Diagnosis of disseminated intravascular coagulation

The variations of the measured dose rate in air should be recognized especially where background radiation is used as a comparative benchmark to assess radiation surveillance and environmental remediation work. In this note, the natural variations of the combined gamma and cosmic-ray background air-dose rate as measured by lithium fluoride thermoluminescence dosimeters are reported. The dosimeters were deployed monthly at locations within 150 km of the Environmental Measurements Laboratory in New York City. Urban and suburban stations were established with simultaneous indoor and outdoor measurements at some locations. Measurements were obtained over 10 to 18 years. The mean air-dose rates from the six outdoor and four indoor stations vary from 50.8 to 123.1 nGy h(-1). The range of the annual dose rates expressed as a percent-difference of the minimum and maximum is 5.3 to 18.0%. Commonly, 1-mo deviations from the long term mean of about +/-10 to +/-25% are observed. An abrupt decrease in the annual dose rate at one of the measurement sites was attributed to a minor relocation of a dosimeter. Structural shielding factors for the first and second floors of a residence are reported. The ground level location of a dosimeter inside another residence apparently resulted in a very high shielding factor. Finally, a gradual decrease of the dose rate at most of the stations is shown to exist (approximately -0.3 nGy h(-1) y(-1) for the outdoor stations). Plausible causes of this trend are briefly discussed.     

Effect of urokinase on disseminated intravascular coagulation

Our study evaluated the possible therapeutic effect of urokinase in treating the microthrombiotic effects of disseminated intravascular coagulation by assisting the activation of endogenous plasminogen. Twenty-six pigs were anesthetized, intubated, mechanically ventilated, and surgically catheterized. Septic shock was induced in all 26 pigs by an intravenous infusion of heat-killed Escherichia coli. The pigs were divided into two sets of experiments: in experiment 2 (n = 14), one-half received an intravenous dose of urokinase 1 h after heat-killed E. coli infusion and in experiment 3 (n = 12) one-half received an intravenous bolus dose and a continuous drip of urokinase 2 h after heat-killed E. coli infusion. The untreated pigs served as controls. Hemodynamic parameters, blood chemistries, and blood gases were analyzed. Urokinase given 1 h after bacterial toxin infusion significantly restored blood flow, resulting in an increase in cardiovascular and pulmonary function and improved survival rate (43% control vs. 100% treated, 24-h experimental period). Treatment given after 2 h showed some significant effect on pulmonary function; however, within 10 h of E. coli infusion, mortality rates in control and treated groups were 100 and 83%, respectively. Early administration of urokinase after onset of disseminated intravascular coagulation restored blood flow and helped resolve organ damage.     

Fatal disseminated intravascular coagulation after autologous islet transplantation

Autologous islet transplantation after pancreatectomy has been used in the surgical management of patients with intractable pain secondary to chronic pancreatitis. Total or near total pancreatectomy invariably leads to exogenous insulin dependence in these patients unless they undergo islet transplantation. Transplantation of autologous islet cells harvested from the patient's pancreas into the liver through portal vein infusion has led to long-term euglycemia in 30% to 50% of patients. We report the development of disseminated intravascular coagulation and fatal hemorrhagic shock in a 36-year-old woman after total pancreatectomy and autologous islet transplantation through retrograde infusion into the splenic vein. We report the clinical and pathological findings and discuss the possible pathophysiological mechanisms involved in the development of disseminated intravascular coagulation after this procedure.     

Tissue factor initiation of disseminated intravascular coagulation in filovirus infection

Filovirus infections in humans and primates cause intrinsic activation of the clotting cascade. Tissue factor, the normal activator of the clotting cascade, is released into the bloodstream from activated leukocytes and viral budding from infected cells. This release of tissue factor, a trans-membrane protein found in large amounts in cells preferred by filoviruses for replication, initiates the hemorrhagic complications characteristic of filovirus infection. These complications contribute to the high mortality rates of filovirus infections. Directing chemotheraputic measures at the release of tissue factor, which causes the hemorrhagic complications, will result in significant reductions of mortality rates in man and primates.     

Death associated with disseminated intravascular coagulation after hip replacement

Sudden-onset disseminated intravascular coagulation (DIC) occurred 3 h after uneventful polymethacrylate bone cement insertion for a revision left Charnley hip replacement. Profuse bleeding caused a hypovolaemic state aggravating existing myocardial ischaemia; as a result death occurred secondary to myocardial infarction 6 h after operation.     

Fibrinogen metabolism and disseminated intravascular coagulation in dengue hemorrhagic fever

In 29 patients with dengue hemorrhagic fever (DHF), 12 with grade 2 and 17 with grades 3 and 4, fibrinogen metabolism was studied by using 125I-fibrinogen; 11 of these patients were studied during shock. Hemostatic studies were also performed to search for evidence of disseminated intravascular coagulation (DIC). Increased intravascular coagulation, as judged by rapid T1/2 of 125I-fibrinogen, as well as evidence of DIC by hemostatic patients with DHF grade 2 had rapid T1/2 and only 17% had DIC. Of the 11 patients studied during shock, 91% had both rapid T1/2 and evidence of DIC, whereas 63% of the 18 patients without shock had rapid T1/2 and only 11% of this latter group had DIC. A correlation between the increased fibrinogen consumption as judged by rapid T1/2 of 125I-fibrinogen, DIC, clinical severity, and shock was demonstrated. The role of DIC in the pathogenesis of DHF is discussed, and heparin is suggested for patients with prolonged shock and severe acidosis when DIC becomes clinically apparent.     

Spontaneous remission of recurring disseminated intravascular coagulation associated with prostatic carcinoma

A 58-year-old patient with metastatic prostatic carcinoma had two well-documented episodes of disseminated intravascular coagulation (DIC) occurring 1 year apart and resolving without heparin therapy. This case illustrates that DIC need not have a poor prognosis and may resolve spontaneously despite progressive cancer. The efficacy of heparin therapy is discussed.     

Activation of coagulation and fibrinolysis in patients with abdominal true aortic aneurysm associated with disseminated intravascular coagulation

Two cases of abdominal true aortic aneurysm (AAA) associated with disseminated intravascular coagulation (DIC) were reported. Case 1 was an 81-year-old male who was admitted because of hematoma on the left leg and in whom was found by MRI an aortic aneurysm of 14 cm in diameter. Coagulation studies indicated DIC by revealing thrombocytopenia, hypofibrinogenemia and increased level of FDP. DIC was well controlled by surgical repair of the aneurysm after the administration of a small dose of heparin. Case 2 was a 60-year-old male who was admitted because of lumbago and hematoemesis and in whom was found by CT and echography an aortic aneurysm of 5.5 cm in diameter. Coagulation studies indicated DIC by revealing thrombocytopenia and an increased level of FDP. On the 2nd hospital day, he suddenly died due to the rupture of the aortic aneurysm. In most of 9 cases with AAA without DIC, plasma levels of thrombin-antithrombin III complex, plasmin-alpha 2 plasmin inhibitor complex and FDP-D dimer were also elevated. These findings indicate that the coagulation and fibrinolysis systems were generally activated in patients with AAA, and that DIC tends to occur in patients with a giant aortic aneurysm or an impending ruptured aneurysm.     

Multiorgan dysfunction and disseminated intravascular coagulation in children receiving lamotrigine and valproic acid

Two children developed multiorgan dysfunction with disseminated intravascular coagulation 9 days after lamotrigine was added to their antiepileptic therapy, which included valproic acid. During the episodes, rhabdomyolysis was detected in one of them, while being seizure-free, suggesting that this adverse reaction may involve muscular tissue.     

Outcome of disseminated intravascular coagulation in relation to the score when treatment was begun. Mie DIC Study Group

We examined 395 patients with disseminated intravascular coagulation (DIC) divided into two groups: non-leukemic and leukemic. In 58% of the patients as a whole, treatment of DIC resulted in complete or partial remission, while exacerbation and death occurred in 31%. The efficacy of DIC treatment in the non-leukemic group was less than that in the leukemic group, indicating that the outcome of DIC depended, in part, on the underlying disease. We examined hemostatic indicators in relation to DIC score: prothrombin time (PT) ratio, FDP, platelet count, and fibrinogen levels were found to be important indicators for the diagnosis of DIC, but not for Pre-DIC. Plasma levels of fibrin-D-dimer, thrombin-antithrombin complex (TAT), and plasmin-plasmin inhibitor complex (PPIC) were significantly increased in pre-DIC. The efficacy of treatment in relation to the DIC score when the treatment was begun showed that greater efficacy was achieved in pre-DIC than in DIC patients. The outcome was poorer with increasing DIC score, suggesting that early diagnosis and early treatment are important. On examining the relationship between outcome and hemostatic indicators, we found that the PT ratio and the levels of antithrombin, plasminogen, PPIC, the PPIC/TAT ratio, and thrombomodulin were related to outcome, suggesting that very high consumption of blood coagulation factors, liver dysfunction, hypofibrinolysis, or organ failure caused a poor outcome. Although the outcome in DIC patients may not depend substantially on plasma levels of TAT and fibrin-D-dimer, we can use these indicators to treat DIC patients at an early stage.     

A case of disseminated intravascular coagulation probably arising from sudden infant death syndrome

The cause of death in a 45-day-old male infant who was found apneic at home and died 21 hours later was disseminated intravascular coagulation (DIC). The patient was admitted to a hospital in a state of cardio-respiratory arrest. The initial diagnosis was interrupted sudden infant death syndrome. The patient remained apneic, and recurrent discharge of bloody stool was the dominant clinical findings. He died without spontaneous respiration being restored. The autopsy revealed hemorrhages in the lungs and the ventricular septum and the free wall of the left ventricle of the heart. Microscopically, fibrin thrombi were noted in the large intestine and heart. The DIC was probably triggered by a widespread endothelial injury caused by severe hypoxia and acidosis originating from the apnea and cardiac arrest lasting longer than 30 min.     

Pig I alpha I appears unmodified in plasma in case of endotoxin-induced disseminated intravascular coagulation

The unrestricted activity of leukocyte proteinases is thought to contribute to the degradation of plasma proteins and thus amplify the coagulation disorders occurring in septic shock. Inter-alpha-inhibitor (I alpha I) is a plasma protein particularly susceptible to their action. Therefore we investigated its behavior in a porcine model of endotoxin shock which reproduces the coagulation changes observed in human sepsis. We did not detect any qualitative or quantitative modification of porcine I alpha I in plasmas collected from pigs after endotoxin infusion. To explain these data, I alpha I was incubated with polymorphonuclear neutrophils (PMN) stimulated by FMLP in the presence of cytochalasin B. We found that, unlike human PMN, porcine cells were unable to proteolyze I alpha I. Moreover, in the incubation medium of pig PMN, triggered either by FMLP or PMA, no measurable elastase activity was evidenced. Therefore, we urge to better take into account species differences in functional responses of PMN, to explain the experimental results obtained in animal models of septic shock.     

Falciparum malaria in an overseas traveler complicated by disseminated intravascular coagulation and pulmonary edema

The fluorescence brightener Rylux BSU (RBSU) showed an affinity for polysaccharide components of cell walls and accumulated in the extension zones of hyphal apices in Basidiobolus ranarum. It inhibited the polarized growth of mycelial hyphae and induced isotropic growth resulting in spherical thick-walled cells up to 456 microm in diameter. On the inner cell wall surface, massive protuberances were formed. The cell wall and protuberances were positive in PAS and the Grocott method and stained with fluorochromes Blankophor BA, Calcofluor, Uvitex 2B, Rylux BSU and FITC-labeled WGA- and ConA-lectins. The WGA-FITC fluorescence intensity of the wall's outermost layer, if not connected with neighbouring cells, and the fluorescence intensity of the innermost layer and of some protuberances mainly in their apical parts were on the average twice higher than the fluorescence intensity of the remaining wall material. RBSU binding to the cell wall material was stable. The process of converting from polarized to isotropic growth was reversible, depending upon contact with RBSU-containing medium. Repeated transfers of cells from RBSU-containing medium to an RBSU-free medium resulted in the development of apical swollen dumbbell-shaped cells.