8. Intestinal obsfgggtruction 2020 2.pptx

Heyyyy

1. Anatomy of small intestine and intestinal obstruction in adults By: Dr Sanchi Gupta Moderator: Dr. Gurpreet Singh

2. AT 3 RD WEEK OF DEVELOPMENT 3 GERM LAYERS ECTODERM: ENCLOSES AMNIOTIC CAVITY MESODERM ENDODERM: ENCLOSES YOLK SAC Development and surgical anatomy of small intestine

3. ectoderm gives rise to the enteric nervous system mesoderm gives rise to the connective tissue, including the wall of the gut tube and the smooth muscle endoderm gives rise to the epithelial lining of the digestive tract, as well as to all of the associated glands and organs such as stomach, the intestines, the lungs, the liver, and the pancreas

4. Anatomy of SMALL INTESTINE The small intestine extends from the pylorus to the ileocaecal junction. It is about 6 metres long. It is divided into: An upper, fixed part, called the duodenum, which measures about 25 cm in length. A lower, mobile part, forming a very long convoluted tube.

5. The circular folds of mucous membrane, plicae circulares , or valves of Kerckring form complete or incomplete circles. The intestinal villi are finger-like projections of mucous membrane.Each villus is covered by a layer of absorptive columnar cells made of microvilli. Intestinal Glands or Crypts of Lieberkühn are simple tubular glands distributed over the entire mucous membrane of the jejunum and ileum.

6. Nerve Supply parasympathetic (vagus) myenteric plexus of Auerbach : containing parasympathetic ganglia between circular and longitudinal muscle coats. Fibres from this plexus form the submucous plexus of Meissner . sympathetic (T9 to T11) Sympathetic nerves are motor to the sphincters and to the muscularis mucosae and inhibitory for peristaltic movements.

7. Duodenum (25 cm) 5cm 7.5 cm 10cm 2.5cm

8. Up to the level of the opening, the duodenum is supplied by the superior pancreaticoduodenal artery, and below it by the inferior pancreaticoduodenal artery. The first part of the duodenum receives additional supply from: a. The right gastric artery. b. The supraduodenal artery of Wilkie, which is usually a branch of the common hepatic artery. c. The retroduodenal branches of the gastroduodenalartery. d. Some branches from the right gastroepiploic artery.

9. Venous Drainage The veins of the duodenum drain into the splenic, superior mesenteric and portal veins. Lymphatic Drainage Mostly pancreaticoduodenal nodes ->hepatic nodes -> coeliac nodes and partly to the superior mesenteric nodes -> intestinal lymph trunk -> cisterna chyli. Nerve Supply Sympathetic nerves from T9-T10 and parasympathetic nerves from the vagus

10. Small intestinal obstruction

11. INTRODUCTION IT IS DEFINED BY THE LACK OF NORMAL TRANSIT OF THE INTESTINAL CONTENT, REGARDLESS OF ETIOLOGY. LACK OF PROPULSIVE ACTIVITY OF GI CONTENT EARLY RECOGNITION AND AGGRESSIVE TREATMENT ARE CRUCIAL

12. Epidemiology 🞇 ABOUT 80–90% OF BOWEL OBSTRUCTIONS OCCUR IN THE SMALL INTESTINE; THE OTHER 10–20% OCCUR IN THE COLON.

13. causes 80-90% bowel obstruction in SB and 10-20% occur in the colon . SBO

14. causes DYNAMIC: In which peristalsis is working against a mechanical obstruction. INTRALUMINAL INTRAMURAL EXTRAMURAL ADYNAMIC: In which there is no mechanical obstruction;peristalsis is absent or inadequate. PARALYTIC ILEUS- PERITONITIS ELECTROLYTE IMBALANCE MESENTRIC ISCHEMIA PSEUDO OBSTRUCTION- PERISTALSIS MAY BE PRESENT IN THE NON PROPULSIVE FORM

15. Intraluminal Fecal impaction Foreign bodies Gallstone Bezoars Worms Intramura l Stricture malignancy Crohn’s Tb Congenital Extramural Extramural bands/adhesion Hernia abscess Volvulus Compression

16. OTHER CAUSES OF MECHANICAL INTESTINAL OBSTRUCTION OBSTRUCTION FROM ENTERIC STRICTURES BOLUS OBSTRUCTION GALL STONES OBSTRUCTION OBSTRUCTION DUE TO TRYCHOBEZOAR OR PHYTOBEZOAR STERCOLITHS WORMS INTUSSUCEPTION

17. Classifications HIGH VS LOW SBO High sbo : vomiting occurs early,is profuse and causes rapid dehydration Distension is minimal Little evidence of dilated small bowel loops on abdominal radiograph y Low sbo: Pain is prominent with cental distension Vomiting is delayed dilated small bowel loops on abdominal radiography

18. PATHOPHYSIOLOGY ABOVE THE OBSTRUCTION PERISTALSIS INCREASED INITIALLY INTESTINE DILATES REDUCTION IN PERISTALTIC STRENGTH(PROTECTIVE BUT LATE) RELATIVE HYPOXIA DISRUPTION OF AUTONOMIC INNERVATION LOCAL EFFECT OF INFLAMMATION BELOW THE OBSTRUCTION NORMAL PERISTALSIS AND ABSORPTION UNTIL IT BECOMES EMPTY IT CONTRACTS AND BECOMES IMMOBILE

19. PATHOPHYSIOLOGY BOWEL DISTENTION GAS ACCUMULATION SWALLOWED AIR FERMENTATION OF SUGARS PRODUCTION OF CO2 BY INTERACTION OF BICARBONATE AND GASTRIC ACID DIFFUSION OF CO2 AND O 2 FLUIDS INGESTED FLUIDS SALIVA, GASTRIC, INTESTINAL JUICES, BILE AND PANCREATIC SECRETION ( NORMALLY 8 -9 LITER )

20. PATHOPHYSIOLOGY DEHYDRATION REDUCED INTAKE REDUCED ABSORPTION INCREASED LOSS(VOMITING AND SEQUESTRATION) SYSTEMIC EFFECT WATER AND ELECTROLYTE LOSSES TOXEMIA CARDIOPULMONARY DYSFUNCTION RENAL FAILURE SHOCK AND DEATH

21. STRANGULATION-OCCURS IN 25% EXTRINSIC COMPRESSION OF ARTERIAL ARCADE PROGRESSIVE DISTENTION EXTENSIVE MESENTERIC VENOUS THROMBOSIS BACTERIA TRANSLOCATION AND PROLIFERATION → SEPTIC COMPLICATIONS .

22. CLOSED LOOP OBSTRUCTION- TWO POINTS ALONG THE COURSE OF A BOWEL ARE OBSTRUCTED AT A SINGLE LOCATION. E.G. HERNIAS , ADHESIONS AND VOLVULUS STRANGULATION OCCURS FROM THE SAME MECHANISM TWIST OF THE BOWEL MESENTERY

23. Diagnosis DISTINGUISH MECHANICAL OBSTRUCTION FROM ILEUS DETERMINE THE ETIOLOGY DISCRIMINATE PARTIAL FROM COMPLETE OBSTRUCTION DISCRIMINATE SIMPLE FROM STRANGULATED OBSTRUCTION

24. Clinical features: History f our cardinal features of IO: colicky abdominal pain distension, vomiting, and constipation Abdominal pain Location Character Severity periodicity Bowel habit Weight loss Previous obstruction Previous abdominal /pelvic surgery Abdominal ca/intraabdominal inflammation Medical condition/radiation/ medication C.F. vary Site of the obstruction Duration of the obstruction Underlying pathology Presence / absence of strangulation

25. CARDINAL CLINICAL FEATURES OF ACUTE OBSTRUCTION ●● ABDOMINAL PAIN ●● DISTENSION ●● VOMITING ●● ABSOLUTE CONSTIPATION PRESENTATION WILL BE FURTHER INFLUENCED BY WHETHER THE OBSTRUCTION IS: ● SIMPLE – IN WHICH THE BLOOD SUPPLY IS INTACT; ● STRANGULATING/STRANGULATED – IN WHICH THERE IS INTERFERENCE TO BLOOD FLOW •

26. LATE MANIFESTATIONS OF INTESTINAL OBSTRUCTION INCLUDE DEHYDRATION OLIGURIA, HYPOVOLAEMIC SHOCK, PYREXIA, SEPTICAEMIA, RESPIRATORY EMBARRASSMENT AND PERITONISM. IN ALL CASES OF SUSPECTED INTESTINAL OBSTRUCTION, THE HERNIAL ORIFICES MUST BE EXAMINED. •

27. Investigations CBC with differential Electrolyte LFT ABG Serum lactate Blood culture

28. STRANGULATION SEVERE CONTINUOUS PAIN TENDERNESS WITH RIGIDITY SHOCK FEVER TACHYCARDIA AFTER RESUSCITATION LAB. → LEUCOCYTOSIS THE PRESENCE OF THESE SIGNS SHOULD ALERT THE SURGEON

29. X-rays ABDOMINAL SERIES SUPINE UPRIGHT LATERAL DECUBITUS FILM ADV MOST VALUABLE IN PATIENTS WHO ARE HEMODYNAMICALLY UNSTABLE AVAILABILITY AND LOW COST DISADV WILL NOT PROVIDE INFORMATION ABOUT THE ETIOLOGY OF OBSTRUCTION MAY BE NORMAL IN PATIENTS WITH EARLY OR PROXIMAL OBSTRUCTION

30. X-ray SBO VALVULAE CONNIVENTES CENTRAL ABDOMEN MULTIPLE AIR FLUID LEVEL PAUCITY/ABSENCE GAS IN THE COLON

31. CT-scan PROVIDE MORE CLINICALLY RELEVANT INFORMATION. LOCALIZE THE OBSTRUCTIVE SITE DEGREE OF OBSTRUCTION CLOSED-LOOP OBSTRUCTION GIVE IDEA OF CHANGES IN BOWEL WALL ISCHAEMIA ,STRANGULATI ON ,MESENTIRC OEDEMA AND THICKENING

32. Ultrasound CRITERIA FLUID-FILLED SMALL BOWEL LUMEN >2.5 CM HISTORICALLY HAD DIAGNOSTIC SENSITIVITY APPROACHING 85%, ADV: INITIAL EVALUATION OF HEMODYNAMICALLY UNSTABLE PATIENTS IN PATIENTS FOR WHOM RADIATION EXPOSURE SHOULD BE AVOIDED, SUCH AS PREGNANT WOMEN DISADV: OPERATOR-DEPENDENT BOWEL GAS ARTIFACT DIFFICULT TO PERFORM IN OBESE PATIENTS

33. CONTRAST STUDIES ENTEROCLYSIS - PARTIAL OBSTRUCTION AFTER FIRST-LINE STUDIES FAILED IT IS NOT COMMONLY PERFORMED BECAUSE IT MAY CAUSE DISCOMFORT AND RELATIVELY HIGH RADIATION EXPOSURE, AND IT IS TIME CONSUMING RARELY PERFORMED IN ACUTE SETTING BARIUM STUDY ; INDICATIONS UNPROVEN LARGE BOWEL OBSTRUCTION OBSTIPATION V S OBSTRUCTION LOCALIZATION IS REQUIRED FOR SURGICAL INTERVENTION

34. GENERAL MANAGEMENT PRE-OPERATIVE CARE ADMISSION: o ACUTE BOWEL OBSTRUCTION SHOULD BE ADMITTED TO THE HOSPITAL o CHRONIC OR INTERMITTENT OBSTRUCTION CAN BE MANAGED AS OUT PATIENT FLUID THERAPY- ISOTONIC FLUID THERAPY AGGRESSIVE K REPLACEMENT • • DIET-NPO BLADDER CATHETERIZATION MONITOR UOP-(>0.5ML/KG/HR) Surgery in under resuscitated patient is associated with increased mortality.

35. General management NGT DECOMPRESSION DECREASES DISTENTION DECREASES NAUSEA AND VOMITING DECREASES RISK OF ASPIRATION ANTIBIOTICS SUSPECTED BOWEL COMPROMISE STANDARD PREOPERATIVE PROPHYLACTIC ANTIBIOTICS INFECTIOUS CAUSE OF NON ADHESIVE SBO I.E. DIVERTICULITIS CONSENT INCLUDING STOMA(MARKING)

36. NON OPERATIVE MANAGEMENT INITIAL MANAGEMENT NPO FLUID RESUSCITATION ELECTROLYTE REPLETION NGT DECOMPRESSION HYPERTONIC WATER-SOLUBLE CONTRAST MONITORING V/S SERIAL ABDOMINAL EXAMINATION( BY THE SAME PERSON ) LABORATORY STUDIES FOLLOW-UP IMAGING NGT OUTPUT DURATION:3-5 DAYS

37. Non operative management WATER SOLUBLE CONTRAST DIAGNOSTIC AND THERAPEUTIC CONTRAINDICATED IN BOWEL COMPROMISE/PREGNANCY NOT FOR NON ADHESIVE SBO NOT EFFECTIVE FOR EARLY SBO PROCEDURE NGT INSERTED STOMACH ASPIRATED TO DRYNESS 100ML OF GASTROGRAFFIN GIVEN THROUGH NGT NGT CLAMPED FOR 2-4HRS KUB TAKEN 6-24HRS

38. NON OPERATIVE MANAGEMENT FAILURE 25% OF PATIENTS REQUIRE SURGERY CLINICAL AND IMAGING DETERIORATION SIGNS OF BOWEL ISCHEMIA SIGNS OF PERITONITIS COMPLETE OBSTRUCTION FAILURE TO REGAIN BOWEL FUNCTION IN 3-5DAYS. 1. ✓ ✓ Outcome Resolutio n Remove NGT Diet initiated ✓ ✓ Patients stable and signs and symptoms of SBO persists Surgery may be required Patients deteriorates Immediate surgical intervention

39. WHEN TO CONVERT TO OPERATIVE MANAGEMENT? WORSENING OF CLINICAL CONDITION CONTINUOUS ABDOMINAL PAIN FEVER TACHYCARDIA LOCALISED/ DIFFUSE ABDOMINAL TENDERNESS LEUKOCYTOSIS NO IMPROVEMENT IN SYMPTOMS ON X RAYS OR CT SCAN SUSPECTED BOWEL COMPROMISE(ISCHEMIA, NECROSIS OR PERFORATION) ✓

40. SURGICALLY CORRECTABLE CAUSE OF OBSTRUCTION, EXCEPT ADHESION CLOSED LOOP OBSTRUCTION VOLVULUS INTUSSUSCEPTION INCARCERATED HERNIA GALLSTONE ILEUS, TUMOR THOSE FOR WHOM THREE TO FIVE DAYS OF NONOPERATIVE MANAGEMENT IS INEFFECTIVE

41. OPERATIVE MANAGEMENT POSITION-SUPINE/LITHOTOMY INCISION-MIDLINE FOR MOST DELIVER THE BOWEL INTO THE WOUND BOWEL SHOULD BE COVERED WITH MOIST SWAB WEIGHT OF FLUID FILLED SHOULD BE SUPPORTED TREATING CAUSE OF OBSTRUCTION AVOID SPILLAGE ASSESS VIABILITY OF THE BOWEL COLOR PERISTALSIS PULSATION AND BLEEDING FROM MARGINAL ARTERIES IF IN DOUBT WRAP IN HOT PACK FOR 10MIN WITH INCREASED OXYGENATION

42. SHORT LENGTHS OF ISCHEMIC BOWEL OR(SHORT QUESTIONABLE VIABILITY + HEMODYNAMICALLY STABLE) RESECTION AND PRIMARY ANASTOMOSIS IF LONG SEGMENT IS QUESTIONABLE SECOND LOOK AFTER 24-48HRS AND RESECT IF NONVIABLE

43. INTRAOPERATIVE INTESTINAL DECOMPRESSION MANUAL RETROGRADE DECOMPRESSION INTO THE STOMACH MAKE THE CLOSURE EASIER, FASTER, AND SAFER. INTRAOPERATIVE PASSAGE OF A LONG NASO INTESTINAL TUBE PERFORMANCE OF A CONTROLLED ENTEROTOMY

44. COMPLICATIONS SEPSIS INTRAABDOMINAL ABSCESS WOUND DEHISCENCE ASPIRATION PNEUMONIA RECURRENCE OF SIGMOID VOLVULUS ELECTROLYTE DISTURBANCE SHORT-BOWEL SYNDROME

45. ADHESIVE BOWEL OBSTRUCTION ABNORMAL FIBROUS BANDS BETWEEN ORGANS OR TISSUES OR BOTH IN THE ABDOMINAL CAVITY THAT ARE NORMALLY SEPARATED. ACQUIRED(MOST COMMON) OR CONGENITAL)E.G. LADD BANDS 93-100% WHO UNDERGO TRANSPERITONEAL SURGERY WILL DEVELOP POST OP ADHESION

46. ACCOUNT OF ~55% TO 80% OF SBO IN INDUSTRIALIZED COUNTRIES. 80% OF ADHESIVE SBO PTS HAVE HX OF PRIOR INTRAABDOMINAL SURGERY 20% HAVE HX OF PERITONITIS OR NO CAUSE INFRA-MESOCOLIC SURGERIES COLONIC, RECTAL, AND GYNECOLOGIC PROCE DURES ✓ ✓ ✓ ✓ Risk SBO 1-10% - appendectomy 6.4 % -open cholecystectomy 10-25% - intestinal surgery 17-25% - restorative proctocolectomy(IPPA)

47. pathophysiology The early balance between fibrin deposition and degradation seems to be the critical factor in adhesion formation.

48. TYPES FIBRINOUS ADHESION-EARLY AVASCULAR AND FLIMSY GET RESOLVED COMPLETELY FIBROUS ADHESION COLLAGENIZED AND VASCULARIZED

49. CLINICAL FEATURES ABDOMINAL PAIN • • • COLICKY RECURRENT EPISODIC DISTENSION CONSTIPATION PREVIOUS SURGICAL SCARS COMMONLY OBSERVED IMAGING ✓ ✓ X-RAY CT-SCAN ✓ ✓ ✓ Gilroy Bevan triad Pain gets aggravated or relieved on change of posture Pain in the region of old scar Tenderness is elicited by pressure over the scar

50. Management GENERAL FLUID AND ELECTROLYTES BOWEL REST NG TUBE URETHRAL CATHETER MONITORING DECIDE ON NON OPERATIVE VS OPERATIVE Management NON OPERATIVE ~ 80% SUCCESS RATE

51. OPERATIVE MANAGEMENT ADHESIOLYSIS • OPEN LAPAROSCOPIC • AT OPERATION, DIVIDE ONLY THE CAUSATIVE ADHESION(S) AND LIMIT DISSECTION • ●● REPAIR SEROSAL TEARS; INVAGINATE (OR RESECT) AREAS OF DOUBTFUL VIABILITY ●● LAPAROSCOPIC ADHESIOLYSIS IN THE HANDS OF ADVANCED LAPAROSCOPIC PRACTITIONERS •

52. PREVENTION GENTLE HANDLING OF BOWEL USE OF GLOVE FREE OF TALC PREVENTION OF SPILLAGE OF CONTENT OF VISCUS METICULOUS HEMOSTASIS CAREFUL PLACEMENT OF DRAIN PULLING OMENTUM OVER BOWEL BEFORE CLOSURE INSTILLATION OF DRUGS I.E. HYALURONIDASE…. LAPAROSCOPIC PROCEDURE

53. Small bowel volvulus

54. SMALL BOWEL VOLVULUS VOLVULUS REFERS TO TORSION OF A SEGMENT OF THE ALIMENTARY TRACT, WHICH OFTEN LEADS TO BOWEL OBSTRUCTION RISK FACTORS ANATOMIC • • • • • LONGER MOBILE MESENTERY NARROW BASE LESS FAT MUSCULAR ABDOMEN PREGNANCY DIETARY LARGE INFREQUENT MEAL

55. DIAGNOSIS SIGN OF SBO IMAGING PLAIN ABDOMINAL X-RAY • • NONSPECIFIC GANGRENOUS • • PNEUMATOSIS PORTAL VENOUS GAS CT-ACCURACY 83% • • WHIRL SIGN GANGRENOUS • • • PNEUMATOSIS PORTAL VENOUS GAS FREE INTRAPERITONEAL FLUID

56. SBV TREATMENT VIABLE SBV SIMPLE DETORSION- RECURRENCE? • • RESECTION??? INTESTINOPEXY??? GANGRENOUS BOWEL SEGMENTAL RESECTION AND PRIMARY ANASTOMOSIS

57. SBV OUTCOME Depends Time of diagnosis Age Physiologic status Associated illness Presence of infarcted bowel Time to surgical intervention Overall mortality 10-30%

58. Postoperative ileus

59. Postoperative ileus Physiologic postoperative ileus usually resolves without serious sequel. Following abdominal surgery bowel dysmotility lasts 0-24hrs in Small bowel 24-48hrs in the stomach 48-72hrs in the colon

60. Prolonged or pathologic When the expected period of time extends beyond normal usually beyond 4-6 days. Should be differentiated from mechanical obstraction and secondry cause of ileus should be considered International panel proposed Normal/obligatory post op ileus -<4days from surgery to until passage of flatus or stool and tolerance of oral diet. prolonged -2 or more of the following on 4 th post op day or after Nausea or vomiting Inability to tolerate an oral diet >24hrs Absence of flatus >24hrs Abdominal distention radiologic confirmation

61. pathophysiology Inflammatory mediators Inhibitory neural(sympathetic) reflexes Neurohormonal peptides i.e. VIP,NO…

62. Risk factors Lower abdominal surgery with large incisions Intestinal manipulation Prolonged surgery Open surgery Delayed enteral/tube feeding Intra-abdominal inflammation Perioperative complication Intraoperative/postoperative bleeding need transfusion Opioids/other medications Hypoalbuminemia/aggressive fluid adminstration

63. Clinical features

64. Plain abdominal films Dilated loop of bowel Should demonstrate air in the colon CT -if the diagnosis is unclear 90-100% sensitivity in distinguishing from mechanical obstruction

65. Treatment Pain management-avoid opioids Maintain normovolemia Electrolyte replacement Bowel rest- clear fluids may be allowed ,if tolerated Bowel decompression Nutrition –TPN may be considered Serial abdominal examination mu-opioids antagonists

66. summary one of the most common intraabdominal problems faced by the general surgeon Early recognition and aggressive treatment are crucial Operating too early, before you rehydrate, or too late, after you have allowed it to strangulate is common mistake.

67. Thank you!!!!