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

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.
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PMID:A case of bacteremia and disseminated intravascular coagulation after the conduit procedure for tetralogy of Fallot with pulmonary atresia. 712 Jun 53

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

In February, 1990, a 49-year-old man was admitted with petechia and gingival bleeding. The peripheral blood showed 5,200 leukocytes/microliters including 73% abnormal promyelocytes and 24,000/microliters platelets. Bone marrow puncture revealed that nucleated cell count was 331,250/microliters including 85.4% abnormal promyelocytes with 46XY, i(17q) chromosome. Coagulation tests revealed DIC. He was diagnosed as having acute promyelocytic leukemia, and he was treated with the BHAC-DMP protocol. He achieved complete remission, and received consolidation therapy and maintenance therapy. However, he relapsed in May, 1991 with 46XY, 16q-, i (17q) chromosome. He was treated with BHAC-MV protocol and again achieved complete remission. In June, 1992, he re-relapsed and 3.6% blasts and 10% abnormal promyelocytes was found in his bone marrow. He was treated for 14 days with 15 mg Aclarubicin without any change. Then he was treated with 60 mg All-trans retinoic acid (ATRA). After administration of ATRA, his peripheral blood leukocyte count increased temporarily but bone marrow suppression continued. Then he received continuous subcutaneous infusion of 24 micrograms/day granulocyte colony-stimulating factor (rhG-CSF). After treatment with ATRA and rhG-CSF, he entered a third complete remission.
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PMID:[Complete remission induced by combined treatment with all-trans retinoic acid (ATRA) and granulocyte colony-stimulating factor (G-CSF) in a patient with relapsed acute promyelocytic leukemia]. 752 43

A few hours after a 15 km march a 19-year-old man developed a fever of 40 degrees C, accompanied by hemoptysis, tarry stools and pain in the thigh. On physical examination there was tenderness and swelling over the shoulders, upper arms and thighs as well as petechiae, bruises, hepatomegaly, pain on percussion over the kidney region and signs of hypovolaemia. There was leukocytosis (18,800/microliters) and increased creatinase activity (3900 U/l, rising to 66,300 U/l after 24 h). The platelet count fell from 147,000 to 11,000/microliters, the fibrinogen level to 0.25 milligrams. On the second day serum creatinine was 4.1 mg/dl, urine volume 50 ml/24 h, urinary myoglobin concentration 120,000 micrograms/l. The Quick value dropped to under 3%, while liver enzymes and bilirubin concentration rose. The rhabdomyolysis caused acute respiratory failure, despite symptomatic treatment of the acute renal failure and consumption coagulopathy, but after 8 weeks of intensive treatment the patient was discharged without symptoms. No cause other than the preceding physical exertion was found for the rhabdomyolysis. Muscle biopsy revealed unspecific changes 4 1/2 months after discharge.
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PMID:[Complications of an idiopathic rhabdomyolysis (Meyer-Betz syndrome) after physical exertion]. 786 81

A 26-year-old male who had been diagnosed as pulmonary tuberculosis three years ago with an antituberculous chemotherapy of only two months, complained of tiredness, exertional dyspnea and fever since a month ago. Bloody sputum, bloody stool and hematuria have developed three days before admission. Petechiae over the body trunk and lower extremities were observed on admission. Peripheral blood examination revealed lymphocytopenia (672/microliters), low hemoglobin content (6.2 g/dl), thrombocytopenia (3,000/microliters), elevated FDP (36.2 micrograms/ml) and D-dimer (25.0 micrograms/ml) values. Chest radiograph showed a massive pleural effusion in the right hemithorax, bilateral pulmonary infiltrates and a cavity on CT scan. Together with positive acid-fast bacilli in sputum, diagnoses of relapsed pulmonary tuberculosis, tuberculous pleurisy associated with DIC (disseminated intravascular coagulation) were made. Left hydronephrosis which was presumed to be a consequence of infundibulum stenosis due to renal tuberculosis, was detected by abdominal ultrasonography. Treatment with antituberculous drugs and protease inhibitors were started with thoracic tube drainage. DIC condition was improved by the 20th hospital day and sputum culture turned to be negative after the 4th week, however, fever up to 38 degrees C continued until the end of the 7th week and a D-dimer which is a representative marker for secondary fibrinolysis, continuously showed a high level up to the 10th week of hospitalization. The patient was uneventful during the three months follow up period after discharge. DIC is a well known complication of sepsis including miliary tuberculosis, whereas it is rarely associated with cavitary tuberculosis and no case of prolonged elevation of D-dimer have been reported.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of pulmonary, pleural, and renal tuberculosis associated with DIC and a prolonged increase in D-dimer]. 804 Oct 60

A 27-year-old woman visited Kanto Teishin Hospital complaining of fever and petechiae in September, 1992. Her fetus had suddenly died in the uterus two weeks before (in the sixth month of pregnancy). Total white blood cell (WBC) count was 3.2 x 10(3)/microliters with 80% promyelocytes. Bone marrow was hypercellular with 90% promyelocytes. Disseminated intravascular coagulation (DIC) was recognized. She was diagnosed as having acute promyelocytic leukemia (APL), and treatment with daily oral administration of all-trans retinoic acid (ATRA) (70 mg/body/day) was begun. On day 4, hemiplegia and aphasia appeared. Broad cerebral infarction was suspected from computed tomography. On day 9, the WBC count increased rapidly, standard chemotherapy was added and she achieved complete remission. ATRA is known to have stimulatory effects on the differentiation of APL cells, but some reports have described thromboembolic events during the administration of ATRA. In this case, ATRA might have affected coagulability resulting in cerebral infarction.
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PMID:[Acute promyelocytic leukemia (APL) resulting in broad cerebral infarction during all-trans retinoic acid (ATRA) treatment]. 813 18

A 64-year-old Japanese man with necrotizing fasciitis is reported. He developed an Enterobacter agglomerans infection in his left leg without any known causative surgery or trauma, although he had acute myelocytic leukemia as a predisposing condition. Uncommonly, the first clinical sign was petechiae. Surgical debridement could not be performed because of pancytopenia due to his original disease and chemotherapy. The patient died, and an autopsy was performed. Severe intravascular coagulation was observed in the cutaneous infected tissues, while little or no disseminated intravascular coagulation was observed in the major internal organs. The local microorganism factors such as necrotoxins were suspected to cause the intravascular coagulation in the infected tissues.
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PMID:Necrotizing fasciitis appearing with petechiae as the first clinical sign. 834 28

A 44-year-old Spanish woman travelled in Kenya without doing correct malarial prophylaxis. Upon her return to Spain, she suffered from Plasmodium falciparum malaria. She was initially treated with chloroquine for three days, but her state worsened and she was admitted to our intensive care unit. On admission, parasitaemia was 22%. She had hyperpyrexia, obtundation, hypotension, tachycardia, tachypnoea, jaundice, digestive haemorrhage, petechiae in her soles, oliguria with elevation of serum uraemia and creatinine, anaemia, thrombocytopaenia, hypoproteinaemia, hyponatraemia, hypocalcaemia, metabolic acidosis and parameters of disseminated intravascular coagulation. She was given quinine, sulfadoxine-pyrimethamine and clindamycin. An exchange transfusion was performed, during which an acute pulmonary oedema appeared, initially with high pulmonary artery wedge pressure. She required mechanical ventilation for 16 days and haemodialysis for 11 days. She remained in coma and had seizures which required diazepam, phenitoin and thiopentone. She received a total amount of 22 units of packed erythrocytes, 55 of platelets and 15 of plasma. After the first week, she had nosocomial infection due to Escherichia coli, Staphylococcus and Pseudomonas aeruginosa and was treated with the corresponding antibiotics. She cured completely. This case report gives us the possibility of discussing on frequent problems in the prevention and treatment of malaria, and on the treatment of severe, life-threatening malaria in the setting of the intensive care unit.
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PMID:[Multiple organ failure in Plasmodium falciparum malaria]. 853 25

We report on a 3 year old girl with acute promyelocytic leukemia (APL) with cerebral infarction due to disseminated intravascular coagulation (DIC) at initial presentation. She was hospitalized because of unconsciousness and petechiae on the chest wall and extremities. Cerebral ischemia and infarction were found on computed tomography scan and magnetic resonance imaging. Peripheral blood content was hemoglobin 7.3 g/dL, white blood cells 1.0 x 10(3) cells/microL (31% blasts) and platelet count was 12 x 10(3) cells/microL. Fragmented erythrocytes were frequently observed on May-Giemsa stained blood smears. Bone marrow aspirates showed normal cellularity, with 60.4% blasts, containing faggot cells. The blasts were positive for peroxidase. Therapy was begun; however, the patient died 1 week after admission.
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PMID:Cerebral infarction in acute promyelocytic leukemia at initial presentation. 877 58

A 44-year-old women was treated for hyperparathyroidism resulting from parathyroid hyperplasia. Several months later, following a flu-like episode, she developed fever, confusion, abdominal pain, and diffuse petechiae, with severe thrombocytopenia and hemolytic anemia. She died on the 11th day of hospitalization. At autopsy she had multiple endocrine neoplasia type I, with two islet cell tumors, adrenal adenoma, pituitary adenoma, and bronchial carcinoid with liver metastasis. Florid visceral microthrombi involved arterioles and capillaries of the heart, including the conduction system. Brain, kidney, pancreas, adrenal, and portal areas of the liver were also heavily involved, but thrombi were rare in the liver sinusoids and the lungs. PAS-positive subendothelial deposits were demonstrated. In spite of the disseminated malignancy, the morphologic and laboratory findings were inconsistent with disseminated intravascular coagulation (DIC), and supported the clinical diagnosis of TTP. To the best of our knowledge this is the first report association of TTP with MEN and raises the question of a genetic linkage and/or hormonal interaction.
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PMID:Fatal thrombotic thrombocytopenic purpura (TTP) presenting concurrently with metastatic multiple endocrine neoplasia (MEN) type I. 887 34


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