1 / 57

Acute intestinal obstruction. Peritonitis. L. Yu. Ivashchuk

Acute intestinal obstruction. Peritonitis. L. Yu. Ivashchuk. Intestinal obstruction is a complete or partial disturbance of intestinal evacuation and peristalsis resulting from various causes which manifests by specific clinical course and morphologic changes of involved part of the bowel.

rickiek
Télécharger la présentation

Acute intestinal obstruction. Peritonitis. L. Yu. Ivashchuk

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. Acute intestinal obstruction. Peritonitis. L. Yu. Ivashchuk

  2. Intestinal obstruction is a complete or partial disturbance of intestinal evacuation and peristalsis resulting from various causes which manifests by specific clinical course and morphologic changes of involved part of the bowel Intestinal obstruction occursapproximately in 9.4 % among urgent abdominal pathology, consisting 1.2 % of all surgical diseases.

  3. Classification (by D.P.Chuhrienko) 1. Dynamic intestinal obstruction: a) paralytic; b) spastic. 2. Mechanical intestinal obstruction: a) strangulation; b) obturation; c) mixed (invagination). II. According to the course of pathological process. 1. Stage of acute disturbance of intestinal evacuation and peristalsis. 2. Stage of hemodynamic disorders of the bowel wall and its mesentery. 3. Stage of peritonitis.

  4. Etiologic and contributing factors • Adhesions (50 %). • Tumours. • Bile stones. • Inflammatory infiltrates in the abdominal cavity. • Internal hernias. • Increasing of abdominal pressure. • Defects of the peritoneum. • Long mesentery of the bowel.

  5. Pathogenesis Intestinal block Accumulation of intestinal contents Distention of intestinal wall Transudation of intestinal juice Vomiting Loss of electrolytes, dehydratation, loss of potassium, loss of proteins Peritonitis Necrosis of the bowel Intoxication, hemodynamic disturbances More higher the obstruction, more severe the pathologic changes

  6. Pathogenesis

  7. Peculiarities of strangulated intestinal obstruction • Transfusion of large quantity of proteins; • Transfusion of erythrocytes and decreasing of volume of circulating blood; • Severe dehydratation, caused by additional edema of the bowel wall; • Rapid necrosis of intestinal wall with subsequent peritonitis and intoxication.

  8. Clinical manifestation It depends on the level of the block, type and degree of obstruction and its cause. 1. Acute onset of the disease. 2. Periodic acute diffuse painof wavelike character which results in shock. 3. Constant vomiting and nausea without any relief. 4. Signs of dehydratation and intoxication (The patient looks anxious, with drawn features, hollowed-eyed, his lips and tongue are dry, with brown fur). 5. Retention of stool and gases.

  9. Objective examination 1. Signs of shock. 2. Distended and asymmetric abdomen. 3. Splashing sound (Sklyarov’s sign). 4. Increased peristalsis in early period with further absence. 5. Wahl’s sign - high tympanic sound over the distended bowel. 6. PR: empty and distended anus and rectal ampoule - (Grekov’s sign). 7. In intestinal strangulation and advanced cases of obstruction - peritoneal signs.

  10. X-ray examination 1. Kloiber's cups (air-fluid level) 2. Intestinal pneumatisation

  11. Periodic acute diffuse pain Constant vomiting and nausea without any relief Retention of stool and gases Abdominal distension On X-ray of theabdomen Kloiber's cups (air-fluid levels) Splashing sound, increased peristalsis Sharp acute diffuse pain Ulcerative anamnesis Absence of hepatic dullness On X-ray of the abdomen air above the liver (air sickle) Rigidity of anterior abdominal wall Differential diagnostics of acute intestinal obstruction with perforative peptic ulcer

  12. Periodic acute diffuse pain Constant vomiting and nausea without any relief Retention of stool and gases Abdominal distension On X-ray of theabdomen Kloiber's cups (air-fluid levels) Splashing sound, increased peristalsis Sharp acute constant girdle pain with irradiation into left scapule Vomiting and nausea without any relief Mayo-Robson symptom Increased serum amylase Increased urinary diastase No retention of stool and gases Abdominal distension only in advanced cases. No increased peristalsis Differential diagnostics of acute intestinal obstruction with acute pancreatitis

  13. Periodic acute diffuse pain Constant vomiting and nausea without any relief Retention of stool and gases Abdominal distension On X-ray of theabdomen Kloiber's cups (air-fluid levels) Splashing sound, increased peristalsis Sharp acute constant pain which results in shock Abdominal distension. Decreased peristalsis Blood stool Concomitant cardiac pathology Peritoneal signs Differential diagnostics of acute intestinal obstruction with mesentericthrombosis

  14. Periodic acute diffuse pain Constant vomiting and nausea without any relief Retention of stool and gases Abdominal distension On X-ray of theabdomen Kloiber's cups (air-fluid levels) Splashing sound, increased peristalsis Acute pain in a right hypohondrium with irradiation to the scapula Muscular tenderness in a right hypohondrium Vomiting by bile and nausea without any relief Ortner's symptom, phrenic symptom, Murphy’s sign Increased serum bilirubin Differential diagnostics of acute intestinal obstruction with acute cholecystitis

  15. Conservative treatment Conservative treatment is indicated only in: 1. Adhesive obstruction without signs of strangulation. 2. Initial stages of invagination. 3. Initial stages of low obturation • Gastric decompression • Siphon enema • Paranephral procaine block • Ganglio- and sympatholytics • Correction of water-electrolyte balance

  16. Surgical treatment is indicated only if no improvement during 3-4 hours of conservative treatment • Wide laparotomy • Procaine block of mesenteric root • Revision of intestine and detecting of the level and cause of obstruction • Decompression of intestine proximal to the obstruction • Assessing of viability of the bowel (peristalsis, colour, vascular pulsation) • Removal of the obstruction (division of adhesions, intestinal resection, collateral anastomosis) • External drainage of intestine(nasogastrointestinal intubation, rectal tube)

  17. Strangulation intestinal obstruction 1. Volvulus, (torsion). 2. Nodulus (knots). 3. Hernial strangulation (incarceration). 4.Invagination (refers to mixed forms of intestinal obstruction) • Causes • Elongation of intestinal loop. • Increasing of abdominal pressure. • Long mesentery of the bowel. • Cicatrical shortening of mesenteric root. • Adhesions • Extensive functional overload of the bowel.

  18. Volvulus (torsion) Small intestine volvulus Clinically manifests by high strangulation intestinal obstruction Cecal volvulus, sigmoid volvulus Clinically: low strangulation intestinal obstruction asymmetric abdomen by palpation enlarged and displaced colon (like balloon) retracted right or left iliac region Treatment:detorsion, division of adhesions, cecopexia, colon resection

  19. Nodulus It is the most severe type of strangulation with manifestation of a high strangulated obstruction which rapidly results in shock, bowel necrosis and peritonitis • Treatment: • very short preoperative period (less 1 hour) • untie of the bowel node (till 4-5 hours from the onset) • resection of the bowel

  20. Invagination It is the insertion of one part of the bowel into the lumen of another • Clinically: • signs of obturation and in advanced cases the strangulation ileus • elastic, painful, tumourlike formation in the abdomen • blood in stool (or during rectal examination) Treatment: desinvagination or resection

  21. Abdominal peritonitis mesenteric thromboses hemoperitoneum pancreatitis postoperative ileus Retroperitoneal phlegmone hematoma renal colic spinal trauma Other cranial trauma acidosis diminished potassium hypoproteinemia uremia Paralytic ileus

  22. Abdominal hepatic colic ascaridosis Retroperitoneal renal colic Other lead poisonong Spastic ileus

  23. Treatment of dynamic ileus 1. Cholynomymetics (Proserin, ubretid). 2. Intravenous infusion of hypertonic solution (10 % NaCl). 3. Hypertonic enema. 4. Oil enema. 5. Gastric decompression. 6. Paranephral novocaine block. 7. Ultrasound stimulation.

  24. ACUTE PERITONITIS

  25. Peritonitis – is the acute or chronic peritoneal inflammation with characteristic local and general changes in the organism and severe dysfunction of vital organs Acute peritonitis complicatesapproximately 0.8-2 % of all “clear” operations, and 20 % of all inflammatory pathology of the abdominal cavity. Mortality rate of peritonitis rises to 70-80 %.

  26. ETIOLOGY As the complication of surgical pathology Appendicitis – 50 % Cholecystitis – 16 % Perforation of gastric ulcer and cancer – 7 % Pancreatitis – 6 % Mesenteric thrombosis – 6 % Colon cancer – 2 % Postoperative peritonitis – 13 % Primary peritonitis Tuberculosis, canceromatosis, pneumonia, streptococcal infection, gonorrhea Toxico-chemical aseptic peritonitis Blood, urine, bile, pancreatic juice

  27. CLASSIFICATION • According to the extension of inflammatory process: • Local – involvement of 1 anatomic area, • Diffuse – involvement of 3-6 anatomic area, • Generalized – involvement of all peritoneum. • According to the character of the exudate: serous, fibrinous, fibrino-purulent, purulent, hemorrhagic, septic. • According to the stages: • Reactive (first 24 hours) maximal manifestation of local signs of the disease; • Toxic (24-72 hours) – gradual reducing of local signs and increasing of general intoxication. • Terminal (after 72 hours) – severe, often unreversable intoxication with vital function decompensation.

  28. PATHOGENESIS • Pathogenic microorganisms • Intoxication • Hypovolemia • Disfunction of vital organs

  29. PATHOGENESIS Bacterial contamination Reactive stage Inflammatory reaction of the peritoneum Exsudation Reabsorption of the microorganisms and toxins Toxic stage Hypovolemia, disturbances of water-electrolytic and protein balance Intoxication Toxic and hypovolemic shock Paralytic ileus Terminal stage Disturbances of vital organ function, polyorganic insufficiency

  30. CLINICAL MANIFESTATIONS Reactive stage • Sharp intensive pain. • Forced patient's position in bed. • Tachycardia 100-120 /min. • Dryness of tongue. • Abdominal tension over the site of inflammatory process or desk-like abdomen. • Peritoneal signs (Blumberg’s sign) • Decrease of peristalsis • X-ray examination could reveal pneumoperitoneum, Kloiber's cups, intestinal pneumatisation, pleurisy, lung atelectases

  31. CLINICAL MANIFESTATIONS Toxic stage • Decrease of pain. • Intensive vomiting. • Positive peritoneal signs (Blumberg’s sign) • Decrease of abdominal tension, abdominal distension. • Absence of peristalsis, paralytic ileus. • Tachycardia >120 /min. • Hypotonia. • Tachypnea. • Increase of body t° (> 38° C). • Dry tongue (like a brush). • Euphoria.

  32. CLINICAL MANIFESTATIONS Terminal stage • Disturbanses of CNS (adynamia, euphoria, psychomotoric excitement). • Facies Hyppocratica (prostration, face with drawn features, hollowed eyes). • Anuria. • Shallow breathing. • Fecal vomiting, absence of peristalsis, abdominal distension paralytic ileus. • Positive peritoneal signs (Blumberg’s sign). • Thread-like pulse (impossible to count), hypotonia. • Cardiac arrhythmia, cardiac failure. • Disturbanses of blood coagulation.

  33. Differential diagnostics

  34. Differential diagnostics

  35. Postoperative peritonitis

  36. Postoperative peritonitis

  37. TREATMENT Peritonitis is the absolute indication for the operative treatment • Tasks: • Removal of the source of inflammation • Evacuation of the exsudate and fibrin • Washing of the abdominal cavity • Satisfactory draining of the abdominal cavity

  38. Surgical treatment • Medial laparotomy • Depending on the cause: • append- or cholecystectomy • suturing of perforative ulcer • resection of the colon with colostomy • reinforcement of anastomosis suture • Sanation and washing of the abdominal cavity • Intestinal intubation • Procaine block of mesenteric root • Drainage of the abdominal cavity, peritoneal lavage

  39. Pre- and postoperative treatment • Antibacterial therapy, anti-inflammatory therapy • Correction of blood rrheology • Immunocorrection • Correction of water-electrolyte and protein balance • Desintoxication • Renewal of peristalsis • Correction of cardiac activity and breathing • Parenteral nutrition

  40. Subdiaphragmatic abscess • Causes: • Surgical operations (operations for stomach cancer and ulcer, pancreatic resections, operations for stomach peritonitis and intestinal obstruction, splenectomy) • Abdominal trauma (hematoma, bile accumulation) • Purulent processes of the organism (paranefritis, liver abscess, pleural empyema) • Classification: • Left-, rightside, bilateral • Intra-, exraperitoneal

  41. Subdiaphragmatic abscess • Clinical manifestation: • Intensive pain in upper part of the abdomen • Phrenicus-sign • Hectic temperature • Intoxication • Restriction of breathing, paradox breathing

  42. Diagnostic: • X-ray of the abdomen and chest • Ultrasound examination • CT scanning

More Related