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

Cerebral infarction due to chronic disseminated intravascular coagulation (DIC) after thromboexclusion for thoracic dissecting aortic aneurysma is described. Chronic DIC may be caused by the delay of thrombus formation at the site of thromboexclusion, and local DIC occurred at that site. It is difficult to find chronic DIC. This case shows that DIC after thromboexclusion for dissecting aortic aneurysma may be one of the causes of recurrent cerebral infarction.
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PMID:Cerebral infarction due to disseminated intravascular coagulation with thromboexclusion for dissecting aortic aneurysma. 279 32

Spontaneous extracranial metastases of glioblastoma multiforme in the absence of previous surgery have been rarely reported (Table 1). We presented an autopsy case of glioblastoma multiforme which spontaneously metastasized to the lungs, bronchial lymph nodes, liver, kidney, heart and spleen. A 68-year-old man was admitted to the Department of Neurosurgery at our hospital with chief complaints of right sided weakness in July 1984. He was well until November 1983, when he noticed weakness of right lower extremity followed one month later by the weakness in the right arm. He was treated at another hospital under the diagnosis of cerebral infarction, but his right sided weakness gradually progressed. In June 1984, a diagnosis of brain tumor was made by the neurological findings and CT scan, and he was transferred to our hospital for further evaluation and treatment. Neurological examination revealed disorientation, bilateral papilledema, right hemiparesis, right hyperreflexia and right hemisensory disturbance. CT scan revealed abnormal low density area in the left fronto-parietal lobe (Fig. 1) with irregular enhanced lesions on contrast CT scan (Fig. 2). Chest x-ray showed abnormal shadow in the right middle and lower lobe (Fig. 3) and a diagnosis of pulmonary infarction was suspected. The clinical states of this patient took downhill course and he expired on July 13, 1984 by the complication of disseminated intravascular coagulation syndrome. The brain weight was 1400 gr. Dura mater and falx cerebri were tightly adherent to the left parietal lobe (Fig. 4). Primary brain tumor was found in the left fronto-parietal region. The tumor was poorly defined with necrosis and hemorrhage (Fig. 5).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Glioblastoma multiforme with extracranial metastases without previous surgery: demonstration of extracranial metastases by peroxidase antiperoxidase staining and clinicopathological study]. 282 54

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

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

Clinicopathologic correlations of nonbacterial thrombotic endocarditis (NBTE) were studied with special reference to their pathogenetic role in cerebral and myocardial infarction. In 2340 cases of consecutive autopsies of the aged, NBTE was observed in 217 cases or 9.3%. The age distribution of NBTE revealed a gradual increase with advancing age. The underlying diseases of NBTE were malignant neoplasm (51.6%), infection (28.3%) and other diseases (20.1%). The incidence of NBTE in each cancer was high in cancers of the colon (16.2%), pancreas (15.2%), gall bladder or bile duct (14.1%) and lung (13.0%). The vegetations of NBTE were found on the aortic valve in 46.1%, on the mitral valve in 40.6% and on the both valves in 8.3%. The incidence of myocardial infarction and scar was 51.2% in the NBTE group, while it was 38.6% in the non-NBTE control group (p less than 0.02). This difference was marked in patients with a small infarction (10.6% vs. 5.3%) and a myocardial scar (30.4% vs. 19.0%). The grade of coronary stenosis was less in the NBTE group than in the control group (p less than 0.001), suggesting that the origin of the myocardial ischemic lesion was embolism from NBTE. The incidence of large cerebral infarction was 14.7% in NBTE and 9.2% in the control group, and that of medium sized cerebral infarction was 35.0% and 23.6% respectively. In this latter group, cortical infarction comprised 57.9% in the NBTE group and 26.6% in the control group. In large cerebral infarction, cerebral atherosclerosis was less severe in NBTE than in the control group (p less than 0.001), also suggesting an embolic mechanism. Disseminated intravascular coagulation was found in 41.9% of NBTE.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nonbacterial thrombotic endocarditis as a cause of cerebral and myocardial infarction. 648 38

The importance of DIC in the management of gynecological malignancy, especially in advanced cases, was stressed on the basis of our experience with 8 cases. The overall incidence of DIC in our series of 366 cases of gynecological malignancies was 2.2%. However, DIC was experienced only in cases of advanced later stages and the recurrence of malignancy, and the incidence of DIC in these two groups were 2.2% and 7.2% respectively. In our 8 cases, DIC seemed to be provoked or worsened by antitumoric chemotherapy, major surgery, radiation therapy, infection, cerebral infarction and massive packed red cell transfusion. At the same time, an exceptional case of fulminating DIC which had probably been provoked by packed red cell transfusion in a patient with advanced but not detected endometrial cancer which developed in a endometriotic uterus was presented.
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PMID:Gynecological malignancies and disseminated intravascular coagulation. 653 11

Ninety five patients with cerebrovascular accidents were studied on their coagulation and fibrinolysis at acute stage of their onset. From the data collected in the present study, following findings were obtained; 1) Hypercoagulable state, which are responsible for the decreased antithrombin III levels, was observed at acute stage of cerebral infarction. 2) Findings from patients with cerebral hemorrhage were normal antithrombin III levels and slightly decreased alpha 2-plasmin inhibitor. These imply the fact of increased fibrinolytic activities. It is suggested that increased fibrinolysis are secondary reaction of cerebral hemorrhage. 3) Findings from patients with subarachnoid hemorrhage showed hypercoagulable state and increased fibrinolytic activities. It is considered that subarachnoid hemorrhage might have mostly a preparatory condition of disseminated intravascular coagulation among cerebrovascular accidents.
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PMID:[Correlation between coagulation and fibrinolysis in patient with cerebrovascular accident at acute stage]. 715 Apr 48

Patients infected with the human immunodeficiency virus (HIV) appear to have a high risk of ischaemic cerebral events. We observed two cases of cerebral infarction in patients with acquired immune deficiency syndrome (AIDS). In the first case, a 38-year-old homosexual with no cardiovascular risk other than smoking presented with rapidly progressive hemiparesia. Brain CT-scan visualized two infarcts in the territory of the right sylvian artery and the arteriography an occlusion of the internal carotid artery. In the second, a 37-year-old homosexual, hospitalization was required for a left-sided pure sensitive epilepsy seizure. There was no cardiovascular risk other than smoking. Magnetic resonance imaging showed parietal ischaemia and thrombus in the left atrium without atrial hypertrophy was seen at transoesophageal echocardiography. In both cases, there was no evidence of endocarditis, dissection of the neck vessels or disseminated intravascular coagulation nor of associated viral or bacterial infectious complication of AIDS. Angiographic findings eliminated cerebral vascularitis. Among the perturbed haemostasis factors previously reported in HIV+ patients, we observed free proteins S deficiency (68 and 43%) and heparin cofactor II deficiency (54 and 40%). Serum albumin was 33 and 32 g/l respectively. Outcome was favourable in both cases with anticoagulant therapy. These coagulation anomalies would not appear sufficient to explain cerebral infarction. Other mechanisms including immune complexed deposition, direct HIV toxicity for endothelial cells or the effect of cytokines on smooth muscles fibres and fibroblasts are probably more important causal factors.
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PMID:[Cerebral infarction in human immunodeficiency virus infection]. 763 44

Neurologic morbidity is observed more frequently in twins than in singletons. Low birthweight and premature birth are observed more frequently in twins but cannot always explain the cause of cerebral palsy, although circumstances related to twinning may cause brain damage. We attempted to select the patients whose brain damages might be caused by circumstances related to twinning and discussed the developmental mechanisms of their brain damages. We divided the cases into 3 groups. One comprised the monozygotic (MZ) twins whose co-twins had died. The second comprised the MZ twins with the complication of the twin-twin transfusion syndrome or discordant twins. The third comprised the MZ twins with concordant co-twins. We postulated that group I and II had complication of the disturbance of fetal circulation, but group III did not. Hydranencephaly (group I) and polymicrogyria (group II) might develop when the disruption occurs at an intermediate stage of morphogenesis (before the 6th month of gestation). In the cases with cerebral infarction (group I), the distribution of the lesions were related to the main vascular territories of the mature form, might be caused by occlusion of blood vessels associated with intrauterine disseminated intravascular coagulation. In the cases of MCE (group I), multiple cavities are present mainly in the white matter, the gray matter having a tendency to be spared. As the distribution of the cavities is not related to the main vascular territories, it was less likely that the lesions was produced by occluded vessels. The death of one fetus might cause severe blood deprivation, leading to hypoxic-ischemic brain insults in the surviving fetus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Pattern of the brain damages and its developmental mechanisms in monozygotic twins]. 766 9

A 27-year-old woman visited Kanto Teishin Hospital complaining of fever and petechiae in September, 1992. Her fetus had suddenly died in the uterus two weeks before (in the sixth month of pregnancy). Total white blood cell (WBC) count was 3.2 x 10(3)/microliters with 80% promyelocytes. Bone marrow was hypercellular with 90% promyelocytes. Disseminated intravascular coagulation (DIC) was recognized. She was diagnosed as having acute promyelocytic leukemia (APL), and treatment with daily oral administration of all-trans retinoic acid (ATRA) (70 mg/body/day) was begun. On day 4, hemiplegia and aphasia appeared. Broad cerebral infarction was suspected from computed tomography. On day 9, the WBC count increased rapidly, standard chemotherapy was added and she achieved complete remission. ATRA is known to have stimulatory effects on the differentiation of APL cells, but some reports have described thromboembolic events during the administration of ATRA. In this case, ATRA might have affected coagulability resulting in cerebral infarction.
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PMID:[Acute promyelocytic leukemia (APL) resulting in broad cerebral infarction during all-trans retinoic acid (ATRA) treatment]. 813 18


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