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Anaphylactic reaction dextran

Iron salts occasionally cause gastrointestinal irritation, nausea, vomiting, constipation, diarrhea, headache, backache, and allergic reactions. The stools usually appear darker (black). Iron dextran is given by the parenteral route Hypersensitivity reactions, including fatal anaphylactic reactions, have been reported with the use of this form of iron. Additional adverse reactions include soreness, inflammation, and sterile abscesses at the intramuscular (IM) injection site Intravenous (IV) administration may result in phlebitis at the injection site When iron is administered via the IM route, a brownish discoloration of tlie skin may occur. Fhtients with rheumatoid arthritis may experience an acute exacerbation of joint pain, and swelling may occur when iron dextran is administered. [Pg.434]

Monitoring and Managing Adverse Reactions When tiie patient is receiving iron dextran, the nurse monitors closely for a hypersensitivity reaction. Epinephrine is kept on standby in tiie event of severe anaphylactic reaction. [Pg.440]

Generally, the major adverse effects associated with colloids are fluid overload, dilutional coagulopathy, and anaphy-lactoid/anaphylactic reactions.24,32 Although derived from pooled human plasma, there is no risk of disease transmission from commercially available albumin or PPF products since they are heated and sterilized by ultrafiltration prior to distribution.24 Because of direct effects on the coagulation system with the hydroxyethyl starch and dextran products, they should be used cautiously in hemorrhagic shock patients. This is another reason why crystalloids maybe preferred in hemorrhagic shock. Furthermore, hetastarch can result in an increase in amylase not associated with pancreatitis. As such, the adverse-effect profiles of the various fluid types should also be considered when selecting a resuscitation fluid. [Pg.203]

Adverse effects of IV iron include allergic reactions, hypotension, dizziness, dyspnea, headaches, lower back pain, arthralgia, syncope, and arthritis. Some of these reactions can be minimized by decreasing the dose or rate of infusion. Sodium ferric gluconate and iron sucrose have better safety records than iron dextran. Iron dextran requires a test dose to reduce the risk of anaphylactic reactions. [Pg.878]

There is a large class of compounds that are capable of releasing histamine. They can be enzymes, toxins, morphine, d-tubocurarine, and polymers such as dextran. Moreover, tissue damage such as trauma, bites, and stress can also cause a release of histamine, and in all probability as a result, an endogenous polypeptide bradykinin is released. Action of all of these listed substances as well as a number of others can facilitate formation of anaphylactic reactions in the organism. [Pg.220]

The parenteral use of complexes of iron and carbohydrates has resulted in anaphylactic-type reactions. Deaths associated with such administration have been reported therefore, use iron dextran injection only in those patients in whom the indications have been clearly established and laboratory investigations confirm an iron-deficient state not amenable to oral iron therapy. Because fatal anaphylactic reactions have been reported after administration of iron dextran injection, administer the drug only when resuscitation techniques and treatment of anaphylactic and anaphylactoid shock are readily available. [Pg.50]

Indications for use of parenteral iron, e.g. as fer-rioxidesaccharate or iron dextran, are in patients on hemodialysis and patients with a disease which prevents absorption from the gastrointestinal tract, in patients who are on long term parenteral nutrition and sometimes in patients with inflammatory bowel disease. Parenteral iron does not raise the hemoglobin level significantly faster than oral therapy and carries a risk of severe adverse reactions. Reactions to intravenous iron include headache, malaise, fever, arthralgias, urticaria and in rare cases anaphylactic reactions, which may be fatal. [Pg.368]

Anaphylactic reactions to dextrans have been reported, for example within 10 minutes after exposure to dextran in hysteroscopy (22). It can be fatal (23). [Pg.1085]

The authors suggested that dextran-reactive antibodies had formed immune complexes with dextran, leading to complement activation and release of mediators of anaphylaxis. There was also evidence of mast cell degranulation. They therefore recommended that titration of dextran-reactive antibodies before administration of dextrans could provide a method of identifying those who are at risk of dextran-induced anaphylactic reactions. [Pg.1085]

The authors suggested that this reaction had been due to a dextran-induced anaphylactic reaction, but were uncertain as to the cause of these observations, as they were not accompanied by immediate symptoms of shock. It is unclear if this case was caused by an antibody reaction. [Pg.1085]

The syndrome of acute hypotension, adult respiratory distress syndrome, non-cardiogenic pulmonary edema, anemia, coagulopathy, and anaphylactic reactions after the administration of dextran 70 is referred to as the dextran syndrome (36-39). Factors other than acute volume overload due to intravascular absorption of dextran are thought to account for the syndrome. A combination of diverse pathophysiological factors may be responsible, namely direct pulmonary toxicity, activation of the coagulation cascade, release of vasoactive mediators, hypotension, pulmonary edema, intravascular intravasation of fluids, dilution of blood, and impaired renal and hepatic clearance. Cases of pulmonary edema are described under the section Respiratory. [Pg.1086]

Ljungstrom KG, Renck H. Metabolic acidosis in dextran-induced anaphylactic reactions. Acta Anaesthesiol Scand 1987 31(2) 157-60. [Pg.1087]

Ahmed N, Falcone T, Tulandi T, Houle G. Anaphylactic reaction because of intrauterine 32% dextran-70 instillation. Fertil Steril 1991 55(5) 1014-16. [Pg.1087]

Large doses of intravenous iron dextran and iron saccha-rate have been compared in a retrospective study of 379 patients who had attended peritoneal dialysis clinics in the past 5 years (12). Of these, 62 were selected to receive intravenous iron based on ferrokinetic markers of iron deficiency, non-adherence to oral iron, ineffectiveness of oral iron, or increased erythropoietin requirements. Intravenous iron was given as two injections of 500 mg each 1 week apart in 61 patients, 33 of whom received iron dextran, 23 iron saccharate, and five both iron dextran and iron saccha-rate. One patient developed anaphylaxis to a test dose of iron dextran and was excluded from further therapy. Blood samples were collected before and 3 and 6 months after iron infusions. Five of the 34 patients who received iron dextran developed minor adverse effects and one had an anaphylactic reaction to the test dose. Of the 23 patients who received iron saccharate, one had an anaphylactic reaction and two had transient chest pain, which subsided without therapy. There were more adverse effects with iron dextran (7.4% of injections) compared with iron saccharate (4.3% of injections), but this difference was not statistically significant. The number of episodes of peritonitis also increased during the 6 months after intravenous iron infusion, especially with iron dextran, compared with the number of episodes during the 6 months before iron infusions, although the difference was not statistically significant. [Pg.1912]

FDA-approved preparations for parenteral therapy include sodium ferric gluconate complex in sucrose (ferrlecit), iron sucrose (venofer), and iron dextran (iNFED, DEXFERRUM). Unlike iron dextran, which requires macrophage processing that may require several weeks, -80% of sodium ferric gluconate is delivered to transferrin with 24 hours. Sodium ferric gluconate has a much lower risk of serious anaphylactic reactions than iron dextran. [Pg.939]

Dextran cyclic imidocarbonate has been used to prepare soluble conjugates of a-amylase from Bacillus amyloliquefaciens and of bovine liver catalase for use in experimental enzyme therapy. The results suggest that by coupling the enzymes with a poorly antigenic macromolecule (dextran) anaphylactic reaction in animals pre-immunized with dextran may be suppressed or eliminated. Trypsin has been immobilized by reaction with dextran cyclic imidocarbonate. [Pg.643]

Hedin H, Richter W, Messmer K, Renck H, Ljungstrom KG, Laubenthal H (1981 b) Incidence, pathomechanism and prevention of dextran induced anaphylactoid/anaphylactic reactions in man. Dev Biol Stand 48 179-189 Hehre EJ, Neill JM (1946) Formation of serologically reactive dextrans by streptococci from subacute bacterial endocarditis. J Exp Med 83 147-162 Hehre EJ, Sugg JY (1950) Serological reactivity of dextran plasma substitute. Fed Proc 9 383... [Pg.620]

Ljungstrom KG, Renck H, Strandberg K, Hedin H, Richter W, Widelof E (1983 a) Adverse reactions to dextran in Sweden 1970-1979. Acta Chir Scand 149 253-262 Ljungstrom KG, Renck H, Hedin H, Richter W, Rosberg B (1983 b) Prevention of dextran-induced anaphylactic reactions by hapten inhibition. I. Scandinavian multicenter study on the effects of 10 ml 15% Dextran 1 administered before Macrodex or Rheomacro-dex. Acta Chir Scand 149 341-348... [Pg.622]

Sorg C, Riide E, Westphal O (1970) Immunological properties of amylose, dextran and polyvinyl alcohol conjugate with polytyrosyl peptides. Eur J Biochem 17 85-90 Spaeth GL, Spaeth EB, Spaeth PG, Lucier AC (1967) Anaphylactic reaction to mannitol. Arch Ophthalmol 78 583-584... [Pg.626]

Wiedersheim M (1957) An investigation of oxyethylstarch as a new plasma volume expander in animals. Arch Int Pharmacodyn tW 111 353-361 Wilkinson AW (1956) Dextran without reactions. Lancet 2 604-606 Wilkinson AW, Storey ID (1953) Reactions to dextran. Lancet 2 956-958 Wisborg K (1975) Anaphylactic reaction induced by infusions of polygeline (haemaccel). Br JAnesth 47 1116-1117... [Pg.628]

It is common practice not to add iron to TPN solutions because of the possibility of physical incompatibility and the risk of anaphylaxis when iron-dextran preparations are used. Fatal anaphylactic reaction secondary to intramuscular iron dextran injections (Becker et al, 1966), as well as other local and systemic reactions following intravenous administration, particularly using the bolus dosage method, have been described (Hamstra et al., 1980). Yet many recent reports attest to the low frequency of the above complications and the apparent safety of using lower doses in nutrient solutions for adults and children (Hamstra et al., 1980 Gilbert et al., 1979 Figueredo and Kaminski, 1979 Halpin et al., 1980 Peters et al, 1980 Reed et al, 1981). Similarly, physical incompatibility problems are less common with the lower doses and lower iron concentrations. As an alternative iron source, ferrous citrate may prove to be a more suitable intravenous iron supplement than dextran (Sayers et al, 1983). [Pg.265]

After injection of dextran, the normal rat develops hyperarania and oedema of the head and extremities as the result of an anaphylactic reaction. Some rats of a single Wistar strain, however, fail to show this reaction. The frequency of nonreacting animals is approximately 23%. Offspring from cross-matings of nonreacting and reacting animals are resistant to dextran. The failure to react to dextran thus seems to be inherited as a recessive trait... [Pg.619]


See other pages where Anaphylactic reaction dextran is mentioned: [Pg.386]    [Pg.407]    [Pg.289]    [Pg.1083]    [Pg.1085]    [Pg.1876]    [Pg.1912]    [Pg.1917]    [Pg.227]    [Pg.830]    [Pg.1816]    [Pg.1817]    [Pg.939]    [Pg.35]    [Pg.595]    [Pg.356]    [Pg.384]    [Pg.235]    [Pg.280]    [Pg.457]    [Pg.92]    [Pg.494]    [Pg.258]   
See also in sourсe #XX -- [ Pg.40 , Pg.70 , Pg.257 , Pg.258 ]




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Anaphylactic reactions

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