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

Two cases of microangiopathic hemolytic anemia in disseminated carcinoma are reported. Both showed the classical features of this illness, namely acute generalized hemorrhagic diathesis, severe hemolytic anemia, thrombocytopenia, fragmentation of erythrocytes in the peripheral blood smear, increased erythropoiesis and megakaryopoiesis or tumor cell invasion in the bone marrow, tumor cell emboli in venules and disseminated intravascular coagulation. In both cases the microangiopathic hemolytic anemia was the first sign of the disseminated carcinoma. Differential diagnosis, pathogenesis and therapy are discussed.
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PMID:[Microangiopathic hemolytic anemia in malignant tumors. 2 cases]. 62 35

Patients with typhoid fever were studied to determine whether disseminated intravascular coagulation (DIC), circulating bacteria, and endotoxemia were responsible for the signs and symptoms of their illnesses. Coagulation tests in 28 patients detected thrombocytopenia in 17, hypofibrinogenemia in nine, and elevated titers of fibrinogen-related antigens in 20. Repeated testing during convalescence showed a return toward normal values. Intestinal bleeding, however, did not correlate with abnormalities of coagulation tests. Thus, DIC occurred commonly but appeared to be a subclinical event in these patients. In 25 patients with positive blood cultures for Salmonella typhi, quantitative cultures detected from less than 10 to 9 x 10(2) bacteria/ml. Limulus tests for endotoxin in plasma were negative in all 21 patients tested. These results indicated that the concentrations of circulating bacteria and endotoxin in typhoid fever are lower than in other Gram-negative bacterial infections and suggested that circulating bacteria and endotoxin do not play a major role in the pathogenesis of typhoid fever.
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PMID:Typhoid fever. Studies of blood coagulation, bacteremia, and endotoxemia. 62 35

Coagulopathy, or non-mechanical hemorrhage, complicated the operative course of 17 of 33 (51.5%) patients suffering severe liver trauma. The highest incidence of non-mechanical hemorrhage (66.7%) occurred in patients undergoing anatomic lobectomy. Serial hemostatic parameters were assessed and thrombocytopenia was the most striking abnormality in patients with non-mechanical hemorrhage. The degree of thrombocytopenia was directly correlated with the number of blood transfusions administered. The mean operative blood transfusion requirement was significantly greater in patients with non-mechanical hemorrhage, 25.1 +/- 2.87 (S.E.M.) units, than in those without, 12.2 +/- 1.83 units (p < 0.001). The bulk of this transfusion was given before the onset of clinically overt coagulopathy. Massive transfusion of stored blood was felt to be the most important factor in causing non-mechanical hemorrhage. Convincing evidence for disseminated intravascular coagulation was lacking, and abnormal fibrinolysis was infrequent and mild when observed. Although uneventful in most, in six patients non-mechanical hemorrhage resulted in excessive blood transfusion, unnecessary operation or death. Infusions of platelet concentrate, fresh frozen plasma, and fresh blood were used to successfully treat most cases of non-mechanical hemorrhage. In all cases, these components were not started until non-mechanical hemorrhage was clinically apparent. The value of prophylactic use of blood components is stressed. Because of troublesome side effects associated with the use of prothrombin complex concentrates, these agents are contraindicated in patients with severe liver injury. After receiving concentrates, one patient developed severe hypotension leading to ventricular fibrillation, two developed transient thrombocytopenia and two others demonstrated multiple pulmonary microthrombi at autopsy, a finding not observed in autopsied patients not receiving the concentrates.
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PMID:Non-mechanical hemorrhage in severe liver injury. 64 75

A patient with laboratory-acquired Rocky Mountain spotted fever (RMSF) and concomitant influenza virus infection was studied from the third day of clinical illness. The course of his illness was marked by petechial rash, thrombocytopenia, and elevation of fibrin split products. No evidence of complement activation was observed. Plasma proteins were elevated in a pattern characteristic of the "acute phase reaction." The patient recovered completely, and vascular collapse or clinically important disseminated intravascular coagulation had developed. In febrile patients who had influenza or a clinically similar noninfluenzal respiratory syndrome, no changes in coagulation, complement, or plasma proteins developed. We conclude that aberrations in the patient's laboratory values reflected RMSF, and that complement played no critical role in his illness.
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PMID:Coagulation and complement studies in Rocky Mountain spotted fever. 64 36

The incidence and type of hemorrhage were studied in 718 patients with solid tumors. All patients were receiving myelosuppressive chemotherapeutic agents. Seventy-five patients (10.4%) experienced one or more episodes of hemorrhage. Bleeding was due to tumor invasion in 25 patients (33.3%), was due to disseminated intravascular coagulation in seven patients (9.3%), and was unrelated to malignant neoplasms or drug treatment in six patients (8%). Thirty-seven patients (49.3%) had hemorrhages associated with drug-induced thrombocytopenia. There was a quantitative relationship between the incidence of hemorrhage and the platelet count for both the thrombocytopenic group and the total group of patients with hemorrhages from all causes. The incidence of hemorrhage was low until the platelet count decreased below 10,000/cu mm.
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PMID:Incidence of hemorrhagic complications in patients with cancer. 66 Jul 90

Twenty cases of moderate thrombocytopenia in young women were examined in an assessment of the nosological status of this form. Parameters enjoying pathogenetic significance were distinguished in some instances: 4 cases displayed dysendocrinopathy, 2 the signs of consumption coagulopathy, 3 an antibody situation attributable to compensated autoimmune thrombocytopenia, and 3 a probable central inhibition of thrombocytopoiesis due to drugs. Since no significant cause could be determined in the remaining 8 cases, it can be said that this syndrome occupies a special place among the forms of chronic thrombocytopenia.
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PMID:[Etiopathogenetic considerations on so-called moderate thrombopenia in young women]. 66 49

As outlined in this paper, the patient with disseminated malignancy suffers many alterations of hemostasis; in addition, hemorrhage or less commonly thrombosis is the final clinical event in many of these patients. Patients with malignancy present a major clinical challenge in this day of new oncological awareness and more aggressive care. Thus, it is important to realize that these alterations of hemostasis do exist and they must be approached in a logical manner with respect to diagnosis as well as efficacious therapy. By far the most common alteration of hemostasis in malignancy is that of hemorrhage associated with thrombocytopenia either drug-induced or from bone marrow invasion. However, hemorrhage due to disseminated intravascular coagulation is also quite common. In addition, many antineoplastic drugs, as well as radiotherapy, may lead to hemorrhage in these patients. Thrombosis, which is also commonly seen in the patient with malignancy, is usually a manifestation of disseminated intravascular coagulation manifest as an intravascular thrombotic rather than an intravascular proteolytic event. When suspecting this, confirmatory laboratory evidence must be sought and the patient treated apropriately. When approaching the patient with malignancy and either hemorrhage or thrombosis, all of the potential defects in hemostasis must be taken into account, defined from the laboratory standpoint, and treated in as precise a manner as possible.
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PMID:Alterations of hemostasis associated with malignancy: etiology, pathophysiology, diagnosis and management. 70 51

We have reviewed 53 cases of disseminated intravascular coagulation (DIC) in the newborn, including 29 cases that were confirmed at autopsy. Factors predisposing to DIC included maternal complications (60%), low Apgar scores (30%), hyaline membrane disease (62%), and sepsis (26%). Diagnostic criteria common to autopsy-proved cases included presence of fibrin degradation products, low factor V activity, a prolonged prothrombin time, and a prolonged partial thromboplastin time and/or thrombocytopenia. There appeared to be no difference in coagulation response or in mortality among patients treated with different therapeutic regimens. Survivors were older gestationally, had higher birth weights, and higher Apgar scores.
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PMID:Disseminated intravascular coagulation in the newborn. 76 May 11

This chapter has provided a review of available literature regarding alterations of hemostasis associated with CPB. The primary pathology of altered hemostasis during CPB appears to be two-fold: (1) a functional platelet defect of unclear etiology, which occurs in virtually all patients, and (2) a primary hyperfibino(geno)lytic defect which occurs in the majority of patients undergoing cardiopulmonary bypass. Significant thrombocytopenia does not appear to be a consistent problem, and is probably a function of perfusion technics; this may, however, be an important source of hemorrhage in some instances. Although hyperheparinemia, heparin rebound, and protamine excess have occasionally been incriminated as sources of hemorrhage during CPB, no well documented cases appear in the literature. Likewise, although DIC gained popularity in early reports of CPB hemorrahge, it appears that this syndrome rarely, if ever, arises as a consequence of CPB alone; it can be seen, however, in CPB patients who are provided a triggerin situation for DIC, such as shock, sepsis, or hemolytic transfusion reaction. It is likely that many reported alterations of hemostasis during CPB which were concluded to represent DIC actually were due to hyperfibino(geno)lysis. The key to prevention of CPB hemorrhage rests simply in obtaining an adequate preoperative workup. Of extreme importance is an adequate history with respect to bleeding tendencies in both patient and family; of equal importance is a careful history regarding antiplatelet drugs. A careful physical examination, searching for clues of a real or potential bleeding diathesis, also can often prevent catastrophic cases of CPB hemorrhage. Lastly, an adequate presurgical laboratory screen must be performed; in addition to the usual prothrombin time, partial thromboplastin time, and platelet count, a thrombin time and standardized template bleeding time must be added. The addition of these two simple modalities will insure against significant defects in fibrinogen, the fibrinolytic system, vascular function, and platelet function. When CPB hemorrhage occurs, simple laboratory screening will usually allow for a quick hemostasis evaluation. The parameters recommended in this review will distinguish between surgical and nonsurgical bleeding and should, therefore, allow for a quick decision regarding necessity for reexploration and the adequacy of hemostasis if reexploration is needed. In addition, this screen will distinguish between difficulties with heparin, protamine, and the fibrinolytic system. The vast majority of nonsurgical hemorrhages during CPB is due to a functional platlet defect, primary hyperfibrino(geno)lysis, or a combination of these. The quick administration of platelet concentrates, while awaiting laboratory evaluation, will control or significantly blunt most instances of CPB hemorrhage. If platelets fail to control bleeding, and reasonable laboratory evidence of primary hyperfibrino(geno)lysis is present, antifibrinolytics should then be used...
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PMID:Alterations of hemostasis associated with cardiopulmonary bypass: pathophysiology, prevention, diagnosis, and management. 79 78

In all of four patients with African trypanosomiasis, thrombocytopenia was present on admission to hospital or developed during the course of the illness. One patient with severe thrombocytopenia died following gastrointestinal haemorrhage shortly after admission to hospital. Kinetic studies in the other three patients showed marked pooling of platelets in the spleen in all, but severe shortening of platelet life-span in only one. Evidence of disseminated intravascular coagulation (DIC) was found in 3 patients, 2 of whom received heparin therapy. These findings provide evidence that thrombocytopenia is a feature of African trypanosomiasis and is due mainly to hypertrophy of the reticuloendothelial system which accompanies the infection. In some patients immune damage to platelets or platelet consumption as part of DIC may be an additional factor contributing to the thrombocytopenia.
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PMID:Thrombocytopenia in trypanosomiasis. 80 67


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