Intestinal ObstructionAssessment 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:-

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

Physiology:(secretion&absorbtion)

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 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

INTESTINAL MOTILITY2) 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 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

Dynamic (Mechanical)

Failure of forward intestinal progression due to organic occlusion:

I. Intraluminal: gallstone,FB,Bezoars,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):

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

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 FUNCTIONALOBSTRUCTION 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

Click icon to add picture

Type1A:comptent

valve

Progress to Type 1B with some SB dilatation

Type2:incomp.valve

and colonic &SB

dilatation

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

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

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)

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. STRICTURESA.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 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.

• 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

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

Gallstone Ileus

Trichobezoars

Ascaris lumbricoides

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 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

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.

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

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%)

INCIDENCESmall Bowel

(85%)

COLON

(15%)

DIAGNOSIS HISTORY

CLINICAL EXAMINATION

PLAIN ABDOMINAL X-RAY

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

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

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 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

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)

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

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

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

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

.

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

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

Small Bowel Large bowel

•Central ( diameter 2.5cm+ vulvulae connventines)•Ileum: may appear tubeless

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

DIAGNOSIS OBJECTIVES

DIAGNOSIS OBJECTIVESFive Questions Should Be Answered:

I. Is The Diagnosis INTESTINAL OBSTRUCTION

II. Mechanical Vs AdynamicIII. 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

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

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

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 OBSTRUCTIONDistal 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

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

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

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

TREATMENT

TREATMENTI. 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 StrangulationClosed-Loop ObstructionComplete ObstructionPnumoperitonium/ 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 ILEUSACUTE COLONIC PSEUDO-OBSTRUCTION

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

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

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

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 Pseudo-obstruction

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 Paul-Mickulicz Procedure With Delayed Anastomosis(After 8-12 Weeks)

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

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

LT.COLONIC CARCINOMASURGICAL 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