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

Preeclampsia occurs in 3-14% of pregnancies and is defined by maternal hypertension with proteinurea, generally associated with edema, coagulation abnormalities, and disseminated intravascular coagulation. The conditions can lead to eclampsia, characterized by hyperreflexia and convulsions. Several organs are afflicted by the condition, most importantly the liver and kidneys. The direct cause of preeclampsia is unknown, but the initial events are linked to abnormalities of placentation. This implies abnormalities in trophoblast invasion and in physiological alterations of placental vessels required for adequate perfusion of the placenta, which leads to ischemia. The mechanisms that link the ischemic placenta to endothelial lesions and to stimulation of vasoconstrictors and inhibition of vasodilators are still subject of speculation. The only treatment of preeclampsia is delivery. Lowering of blood pressure and prevention of eclampsia with magnesium sulfate is indicated in severe preeclampsia. Despite numerous studies attempting to elucidate the exact etiopathogenesis of this complex multifactorial disease, prediction or prevention methods of preeclampsia are not available.
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PMID:Preeclampsia: a danger growing in disguise. 1849 5

The diagnosis of disseminated intravascular coagulation (DIC) should encompass both clinical and laboratory information. The International Society for Thrombosis and Haemostasis (ISTH) DIC scoring system provides objective measurement of DIC. Where DIC is present the scoring system correlates with key clinical observations and outcomes. It is important to repeat the tests to monitor the dynamically changing scenario based on laboratory results and clinical observations. The cornerstone of the treatment of DIC is treatment of the underlying condition. Transfusion of platelets or plasma (components) in patients with DIC should not primarily be based on laboratory results and should in general be reserved for patients who present with bleeding. In patients with DIC and bleeding or at high risk of bleeding (e.g. postoperative patients or patients due to undergo an invasive procedure) and a platelet count of <50 x 10(9)/l transfusion of platelets should be considered. In non-bleeding patients with DIC, prophylactic platelet transfusion is not given unless it is perceived that there is a high risk of bleeding. In bleeding patients with DIC and prolonged prothrombin time (PT) and activated partial thromboplastin time (aPTT), administration of fresh frozen plasma (FFP) may be useful. It should not be instituted based on laboratory tests alone but should be considered in those with active bleeding and in those requiring an invasive procedure. There is no evidence that infusion of plasma stimulates the ongoing activation of coagulation. If transfusion of FFP is not possible in patients with bleeding because of fluid overload, consider using factor concentrates such as prothrombin complex concentrate, recognising that these will only partially correct the defect because they contain only selected factors, whereas in DIC there is a global deficiency of coagulation factors. Severe hypofibrinogenaemia (<1 g/l) that persists despite FFP replacement may be treated with fibrinogen concentrate or cryoprecipitate. In cases of DIC where thrombosis predominates, such as arterial or venous thromboembolism, severe purpura fulminans associated with acral ischemia or vascular skin infarction, therapeutic doses of heparin should be considered. In these patients where there is perceived to be a co-existing high risk of bleeding there may be benefits in using continuous infusion unfractionated heparin (UFH) due to its short half-life and reversibility. Weight adjusted doses (e.g. 10 mu/kg/h) may be used without the intention of prolonging the APTT ratio to 1.5-2.5 times the control. Monitoring the APTT in these cases may be complicated and clinical observation for signs of bleeding is important. In critically ill, non-bleeding patients with DIC, prophylaxis for venous thromboembolism with prophylactic doses of heparin or low molecular weight heparin is recommended. Consider treating patients with severe sepsis and DIC with recombinant human activated protein C (continuous infusion, 24 microg/kg/h for 4 d). Patients at high risk of bleeding should not be given recombinant human activated protein C. Current manufacturers guidance advises against using this product in patients with platelet counts of <30 x 10(9)/l. In the event of invasive procedures, administration of recombinant human activated protein C should be discontinued shortly before the intervention (elimination half-life approximately 20 min) and may be resumed a few hours later, dependent on the clinical situation. In the absence of further prospective evidence from randomised controlled trials confirming a beneficial effect of antithrombin concentrate on clinically relevant endpoints in patients with DIC and not receiving heparin, administration of antithrombin cannot be recommended. In general, patients with DIC should not be treated with antifibrinolytic agents. Patients with DIC that is characterised by a primary hyperfibrinolytic state and who present with severe bleeding could be treated with lysine analogues, such as tranexamic acid (e.g. 1 g every 8 h).
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PMID:Guidelines for the diagnosis and management of disseminated intravascular coagulation. British Committee for Standards in Haematology. 1922 77

Varicella-associated purpura fulminans (PF) is a rare complication to varicella infection. The condition is due to autoantibodies directed against protein S which forms part of the anticoagulation system. Lack of protein S leads to disseminated intravascular coagulation in the small vessels, which causes thrombosis and ischemia. Despite early treatment, amputation and skin-grafting is often necessary. In this case story, we give a brief review of the pathogenesis and possible modes of treatment. Knowledge of PF is necessary since early treatment may be life-saving.
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PMID:[Purpura fulminans]. 2061 77

Early activation of coagulation is common after traumatic brain injury. Its origin is probably mainly intracerebral, due to tissue factor release from the injured brain. Abnormalities in blood coagulation tests are associated with poor neurological prognosis. Coagulation activation may induce disseminated intravascular coagulation and fibrinolysis. Disseminated intravascular coagulation is linked to brain ischemia caused by intravascular microthrombosis. This review will focus on pathophysiology of coagulation disorders after traumatic brain injury, and on their implications for therapeutic approaches.
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PMID:[Coagulation disorders after traumatic brain injury: pathophysiology and therapeutic implications]. 2065 67

We review our baboon models of Escherichia coli sepsis that mimic, respectively, the shock/disseminated intravascular coagulation (DIC) and organ failure variants of severe sepsis, and analyse the pathophysiologic processes that are unique to each. The multi-stage, multi-factorial characteristics of severe sepsis develop as a result of the initial insult, which - depending on its intensity - activates components of the intravascular compartment leading to overwhelming shock/DIC; or initiates a sequence of events involving both the intra- and extravascular (tissues) compartments that lead to organ failure. In the latter case, the disorder passes through two stages: an initial inflammatory/coagulopathic intravascular first stage triggered by E. coli, followed by an extravascular second stage, involving components unique to each organ and triggered by ischemia/reperfusion (oxidative stress and histone release). Although a myriad of overlapping cellular and molecular components are involved, it is the context in which these components are brought into play that determine whether shock/DIC or organ failure predominate. For example, inflammatory and thrombotic responses amplified by thrombin in the first case whereas similar responses are amplified by complement activation products in the second. Rather than blocking specific mediators, we found that attenuation of the thrombin and complement amplification pathways can effectively reverse the shock/DIC and organ failure exhibited by the LD(100) and LD(50) E. coli models of severe sepsis, respectively. Translation of these concepts to successful intervention in the respective baboon models of E. coli sepsis and the application to their clinical counterparts is described.
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PMID:Pathophysiology, staging and therapy of severe sepsis in baboon models. 2197 70

Sepsis is often associated with haemostatic changes ranging from subclinical activation of blood coagulation (hypercoagulability), which may contribute to localized venous thromboembolism, to acute disseminated intravascular coagulation (DIC), characterized by widespread microvascular thrombosis and subsequent consumption of platelets and coagulation proteins, eventually causing bleeding manifestations. The key event underlying this life-threatening complication is the overwhelming inflammatory host response to the infectious agent leading to the overexpression of inflammatory mediators. The latter, along with the micro-organism and its derivatives are now believed to drive the major changes responsible for massive thrombin formation and fibrin deposition, namely 1) the aberrant expression of the TF by different cells (especially monocytes-macrophages), 2) the impairment of physiological anticoagulant pathways, orchestrated mainly by dysfunctional endothelial cells (ECs) and 3) the suppression of fibrinolysis due to overproduction of plasminogen activator inhibitor-1 (PAI-1) by ECs and likely also to thrombin-mediated activation of thrombin-activatable fibrinolysis inhibitor (TAFI). The ensuing microvascular thrombosis and ischemia are thought to contribute to tissue injury and multiple organ dysfunction syndrome (MODS). Recent evidence indicates that extracellular nuclear materials released from activated and especially apoptotic or necrotic cells, e.g. High Mobility Group Box-1 (HMGB-1) and histones, are endowed with cell toxicity, proinflammatory and clot-promoting properties and thus, during sepsis, they may represent late mediators that propagate further inflammation, coagulation, cell death and MODS. These insights into the pathogenesis of DIC and MODS may have implications for the development of new therapeutic agents potentially useful for the management of severe sepsis.
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PMID:Sepsis, thrombosis and organ dysfunction. 2206 11

Symmetrical peripheral gangrene (multilimb ischemia without large artery occlusion) is a rare condition usually associated with disseminated intravascular coagulation, hemodynamic compromise, and/or sepsis. However, it has not been described in patients on extracorporal membrane oxygenation (ECMO). Over a 5 year period, four pediatric patients developed symmetrical peripheral gangrene on ECMO after cardiac surgery. They subsequently died and came to autopsy. History, physical examination, and laboratory studies were examined. Gross and microscopic autopsy material was reviewed. Patients were 11 days to 13 years old. Extracorporal membrane oxygenation duration was 11-22 days, and limb ischemia began 2-4 days before death. Three patients had rapid onset, with ischemia developing in <48 hours. In the fourth, ischemic changes began as focal lesions and gradually spread. Two patients were septic. Three had evidence of other end-organ damage. Pressors were used in 3 patients before the limb ischemia. Autopsies disclosed ischemic changes involving all limbs, with confluent ecchymoses. In a detailed examination in 1 case, large arteries of the extremities were patent. Involved skin and soft tissue showed bland fibrin thrombi in the microcirculation, with tissue necrosis and hemorrhage. This report describes the first 4 cases of symmetrical peripheral gangrene complicating ECMO. The 4 pediatric patients all had recent surgery for congenital cardiac disease, and all had significant exposure to ECMO prior to developing limb ischemia. Symmetrical peripheral gangrene is an unusual complication of ECMO that may arise in the setting of disseminated intravascular coagulation, sepsis, or other hemostatic and/or hemodynamic imbalance.
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PMID:Symmetrical peripheral gangrene in four pediatric cardiac surgery patients receiving extracorporeal membrane oxygenation. 2240 Apr 89

We present a dramatic case of a patient presenting with disseminated intravascular coagulation related to meningococcal sepsis who developed heparin-induced thrombocytopenia following heparin administration during continuous renal replacement therapy. Association of these two prothrombotic conditions led to severe limbs ischemia and finally to bilateral legs amputation. We stress the importance of suspect heparin-induced thrombocytopenia in intensive care unit patients, especially when an improvement of other coagulation parameters is observed, and heparin therapy was started.
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PMID:Meningococcemia and heparin-induced thrombocytopenia: a dangerous combination. 2306 21

Iatrogenic vascular injury rarely occurs during lumbar disc surgery and can be fatal if it is not recognized instantly. In this paper we aim to introduce three iatrogenic vascular injuries that occurred during the lumbar disc surgery. The first case was consulted because of the sudden hypotension attack during lumbar disc surgery. The left common iliac artery and bilateral common iliac vein injuries were detected in emergency laparotomy, and repaired primarily. The second case was consulted to our clinic because of the hypotension attack at the first postoperative day. Left common iliac artery and vein injuries were diagnosed by CT angiography. Left common iliac vein was ligated and left common iliac arterial injury was repaired primarily by laparotomy. The third case was referred to our clinic for left lower extremity ischemia. Left common iliac artery injury was diagnosed by simple physical examination. Reconstruction by PTFE graft interposition was performed. The first patient died due to disseminated intravascular coagulation at the early postoperative period. Pulmonary embolus developed in the iliac vein ligated patient but was well treated by anticoagulant therapy. The last patient was discharged without any problem. Two of the patients are well on long-term follow-up.
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PMID:Iatrogenic major vascular injury during lumbar discectomy: report of three cases. 2375 80

Necrotizing fasciitis (NF) and purpura fulminans (PF) are conditions with extensive septic skin necroses that are associated with significant morbidity and mortality. NF is caused by fulminant bacterial spread on the superficial muscle fascia, Group A streptococcus being the main microorganism responsible for it. The major challenge NF poses is timely recognition. Although crucial for patient survival, early diagnosis is difficult because paucity of specific early findings does not allow setting NF apart from other, less severe, differential diagnoses. Surgical therapy consists of early and aggressive debridement of all affected tissue, even if large disfiguring wounds are left back. The responsible microorganism for PF in children is predominantly Neisseira meningitidis. Endotoxin triggered misbalance of anticoagulant and procoagulant activities of endothelial cells leads to disseminated intravascular coagulation (DIC) followed by microvascular thrombosis and bleeding, resulting in hemorrhagic skin infarction and limb ischemia. Although survival in PF is not dependent on surgery, and surgery plays not a key role in the early phase of the disease, early surgical consult to assess if limb perfusion can be improved to achieve limb salvage is still absolutely necessary. Debridement should be postponed until clear demarcation has established. Large defects after NF and PF can be successfully reconstructed with vacuum-assisted fixation of Integra (Integra LifeSciences Corporation, Plainsboro, New Jersey, United States) artificial skin before split-thickness skin grafting. This provides good functional and cosmetic results as well as good stump coverage in case of amputation in PF.
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PMID:Management of septic skin necroses. 2400 50


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