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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

DIC is a hemorrhagic syndrome frequently encountered as a complication in severe gram-negative bacterial sepsis. An animal model for sepsis-associated DIC was developed in order to permit study of the appearance and development of this syndrome in relation to the entire disease process. Rhesus monkeys (4 to 6 kg) were infected by intravenous injection of 10(9) Salmonella typhimurium organisms and studied for a period of 7 to 10 days following infection. Ten of 23 infected monkeys developed petechial rash characteristic of DIC, which appeared on days 1 to 2 infection and lasted 4 to 5 days. In the group of monkeys developing rash, activation of coagulation was suggested by an 80% decrease in platelet count and 20% to 30% increases in PT and APTT. Fibrinolytic system activation was indicated by the appearance of FDP. Kinin system activation was evidenced by decreases in both prekallikrein nad kininogen. Changes in laboratory tests suggestive of subclinical DIC were also noted in infected monkeys which did not develop a rash. Pathologic evidence of DIC was obtained through observation of numerous fibrin thrombi in the kidneys of the only monkey which died in the course of infection. Occurrence of DIC in association with this experimental infection in rhesus monkeys was established on the basis of clinical, laboratory, and pathologic criteria. Expression of the syndrome on days 1 to 2 following infection correlated with the period of increasing bacteremia.
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PMID:Model for disseminated intravascular coagulation: bacterial sepsis in rhesus monkeys. 9 3

The newborn infant, particularly when premature, has a haemostatic mechanism which may not be entirely capable of withstanding the onslaughts of trauma, infection, asphyxia or other complications of the neonatal period. He is at risk of local or diffuse haemorrhage, which may at times be serious or even life-threatening. The cause of haemorrhage during the newborn period can generally be ascertained by a careful history and brief physical examination directed toward recognition of any predisposing factors or underlying diseases. Screening laboratory tests can usually be correctly interpreted as long as certain laboratory artifacts and physiological peculiarities of the neonatal coagulation mechanism are kept in mind. Diagnosis of and therapy for vitamin K deficiency and haemophilia in the healthy-appearing neonate is generally carried out with little difficulty. The seriously ill neonate with bacterial sepsis, respiratory distress syndrome, or extreme immaturity presents greater problems, for laboratory tests may be more difficult to obtain and interpret and underlying conditions may be untreatable. DIC occurs commonly in such neonates, and transfusion therapy, with or without heparin, is often unsuccessful. A persistent dilemma are those neonates with fatal intravascular haemorrhage, in whom definable haemostatic abnormalities are few and transfusion therapy is futile.
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PMID:Neonatal coagulation: normal physiology and pathophysiology. 35 Apr 67

We conclude that DIC can occur as a result of sickle cell crisis in the absence of sepsis and we recommend that patients with sickle cell disease, particularly those with hemoglobin SC disease, presenting in crisis should be considered at risk for the development of disseminated intravascular coagulation. With symptomatic treatment and improvement of the crisis, our patient's coagulopathy resolved.
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PMID:Disseminated intravascular coagulation in sickle cell crisis. 43

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

In childhood hyperpyrexia is the most important factor causing the irreversibility of shock. The combination of high fever and circulatory impairment is more frequent during the first years of life. This behaviour is due to the high resistance of the arterial system in infancy. Marked general vasoconstriction increases the risk of a reduction in circulation and of heat loss, and causes hypoxia and rise of fever. The further course of shock is largely determined by microcirculatory failures. Under hyperpyrexia the disturbance of homeostasis can be intensified by shivering, blocking of perspiratio sensibilis, hyperosmolarity, brain edema, and DIC. In most cases of meningococcal sepsis shock and DIC begin with vasoconstrictive centralisation of circulation. The high-output-shock is extremely rare in children with high fever. The control of all important functions of a febril child in shock is the best baseline for the treatment. It is necessary in all shock patients in hyperpyrexia to reduce the fever and to repair the peripheral circulation. The therapy consists of antipyretic drugs, physical cooling, infusions of buffer-bases, dopamine, antibiotics and so on. In DIC heparin or streptokinase are indicated. In severe circulatory impairment combined with high fever prednisone is useful, in brain edema dexamethasone. The fatality rate of our cases has been diminished by a systematic therapy of hyperpyrexia and shock from 10 to 3 percent.
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PMID:[Hyperpyrexia and shock (author's transl)]. 77 99

This chapter has provided a review of available literature regarding alterations of hemostasis associated with CPB. The primary pathology of altered hemostasis during CPB appears to be two-fold: (1) a functional platelet defect of unclear etiology, which occurs in virtually all patients, and (2) a primary hyperfibino(geno)lytic defect which occurs in the majority of patients undergoing cardiopulmonary bypass. Significant thrombocytopenia does not appear to be a consistent problem, and is probably a function of perfusion technics; this may, however, be an important source of hemorrhage in some instances. Although hyperheparinemia, heparin rebound, and protamine excess have occasionally been incriminated as sources of hemorrhage during CPB, no well documented cases appear in the literature. Likewise, although DIC gained popularity in early reports of CPB hemorrahge, it appears that this syndrome rarely, if ever, arises as a consequence of CPB alone; it can be seen, however, in CPB patients who are provided a triggerin situation for DIC, such as shock, sepsis, or hemolytic transfusion reaction. It is likely that many reported alterations of hemostasis during CPB which were concluded to represent DIC actually were due to hyperfibino(geno)lysis. The key to prevention of CPB hemorrhage rests simply in obtaining an adequate preoperative workup. Of extreme importance is an adequate history with respect to bleeding tendencies in both patient and family; of equal importance is a careful history regarding antiplatelet drugs. A careful physical examination, searching for clues of a real or potential bleeding diathesis, also can often prevent catastrophic cases of CPB hemorrhage. Lastly, an adequate presurgical laboratory screen must be performed; in addition to the usual prothrombin time, partial thromboplastin time, and platelet count, a thrombin time and standardized template bleeding time must be added. The addition of these two simple modalities will insure against significant defects in fibrinogen, the fibrinolytic system, vascular function, and platelet function. When CPB hemorrhage occurs, simple laboratory screening will usually allow for a quick hemostasis evaluation. The parameters recommended in this review will distinguish between surgical and nonsurgical bleeding and should, therefore, allow for a quick decision regarding necessity for reexploration and the adequacy of hemostasis if reexploration is needed. In addition, this screen will distinguish between difficulties with heparin, protamine, and the fibrinolytic system. The vast majority of nonsurgical hemorrhages during CPB is due to a functional platlet defect, primary hyperfibrino(geno)lysis, or a combination of these. The quick administration of platelet concentrates, while awaiting laboratory evaluation, will control or significantly blunt most instances of CPB hemorrhage. If platelets fail to control bleeding, and reasonable laboratory evidence of primary hyperfibrino(geno)lysis is present, antifibrinolytics should then be used...
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PMID:Alterations of hemostasis associated with cardiopulmonary bypass: pathophysiology, prevention, diagnosis, and management. 79 78

A case of pneumococcal sepsis with DIC is reported. The patient had hyposplenism from thorium dioxide administration 23 years previously. Evidences of consumptive coagulopathy were verified by clinical manifestations of shock, generalized petechiae, abnormal hemostatic studies, and autopsy findings. The possible pathogenetic mechanism(s) of DIC in hyposplenism and pneumococcemia are reviewed.
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PMID:Hyposplenism and disseminated intravascular coagulation (DIC) in fulminant pneumococcal sepsis. 88 88

Combination chemotherapy with adriamycin and DTIC was used in 102 evaluable patients under 15 years of age who had previously treated metastatic solid tumors. Responses, defined as 50% or more reduction in all tumor masses, occurred in 10 out of 27 patients with neuroblastoma, 3 out of 8 patients with Wilms tumor, 7 out 15 patients with Ewing sarcoma, 2 out of 6 patients with osteosarcoma, 5 out of 13 patients with rhabdomyosarcoma, and 15 out of 33 patients with miscellaneous tumors which included a patient who had a complete regression of an extensive juvenile angiofibroma. Response rate to combination chemotherapy with adriamycin and DTIC in patients with Ewing sarcoma was significantly superior to the response rate obtained with adriamycin alone in another Southwest Oncology Group Study. Major toxicity included nausea, vomiting, myelosuppression, high incidence of pneumocystis carinii pneumonia (5 patients) and congestive heart failure (4 patients). There was 7 drug-associated deaths due to sepsis (1), pneumocystis carinii pneumonia (4), and congestive heart failure (2).
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PMID:Combination chemotherapy with adramycin (NSC-123127) and dimethyl triazeno imidazole carboxamide (DTIC) (NSC-45388) in children with metastatic solid tumors. 95 60

A 13-year-old girl was admitted to a hospital because of fever and sore throat. Staphylococcus aureus was obtained on blood culture, and she was treated with antibiotics under the diagnosis of sepsis and DIC. Echocardiography showed huge vegetation attached to the posterior leaflet of mitral valve and severe mitral regurgitation. CT scan revealed multiple heterogeneous high density areas in her brain. She was transferred to our hospital for further examination and treatment. Large verrucae on the mitral valve, severe regurgitation and repeated embolism urged us to the emergency mitral valve replacement. Debridement of abscess on the posterior wall of the left atrium and ventricle necessitated patch plasty of those structures and mitral ring as well. Operative and postoperative examination showed mycotic aneurysm of right coronary artery, multiple brain hemorrhage, arterial obstructions of extremities and splenic infarction. Sooner she recovered except for slight macular degeneration caused by retinal embolism.
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PMID:[A case of infective endocarditis with multiple embolic complications]. 140 96

The syndrome of symmetrical peripheral gangrene is characterised by distal ischaemic damage in two or more extremities, without large vessel obstruction. Four patients with bilateral pedal ischaemia are described and their haemodynamic profiles presented. In all four cases the syndrome developed in association with noradrenaline administration, sepsis and DIC, despite a high cardiac output and a low calculated systemic vascular resistance index. Early treatment with epoprostenol was instituted in the final case and was successful.
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PMID:Symmetrical peripheral gangrene: association with noradrenaline administration. 146 85


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