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Adhesive Biomaterials for Tissue Repair and Reconstruction
Published in Severian Dumitriu, Valentin Popa, Polymeric Biomaterials, 2020
The limitations of traditional approaches for wound closure are best illustrated by current rates of adverse events following common surgical procedures. For example, gastrointestinal anastomotic closures demonstrate a leakage rate of 3%–15%, resulting in dire clinical consequences (infection, hemorrhage) and a 2%–3% mortality rate for patients undergoing abdominal surgeries [1,2]. Leaking fluids can escape between suture or staple lines; fluids can also leak through needle holes and staple punctures created by the placement of sutures and staples. A slight seepage of intestinal contents can lead to local contamination and infection, abscess formation, and fulminant bacterial peritonitis. Likewise, a small oozing blood vessel can permit significant blood loss. Moreover, in patients undergoing a potentially curative surgery for colorectal cancer, the presence of gastrointestinal anastomotic leakage is associated with a lower 5 year survival rate (44.3% in patients with leakage versus 64.0% in patients without leakage), even when there are no immediate clinical consequences of wound leakage [3]. Failure to achieve robust tissue closure thus carries both short-term and long-term risks.
paniculata (C.B. Clarke) Munir Leaves on Various Gastric Aggressive Factors
Published in Parimelazhagan Thangaraj, Phytomedicine, 2020
P. S. Sreeja, K. Arunachalam, Parimelazhagan Thangaraj
The etiology of the gastric ulcer is pluricausal. An imbalance between antagonistic and protective factors starts the ulcerogenic process, and the gastric ulcers arise due to the exposure of the gastric mucosa constantly to harmful stimuli, such as acid-peptic juice. The presence of the excess gastric acid secretion and pepsin are one among the endogenous effects of the ulcer. The gastric acid gets secreted from the parietal cells of the epithelial layer into the lumen, which is activated by many factor receptors, like histamine, acetylcholine, and gastrin that receive the stimulus from the central nervous system by stress, smell, taste, etc. of various substances. This gastric acid activates the conversion of the pepsinogen into pepsin optimally at pH < 3.5, whereas at pH > 5, this gets inactivated/denatured. Hence, at low pH (high H+ ions), the highest secretion of acid and pepsin causes mucus and cellular damage. At this situation, the mucosal lining is breached and the epithelial layer gets perforated, which eventually results in the penetration of the stomach content, including acidic fluid into the abdominal cavity, causing intense pain, local peritonitis, that can become generalized, and finally leads to a systemic inflammatory response syndrome and sepsis, with the risk of multiorgan failure and death. In the presence of stress, there is an increase in the secretion of gastric acid and pepsin, with the involvement of two pathways, the hypothalamic-pituitary-adrenal axis and the sympathoadrenal system. Besides, the presence of glucocorticoids and catecholamines in the microcirculation of gastric tissue also provokes ischemia and tissue necrosis in the stomach, consequently, the appearance of gastric ulcers (Saavedra et al. 2011; Yandrapu and Sarosiek 2015).
Potential clinical value of catheters impregnated with antimicrobials for the prevention of infections associated with peritoneal dialysis
Published in Expert Review of Medical Devices, 2023
Hari Dukka, Maarten W. Taal, Roger Bayston
Peritonitis is a very common complication of PD and is associated with significant risk of technique failure and transfer to HD and also increased mortality. Global peritonitis rates are variable, ranging between 0.16 episodes per patient-year to 0.4 episodes per patient-year [16]. The International Society of Peritoneal Dialysis (ISPD) recommendation is to keep peritonitis rates below 0.4 episodes per patient-year. The signs and symptoms of peritonitis commonly include abdominal pain, cloudy dialysis fluid, fever, diarrhea, and vomiting. Diagnostic criteria for peritonitis are: 1) clinical signs and symptoms of peritonitis present, 2) dialysis effluent white cell count >100/µL or >0.1 × 109/L (after a dwell time of at least 2 hours), with >50% polymorphonuclear leukocytes, 3) positive bacterial culture of dialysis effluent. A diagnosis is made if at least two criteria are met [16]. There are several risk factors for developing PD peritonitis, including constipation, inadequate hand hygiene, medical procedures such as colonoscopy, colposcopy, and dental work [16,17]. Any surgical procedure holds similar risks and it is recommended to drain dialysis fluid completely from peritoneum before any procedure, to avoid bacterial translocation into the dialysis fluid. Other factors associated with the risk of peritonitis are obesity, hypoalbumiemia, hypokalemia, chronic obstructive pulmonary disease, and smoking. Nephrology centers provide training to patients to enable them to perform dialysis fluid exchanges using an aseptic technique, but as the process involves manually connecting the bags to the PD catheter there remains a risk of introduction of organisms by touch contamination [17]. Being a new starter on PD is another risk factor. The risk of developing peritonitis was 55% in the first year after starting PD and 89% within the first 3 years in one study [18]. This may be due to lack of patient experience in doing PD using aseptic techniques.