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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 clinical and laboratory characteristics of a severe form of hemorrhagic fever with renal syndrome (HFRS) in Greece are presented. Twenty-seven patients with serologically confirmed HFRS were studied; 10 required renal dialysis, six had hemorrhagic manifestations, and four died. In patients with hemorrhagic manifestations, the platelet counts were generally less than 100,000 cells/microL. In three patients findings were compatible with disseminated intravascular coagulation. Laboratory investigation showed a consistent rise in levels of serum urea nitrogen and creatinine beginning on the fifth or sixth day of illness and reaching a maximum level between the ninth and 12th days of illness. The disease in Greece more closely resembles the Asian form of HFRS (Korean hemorrhagic fever) than the Scandinavian form of the disease (nephropathia epidemica) because of the high mortality rate, the occurrence of hemorrhagic manifestations, and the severity of the clinical disease.
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PMID:Hemorrhagic fever with renal syndrome in Greece: clinical and laboratory characteristics. 256 79

Hantaviruses, the causative agents of HFRS, have become more widely recognized. Epidemiologic evidence indicates that these pathogens are distributed worldwide. People who come into close contact with infected rodents in urban, rural and laboratory environments are at particular risk. Transmission to man occurs mainly via the respiratory tract. The epidemiology of the hantaviruses is intimately linked to the ecology of their principal vertebrate hosts. Four distinct viruses are now recognized within the hantavirus genus and that number is likely to increase to six very soon; however, further investigations are necessary. Much more work is still needed before we fully understand the wide spectrum of clinical signs and symptoms of HFRS as well as the pathogenicity of the different viruses in the hantavirus genus of the Bunyaviridae family. HFRS is difficult to diagnose on clinical grounds alone and serological evidence is often needed. A fourfold rise in IgG antibody titer in a 1-week interval, and the presence of the IgM type of antibodies against hantaviruses are good evidence for an acute hantavirus infection. Physicians should be alert for HFRS each time they deal with patients with acute febrile flu-like illness, renal failure of unknown origin and sometimes hepatic dysfunction. Especially the mild form of HFRS is difficult to diagnose. Acute onset, headache, fever, increased serum creatinine, proteinuria and polyuria are signs and symptoms compatible with a mild form of HFRS. Differential diagnosis should be considered for the following diseases in the endemic areas of HFRS: acute renal failure, hemorrhagic scarlet fever, acute abdomen, leptospirosis, scrub typhus, murine typhus, spotted fevers, non-A, non-B hepatitis, Colorado tick fever, septicemia, dengue, heartstroke and DIC. Treatment of HFRS is mainly supportive. Recently, however, treatment of HFRS patients with ribavirin in China and Korea, within 7 days after onset of fever, resulted in a reduced mortality as well as shortened course of illness.
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PMID:Hemorrhagic fever with renal syndrome. 257 14

Clinical symptoms and laboratory measures of renal and liver function, coagulation, and inflammatory parameters were prospectively studied in 74 hospitalized patients (14-74 years of age) with serologic evidence of nephropathia epidemica. The most common clinical findings were acute onset of symptoms, fever (greater than or equal to 38 degrees C), thirst, headache, nausea, back pain, vomiting, myalgia, and abdominal pain. Twenty-seven patients (37%) had hemorrhagic manifestations, i.e., epistaxis, melena, hematemesis, petechial bleeding, macroscopic hematuria, or metrorrhagia. Disseminated intravascular coagulation developed in four patients. Fifty-one percent had thrombocytopenia. Proteinuria was recorded for all patients, while hematuria and glucosuria were noted for 85% and 58%, respectively. Serum creatinine levels were elevated in 71 (96%) of the patients. Levels of C-reactive protein or erythrocyte sedimentation rates were elevated in all cases, usually to levels found in serious bacterial diseases. Sixty-six (89%) of the patients were followed for up to 7 months, at which time all had recovered clinically. No patient died or required dialysis. We conclude that nephropathia epidemica in Sweden has a clinical picture similar to that of hemorrhagic fevers in other parts of the world, but with a milder course and a better prognosis.
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PMID:Clinical characteristics of nephropathia epidemica in Sweden: prospective study of 74 cases. 257 3

A veterinarian dealing with critical and trauma patients must be proficient with techniques for tracheostomy, thoracostomy tube placement for chest drainage, diagnostic peritoneal lavage, and autotransfusion. The utilization of these techniques may be life-saving in the critical patient. A tracheostomy is indicated in any patient with upper airway obstruction that cannot be managed with supplemental oxygen and/or orotracheal intubation. A tracheostomy tube with an inner cannula is preferred. Tracheostomy tubes should be cleaned at 3- to 4-h intervals, and methods should be employed to decrease thick tracheal secretions and to remove them from the trachea. A patient with a tracheostomy tube should be monitored continuously. A thoracostomy tube is indicated in any patient with large and/or continuous accumulation of air, blood, fluid, or chyle in the pleural space. The thoracostomy tube should be at least the same size as the patient's main stem bronchus. The thoracostomy tube is placed aseptically at the seventh intercostal space at the junction of the upper one third and lower two thirds of the lateral chest wall. Fluid or air may be removed from the chest intermittently with a three-way stopcock attached to the thoracostomy tube and a 60-ml syringe. If continuous drainage is needed, a continuous underwater seal and suction system should be used. Diagnostic abdominal paracentesis and peritoneal lavage are useful techniques in the determination of abdominal trauma, hollow viscus rupture, peritonitis, hepatic trauma, and urinary system trauma. When a multiholed catheter and lavage are used, the accuracy of detecting abdominal trauma is 95 per cent. When only needle paracentesis is used, the accuracy drops to 47 per cent. Abdominal lavage fluid can be analyzed for bacteria, whole blood, white blood cells, free bilirubin, creatinine, blood urea nitrogen, amylase, alkaline phosphatase, and alanine aminotransferase. Large volumes of whole blood recovered from abdominal or thoracic paracentesis can be reinfused into the patient if needed, providing it is not contaminated or markedly hemolyzed. The blood should be collected aseptically into blood bottles or bags. If the bleeding is ongoing or the blood only a few hours old, anticoagulants should be used. If the hemorrhage is several hours old, then clotting and defibrination has already occurred and the blood can be collected into "dry" bags or bottles. Before use, abdominal blood should be analyzed for urine, bile or fecal contamination. Blood collected from the thoracic cavity is much less likely to be contaminated. Autotransfused blood is administered through a standard blood administration set.
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PMID:Critical care surgical techniques. 268 82

A new reproducible animal model of sepsis was established to investigate interrelationship between disseminated intravascular coagulation (DIC) and multiple organ failure (MOF). Sepsis was induced by injecting fecal suspension into bile duct of rabbits, in which the amount of endotoxin in circulating blood was gradually increased and manifestations of sepsis were confirmed. During 9 hours' observation period, an occurrence of hypercoagulable state leading to DIC was evidenced by the abnormal hemostaseological parameters. Simultaneously the elevation of plasma bilirubin and creatinine levels was observed, indicating the presence of liver and kidney failure, which was confirmed by the histological examination. Thereby, the present sepsis model complicates DIC and MOF with high reproducibility, which is relevant to sepsis seen in clinical patients.
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PMID:Sepsis model with reproducible manifestations of multiple organ failure (MOF) and disseminated intravascular coagulation (DIC). 272 56

The case is presented of a 36-year-old secundipara with the uterine myoma and a mild form of EPH gestosis. She became icteric and anuric on the sixth day after a spontaneous vaginal delivery and an apparently uneventful early puerperium. Blood coagulation tests were characteristic of disseminated intravascular coagulation (DIC). Since it is postulated that the appearance of DIC could be connected with the probable necrosis of a preexisting uterine myoma, abdominal hysterectomy was performed on the 8th puerperal day. Because of a persisting acute renal failure with highly elevated BUN levels and creatinine, the patient was subjected to haemodialysis every day during the next 73 days. After 3 months of this treatment she was discharged from hospital with a reduced but satisfactory renal function. The pathogenesis of DIC and acute renal failure following necrosis of the uterine myoma is discussed.
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PMID:[Acute renal failure following necrosis of a myoma in the puerperium]. 273 39

The toxicity of hemoglobin solutions was studied in the context of their ability to activate serum complement (C). Three bovine polymerized hemoglobin solutions (BPHSs) with different degrees of purity were used for experiments in vitro and in vivo. BPHS-1 contained bacterial endotoxins (E) (5 EU/ml) and stromal phospholipids (PLs) (1.2 mg/dl), BPHS-2 contained only PLs (2.0 mg/dl), while BPHS-3 was completely free of both contaminants. C-activation was studied by the direct measurement of C3a, C4a, and C5a des Arg fragments, using commercially available RIA kits. During 1 hour of incubation with fresh monkey plasma, BPHS-1 and -2 activated both pathways of C, while BPHS-3 caused no activation of any factor. In vivo, Hb solutions were used to replace one-third of blood volume in three groups of six Coebus monkeys each, while fresh homologous plasma was used in a control group of four animals. Impure solutions activated the alternative pathway of C and caused significant reactions of the circulating blood (thrombocytopenia, leukopenia, and disseminated intravascular coagulation) associated with multiorgan dysfunction (cardiac arrhythmias, hypoxemia, reduction of renal clearance of endogenous creatinine, and elevation of liver enzyme SGPT). The pure solution neither activated C nor caused any reaction in the circulating blood. However, it caused a moderate degree of direct tissue injury, evidenced by transient reduction of creatinine clearance and elevation of SGPT. These observations suggest that impure and pure Hb solutions carry separate mechanisms of toxicity. Complement, activated by toxic impurities, plays an active role in the toxicity of impure solutions. C-activation in vitro could be used as a screening test of biocompatibility.
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PMID:Complement activation and the toxicity of stroma-free hemoglobin solutions in primates. 316 73

The state of microcirculation and blood rheology was studied in 32 patients with chronic renal insufficiency. Improved microcirculation and the reduction of clinico-laboratory indices of the DIC-syndrome were noted against a background of heparin and antiaggregant therapy in patients on programmed hemodialysis as well as in patients receiving systemic conservative therapy. In both groups of patients blood pressure decreased in parallel with a decrease in the level of creatinine and urea; a tendency toward improved renal function was noted.
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PMID:[Correction of blood rheological disorders in patients with chronic kidney failure using heparin and antiaggregants]. 317 33

A total of 29 patients with chronic renal insufficiency (CRI) were investigated. Noticeable disorder of erythrocytic deformability (ED) was detected in half of them. The expression of arterial hypertension showed correlation with a degree of ED disorder. A possibility of the main role of ED disorder in the development and progression of arterial hypertension was discussed. ED disorder was found to correlate with a degree of expression of laboratory signs of the DIC-syndrome and was practically unassociated with the blood level of creatinine.
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PMID:[Relation between arterial hypertension and disorder of erythrocyte deformability in patients with chronic renal failure]. 320 74

Four solutions of bovine polymerized hemoglobin (BPHS) and rabbit plasma were used to replace one-third of the blood volume in five groups of rabbits. The first three solutions were "impure" because of the presence of stromal phosphatidyl-ethanolamine and phosphatidyl-serine in BPHS-1, environmental endotoxins in BPHS-2, and a large amount of higher molecular weight hemoglobin-glutaraldehyde polymers in BPHS-3. These solutions caused a 33 per cent mortality rate and significant morbidity which was characterized by hemodynamic instability, respiratory and renal insufficiency, elevation of hepatic enzyme levels, thrombocytopenia, leukopenia, disseminated intravascular coagulation (DIC) and activation of the alternate pathway of complement. Histopathologic changes found in the heart, lungs, liver, spleen and kidney were characterized by a combination of ischemic and inflammatory lesions. Fibrin thrombi were visible by immunofluorescence in the microcirculation. In contrast, the fourth solution (BPHS-4) was free of the aforementioned impurities; caused no deaths and minimal morbidity, which was limited to elevated levels of serum glutamic pyruvic transaminase and reduction of creatinine clearance; no DIC or complement activation, and mild histopathologic changes which were exclusively ischemic in nature. The results of this study indicated that the toxicity of polymerized hemoglobin solutions is due principally to the presence of impurities. Pure hemoglobin does exhibit mild toxicity when compared with a control solution which is most likely due to a vasoconstrictor effect of oxyhemoglobin.
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PMID:Toxicity of polymerized hemoglobin solutions. 334 50


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