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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 appearance of lesional edema in the region of the alveolar wall constitues the initial phenomenon of involvement of the pulmonary parenchyma during shock lung, fat embolism, DIC and post perfusion lung syndrome. The alveolar septum reacts in a monomorphous manner to these various agressions, although the responsible physiopathological factors are numerous and varied. The lung in E.C.C. represents a vertiable experimental post-agressive lung. It has been studied in man from the clinical, radiological, hemodynamic and anatomopathological standpoints. The modifications found enable one to better understand the etiological factors intervening in the other post-agressive lungs.
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PMID:[Pulmonary edema due to shock, fat embolism, disseminated intravascular coagulation and post extracorporeal circulation]. 0 70

Cerebral fat embolism was established as the cause of death in a 34-year-old man with acute pancreatitis. Encephalopathy complicating pancreatitis may be due to hypoxia secondary to pulmonary fat embolism, cerebral fat embolism, or the complicating syndromes of disseminated intravascular coagulation or hyperosmolality.
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PMID:Pancreatic encephalopathy. 32 Jun 76

The clinical course and radiographs of 30 patients with fat embolism syndrome were reviewed. In all cases the classic triad of neurologic dysfunction, respiratory insufficiency, and petechiae were present. Three responses to embolized fat were noted. The hyperacute response was seen in two patients with paradoxical embolization of fat to the systemic circulation. A "classic response" was noted in 18 patients with transient respiratory compromise and variable radiographic findings. The two deaths in the group responding in the classical manner were attributed to massive pulmonary emboli. The third response, noted in ten patients, consisted of a chest radiograph compatible with pulmonary edema in the clinical setting of the adult respiratory distress syndrome. In this group the degree of respiratory dysfunction and pulmonary damage correlated with the development of disseminated intravascular coagulation. Pathologic correlations are presented and the mechanisms by which embolic fat produces tissue damage are discussed.
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PMID:The three syndromes of fat embolism: pulmonary manifestations. 45 28

Combined injuries occur in a great number. More than half of the deaths in accidents are caused by combined injuries. In more than 70 per cent of these, brain injury is the decisive lethal factor. Shock, respiratory disturbances, signs of fat embolism, coagulation disturbances have to be assessed first. The primary shock therapy begins with the filling up of the volume by colloid solutions. If internal bleedings are the cause of the shock, they must be treated first. Respiratory insufficiencies are mainly due to thorax injuries. Although systematic treatment cannot remove the fact of a fat embolism, it can keep its pathophysiological consequences within certain limits. Among the coagulation disturbances, special attention should be paid to the consumption coagulopathy. As regards the brain, attention should be paid to the increase in intracranial pressure as well as to increase in body temperature, decrease in oxygen saturation, and the like, the combination of which often has a deleterious effect. In the timing, the shock therapy is followed by an orientating examination (including state of consciousness, possible internal haemorrhages, bone fractures, etc.), provisional immobilisation, pain relieving and, when required, sedation. Intracranial complications must be looked for in all their phases. Osteosynthesis is not carried out as part of the primary treatment but usually only one week later. Open brain injuries have no priority but intracranial haematomas have an absolute priority. Surgical treatment of liquor fistulas should only be carried out in the acute phase when extensive impression fractures are present at the same time.
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PMID:[Timing in the treatment of multiple injuries]. 55 Jun 45

Forty-five patients with multiple injuries treated at an intensive care unit were studied prospectively. The patients were divided into two groups: the severely injured (no mortality) and critically injured (56% mortality). Treatment was started within two hours from the accident in all cases. The following coagulation parameters were measured for eight days: euglobulin lysis time (ELT), thromboelastography (TEG), vecalcification time (RECA), partial thromboplastin time (PTT), factor V, factor VIII, Normotest, Thrombotest, thrombin time, fibrinogen and platelets. Severe coagulation disorders were observed in one-third of the patients 12-48 hours after trauma. The abnormalities were more pronounced in patients who had sustained very severe injuries and arrived in a state of shock. The ELT was shortened 0-6 hours after the accident and accelerated coagulation was indicated simultaneously by decreased PTT, RECA, and r-values as well as by elevated Thrombotest and factor VIII values. The factor V and fibrinogen levels were initially lowered. Low platelet values at 2-4 days, prolonged thrombin and r-times, secondary decrease of fibrinogen FV, FVIII, and low Thrombotest values suggested disseminated intravascular coagulation associated with complications, such as fat embolism and "shock lung" syndromes. General bleeding tendency with high mortality was observed in 16% of the patients.
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PMID:Coagulation disorders in severely and critically injured patients. 60 16

If the underlying pathology of the syndrome of fat embolism is the presence of circulating emboli of neutral fat with adherent platelets and red blood cells, then one could expect certain changes in normal vascular cellular elements and fat metabolism, with resultant alterations in pulmonary function. In our series of 118 patients with fractures of the lower limbs we found that more than half of them exhibited hypoxemia as well as a decrease in the hematocrit and platelet counts with a concomitant increase in platelet adhesiveness. In addition, those patients with hypoxemia showed increased fibrinogen degenerative product levels indicating an increased fibrinolysis. We found only a slight temporary rise in the serum triglycerides, but the nonesterified fatty acid levels rose sharply over the first three days following trauma associated with an increase in serum lipase. Our study demonstrated that this increase in serum lipase occurred slightly before the peaking tendency observed in the nonesterified fatty acids. Following trauma, fat emboli with adherent platelets and other vascular cellular elements are formed; we would expect that these emboli would lodge in the capillaries and small vessels of the lung, thereby producing a physiological shunt. An increase in the A-aDo2 confirmed this hypothesis and was associated with a decrease in the arterial oxygen level in over half the patients studied. Although 58 of our patients showed evidence of hypoxemia associated with a fall in hematocrit and platelet count, not one of them showed clinical signs and symptoms of the fat embolus syndrome. This study suggests that a subclinical form of fat embolism does exist. What causes a small percentage of those patients with subclinical fat embolism to progress to a clinical fat embolism is still unknown. The majority of our patients spontaneously returned to normal within 5 days. Reviewing the results of those patients who developed hypoxemia and the two patients who developed clinical fat embolism, there seems to be no indication of what causes the progression. Hypotension and shock do not seem to be relevant to the progression of the subclinical condition. Not one of 110 reviewed had evidence of shock or persistent hypotension, yet 58 of these patients developed changes in arterial saturation, vascular elements, and evidence of disseminated intravascular coagulation.
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PMID:Alterations in pulmonary function, coagulation and fat metabolism in patients with fractures of the lower limbs. 125 90

Altered clotting encompasses a wide spectrum of clinical conditions ranging from bleeding disorders to abnormal clot formation. DIC is an abnormal overstimulation of the normal coagulation process resulting from several clinical conditions that illustrate these extremes. In orthopaedic patients, DIC can develop following trauma (crush injuries), tissue necrosis, fat embolism, gram-negative or gram-positive sepsis, and venous stasis (bedrest). Because of its occurrence as a secondary process and its subtle development, DIC can elude early recognition, diagnosis, and treatment.
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PMID:Disseminated intravascular coagulation: a nursing challenge. 260 99

In our opinion, this clinical study demonstrates the intravascular formation of globules, macroglobules and their aggregations both in the association with the type of general anaesthesia and with the operative osteosynthesis of long bones. Within the framework of this study changes in the level of lactic acid in blood serum and of total ketosubstances in blood were followed as well as the levels of total lipids, triglycerides, phospholipides, serum lipase, non-esterified and esterified fatty acids, changes in blood coagulation and 17-ketosteroides in blood. The observed changes supported the opinion that the development of fat globulemia was associated with humoral and physicochemical changes in blood. Repeated evaluations of fat globulemia in plasma are important for studies on pathogenesis and development of fat embolism. In practice, they help: to diagnose especially subclinical forms of fat embolism with non-marked clinical symptoms; to define a suitable term of both primary and delayed operation performed in the period of ending katabolic phase after severe trauma; to define an optimum time for the indication of osteosynthesis to the end of manifest fat embolism; to control positive effects of drugs used for the prophylaction and treatment of fat embolism. In this way it is possible to objective the effectiveness of a rational prophylaxis and treatment of fat embolism. Following factors contribute to macroglobulamia and to manifestation of F. E.: injuries to bones, tissues and organs; stress, posttraumatic shock; severe hemorrhagic hypotension; posttraumatic hypercoagulation with possible binding to the development of a consumption coagulopathy; heavy changes of acid-base balance; increase of catecholamines in plasma; hormonal and general metabolic disturbances; posttraumatic dyslipidemia with special regard to the decrease of beta-lipoproteins and of lipoproteinlipase activity together with the increase of lipoproteins having a very low density and with the occurrence of a significant lipoprotein coalescence. The prospective study on the globulemia changes is based on the following examinations: in 76 injured patients: a short time observation (24 hours) of the globulemia changer after osteosyntheses in general anesthesia. The operative interventions were usually performed 6 to 8 days after injury. in 60 injured patients with fractures (single or multiple fractures, fractures in polytrauma patients): a long-time observation (28 days) of the globulemia changes.
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PMID:Fat globulemia in early diagnostics of traumatic fat embolism. 308 41

Fat embolism is a known complication of marrow infarction in patients with sickle cell disease (Hb S/S and Hb S/C) disease. It should be considered in sickle cell crisis when there is deterioration in respiratory function, a fall in arterial PO(2), a normoblastaemia, and a thrombocytopenia in the peripheral blood. We now report a patient in whom the diagnosis was confirmed in life by identifying fat in the sputum, demonstrating disseminated intravascular coagulation, and using a double isotope technique to distinguish recent from old marrow infarction. Use of these features enabled an early diagnosis to be made which led to a successful outcome in a potentially fatal condition.
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PMID:Fat embolism in sickle cell disease. 473 65

The pathophysiologic mechanism of fat embolism syndrome (FES) has been thought to depend on mechanical blockage of capillaries by fat emboli or on the toxic effect of free fatty acids on the capillary endothelium. Aggregation of platelets, microembolism, disseminated intravascular coagulation, and vasoactive amines are considered to be involved. The question of why some patients develop fat embolism while other patients with similar injuries do not remains to be solved. Blood tests in ten patients who developed FES and their reaction to stress were compared to the same tests in ten patients with similar injuries without FES at least 1 year after trauma. The following were measured: blood Hb, leucocytes, platelets, protein and lipid electrophoresis, ACTH, cortisol, TSH, GH, insulin, glucose, NEFA, certain coagulation and fibrinolytic studies, alpha 1 antitrypsin, and antithrombin III. The platelet values, especially after stress, and P + P values were higher in the FES-patients. The alpha-beta lipoprotein ratio was lower and the blood glucose values were higher in half of those FES-patients in whom a diabetic heredity was discovered. The U-catecholamines were also somewhat higher in the FES-patients. Disturbances of the lipid and carbohydrate metabolism as well as a high platelet count and high P + P values may predispose to thrombosis and DIC. More numerous petechiae in Rumpel-Leede's stasis test in fat embolism patients suggest increased capillary fragility. Low growth hormone values in FES-patients and a different cortisol reaction to stress compared to control patients suggests a disturbed neurohumoral regulation in FES.
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PMID:Stress hormones, lipids, and factors of hemostasis in trauma patients with and without fat embolism syndrome: a comparative study at least one year after severe trauma. 735 96


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