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Surgical Endoscopy Jan 2011Laparoscopic surgery has been incorporated into common surgical practice. The peritoneum is an organ with various biologic functions that may be affected in different... (Review)
Review
BACKGROUND
Laparoscopic surgery has been incorporated into common surgical practice. The peritoneum is an organ with various biologic functions that may be affected in different ways by laparoscopic and open techniques. Clinically, these alterations may be important in issues such as peritoneal metastasis and adhesion formation.
METHODS
A literature search using the Pubmed and Cochrane databases identified articles focusing on the key issues of laparoscopy, peritoneum, inflammation, morphology, immunology, and fibrinolysis.
RESULTS
Laparoscopic surgery induces alterations in the peritoneal integrity and causes local acidosis, probably due to peritoneal hypoxia. The local immune system and inflammation are modulated by a pneumoperitoneum. Additionally, the peritoneal plasmin system is inhibited, leading to peritoneal hypofibrinolysis.
CONCLUSION
Similar to open surgery, laparoscopic surgery affects both the integrity and biology of the peritoneum. These observations may have implications for various clinical conditions.
Topics: Acidosis; Animals; Carbon Dioxide; Cell Adhesion Molecules; Cell Hypoxia; Cytokines; Epithelium; Fibrinolysin; Fibrinolysis; Humans; Intercellular Signaling Peptides and Proteins; Laparoscopy; Macrophages, Peritoneal; Mice; Neoplasm Seeding; Peritoneal Cavity; Peritoneal Neoplasms; Peritoneum; Peritonitis; Pneumoperitoneum, Artificial; Tissue Adhesions; Wound Healing
PubMed: 20552372
DOI: 10.1007/s00464-010-1139-2 -
Annals of Surgery Jul 1996The authors review current definition, classification, scoring, microbiology, inflammatory response, and goals of management of secondary peritonitis. (Review)
Review
OBJECTIVE
The authors review current definition, classification, scoring, microbiology, inflammatory response, and goals of management of secondary peritonitis.
SUMMARY BACKGROUND DATA
Despite improved diagnostic modalities, potent antibiotics, modern intensive care, and aggressive surgical treatment, up to one third of patients still die of severe secondary peritonitis. Against the background of current understanding of the local and systemic inflammatory response associated with peritonitis, there is growing controversy concerning the optimal antibiotic and operative therapy, intensified by lack of properly conducted randomized studies. In this overview the authors attempt to outline controversies, suggest a practical clinical approach, and highlight issues necessitating further research.
METHODS
The authors review the literature and report their experience.
RESULTS
The emerging concepts concerning antibiotic treatment suggest that less-in terms of the number of drugs and the duration of treatment-is better. The classical single operation for peritonitis, which obliterates the source of infection and purges the peritoneal cavity, may be inadequate for severe forms of peritonitis; for the latter, more aggressive surgical techniques are necessary to decompress increased intra-abdominal pressure and prevent or treat persistent and recurrent infection. The widespread acceptance of the more aggressive and demanding surgical methods has been hampered by the lack of randomized trials and reportedly high associated morbidity rates.
CONCLUSIONS
Sepsis represents the host's systemic inflammatory response to bacterial peritonitis. To improve results, both the initiator and the biologic consequences of the peritoneal infective-inflammatory process should be addressed. The initiator may be better controlled in severe forms of peritonitis by aggressive surgical methods, whereas the search for methods to abort its systemic consequences is continuing.
Topics: Abdomen; Abscess; Anti-Bacterial Agents; Combined Modality Therapy; Humans; Peritonitis
PubMed: 8678610
DOI: 10.1097/00000658-199607000-00003 -
Frontiers in Immunology 2024Peritoneal dialysis is a widely used method for treating kidney failure. However, over time, the peritoneal structure and function can deteriorate, leading to the... (Review)
Review
Peritoneal dialysis is a widely used method for treating kidney failure. However, over time, the peritoneal structure and function can deteriorate, leading to the failure of this therapy. This deterioration is primarily caused by infectious and sterile inflammation. Sterile inflammation, which is inflammation without infection, is particularly concerning as it can be subtle and often goes unnoticed. The onset of sterile inflammation involves various pathological processes. Peritoneal cells detect signals that promote inflammation and release substances that attract immune cells from the bloodstream. These immune cells contribute to the initiation and escalation of the inflammatory response. The existing literature extensively covers the involvement of different cell types in the sterile inflammation, including mesothelial cells, fibroblasts, endothelial cells, and adipocytes, as well as immune cells such as macrophages, lymphocytes, and mast cells. These cells work together to promote the occurrence and progression of sterile inflammation, although the exact mechanisms are not fully understood. This review aims to provide a comprehensive overview of the signals from both stromal cells and components of immune system, as well as the reciprocal interactions between cellular components, during the initiation of sterile inflammation. By understanding the cellular and molecular mechanisms underlying sterile inflammation, we may potentially develop therapeutic interventions to counteract peritoneal membrane damage and restore normal function.
Topics: Humans; Peritoneal Dialysis; Peritoneum; Animals; Stromal Cells; Cell Communication; Inflammation; Peritonitis
PubMed: 38779674
DOI: 10.3389/fimmu.2024.1387292 -
American Journal of Physiology. Renal... Jun 2021Peritonitis, due to a fungal or bacterial infection, leads to injury of the peritoneal lining and thereby forms a hazard for the long-term success of peritoneal dialysis...
Peritonitis, due to a fungal or bacterial infection, leads to injury of the peritoneal lining and thereby forms a hazard for the long-term success of peritoneal dialysis (PD) and remains a lethal complication in patients with PD. This study investigated whether C1 inhibitor (C1-INH) could protect against the progression of peritoneal injuries with five daily administrations of zymosan after mechanical scraping of the rat peritoneum to mimic fungal peritonitis. Severe peritoneal injuries were seen in this model, accompanied by fibrinogen/fibrin exudation and peritoneal deposition of complement activation products such as activated C3 and C5b-9. However, intraperitoneal injection of C1-INH decreased peritoneal depositions of activated C3 and C5b-9, ameliorated peritoneal thickening, reduced the influx of inflammatory cells, and prevented the production of peritoneal fibrous layers with both one and two doses of C1-INH each day. Our results suggest that C1-INH might be useful to protect against peritoneal injuries after causes of peritonitis such as fungal infection. This clinically available agent may thus help extend the duration of PD. Peritoneal injuries associated with peritonitis comprise an important issue to prevent long-term peritoneal dialysis (PD) therapy. Here, we showed that C1 inhibitor (C1-INH), as an anticomplement agent, protected against peritoneal injuries in a peritonitis animal model related to fungal infection. Therefore, C1-INH might be useful to protect against peritoneal injuries after peritonitis due to fungal infection. This clinically available agent may thus help extend the duration of PD.
Topics: Animals; Complement C1 Inhibitor Protein; Epithelial Cells; Epithelium; Fibrin; Fibrinogen; Male; Peritoneum; Peritonitis; Rats; Rats, Sprague-Dawley; Zymosan
PubMed: 33818127
DOI: 10.1152/ajprenal.00600.2020 -
Postgraduate Medical Journal Jun 2007Spontaneous bacterial peritonitis (SBP) is the infection of ascitic fluid in the absence of any intra-abdominal, surgically treatable source of infection. Despite timely... (Review)
Review
Spontaneous bacterial peritonitis (SBP) is the infection of ascitic fluid in the absence of any intra-abdominal, surgically treatable source of infection. Despite timely diagnosis and treatment its reported incidence in ascitic patients varies between 7-30%. Ascitic paracentesis remains the chief diagnostic procedure. Automated cell counters have the same diagnostic accuracy as the manual measurement of white cells. Lately, the use of leucocyte reagent strips (dipsticks) has emerged as a useful alternative. Examination of the fluid is not complete unless the sample is inoculated in blood culture bottles. Treatment is currently with third-generation cephalosporins or oral quinolones. Following a single episode of SBP patients should have long term antibiotic prophylaxis.
Topics: Albumins; Anti-Bacterial Agents; Bacterial Infections; Humans; Peritonitis
PubMed: 17551068
DOI: 10.1136/pgmj.2006.056168 -
The Journal of Vascular Access Nov 2022Peritoneal dialysis associated infections are common and associated with high morbidity and mortality, if not treated in a timely manner. is an uncommon pathogen in... (Review)
Review
Peritoneal dialysis associated infections are common and associated with high morbidity and mortality, if not treated in a timely manner. is an uncommon pathogen in peritoneal dialysis associated infections, but is resistant to standard antimicrobial therapies used. Here we present a case of a 56 year-old male with end stage kidney disease on peritoneal dialysis for 7 years who developed a exit-site infection. Peritonitis and peritoneal dialysis catheter tunneled line infections were ruled out and he was treated with linezolid, amikacin, and azithromycin. He required peritoneal dialysis catheter removal and hemodialysis conversion. Antibiotics were de-escalated based on inducibility and antibiotic sensitivities. Linezolid and amikacin were continued for approximately 7 total weeks, with complete resolution of the infection. Further research is needed to refine challenges in the management of exit-site infections, including risk factors for development of , optimal selection of empiric antibiotic therapies, duration of antibiotics, and peritoneal dialysis catheter re-insertion timing.
Topics: Male; Humans; Middle Aged; Mycobacterium abscessus; Linezolid; Amikacin; Azithromycin; Peritoneal Dialysis; Mycobacterium Infections, Nontuberculous; Peritonitis; Anti-Bacterial Agents
PubMed: 33985367
DOI: 10.1177/11297298211015083 -
Mediators of Inflammation 2012The success of peritoneal dialysis (PD) is dependent on the structural and functional integrity of the peritoneal membrane. The mesothelium lines the peritoneal membrane... (Review)
Review
The success of peritoneal dialysis (PD) is dependent on the structural and functional integrity of the peritoneal membrane. The mesothelium lines the peritoneal membrane and is the first line of defense against chemical and/or bacterial insult. Peritonitis remains a major complication of PD and is a predominant cause of technique failure, morbidity and mortality amongst PD patients. With appropriate antibiotic treatment, peritonitis resolves without further complications, but in some PD patients excessive peritoneal inflammatory responses lead to mesothelial cell exfoliation and thickening of the submesothelium, resulting in peritoneal fibrosis and sclerosis. The detrimental changes in the peritoneal membrane structure and function correlate with the number and severity of peritonitis episodes and the need for catheter removal. There is evidence that despite clinical resolution of peritonitis, increased levels of inflammatory and fibrotic mediators may persist in the peritoneal cavity, signifying persistent injury to the mesothelial cells. This review will describe the structural and functional changes that occur in the peritoneal membrane during peritonitis and how mesothelial cells contribute to these changes and respond to infection. The latter part of the review discusses the potential of mesothelial cell transplantation and genetic manipulation in the preservation of the peritoneal membrane.
Topics: Animals; Cell Membrane; Defensins; Epithelium; Fibrosis; Human Umbilical Vein Endothelial Cells; Humans; Inflammation; Nod Signaling Adaptor Proteins; Peritoneal Dialysis; Peritoneum; Peritonitis; Toll-Like Receptors
PubMed: 22577250
DOI: 10.1155/2012/484167 -
Peritoneal Dialysis International :... 2016♦
UNLABELLED
♦
BACKGROUND
Burkholderia cepacia is a hardy bacterium with intrinsic resistance to multiple antibiotics and high transmissibility. Opportunistic healthcare-associated B. cepacia infections among immunocompromised or critically ill patients have been reported, but there is limited data on the clinical characteristics and treatment outcomes of exit-site infection (ESI) in peritoneal dialysis (PD) patients. ♦
PATIENTS AND METHODS
Patients who suffered from B. cepacia ESI from 1 January 2004 to 31 December 2014 were reviewed. The clinical characteristics and treatment outcomes of the patients and the antibiotic susceptibility patterns of the bacterial isolates were analyzed. ♦
RESULTS
Twenty-two patients were included for analysis. Eight patients (36.4%) had medical conditions which impaired host immunity, while 7 (31.8%) had pre-existing skin abnormalities. Three patients (13.6%) progressed to tunnel-tract infection and another 3 patients (13.6%) developed associated peritonitis. Fifteen patients (68.2%) responded to medical treatment while 7 (31.8%) required catheter removal. Eleven patients (50.0%) had recurrent B. cepacia ESI, which occurred at 7.8 months (95% confidence interval [CI] 0.1 - 19.4 months) after the first episode. Most B. cepacia strains were susceptible to ceftazidime (95.5%), piperacillin/tazobactam (95.5%), and piperacillin (90.9%). Besides aminoglycosides (80 - 100%), high rates of resistance were also observed for ticarcillin/clavulanate (90.9%). ♦
CONCLUSION
Burkholderia cepacia ESI is associated with low rates of tunnel-tract infection or peritonitis, but the risk of recurrence is high. Most cases can be managed with medical treatment alone, although one third of patients might require catheter removal.
Topics: Aged; Anti-Bacterial Agents; Burkholderia Infections; Burkholderia cepacia; Catheter-Related Infections; Catheters, Indwelling; Device Removal; Drug Resistance, Bacterial; Female; Humans; Kidney Failure, Chronic; Male; Middle Aged; Peritoneal Dialysis; Peritonitis; Retrospective Studies; Treatment Outcome
PubMed: 26493755
DOI: 10.3747/pdi.2015.00122 -
Digestive Diseases (Basel, Switzerland) 2005Spontaneous bacterial peritonitis (SBP) is a bacterial infection of ascitic fluid in patients with decompensated cirrhosis. The modifier 'spontaneous' distinguishes this... (Review)
Review
Spontaneous bacterial peritonitis (SBP) is a bacterial infection of ascitic fluid in patients with decompensated cirrhosis. The modifier 'spontaneous' distinguishes this from surgical peritonitis. The infecting organisms are usually enteric gram-negatives which have translocated from the bowel. Symptoms of infection occur in most patients with SBP, including fever, abdominal pain, mental status changes, and ileus. A high index of suspicion should exist for SBP in patients with cirrhosis and ascites. Diagnostic abdominal paracentesis can be undertaken with minimal risk and should be performed in all patients admitted to the hospital, during times of worsening clinical appearance, or when gastrointestinal bleeding occurs. The ascitic fluid polymorphonuclear cell count is the most sensitive test in evaluating for infection. Cultures of the ascitic fluid are helpful in identifying the organism and are best performed by bedside injection of blood culture bottles. Ascites total protein, lactate dehydrogenase, and glucose levels can assist in distinguishing SBP from secondary peritonitis. Empirical therapy is recommended after paracentesis if suspicion for infection exists. Cefotaxime is the best-studied antibiotic for this purpose and has excellent penetration into ascites with no nephrotoxicity. Prophylaxis should be limited to high-risk settings. Mortality rates in SBP have declined dramatically, largely due to earlier detection and improved therapy.
Topics: Anti-Bacterial Agents; Ascites; Gram-Negative Bacterial Infections; Humans; Liver Cirrhosis; Paracentesis; Peritonitis; Prognosis
PubMed: 15920324
DOI: 10.1159/000084724 -
The Veterinary Record Apr 2021Parietal fibrinous peritonitis (PFP) is a complication of laparotomy in cattle, consisting of fluid and fibrin accumulation within a fibrous capsule between the parietal... (Review)
Review
BACKGROUND
Parietal fibrinous peritonitis (PFP) is a complication of laparotomy in cattle, consisting of fluid and fibrin accumulation within a fibrous capsule between the parietal peritoneum and the abdominal muscles. Since scientific information on PFP is scarce, we aim to collect available information to help practitioners in its diagnosis and treatment, and to formulate research perspectives.
METHODS
PubMed and GoogleScholar databases were scanned using "cattle" or "bovine", and one of the following keywords: "seroma", "parietal fibrinous peritonitis", "retroperitoneal abscess", or "wound infection".
RESULTS
Although scientific information is often anecdotal, two recent larger studies shed more light on PFP symptoms, diagnosis and treatment. Symptoms vary according to the cavity's localisation and size, and include anorexia, weight loss and an inflammatory status. Rectal palpation is strongly indicative, but the definitive diagnosis is made by ultrasound. Trueperella pyogenes and Escherichia coli are frequently isolated germs, although it remains unclear whether they are primary or secondary agents. Good survival rates were reported after surgical drainage.
CONCLUSION
Although the diagnosis and treatment seem clear, the exact pathogenesis of PFP should be the focus of ongoing research. This can be achieved by epidemiological data analysis focusing on risk factors like surgery technique, housing and ration.
Topics: Animals; Cattle; Cattle Diseases; Laparotomy; Peritonitis
PubMed: 33729566
DOI: 10.1002/vetr.30