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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bacterial translocation (BT) occurs transiently after thermal injury and may result from an ischemic intestinal insult. To evaluate continued intestinal ischemia in the ongoing BT associated with sepsis after injury, rats were randomized to (1) 30% burn injury with Pseudomonas wound infection (BI), (2) BI + fluid resuscitation (BI + Fluid), (3) BI after allopurinol pretreatment to inhibit xanthine oxidase (BI + Allo), or (4) BI after azapropazone pretreatment to inhibit neutrophil degranulation (BI + Aza). On postburn days (PBD) 1, 4, and 7, animals were studied for evidence of BT and intestinal lipid peroxidation. BI + Fluid, BI + Allo, and BI + Aza significantly (p less than 0.05) reduced rates of BT and ileal lipid peroxidation acutely after thermal injury (PBD 1) compared to BI. All four groups had equally high rates of BT associated with the onset of sepsis (PBDs 4 and 7), without evidence of further intestinal lipid peroxidation. These data indicate that the chronic gut barrier failure associated with sepsis after injury occurs independently of continued intestinal ischemia.
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PMID:Differential pathophysiology of bacterial translocation after thermal injury and sepsis. 206 68

Thermal injury is associated with functional alterations of multiple organ systems, including the gastrointestinal tract. To study the effects of ongoing infection after thermal injury on bowel mass, composition, and blood flow, male Wistar rats were randomized to receive either 30% scald burn, 30% scald burn with Pseudomonas aeruginosa wound inoculation, sham burn, or sham burn with pair feeding to burned and infected animals. On days 3 and 7 after injury, intestinal blood flow was measured with 51Cr-labeled microspheres, and intestinal mass and composition were analyzed. Burned and infected animals demonstrated a chronic loss of small bowel mass not seen in burned animals without infection by day 7 after injury. Compositional alterations of the small bowels of burned and infected animals included protein wasting similar to but occurring earlier than that seen with anorexia alone and significantly decreased deoxyribonucleic acid and ribonucleic acid content, whereas tissue water content remained unchanged. These chronic intestinal alterations in the burned and infected group could not be explained by ongoing ischemia because intestinal blood flow in these animals was not significantly altered at either time point, implying mediation by other pathophysiologic mechanisms.
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PMID:Additive effects of thermal injury and infection on the small bowel. 236 Jan 91

Necrotizing dermatitis in patients being treated with cancer chemotherapeutic agents can be of several types. Microbial causes can include a variety of bacteria and fungi, the most common being Pseudomonas aeruginosa. Gangrene from occlusive causes is not uncommon among cancer patients with coexisting atheromatous, thromboembolic, or obliterative vascular disease. Toxic gangrene is most commonly caused by extravasation of intravenously administered cytotoxic antineoplastic drugs but has also been associated with the use of coumarin congeners and the bite of the brown recluse spider. Pyoderma gangrenosum is an idiopathic condition that has been reported in association with myeloproliferative disorders. Finally, necrosis can be caused by the neoplasm itself, when its growth is so great that blood vessels are compressed and ischemia of the surrounding tissue results.
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PMID:Necrotizing dermatitis in patients receiving cancer chemotherapy. 346 38

The normal bacterial flora of the skin represents an important host defense mechanism against invasion by potentially pathogenic organisms. This flora is primarily composed of aerobic diphtheroids (Corynebacterium species), anaerobic diphtheroids (Propriono-bacterium acnes), and coagulase-negative staphylococci. Gram-negative bacilli may be present in limited numbers in intertriginous areas. Localized cutaneous infections occur in ostensibly normal hosts, often after trivial trauma, examples being streptococcal or staphylococcal impetigo, staphylococcal furunculosis, or more unusual infections due to agents such as Mycobacterium marinum. When the skin is injured more extensively by trauma, burns, ischemia with ulceration, or iatrogenic manipulations, or when host immunologic defenses are suppressed, more severe infections are likely to supervene, and the threat of systemic dissemination of infecting microorganisms increases. Cutaneous infection in immunosuppressed hosts may involve the same pyogenic bacteria that affect normal subjects or it may involve a variety of opportunistic invaders, including herpes viruses, gram-negative bacilli, mycobacteria, and deep or superficial mycoses. The skin may also be affected by infections whose primary site lies elsewhere in the body. Cutaneous manifestations may be secondary to hematogenous seeding of the causative agent or to the effects of toxins or immune complexes. Certain microbial agents may initiate a wide variety of cutaneous lesions, depending on route of infection and the status of the host. Thus, cutaneous lesions attributable to Pseudomonas aeruginosa range from "green nail syndrome" and self-limited folliculitis to ecthyma gangrenosum. Similarly, group A streptococci may produce pyoderma, cellulitis, lymphangitis, erysipelas, or scarlet fever. We recently described a syndrome of recurrent cellulitis in the saphenous vein donor extremities of patients who have undergone coronary artery bypass grafts. Most patients have associated tinea pedis. The pathophysiologic aspects of this syndrome are probably multifactorial, involving compromise of lymphatic or venous drainage, bacterial infection, elaboration of bacterial toxins, and hypersensitivity to bacterial or fungal products, or both. Coagulase-negative staphylococci are exhibiting a more prominent pathogenic potential than heretofore. When they infect immunosuppressed hosts or patients with indwelling intravascular catheters or cardiac prostheses, coagulase-negative staphylococci may cause life-threatening disease.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cutaneous infections: microbiologic and epidemiologic considerations. 637 67

Chronic, excruciatingly painful ulcerations of the lower extremities in patients with homozygous sickle cell anemia (HbSS) present a frustrating clinical problem for the reconstructive surgeon. Despite adequate wound care and skin grafting, there is a dismally high incidence of recurrence. Furthermore, there is a paucity of reliable locoregional fasciocutaneous, muscle, and myocutaneous flaps in the ankle region. Free-tissue transfer has become the procedure of choice for reconstruction of the lower third of the leg. However, in sickle cell anemia, does the obligate period of flap ischemia inherent in free-tissue transfer inevitably doom a flap to failure? We present our multidisciplinary experience over 55 months with five free flaps in four homozygous sickle cell anemia patients 21 to 38 years old who had chronic nonhealing leg ulcerations. Special perioperative measures included exchange transfusion to lower hemoglobin S to below 30 percent, maintaining the hematocrit at 31 to 35 percent, intraoperative flap washout and perfusion with warm heparinized saline-dextran solution, administration of dextran and aspirin intraoperatively and postoperatively, prophylactic topical and systemic anti-Pseudomonas antibiotics, supplemental oxygen, and warm ambient room temperature. Flaps included the latissimus dorsi muscle (two patients), the temporoparietal fascia (one patient), and "split" omentum for bilateral lower limb salvage (one patient). Successful free-tissue transfer was accomplished in all patients. One patient suffered gradual partial occlusion of the microcirculation by sickled erythrocytes following a transient hypothermic, hypotensive episode. Sufficient flap tissue survived to permit skin grafting with an excellent result. Pseudomonas infection occurred in two patients (three flaps).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lower limb salvage by microvascular free-tissue transfer in patients with homozygous sickle cell disease. 756 93

Success in lung transplantation has been hindered by airway complications, usually as a result of anastomotic ischemia and stenosis. We report our experience with expanding metal stents in managing airway stenoses after lung transplantation. From April 1984 through November 1993, 46 single lung, 5 double lung, and 154 heart-lung transplantations were performed at Papworth Hospital. All patients received immunosuppression with azathioprine, cyclosporine, methylprednisolone, and induction antithymocyte globulin. Fourteen patients (nine single lung, two double lung, and three heart-lung) had an airway stenosis requiring a stent. The most common features were shortness of breath, wheezing or stridor, and a fall in pulmonary function tests (11 patients). Three patients had pneumonia. Airway stenosis was diagnosed on bronchoscopy an average of 61 days after transplantation (range 3 to 245 days). Stent placement occurred an average of 18 days after the diagnosis (range 2 to 84 days). One heart-lung transplant recipient received a silicone rubber stent. All other patients received expanding metal stents. Six patients required multiple stent placements. After stent placement the average increase in the forced expiratory volume in 1 second was 117%. Infection complicated the stenoses in 12 patients. Pseudomonas aeruginosa and Aspergillus fumigatus were the most common pathogens, each occurring in six cases. Multiple pathogens were isolated in seven cases. Three patients died as a direct consequence of their airway problems. Two died of pneumonia despite stenting, and a third died of acute occlusion of the silicone rubber stent. Expanding metal stents are an effective treatment of airway stenoses in lung transplant recipients. Patients with suspected airway problems should be referred for early bronchoscopy with the potential for stent placement.
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PMID:Airway stenoses after lung transplantation: management with expanding metal stents. 780 17

Leukocyte (WBC) adherence to endothelial cells (EC) has been implicated in the pathogenesis of microvascular injury. WBC-EC adherence is largely dependent on interaction between the WBC-CD18 complex and the endothelial ligand, intercellular adhesion molecule-1 (ICAM-1). Administration of monoclonal antibodies directed against CD18 and/or ICAM-1 inhibit WBC-EC adherence and have been reported to modulate ischemia-reperfusion and inflammatory injury. We asked the question, does inhibition of WBC-EC adherence by administration of monoclonal antibody directed against either CD18 (R15.7) or against ICAM-1 (R6.5) increase susceptibility to infection. New Zealand white rabbits were shaved and injected subcutaneously on their dorsum with Staphylococcus aureus (ATCC No. 25923) at two sites each with 10(9), 10(8), 10(7), and 10(6) colony-forming units (CFUs). A second set of rabbits were injected subcutaneously with Pseudomonas aeruginosa (ATCC No. 27853) at two sites each of 10(8) and 10(7) CFUs. Animals were monitored for 1 week with daily determination of weight, temperature, WBC counts, hematocrit, and gross evidence of abscess formation. There were three blinded experimental groups; animals given R15.7 (2.0 mg/kg), animals given R6.5 (2.0 mg/kg), and controls given saline (2.0 ml/kg). Administration of the anti-CD18 antibody, R15.7, resulted in significantly increased rates of abscess formation following innoculation with S. aureus and with P. aeruginosa, compared to controls and to the animals given the antibody to ICAM-1, R6.5. The administration of R6.5 did not increase the incidence or severity of abscess formation.
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PMID:Inhibition of leukocyte adherence and susceptibility to infection. 810 Dec 45

Although many new antibiotics became available for clinical use, intractable bacterial infections are still major cause of morbidity and mortality in surgical patients. The infections are attributable to multiple factors. Surgical stress such as extensive burns and major surgery results in the depressed host-defense function, which is mediated by cytokine responses. Necrotic tissue, ischemia, hematoma, cholelithiasis, foreign bodies, indwelling catheters, intra-tracheal tubes, and other medical devices are local factors making infection resistant to ordinary chemotherapy. Multi-resistant bacteria such as methicillin resistant Staphylococcus aureus and Pseudomonas, and ampicillin resistant enterococci are the main bacteria causing the infections. 32% of surgical specimens isolated two or more bacteria, making the chemotherapy difficult in clinical setting. Importance of surgical drainage, removal of necrosis and the devices are emphasized.
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PMID:[Intractable bacterial infections in surgical patients]. 812 4

P-selectin is a major component in the early interaction between platelets, endothelial cells, and inflammatory cells in the initial phases of the innate immune response. The major ligand for P-selectin is P-selectin glycoprotein ligand-1 (PSGL-1) and this ligand is expressed on the surface of monocyte, lymphocyte, and neutrophil membranes. A truncated form of recombinant human P-selectin glycoprotein ligand-1 has been covalently linked to immunoglobulin G (rPSGL-Ig) and this fusion peptide functions as a competitive inhibitor of PSGL-1. As an inhibitor of neutrophil-endothelial cell adherence, rPSGL-Ig is in early clinical development for the treatment of ischemia reperfusion injury. To determine the potential for deleterious effects from inhibition in P-selectin-mediated neutrophil attachment in the presence of bacterial infection, the effects of therapeutic doses of rPSGL-Ig were tested in three standard laboratory sepsis models. The experimental models included: the murine systemic Listeria monocytogenes infection model, the Pseudomonas aeruginosa bacteremia model in neutropenic rats, and the cecal ligation and puncture (CLP)-induced peritonitis model in rats. Recombinant human PSGL-Ig had no adverse effects on mortality or immune clearance in systemic bacterial infection in any of the three infection models. The PSGL-1 inhibitor did significantly decrease local neutrophil infiltration and bacterial clearance in the peritoneum following CLP, but this did not increase the systemic levels of proinflammatory cytokines, the quantitative levels of bacteremia, or the overall mortality rate following CLP. The results indicate that rPSGL-Ig did not exacerbate infection in these experimental sepsis models.
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PMID:Evaluation of the safety of recombinant P-selectin glycoprotein ligand-immunoglobulin G fusion protein in experimental models of localized and systemic infection. 1130 27

The aim of this study was to report on 8 patients with all different non-ischemic etiologies for portal-venous gas and to discuss this rare entity and its potentially misleading CT findings in context with a review of the literature. The CT examinations of eight patients who presented with intrahepatic portal-venous gas, unrelated to bowel ischemia or infarction, were reviewed and compared with their medical records with special emphasis on the pathogenesis and clinical impact of portal-venous gas caused by non-ischemic conditions. The etiologies for portal-venous gas included: abdominal trauma ( n=1); large gastric cancer ( n=1); prior gastroscopic biopsy ( n=1); prior hemicolectomy ( n=1); graft-vs-host reaction ( n=1); large paracolic abscess ( n=1); mesenteric recurrence of ovarian cancer superinfected with clostridium septicum ( n=1); and sepsis with Pseudomonas aeruginosa ( n=1). The clinical outcome of all patients was determined by their underlying disease and not negatively influenced by the presence of portal-venous gas. Although the presence of portal-venous gas usually raises the suspicion of bowel ischemia and/or intestinal necrosis, this CT finding may be related to a variety of non-ischemic etiologies and pathogeneses as well. The knowledge about these conditions may help to avoid misinterpretation of CT findings, inappropriate clinical uncertainty and unnecessary surgery in certain cases.
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PMID:Portal-venous gas unrelated to mesenteric ischemia. 1204 50


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