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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Transfusion of blood components is usually required in the management of critically ill patients. However, pathologic interactions between blood products and organ function may result from transfusion reactions. Emerging understanding of the mediation and interruption of clinical inflammatory responses is applicable to severe transfusion reactions. The pathophysiology of four types of severe transfusion reactions are reviewed: a) acute hemolysis; b) bacterial contamination of blood components; c) transfusion-related acute lung injury (TRALI); and d) anaphylaxis. Acute hemolytic reactions are often caused by preventable errors in sample or patient identification. Renal toxicity, coagulopathy, and hypotension may result from circulating red cell stroma and immune-complex activation of complement and cytokine secretion. Bacterial contamination of blood components has caused patient sepsis in many cases; platelets stored at 20 degrees to 24 degrees C are of particular concern. Careful blood collection and handling is essential for prevention. TRALI is manifested by acute respiratory distress, which is usually caused by infusion of plasma containing antibodies against the patient's leukocytes. Complement activation and cytokine stimulation cause edema and neutrophil accumulation in the lungs. Anaphylactic reactions may result from patient immunoglobulin (Ig)E antibodies against donor plasma constituents. IgA-deficient patients are at risk for anaphylactic reactions if these patients develop anti-IgA antibodies. Vasoactive or complement-activating factors in a blood product may also cause anaphylactoid reactions in some patients.
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PMID:The pathophysiology and organ-specific consequences of severe transfusion reactions. 780 6

Amonafide is a substituted benzisoquinolinedione that exerts its cytotoxicity through effects on macromolecular synthesis and intercalation of DNA. In this trial, 44 patients with advanced colorectal cancer and without prior chemotherapy received amonafide at a starting dose of 300 mg/m2 intravenously over one hour, on a daily x 5 schedule every 3 weeks. Toxicities of grade 3 or above included granulocytopenia, thrombocytopenia, sepsis, anaphylaxis and transient aphasia. Forty-seven % of patients had grade 3 or higher toxicity of any type. There were no complete or partial responses for an overall response rate of 0%, with a 95% confidence interval of 0-9%. The level of toxicity observed on this trial suggests an appropriate dose intensity of amonafide, despite lack of knowledge of patients' acetylator phenotypes.
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PMID:Phase II trial of amonafide in advanced colorectal cancer: a SouthWest Oncology Group study. 845 14

Over the past century, the treatment of various forms of circulatory shock has included fluid resuscitation with either crystalloidal or colloidal solutions. Despite decades of investigation, there still is considerable controversy over the beneficial and adverse effects of each fluid type. Most authors agree that the initial resuscitation of any form of shock should be performed with crystalloid solutions. Trauma resuscitation uses crystalloid therapy almost exclusively. Much controversy exists when the shock state involves increased microvascular permeability, such as seen in sepsis, anaphylaxis, and burns. Concerns involve increased permeability pulmonary edema and whether colloid or crystalloid therapy may contribute to its formation. Regardless of fluid type used for resuscitative efforts, it is essential to ensure adequate invasive and noninvasive monitoring to guide therapy. Endpoints to resuscitation should include stabilization of vital signs, adequate urine output, adequate cardiac output, and evidence of supply-independent oxygen consumption. Side effects of aggressive fluid loading are frequent and include intravascular volume overload, pulmonary edema, increased myocardial water content, brain swelling, gastrointestinal ischemia, and massive systemic edema. These complications can best be minimized by careful fluid titration, using physiologic and hemodynamic endpoints.
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PMID:Fluid resuscitation in circulatory shock. 849 Jul 65

A 14-year-old girl with perinatally acquired human immunodeficiency virus infection had fatal intravascular hemolysis after intravenous administration of ceftriaxone. Laboratory studies confirmed the presence of an antibody against ceftriaxone in the serum and on the patient's red blood cells. No evidence of sepsis, glucose-6-phosphate dehydrogenase deficiency or anaphylaxis was found.
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PMID:Ceftriaxone-related fatal hemolysis in an adolescent with perinatally acquired human immunodeficiency virus infection. 970 22

Distributive shock is defined as circulatory insufficiency induced by excessive dilatation of the peripheral vasculature or maldistribution of cardiac output. Septicemia, systemic inflammatory response syndrome, anaphylaxis, injuries to the central nervous system, and drug intoxication are causative factors of shock. Circulatory derangements induced by bacterial infection have been divided into hyperdynamic and hypodynamic shock. Administration of inotropic drugs, vasopressors, and/or vasodilators are primary treatments in this type of shock. Continuous infusion of norepinephrine to maintain blood pressure or administration of inoptropes such as dopamine or dobutamine are recommended to improve tissue perfusion. High-dose intravenous epinephrine is required to reestablish cardiac function, followed by continuous infusion of norepinephrine in severe anaphylactic shock. Vasoconstrictors such as norepinephrine, vasopressin, or amaminone are administered to maintain vascular tone in shock caused by nerve damage or drug overdose.
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PMID:[Distributive shock and it's therapy by cardio-vascular acting drugs]. 1057 Jul 79

This was a great save. The crew could easily have missed the presentation of anaphylaxis and let the window for treatment with epinephrine slip away. This patient was in anaphylactic shock. There were no signs that supported a traumatic injury, and that, combined with diaphoresis, urticaria and tachycardic central pulse, contributed to the suspicion of anaphylaxis. Anaphylaxis is classified as distributive shock. This type of shock is caused by profound systemic vasodilation, and the heart is unable to increase output enough to maintain blood pressure. Other causes of distributive shock include sepsis and spinal cord injury. It is rare to have both hypotension and wheezing in such cases. In an anaphylactic reaction, an allergen, such as a food protein, medication, insect venom or latex, is introduced into the body. The mast cells of the immune system have a protein on their surface called IgE antibodies (Immunoglobulin E). The mast cells are filled with histamines [table: see text] and leukotrienes, which are chemical mediators. These are released when the allergen reacts with the IgE antibodies. When these mediators are released, they cause smooth-muscle constriction in the respiratory and gastrointestinal tracts, resulting in wheezing, stridor, nausea, vomiting and diarrhea. They also cause vascular dilation, leading to edema and urticaria. Most patients will present with either profound vascular effect (shock) or wheezing; this is a rather rare presentation of a patient having both. The medication best suited to counteract the effects of these medicators is epinephrine. Epinephrine is an alpha- and beta-agonist, acting to constrict the vasculature and dilate the smooth muscles in the bronchial tree. Antihistamines can alleviate symptoms of anaphylaxis, but should only be used in addition to epinephrine, not as a substitute. In life-threatening reactions, epinephrine must be given quickly and in a form that the body can distribute. Use of the subcutaneous route with a solution mixed at 1:1,000 dilution is appropriate in most patients, but if the patient is in profound shock and not perfusing the skin (pale, cold, clammy skin), then a more diluted concentration must be given i.v. at a slow rate (1 cc every minute of the 1:1,000 dilution) until the patient recovers. If i.v. access is delayed or not available, give the 1:1,000 dilution intramuscularly, in the tongue or down the endotracheal tube. Refer to your local protocols for dosage, but the usual dose of epinephrine is 0.3-0.5 mg, or 0.01 mg/kg in a child. There are more than 40 million people in the U.S. with allergic histories that place them at risk for developing anaphylaxis. Each year over 5,000 deaths are attributed to anaphylaxis. The risk of death from anaphylaxis increases with a more rapid onset of signs and symptoms. Up to 25% of patients will experience a biphasic reaction. This means there is a recurrence of symptoms several hours after the initial reaction, and it is prudent to observe patients for a period of time following their initial treatment.
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PMID:Bugged. 1277 12

Using meta-analysis methodology, we compared the clinical outcomes for 769 patients with hepatic cystic echinococcosis treated with percutaneous aspiration-injection-reaspiration (PAIR) plus albendazole or mebendazole (group 1) with 952 era-matched historical control subjects undergoing surgical intervention (group 2). The rate of clinical and parasitologic cure (P<.0001) was greater in patients receiving PAIR plus chemotherapy. Disease recurrence (P<.0001), major complications (anaphylaxis, biliary fistula, cyst infection, liver/intra-abdominal abscess, and sepsis; P<.0001), minor complications (P<.0001), and death (P<.0824) occurred more frequently among surgical control subjects. Fever (P<.002) and minor allergic reactions subjects (P<.0001) were more common among PAIR-treated subjects. The mean durations of hospital stay were 2.4 days for group 1 and 15.0 days for group 2 (P<.001). Compared with surgery, PAIR plus chemotherapy is associated with greater clinical and parasitologic efficacy; lower rates of morbidity, mortality, and disease recurrence; and shorter hospital stays.
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PMID:Percutaneous aspiration-injection-reaspiration drainage plus albendazole or mebendazole for hepatic cystic echinococcosis: a meta-analysis. 1452 72

Group B streptococcus (GBS) is a leading cause of morbidity and mortality among newborns. Universal screening for GBS among women at 35 to 37 weeks of gestation is more effective than administration of intrapartum antibiotics based on risk factors. Lower vaginal and rectal cultures for GBS are collected at 35 to 37 weeks of gestation, and routine dindamycin and erythromycin susceptibility testing is performed in women allergic to penicillin. Women with GBS bacteriuria in the current pregnancy and those who previously delivered a GBS-septic newborn are not screened but automatically receive intrapartum antibiotics. Intrapartum chemoprophylaxis is selected based on maternal allergy history and susceptibility of GBS isolates. Intravenous penicillin G is the preferred antibiotic, with ampicillin as an alternative. Penicillin G should be administered at least four hours before delivery for maximum effectiveness. Cefazolin is recommended in women allergic to penicillin who are at low risk of anaphylaxis. Clindamycin and erythromycin are options for women at high risk for anaphylaxis, and vancomycin should be used in women allergic to penicillin and whose cultures indicate resistance to clindamycin and erytbromycin or when susceptibility is unknown. Asymptomatic neonates born to GBS-colonized mothers should be observed for at least 24 hours for signs of sepsis. Newborns who appear septic should have diagnostic work-up including blood culture followed by initiation of ampicillin and gentamicin. Studies indicate that intrapartum prophylaxis of GBS carriers and selective administration of antibiotics to newborns reduce neonatal GBS sepsis by as much as 80 to 95 percent.
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PMID:Prevention of group B streptococcal disease in the newborn. 1576 20

Propofol is a potent lipophilic anesthetic that was initially formulated in Cremophor El for human use. Because of the occurrence of Cremophor EL anaphylaxis and improvements in the quality of lipid emulsions, it was ultimately brought to market as 1% propofol formulated in 10% soybean oil emulsion. Emulsions represent complex formulation compositions whose suitability for intravenous administration is dependent on a number of factors. Despite the success of propofol emulsions, drawbacks to such formulations include inherent emulsion instability, injection pain, a need for antimicrobial agents to prevent sepsis, and a concern of hyperlipidemia-related side effects. Efforts to overcome such drawbacks have involved the development of propofol emulsions with altered propofol and lipid contents, the addition of different excipients to emulsions for antimicrobial activity, and study of nonemulsion formulations including propofol-cyclodextrin and propofol-polymeric micelle formulations. In addition, a number of propofol prodrugs have been made and evaluated.
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PMID:Propofol: the challenges of formulation. 1619 80

We report 14 older patients with aplastic anaemia (AA) who were treated with 'low dose' antithymocyte globulin (ATG). The aims of the study were to assess the efficacy and safety of reduced dose ATG in patients over the age of 60 years. Median age was 71 years (range 62-74 years). At the study endpoint (response to treatment at 6 months) 12 patients were evaluable. All patients received lymphoglobuline (horse ATG; Genzyme) at a dose of 0.5vials/10kg/day for 5 days (5mg/kg/day, equivalent to one-third of the standard dose). There were no deaths attributed to ATG. Two patients died during follow-up, from sepsis and anaphylaxis following platelet transfusion, respectively. Only one of the 12 evaluable patients responded to treatment and remains transfusion independent at 14 months after ATG. These results suggest that this lower dose of ATG, though well tolerated, had low efficacy in the treatment of AA.
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PMID:Low dose antithymocyte globulin for the treatment of older patients with aplastic anaemia. 1653 Feb 66


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