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

An infant, aged seven months, developed toxic shock with acute renal failure as a sequel to the development of hypertonic dehydration. The anuric phase persisted despite treatment of the dehydration and diuretic infusions. The coagulation tests showed signs of disseminated intravascular coagulation and so the child was given fibrinolytic therapy for 36 hours following initial heparinization. Excretion of urine recommenced 8 hours after the initiation of fibrinolytic therapy. Peritoneal dialysis was carried out in parallel with the fibrinolytic treatment without haemorrhagic complications. It was possible to terminate dialysis on the fourth day already and renal function subsequently recovered completely.
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PMID:[Disseminated intravascular coagulation and acute renal failure in an infant. Treated with streptokinase and peritoneal dialysis (author's transl)]. 121 46

On the basis of three case histories we discuss the menstrual toxic shock syndrome (TSS), characterised by multi-organ involvement, fever, exanthema and shock. The symptoms are provoked by a toxin (TSST-1), a product of certain St. aureus strains. Rapid recognition is important in order to prevent complications such as the adult respiratory distress syndrome, disseminated intravascular coagulation or ventricular fibrillation. It appears that a tampon can lower the magnesium concentration in the vagina by a process of ion exchange, thus creating an environment that favours the production of TSST-1 by St. aureus. This knowledge may lead to preventive measures in the production of tampons in the future.
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PMID:[Tampon disease, still not past tense]. 156 Aug 69

Acute infections with group A beta-hemolytic streptococcus normally take a favourable course under therapy with penicillin. Only in a few cases has a completely different manifestation been described with multisystem failure similar to toxic shock syndrome induced by Staphylococcus aureus. We report on 4 patients (1990/91) who showed this manifestation in spite of immediate antibiotic therapy. In 3 patients the suspected portal of entry was the skin, in 1 patient it was unknown. Group A streptococci were grown from blood cultures from all 4 patients. Without an underlying immune deficiency all 4 patients (age 22, 24, 38 and 51) went into septic shock with high fever, hepatic and renal impairment, diarrhea, DIC and cerebral confusion. 2 patients died within a few days after developing acute respiratory distress syndrome and cerebral edema. All strains isolated from the patients were penicillin-sensitive, group A streptococci. 3 of them were M-type 1, which are known to be more invasive. The bacteremia by itself is not sufficient to explain all complications and the high mortality rate. It is probable that streptococcal toxins, such as pyrogenic exotoxin A, streptolysin O, or a new unknown one, play a decisive role.
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PMID:[Toxic shock syndrome in infection due to Streptococcus pyogenes]. 173 21

The most frequent cause of toxic shock in our area is meningococcal sepsis. It is currently assumed that endotoxin produce by this bacteria, a lipopolysaccharide with toxic properties, is able to trigger shock and DIC by stimulating both arachidonic acid pathways, among other actions. Previous studies in our laboratory demonstrated significant differences (p +/- 0.001) in the amounts of endotoxins released in vitro by strains from patients and healthy carriers and statistically related criteria of severity with mortality in 256 patients in our center over the last 10 years. In the present study we attempted to establish whether plasma levels of endotoxin were correlated with the severity of the disease. We studied 32 patients with meningococcal sepsis, dividing the subjects into two groups: those in whom six or more criteria of severity were present, and those in whom less than six criteria were found. Blood levels of endotoxin were determined upon admission and after the administration of antibiotics (penicillin and chloramphenicol) using the limulus test with a chromogenic substrate (Coatest, Endotoxin, Kabivitrum, Sweden). Levels of endotoxins were significantly higher in patients with more than six criteria of severity both upon admission (0.6 +/- 0.03) ng/ml) and 4 h. afterward (0.74 +/- 0.006 ng/ml) in comparison to children in whom the clinical picture was less serious (0.27 +/- 0.18 ng/ml and 0.27 +/- 0.18 ng/ml and 0.27 +/- 0.16 ng/ml7 t = 5.8 y t = 5.6 respectively. Endotoxin levels were highest in patients presenting shock, disseminated intravascular coagulation in the hypocoagulability phase and more than 8 criteria.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Studying the levels of endotoxemia in meningococcal sepsis. Its relations to pregnancy and antibiotic treatment]. 188 9

The results of the clinico-morphological examination of the bacteriologically confirmed meningoencephalitis in 12 autopsy cases are presented. The gravity of the clinical course of the pneumococcus meningoencephalitis is due to infectious-toxic shock the main morphological manifestation of which is disseminated intravascular coagulation. Neurotoxicosis symptoms prevailed in the clinical picture of the infectious-toxic shock even though the morphological changes characteristic of shock were found in the brain as well as in the internal organs particularly in the adrenals, lungs and kidneys. The peculiar feature of the disseminated intravascular coagulation was the domination of the hypercoagulation stage with the variety of intravascular fibrin formations (fibrin, hyaline, globular thrombi, prethrombi, fibrinous threads).
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PMID:[The pathological anatomy of pneumococcal meningoencephalitis in adults]. 233 87

Infectious toxic shock, acute renal and acute hepatorenal insufficiency are the principal morphoclinical syndromes in malignant forms of icterohemorrhagic leptospirosis. The major complications of acute renal and hepatorenal failure are pyoseptic involvements of the lungs, heart, and pancreas. Direct or indirect signs of the DIC syndrome and intravascular platelet aggregation are characteristic of all the principal clinical syndromes of malignant forms of leptospirosis.
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PMID:[Clinico-morphologic characteristics of leptospirosis with hemorrhagic syndrome]. 234 4

A relationship between PM severity and early onset of dramatic microcirculatory disorders of the brain and viscera leading to DIC syndrome and infective toxic shock has been reported in a clinicomorphological study of 12 PM cases. Being the main PM target, the brain is afflicted more seriously. The related shock has specific features: toxicosis and brain swelling. They should be taken into consideration when performing reanimation.
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PMID:[Clinico-morphologic characteristics of pneumococcal meningoencephalitis]. 262 24

Report on the first case of streptococcal toxic shock syndrome in the GDR. The patient was a 54-year-old female. One week before admission to the hospital she cut her finger. The day before admission to the hospital she presented with a painful left shoulder. Demarcation followed, and Streptococcus pyogenes (group A streptococci) was isolated from this area. The temperature rose to more than 40 degrees C and she became confused, hypotensive and anuric. There was evidence for disseminated intravascular coagulation. She died 23 h after admission. Clinical course and laboratory parameters resembles staphylococcal toxic shock syndrome, except a diarrhoea. The streptococcal strain produced a large amount of erythrogenic toxin type B (more than 20 ng/ml), but not erythrogenic toxins A or C. Erythrogenic toxins of Streptococcus pyogenes seem to play the same role in the development of streptococcal toxic shock syndrome as the toxic shock syndrome 1 (TSST-1) in staphylococcal toxic shock syndrome.
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PMID:[Streptococcus-induced syndrome of toxic shock (streptococcal toxic shock syndrome)]. 269 6

Phosphatidylinositol-specific phospholipase C (PIPLC), an enzyme that can specifically release phosphatidylinositol-linked proteins from host cells, is one of the extracellular enzymes produced by Staphylococcus aureus. To investigate whether PIPLC might be a virulence factor, we assessed PIPLC production by S. aureus strains that had been isolated from healthy carriers and from infected patients with or without toxic shock syndrome. Although none of five vaginal isolates from healthy women was a PIPLC producer, only 10 of 32 selected pathogenic strains that caused significant infections or toxic shock syndrome elaborated PIPLC enzyme activity. Seven of 24 toxic-shock-associated strains, compared with 3 of 8 non-toxic-shock-associated strains, were positive for PIPLC. The majority of strains that produced PIPLC were negative for toxic shock syndrome toxin 1 (P less than 0.05); this association between PIPLC production and strains negative for toxic shock syndrome toxin 1 was even stronger among strains isolated only from patients with toxic shock syndrome (P less than 0.01). Among all 32 pathogenic isolates, PIPLC-producing S. aureus strains were isolated from four of four patients developing adult respiratory distress syndrome and four of five patients with disseminated intravascular coagulation, suggesting a significant association between PIPLC production and adult respiratory distress syndrome and/or disseminated intravascular coagulation (P less than 0.002). On the basis of these results, we propose that PIPLC is a virulence factor of S. aureus and is implicated in the development of adult respiratory distress syndrome and disseminated intravascular coagulation.
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PMID:Phosphatidylinositol-specific phospholipase C, a possible virulence factor of Staphylococcus aureus. 280 68

A 50-year-old woman was admitted as an acute medical emergency and was diagnosed as having toxic shock syndrome. Thirty-six hours after admission she went into hepato-renal failure and had disseminated intravascular coagulation. She developed severe laryngeal oedema, a complication which has not been reported previously, and was intubated with great difficulty. She recovered from this, but died 5 weeks after the presentation of a pulmonary embolus.
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PMID:Toxic shock syndrome complicated by laryngeal oedema. 686 87


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