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

Two cases of fulminating pneumococcal septicemia (FSP) are reported, and 47 confirmed cases were discovered after a review of the published literature. The syndrome is that of a malignant infection with fever, collapse, and disseminated intravascular coagulation, with a rapid mortal outcome in most cases. Etiologically, FSP is usually the consequence of functional or anatomical asplenia, and the relative frequency of this affection after splenectomy following trauma confirms this observation. Lack of a splenic filter and a deficiency in the phagocytic system are the reasons for microbial proliferation in the blood, and the lymphocytic defence mechanisms are inactive because of the absence of any focus of infection.
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PMID:[Fulminating pneumococcal septicemia (author's transl)]. 22 89

Review of clinical and pathologic data from ten fatal cases of Rocky Mountain spotted fever (RMSF) revealed the importance of acute renal failure in the clinical course and of multifocal perivascular interstitial nephritis as the principal pathologic lesion. In nine cases, Rickettsia rickettsii were demonstrated by immunofluorescence in the areas of vasculitis. Evidence was lacking for the role of disseminated intravascular coagulation, glomerulonephritis, or myoglobinuria in the pathogenesis of acute renal failure in these cases. Rickettsia-induced vascular injury led to acute renal failure by several mechanisms. Hypovolemia early in the course resulted in reversible, prerenal azotemia. Transient hypotension in midcourse produced acute tubular necrosis. In fulminant cases, preterminal circulatory collapse was associated with coma and oliguria. The interstitial nephritis could not be demonstrated conclusively to contribute to the acute renal failure.
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PMID:Acute renal failure in Rocky Mountain spotted fever. 43 98

Over a period of 10 months (august 1975 to may 1976), the authors observed 6 successive accidents during the Shirodkar manoeuvre during operations for sterility of tubal origin: 1) 4 cases involved disturbances in haemostasis only, clinical manifestations being seen in only one case. In the laboratory, these quite atypical manifestations suggested either fibrinolysis or disseminated intravascular coagulation. 2) In 2 cases there was cardiovascular collapse with cardiac arrest. In the first patient, cardiac arrest was followed by a period of coagulopathy quite similar to those seen previously. In the second case resuscitation failed, leading the authors to abandon use of the Shirodkar manoeuvre, which brought the study to an end. We are unable to provide any satisfactory pathological interpretation of these complications, thought two factors are worthy of consideration:--The hydrocortisone suspension used;--The uterine trauma related to peroperative manipulations.
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PMID:[Tubal sterility: Disturbances in haemostasis and cardiac arrest during the shirodkar manoeuvre (author's transl)]. 64 47

A patient with laboratory-acquired Rocky Mountain spotted fever (RMSF) and concomitant influenza virus infection was studied from the third day of clinical illness. The course of his illness was marked by petechial rash, thrombocytopenia, and elevation of fibrin split products. No evidence of complement activation was observed. Plasma proteins were elevated in a pattern characteristic of the "acute phase reaction." The patient recovered completely, and vascular collapse or clinically important disseminated intravascular coagulation had developed. In febrile patients who had influenza or a clinically similar noninfluenzal respiratory syndrome, no changes in coagulation, complement, or plasma proteins developed. We conclude that aberrations in the patient's laboratory values reflected RMSF, and that complement played no critical role in his illness.
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PMID:Coagulation and complement studies in Rocky Mountain spotted fever. 64 36

Four cases of intravascular coagulation associated with a state of acidosis in diabetics were observed in 57 patients with diabetic acidosis and 19 with lactic acidosis, in a series of 112 cases of consumption coagulopathy admitted to a department of medical resuscitation. In three cases the coagulopathy was found only on investigation; in one there were clinical and anatomic signs. The coagulopathy may be found either during the phase of recovery from ketoacidosis, or during the course of severe lactic acidosis, particularly during a recurrence of this form of acidosis. In spite of the unfavorable outcome in 3 of the 4 cases, the abnormal findings of coagulopathy reverted toward normal along with successful metabolic corrections. The factors responsible for consumption coagulopathy are acidosis, collapse, generalised systemic reactions and alterations of platelet function, of coagulation, of the balance between fibrin deposition and lysis and of lipid levels, all characteristic of diabetes. The clinical effects of this coagulopathy seldom become apparent but provide a possible explanation of some of the complications of diabetic ketoacidosis, particularly certain hemorrhagic or thrombotic events, as well as certain visceral complications, especially those affecting renal, pulmonary and cerebral areas.
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PMID:[Consumption coagulopathy and acidosis in the diabetic patient (author's transl)]. 82 99

Venom from newborn Bothrops asper snakes has higher lethal, hemorrhagic, edema-forming, proteolytic and defibrinating activities than venom from adult B. asper specimens. Electrophoretic analysis confirmed the variation between these venoms. Intramuscular injection of 100 micrograms of venom from newborn specimens in mice induced defibrination, together with moderate increments of serum levels of lactate dehydrogenase, creatine kinase, hemoglobin and total proteins. A conspicuous hemorrhage developed in injected muscle rapidly after envenomation, probably due to a drastic alteration in capillaries and larger blood vessels. Other histological alterations included moderate myonecrosis, lung collapse and prominent renal damage, characterized by tubular necrosis and hyalinization. Polyvalent antivenom effectively neutralized lethal, hemorrhagic and indirect hemolytic activities of newborn B. asper venom, although requiring higher antivenom doses than neutralization of venom from adult B. asper.
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PMID:Pathological and biochemical changes induced in mice after intramuscular injection of venom from newborn specimens of the snake Bothrops asper (Terciopelo). 144 Jun 47

Vitamin E pretreatment significantly prevented E. coli-induced Disseminated Intravascular Coagulation (DIC) in rats (1). DIC, a reduction in fibrinogen and a falling platelet count and diffuse haemorrhage are part of the clinical features of Haemorrhagic Shock Encephalopathy Syndrome (HSES), recognised as a disease entity in the 1980s (2). At the SIDS Conference 1974 Reisinger described the effect of Escherichia coli (E. coli) endotoxin on the rabbit (3). An early effect was a reduction in fibrinogen and a falling platelet count, resulting in the release of relatively large amounts of the neuro-transmitter serotonin, stored in platelets (3, 4). Fibrinogen inhibited the release of serotonin from platelets (24). Serotonin is released from platelets during platelet aggregation (14). Platelet aggregation is inhibited by vitamin E (1). Serotonin is a neuro-transmitter associated with deep sleep, respiratory movements and cardiovascular collapse (3). Death at a later stage involved vascular permeability, edema and haemorrhage. After fibrin-platelet clots had formed DIC was present in lungs, kidneys and other organs (3). Medical researchers in Australia linked almost half of SIDS victims with a poisonous strain of intestinal E. coli bacteria (5). Dietary selenium in the intestinal villous tip is considered a daily modulator of cytochrome P450-dependent metabolism of drugs and toxins absorbed by intestinal mucosa (6). Villous atrophy occurs in HSES (2).
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PMID:Sudden infant death syndrome (SIDS) and the immune response. 146 Nov 72

A retrospective review of 114 solid organ donors over a 6-year period (1982-1987) was undertaken to identify problems in organ donor management and determine outcome of donated organs. Admission GCS was less than or equal to 4 in 84% of the donors. Complications included hypotension (81%), multiple transfusion requirements (63%), diabetes insipidus (53%), DIC (28%), arrhythmias (27%), cardiac arrest requiring CPR (25%), pulmonary edema (19%), hypoxia (11%), acidosis (11%), seizures (10%), and positive bacterial cultures (10%). Only 18% of organs were procured within 3 hours of brain death; 23% were procured more than 6 hours later. Six patients excluded from this study suffered cardiovascular collapse before their organs could be retrieved. From 114 organ donors, consent was obtained to procure 224 kidneys, 77 livers, 62 hearts, 35 pancreata, and ten heart-lung units. All 224 donated kidneys were procured and 202 were ultimately transplanted. Of 77 donated livers, 32 were procured; 31 transplanted. Of 62 donated hearts, 38 were procured; 29 transplanted and nine used for valves. Ten heart-lung units were donated; six were procured and transplanted. Of 35 donated pancreata, 11 were procured; only five were transplanted. Reasons for failure of donated organs to be procured or transplanted included abnormal organ characteristics, lack of compatible recipients, unavailability of surgical teams, organ injury during procurement, intraoperative arrest, and anatomic limitations precluding multiple organ procurement. This study identifies characteristics of organ donors and common organ-threatening complications. Rapid and continuing resuscitation of clinically brain dead trauma victims is mandatory.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Organ donor management and organ outcome: a 6-year review from a Level I trauma center. 235 1

Acute renal failure complicates the course in 5% to 30% of victims of severe viper poisoning. No consensus exists on the single mechanism causing acute renal failure after viper bite. It is known, however, that viper venom induces several clinical abnormalities that favor the development of acute renal failure. These alterations include a varying degree of bleeding, hypotension, circulatory collapse, intravascular hemolysis, and disseminated intravascular coagulation with or without microangiopathy. A direct cytotoxic action of snake venom on the kidney is suspected, but convincing evidence is still lacking. Severe hypocomplementemia is consistently present, but I doubt its role in the causation of renal lesions. Hypersensitivity to venomous or antivenomous protein occasionally causes acute renal failure. In sea snake poisoning, myonecrosis and myoglobinuria appear to play the predominant pathogenetic role. The renal lesions of clinical significance in envenomed patients are acute tubular and patchy or diffuse cortical necrosis. Glomerulonephritis, interstitial nephritis, and papillary necrosis have been reported in rare patients. I trust that this overview of the clinical and basic-science aspects of snake-bite-induced acute renal failure will prompt investigators to further define the pathogenetic mechanisms involved. Lessons learned may aid patients with acute renal failure of diverse causes, both here in India and around the world.
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PMID:Snake-bite-induced acute renal failure in India. 265 63

Endotoxins (lipopolysaccharides, LPS) are potent bacterial poisons always present within the intestines in considerable amounts. Several pathophysiological conditions such as hypovolaemia, hypoxia, intestinal ischaemia, burns and radiation lead to a breakdown in the barrier and depending upon the extent of the injury, endotoxins enter the systemic circulation in increasing amounts. Antibiotics do not inactivate the endotoxins which continue to exert their toxic effects leading to nausea, vomiting, diarrhoea, fever, disseminated intravascular coagulation, vascular collapse and organ failure. When nonabsorbable antibiotics are given prior to the insult, systemic endotoxaemia is prevented. Immunotherapy, using anti-lipopolysaccharide IgG, inactivates plasma endotoxins, destroys gram-negative bacteria and opsonises them and may become a major form of therapy. An outline of endotoxin and anti-lipopolysaccharide and its importance to the anaesthetist and intensive care specialist is presented.
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PMID:Endotoxins and anti-endotoxins (their relevance to the anaesthetist and the intensive care specialist). 265 93


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