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

Six children, out of twelve in a neonatal unit suffered from group D salmonellosis. Two patients presented in addition to intestinal manifestations massive extraintestinal symptoms, both with septicemia and meningitis. One patient died on the fourth day from massive disseminated intravascular coagulation and pyocephalus. The other patient had a complete recovery after an antibiotic therapy with chloramphenicol and ampicillin. As the source of infection the mother of case 1 was identified. In her stools salmonella group D were cultured. Cultures of the ward-personals, stool and the food were negative. It should be mentioned that only children fed with artificial food suffered from salmonellosis; whereas children on breastmilk had an unremarkable clinical course and consistantly negative stoolcultures.
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PMID:[Salmonella-meningitis in the newborn (author's transl)]. 46 Feb 61

3 cases of severe septic shock are described; a 5 month old girl with congenital hyposplenia, a 2 3/12 year old boy splenectomized because of microspherozytosis and a 11 6/12 year old boy splenectomized because of Hodgkin's disease. In 2 cases pneumococci were found in the blood cultures. In all 3 cases the coagulation analysis showed a consumption coagulopathy. Intravenous streptokinase treatment was applied in addition to general treatment for shock and antibiotic therapy. 2 patients survived and made a complete recovery, whereas the 2 year old boy died. The histological findings showed a severe DIC. In the Department of Surgery, Innsbruck, 44 children have been splenectomized during the last 6 years, 38 of whom we were able to follow up on for an average of 3.3 years. After an average of 1.2 years following splenectomy, 4 patients (including the 3 cases mentioned above) contracted acute septicaemia; a further patient also incurring a probable sepsis with DIC. 3 of these 5 children died, representing a morbidity rate of 13% and a mortality rate of 8%. The mortality rate is thus as high as that caused by the primary disease, indicating the urgency of prophylaxis for infections of this kind. 3 prophylactic forms of treatment are suggested: protection with penicillin, active immunization with polyvalent pneumococcal antigen and spleen preservation whenever possible.
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PMID:[Asplenia and DIC (author's transl)]. 47 21

A male patient was admitted to hospital 12 h after self-poisoning with mercuric chloride. He suffered multiple complications including acute renal failure, ulcerative colitis, anaemia, disseminated intravascular coagulation, chronic sepsis and severe weight loss. Initially he responded well to resuscitative measures and intensive supportive therapy, which included ventilation of the lungs, haemodialysis, dimercaprol, antibiotics, parenteral feeding and gastrointestinal surgery. Unfortunately the sepsis was never satisfactorily eradicated despite satisfactory serum concentrations of the appropriate antibiotics. On day 43 after poisoning he had a grand mal fit; after this there were focal neurological signs and on lumbar puncture he was found to have a raised protein concentration and raised pressure in his cerebrospinal fluid. The condition of the patient rapidly deteriorated and on day 47 he died. Post-mortem examination revealed a large cerebellar abscess. The literature on mercury poisoning is reviewed.
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PMID:A case of poisoning with mercuric chloride. 49 32

Among 592 infants examined at autopsy during a four-year period, 32 (5.4%) had cerebral infarcts. Excluded were cases of traumatic hemorrhages and softening, periventricular leukomalacia, venous lesions, and any mass, including encephaloceles, with arterial distortion and infarction. Histological abnormalities were similar to those of infarcts in adults. Relatively advanced histopathological changes in some infants living only a few hours indicated that some infarctions may have occured in utero. The most common cause of arterial occlusion was embolization, with sepsis and disseminated intravascular coagulation playing a major role. The brains of term neonates were more frequently involved than those of premature infants. Multiple small infarcts occurred more often in premature infants. In most cases autonomic dysfunction with prolonged apnea, episodic seizures, and metabolic acidosis were the major associated clinical features, rather than focal neurological deficits. Similar cerebral infarcts in infants who survive with less severe systemic complications may lead to porencephaly, hemiplegia, mental and motor retardation, and recurrent seizures.
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PMID:Cerebral infarcts with arterial occlusion in neonates. 53 48

This paper has reported two deaths occurring in young adults who had undergone splenectomy for trauma several years before developing pneumococcal sepsis. Tissues at autopsy demonstrated a disproportionate autolysis for the postmortem interval. One victim also showed diffuse serosal hemorrhages, presumably as a result of disseminated intravascular coagulation. Both showed evidence of residual splenic implants but such implants clearly did not provide protection against sepsis. The mechanisms whereby the spleen protects from sepsis appear to be that of a mechanical filter and an immunological organ producing antibody or antibody-like substance. How much splenic tissue and what relationships to the system circulation are necessary to provide protection remain undiscovered.
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PMID:Sudden death and sepsis after splenectomy. 54 39

Organisms of the genus Bacteroides represent the major group of obligate anaerobes involved in human infections. Bacteroides usually cause either bacteremia or localized abscesses. Of the numerous species of Bacteroides, Bacteroides fragilis is the single most frequent clinical isolate. B. fragilis and Bacteroides melaninogenicus have chemically incomplete lipopolysaccharides as compared with the lipopolysaccharides (endotoxins) of aerobic bacteria, and the lipopolysaccharides of Bacteroides lack the biologic potency characteristic of endotoxin. This inactivity may account for the very infrequent occurrence of disseminated intravascular coagulation or purpura that can accompany sepsis due to these organisms. Furthermore, strains of B. fragilis have an immunologically common capsular polysaccharide. In an animal model of intraabdominal sepsis, the encapsulated strains caused abscesses when given without other organisms, but abscess formation from unencapsulated strains of Bacteroides generally required the administration of a synergistic aerobe. The abscesses caused by encapsulated strains were shown to be directly attributable to the capsular polysaccharide, which is an important virulence factor of this organism. Patients or experimental animals infected with B. fragilis develop antibodies to the capsular polysaccharide, and these antibodies can be detected in a radioactive antigen-binding assay.
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PMID:Surface antigens as virulence factors in infection with Bacteroides fragilis. 54 84

The morphologic and clinical findings in seven fatal cases of meningococcal septicemia are described and interpreted in light of recent experimental and clinical studies. We include evidence that suggests the disease has two distinct pathogenetic mechanisms. First, a shock-like terminal phase is associated with the development of widespread pulmonary microvascular thrombosis. These thrombi, composed largely of platelets and leukocytes, produce severe cor pulmonale that cannot be prevented with heparin sodium treatment. Meningococcal endotoxin also produces disseminated intravascular coagulation, which includes the rapid consumption of fibrinogen and the formation of fibrin thrombi in adrenal and renal glomerular capillaries, causing hemorrhagic infarction of the adrenal glands and renal cortical necrosis. This secondary phase of the disease can be modified with heparin therapy, but its control does not improve survival because the parenchymal lesions produced are not immediately life threatening.
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PMID:Fatal meningococcal septicemia. 57 4

Two cases of infants with shock are presented. Cardiac output was determined in both with dilution dye using an auricular oxymeter, with three determinations: at 0, 30 and 60 minutes while receiving intranvenous fluids. At the same time, blood gases and blood lactatewere determined. The first case showed hypodynamic shock secondary to hypovolemia due to severe dehydration, associated to low central venous pressure, low arterial tension, increased peripheral resistance and increased arteriovenous difference of oxygen. The second case was a newborn with sepsis and disseminated intravascular coagulation with hyperdynamic shock with very high cardiac output, low peripheral resistance and low arteriovenous difference of oxygen. Both cases had an initial increase of lactate and a mild decrease at the end of the period of clinical observation.
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PMID:[Hemodynamometabolic changes in shock in infants. Report of 2 cases]. 62 52

Fulminant pneumococcal infections are rare in teen-agers with sickle cell anemia. A 16-year-old black male with sickle cell anemia was treated as an outpatient for cryptogenic pain crisis, which delayed antibiotic therapy for primary pneumococcal septicemia for seven hours. This patient did not appear ill upon initial presentation but rapidly developed disseminated intravascular coagulation and died.
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PMID:Concurrent primary pneumococcemia, disseminated intravascular coagulation, and sickle cell anemia. 66 36

A factor V inhibitor arose in a 79-year-old man within 1 month of an operation for a fractured leg. Absorption studies with solid-phase antibodies to human immunoglobulins showed the inhibitory activity to be primarily in the IgG class, but also in the IgA class, of immunoglobulins. This is the first report of an IgA immunoglobulin with factor V inhibitory activity. While the inhibitor was present, and at a time when no circulating Factor V activity was detectable, the patient developed septicemia and disseminated intravascular coagulation. The mechanism sustaining disseminated intravascular coagulation despite the absence of circulation factor V activity remains unexplained. The factor V inhibitor disappeared within 5 months of its initial detection. Possible origins of factor V inhibitors are discussed.
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PMID:Factor V antibody and disseminated intravascular coagulation. 67 79


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