Peritonitis infections

PG-1 IntraBiotics (Mountain View, CA, USA) Peritoneal infections Phase III... 

Peritonitis infection of ascitic fluid, characteristically by gram negative organisms without an obvious cause, is common in patients with increasing ascites, and is diagnosed by raised ascitic polymorphonuclear cell counts. Treatment with third generation cephalosporins, or amoxicillin and clavulanic acid is effective. Concurrent albumin supplementation helps prevent renal failure. 

Accessory measures insertion of a peritoneo-venous shunt to allow transfer of ascitic fluid to the venous compartment has largely been abandoned due to frequent shunt obstruction, peritoneal infection and the occurrence of encephalopathy. TIPS is as effective in relieving ascites as paracentesis with albumin replacement, but shunts can quickly become obstructed, and hepatic encephalopathy is a common complication. 

Kretschmar M, Hube B, Bertsch T, Sanglard D, Merker R, Schroder M, Hof H, Nichterlein T Germ tubes and proteinases are virulence factors of Candida albicans in murine peritonitis. Infect Immun 1999 67 6637-6642. 

The physiologic characteristics of the peritoneal cavity determine the nature of the response to infection or inflammation within it. The peritonemn is lined by a highly permeable serous membrane with a smface area approximately that of skin. The peritoneal cavity is lubricated with less than 100 mL of sterile, clear yellow fluid, normally with fewer than 300 ceUs/mm, a specific gravity below 1.016, and protein content below 3 g/dL. These conditions change drastically with peritoneal infection or inflammation, as described below. 

Trichuris trichiura May penetrate gut wall and cause peritonitis Infection by food contaminated with eggs ... 

Mixed infections Multiple organisms may be involved in some infections. For example, peritoneal infections may be caused by several pathogens (eg, anaerobes and coliforms) a combination of drugs may be required to achieve coverage. Skin infections are often due to mixed bacterial, fungal, or viral pathogens. 

Mice are utilized for testing antiseptics for appHcation to cuts, wounds, and incisions (339). The test bacteria, type 1 pneumococcus and hemolytic streptococcus, ate appHed to the taHs of anaesthetized mice. The tip of the taH is then dipped into the antiseptic for 2 min, after which one-half inch of the taH is removed and inserted into the peritoneal cavity and the incision is closed. If after 10 days the animals survive, the product is considered satisfactory for use as a skin antiseptic. The blood of dead animals is sampled and streaked on blood agar for confirmation of infection from the test bacteria as the cause of death. Since lack of toxicity is another requirement of a product to be appHed to wounds, this test has been combined with a toxicity test (340). 

In severe cases, or those refractory to treatment, truncal and limb weakness may be accompanied by involvement of masticatory, bulbar, and respiratory muscles. However the most life-threatening clinical manifestations are those affecting the gastrointestinal tract, since stomach ulceration can occur and death from perforation and peritonitis are not unknown. Medication with steroidal antiinflammatory agents is necessary but weakens the childrens resistance to infection, so that systemic spread of usually self-limiting disorders, such as candidiasis, may occasionally occur. 

As the name implies, these organisms grow in pairs, otherwise they are similar to streptococci and are now referred to as streptococci. Streptococcus pneumoniae is the causal agent of acute lobar pneumonia and also of meningitis, peritonitis and conjunctivitis. This organism can also initiate an invasive infection. 

Immunological tests were performed for studying the reactive of peritoneal-exudative cells, especially peritonial macrophages, which are the main effector cells involved in natural resistance (host defence system) against bacterial infection. 

Superior mesenteric artery syndrome Enteric infections Inflammatory bowel diseases Pancreatitis Appendicitis Cholecystitis Biliary colic Gastroparesis Postvagotomy syndrome Intestinal pseudo-obstruction Functional dyspepsia Gastroesophageal reflux Peptic ulcer disease Hepatitis Peritonitis Gastric malignancy Liver failure... 

Complications associated with PD include mechanical problems related to the PD catheter, metabolic problems associated with the components of the dialysate fluid, damage to the peritoneal membrane, and infections (Table 23-10). Strategies to manage infectious complications of PD are discussed below. 

Peritonitis Exit-site infections Tunnel infections... 

The preferred route of administration is intraperitoneal (IP) rather than IV to achieve maximum concentrations at the site of infection. Antibiotics can be administered IP intermittently as a single large dose in one exchange per day or continuously as multiple smaller doses with each exchange. Intermittent administration requires at least 6 hours of dwell time in the peritoneal cavity to allow for adequate systemic absorption and provides adequate levels to cover the 24-hour period. However, continuous administration is better suited for PD modalities that require more frequent exchanges (less than 6-hour dwell time). The reader should refer to the ISPD guidelines for dosing recommendations for IP antibiotics in CAPD and automated PD patients.49 The dose of the antibiotics should be increased by 25% for patients with residual renal function who are able to produce more than 100 mL urine output per day. 

Exit-site infections present with purulent drainage at the site. Erythema may or may not be present with an exit-site infection. Tunnel infections are generally an extension of the exit-site infection and rarely occur alone. Symptoms of a tunnel infection may include tenderness, edema, and erythema over the tunnel pathway, but are often asymptomatic. Ultrasound can be used to detect tunnel infections in asymptomatic patients. Exit-site infections caused by S. aureus and P. aeruginosa often spread to tunnel infections and are the most common causes of catheter-infection-related peritonitis. 

Treatment Exit-site infections may be treated immediately with empiric coverage, or treatment may be delayed until cultures return. Empiric treatment of catheter-related infections should cover S. aureus. Coverage for P. aeruginosa should also be included if the patient has a history of infections with this organism.49 Cultures and sensitivity testing are particularly important in tailoring antibiotic therapy for catheter-related infections to ensure eradication of the organism and prevent recurrence or related peritonitis. 

Prevention of peritonitis and catheter-related infections starts when the catheter is placed. The exit site should be properly cared for until it is well healed before it can be used for PD. Patients should receive proper instructions for care of the catheter during this time period, which can last up to 2 weeks. Patients should also be instructed on the proper techniques to use for dialysate exchanges to minimize the risk of infections during exchanges, which is the most common cause of peritonitis. 

Intranasal S. aureus increases the risk of S. aureus exit-site infections, tunnel infections, peritonitis, and subsequent catheter loss.49 Several measures have been used to decrease the risk of peritonitis caused by S. aureus, including mupirocin cream applied daily around the exit site, intranasal mupirocin cream twice daily for 5 days each month, or rifampin 300 mg orally twice daily for 5 days, repeated every 3 months.49 Mupirocin use is preferred over rifampin to prevent the development of resistance to rifampin, although mupirocin resistance has also been reported.49 Other measures that have been used to decrease both S. aureus and P. aeruginosa infections include gentamicin cream applied twice daily and ciprofloxacin otic solution applied daily to the exit site.49... 

Clinical improvement should be seen within 48 hours of initiating treatment for peritonitis or catheter-related infections. Perform daily inspections of peritoneal fluid or the exit site to determine clinical improvement. Peritoneal fluid should become clear with improvement of peritonitis and erythema and discharge should remit with improvement of catheter-related infections. If no improvement is seen within 48 hours, obtain additional cultures and cell counts to determine the appropriate alterations in therapy. 

Evaluate the patient for complications associated with dialysis. Does the patient develop hypotension or cramps during hemodialysis Does the patient have symptoms consistent with peritonitis or a catheter infection ... 

Piraino B, Bailie GR, Bernardini J, et al. ISPD guidelines/recommen-dations peritoneal dialysis-related infections recommendations 2005 update. Perit Dial Int 2005 25 107-131. 

Peritonitis may be classified as primary, secondary, or tertiary. Primary peritonitis, also called spontaneous bacterial peritonitis, is an infection of the peritoneal cavity without an evident source of bacteria from the abdomen.1,2 In secondary peritonitis, a focal disease process is evident within the abdomen. Secondary peritonitis may involve perforation of the gastrointestinal (GI) tract (possibly because of ulceration, ischemia, or obstruction), postoperative peritonitis, or posttraumatic peritonitis (e.g., blunt or penetrating trauma). Tertiary peritonitis occurs in critically ill patients and is infection that persists or recurs at least 48 hours after apparently adequate management of primary or secondary peritonitis. 

O Primary peritonitis develops in up to 25% of patients with alcoholic cirrhosis.3 Patients undergoing continuous ambulatory peritoneal dialysis (CAPD) average one episode of peritonitis every 2 years.4 Secondary peritonitis may be caused by perforation of a peptic ulcer traumatic perforation of the stomach, small or large bowel, uterus, or urinary bladder appendicitis pancreatitis diverticulitis bowel infarction inflammatory bowel disease cholecystitis operative contamination of the peritoneum or diseases of the female genital tract such as septic abortion, postoperative uterine infection, endometritis, or salpingitis. Appendicitis is one of the most common causes of intraabdominal infection. In 1998, 278,000 appendectomies were performed in the United States for suspected appendicitis.5... 

Many of the manifestations of intraabdominal infections, particularly peritonitis, result from cytokine activity. Inflammatory cytokines are produced by macrophages and neutrophils in... 

Bacteria such as E. coli appear responsible for the early mortality from peritonitis, whereas anaerobic bacteria are major pathogens in abscesses, with B. fragilis predominating.15 Enterococcus can be isolated from many intraabdominal infections in humans, but its role as a pathogen is not clear.16... 

Intraabdominal infections have a wide spectrum of clinical features. Peritonitis usually is easily recognized, but intraabdominal abscess often may continue for long periods of time. Patients with primary and secondary peritonitis present quite differently. 

The treatment of intraabdominal infection most often requires the coordinated use of three major modalities (1) prompt drainage, (2) support of vital functions, and (3) appropriate antimicrobial therapy to treat infection not eradicated by surgery. Antimicrobials are an important adjunct to drainage procedures in the treatment of secondary intraabdominal infections however, the use of antimicrobial agents without surgical intervention usually is inadequate. For most cases of primary peritonitis, drainage procedures may not be required, and antimicrobial agents become the mainstay of therapy. 

In the early phase of serious intraabdominal infections, attention should be given to preserving major organ system function. With generalized peritonitis, large volumes of intravenous (IV) fluids are required to maintain intravascular volume, to improve cardiovascular function, and to ensure adequate tissue perfusion and oxygenation. Adequate urine output should be maintained to ensure appropriate fluid resuscitation and to preserve renal function. A common cause of early death is hypovolemic shock caused by inadequate intravascular volume expansion and tissue perfusion. 

Primary peritonitis is treated with antimicrobials and rarely requires drainage. Secondary peritonitis requires surgical removal of the inflamed or gangrenous tissue to prevent further bacterial contamination. If the surgical procedure is sub-optimal, attempts are made to provide drainage of the infected or gangrenous structures. 

Intraperitoneal (IP) administration of antibiotics is preferred over IV therapy in the treatment of peritonitis that occurs in patients undergoing continuous ambulatory peritoneal dialysis (CAPD). The International Society of Peritoneal Dialysis (ISPD) recently revised its guidelines for the diagnosis and pharmacotherapy of peritoneal dialysis (PD)-associated infections.24 The guidelines provide dosing recommendations for intermittent and continuous therapy based on the modality of dialysis [CAPD or automated peritoneal dialysis (APD)] and the extent of the patient s residual renal function. 

Acute intraabdominal contamination, such as after a traumatic injury, may be treated with a very short course (24 hours) of antimicrobials.25 For established infections (i.e., peritonitis or intraabdominal abscess), an antimicrobial course limited to 5 to 7 days is justified. Under certain conditions, therapy for longer than 7 days would be justified, e.g., if the patient remains febrile or is in poor general condition, when relatively resistant bacteria are isolated, or when a focus of infection in the abdomen still may be present. For some abscesses, such as pyogenic liver abscess, antimicrobials may be required for a month or longer. 

Whether diagnosed with primary or secondary peritonitis, monitor the patient for relief of symptoms. Once antimicrobials are initiated and the other important therapies described earlier are used, most patients should show improvement within 2 to 3 days. Successful antimicrobial therapy with resolution of infection will result in decreased pain, manifested as resolution of abdominal guarding and decreased use of pain medications over time. The patient should not appear in distress, with the exception of recognized discomfort and pain from incisions, drains, and a nasogastric tube. 

For patients with primary peritonitis, if peritoneal dialysate cultures were positive initially, repeat cultures should be negative. For patients with secondary peritonitis, monitor the amount of fluid draining if a drain was placed. The volume of drainage should lessen as the infection resolves. Repeat abdominal radiographs should return to normal. 

Treatment regimens for intraabdominal infection can be judged as successful if the patient recovers from the infection without recurrent peritonitis or intraabdominal abscess and without the need for additional antimicrobials. A regimen can be considered unsuccessful if a significant adverse drug reaction occurs, reoperation or percutaneous drainage is necessary, or patient improvement is delayed beyond 1 or 2 weeks. 

Dougherty SH. Antimicrobial culture and susceptibility testing has little value for routine management of secondary bacterial peritonitis. Clin Infect Dis 1997 25(suppl 2) S258-261. 

Erosion of liver abscesses can result in peritonitis. Liver abscesses that are located in the right lobe can spread to the lungs and pleura. Pericardial infection, although rare, may be associated with extension of the amebic abscesses from the liver. 

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