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.     

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.     

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.     

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.     

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.     

Fatal eosinophilic disease following autologous bone marrow transplantation

A 15-year-old girl developed massive, fatal eosinophilic disease following autologous bone marrow transplantation (BMT) for Hodgkin's disease (HD). Prior to autologous BMT, the erythrocyte sedimentation rate (ESR) was elevated, with active HD, but eosinophilia was absent. Post-autologous BMT, ESR and peripheral eosinophilia were observed to correlate with respiratory symptoms. Initial evaluation revealed no recurrent tumor, infection or other identifiable etiology. A diagnosis of chronic eosinophilic pneumonia was made following lung biopsy. A complete response was initially achieved with steroid therapy; however, when steroid therapy was tapered, the eosinophilia and elevated ESR recurred with worsening respiratory symptoms. Terminally, severe pulmonary disease developed and recurrent HD was found in lung, lymph nodes and bone marrow. During episodes of eosinophilia, the patient's serum stimulated her bone marrow as well as control marrow to produce predominantly eosinophilic colonies. Eosinophilic colony production was not observed with patient's sera obtained prior to or during autologous BMT or with control sera. This patient died of eosinophilic inflammatory disease following autologous BMT. The etiology of this disease was not definitely identified but appeared to be due to an eosinophilic-stimulating factor which developed after autologous BMT.     

Partial splenic embolization for treatment of disseminated intravascular coagulation in lymphangiomatosis

A 1-year-old boy presented with pericardial effusion, pulmonary infiltrates, and disseminated intravascular coagulation; lung biopsy indicated pulmonary lymphangiomatosis. He did not respond to medical therapy and was a poor surgical candidate; therefore, he underwent partial splenic embolization. The procedure resulted in a complete disappearance of the DIC and marked improvement in his cardiorespiratory status. He continues to thrive and is transfusion-independent 2 years after the procedure.     

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.     

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.     

A case of bacteremia and disseminated intravascular coagulation after the conduit procedure for tetralogy of Fallot with pulmonary atresia

A case undergoing conduit procedure for tetralogy of Fallot with pulmonary atresia was complicated postoperatively by bacteremia due to non-fermentative Gram-negative rods and by disseminated intravascular coagulation. He was able to be cured without any sequela. The patient was a 16-year-old male, who had undergone Blalock-Taussig anastomosis in his infancy. The present operation was carried out as follows: ventricular septal defect was closed with a Teflon-patch and discontinuity between the right ventricle and the pulmonary artery was corrected using a Hancock's valved conduit. Two weeks after the operation, pleural effusion in the right chest cavity was shown by a chest X-ray film. On the 32nd postoperative day, high fever with chills occurred, and subsequently developed pulmonary edema, shock and hemorrhagic tendencies with petechia. Pseudomonas aeruginosa, Flavobacterium and Alcaligenes faecalis were detected by the culture of pleural effusion. The platelet count decreased to about 10,000/microliters. Carbenicillin, tobramycin and minocycline were administered for the infection, and heparin and aprotinin were used for disseminated intravascular coagulation. By these treatments for about 6 months, the patient became well and was discharged without any sequela.     

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.     

Disseminated intravascular coagulation

The diagnosis of disseminated intravascular coagulation associated with intracranial pathology is discussed. This pathological entity is characterized by a diffuse bleeding diathesis. Laboratory studies suggest a consumption of all clotting and fibrinolytic factors with an elevation of fibrin split products as a sign of the fibrinolytic activity. The treatment consists of the administration of packed platelets and fresh frozen plasma to replace the consumed coagulation factors. Heparinization is recommended early to prevent further consumption of coagulation factors and epsilon-aminocaproic acid is recommended later after acute fibrinolysis is diagnosed. Constant coaguloanalytic monitoring is necessary. Although the etiology with massive injury to brain tissue is possibly secondary to autotransfusion of brain tissue thromboplastin, other causes such as hypotension, anoxia, acidosis and hemolysis must be considered.