A Slide on INTESTINAL or bowel OBSTRUCTION.pptx

EricaMaarDer 61 views 23 slides Aug 13, 2024
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About This Presentation

A slide on Intestinal obstruction


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I NTESTINAL OBSTRUCTION

outline Introduction Epidemiology Etiology Pathophysiology Signs and symptoms Diagnosis management

I ntroduction Intestinal obstruction, one of the commonest surgical emergencies, is a condition in which there is stoppage of the onward passage of intestinal contents - gas, digestive juices and food There is either significant impairment or complete impairment of the flow of materials in the intestines. Obstruction could be mechanical or paralytic Mechanical (or dynamic) ileus, due to mechanical obstruction of the intestinal canal, is associated with abdomi n al pain. Paralytic (or adynamic ) ileus, due to paralysis of the intestinal musculature, is characterized by the absence of pain. Could be caused by low potassium or peritonitis

Mechanical obstruction is of 3 types: , l. Acute, i.e. of sudden onset. Usually occurs in small bowel obstruction Severe central abdominal pain, distension and early vomiting and constipation 2 . Chronic, i.e. of slow, progressive severity . usually seen in large bowel obstruction with lower abdominal colic and absolute constipation, followed by distention 3 . Acute-on-chronic, i.e. chronic obstruction suddenly becoming acute by the obturation of the already narrowed intestinal canal . Usually occurs in large bowel but gradually involve the small intestine Early symptoms are pain and constipation, if small intestines are involved, vomiting and distension

Acute obstruction 1. Site of obstruction. The site of 'obstruction is its position relative 10 the ampulla of Vater . It may be ( i ) High, i.e. relatively near to the ampulla-jejunum and proximal ileum - with rapid loss of water and electrolytes; or (ii) Low i.e. relatively distant from the ampulla-distal ileum and colon - with relatively late onset of fluid and electrolyte imbalances but early onset of distension

2. Nature of obstruction Simple obstruction. The bowel lumen is occluded with no impairment of the blood supply to the bowel, e.g. obstruction due to intra-abdominal adhesions which may improve on conservative treatment alone. Other examples are uncommon causes such as ball of worms, gallstones and bezoars, (ii) Strangulation obstruction, e.g. strangulated inguinal hernia, volvulus or inus susception . In addition to the occlusion of the lumen, the blood supply to the segment of bowel involved is also cut off. Pure strangulation without occlusion of the bowel lumen occurs in mesenteric thrombosis or embolism. (iii) Closed loop obstruction. The obstructed loop is "closed" at both ends so that nothing can escape from it proximally or distally. The blood supply of the bowel wall may be impaired. Closed loop obstruction occurs in a pure form in obstruction of the colon with a competent ileocaecal valve

ETIOLOGY Intramural(from the wall of the intestines) : congenital, tumor, hematoma, inflammatory Extramural(outside the wall): adhesion, volvulus, hernia, abscess, hematoma Lumen obstruction(from the wall): stone meconium, foreign body, impaction Causes of intestinal obstruction Adhesions-40% Tumors-15% Inflammatory-15% Obstructed hernia-12% Intraluminal-10% Others-8%

Mechanical obstruction intramural TB ( ileo-caecal tuberculosis) Inflammatory lesions - diverticulitis, Crohn's disease Tumors Sticture Congenital (Atresia, Anorectal anomalies) Intussusception Aganglionic megacolon Mechanical obstruction intraluminal Gallstones Foreign bodies Bezoars Worms(Ascariasis) Impacted faeces etiology

Mechanical obstruction ( extraluminal ) Bands Adhesions Abscess Hernia Compression volvulus

P athophysiology 1. Simple Obstruction I n the bowel below the site of obstruction, normal peristalsis and absorption continue until the contents are absorbed or passed out. The bowel then collapses. Above the obstruction the bowel becomes distended . Peristalsis is vigorous for several days but if the obstruction is not relieved, then increasing distension leads ultimately to loss of peristaltic activity Distension: The distension results from accumulation of gases and fluids. The gasesĀ· nitrogen (70%), carbon dioxide (6-9%), oxygen (10%), hydrogen (I%), methane (1 %), hydrogen sulphide (1-10%)- are mostly from swallowed air. But some are products of putrefaction and fermentation of intestinal contents by bacteria and some result from diffusion from the blood The fluids are essentially digestive juices - saliva, gastric juice, bile, pancreatic and intestinal secretions - which accumulate partly due to decreased absorption and increased secretion

Dehydration And Electrolyte Imbalance These are due to vomiting, accumulation of gastrointestinal secretions in the bowel lumen, sequestration of fluid in the bowel wall and peritoneal cavity, diminished oral intake and decreased absorption. Most of the gastro-intestinal secretions - normally amounting to 7-10 litres in 24h but increased in obstruction - is lost to the body through vomiting and/or sequestration in the obstructed gut. There is also loss of E.C.F . into the peritoneum and the bowel wall. This results in hypovolaemia - dehydration or shock- hyponatraemia , hypokalaernia , hypochloraemia and renal failure

2. Strangulation Obstruction In addition to the effects of simple occlusion, obstruction of the blood supply has profound consequences . When the pressure of the occluding band exceeds the venous pressure, venous engorgement of gut wall occurs. ( i ) If the strangulated loop is long, this may lead to sequestration of large quantities of blood from the circulation with consequent hypovolemia , shock and death. The bowel wall becomes cyanosed The venous engorgement leads also to outpouring of fluid, dilatation of intramural lymph channels that provide a pathway for carrying multiplying bacteria (particularly E. coli) and their products ( exo -and endo-toxins) from the mucosal surface deep into the muscularis and to the serosa, peritoneal cavity and circulation. This may lead to endotoxic shock, septicaemia or peritonitis.

The occluding band may be tight enough to obstruct the arterial supply or the artery may go into spasm as a reflex response to the venous congestion. Infarction of the bowel wall then results. Necrosis of tissues is also hastened by thrombosis of intramural and mesenteric veins resulting from the stasis of venous engorgement. Hypoxia or anoxia also enhances the growth of anaerobic bacteria such as Clostridia and Bacteroides Distension of the involved loop and the disintegration of mural structures due to intramural blood accumulation may cause perforation with secondary peritonitis. (vi) The bowel is at first-congested and bright red later becoming purplish. As gangrene sets in by about 6h, it becomes black (Fig.34-ld), green or grey due in part to

3. Closed Loop Obstruction The afferent and efferent limbs of the bowel are both obstructed. It is seen typically in obstruction of the colon. A competent ileocaecal valve allows gases and liquid faeces to enter the caecum but not to leave it. The rich bacterial flora adds to the production of a lot of gases. Distension thus increases rapidly and with rising intraluminal pressure ernbarrasses the circulation. The bowel becomes necrotic, first in the caecum where distension is usually greatest. Perforation allows free escape of faeces and bacteria with fulminating peritonitis

Risk factors of bowel obstruction Previous abdominal or pelvic surgery ( risk for adhesion formation ) Intestinal inflammation ( Crohn disease ) History of or increased risk for neoplasm History of foreign body ingestion

Physical examination Abdominal inspection auscultation percussion palpation Digital rectal examination

Signs and Symptoms Abdominal pain(first symptom) Small bowel obstruction-central pain Large bowel obstruction- hypogastric pain Vomiting Absolute constipation Distention Visible peristalsis Hernial orifices and rectum Scars(post surgical adhesions) Rebound tenderness General signs of dehydration

Investigations Plain abdominal X-ray Abdominal CT , if suspicion exist despite negative radiography FBC Creatinine and Electrolyte ( sodium, potassium and chloride) Colonoscopy /Sigmoidoscopy Barium enema

C omplications : I. Shock ( i ) Hypovolemic - Loss of E.C.F. and/or sequestration of blood. (ii) septic shock. 2 . Dehydration. 3 . Electrolyte and metabolic imbalance. ( i ) Hypokalemia (ii) Hyponatremia . (iii) Alkalosis or acidosis. 4 . Peritonitis. 5 . Septicemia 6 . Renal failure

TREATMENT GOALS OF TREATMENT 1. Correction of fluid, electrolyte and metabolic imbalances Using crystalloids(ringers lactate or DNS and dextrose), KCl is added when urine output is over 30ml/h.. In severe strangulation, blood transfusion may be necessary Nasogastric decompression Sedation/analgesia Pethidine 100mg or morphine 10-15mg Antibiotic therapy Ceftriaxone + metronidazole or cefuroxime or ciprofloxacin

CONSERVATIVE THERAPY laparotomy if obstruction continues SURGERY Management is based on the etiology Resection and anastomosis (R&A); malignant enteric strictures, diverticulitis, caecal /sigmoid volvulus Palliative gastrojejunostomy ;duodenal lesion not removable Laparotomy ;complete SBO Enterotomy and cholecystectomy ; gall stone obstruction Colostomy with R&A; colon cancers Ileostomy

Criteria for immediate surgery Bowel ischemia , necrosis or perforation Closed-loop obstruction ( including volvulus ) Acute incarcerated hernia Intussusception Gallstone ileus Foreign body ingestion Localized small bowel tumor
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