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

Abdominal pain and Tenderness 14/03/02 STEVENSIULearning Objectives 1Describe the anatomy and physiology of the peritoneum, including the innervations 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 – 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 the spinal nerves not sympathetic nerves→ 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 pathogenic 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.Seeding→ The exact pathogenic mechanism is unknown. Bacterial seeding is believed to involvehaematogenous 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 phagocyticproperties of neutrophils in advanced liver cirrhosis 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 hepaticencephlopathy in patient with ascitesLearning Objective 3Outline intra- abdominal lesions 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:Bowel1.Appendicitis (By farthe most common)2.Diverticulitis3.Bowelstrangulations Chemical1.Ruptured pepticulcer2.Cholecystitis3.Acute pancreatitisOthers1.Acute salpingitis2.Abdominal trauma3.Peritoneal dialysisLearning Objectives 4Outline the causes of chemical peritonitisChemical peritonitis 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.Learning objective 5Compare the clinical features of localized and generalized peritonitis. In particular discuss the haemodynamic consequences of generalized peritonitisInvestigations1.Confirm the diagnosis of LP or GP2.Determine the cause of LP or GPHaemodynamic consequencesHypovolumic and septic Shock→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 tosepticemia. High level of circulatory 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. Theperfusion to the kidneys is also reduced leading to oligouria.Learning Objective 6Discuss the pathogenesis of intra-abdominal abscesses. Outline the role of imaging in the management of such abscesses.Management1.Ultrasounds and abdominal X rays → elevation of the diaphragm with a fluid level below or aneffusion aboveLearning Objectives 7Outline the factors predisposing to the development of diverticular disease, emphasizing the role of diet. Describe the clinical presentation and complications of diverticular disease.Diverticular diseaseDefinition∙Acquired deformity where the mucosa and submucosa herniate through the underlying muscularis;95% of which occurs in the sigmond colon.Aetiology∙Affects 10% of American population, incidence increases from the age of 40.∙Functional aetiological factors → diet of highly refined foods and low fibre a/w modern affluent life∙Structural aetiological factors→ associated with connective tissue diseases such as Ehler-Danlos and Marfan’s sy ndromeClinical presentation1.Chronic constipation with diarrhoea and flatulence→ 80%2.Intermittent and unpredictable gripping lower abdominal painPathophysiology and Clinicopathological correlation1.Decreased dietary fibre means that the forward propulsion of the faeces more difficult at normaltransmural 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 contractions, which causes the intermittent and unpredictablegripping 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 pressure 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 →most common cause of painless lower GIT bleeding in the elderly. It iscaused by rupture and bleeding of the colonic intramural arteries.2.Diverticulitis→ stagnant faecal material causes inflammation of the wall of the diverticulum. Patientdevelops abdominal pain and fever. It may progress to abscess formation and perforation.Learning Objectives 8Discuss the differential diagnosis of right 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.Raised pressure impedes mucosal blood flow and contributes to mucosal ischaemic damage4.Damaged mucosa predisposes to enteric bacterial invasion. The subsequent inflammation responsecauses further ischaemia in a feed forward manner.5.In early acute appendicitis, inflammatory mural exudate and the smooth muscle contractionsagainst 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 pyelospasm and inhibition of caecal peristalsis cause anorexia and constipationrespectively. Vomiting is rare due to anorexia.7.Release of inflammatory cytokines such as IL-1 and INF alpha causes systemic symptoms such asfever (<38 degrees), leucocytosis and raised coagulation factors.8.After a few hours, serosal fibrinosuppurative exudate stimulates the parietal peritoneum which hassomatic 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 anappendiceal mass, which makes surgical removal difficult.2.At the stage, the appendix may become gangrenous and predisposes to rupture. Contained ruptureinto the appendiceal mass predisposes to periappendiceal abscess. Uncontained rupture into the peritoneum causes localized peritonitis and general peritonitis. Generalized peritonitis can lead to the fatal complication of GN septicaemia.3.Pyogenic microorganisms may enter the appendiceal vein, resulting in pyelophlebitis and liverabscesses.4.Residual abscesses in the paracolic gutter, subphrenic and pelvic regions may occur due to poordrainage of the fibrinosuppurative maternal5.Adhesion and bowel obstruction occurs months/ years after the appendicitis. Granulation tissuecan form between loops of bowel and appendix. Such adhesion can causes strangulations of bowel when another loop is trapped between adhered loop and appendix.。