ACUTE INTESTINAL OBSTRUCTION.pptx

acute intestinal obstruction

1. INTESTINAL OBSTRUCTION DR P SRINIVASA SUDHAKAR

2. When there is pathological interference with the normal progression of the intestinal luminal contents distally, the condition is called intestinal obstruction. Such obstruction may be due to mechanical obstruction of the intestine when it is called mechanical obstruction . It may also occur from paralysis of the intestinal muscle so that the peristalsis of the intestine is lost, so is the progression of the intestinal contents. This is paralytic ileus .

3. AETIOLOGY A. Mechanical Obstruction.— This includes : 1. OBSTRUCTION IN THE LUMEN may be caused by ( i ) Meconium , (ii) Bezoars which may be trichobezoar (hair) or phytobezoar (fruit and vegetable fibres), (iii) gallstones, (iv) polypoid tumour of the bowel, (v) intussusception , (vi) impaction of barium or worms.

4. TRICHOBEZOAR

5. PHYTOBEZOAR

6. OBSTRUCTION ILIUS DUE TO GALL STONES

7. POLYPOID TUMOUR OF THE BOWEL

8. OBSTRUCTION DUE TO WORMS

9. 2. LESIONS OF THE BOWEL WALL also cause intestinal obstruction These can be classified into — (a) Congenital.—This includes ( i ) Atresia and stenosis ; (ii) Megacolon ( Hirschsprung’s disease), (iii) Meckel’s diverticulum ; (iv) Imperforate anus; (v) Diverticuli . (b) Traumatic. (c) Inflammatory.— (i) Crohn’s disease; (ii) Ulcerative colitis (rare); (iii) Diverticulitis (rare). (d) Neoplastic .— Various tumours of the small intestine and large instestine also cause obstruction. (e) Miscellaneous.— ( i ) Radiation therapy; (ii) Iatrogenic stricture following intestinal anastomosis ; (iii) Potassium induced stricture.

10. ATRESIA

11. MEGACOLON (HIRSCHSPRUNG’S DISEASE)

12. Meckel’s diverticulum

13. IMPERFORATE ANUS

14. 3. LESIONS EXTRINSIC TO THE BOWEL are important causes of intestinal obstruction. These are : Adhesive band constriction or angulation by adhesion.— This is a leading cause of small intestinal obstruction. This may follow previous surgery or inflammation. Adhesions may produce kinking or angulation of the intestine or create bands of tissue that compress the bowel. (b) External hernia is the second common cause of mechanical small intestinal obstruction. Inguinal, femoral, umbilical and incisional hernia are important causes of bowel obstruction.

15. EXTERNAL HERNIAS

16. (c) Volvulus .— This is a separate entity. (d) Extrinsic masses e.g. ( i ) Haematomas and abscess may press on the bowel and cause obstruction ( Neoplasms outside the bowel can also press on it to cause obstruction, (iii) Annular pancreas, (iv) Abnormal vessels may cause such obstruction, which of course is extremely rare.

17. VOLVULUS

18. ANNULAR PANCREAS

19. B. Paralytic ileus .— The causes of paralytic ileus can be divided into two categories; (a) Abdominal causes and (b) Systemic causes. Abdominal causes include intestinal distension, (ii) peritonitis and (iii) retroperitoneal lesions retroperitoneal haemorrhage, retroperitoneal sarcoma, distension of the ureter etc. (b) Systemic causes include electrolyte imbalance particularly hypokalaemia and toxaemias.

20. CLASSIFICATION of intestinal obstruction can also be made as follows : 1. Simple mechanical obstruction in which there is obstruction but blood supply to the intestine remains intact. 2. Strangulated obstruction, in which the mesenteric vessels are occluded besides the usual mechanical obstruction. This is a dangerous condition and should be operated on without delay. 3. Closed loop obstruction when both limbs of the loop are obstructed so that there is neither progression nor regurgitation.

21. Intestinal obstruction can be further classified into: A cute obstruction Chronic obstruction Acute-on- chronJc obstruction

22. ( i ) A cute obstruction Which is an obstruction to the small bowel and is characterised by central abdominal pain, early vomiting, central abdominal destension constipation.

23. (ii) Chronic obstruction When obstruction is confined to the large bowel and is characterised lower abdominal colic, absolute constipation and later on distension

24. (iii )Acute-on- chronJc obstruction Which starts in the large bowel but gradually involves the small intestine. Early pain and constipation are the symptoms to starts with but when the small intestine is involved it is characterised by vomiting and general abdominal distension.

25. PATHOLOGY BOWEL MOTILITY :- When the intestine is obstructed, the part of the intestine above the obstruction shows vigorous peristalsis to overcome the obstruction. This continues from 2 to 6 days. The more distal is the obstruction, the more vigorous is the peristalsis and longer does it remain. If the obstruction is not relieved, increasing distension of the intestine ensues and a time comes when peristalsis ceases and the obstructed intestine remains flaccid and paralysed.

26. PATHOLOGY For a few hours the intestine below the obstruction shows normal peristalsis and absorption. This will empty its contents and later on it becomes immobile, contracted and pale.

27. PATHOLOGY DISTENSION :- In case of intestinal obstruction accumulation of fluid and gas proximal to the obstruction occurs. This produces distension of the intestine proximal to the obstruction. Ingested fluid, digestive secretion and intestinal gas play the major role to form this distension.

28. PATHOLOGY Fluid and electrolyte imbalance :- Large volume of saliva, gastric secretion, bile and pancreatic juice enter the gut daily. These are mainly absorbed in the small intestine. Distension increases intestinal secretion and decreases absorption. This phenomenon results in increased fluid accumulation in the bowel proximal to the obstruction.

29. PATHOLOGY Besides ingestion of fluid, various digestive juices comprise about 8000 ml/day. Saliva 1500 ml, gastric juice 2500 ml, bile and pancreatic juice 1000 ml. and intestinal juice 3000 ml. Accumulation of such huge amount of fluid along with repeated vomiting causes severe metabolic disturbances. Particularly in proximal obstruction there is relatively more vomiting and this leads to losses of water, sodium, chloride, hydrogen and potassium ions producing dehydration with hypochloraemia , hypokalaemia and metabolic alkalosis.

30. PATHOLOGY Distal small bowel obstruction may cause loss of large quantities of fluid, but the abnormalities of serum electrolyte values are less dramatic, probably because of hydrochloric acid losses are less. With dehydration the-e will be oliguria , haemo -concentration and azotemia ( high levels of nitrogen ). If dehydration continues, there will be reduced cardiac output, low central venous pressure, hypotension and hypovolaemic shock. Distension of the abdomen will lead to elevation of the diaphragm to impair proper ventilation.

31. PATHOLOGY Intestinal gas:- Much of the distension is caused by gas accumulation in the intestine proximal to the obstruction. This mainly consists of: ( i ) gas swallowed from the atmospheric air, (ii) diffusion from blood into the bowel lumen ( carbondioxide from neutralisation of bicarbonate) and (iii) organic gases (hydrogen sulphide, ammonia, amines and hydrogen) from bacterial fermentation (10%). Swallowed air is the most important source of gas in causing intestinal distension. While the oxygen and carbon dioxide are absorbed, nitrogen is not absorbed by intestinal mucosa.

32. PATHOLOGY BACTERIAL PROLIFERATION :- During intestinal obstruction there is rapid proliferation of intestinal bacteria. Normally the small intestine contains very small quantity of bacteria and may be considered as almost sterile. Normal peristalsis with continued progression of luminal content minimises small intestinal bacterial flora. But during small intestinal obstruction, whatever may be the cause, bacteria proliferate rapidly.

33. PATHOLOGY That is why, intestinal contents become faeculent ’ during obstruction. As the bacteria or bacterial toxins cannot cross normal intestinal mucosa the bacteria in the small intestine probably play no role in the ill effects of simple mechanical small intestinal obstruction.

34. PATHOLOGY Strangulated obstruction :- Strangulation develops when the circulation to the obstructed intestine is impaired. This frequently occurs secondary to ( i ) Adhesive band obstruction, (ii) Hernia, (iii) Volvulus or (iv) I ntussusception . If the obstructed distending bowel is held by unyielding adhesive bands or hernial rings strangulation may occur. Similarly in volvulus or intussusception , the mesenteric vessels are occluded by twisting of the mesentery. In strangulated obstruction the patient suffers from all the ill effects of simple obstruction plus to the effects of strangulation.

35. PATHOLOGY Distension:- Distension in case of strangulated obstruction is different from simple obstruction. Unlike on-strangulated obstruction, early distension of the proximal intestine is absent. In fact for a few minutes several hours the proximal intestine contracts. After this, vigorous peristalsis occurs in the proximal segment without any distension. When gangrene is imminent, retrograde thrombosis of the related tributaries of the mesenteric vein will cause distension of both the proximal and distal segments of the strangulated intestine. For a considerable time the strangulated segment alone distends. The greatest distension occurs when the venous return is completely impaired and the arterial supply continues uninterrupted.

36. PATHOLOGY The onset of gangrene :- Gangrene does not occur till the venous return is completely occluded. At this time the colour of the intestine changes from purple to black. Gradually the arterial supply is also impeded. Now the serous coat loses its glistening appearance, the mucous membrane becomes ulcerated and thus wet gangrene develops.

37. PATHOLOGY Loss of blood volume:- In addition to the accumulation of fluid and gas in the obstructed loops, blockage of venous outflow from the strangulated segment will cause extravasation of bloody fluid into the bowel. So strangulation causes loss of blood and plasma. This loss of blood and plasma will cause shock particularly the patient is already dehydrated. The amount of loss of blood volume will depend upon the length of the strangulated segment. If strangulation produces gangrene, peritonitis with its sequelae will occur. Rupture perforation of strangulated segment is possible.

38. PATHOLOGY Transmigration of bacteria and toxin:- In addition to the loss of blood volume, another important factor in strangulated obstruction is production of toxic material in the strangulated bowel. As mentioned above, the bacteria proliferate and produce toxic material within the strangulated segment. When the intestine mucous membrane is normal this toxic material is not absorbed, but when the wall of the intestine becomes partly devitalised, both bacterial toxin and the products of tissue autolysis pass through the wall of intestine into the peritoneal cavity, whence these are absorbed into the circulation. So if the strangulation is external, it is far less dangerous than intra peritoneal strangulation

39. PATHOLOGY Closed-loop obstruction:- When both afferent and efferent limbs of a loop of bowel are obstructed, it is called closed-loop obstruction. It is dangerous as this type of obstruction very rapidly becomes strangulated even before the usual manifestations of intestinal obstruction. Obstruction to blood supply occurs either from the same mechanism which produces such obstruction or by the twist of the bowel on the mesentery. Development of distension and onset of gangrene are almost same as strangulated obstruction described above

40. PATHOLOGY Closed-loop obstruction

41. PATHOLOGY Colon obstruction:- In general, effects of colon obstruction is usually much less dramatic than the effects of small bowel obstruction. If the ileocaecal valve is competent colon obstruction will lead to closed-loop obstruction. In this case pressure within the caecum becomes quite high to compress blood vessels within its wall. Stercoral ulcers develop, followed by even perforation. If the ileocaecal valve is incompetent, signs of small bowel distension may accompany colon obstruction.

42. PATHOLOGY Otherwise colon obstruction is less dangerous as it produces less fluid and electrolyte imbalance than small bowel obstruction. Further colon obstruction usually does not strangulate except cases of volvulus .

43. CLINICAL FEATURES The important symptoms of simple mechanical intestinal obstruction are: ( i ) Abdominal pain, (ii) Vomiting, (iii) Failure to pass gas (flatus) or faeces per rectum and (iv) abdominal distension.

44. ( i ) Abdominal Pain This is the first symptom and usually starts suddenly. The pain is typically cramp like. This cramping pain is felt synchronously with hyperperistalsis . The pain is represented by severe cramps with intervals of 4 to 5 minutes in proximal intestinal obstruction and with more intervals (15 to 20 minutes) in distal obstruction . In between attacks the patient is often free from pain.

45. ( i ) Abdominal Pain The pain is diffuse, poorly localised and is felt across the upper abdomen in high obstruction, at the level of the umbilicus in low ileal obstruction, in the lower abdomen in colon obstruction and in the perineum in case of rectosigmoid obstruction. When obstruction is not relieved the characteristic abdominal colicky pain may stop by itself and will be replaced steady generalised abdominal discomfort.

46. ( i ) Abdominal Pain It must be remembered that continuous severe pain without any quiescent period is usually indicative of strangulation. In paralytic ileus there is no typical colicky pain of mechanical obstruction, but there may be steady generalised abdominal discomfort.

47. (ii) Vomiting There may be early vomiting which is ‘reflex’ and is followed by a quiescent period of variable length before ‘actual’ vomiting starts. This interval depends on the site of obstruction and is short in high obstruction and long (every day or two) in low small bowel obstruction. With high obstruction vomiting is more frequent and copious and may cause some relief by decompressing the obstructed bowel. With low small bowel obstruction vomiting is less frequent and does not cause any relief. In this case vomiting may be ‘ faeculent ’ because of large bacterial population of distal small bowel.

48. (ii) Vomiting In acute small intestinal obstruction, the character of the vomitus alters . Initially it contains partly digested food next it becomes yellow or green from regurgitation of bowel and finally it becomes faeculent . In colon obstruction reflex vomiting is absent and vomiting does not occur until due to incompetent valve the small bowel is retro gradely involved. When the ileocaecal valve is competent vomiting is absent in colon obstruction

49. (iii) Constipation Failure to pass gas (flatus) or faeces through the rectum is an important symptom of intestinal obstruction. But it must be remembered that it becomes evident only after the bowel distal to the obstruction has been evacuated. So there may be one or two natural actions of bowel after the onset of attack before constipation develops.

50. (iii) Constipation It should be remembered that in a few conditions of intestinal obstruction there may not be constipation e.g. Richter’s hemia , mesenteric vascular occlusion and intestinal obstruction with pelvic abscess.

51. (iv) Distension In early case of small intestinal obstruction there may not be any abdominal distension. Distension is much less in high small bowel obstruction. In low small bowel obstruction centrally placed distension becomes evident but late. Visible peristalsis may be present, if the abdomen is inspected very carefully. This is evident in the proximal loops. Borborygmi may be quite loud and may not require a stethoscope to hear it. In auscultation, sound of hyperperistalsis coinciding with attack of colic is definite evidence of intestinal obstruction.

52. PHYSICAL EXAMINATION Tachycardia and hypotension indicate severe dehydration and/or peritonitis. The degree of dehydration is estimated by examination of the skin turgor and moisture of the mucous membrane. Fever suggests strangulation. In strangulated obstruction patient appears very ill during this early period.

53. INSPECTION In early stage visible peristalsis may be the only sign present particularly in these individuals with long standing obstruction. One must look for surgical scars, indicative of previous surgery (which indicates adhesion or cancer).

54. INSPECTION Abdominal distension is a late sign of intestinal obstruction. But one must exclude distension due to ascites . In the latter case there will be fluid thrill, shifting dullness and fullness in the flanks. All hernial orifices must be inspected. This will diagnose many obscure hernias (even strangulated) to be the cause of intestinal obstruction.

55. PALPATION During colic there may be muscle guarding. Slight tenderness may be present between attacks of pain. Tenderness and rigidity at the site of obstruction usually indicate strangulation. Rebound tenderness suggests peritonitis and likelihood of strangulation. Abdomen should be thoroughly palpated to exclude presence of mass (lump) which may be present in intussusception , neoplasms and abscesses. Again all the hernial orifices should be palpated to exclude presence of hernia (impulse on coughing should be tried)

56. PERCUSSION Tenderness on light percussion suggests strangulation.

57. AUSCULTATION It is of great value. In simple mechanical obstruction — during attacks of colic the bowel sounds become loud, high-pitched and metallic. In paralytic ileus occasional isolated bowel sound may be heard. In presence of strangulation, bowel sound is completely absent at that region.

58. RECTAL EXAMINATION Rectal Examination should be performed in all cases of intestinal obstruction. Presence of mass on rectal examination within or outside the lumen will give a clue to the diagnosis. Most of rectal cancers are within the reach of the rectal examination finger. It should be noted presence or absence of faeces in the rectum. Absence of faeces means the obstruction is higher up. If present, it should be studied for presence of occult blood, which indicates mucosal lesion e.g. cancer, intussusception or infarction.

59. Sigmoidoscopy examination should be done if colonic obstruction is suspected.

60. SPECIAL INVESTIGATIONS 1. BLOOD EXAMINATION 2. RADIOLOGICAL EXAMINATIONS BARIUM ENEMA Intravenous urography may be indicated to exclude presence of ureteric calculi (which has not been visualised straight X-ray), which may cause marked paralytic ileus .

61. MANAGEMENT Principle of treatment of intestinal obstruction includes : ( a) fluid and electrolyte therapy , ( b) decompression of the bowel and ( c) timed surgical intervention to relieve the obstruction.

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