pressure

PATHOPHYSIOLOGY

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

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

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

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

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)

Colonic obstruction
Type1A:comptent

valve
Progress to Type 1B with some SB dilatation

Type2:incomp.valv
e and colonic &SB dilatation

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

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.

PATHOPHYSIOLOGY:(SYSTEMIC EFFECTS)
So;EARLY:BP is maintained but there
signs of EC .Dehydration:dry tongue;sunken eyes;loss of skin texture ;oligourea
and prerenal uraemia

LATER:there is HYPOVOLAEMIC SHOCK

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)

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.

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

ETIOLOGY

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

I.

ADHESIONS

B.Inflamatory:
Cholecystitis Appendicitis PID

T.B
Peritonitis

C. Radiation D. F.B and Drugs

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)

ADHESIVE INTESTINAL OBSTRUCTION

ADHESIVE INTESTINAL OBSTRUCTION

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)

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

STRANGULATED SMALL BOWEL LOOP(STRANGULATED ING.H.)

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

IV. STRICTURES
A.Congenital: Intestinal Atresia
B. Inflammatory:
Crohns Disease Tuberculosis

Drugs :enteric-coated KCLtab. ;NSAIS drugs

C. Neoplastic:
Lymphoma Carcinoid

V.

VOLVULUS

Small Bowel volvulus ;when loop of small

A. congenital bands:

bowel is twisted around unyielding band.360 degree rotation cause closed-loop obstruction:

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.

MALROTATION & NEONATAL VOLVULUS Treatment:

The volvulus is reduced, the transduodenal band(Ladds 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.

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

INTUSSUSCEPTION

JEJUNO-JEJUNAL INTUSSESCEPTION(IN ADULT)

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

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

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

SIGMOID VOLVULUS

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

III. STRICTURES(BENIGN):
I. Diverticular

II. Inflammatory(IBD)
III.Ischemic

IV.Intussussception:Due to colonic polyps V. External Hernia VI.Faecal impaction

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

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

II.

ACUTE COLONIC PSEUDOOBSTRUCTION

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

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

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.
of pre-existing athr. of visc.A Hypercoagulopathy

2. Trombotic(20%) due to acute thrombosis on top

3. Venous Thrombosis: Sec.to

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

INCIDENCE
Small Bowel (85%)
Adhesions(80%)
Hernia(10%) Tumors(5%) Miscellan.(5%)

COLON (15%)
Cancer (75%) Diverticulos.(10%) Volvulus(10%) Miscellan.(10%)
In Eastern Countries& Middle East volvulus accounts for > 50% of causes of colon obstruction

DIAGNOSIS
HISTORY

CLINICAL EXAMINATION
PLAIN ABDOMINAL X-RAY

I.
1. PAIN

HISTORY

The four cardinal symptoms are:

2. VOMITING 3. ABDOMINAL DISTENSION

4. ABSOLUTE CONSTIPATION
These clinical features and also the clinical

course vary according to the LEVEL &CAUSE

of obstruction

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

and liquid stool

gas

This is seen in partial bowel obstruction either small bowel or colon

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

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 painfree 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

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(closedloop obstruction)

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

4) ABDOMINAL DISTENTION
It varies according to level of obstruction :

In HIGH SB.Obst.and EARLY mesenteric

ischemia;There is minimal distention DISTENSION

In LOW SB.Obstruction.(and caecal obstruction.) there is PROMINENT CENTRAL

In colonic obstruction:LATE DISTENSION

in flanks and upper abdomen

mainly

However; MARKED ABDOMINAL DISTENSION IN :

Obstructing lt colonic ca.(comp. ileocaecal valve)

Sigmoid volvulus
Hirschprung disease

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)

II.

EXAMINATION LOCAL
Scares; Distension; Hernial orifices

1) Inspection: 2) Palpation:
Localized tenderness; and rebound tenderness in impending strangulation Localized guarding; in perforation and peritonitis Localized tender Mass; in Neoplasm and Inflamm.

Phlegmon

II.

EXAMINATION LOCAL

3) Percussion: Tympantic Abdomen(gas filled

loops)

4) Auscultation: EARLY; Frequent; high pitched

5) Careful Exam. Of HERNIAL ORIFICES

bowel sounds. LATER; OR STRANGULATION; silent abdomen

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

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

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)

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

THE DIFFERENCE BETWEEN SMALL AND LARGE BOWEL OBSTRUCTION

Large bowel Peripheral ( diameter 5cm+) Presence of haustration
Presence of solid faeces

Small Bowel Central ( diameter 2.5cm+ vulvulae

connventines)

Ileum: may appear tubeless

DIAGNOSIS OBJECTIVES

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

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

II. IS MECHANICAL VS ADYNAMIC

Adynamic(Ileus)
History of major surgery/ Trauma/Sepsis Usually NO PAIN(or mild abdominal discomfort) Diffuse marked abd.distention Continue to pass air and diarrheaa

Mechanical
NO Early episodes of sever colic.Later sharp constant pain(due distension and sec.perist.Failure Distention; less NO air or faeces

ADYNAMIC
Bowel sounds: Hypoactive Abd.X-Ray:diffuse distended SB loops colon also distended with GAS in RECTUM Gastrograffine SB follow-through: confirmatory

MECHANICL
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

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)

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

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)

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)

V. THE LIKELY CAUSE OF OBSTRUCTION

This Depends Upon
:

Clinical Course Of Obstruction Anatomical Level Of Obstruction Age Of The Patient

AGE-RELATED COMMON OBSTRUCTING LESIONS

Neonates
Meconium Ileus Cong.Intes.Atresia Volv.Neonatorum Hirschsprung Dis.

Infants& Children
Ileocaecal Intussessception Ing.Hernia Meckles Diverticulum Adhesions Hirschsprungs Disease Foreign Bodies

Cong.Anorectal Anomalies
Neonatal Necrotising Enterocolitis

AGE-RELATED COMMON OBSTRUCTING LESIONS

Young Adult
Adhesions Hernia Meckeles Diverticulum Strictures (Crohns D.) Intussessc.(Polyp) Colonic Rare (volv. Or Carcinoma)

Middle Age
Adhesions Hernia Strictures (Crohns)

Intussessception
Colonic (common): Volvulous Carcinoma Diverticulitis

AGE-RELATED COMMON OBSTRUCTING LESIONS

OLD AGE (>65 Y.):

SMALL BOWEL OBSTRUCTION:

Adhesions ;Hernia ;Gall Stone Ileus Small Bowel Tumers Obstructing carcinoma Sigmoid volvulus Diverticulitis Faecal Impaction Acute Colonic Psedoobstruction Acute Mesentric Vascular Occlusion

Colonic Obstruction:

TREATMENT

TREATMENT
I. URGENT RESUSCITATION II. CLOSE PATIENT MOINTORING III.THE NEED&TIMING OF SURGERY

IV.PRINCIPLES OF DEFINITIVE SURGICAL INTERVENTION

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

II.

INDICATIONS OF SURGICAL INTERVENTION

1. URGENT:
Strangulation / Suspected Strangulation Closed-Loop Obstruction Complete Obstruction Pnumoperitonium/ Peritonitis

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

3.

NOT TO OPERATE

PARALYTIC ILEUS ACUTE COLONIC PSEUDOOBSTRUCTION

A. CONTINUE CONSERVATIVE
Adhesive SB. Obstruction Provided: Pain Is
Settled& Radiological Improvement
Likely

Immediate Postop.Periode: Where P. Ileus Is Disseminated Malignancy OR Extensive Radiation Enteritis Where Prognosis Is Bad Patients With History Of IBD: When
Preservation Of Bowel Length Is Major Concern

B. INVESTIGATE WITH CONTRAST STUDIES

1)SB. Gastrograffine Followthrough/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

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 Pseudoobstruction

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

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

4) FIBRE-OPTIC COLONOSCOPY
In colonic Obstruction:
Differentiate Mechanical From Pseudo-obstruction Confirm Mechanical Cause& Biopsy From LESION

Colonoscopic Decompression In Pseudoobstruction

IV. DEFINITIVE SURGICAL INTERVENTION

PRINCIPLES: Decompress The Bowel Resect Obstructing Lesion / Ischemic Bowel Restore Intestinal Continuity

 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

 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

 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

 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 PaulMickulicz Procedure With Delayed Anastomosis(After 8-12 Weeks)

2) One-Stage Procedure ; Primary ResectionAnastomosis ( On-Table Colonic Lavage)

SURGICAL OPTIONS : OBSTRUCTED LT.COLONIC CA.

3) Total Colectomy With Ileo-Rectal Anastomosis 4) Subtotal Colectomy With IleoSigmoid Anastomosis
In Closed-Loop Or Ischemic / Gangrenous Caecum They Have Low Morbidity& Mortality And Remove synchronous colonic Lesions And Avoid Metachronous Lesions

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

THANK YOU