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1. Hommes DW, Bura A, Mazzolai L, Biller HR, ten Cate JW: Subcutaneous heparin compared with continuous intravenous heparin administration in the initial treatment of deep vein thrombosis. Ann Intern Med 1992; 116: 279-284 Eisenberg PR: Role of heparin in coronary thrombolysis. Chest.
Organization to Assess strategies for Ischemic Syndromes OASIS-2 ; Trial Investigators. Effects of recombinant hirudin lepirudin ; compared to heparin in preventing death, myocardial infarction, refractory angina and revascularization procedures in patients with acute myocardial ischemia without ST elevation: A large international randomized double blind study. Lancet 1999; 353: 429-438. Eikelboom JW, Anand SS, Mehta SR, Weitz JI, Yi C, Yusuf S. Prognostic significance of thrombocytopenia during hirudin and heparin therapy in acute coronary syndrome without ST elevation: Organization to Assess Strategies for Ischemic Syndromes OASIS-2 ; Study. Circulation 2001; 103 5 ; : 643-650. Mehta SR, Chrolavicius S, Afzal R, Pogue J. Granger CB, Budaj A, Peters RJ, Bassand JP, Wallentin L, Joyner C, Fox KA, for the OASIS-6 Trial Group. Effects of fondaparinux on mortality and reinfarction in patients with acute ST-segment elevation myocardial infarction: the OASIS-6 randomized trial. JAMA 2006; 295: 15 Yusuf S, Mehta SR, Chrolavicius S, Afzal R, Pogue J, Granger CB, Budaj A, Peters RJ, Bassand JP, Wallentin L, Joyner C, Fox KA: Fifth Organization to Assess Strategies in Acute Ischemic Syndromes Investigators. Comparison of fondaparinux and enoxaparin in acute coronary syndromes. N Engl J Med 2006; 354 14 ; : 1464-1476. Yusuf S, Zhao F, Mehta SR, Chrolavicius S, Tognoni G, Fox KAA for the CURE Investigators. The Clopidogrel in Unstable angina to prevent Recurrent Events Trial CURE ; Investigators. Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation. N Engl J Med 2001; 345: 494-502
Condensed for weeks and do not dissolve in the extracellular medium. We also note that to dissolve a proteoglycan matrix, the linkage between heparin chains and the core protein must be cut. These observations suggest that the proteoglycan gel is a cross-linked molecular network Fig. 5, C ; . It not known if this cross-linking between heparin chains and proteins is chemical in nature or if it involves physical entanglements of individual heparin polymers. Regardless of the nature of this cross-linking, it must be strong enough to enable the matrix to withstand the large stretching forces that occur upon swelling. A force that a swelling matrix can exert was directly measured, and the associated swelling pressure was determined to be ; 12 bar Nanavati and Fernandez, 1993 ; . On the other hand, we know that the matrix is only weakly cross-linked because large molecules such as concanavalin A ; 5 nm length ; can easily penetrate it Oberhauser and Fernandez, unpublished observation ; . In addition, AFM measurements of the elastic modulus of the matrix confirmed that the matrix behaves as a weakly crosslinked ion exchanger Parpura and Fernandez, 1996 ; . We therefore assume that in the swollen matrix there is a single heparin molecule per ; 100 nm2 of the granule surface and that such a molecule is attached to the matrix at two points at least, and therefore is subjected to tensile forces upon swelling of the matrix see Fig. 5 D ; . Then, a pressure of 12 bar corresponds to a stretching force of 120 pN per single heparin molecule. From this rough estimate we clearly see that the forces within the swollen matrix are of such a magnitude that they can affect the conformation of pyranose rings in heparin. Hence, it is likely that during exocytosis the sugar residues of heparin undergo force-induced conformational transitions. It is therefore possible that these conformational transitions have biological significance in regulating release of many molecules that are bound to heparin. In Fig. 4 we describe the mechanism of release that, in addition to ion.
Heparin flush solution
4. Antilipid Therapy: all patients should have a lipid profile within 24 hours of admission for ACS. - statin: start as first-line therapy post-ACS especially if TC 200 mg dL or LDL 100. - Niaspan: start as second agent if HDL 40 mg dL or LDL 100 mg dL on statin, unless patient has poorly controlled DM. Dosage: start at 500 mg q.h.s. and titrate up to 2 q.h.s. - fibrate: second-line agent for diabetics with low HDL and or high triglycerides on statin. Dosage: gemfibrozil 600 mg b.i.d. or fenofibrate 200 mg daily - Lipid profile and SGPT at 6 weeks following initiation of therapy or dosage increase. 5. Transfusion: Transfuse as needed to keep hgb 10 gm post ACS. 6. Diabetic Therapy: Patients with admitting BS 175 with ACS should be started on an insulin drip per protocol ; for first 24. Endocrine consult will be initiated for all patients started on insulin drip, especially if they have no primary care physician on staff. Also, stop metformin if PCI planned. 7. Renal Disease: If a cardiac catheterization or PCI is anticipated and creat 2.0, then start hydration with normal saline the night before cath and start acetylcysteine Mucomyst ; 600 mg p.o. b.i.d x 4 doses. 8. Tobacco Abuse: Smoking cessation is discussed with patient prior to discharge. 9. Folate therapy: consider MVI daily. 10. Consider nicotine patch if indicated but would try to avoid if coronary spasm is suspected or if significant unrevascularized coronary disease. 11. Dietary Advice: Education on low fat diet. 12. Cardiac Rehab: Referral to start immediately post discharge. II. Percutaneous Coronary Intervention PCI ; 1. Antiplatelet agents: A. Oral - ASA: started before PCI at 325 mg and continue indefinitely in all patients post-PCI. - Clopidogrel load with 300 mg if not on prior to PCI ; and then 75 mg daily Continue 12 months: all stents, including coated stent, and brachytherapy. B. Intravenous - Eptifibatide: bolus 180 mcg kg IV x started immediately prior to PCI. if started before PCI, then continue for 12-18 hours post-PCI. if started at time of PCI, then continue for 12-18 hours post-PCI. if large thrombus burden at time of PCI, the interventionalist may order for 18 hour infusion will specify duration of infusion ; . 2. Options for Anticoagulation: - Unfractionated heparin UFH ; : bolus 60 U kg and then 12 U kg hr. - Lepirudin: use as replacement for UFH if suspected HIT syndrome. - Low molecular weight heparin LMWH ; : A. PCI within 8 hours of last LMWH: no additional doses. B. PCI between 8-12 hours: 0.3 mg kg IV enoxaparin. C. PCI 12 hours: standard dose enoxaparin 1.0 mg kg IV ; . post-cath: pull sheath 8 hours after last dose if Perclose not utilized. pre-CABG: no LMWH 12 hours prior to surgery. 3. Folate therapy: Folgard folate 800 mcg, B 12, pyridoxine 10 mg ; daily. for 6 months, especially PCI without stent placement. 4. Transfusion: - If acute coronary syndrome, transfuse as needed to keep hgb 10 gm hct 30% ; . - If stable asymptomatic patient no ACS: transfuse for hgb 8 gm hct 24.
Low molecular weight heparin metabolism
Geerts WH, Pineo GF, Heit JA, et al. Prevention of Venous Thromboembolism. The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. CHEST 2004; 126: 338S400S, Suppl 3 ; . Prevention of Venous thromboembolism: International Consensus Statement Guidelines compiled in accordance with the scientific evidence. Under the auspices of the cardiovascular Disease Educational and Research Trust, and the International Union of Angiology. International Angiology 2001; 20: 1-37. h t t p Thromboprophylaxis no037 accessed July 2006 ; . Nicolaides AN, Fareed J, Kakkar AK, Breddin HK, Goldhaber SZ, Hull R, et al. Prevention and treatment of venous thromboembolism. International Consensus Statement Guidelines according to scientific evidence ; . Int Angiol Jun 2006; 25: 101-61. : nccn professionals physician gls PDF vte. pdf accessed July 2006 ; . Prandoni P, Lensing AW, Cogo A, et al. The long term Clinical Course of Acute Deep Vein Thrombosis. Ann Intern Med 1996; 125: 1-7. Agarwala S, Bhagwat A, Sharma A, et al. Local and general factors are the likely cause of venous thrombosis in lower limb arthroplasty. Thromb Haemost 2004; 92: 1167-9. Geerts WH, Heit JA, Claget GP, et al. Prevention of Venous Thromboembolism. CHEST 2001; 119: 132-75S. Samama MM, Cohen AT, Darmon JY, et al. A comparison of Enoxaparin with placebo for the prevention of venous thromboembolism in acutely ill medical patients. Prophylaxis in Medical Patients with Enoxaparin Study Group. N Engl J Med 1999; 341: 793-800. Todi Sk, Sinha S, Chakarborty A, et al. Utilization of DVT Prophylaxis in medical Surgical Intensive care units. Indian Journal of Critical Care Medicine 2003; 7: 103-5. Hirsh J, Warkentin TE, Shanghnessey SG, et al. Heparin and LMWH: Mechanism of action, Pharmacokinetic dosing, Monitoring efficacy and safety. CHEST 2001; 119 Suppl-64S94S ; . Creager MA, Dzau VJ. Vascular diseases of the extremities, in Fauci AS, Martin JB, Braunwald E, et al ed ; Harrisons Principles of Internal Medicine 14 edition, 2001; pp 1403. Lindblad B, Bergqvist D, Nordstrom M, Kjellstrom T, Bjorgell O, Nylander G, Sternby NH, Anderson H. [A survey in Malmo. The frequency of venous thromboembolism has not changed during the last 30 years] Lakartidningen 1992; 89: 2941-2, Claget GP, Anderson FA jr, Heit J, et al. Prevention of Venous Thromboembolism. CHEST 1995; 108 Suppl: 312S-334S ; . Piovella F, Wang CJ, Lu H, Lee K, et al. Deep-vein thrombosis rates after major orthopedic surgery in Asia. An epidemiological study based on post-operative screening with centrally adjudicated bilateral Venography. J Thromb Haemost 2005; 3: 2664-70. Dhillon KS, Askander A, Doraiswamy S. Post Operative DVT in Asian Patients is not a rarity: A prospective study of 88 patients with no Prophylaxis. Journal of Bone Joint Surgery Br 1996; 78: 42730. Kin YH, Suh JS. Low Incidence of Deep Vein Thrombosis after Cementless Total Hip Arthoplasty. J Bone Joint Surg 1988; 70: 878-82.
Heparin storage condition
I do remember an incident in which we had cannulated and the heparin was sort of lying on the nursing tray, and I had indicated to the perfusionist to go on pump, and the nurse mentioned that, oh, we had not given the heparin yet. And so we gave the heparin and then we went on pump. Q: Had you gone on pump without giving the heparin, what are the potential consequences? A: Hopefully, we wouldn't have done that, because the perfusionist's job, before he turns on the pump, is to be sure there is an ACT, and an ACT had not been measured. One of the checks and balances in the system is the perfusionist's responsibility is to be sure that the ACT is greater than 400 seconds before going on pump. At any rate, if you were to go on pump without heparinizing, you run the risk of clotting the system, pump and cannulas. Evidence, page 25, 805 and hepsera.
Based on the revised evidence, we may conclude that low-molecular-weight heparins have class I recommendation in the treatment of acute coronary syndromes ie, indication based on evidence obtained in randomized studies properly delineated with clinically relevant outcomes and statistical power ; . To date, enoxaparin is the only low-molecular-weight heparin that has proved to be superior to unfractionated heparin, dalteparin and nadroparin being at least as effective as the unfractionated heparin fig. 1 ; . This suggests that enoxaparin should be part of the current.
Prolongation of aptt during therapy with enoxaparin to the same extent as with unfractionated heparin should only be used as a criteria of overdose and herceptin.
87. Package Insert. Tinzaparin [Innohep]. Wilmington, DE. DuPont Pharma, July 2000. 88. Package Insert. Enoxaparin [Lovenox]. Bridgewater, NJ. Aventis Pharmaceuticals Inc. November 2005. 89. Package Insert. Dalteparin [Fragmin]. Kalamazoo, MI, Pharmacia & Upjohn Company, March 2004. 90. Package Insert. Heparin Sodium Injection, USP. Deerfield, IL. Baxter Healthcare Corp. December 2004. 91. Lim W, Crowther MA, Eikelboom JW. Management of antiphospholipid antibody syndrome: a systematic review. JAMA. 2006; 295: 1050-1057. Hutten BA, Prins MH, Gent M, et al. Incidence of recurrent thromboembolic and bleeding complications among patients with venous thromboembolism in relation to both malignancy and achieved international normalized ratio: a retrospective analysis. J Clin Oncol. 2000; 18: 3078-3083. Meyer G, Marjanovic Z, Valcke J, et al. Comparison of lowmolecular-weight heparin and warfarin for the secondary prevention of venous thromboembolism in patients with cancer: a randomized controlled study. Arch Intern Med. 2002; 162: 1729-1735. Hull RD, Pineo GF, Mah AF, et al. A randomized trial evaluating long-term low-molecular-weight heparin therapy for three months versus intravenous heparin followed by warfarin sodium [abstract]. Presented at the 19th meeting of the International Society of Thrombosis and Haemostasis ISTH ; . December 9, 2002. 95. Hylek EM, Heiman H, Skates SJ, et al. Acetaminophen and other risk factors for excessive warfarin anticoagulation. JAMA. 1998; 279: 657-662. Bona RD, Hickey AD, Wallace DM. Warfarin is safe as secondary prophylaxis in patients with cancer and a previous episode of venous thrombosis. J Clin Oncol. 2000; 23: 71-73. REF-5.
Pharmacy managed weight based heparin protocol
1. Jones GR, Hashim R, Power DM. A comparison of the strength of binding of antithrombin III, protamine and poly l-lysine ; to heparin samples of different anticoagulant activities. Biochim Biophys Acta. 1986; 883: 69-76. Metz S, Horrow JC. Protamine and newer heparin antagonists. In: Stoelting RK, ed. Pharmacology & Physiology in Anesthetic Practice. JB Lippincott Co, Philadelphia, PA; 1994: 1-15. 3. Porsche R, Brenner ZR. Allergy to protamine sulfate. Heart Lung. 1999; 28: 418-428. Weiler JM, Gellhaus MA, Carter JG, et al. A prospective study of the risk of an immediate adverse reaction to protamine sulfate during cardiopulmonary bypass surgery. J Allergy Clin Immunol. 1990; 85: 713-719. Levy JH, Zaidan JR, Faraj B. Prospective evaluation of risk of protamine reactions in patients with NPH insulin-dependent diabetes. Anesth Analg. 1986; 65: 739-742. Morel DR, Lowenstein E, Nguyenduy T, et al. Acute pulmonary vasoconstriction and thromboxane release during protamine reversal of heparin anticoagulation in awake sheep: Evidence for the role of reactive oxygen metabolites following nonimmunological complement activation. Circ Res. 1988; 62: 905-915. Sela M. Antigenicity: Some molecular aspects. Science. 1969; 166: 1365-1374. Yang VC, Port FK, Kim JS, Teng CL, Till GO, Wakefield TW. The use of immobilized protamine in removing heparin and preventing protamine-induced complications during extracorporeal blood circulation. Anesthesiology. 1991; 75: 288-297. Chang LC, Lee HF, Yang Z, Yang VC. Low molecular weight protamine as nontoxic heparin low molecular weight heparin antidote. I ; : Preparation and characterization. AAPS PharmSci. 2001; 3 2 ; article 17 : pharmsci scientificjournals pharmsci journal 01 17 ; . 10. Byun Y, Singh VK, Yang VC. Low molecular weight protamine: A potential nontoxic heparin antagonist. Thromb Res. 1999; 94: 53-61. Mayer MM. In: Kabat EA, Mayer MM, immunochemistry. Thomas, Springfield, IL; 1961: 113. eds and hms.
200 ng ml equivalent to 13.3 nM, with increasing concentrations of soluble recombinant receptor polypeptides, prior to plating out aliquots 100 l ; in heparinBSA complex coated wells. For sIL-2R, up to 37 nM was used, this maximal concentration corresponding to the dissociation constant for the binding of this receptor to IL-2 Myszka et al., 1996 ; . As shown in Figure 3, there was no apparent competition for subsequent heparin binding. Indeed at the highest concentration of sIL-2R employed, there is a statistically significant increase p 0.005, by Student's t test ; in heparin binding. In the case of the lower affinity polypeptide, sIL-2R, Kd 400 nM Myszka et al., 1996 ; , the use of concentrations equal to the Kd is impractical. However, similarly preincubation with up to 40 sIL-2R, showed no evidence of competition, again a modest but statistically significant p 0.005 ; increase in binding is observed. Therefore, these data provide no evidence of competition between these receptor subunits and heparin for the binding of IL-2. The effect of heparin on the binding of IL-2 to its receptor was also examined in a bioassay involving the IL-2dependent cell line, CTLL-2. As shown in Figure 4A, the presence of 100g ml heparin neither inhibited nor enhanced the proliferative response of these cells to rhIL-2 in vitro. Moreover, pretreatment of the cells with heparinase II also had no detectable effect Figure 4B ; . Taken overall, our data strongly suggests that the binding of heparin to IL-2 does not affect receptor interactions. Heparin binding properties of rhIL-2 mutants We sought to establish the effect of single amino acid substitutions on the binding of rhIL-2 to heparin. Four different purified rhIL-2 muteins R38A, K43E, T51P, and Q126D ; Sauve et al., 1991; Buchli and Ciardelli, 1993; Chang et al., 1995 ; were investigated. We first performed direct ELISA by adding increasing concentrations, 0200 ng ml, of each analog or wild type rhIL-2 to uncoated plate wells, with binding detected by 511.
Heparin overdose in texas
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REFERENCES: 1. Data on file, Rh# ne-Poulenc Rorer Pharmaceuticals Inc. 2. Turple AGO. Levine MN, Hirsh J, et al: A randomized controlled trial ofa Iow'molecular-weight heparin Ienoxaparinl to prevent deep-vein thrombosis in patients undergoing elective hip surgery. N EngIJ Med.
[May 30, 2000: Aventis Pharmaceuticals]: precautions: geriatric use: new subsection. Accessed September 11, 2003, at : fda.gov medwatch safety 2000 may00 #lovenox. ; 2. FDA MedWatch. LOVENOX enoxaparin sodium ; injection [January 9, 2002: Aventis]: warnings. Accessed September 11, 2003, at : fda.gov medwatch SAFETY 2002 jan02 #lovenox. ; 3. Dolovich LR, Ginsberg JS, Douketis JD, Holbrook AM, Cheah G. A meta-analysis comparing low-molecular-weight heparins with unfractionated heparin in the treatment of venous thromboembolism: examining some unanswered questions regarding location of treatment, product type, and dosing frequency. Arch Intern Med 2000; 160: 181-8 and humira.
Products with omega-3 oils rose nearly 8% vs. a year ago and 39% compared to 2001. Fibre content is another fast-growth health claim, up 18% in one year and up 50% vs. 2001. This label is mostly used in breakfast cereals and bread products. Products with an organic claim UPC-coded products only ; grew by nearly 18% in one year and 60% since 2001. Top-selling products include fresh produce, dairy products, and eggs. ACNielsen predicts organic brands will expand into many processed food categories.
Luation. Thromb Haemost 1998; 97: 259-63. The Enoxaparin Clinical Trial Group. A multicenter clinical trial comparing once-and twice-daily subcutaneous enoxaparin and intravenous heparin in the treatment of acute deep vein thrombosis. 39th annual meeting and exposition of the American Society of Hematology; San Diego, CA, USA; 1997 December 5-9, Abstract 1305. 31. Charbonnier BA, Fiessinger JN, et al. Comparison of a once daily with twice daily subcutaneous low molecular weight heparin regimen in the treatment of deep vein thrombosis. Thromb Haemost 1998; 79: 897-901. Levesque H, et al. Evaluation of hospital cost of six days of treatment of deep venous trombosis. Comparison of subcutaneous nadroparin and intravenous heparin in 40 patients. Therapie French ; 1999; 49 2 ; : 101-5. 33. O'Brien B, Levine M, Willan A, et al. Economic evaluation of outpatient treatment with low-molecular-weight heparin for proximal vein thrombosis. Arch Intern Med 1999; 159: 2298-304. Boccalon H, Elias A, Chale JJ, et al. For the Vascular MidiPyrenees Network Group. Clinical outcome and cost of hospital vs home treatment of proximal deep vein thrombosis with a low-molecular-weight heparin. Arch Intern Med 2000; 160: 1769-73. Kovacs MJ, Anderson D, Morrow B, et al. Outpatient treatment of pulmonary embolism with dalteparin. Thromb Haemost 2000; 83: 209-11. Grau E, Real E, Pastor E, et al. Home treatment of deep vein thrombosis: a two-year experience of a single institution. Haematologica 1998; 83: 438-41. EFS Group European Fraxiparine Study Group ; . Comparisonof a low molecular weight heparin and unfractionated heparin for the prevention of deep vein thrombosis in patients undergoing abdominal surgery. Br J Surg 1998; 75: 1058-63. Gould MK, Dembitzer AD, et al. Low-molecular-weight heparins compared with unfractionated heparin for treatment of acute deep venous thrombosis. A meta-analysis of randomized, controlled trials. Ann Intern Med 1999; 130: 800-9. Dolovich LR, Ginsberg JS, et al. A meta-analysis comparing low-molecular-weight heparins with unfractionated heparin in the treatment of venous thromboembolism. Arch Intern Med 2000; 160: 181-8. Lopaciuk S, Bielska-Falda H, et al. Low molecular weight heparin versus acenocoumarol in the secundary prophylaxis of deep vein thrombosis. Thromb Haemost 1999; 81: 26-31. Gonzales-Fajardo JA, Arreba E, Castrodeza J, et al. Venographic comparison of subcutaneous low-molecular-weight heparin with oral anticoagulant therapy in the long-term treatment of deep venous thrombosis. J Vasc Surg 1999; 30: 283-92. Veiga F, Escriba A, et al. Low molecular weight heparin enoxaparin ; versus oral anticoagulant therapy acenocoumarol ; in the long-term treatment of deep venous thrombosis in the elderly: a randomized trial. Thromb Haemost 2000; 84: 559-64. Monreal M. Long-term treatment of venous thromboembolism with low-molecularweight heparin. Curr Opin Pulm Med 2000; 6: 326-9. Howard AW, Aaron SD. Low molecular weight heparin decreases proximal and distal deep venous thrombosis following total knee arthroplasty. A meta-analysis of randomized trials. Thromb Haemost 1998; 79: 902-6. Hawkins DW, Langley PC, Krueger KP. Pharmacoeconomic model of enoxaparin versus heparin for prevention of deep and hyaluronan.
Coumadin and heparin induced thrombocytopenia
Antiplatelet therapy combined with intravenous heparin followed by oral anticoagulation was utilized in an attempt to overcome the problem of stent thrombosis. This approach reduced the frequency of stent thrombosis, but was associated with a marked increase in haemorrhagic complications, notably bleeding requiring blood transfusion and puncture site complications requiring surgical repair13"51. In addition, such an approach requires prolonged hospitalization at considerable financial cost. In the recent Benestent Study, subacute stent thrombosis occurred in 3-5% of patients, and serious vascular complications requiring transfusion and heparin.
It is expected that with the new 2% pension formula, the shortfall should eventually take care of itself. In fact, if interest rates rise and stock market returns continue to improve, the shortfall could disappear in as little as a couple of years. As soon as this happens, the Trustees can start looking at bonuses or benefit improvements. On the other hand, the shortfall could last as long as 10 years, or more. In fact, if interest rates and market returns decline, we might have to look at more changes to the plan and hydralazine.
Contaminated heparin china
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Heparin drip rate protocol
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