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

Activation of the kallikrein-kinin system, as indicated by increased plasma kallikrein and depleted plasma kininogen, prekallikrein, and kallikrein inhibitor, was observed in five patients with Rocky Mountain spotted fever. Four of the patients had petechial rashes characteristic of vasculitis. Three patients had alterations in coagulation consistent with disseminated intravascular coagulation, although no hemorrhagic syndrome was found. Our data, along with the known physiologic actions of kinins, suggest a possible role for the kallikrein-kinin system in the pathophysiology of vasculitis, disseminated intravascular coagulation, circulatory shock, and other complications of infection with Rickettsia rickettsii.
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PMID:Activation of the kallikrein-kinin system in Rocky Mountain spotted fever. 30 54

Review of clinical and pathologic data from ten fatal cases of Rocky Mountain spotted fever (RMSF) revealed the importance of acute renal failure in the clinical course and of multifocal perivascular interstitial nephritis as the principal pathologic lesion. In nine cases, Rickettsia rickettsii were demonstrated by immunofluorescence in the areas of vasculitis. Evidence was lacking for the role of disseminated intravascular coagulation, glomerulonephritis, or myoglobinuria in the pathogenesis of acute renal failure in these cases. Rickettsia-induced vascular injury led to acute renal failure by several mechanisms. Hypovolemia early in the course resulted in reversible, prerenal azotemia. Transient hypotension in midcourse produced acute tubular necrosis. In fulminant cases, preterminal circulatory collapse was associated with coma and oliguria. The interstitial nephritis could not be demonstrated conclusively to contribute to the acute renal failure.
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PMID:Acute renal failure in Rocky Mountain spotted fever. 43 98

Of 35 newborn infants who died from an infection 19 had postmortem evidence of massive pulmonary hemorrhage. All but 1 of the 19 had evidence of antimortem formation of intravascular fibrin clots in lung tissue. Seventeen infants had low platelet counts. Of the 11 infants in whom coagulation studies were done, 8 had evidence of disseminated intravascular coagulation (DIC) during life. Vasculitis in the lungs, associated with fibrin clots and hemorrhages, was detected in two infants. It is postulated that sepsis is an important cause of hemorrhage in the newborn, probably as a result of the development of DIC.
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PMID:Massive pulmonary hemorrhage in neonatal infection. 76 37

A patient developed disseminated intravascular coagulation with purpura fulminans 1 month after starting Dilantin therapy for a seizure disorder. In addition, the patient developed exfoliative dermatitis, hepatitis, cutaneous vasculitis, and microangiopathic hemolytic anemia. She was successfully treated with adrenal steroids and heparin for her purpura fulminans. The hepatitic dermatologic, along with hemorrhagic, complications of Dilantin are reviewed, and the possible origin of the vasculitis and disseminated intravascular coagulation is discussed.
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PMID:Dilantin-induced disseminated intravascular coagulation with purpura fulminans. A case report. 114 59

About 15% of patients with cancer have cerebrovascular lesions, resulting from 4 kinds of disorders sometimes intermingled in advanced disseminated cancer: coagulation disorders, direct effects of the tumor, infections and therapeutic measures. Infarction, hardly less frequent than hemorrhage, mostly complicates lymphoma and carcinoma. Hypercoagulation states, such as chronic disseminated intravascular coagulation, nonbacterial thrombotic endocarditis, and nonmetastatic cerebral venous thrombosis account for about 50% of cases. Tumor emboli, as seen in intravascular malignant lymphomatosis, arteritis related to aspergillus, granulomatous angiitis with or without herpes zoster and radiation-induced atherosclerosis are rarer. Cerebral hemorrhages, excluding bleeding from the metastases of choriocarcinoma and melanoma are mainly associated with leukemia by acute disseminated intravascular coagulation as in promyelocytic leukemia, by leukostasis or by pancytopenia. Both infarction and hemorrhage rarely reveal the neoplasia. Lesions are often small and disseminated, and therefore produce a picture of diffuse acute or subacute encephalopathy rather than acute focal deficits. Finally, there may be no relationship between the cerebrovascular event and the neoplasia, and atherosclerosis or traumatic subdural hematoma may well be the causal factor.
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PMID:[Cerebrovascular complications of cancers]. 130 55

We encountered a patient who was diagnosed as rheumatoid arthritis (RA) at 15 years old and developed malignant RA (MRA) within one year. He suffered from mononeuritis multiplex and cutaneous infarction. Despite of treatment including steroid pulse therapy, neuritis progressed. Lung infiltration, pancreatitis and intestinal bleeding were accompanied. He died of disseminated intravascular coagulation on 153 days after admission. Autopsy revealed systemic rheumatoid vasculitis in coronary artery, pancreas, liver, small and large intestine, kidney and lung. These severe vasculitis occurred in young RA patient are rare case and it is important to consider the therapy and prognosis.
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PMID:[An autopsy case of malignant rheumatoid arthritis (MRA) which was difficult to distinguish from polyarteritis nodosa (PN)]. 135 57

The causes of acute renal failure (ARF) and results of its treatment are analyzed in 34 patients aged 15 to 51 years with exacerbation of chronic glomerulonephritis (CGN). Of these, 20 patients presented with lupoid GN, 11 with Bright's GN, and 3 had GN associated with systemic vasculitis (2 of them also had mixed cryoglobulinemia). All the patients underwent clinical treatment that lasted from January 1, 1986 to December 31, 1990. In 15 patients, ARF was due to the activity of the underlying disease or development of its complications (nephrotic crisis, disseminated intravascular coagulation, cryoglobulinemia); in 15 patients, it was determined by complications induced by drug treatment (diuretics, antibiotics, nonsteroid antiinflammatory drugs), and in 4 patients, by complications related to invasive examinations (radiographic contrast studies) and treatment (isolated ultrafiltration). The authors hold that superaddition of progressive tubular disorders, rapid decrease of the rate of glomerular filtration accompanied by the growth of serum creatinine form the basis for ARF to be diagnosed in such patients. Identification of the cause of ARF and delimitation of whether the pathological process is renal or prerenal in CGN patients is required for rational treatment prescription.
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PMID:[Acute kidney failure in patients with chronic glomerulonephritis]. 144 Mar 33

The purpose of the study was to explore hemostasis in children suffering from hemorrhagic vasculitis (HV) by means of the new amidolytic methods using chromogenic substrates. The patient's plasma was studied for the content of thrombin, trypsin, factor Xa, AT-III, kallikrein, plasmin, free heparin, urokinase, factor 3 of platelets, prothrombin and Willebrand's factor. 69 children with HV were entered into the study. All of them were examined during crises. In cutaneous HV, the content of trypsin decreased 3-fold, the content of factor Xa increased 5-fold; there was a negligible increase in the plasmin and AT-III levels; the content of kallikrein rose 2-fold, that of urokinase 60-fold; the release of platelet factor 3 was intensified 1.5-fold, the activity of prothrombin 3-fold. These data indicate that in cutaneous HV, blood coagulation increased. However, the signs of disseminated intravascular coagulation were lacking because of the high blood anticoagulant activity. In mixed HV, the phase of hypercoagulation was not made for by the blood anticoagulant activity, since the latter one was depleted. The capillary toxic nephritis may give rise to disseminated intravascular coagulation associated with the depletion of the anticoagulant component. The gravity of HV and its complications can be predicted according to the characteristics of the anticoagulant component of hemostasis, especially according to the levels of urokinase and AT-III.
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PMID:[State of hemostasis in hemorrhagic vasculitis in children]. 151 26

A 47-year-old woman with progressive systemic sclerosis developed disseminated intravascular coagulation in the course of her terminal illness. She also had complicating necrotizing angiitis and generalized lymphadenopathy. The likely relationship between disseminated intravascular coagulation and vasculitis is discussed.
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PMID:Disseminated intravascular coagulation in a patient with progressive systemic sclerosis associated with necrotizing angiitis and generalized lymphadenopathy. 168 85

The authors report the clinicopathological findings in six cases of bacterial intracranial aneurysms. All patients received appropriate high-dose antibiotics, and four were treated surgically. One patient with multiple aneurysms of the main trunks died of disseminated intravascular coagulation. Autopsy disclosed no apparent aneurysm or inflammatory cell infiltration, but a partially interrupted internal elastic lamina and thickened intima were disclosed at the angiographical aneurysm sites. These findings suggest that 1) appropriate high-dose antibiotics are effective against inoperable bacterial aneurysms in the main trunks, 2) new aneurysms may be formed in patients with cyanotic congenital heart disease, because bacterial emboli can directly reach the cerebral circulation and reimplant on the fragile arterial walls after vasculitis. Histological examination of aneurysmal walls revealed inflammatory cell infiltration after resolution of clinical endocarditis. This suggests that both appropriate high-dose antibiotic therapy and surgery should be considered in patients with distal bacterial aneurysms.
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PMID:Clinicopathological study of bacterial intracranial aneurysms. 172 79


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