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  1. 1. Intestinal Obstruction Assessment And Management DR. Moh.Hazem El-Foll FRCS ED.UK. Consultant General Surgeon KJO Hospital KSA
  2. 2. 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
  3. 3. 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
  4. 4. 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
  5. 5. 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
  6. 6. 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
  7. 7.  Dynamic (Mechanical)  Failure of forward intestinal progression due to organic occlusion: I. Intraluminal: gallstone,FB,Bezoa rs,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):
  8. 8. 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
  9. 9. INTESTINAL OBSTRUCTION COULD BE: I.Simple:Luminal Obstruction with NO interference of mesenteric blood supply II.Strangulated:There is interference of mesenteric blood supply
  10. 10. 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
  11. 11. 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)
  12. 12. Closed Loop Obstruction: Bowel loop trapped in hernial sac or twisted around unyieldind band with increase in intraluminal pressure
  14. 14. 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
  15. 15. 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
  16. 16. 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
  17. 17. 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
  18. 18. 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)
  19. 19. Colonic obstruction Type1A:comptent valve Progress to Type 1B with some SB dilatation Type2:incomp.valv e and colonic &SB dilatation
  20. 20. 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
  21. 21. 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.
  22. 22. 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)
  23. 23. 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.
  24. 24. 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
  25. 25. ETIOLOGY
  26. 26. 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
  27. 27. I. ADHESIONS B.Inflamatory:  Cholecystitis  Appendicitis  PID  T.B  Peritonitis C. Radiation D. F.B and Drugs
  28. 28. 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)
  31. 31. 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)
  32. 32. 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
  34. 34. 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
  35. 35. IV. STRICTURES A.Congenital: Intestinal Atresia B. Inflammatory:  Crohns Disease  Tuberculosis  Drugs :enteric-coated KCLtab. ;NSAIS drugs C. Neoplastic:  Lymphoma  Carcinoid
  36. 36. 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.
  37. 37. • 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
  38. 38. 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
  41. 41. 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
  42. 42. 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
  43. 43. 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 
  45. 45. 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
  46. 46. III. STRICTURES(BENIGN): I. Diverticular II. Inflammatory(IBD) III.Ischemic IV.Intussussception:Due to colonic polyps V. External Hernia VI.Faecal impaction
  47. 47. 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
  48. 48. 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
  49. 49. 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
  50. 50. 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
  51. 51. 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
  52. 52.  Cancer (75%)  Diverticulos.(10%)  Volvulus(10%)  Miscellan.(10%)  In Eastern Countries& Middle East volvulus accounts for > 50% of causes of colon obstruction  Adhesions(80%)  Hernia(10%)  Tumors(5%)  Miscellan.(5%) INCIDENCE Small Bowel (85%) COLON (15%)
  54. 54. 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
  55. 55. 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
  56. 56. D.INTERMITTENT :  These are recurrent acute attacks of acute small bowel obstruction which are relieved spontaneously  This is almost invariably due to adhesions
  57. 57. 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
  58. 58. 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)
  59. 59. 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
  60. 60. 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
  61. 61. 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)
  62. 62. 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 .
  63. 63. 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
  64. 64. 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
  65. 65. 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)
  66. 66. 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
  67. 67. THE DIFFERENCE BETWEEN SMALL AND LARGE BOWEL OBSTRUCTION Small BowelLarge bowel •Central ( diameter 2.5cm+ vulvulae connventines) •Ileum: may appear tubeless •Peripheral ( diameter 5cm+) •Presence of haustration •Presence of solid faeces
  69. 69. 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
  70. 70. 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
  71. 71.  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
  72. 72.  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
  73. 73. 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)
  74. 74. 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
  75. 75. 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)
  76. 76. 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)
  77. 77. V. THE LIKELY CAUSE OF OBSTRUCTION This Depends Upon :  Clinical Course Of Obstruction  Anatomical Level Of Obstruction  Age Of The Patient
  78. 78.  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
  79. 79.  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
  80. 80. 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
  81. 81. TREATMENT
  84. 84. II. INDICATIONS OF SURGICAL INTERVENTION 1.URGENT: Strangulation / Suspected Strangulation Closed-Loop Obstruction Complete Obstruction Pnumoperitonium/ Peritonitis
  85. 85. 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
  87. 87. 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
  88. 88. 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
  89. 89. 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
  90. 90. 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
  91. 91. 4) FIBRE-OPTIC COLONOSCOPY  In colonic Obstruction:  Differentiate Mechanical From Pseudo-obstruction  Confirm Mechanical Cause& Biopsy From LESION  Colonoscopic Decompression In Pseudo- obstruction
  92. 92. IV. DEFINITIVE SURGICAL INTERVENTION PRINCIPLES:  Decompress The Bowel  Resect Obstructing Lesion / Ischemic Bowel  Restore Intestinal Continuity
  93. 93. 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
  94. 94.  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
  95. 95.  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
  96. 96.  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)
  97. 97. 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
  98. 98. 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
  99. 99. THANK YOU