Spontaneous Bacterial Peritonitis - GeoCities自发性细菌性腹膜炎-地理

1、Abdominal pain and Tenderness 14/03/02 STEVENSIU Peritonitis = Inflammation of the peritoneum (Primary) Spontaneous Bacterial Peritonitis(Secondary) PeritonitisChemical Peritonitis Bacterial peritonitisLearning Objectives 1Describe the anatomy and physiology of the peritoneum, including the innervat

2、ions of the visceral and parietal layersThe peritoneum is a continuous, transparent serous membrane that lines the abdominopelvic cavity and invests the viscera. It consists of two continuous layers.1. Parietal peritoneum- lining the internal surface of the abdominopelvic wall.2. Visceral peritoneum

3、 investing the visceraVisceral peritoneum supplied small type C pain fibers and can only response to chronic-aching suffering type of pain. These fibers can response to ischaemia, chemical stimuli, and spasm of a hollow viscus and over distention of a hollow viscusParietal peritoneum is supplied by

4、the spinal nerves not sympathetic nervesà sharp localized somatic painLearning objectives 2Discuss conditions predisposing to spontaneous bacterial peritonitis (SBP)SBP= The inflammation of the peritoneum without a clear event such as bowel perforation that would account for the entry of the pa

5、thogenic organism Liver Cirrhosis is the main predisposing factor. Other conditions leading to ascites e.g. Fulminant hepatic failure, Congestive heart failure, liver metastases can also predispose to SBP.Pathogenesis1. Seedingà The exact pathogenic mechanism is unknown. Bacterial seeding is be

6、lieved to involve haematogenous spread of organisms in a patient in whom diseased liver and altered portal circulation result in a defect in the usual filtration.2. Growth-> The reduced levels of complement cascade and reduced opsonic and phagocytic properties of neutrophils in advanced liver cir

7、rhosis in an excellent culture medium provided by the ascitic fluids, promote the growth of the organisms.Symptoms1. Fever, Hypotension, Decreased or absent bowel sounds, Abdominal Pain and Abrupt onset of hepatic encephlopathy in patient with ascitesLearning Objective 3Outline intra- abdominal lesi

8、ons that may be complicated by bacterial peritonitisBacterial peritonitis is due to entry of bacteria into the peritoneal cavity from a perforation in the GIT or from an external penetrating wound. E.Coli and Bacteroides are the most common causative agents. Common source of bacterial entry are:Bowe

9、l1. Appendicitis (By far the most common)2. Diverticulitis3. Bowel strangulationsChemical1. Ruptured peptic ulcer2. Cholecystitis3. Acute pancreatitisOthers1. Acute salpingitis2. Abdominal trauma3. Peritoneal dialysisLearning Objectives 4Outline the causes of chemical peritonitisChemical peritonitis

10、 is due to the escape of bile, contents of the gastrointestinal tract, or pancreatic juice into the peritoneal cavity; the contents of the fluid causes chemical injury, shock, and peritoneal exudation prior to occurrence of any associated infection.Causative substanceAgent agentsAssociated Intra abd

11、ominal lesionsMechanismGIT content HClRuptured peptic ulcersRuptured peptic ulcer can discharge 1.5 M HCl into the peritoneum cavity, which can damage the peritoneal lining and predisposes to super imposing bacterial infectionBileBile saltsà emulsification and digestion of fats.Cholecystitis

12、83; Gallstone obstruction exposes the epithelium to the detergent action of bile. The inflammatory response raises intra luminal pressure that predisposes to mucosal ischaemic damage. Secondary bacterial infection causes suppurative and gangrenous cholecystitis and ultimately rupture. Rupture leads

13、to the discharge of bile into the peritoneal cavity.Pancreatic juicesPancreatic enzymes e.g. trypsin, elastase, amylases and lipasesAcute oedematous pancreatitis (Mild) to Acute haemorrphagic pancreatitis (severe with 15-20 % mortality)Autodigestion of the pancreas and the surrounding tissue by acti

14、vated proteolytic enzymes causes the to discharge of the digestive enzymes into the peritoneal cavity. Haemorrhage and fatty acids results in globules of free fat may be found floating in the peritoneal fluid, leading to frank suppurative exudate after 24-48 hoursLearning objective 5Compare the clin

15、ical features of localized and generalized peritonitis. In particular discuss the haemodynamic consequences of generalized peritonitisClinical FeaturesLocalized GeneralizedAbdominal pain and tendernessLimited to the area of inflammationDiffuseRigidity + GuardingPresentPresent Rebound tendernessMinim

16、alObviousPositionMotionless, knees drawn upExacerbation factorsCoughing and SneezingBowel SoundsMay be presentAbsentSymptoms of shock - hypotension, Tachycardia and oligouriaMinimal EvidentFBCSlight LeucocytosisMarked Leucocytosis >20,000/L commonInvestigations1. Confirm the diagnosis of LP or GP

17、2. Determine the cause of LP or GPInvestigationPurposeFBCLeucocytosis in inflammatory conditions e.g. appendicitis, also to differentiate between LP or GPAmylase > 5 x à Acute pancreatitisErect chest X-rays Look for free gas under the diaphragm -à ruptured peptic ulcers or bowel perfora

18、tionsPlain Abdominal X raysDilation of the large and small bowel with oedema of the small bowel wall.Paralytic ileus - obstruction of the bowel due to paralysis of the bowel wall, usually as a result of localized or generalized peritonitis or shockCT scanAppendicitisHaemodynamic consequences Hypovol

19、umic and septic Shockà 1. The normal 7-8 L of fluids are not absorbed from the distal bowel and colon. 2. High volume of inflammatory exudate.3. Decreased oral intake4. The peritoneum also provides a large surface area for the absorption of GN endotoxin, leading to septicemia. High level of cir

20、culatory endotoxins can lead to widespread exudation and activation of the coagulation cascade, leading to DIC.5. The contraction of the circulation volume leads to hypotension and reflex tachycardia. The perfusion to the kidneys is also reduced leading to oligouria. Learning Objective 6Discuss the

21、pathogenesis of intra-abdominal abscesses. Outline the role of imaging in the management of such abscesses.Spillage from a colonic source e.g. appendicitis, pancreatitisAcute inflammatory response produces the characteristic neutrophil infiltration with fribinosupprative exudate. A fibrinous wall of

22、ten surrounds the central necrotic material, leading to the abscess formation. Macroscopically, the glistening peritoneal surface has become dull. And creamy in colourLocalized peritonitisà localized by omentum and viscera to a small area Generalized peritonitisà Exudate often accumulates

23、to form subphrenic abscess or pelvic abscess.Subphrenic abscess pus between the diaphragm and liver; common complication after perforation of the stomach, duodenum and gall bladder. May cause dullness at the lung base, tenderness over the lower ribs posteriorly.Pelvic abscess forms in the lower part

24、 of the peritoneal cavity in front of the rectum. Abscess may irritate can Polyuria and incomplete bowel emptying; tender mass during PR or PV.Management1. Ultrasounds and abdominal X rays à elevation of the diaphragm with a fluid level below or an effusion aboveLearning Objectives 7Outline the

25、 factors predisposing to the development of diverticular disease, emphasizing the role of diet. Describe the clinical presentation and complications of diverticular disease.Diverticular disease Definition· Acquired deformity where the mucosa and submucosa herniate through the underlying muscula

26、ris; 95% of which occurs in the sigmond colon.Aetiology · Affects 10% of American population, incidence increases from the age of 40.· Functional aetiological factors à diet of highly refined foods and low fibre a/w modern affluent life· Structural aetiological factorsà asso

27、ciated with connective tissue diseases such as Ehler-Danlos and Marfans syndromeClinical presentation1. Chronic constipation with diarrhoea and flatulenceà 80%2. Intermittent and unpredictable gripping lower abdominal painPathophysiology and Clinicopathological correlation1. Decreased dietary f

28、ibre means that the forward propulsion of the faeces more difficult at normal transmural pressure more difficult. Reduced propulsion leads to constipation. Secondary bacterial liquecifaction of the retained faceal material leads to diarrhoea and flatulence.2. The subsequent increased peristaltic con

29、tractions, which causes the intermittent and unpredictable gripping lower abdominal pain. The pain may last for hours to days with sudden relief upon passing flatus and flatulence.3. The peristaltic contractions also cause an increased in intraluminal pressure and muscular hypertrophy. The raise pre

30、ssure causes the herniation of mucosa through the weaker points of the muscular wall, which are located between the mesenteric and antimesenteric teniae.Complications1. Diverticular Bleeding à most common cause of painless lower GIT bleeding in the elderly. It is caused by rupture and bleeding

31、of the colonic intramural arteries. 2. Diverticulitisà stagnant faecal material causes inflammation of the wall of the diverticulum. Patient develops abdominal pain and fever. It may progress to abscess formation and perforation. Learning Objectives 8Discuss the differential diagnosis of right

32、iliac fossa pain, describe the presentation and complications of acute appendicitis (AA).Pathophysiology and Clinical Presentation1. AA is initiated by the obstruction of the appendiceal lumen, most commonly by facolith.2. Continual secretion by the mucosal glands raises the intraluminal pressure.3.

33、 Raised pressure impedes mucosal blood flow and contributes to mucosal ischaemic damage4. Damaged mucosa predisposes to enteric bacterial invasion. The subsequent inflammation response causes further ischaemia in a feed forward manner.5. In early acute appendicitis, inflammatory mural exudate and th

34、e smooth muscle contractions against an obstructive lumen stimulate the visceral afferent pain fibres. The visceral pain is referred to a T10 dermatome distribution, causing the epigastric pain. The pain is colicky due to the periodic peristaltic contraction of appendiceal smooth muscles.6. Reflex p

35、yelospasm and inhibition of caecal peristalsis cause anorexia and constipation respectively. Vomiting is rare due to anorexia.7. Release of inflammatory cytokines such as IL-1 and INF alpha causes systemic symptoms such as fever (<38 degrees), leucocytosis and raised coagulation factors.8. After

36、a few hours, serosal fibrinosuppurative exudate stimulates the parietal peritoneum which has somatic innervations, resulting in localized constant pain in the RIF and muscle guarding over the appendix. Complications1. Serosal fibrinosuppurative exudate is likely to cause adhesion to the greater omentum forming an appendiceal mass, which makes surgical removal difficult.2. At the stage, the appendix may become gangrenous and predisposes to rupture. Contained rupture into the appendiceal mass predisposes to periappendiceal abscess. Uncontained ruptur