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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hematologic dysfunction occurs commonly in patients with malignancy. Over half are anemic, often because of acute or chronic blood loss, marrow involvement by the malignancy, marrow suppressive effects of chemotherapy or radiation therapy, or because of the anemia of chronic disease. Less frequently, anemia may result from red cell aplasia, folate or B12 deficiency, hemolytic processes, or hypersplenism. Occasional patients may become polycythemic because of erythropoietin-producing tumors such as renal adenocarcinomas or cerebellar hemangiomas. Elevation of the white cell count is commonly seen, especially in patients with lung cancer. Monocytosis and thrombocytosis, which may be early signs of an underlying malignancy, are also very common and occur in up to half of patients. Thrombocytopenia is commonly a result of therapy or marrow replacement; a few patients may have a syndrome resembling immune thrombocytopenic purpura. Abnormalities of coagulation are present in many patients, and may lead to superficial or deep venous thromboses, pulmonary emboli, nonbacterial thrombotic endocarditis with arterial emboli, bleeding, or acute disseminated intravascular coagulation. A sound understanding of the potential hematologic complications that can result from the malignant process is essential to the clinician caring for cancer patients.
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PMID:Hematologic manifestations of malignancy. 268 Mar 58

A 3-month-old male infant died of tricuspid valve nonbacterial thrombotic endocarditis complicating disseminated intravascular coagulation. The vegetations were so extensive as to cause tricuspid atresia and led to congestive right ventricular failure terminating in death. The diagnosis was made only at post mortem.
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PMID:Endocarditis in an infant causing "tricuspid atresia". 270 18

To evaluate the early and late results of mitral valve replacement and reconstruction for mitral insufficiency due to ruptured chordae tendineae respectively, 74 consecutive cases were analyzed. Fifty-five (74.3%) of the patients were men, and the mean age was 48 +/- 12 years old (range 16 to 76). The causes of the mitral disease were idiopathic in 50 (67.6%), rheumatic in 7 (9.4%) and infective endocarditis in 11 (14.9%) patients. In idiopathic 50 cases, 24 had mitral valve prolapse and 16 had both mitral valve prolapse and hypertension. Forty-one (55.4%) of the patients were in NYHA functional class III or IV preoperatively. Thirty (40.5%) cases underwent surgery within one year after their initial symptoms of heart failure onsets including six emergency operation cases due to uncontrollable acute lung edema. Chordae to anterior mitral leaflet were ruptured in 31 (a5, m16, p10)[41%] patients, to the posterior mitral leaflet in 45 (a4, m23, p18)[59%], and to both leaflets in one patient. Mitral valve replacement was performed in 68 patients (91.9%) and 6 patients (8.1%) underwent mitral valve repairs. Twenty cases underwent associated procedures that included tricuspid valve annuloplasty in 8, aortic valve replacement in 5 and myocardial revascularization in 4 cases. There were two operative deaths (2.4%); both occurred after replacement, left ventricular rupture in one and DIC in one. Mean follow-up period was 4.5 years (range 1 to 17) in 67 cases. There were four late deaths; all occurred after replacement. However five patients sustained mild mitral insufficiency after mitral valve repair including one that became worse of regurgitation three years after isolated Kay's annuloplasty, there were no cases that had needed reoperation and no late death after reconstruction. Left ventricular function and pulmonary arterial pressure were almost normalized in more than 90% cases postoperatively. Our data indicated that mitral valve reconstruction (McGoon's plus Kay's method as standardized maneuver) was the procedure of choice for selected patients with mitral insufficiency owing to ruptured chordae tendineae to the posterior mitral leaflet, including more limited patients with ruptured chordae to the anterior mitral leaflet.
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PMID:[Mitral insufficiency due to ruptured chordae tendineae--clinical features, early and late results of valve replacement and repair]. 273 33

This is a case report of a 61-year-old man, suffering from infective endocarditis of mitral valve in association with DIC and intracerebral hemorrhage. He was treated symptomatically and conservatively for 80 days after the onset of the DIC. His multiple cerebral hematomas gradually disappeared 2 months after conservative management. Then the diseased mitral valve was replaced with a Duromedics valve. He is doing well at present. In a review of the literature it appears that there is some room for surgical intervention in endocarditis despite the complication of coagulopathy. We feel that one of the most serious complications of infective endocarditis is DIC. Operative management of endocarditis with this complication is recommended to be followed by medical management.
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PMID:[Successful surgical treatment of infective endocarditis complicated with DIC and intracerebral hemorrhage]. 279 82

A 40-year-old woman was admitted to our hospital because of left hemiplegia. She was affected with myocardial infarction and cerebral infarction. Echocardiogram revealed that the aortic and mitral valves had thick and uneven echoes suggesting vegetations. Judging from the finding that repeated blood cultures were negative, we had considered in her lifetime that myocardial and cerebral infarctions were due to embolization associated with nonbacterial thrombotic endocarditis (NBTE). At autopsy, histological diagnosis was made as ovarian cancer with disseminated intravascular coagulation. From the clinical course and the histological findings, we diagnosed this patient as NBTE.
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PMID:Cerebral and myocardial infarction induced by nonbacterial thrombotic endocarditis in a patient with ovarian cancer: report of a case. 305 70

Platelet-bacterial interactions were examined in vitro by incubating organisms isolated from patients with septicemia with normal platelet-rich plasma. The potency of various species of gram-positive and gram-negative bacteria to induce irreversible platelet aggregation was then determined in an aggregometer. The aggregation curves produced by the bacteria resembled the normal platelet response to collagen and were impeded by the presence of aspirin. Strains of Staphylococcus aureus and Pseudomonas aeruginosa isolated from 25 different patients produced maximum increases in light transmission and irreversible platelet aggregation with relatively rapid mean aggregation times; six of these patients had clinical and laboratory evidence of disseminated intravascular coagulation. In contrast, isolates of alpha streptococcus and Staphylococcus epidermidis induced irreversible platelet aggregation much less commonly and were associated with considerably longer mean aggregation times. None of the latter group of patients had evidence of disseminated intravascular coagulation. Isolates of bacteria from a small number of patients with subacute bacterial endocarditis uniformly induced irreversible platelet aggregation. Addition of paired bacterial isolates to normal platelet-rich plasma demonstrated a synergistic aggregation response. These data suggest that a relative hierarchy exists in bacterial strain potency to induce irreversible platelet aggregation. The rapidity and degree of aggregation in vitro correlated well with the clinical and laboratory evidence for subacute bacterial endocarditis and disseminated intravascular coagulation in vivo. These observations may provide useful adjunctive laboratory information to help establish the diagnosis of subacute bacterial endocarditis, especially in the clinical setting where the classical findings of endocarditis are not obvious during initial presentation.
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PMID:In vitro correlation of platelet aggregation with occurrence of disseminated intravascular coagulation and subacute bacterial endocarditis. 310 30

The enterococci, members of the group D streptococci and the predominant aerobic streptococci of the gastrointestinal and female genital tracts, have long been recognized as significant pathogens in infective endocarditis. Over the past 2 decades, enterococci have become increasingly important nosocomial pathogens, related to their intrinsic resistance to many antibiotics, especially the cephalosporins, and the greatly increased use of antimicrobial therapy in hospitals. Recent reports have documented an alarming increase in the frequency of high-level resistance to aminoglyclosides, and strains resistant to ampicillin by production of a beta-lactamase and to vancomycin have now been encountered. We have reviewed the clinical features and course of 153 cases of enterococcal bacteremia occurring in a university hospital over the 14-year period, 1970 to 1983, 1) to understand better the importance of enterococci as human pathogens, 2) to identify the clinical features of enterococcal bacteremia, 3) to isolate those findings that help to identify associated endocarditis, and 4) to develop guidelines for more effective antimicrobial therapy of bacteremic enterococcal infections. The annual incidence of enterococcal bacteremia in our center rose three-fold over the period reviewed. In 65 cases (42%), bacteremia was polymicrobial, caused by Enterococcus and at least 1 other microorganism, usually an aerobic gram-negative bacillus. Most bacteremias were nosocomial and derived from infections of the urinary tract (29 cases), intravenous catheters (24 cases), intra-abdominal infections or surgical wounds (46 cases), burn wounds (25 cases), or cholangitis (21 cases); only 1 case originated from a pneumonia. Endocarditis was identified in association with 12 of 35 community-acquired bacteremias, but only 1 of 118 bacteremias acquired in the hospital (P less than .001). Endocarditis was also significantly associated with pre-existent valvular heart disease and cryptogenic bacteremia, and was negatively associated with polymicrobial enterococcal bacteremia (no endocarditis in 65 cases, P less than .001). Isolated enterococcal bacteremia produced an indolent infection rarely associated with shock (3 of 64 cases evaluated, all cases due to valve destruction by endocarditis); conversely, with polymicrobial enterococcal bacteremia, primarily with gram-negative bacilli, shock or disseminated intravascular coagulation developed in 50% of cases (P less than .001).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Enterococcal bacteremia: clinical features, the risk of endocarditis, and management. 313 90

A 6-year-old male Doberman Pinscher developed multiple organ infarctions secondary to vegetative endocarditis. Clinical signs included fever, nystagmus, head-tilt, inappetence, dehydration, hematuria, and dysuria. The dog was azotemic and anemic and had a high WBC count and high liver enzyme activities. Disseminated intravascular coagulation was diagnosed on the basis of thrombocytopenia and prolonged activated clotting times. Vegetative mitral valvular lesions were evident on M-mode echocardiography. The dog underwent diuresis with physiologic saline solution and was treated parenterally with antibacterial and anticoagulant agents. Surgery was performed to remove an infarcted kidney and an infarcted spleen and to relieve urethral obstruction caused by a large blood clot. Gram-positive cocci were noticed in the biopsy specimens. Mortality associated with organ infarctions secondary to bacterial endocarditis is high, and combined medical and surgical therapy is rarely reported. This dog survived and was alive 38 months after surgery.
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PMID:Medical and surgical management of multiple organ infarctions secondary to bacterial endocarditis in a dog. 320 56

Cerebral infarcts in 3 patients revealed the presence of disseminated intravascular coagulation (DIVC) of cancerous origin before any clinical manifestations of the neoplasm. Neurologic manifestations of these consumption coagulopathies almost constantly produce a picture of diffuse encephalopathy, expression of disseminated microinfarcts; however, transient or constituted focalized ischemic accidents by occlusion of a medium sized artery are also possible, and this in the absence of non-bacterial thrombotic endocarditis. Biologic diagnosis of DIVC is not always simple, and screening tests (platelet count, prothrombin and fibrinogen levels) can remain within normal limits during chronic forms, as a result of a subjacent inflammatory syndrome, frequently associated with cancer. Two other specific serum tests are therefore of fundamental interest: assay of fibrin degradation products and tests for soluble complexes.
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PMID:[Cerebral ischemic accidents and chronic disseminated intravascular coagulation of cancerous origin]. 338 Oct 47

Skin lesions, an important clue to the cause of septicemia, result from five main processes: (1) disseminated intravascular coagulation and coagulopathy; (2) direct vascular invasion and occlusion by bacteria or fungi; (3) immune vasculitis and immune complex formation; (4) emboli from endocarditis; and (5) vascular effects of toxins. Disseminated intravascular coagulation probably plays only a minor role in pathogenesis. Vascular invasion by bacteria may result in a severe inflammatory reaction, as in meningococcemia, or in a minimal reaction, as in ecthyma gangrenosum. Gram-stained smears of scrapings from the base of skin lesions--a frequently neglected procedure--is an important diagnostic adjunct. Skin biopsies are particularly important in the diagnosis of Rocky Mountain spotted fever and infections caused by Candida.
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PMID:Skin clues in the diagnosis of life-threatening infections. 351 82


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