Intestinal Obstruction Assessment And Management DR. Moh.Hazem El-Foll FRCS ED.UK. Consultant General Surgeon KJO Hospital KSA
Jan 28, 2015
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
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