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Query: UMLS:C0012739 (
disseminated intravascular coagulation
)
8,673
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The intricacies of the pathophysiology of eclampsia are still unknown. The major symptoms of our 37 year old para 3 are convulsions, hypertension, complete
anuria
and gastro-intestinal haemmorhage as a result of disseminated ;ntra-vascular coagulation (
D.I.C.
). The interdisciplinary therapeutic measures are discussed, in the course which special attention is given to the favourable influence of dopamine on renal failure and the complicating gastro intestinal haemmorhage.
...
PMID:[Intensive care medicine in severe eclampsia (author's transl)]. 31 2
Primary malignant nephrosclerosis shows a haemolytic-uraemic symptomatology and can be differentiated from secondary malignant nephrosclerosis on clinical and histological grounds. The disease was observed in 4 patients: a 25-year-old man and 3 women aged 19, 28 and 49 years. The disease is characterized by a fulminating course, malignant hypertension with progressive retinopathy, and development of progressive renal failure with subsequent irreversible
anuria
. In addition haemolytic anaemia or posthaemolytic states as well as
consumption coagulopathy
occur. In 2 cases schizozytes and in particular helmet-shaped forms could be demonstrated. On histology an obliterating necrotizing vascular change is seen which is limited to the kidneys as was demonstrated in one case by angiography. Therapeutic attempts included antibiotics, steroids, heparin, streptokinase, antihypertensive drugs, and haemodialysis. The 3 female patients died, the man survived after bilateral nephrectomy.
...
PMID:[Primary malignant nephrosclerosis (author's transl)]. 112 2
Under the proper experimental conditions,
disseminated intravascular coagulation
,"an intermediary mechanism of disease," results in the classic endotoxin-induced generalized Shwartzman reaction. Other substances, such as liquoid, a highly negatively charged anticoagulant, trigger a generalized Shwartzman reaction-like phenomenon in rabbits. We studied the effects of a single high intravenous dose of liquoid (12.5 mg.) upon the rat's coagulation and complement systems and their correlation with the kidney morphology by light, fluorescence, and electron microscopy. Thrombin time was prolonged; fibrinogen, plasminogen, and factors VIII and XII concentrations were markedly decreased, whereas fibrin degradation products were increased in the experimental animals when compared with the saline-injected controls (p greater than 0.001). Total hemolytic complement, hemolytic activity of terminal components (C3 to C9), and C3 protein concentration were significantly reduced (p greater than 0.001). The liquoid-injected rats developed cortical necrosis and manifested oliguria and
anuria
, with elevated blood urea nitrogen levels, when survival was longer than 3 hours. Histologically, thrombi of fibrin-like material filled the glomerular capillaries. Deposits of fibrin, and also of immunoglobulin G and C3, were readily identifiable by specific immunofluorescence, Linear or granular fluorescent deposits (or both) along the glomerular basement membranes and in the mesangium were observed. Electron microscopy demonstrated necrosis of glomeruli and abundant thrombi of fluffy, compact granular, or fibrillar electron-dense material. No typical fibrin periodicity was detected. These experiments support the concept of activation of the coagulation and the complement systems. We postulate that liquoid produced not only a consumptive coagulopathy in the rat but also a direct or perhaps anindirect activation of complement. Whether this latter has occurred through the classic or an alternate pathway remains to be elucidated.
...
PMID:Disseminated intravascular coagulation induced by liquoid in the rat. I. Correlation of hematologic and complement abnormalities with renal lesions studied by light, fluorescence, and electron microscopy. 112 10
A previously healthy 55-year-old man with nephropathia epidemica (NE) developed
disseminated intravascular coagulation
,
anuria
and shock and died on day 6 of his disease. By use of indirect immunofluorescence technique and ELISA, specific serum IgM antibodies against Puumala virus could be detected, thus confirming the clinical diagnosis. This case demonstrates that NE in Scandinavia is a potentially lethal disease.
...
PMID:A Swedish fatal case of nephropathia epidemica. 168 93
A 22 year old female developed preeclampsia with fetal death in utero. After cesarean section she developed uterine inertia and acute hemorrhagic anemia complicated by sepsis,
disseminated intravascular coagulation
and total
anuria
for 4 weeks. She was treated with hemodialysis. The second patient, a 49 year old man developed sepsis and intravascular coagulation after a dog bite. Acute renal failure with a 3 week total
anuria
followed. He was initially treated with peritoneo dialysis. Renal biopsy showed evidence of renal cortical necrosis in both patients.
...
PMID:[Acute kidney failure due to kidney cortex necrosis. 2 clinical cases of surviving patients]. 184 56
We observed 73 patients with the hemolytic uremic syndrome (HUS) in 9 years (1980-1988), comprising 34% of patients with acute renal failure treated over the same period. There were 53 boys and 20 girls; 59% were below the age of 2 years and 33% between 2 and 5 years. Acute, usually severe dysentery, responding poorly to various antibiotics, was the prodromal illness in 80%, whereas 12% had watery diarrhea. Most patients had severe renal involvement with
anuria
in 56% and oliguria in 30%. A polymorphonuclear leukocytosis was present in 85% of cases, but had no correlation with the highest levels of blood urea. Coagulation abnormalities suggesting
consumption coagulopathy
were found in 24 of 30 cases. The results of stool culture showed Shigella species in 7 cases and nontyphoidal Salmonella in 9. Escherichia coli were isolated in 11 cases, but were not further characterized. Renal biopsy showed total or patchy cortical necrosis in 20 of 50 cases. The patients were managed with supportive care, including transfusion of fresh blood or plasma and dialysis as required. The mortality was 60%, being chiefly related to the duration of renal failure and presence of renal cortical necrosis, whereas persistent dysentery and infections were complicating factors. The presence of convulsions and coagulation defects had no relation to the outcome. Our observations indicate that HUS in children in northern India is mostly related to dysentery, likely to be shigellosis, and is usually associated with severe renal damage and a high death rate.
...
PMID:Hemolytic uremic syndrome in children in northern India. 186 81
Plasmapheresis (PP) was applied to the treatment of 5 children aged 6-14 years with the crush syndrome. The multimodality treatment using antibiotics, erythrocytic mass, rheologically active preparations, hemodialysis and blood rheologically active preparations, hemodialysis and hemoperfusion carried out for 6-7 days before PP did not bring about any appreciable improvement of the patients' status. The patients failed to get rid of
anuria
and manifested the signs of increasing intoxication. The treatment with PP consisted of 1 to 6 procedures, in the course of which 70 to 85 of the design volume of the circulating plasma was removed. The use of PP resulted in the disappearance of myoglobin from the patients' blood and urine, in the normalization of the coagulogram, a considerable decrease of the content of medium molecules, and in the appearance of the first urine towards the end of the procedure. Thus, the introduction of PP into multimodality treatment of the crush syndrome made it possible to eliminate
anuria
,
disseminated intravascular coagulation
, and to noticeably reduce intoxication and to clear the blood off myoglobin.
...
PMID:[Experience with the use of plasmapheresis in the combined treatment of children with the crush syndrome]. 233 28
The terms "consumption coagulopathy" and "disseminated intravascular coagulation" are used synonymously, though the former expression refers to the process of consuming the haemostatic potential, whereas the latter is based upon the generalized formation of microthrombi. Both terms apply to an acquired disturbance of blood clotting leading to an increased turnover of coagulation factors and platelets by which the production sites are being exhausted. Such a process is triggered off by generalized activation of the haemostatic system: after a period of hypercoagulability, haemostasis changes into hypocoagulability with subsequent haemorrhagic diathesis. Additionally, the generalized activation of the haemostatic system leads to a formation of microthrombi in the microcirculation. Since consumption coagulopathies are bound to be secondary disorders, any underlying disease prone to lead to
disseminated intravascular coagulation
, should be treated as early and as intensively as possible. Solely by this and by restoring circulatory functions impaired by the underlying disease, it is possible in the majority of cases to stop the consumptive coagulopathy and to repair its sequelae. The shock frequently going along with a
consumption coagulopathy
requires immediate therapy: correction of hypothermia, treatment of acid-base and electrolyte disorders as well as fighting against hypovalaemia,
anuria
, and uraemia. Dextran does not serve only as plasma expander, but also corrects hypercoagulability and improves the rheological qualities of circulating blood. If these measures fail to stop the consumptive reaction of blood coagulation and/or fail to restore microcirculation in vital organs, indication for the use of anticoagulants or fibrinolytic drugs is given.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:[Therapy of consumption coagulopathies]. 307 Mar 63
Three cases of hypotension are described that followed rapid evacuation of persistent unilateral pneumothorax. Common features included the presence of a pneumothorax for approximately one week before treatment commenced and profuse unilateral reexpansion edema, a rising hematocrit reading, hypotension, and
anuria
after evacuation of the pneumothorax in spite of a relatively normal pulmonary capillary wedge pressure. In one case, cardiac output was measured and found to be low (1.54 and 1.65 L/min/sq m), with a pulmonary capillary wedge pressure of 10 to 14 mm Hg. Death due to cardiovascular collapse occurred in one patient; ischemic colitis, acute renal failure,
disseminated intravascular coagulation
, and ischemic necrosis of both humeral heads occurred in another. The cases presented and the literature reviewed suggest that cardiovascular compromise was the end result of the combined effects of intravascular volume depletion and myocardial depression.
...
PMID:Reexpansion hypotension. A complication of rapid evacuation of prolonged pneumothorax. 394 Jul 93
Therapeutic measures for acute pancreatitis depend on the severity of the disease and its complications. Since complications of acute pancreatitis may develop at any time, patients should be admitted to an intensive care unit for assessment (and frequent reassessment) of the severity of the disease and the development of complications. Basic therapy should include relief of pain, total fasting, nasogastric suction, parenteral replacement of fluids, electrolytes, albumin and blood, and antibiotics. Hyperglycaemia should be corrected and heparin should be given in cases of
disseminated intravascular coagulation
. In renal insufficiency, peritoneal dialysis is important, and in respiratory complications, humidified oxygen or artificial ventilation including positive and expiratory pressure therapy should be applied. Although the effect of peritoneal dialysis has been proven only in animal experiments and in retrospective studies in man, it is recommended in severe cases for shock therapy and for correction of electrolyte imbalance when ascites is present, even before
anuria
occurs. Conservative treatment measures in chronic pancreatitis are limited to the management of pain and of exocrine and endocrine pancreatic insufficiency.
...
PMID:Acute and chronic pancreatitis. An update on management. 608 59
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