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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The histologic spectrum, pathogenesis, and clinical correlates of tracheobronchial and pulmonary lesions were studied by autopsy in six children and 27 adult burn victims. The burns covered a mean total body surface area of 57.7 +/- 23%. The mean survival time was 17.6 +/- 14.3 days. Patients over 60 years tended to survive longer than younger adults, but older patients had less extensive burns (P less than .01). Moderate or severe renal failure was an important clinical complication in 19 patients (58%). Diffuse alveolar damage (DAD) was observed in 16 patients, acute bronchopneumonia in seven patients, and necrotizing pneumonia in seven patients. Both DAD and pneumonia coexisted in 11 patients. Children most consistently developed pneumonia, 6 out of 6 versus 4 out of 17 younger adults (P less than .05). Factors which may have contributed to the pathogenesis of DAD included septicemia (12 patients), hypotension (nine patients), necrotizing pneumonia (six patients), and oxygen toxicity (four patients), in addition to the common presence of inhalational injury. The onset of DAD appeared late in eight patients with long survival periods, suggesting causal factors other than inhalational injury. However, survival rate did not differ in patients with or without DAD, and there was no correlation between DAD and the extent of burns. Airway lesions reflected the length of survival and showed the following sequence of changes: (1) mucosal necrosis and denudation, (2) acute inflammation and ulceration, and (3) squamous metaplasia. Endotracheal intubation injury and superinfection were confounding factors beyond the first few days of survival.
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PMID:Respiratory tract pathology in patients with severe burns. 224 34

Despite improved surgical techniques and advances in immunosuppressive therapy, posttransplant mortality rates remain significantly high in lung transplant patients. Since 1985, 3 of 6 single lung recipients, 3 of 3 double lung recipients, and 4 of 7 heart-lung recipients have died and undergone autopsy. We reviewed the autopsy findings in these patients to determine the type and frequency of pathologic processes associated with mortality. One or more infectious processes was found in every patient at autopsy. Gram-negative bacterial pneumonia and sepsis, found in 7 and 8 of 10 autopsy cases, respectively, were by far the most frequent contributing factors to mortality. Epstein-Barr virus infection was demonstrated in one patient using polymerase chain reaction amplification. Acute transplant rejection was found in only 2 patients and therefore is a much less common factor in the death of lung transplant recipients. Diffuse alveolar damage occurred in 6 patients and bronchiolitis obliterans occurred in 3 patients. These latter two processes may have different etiologies in different patients.
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PMID:Factors contributing to mortality in lung transplant recipients: an autopsy study. 265 22

Diffuse alveolar damage (DAD) is usually considered a generalized lung process. During five years the authors observed 83 patients with generalized DAD in 827 adult autopsies (10.1%) and 10 patients with identical, but localized, lesions. The authors propose the term regional alveolar damage (RAD) to designate localized "DAD." RAD was unilateral in six patients and most frequently involved the upper lobe. All ten patients had chronic systemic diseases and presented with life-threatening illnesses. The probable causes of RAD were multifactorial and included hypotensive shock, septicemia, pneumonia, hyperoxia, and pancreatitis. All patients developed respiratory failure, requiring supplemental oxygen and, in nine patients, mechanical ventilation. Chest roentgenograms revealed alveolar or combined alveolar and interstitial infiltrates that corresponded to the lesions found at autopsy. The reasons for localization of RAD within the lung are unclear, but the presence of proliferative lesions and frequent involvement of the upper lobe suggests that RAD is not simply an early phase of DAD and implicates additional pathogenetic factors.
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PMID:Regional alveolar damage (RAD). A localized counterpart of diffuse alveolar damage. 266 70

A 42-year-old, African-American man presented with a 2-month history of weight loss and fever for 2 weeks. Presumptive diagnoses of human immunodeficiency virus infection (HIV) and acquired immunodeficiency syndrome were made on the basis of a CD4 lymphocyte count of 23 lymphocytes/mL. Chest x-ray revealed right paratracheal adenopathy and a miliary pattern. The etiology of the patient's pulmonary infection was not known, but tuberculosis was an important consideration. Over 5 days, the pulmonary infection progressed and was complicated by acute respiratory distress syndrome (ARDS), septic shock, and death, despite vigorous antibiotic and supportive therapy. Serologic tests for HIV infection were reported as positive after the patient's demise. The etiology of the patient's pulmonary infection, ARDS, and sepsis was not known until autopsy study revealed enumerable yeast-like cells of Blastomyces dermatitidis in the extensively consolidated lungs and in disseminated foci of infection in most other major organs. Diffuse alveolar damage was closely associated with the pulmonary blastomycosis. Electron microscopic study of the yeast-like cells of B. dermatitidis in the autopsy lung obtained and fixed 5 days after the patient's death revealed excellent preservation of viable organisms.
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PMID:Disseminated blastomycosis and acquired immunodeficiency syndrome: a case report and ultrastructural study. 888 26

Immunological interventions in endotoxemia and sepsis have been tested in experimental and clinical studies. Our group evaluated the effects of an immunoglobulin (Ig)M-enriched solution in an established model of Gram-negative bacteraemia. Ten New Zealand White rabbits (2-3 kg) were randomized to a treatment or control group. In both groups, LPS was infused at a rate of 40 mg kg(-1) h(-1). Immunoglobulin M-enriched solution (Pentaglobin; 2 mL kg(-1) h(-1)) was applied in the intervention group 15 min after beginning LPS infusion. 1 x 10(8) colony forming units of Escherichia coli were injected 30 min after LPS infusion was commenced. Baseline hemodynamic and respiratory parameters, blood E. coli concentration (30 min before and 1, 15, 30, 60, 90, 120, and 180 min after E. coli injection), polymorphonuclear neutrophil oxidative burst activity, and phagocytosis dead space (both 30 min before and 1, 15, 60, 120, and 180 min postinjection) were measured. Ex vivo phagocytosis activity was measured in a separate experiment and evaluated by electron microscopy. Diffuse alveolar damage (DAD) was measured. Organ colonization (kidney, lung, liver, spleen) was assessed in aseptic organ samples. Hemodynamic parameters did not differ between the two groups. Bacterial blood clearance was not influenced by application of IgM-enriched solution. Liver and spleen colonization was significantly reduced in the IgM group. Immunoglobulin M-enriched solution reduced in vitro residual phagocytosis capacity at 30, 90, and 180 min and improved respiratory burst at 180 min. Correspondingly, ex vivo phagocytosis activity as documented by electron microscopy was increased in the IgM group. The sum of all weighted DAD scores (except overdistension) was significantly better in the IgM group (23+/-5 vs. 30+/-8). Immunoglobulin M-enriched solution significantly improved six of seven DAD score parameters and reduced liver and spleen E. coli count. Residual phagocytosis capacity was significantly decreased in the IgM group, whereas burst activity was increased, pointing to an increased in vivo phagocytosis efficiency. Short-term IgM-enriched solution intervention had an especially beneficial effect on LPS-induced pulmonary histological changes.
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PMID:Effects of IGM-enriched solution on polymorphonuclear neutrophil function, bacterial clearance, and lung histology in endotoxemia. 1766 45