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

Septicemia is a rare complication of platelet transfusion. A case is reported of transfusion-associated septicemia in a 66-year-old man who received a 10-unit pool of platelets. During transfusion, he experienced rigors, wheezing, dyspnea, and fever. A total of four blood cultures drawn 10 and 36 hours after discontinuation of the transfusion grew Staphylococcus epidermidis. Culture of the residual platelet pool yielded S. epidermidis with a colony count of 10(5) organisms per mL. Strain identity of all four blood isolates and the platelet pool isolate was confirmed by gel electrophoresis of EcoRI and HindIII restriction digests of whole-cell DNA. There have been 31 prior reported cases of platelet transfusion-associated septicemia, of which 9 have been caused by coagulase-negative staphylococci. Systemic reactions to platelet transfusions should prompt consideration of transfusion-associated bacteremia as the cause.
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PMID:Staphylococcus epidermidis bacteremia from transfusion of contaminated platelets: application of bacterial DNA analysis. 141 88

The natural course of post myocardial infarction ventricular septal defect is towards cardiogenic shock and death. 50% in the first week, over 90% a year latter. Between 1973-1989, 28 patients where operated on. Before surgery 14 patients (53%) where in Killip IV, 5 patients (19%) in III, 5 patients (19%) in II and 2 patients in I. The repair was accomplished under hypothermia and cardioplegia, with the insertion of a Teflon patch to close the defect in 20 patients (70%). Complementary procedures (CABG, Pacemaker, repair of dissections) were performed in 12 patients (47%). Three patients (10%) could not be weaned from the pump; another 10 (36%) died before discharge: 2 with multisystem failure and sepsis, the other 8 with cardiogenic shock (4 with residual VSD). The only independent predictor of operative mortality, by univariate analysis, was preoperatory cardiogenic shock. All 15 survivors (100%) where followed between 5 months and 14.5 years (mean 104.5 months). Two patients died at 4 years, one at 10, another at 10.5 years. The actuarial probability of being alive after discharge was 100% at 4 years, 75% at 5, and 50% at 10 years. At last follow up only 2 patients had mild dyspnea, the remaining where asymptomatic. Surgical treatment provides an opportunity to improve this otherwise dismal survival and offers a surprising good long term result. An early diagnosis and efficient repair, before the onset of cardiogenic shock, should provide better results.
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PMID:[Interventricular rupture following myocardial infarction. Surgical treatment and long-term follow-up]. 147 Jul 42

A 65-year-old man, who had been treated for multiple myeloma (MM) since 1986, was admitted because of loss of consciousness in September 1989. An electrocardiogram taken just before admission showed a sinus arrest, junctional escaped rhythm, and marked bradycardia. The diagnosis of sick sinus syndrome (SSS) was made. Soon a temporary pacemaker was inserted, and the dyspnea ameliorated. However on the second day in the hospital, he had a high fever and Staphylococcus aureus was detected in the cultured blood. A diagnosis of septicemia was made, and the pacemaker was removed. He was then treated with beta-stimulants, but died in November 1989. Necropsy revealed cardiomegaly and microscopic examination showed amyloid deposits in the sinoatrial node, and the walls of the ventricles and coronary arteries. Although amyloidosis is often a complication of MM and the heart is frequently affected, SSS caused by amyloidosis associated with MM is quite unusual. In such patients, the use of a pacemaker is controversial, because amyloid deposits are occasionally accelerated by insertion of a pacemaker and for patients with hematological disorders, septicemia associated with pacemaker insertion may prove fatal.
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PMID:[Sick sinus syndrome caused by amyloidosis associated with multiple myeloma]. 160 20

We report a case of idiopathic crescentic glomerulonephritis with pulmonary hemorrhage associated with anti-myeloperoxidase antibodies (anti-MPO ab). A 74 year-old female was admitted to our hospital because of rapidly progressive glomerulonephritic syndrome and dyspnea with bloody sputum. On admission anti-MPO ab, one of anti-neutrophil cytoplasmic antibodies, were detected but anti-GBM antibodies and immune complexes were not detected. Renal biopsy showed crescentic glomerulonephritis and lung biopsy showed massive alveolar hemorrhage. Both tissue had pauci-immune deposit by immunofluorescence microscopy. Hemodialysis and steroid administration were started. Pulmonary hemorrhage was improved remarkably, but renal failure progressed rapidly to end stage kidney, then hemodialysis was continued. Although subsequent 3 years uneventful maintenance hemodialysis had been performed, she admitted to our hospital again because of progressive dyspnea with hemoptysis after upper respiratory tract infection. On admission anti-MPO ab were detected again and steroid administration was started. Pulmonary hemorrhage was improved with decreased anti-MPO ab titer. While tapering the dosis of steroid, anti-MPO ab again increased and pulmonary hemorrhage recurred. Although pulse methylprednisolone therapy and plasma exchange were performed, respiratory failure progressed rapidly and she died of sepsis. Postmortem examination showed no evidence of systemic vasculitis. In this case, titer of anti-MPO ab was associated with not only idiopathic crescentic glomerulonephritis but also with pulmonary hemorrhage. We tried to detect enzymatically active MPO in serum. Titer of serum MPO was also associated with disease activity and anti-MPO ab. It is suggested that both anti-MPO ab and serum MPO are closely related to the pathogenesis of idiopathic crescentic glomerulonephritis and pulmonary hemorrhage.
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PMID:[A case of anti-myeloperoxidase antibodies-associated idiopathic crescentic glomerulonephritis with pulmonary hemorrhage]. 166 75

An 18-year-old man was admitted to Hamamatsu University Hospital on February 15, 1985, with high fever, vesicular and papular rash involving the skin and mouth, conjunctivitis, productive cough and dyspnea. A diagnosis of Stevens-Johnson syndrome was made by skin biopsy, and chest X-ray showed an infiltrate in the right lower lung filed. Despite treatment with corticosteroids and antibiotics, the mucocutaneous lesions did not heal, and the pneumonia progressed to both lung fields. Because the patient had developed dyspnea, a tracheotomy was performed, mechanical ventilatory support was instituted, and high-dose corticosteroid therapy was started. However, jaundice due to intrahepatic cholestasis, hematuria, hematochezia, sepsis, and subcutaneous and mediastinal emphysema ensued, and the patient died of respiratory failure on March 1. Postmortem examination of the lung demonstrated diffuse alveolar damage. The complement-fixation titer for Mycoplasma was 1:64, compared with a level of less than 1:4 on admission. This case was though to be one of fulminant Mycoplasma pneumoniae infection presenting with Stevens-Johnson syndrome, respiratory failure and other extra-pulmonary complications.
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PMID:[Fulminant mycoplasma pneumoniae infection presenting with Stevens-Johnson syndrome & respiratory failure]. 175 8

In Japan, we experienced the first case of Hafnia alvei septicemia with shock and disseminated intravascular coagulation (DIC) in an adult with postoperative lung cancer. A 63 year-old male, who had been followed up in our department since 1987, was admitted to our hospital with the complaints of fever, hemoptysis and dyspnea on June 25, 1989. After admission, he was treated with sulbactam/cefoperazone 4 g/day intravenously for suspicion of respiratory-tract infection. After antibiotic administration, the fever subsided and the general condition became almost good. The patient experienced fever again after the antibiotic was stopped. For this reason subsequent Clavulanic acid/Amoxicillin, Flomoxef, and Ceftazidime was administered, but was not effective. Therefore septicemia was suspected and blood culture was done. The bacteria isolated from blood culture was identified as Hafnia alvei. Hafnia alvei is a gram-negative organism belonging to the Enterobacteriaceae family and quite rare pathogen in human.
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PMID:[Hafnia alvei septicemia with shock and DIC in an adult with postoperative lung cancer]. 176 1

The case of a 52 year old man, whose initial clinical manifestations were dyspnea, bloodstained sputum and malaise is reported. After the initial cancer hypothesis, a diagnosis of diffuse primary tracheo-bronchial amyloidosis was made. The amyloid substance present was not of A A type and the plasma cells next to the deposits were polyclonal. The piece-meal removal of the masses by bronchoscopy led to profuse bleeding. The patient died with sepsis. The clinical, pathological and therapeutical aspects of lower respiratory tract amyloidosis are reviewed.
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PMID:[Diffuse tracheo-bronchial amyloidosis]. 176 15

Ten patients with severe hematologic malignancies (four with acute leukemia, three with multiple myeloma, one with prolymphocytic leukemia, one with malignant lymphoma and one with blastic crisis of chronic myelogenous leukemia) developed respiratory failure during the period between April 1986 and May 1990. Clinically, the patients manifested high-fever, dyspnea refractory to oxygen therapy, diffuse pulmonary rales and severe hypoxemia without evidence of cardiogenic pulmonary edema. Chest roentgenograms displayed diffuse alveolar infiltrates. Respiratory failure occurred as early as 48 hours and as late as 66 days after the administration of intensive anti-neoplastic chemotherapy. At that time leukocyte count was between 100/microliters and 54,900/microliters. Marked leukocytosis was observed in two patients with AML and PLL. Respiratory failure was preceded by sepsis in one patient with AML and by pneumonia in nine patients. DIC was diagnosed in four patients. All patients treated with high dose methyl prednisolone (mPSL) within 12 hours after the onset of respiratory failure. Only one patient required assisted ventilation. High dose mPSL had significant effect on seven of ten patients. But three patients died from progressive respiratory failure, sepsis, pneumonia and multi-organ failure.
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PMID:[Clinical investigation on acute respiratory failure in patients with severe hematologic malignancy]. 194 22

A guideline for early diagnosis of metabolic disorders affecting central nervous system during neonatal and early infancy was presented. Clinical manifestations associated with inborn errors of metabolism in the neonatal period are poor feeding, vomiting, diarrhea, abnormalities in muscle tonus, dyspnea, convulsion, coma and so on, and these are not specific to each disorder. However, such symptoms or signs as described below have often intimate relation to metabolic disorders: (1) previous children died of undetermined causes during early infancy; (2) complication of sepsis; (3) onset in the early neonatal period; (4) developmental and growth retardation. When newborns and infants have these symptoms or signs, we should start simple screening studies immediately for metabolic disorders, including CBC, hepatic function tests, blood glucose, lactate, pyruvate, ketone bodies, ammonia, blood gas analysis, urinalysis (including non-glucose reducing substance tests and FeCl3 reaction) and so on. As for CBC, we have to make our own effort to find spherocytosis and vacuoles in lymphocytes. Family history, especially the mother's personal history, is indispensable. During physical examinations, we must pay attention to facial appearance, skin color, macroglossia, hair abnormalities, peculiar odor of the urine and hepatosplenomegaly. When abnormality is found in these clinical signs or simple laboratory examinations, we should not hesitate to start dietary treatment even if special examinations for differential diagnosis are on the way.
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PMID:[CNS disorders caused by metabolic disorders]. 201 2

A malignant non-Hodgkin lymphoma (Cb-Cc) stage IVb was diagnosed in a man of 71 years of age. He was subjected to polychemotherapy. The mediastinum was irradiated. Cortisone therapy was performed because of irradiation pneumonitis. A highly febrile disease pattern developed with increasing dyspnoea while displaying the signs and symptoms of a miliary pulmonary disease. The treatment course was directed at combatting miliary tuberculosis. The patient died from cardiorespiratory failure. The postmortem examination supplied proof of cryptococcal sepsis. The differential diagnosis is discussed.
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PMID:[Cryptococcal sepsis simulating miliary tuberculosis in malignant lymphoma]. 203 Oct 47


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