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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 article is based on the analysis of the hemocoagulation system in 205 patients (91 with contusion of the brain without compression and 114 with compression). Evaluation of the clinical signs, hemocoagulation disorders, and pathophysiological data revealed 89 (43.4%) cases of the disseminated intravascular coagulation syndrome. Besides other factors, exhaustion of the functioning of the anticoagulation ability of the blood in increased functioning of the coagulation system promoted the development of the syndrome. The syndrome was encountered mostly in the mesencephalobulbar (in 33 among 42 cases) and the diencephalic (in 17 of 37 cases) forms of brain lesions and in subdural hematomas (in 33 among 47 cases). Total mortality was 30.2% (62 among 205), disseminated intravascular coagulation syndrome mortality was 55% (49 among 89 cases).
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PMID:[The DIC syndrome in severe trauma to the skull and brain]. 166 45

The von Willebrand factor (vWF) has gained considerable interest in recent years as a marker of endothelial cell activation or insult and by virtue of its interactions with platelets and vessel walls. Altered patterns of vWF multimers were found to occur frequently in patients with thrombotic thrombocytopenic purpura in the acute and chronic stages. This disorder shares some clinical and laboratory findings with pre-eclampsia, including thrombocytopenia. Recent studies have also suggested that abnormalities of endothelial cell metabolism play a central role in the pathophysiology of pre-eclampsia. In order to determine if vWF could be instrumental in the disease process and the thrombocytopenia of pre-eclampsia we analyzed the ante- and postpartum structural and functional distribution of vWF. This data was correlated with hematological parameters such as platelet counts and the clinical severity of the disease. We found no consistent changes of vWF in association with thrombocytopenia or clinical severity. However, functional vWF was lower in postpartum samples of severely affected pre-eclamptics as compared to normal controls. This finding may reflect endothelial cell exhaustion after stimulation or cellular injury. Elevated titers of fibrin split products and thrombocytopenia were evident in severe pre-eclampsia, as seen in DIC, despite factor VIII coagulant levels within the normal range. Our data is consistent with the hypothesis of endothelial cell dysfunction in pre-eclampsia. However, the mechanism of thrombocytopenia in this disorder does not appear to be related to alterations in the structure or biological function of vWF.
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PMID:The role of von Willebrand factor in pre-eclampsia. 180 15

Hypertension in pregnancy remains a major cause of maternal and fetal morbidity and mortality. It is a late manifestation of a multifactorial, multisystem disease, initiated very early in pregnancy, the features of which suggest an inadequate maternal response to pregnancy. There is a genetic susceptibility to pre-eclampsia. Endothelial cell dysfunction in response to an unknown factor(s) may evoke some of the hormonal anomalies. In established severe disease there is volume contraction, reduced cardiac output, enhanced vascular reactivity, platelet exhaustion and disseminated intravascular coagulation in addition to the hypertension. Delivery is associated with resolution of the hypertension. Pharmacological treatment is most suitable for early-onset, severe disease when an attempt to delay delivery is indicated. Methyldopa or beta-blockers and/or vasodilators may be used. ACE inhibitors are contra-indicated. Low-dose aspirin may be useful in prophylaxis.
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PMID:Pre-eclampsia--the 'disease of theories'. 791 88

12 surgical critically ill patients were studied for a better management of perioperative coagulation dysfunction. Their primary disease, clinical manifestation as well as some coagulation tests before and after therapy were retrospectively analysed. The result showed that secondary disseminated intravascular coagulation (DIC) is the main type of perioperative coagulation disorder, especially in decompensated hepatopathy and severe sepsis patients. It should be emphasized that: control of primary disease, effective drainage of focus, strict indication for 2nd surgical hemostasis and correct operation are required. For those hepatopathy with hypofibrinogenemia, some hemostatic drugs should be prohibited or very carefully used, in order to avoid the activation of plasmin and the exhaustion of fibrin. The early administration of heparin and aprotinin after the supplement of fibrinogen has shown a great potential benifit to stop the cascade of hypercoagulation and hyperplasminogenemia by enhancing the level of AT-III and fibrinogen in plasma.
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PMID:[Management of coagulation dysfunction in critically surgical patient]. 959 75

The body's ability to regulate core temperature depends on both host (internal) and environmental (external) factors. Although athletes are commonly thought to be most at risk for heat illnesses, children and the elderly are particularly vulnerable. Heat cramps, which are caused by fluid and electrolyte imbalances, are treated with massage, and fluid and electrolyte replacement. Heat exhaustion occurs both as water- and sodium-depleted types, with associated symptoms such as malaise, vomiting, and confusion. Treatment involves taking the affected person to a cool environment and replacing fluids and electrolytes if needed. In more serious cases, intravenous hydration may be necessary, although monitoring of serum sodium levels is important to prevent cerebral edema. If not treated promptly, heat exhaustion may evolve into heatstroke, a deadly form of heat illness. Heatstroke occurs in classic and exertional forms and is present when the core body temperature exceeds 40 degrees C (104 degrees F). The patient may experience cardiac arrhythmias, rhabdomyolysis, serum chemistry abnormalities, disseminated intravascular coagulation, and death. Heatstroke is a medical emergency that should be treated immediately with temperature-lowering techniques such as immersion in an ice bath or evaporative cooling. Fluid resuscitation is important but should be closely monitored, and renal function may need to be protected with mannitol and diuretics. It is important to be vigilant for heat illnesses because they occur insidiously but progress rapidly.
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PMID:Evaluation and treatment of heat-related illnesses. 1272 45

The acronym DIC is commonly interpreted as "death is coming". This pessimistic view emphasizes the deficiency of available treatment options following diagnosis of disseminated intravascular coagulation. Clinically, DIC manifests as a systemic hemorrhagic disorder associated with widespread activation and eventual exhaustion of the coagulation system, although events underlying DIC also involve effectors of inflammation. DIC can be associated with diverse conditions including sepsis and major trauma and, when identified, signifies a significant worsening in prognosis and expected mortality. Although recent clinical studies have shown that activated protein C reduces mortality in patients with severe sepsis, there is a need for further investigation and a better understanding of the underlying mechanisms.
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PMID:Alternative treatments for disseminated intravascular coagulation. 1533 73

The acronym DIC is commonly interpreted as "death is coming." This pessimistic view emphasizes the deficiency of available treatment options following diagnosis of disseminated intravascular coagulation. Clinically, DIC manifests as a systemic hemorrhagic disorder associated with widespread activation and eventual exhaustion of the coagulation system, although events underlying DIC also involve effectors of inflammation. DIC can be associated with diverse conditions including sepsis and major trauma and, when identified, signifies a significant worsening in prognosis and expected mortality. Although recent clinical studies have shown that activated protein C reduces mortality in patients with severe sepsis, there is a need for further investigation and a better understanding of the underlying mechanisms.
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PMID:Alternative treatments for disseminated intravascular coagulation. 1554 51

Heat exhaustion and heatstroke are part of a continuum of heat-related illness. Both are common and preventable conditions affecting diverse patients. Recent research has identified a cascade of inflammatory pathologic events that begins with mild heat exhaustion and, if uninterrupted, can lead eventually to multiorgan failure and death. Heat exhaustion is characterized by nonspecific symptoms such as malaise, headache, and nausea. Treatment involves monitoring the patient in a cool, shady environment and ensuring adequate hydration. Untreated heat exhaustion can progress to heatstroke, a much more serious illness involving central nervous system dysfunction such as delirium and coma. Other systemic effects, including rhabdomyolysis, hepatic failure, arrhythmias, disseminated intravascular coagulation, and even death, are not uncommon. Prompt recognition and immediate cooling through evaporation or full-body ice-water immersion are crucial. Physicians also must monitor electrolyte abnormalities, be alert to signs of renal or hepatic failure, and replace fluids in patients with heatstroke. Most experts believe that physicians and public health officials should focus greater attention on prevention. Programs involving identification of vulnerable individuals, dissemination of information about dangerous heat waves, and use of heat shelters may help prevent heat-related illness. These preventive measures, when paired with astute recognition of the early signs of heat-related illness, can allow physicians in the ambulatory setting to avert much of the morbidity and mortality associated with heat exhaustion and heatstroke.
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PMID:Management of heatstroke and heat exhaustion. 1595 43

Reductions in serum levels of Gc globulin, a hepatically synthesized component of the extracellular actin scavenger system responsible for complexing circulating actin and attenuating intravascular microthrombus formation, are associated with poor outcome in acute liver failure. Clinically applicable assays of the important actin-free fraction (Af-Gc) have not been available until now. We measured actin-free Gc globulin levels with a novel, rapid assay in 61 cases of acute liver failure (ALF) and in 91 patients with cirrhosis (40 of whom were clinically unstable with extrahepatic organ dysfunction), and studied associations with liver dysfunction, extrahepatic organ dysfunction, indices of disseminated coagulation, and outcome. Reductions in Af-Gc levels mirrored hepatic dysfunction and organ dysfunction in both groups, and discriminated patients with poor prognosis from those with good prognosis in the ALF cohort. Levels were lowest in patients with ALF (10% of control values), but levels were also markedly reduced in both unstable (28%) and stable (44%) patients with cirrhosis. Associations with markers of disseminated intravascular coagulation were seen in both groups, most notably in the cirrhosis cohort, supporting a pathophysiological role for reduced Af-Gc in the evolution of organ dysfunction. In acetaminophen-induced ALF, Af-Gc identified patients with poor prognosis as well as did the Acute Physiology and Chronic Health Evaluation (APACHE II) score (area under the receiver operating characteristic curve, 0.7), and in cirrhosis, Af-Gc was an independent predictor of mortality by multifactorial analysis. In conclusion, the importance of Af-Gc reductions in the development of multiple organ dysfunction in ALF and cirrhosis is highlighted, probably resulting from reduced hepatic production and peripheral exhaustion of this arm of the extracellular actin scavenger system.
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PMID:Actin-free Gc globulin: a rapidly assessed biomarker of organ dysfunction in acute liver failure and cirrhosis. 1776

Disseminated intravascular coagulation (DIC) is a syndrome that may complicate a variety of diseases, including malignant disease. DIC is characterized by widespread, intravascular activation of coagulation (leading to intravascular fibrin deposition) and simultaneous consumption of coagulation factors and platelets (potentially resulting in bleeding). Clinically, DIC in cancer has, in general, a less fulminant presentation than the types of DIC complicating sepsis and trauma. A more gradual, but also more chronic, systemic activation of coagulation can proceed subclinically. Eventually, this process may lead to exhaustion of platelets and coagulation factors, and bleeding (e.g. at the site of the tumour) may be the first clinical symptom indicating the presence of DIC. In some cases, the clinical presentation of DIC in cancer may be reminiscent of thrombotic microangiopathies, which is understandable in view of the role of the endothelium in both conditions. The therapeutic cornerstone of DIC is treatment of the underlying disorder, but supportive treatment specifically aimed at the haemostatic system may be required.
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PMID:Disseminated intravascular coagulation in cancer patients. 1928 79


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