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

Five cases of disseminated meningococcal disease due to serogroup W135 Neisseria meningitidis are presented. The cases ranged in age from 16 months to 23 years, and spanned a clinical spectrum from mild meningitis without rash or evidence of meningococcal septicemia to severe meningoencephalitis with fulminant meningococcemia, disseminated intravascular coagulation, and death. These cases demonstrate that serogroup W135 N meningitidis is fully pathogenic for man and capable of producing the full spectrum of disseminated meningococcal disease associated with other serogroups. Since this serogroup has recently emerged as a significant cause of disease in Europe, attention should be focused on the correct serogroup designation of strains of N meningitidis isolated from clinical material and reported as "nongroupable" by clinical laboratories, so that additional clinical and epidemiologic information may be obtained.
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PMID:Disease due to serogroup W135 Neisseria meningitidis. 11 72

Pneumonia is one of the most serious infections in the neonate and is responsible for a large percentage of neonatal mortality. Pneumonia in a premature or term infant who is debilitated by an underlying problem such as hyaline membrane disease carries an extremely high morbidity and mortality. Since most of the bacterial pneumonias are treatable, early recognition and diagnosis and vigorous treatment are essential. X-ray findings, though helpful, serve only as a guideline. Prognosis is adversely affected if pneumonia results in generalized sepsis, leading to meningitis, disseminated intravascular coagulation, and osteomyelitis. Prompt antibiotic treatment should be begun before the etiologic agent or drug susceptibility is known.
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PMID:Acute pneumonia in the newborn: changing picture. 32 96

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

Two elderly patients presented with symptoms suggestive of occult temporal arteritis. Both were treated with high doses of corticosteroids although subsequent biopsies of the arteries did not show evidence of arteritis. After 5 months of corticosteroid therapy, the first patient died of Gram-negative bacterial pneumonia and cystitis and disseminated intravascular coagulation. The second patient, six days after the biopsy, died of pneumococcal meningitis which had presumably spread from a focus about the left optic nerve. In the first patient, necropsy studies showed that the loss of vision appeared to be due to arteriosclerosis of the nutrient vessels of the optic nerve while in the second patient, the visual symptoms appeared to be due to a localized optic perineuritis. Corticosteroid therapy in elderly patients carries a high morbidity, as is illustrated by the first case and may mask unsuspected underlying disease processes, as presumably occurred in the second. We discuss the importance of obtaining a biopsy diagnostic of temporal arteritis in order to justify the continuation of corticosteroid therapy and the significance of a negative biopsy.
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PMID:Complications of corticosteroid therapy in presumptive temporal arteritis. 107 27

We report a retrospective, clinicopathologic study of 139 patients who died during treatment of a severe burn. Fifty-three percent of the patients had central nervous system (CNS) complications-infections, cerebral infarcts and hemorrhages, metabolic encephalopathies, central pontine myelinolysis, and cerebral trauma. Children and adults were equally affected. Sixteen percent of the patients had a CNS infection. Candida species, Staphylococcus aureus and Pseudomonas aeruginosa caused almost 80% of them. S. aureus and candida caused cerebral microabscesses and septic infarcts. P. aeruginosa caused meningitis and infarcts due to meningitis. CNS infections arose as a result of spread from a systemic source. The major risk factors for CNS infection were an extensive burn, S. aureus endocarditis, and a burn wound infection due to candida or P. aeruginosa. Patients with burns of less than 30% of the surface area of their body, those without a systemic infection, and those in the first week after their burn were at low risk. Eighteen percent of the patients had cerebral infarcts. In almost half the patients, the infarcts were caused by septic arterial occlusions or other complications of the burn, viz, disseminated intravascular coagulation (DIC) and septic shock. In only one-third of the patients were infarcts due to atherosclerosis, atrial fibrillation, or other causes prevalent in the general population. Intracranial hemorrhages were only one-fifth as frequent as infarcts and were due to DIC and thrombocytopenia, caused by bacteremia. Diagnosis during life was difficult, because the neurologic picture of focal cerebral lesions and meningitis was indistinguishable from that of metabolic encephalopathies, and because many patients had more than 1 neurologic complication. However, our results suggest that a clinical approach that includes analysis of risk factors for CNS infection, cerebral imaging, examination of cerebrospinal fluid, and tests for DIC can lead to a neurologic and microbiologic diagnosis in most patients.
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PMID:Central nervous system complications of thermal burns. A postmortem study of 139 patients. 152 3

Vitamin K deficient hemorrhagic diathesis is well known as a cause of infantile intracranial hemorrhage. Its occurrence, however, as a post-surgical complication is rare and has never been reported previously. Two cases are presented here which illustrate the existence of such a hazard. Case 1. A 73-year-old woman admitted with subarachnoid hemorrhage (WFNS IV) underwent microsurgical exploration of a left internal carotid aneurysm, and neck clipping of the aneurysm was performed. She had an uneventful postoperative course, but her neurological condition deteriorated suddenly on the fifth postoperative day. CT scan revealed a large epidural hematoma. Case 2. A 6-year-old boy was admitted due to the dysfunction of a ventriculo-peritoneal shunt system that had previously been placed for hydrocephalus. This dysfunction was thought to be caused by meningitis. Twelve days after ventricular drainage and antibiotic therapy, sudden intraventricular hemorrhage occurred. In both cases, PT and APTT were markedly prolonged, FDP slightly increased and fibrinogen slightly decreased. SFMC was positive in case 2. After the administration of vitamin K, PT and APTT were immediately normalized. Recent reports emphasize the adverse effect of antibiotics that leads to vitamin K deficient hemorrhagic diathesis, especially, in patients in a cachectic state. In these two cases, such a cachectic condition was not observed. We presume that the cause of vitamin K deficiency would be, along with the administration of antibiotics, a preliminary condition of disseminated intravascular coagulation which is encountered in some neurological disorders including subarachnoid hemorrhage. We conclude that attention should be paid for these pitfalls in perioperative neurosurgical care.
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PMID:[Postoperative intracranial hemorrhage due to vitamin K deficiency: report of two cases]. 173 30

Meningococcal sepsis with cardiovascular manifestations is one of the leading causes of pediatric intensive care admission (14.85%) in our area. We carried out a two phase study over period of 10 years from 1979 to 1988, involving a retrospective analysis of clinical and analytical manifestations in order to determine a prognostic score of the severity of meningococcal infections in our area. A total of 86 cases were studies over a two year period. After establishing the prognostic score, we applied a previously assayed therapeutic protocol, based on the number of criteria of severity, in 170 children selected as having the same criteria. The factors of seriousness considered were: Appearance of the first symptoms less than 12 h. previously, appearance of petechia less than 6 h. previously, hyperthermia, shock at admission, absence of meningitis, fulminating course of purpura and convulsions, leukopenia less than or equal to 5,000 mm3, prothrombin activity less than or equal to 45%, platelets less than or equal to 75,000 mm3, fibrinogen less than or equal to 250 mgrs% and FPD greater than 40 micrograms/ml (p less than or equal to 0.01 (CHI SQUARE]. In the first phase of study, overall mortality was associated with the presence of three criteria, and was highest when more than seven criteria were present. The results indicate that mortality from meningococcal sepsis is linked to fulminating deterioration of hemodynamics and DIC.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Meningococcal sepsis in our area. Study of the disease severity factors and therapeutic management over a 10-year period]. 188 8

The infant or child who presents to the Emergency Department with bacterial meningitis may have nonspecific vague symptoms with few signs of serious illness. However, the disease is often rapidly progressive and life-threatening, and may be associated with respiratory failure, circulatory failure, increased intracranial pressure, disseminated intravascular coagulation, or convulsions, any of which may lead to a fatal outcome. It is important for the triage technician in an Emergency Department to cautiously inspect each young patient who presents with illness, carefully considering whether the presenting syndrome of symptoms and signs might be consistent with early meningitis. If the young patient is triaged in a nonemergent category, then periodic assessments of the patients waiting to be seen may ensure that, when the infant or child with an obscure presentation develops evidence suggesting this diagnosis, the triage technician will promptly notify the appropriate definitive care providers who assume responsibility for immediate definitive evaluation and stabilization. Changes in delivery of lifesaving care to the life-threatened child are being impacted by current advances in the understanding of the biochemical basis of disease at the cellular and subcellular levels. Endotoxin release into the blood causes increased production of kinins, which results in vasodilatation and increased vascular permeability. Members of the leukotriene family may also enhance vascular permeability as well as produce augmented leukocyte aggregation to vascular endothelium, vasoconstriction, and bronchoconstriction. Endotoxin activates the complement cascade and induces platelets to form reversible aggregates that may be trapped in the pulmonary microcirculation; and endotoxemia-activated platelets release serotonin, which may be associated with pulmonary hypertension. Now that we have antibiotics that are effective against organisms whose degradation produces endotoxin, there is interest in lessening the host inflammatory response to endotoxin through use of dexamethasone as an anti-inflammatory agent. Clinical trials have revealed that patients who received dexamethasone became afebrile earlier and were less likely to acquire deafness after bacterial meningitis. Because administration of antibiotics is the current specific medical therapy for this life-threatening microbial invasion, it is reasonable to continue to strive to shorten the interval between recognition of disease and specific therapy. However, new studies suggest that consequences of the complex host inflammatory response (at the cellular and subcellular level) to microbial invasion and endotoxin release from bacterial degradation are increasingly important in determining survival or severity of morbidity. Therapeutic intervention with specific antibiotics and steroid anti-inflammatory agents for modulating host responses enhances outcome.
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PMID:Emergency department stabilization of pediatric patients with bacterial meningitis. Current advances. 189 92

We have studied the activation state of the fibrinolytic system in 39 patients with systemic meningococcal disease (SMD). Patients defined as having fulminant septicemia (n = 13) with high (greater than 700 ng/L) levels of endotoxin (LPS) in plasma and severe coagulopathy, had significantly lower functional levels of plasminogen (P less than 0.05) and alpha-2-antiplasmin (P less than 0.01) and higher antigen levels of plasminogen activator inhibitor 1 (PAI-1) (P less than 0.01), and fibrin degradation products (FDP) (P less than 0.01), but not of PAI-2 (P greater than 0.1) as compared with less severely ill patients (meningitis and meningococcemia) (n = 25). A positive correlation existed between the admission (maximum) levels of LPS and PAI-1 (r = 0.86, P less than 0.0001). Decreasing admission levels of platelets were associated with increasing levels of PAI-1 (r = -0.55, P less than 0.001). After initiation of treatment with antibiotics and fresh frozen plasma, the PAI-1 levels declined rapidly. PAI-1 levels greater than 360 micrograms/L on admission predicted the development of a severe septic shock combined with renal impairment correctly in 12 of 13 patients (92%). None of 25 patients without multiple organ failure had PAI-1 levels greater than 260 micrograms/L. PAI-1 levels greater than 1850 micrograms/L were associated with 100% fatality. The results suggest that in the early phase of fulminant meningococcal septicemia an extensive plasmin generation occurs. On admission, however, high levels of PAI-1 seem to inhibit the plasmin generation, and thereby promote DIC.
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PMID:Plasminogen activator inhibitor 1 and 2, alpha-2-antiplasmin, plasminogen, and endotoxin levels in systemic meningococcal disease. 231 89

A 26-year-old man, in daily contact with pigs was admitted to hospital with septic shock which appeared to be caused by Streptococcus suis type 2 infection. Despite immediate antibiotic therapy a multiple organ failure developed, with ARDS, cardiac failure, disseminated intravascular coagulation and acute renal failure. Streptococcus suis infection is a zoonosis. The bacterium can be isolated from the tonsils of a significant part of the Dutch pig population. Mainly people who are in close contact with pigs or pork become infected. Usually meningitis develops. Sepsis, as this case, is rare and often fatal.
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PMID:[Fulminant sepsis caused by Streptococcus suis]. 238 12


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