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Intestinal obstruction neo
- 1.
- 2. 1. Dynamic - mechanical obstruction 1.Adynamic- – Peristalsis –absent – Peristalsis -non- propulsive form
- 4. Pathology Proximal to obstruction –Altered mobility – Distension Distal to obstruction – Normal peristalsis – Absorption
- 5. Pathology Proximal to obstruction –Altered mobility – Distension – Dilates – flaccid – Paralysis • Exhaustion • to prevent Viability
- 6. Distension Gas – Swallowed air –Diffusion from blood – Products of digestion and bacterial activity – O2 & CO2 reabsorbed – Nitrogen 90% and H2S Fluid – Digestive juice – No absorption of food
- 7. • Electrolyte imbalance –Reduced intake – Defective intestinal absorption – Vomitintg – sequestration
- 8. • Distal toobstruction – Normal peristalsis – Absorption – Empty and contracted – immobile
- 9. • Veins compressedfirst - Edema and hemorrhages • Arterial compression – Haemorrhagic infarction • Translocation of bacteria, toxins and systemic absorption
- 10. Strangulation External Internal • Smaller absorptive surface •Short segment – Less blood and fluid loss • Larger absorptive surface • Large segment – More blood and fluid loss - shock
- 11. Closed loop obstruction •Obstruction both at proximal and distal point – Strangulated loops – Colonic obstruction with a competent ileocecal valve
- 12. Special types • Internalhernia • Entric stricture • Bolus obstruction • Adhesion and bands • Intussusception • volvulus
- 13. Clinical features • Classicalqurtet 1. Pain 2. Vomiting 3. Distension 4. Constipation
- 14. pain • Colicky • Mildconstant diffuse • severe
- 15. vomiting • Proximal- morevomiting • With time – Undigested food to faeculant
- 16. distension • More distal-more distension
- 17. constipation • Absolute • Relative •Absent in – Richter’s hernia – Gall stone obstruction – Mesentric vascular obstruction – obstruction with pelvic abscess – Partial obstruction- faecolith, neoplasm
- 18. Levels • Small bowelobstruction – High – low • Large bowel obstruction
- 19. Levels • Small bowelobstruction- High – Early vomiting – Rapid dehydration – Minimal distension – X ray -fluid level ?
- 20. Levels • Small bowelobstruction- low – Pain- prominent – Late vomiting – Central distension – X ray -fluid level - multiple
- 21. Levels • Large bowelobstruction – Early distension, severe – Late vomiting, dehydration – Pain mild – X ray –caecum , ascending colon distended
- 22. Nature of presentation •Acute- SB, sudden onset of pain • Chronic- LB, constipation, distension • Acute on Chronic- recurrant • Subacute- constipation?
- 23. Other features • Dehydration •Hypokalemia • Pyrexia – Ischemia/perforation/Inflammatory obs. • Hypothermia • Abdominal tenderness
- 24. Type of presentation •Simple – Intact blood supply • Strangulated – Compromised blood supply
- 26. Signs of strangulation •Continous pain • Localised tenderness, rigidity, rebound tenderness • Shock • Does not respond to conservative management
- 27. Radiology • X –ray abdomen Erect Air fluid levels • X – ray abdomen Supine Distended bowel
- 29. Small bowel • Centraland transverse lie • Jejunum – Valvulae conniventes (concertina / Stack of coins) • Ileum – Characterless • Colon – Haustral folds
- 30. Treatment • Gastrointestinal drainage •Fluid and electrolyte replacement • Relief of obstruction
- 31. Timing of surgery •Emergent Obstructed/strangulated Ext hernia Internal intestinal strangulation Acute obstruction • Other cases Atleast within 24 hrs • Adhesions upto 72hrs
- 32. Principles of Surgicalintervention • Mt. of the segment at the site of obstruction • The distended proximal bowel • Underlying cause of obstruction
- 33. assessment • Site ofobstruction • Nature of obstruction • Viability of gut
- 34. Site of obstruction Caecum DilatedNot dilated Large bowel Small bowel Trace distally Trace proximally
- 35.
- 36. Viability of bowel Viable Darkcolor – Light Dark persists Mesentery bleeds on pricking No bleeding Peritoneum – Shiny Dull & Lustreless Int Musc – Firm, Peristalsis seen Flabby, thin, friable Non viable Mesenteric pulsation + Absent
- 37. Doubtful – Resectedends as stomas No resection / Multiple ischaemic areas (Mesenteric Vasc Occlusion) 2nd look laparotomy after 24-48hrs
- 38. Surgical procedure • Adhesiolysis •Excision / Resection • Bypass / Proximal decompression
- 39. Operative decompression • Compromiseof Exposure / Viability / Closure • Septic complications of spillage • Savage’s decompressor / NG tube • Replace fluid
- 40. Large bowel obstruction Caecumto Prox trans colon – Rt. Hemicolectomy, if resectable – Ileotransverse bypass if not resectable Splenic flexure – Extended Rt.Hemicolectomy
- 41. Left colon /Rectosigmoid • Decompression proximal colostomy • Resection with – Anastamosis with covering colostomy – Paul Mikulicz procedure – Hartmann’s procedure
- 42.
- 43. SPECIAL TYPES • internalhernia • Enteric Stricture • Bolus obstruction – Gallstone – Food – Bezoars • Adhesion and bands • Intussusception • volvulus
- 44. INTERNAL HERNIA • Internalhernia – Retroperitoneal fossa • Duodenal fossa- – Left – right • Caecal/appendicaeal fossa – Superior – Inferior – retrocaecal • Intersigmoid fossa – Congenital peritoneal defect • Foramen of winslow • Hole in mesentry, mesocolon, broad ligament – Diaphragmatic hernia
- 45. • Duodenal fossa- –Left – right
- 46. • Caecal/appendicaeal fossa –Superior
- 47. • Caecal/appendicaeal fossa –Inferior
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- 50.
- 51. • Release theconstriction agent by division • Donot- • Duodenal fossa- • Foramen of winslow • Hole in mesentry, mesocolon, broad ligament • Decompress and reduce
- 52. Enteric Stricture • Benign –TB – Chrohn’s • Malignant – Lymphoma – Ca – sar
- 53. Enteric Stricture • t/t –RA – stricturoplasty
- 54. bolus • Gall stone •Food • Bezoars • Stercolith • worms
- 55. Gall stone • Fistula •60 cm proximal to IC • Ball valve effect • t/t – Crush – Milk – Enterotomy – Faceted stone
- 56. food • Post gastrectomy •t/t – same
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- 58.
- 59. worms • Ascariasis • Followanti helminthic therapy • perforation • X ray- medusa head • t/t
- 60. Adhesions • Most commoncause • Difficult to differentiate from paralytic ileus
- 61. Causes • Ischaemic areas •Foreign material – Talc – Starch – gauze – silk • Infection – Peritonotis – TB • Inflammatory conditions- • Radiation enteritis • Drugs – Practolol
- 62. Peritoneal irritation Local fibrinproduction Adhesion between apposed surfaces Early fibrinous adhesions Late fibrous adhesions
- 63. Prevention • Good Surgicaltechnique • Peritoneal wash • Minimizing contact with gauze • Covering anastamosis & raw peritoneal surfaces
- 64. Classification • Early /Flimsy • Late/ Dense
- 65. Bands • Congenital • Acquired –Peritonitis – Greater omentum adherent to parietes
- 66. Treatment • Conservative – NPO –RT aspiration – IV fluids – Vital signs & Abd. girth monitoring – Signs of strangulation – Maximum 72hrs
- 67. Surgery • Adhesiolysis – Onlythose causing obstruction – Covering with omental grafts – Constriction sites
- 68. Recurrent adhesive obstruction •Repeat Adhesiolysis • Noble’s plication procedure • Charles phillip Transmesenteric plication • Intestinal intubation
- 69. intussusception • Telescoping • Proximalto distal • Children- 5-10 yr • follow URTI • weaning
- 70.
- 71.
- 72. • Strangulating • t/t •Radiological reduction • Sx
- 73. volvulus • Primary – Volvulusneonatorum – Sigmoid – Caecal – Gastric – midgut • Secondary
- 74.
- 75. • X-ray • Innertube • Cofee bean • t/t • Endoscopic reduction • Sx
- 76.
- 77. Compound volvulus • Ileosigmoidknotting