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Feedback for danaparoid as a treatment for View pubmed citation view isi citation search isi for citing articles 8 or more ; related articles publication history issue online: 22 dec 2003 accepted 27 march 2001 home list of issues table of contents article abstract bjog: an international journal of obstetrics and gynaecology volume 109 issue 4 page 466-468, april 2002 to cite this article: yin ling woo, shuba allard, hannah cohen, elizabeth letsky, michael de swiet 2002 ; danaparoid thromboprophylaxis in pregnant women with heparin-induced thrombocytopenia bjog: an international journal of obstetrics and gynaecology 109 4 ; , 466– 468 doi: 1 1111 j 71-052 200 0005 x prev article next article abstract case report danaparoid thromboprophylaxis in pregnant women with heparin-induced thrombocytopenia yin ling woo a a west suffolk hospital, bury st.

In contrast to quinine-induced immune thrombocytopenic purpura or thrombotic thrombocytopenic purpura TTP ; with absent ADAMTS-13 activity, HIT typically gives a more moderate thrombocytopenia Figure 1 ; .13, 14 Miscellaneous Sequelae of HIT Some clinical features are relatively specific for HIT, including skin lesions at heparin injection sites, 15, 16 acute systemic reactions after intravenous bolus heparin, 15, 17 and adrenal hemorrhagic necrosis.15, 18 Heparin-induced skin lesions occur in about 10% to 20% of patients who develop HIT in association with subcutaneous UFH or LMWH injections.15, 16 Both necrotizing and nonnecrotizing lesions erythematous plaques ; are reported. Not all patients who develop heparinFigure 2. Bilateral adrenal hemorrhagic infarction complicating heparin-induced thrombocytopenia HIT ; . induced skin lesions develop thrombocytopeThe patient, a 52-year-old female with serious injuries sustained in a motor nia, but among those who do, arterial thrombovehicle accident, had a high pretest probability for HIT, based upon clinical sis is especially common. events that occurred during the first 10 hospital days. The pretest probability Giving an intravenous heparin bolus to a score 4 T's clinical scoring system ; was 8 the maximum score ; , based patient with circulating HIT antibodies can trigupon 55% platelet count fall 2 points ; that began on day 5 of heparin therapy and that preceded the second operation 2 points ; , with thrombotic manifesger abrupt onset of an acute systemic reaction tations bilateral adrenal infarction and deep-vein thrombosis; 2 points ; 5 to 30 minutes later or up to hours after without other apparent explanation 2 points ; . The clinical diagnosis was 15, 17 subcutaneous UFH or LMWH injection ; . supported by strong positive testing for HIT antibodies 99% serotonin Various inflammatory fever, chills, flushing ; , release; normal 10%; 2.245 optical density units in an in-house anti-PF4 heparin ELISA that detects IgG class antibodies; normal 0.450 units ; . cardiorespiratory tachycardia, hypertension, Coagulopathy elevated INR ; and leukocytosis were attributed to HIT and the tachypnea, dyspnea, cardiac or respiratory arearly stages of adrenal crisis, respectively, and both abnormalities resolved rest ; , neurologic pounding headache, transient with danaparoid anticoagulation and corticosteroids. The patient was global amnesia ; , and or gastrointestinal largeswitched from prophylactic-dose to therapeutic-dose danaparoid when routine duplex ultrasound detected a subclinical DVT involving a small area of volume diarrhea ; signs and symptoms can octhe left femoral and popliteal veins. cur. An abrupt platelet count drop accompaAbbreviations: bid, twice-daily; DVT, deep-vein thrombosis; sc, subcutaneous; nies these reactions. UFH, unfractionated heparin. Adrenal hemorrhagic necrosis occurs in 3 to 5% HIT patients, and is characterized by Cerebral hemorrhagic infarction can also represent a abdominal or flank pain; when necrosis is bilateral, death paradoxical "hemorrhagic" complication of HIT that repfrom adrenal crisis can result, which is preventable with timely use of corticosteroids.15, 18 The pathogenesis is adrenal vein resents the final common pathway of cerebral venous dural sinus ; thrombosis.15, 19 This sequela occurs in less than thrombosis, with secondary hemorrhagic infarction. Figure 2 shows the clinical course of a patient who 1% of patients with HIT. developed thrombocytopenia and bilateral adrenal hemorrhage during LMWH use. A superficial analysis might sug- Coumarin-induced Microthrombosis gest HIT to be unlikely--after all, hemorrhage is not a fea- There are two forms of coumarin-induced necrosis, the clasture of HIT, LMWH is not a common cause of HIT, and sic syndrome of skin necrosis non-acral dermal and subthese events occurred in a post-trauma patient who had dermal necrosis ; and venous limb gangrene acral necrosis 1 undergone two major operations. Yet, when one considers of a limb, usually one affected by DVT ; . Coumarin-induced necrosis complicating HIT is much more likely to manifest that the patient received a dose of UFH, that the timing of 3 onset of thrombocytopenia was precisely 5 days after this as venous limb gangrene. The pathogenesis is a profound disturbance in procoagulant-anticoagulant balance, namely single UFH injection, that a large platelet count fall occurred otherwise inexplicably on the day before the second interaction of HIT-associated hypercoagulability increased operation, and that adrenal hemorrhage is a manifestation of thrombin generation ; and coumarin-induced compromise adrenal vein thrombosis, then it is clear that the patient has a of the protein C natural anticoagulant pathway. Microthrombosis results from impaired ability of protein C to high pretest probability for HIT. downregulate thrombin in the microcirculation. 410 American Society of Hematology.

Effect on proximal DVT: There was no significant difference between OAC and aspirin RR 0.87, CI: 0.57 to 1.35, four studies ; Figure 70, Appendix E ; . Effect on major bleeding: There was no significant difference between groups RR 5.08, 95% CI: 0.61 to 42.28, one study ; Figure 71, Appendix E ; . OAC vs dextran We identified one systematic review374 and two additional RCTs216, 316 with a total of 990 participants from 6 RCTs Evidence Table 32, Appendix D ; . Effect on DVT: There was no significant difference between OAC and dextran RR 0.91, 95% CI: 0.53 to1.56, five studies ; Figure 72, Appendix E ; . There was heterogeneity within the results 2 on 4 13.82, p 0.008 ; caused by the inclusion of one study165 which used dextran 40 the other studies used dextran 70 ; . This study found a significant benefit of OAC over dextran 40 RR 0.40, 95% CI: 0.22 to 0.75 ; , whereas the difference was not significant for OAC vs dextran 70 RR 1.24, 95% CI: 0.69 to 2.23, four studies ; . Effect on pulmonary embolism: There was no significant difference between dextran and OAC RR 0.50, 95% CI: 0.22 to 1.13, four studies ; Figure 73, Appendix E ; . Effect on proximal DVT: OAC reduced the risk of proximal DVT by 71% compared to dextran RR 0.27, 95% CI: 0.10 to 0.78, two studies ; Figure 74, Appendix E ; . Effect on major bleeding: It was not possible to obtain a reliable estimate of effect due to the low number of events observed RR 3.78, 95% CI: 0.68 to 21.04, two studies ; Figure 75, Appendix E ; . 6.2.2.10 OAC vs danaparoid We identified one systematic review with two RCTs with a total of 777 participants374 Evidence Table 33, Appendix D ; . Effect on DVT: There were significantly more DVT in the OAC group compared to the danaparoid group RR 2.14, 95% CI: 1.53 to 2.99, two studies ; Figure 76, Appendix E ; . Effect on pulmonary embolism: There was no significant difference found between OAC and danaparoid RR 3.03, 95% CI: 0.32 to 28.94, two studies ; Figure 77, Appendix E ; . Effect on proximal DVT: There was no significant difference found between OAC and danaparoid and dandelion.

1. Hirsh J, Dalen JE, Deykin D, Poller L. Heparin: mechanism of action: pharmacokinetics, dosing considerations, monitoring, efficacy, and safety. Chest. 1992; 102 suppl ; : 337S351S. 2. Freedman MD. Pharmacokinetics, clinical indications, and adverse effects of heparin. J Clin Pharmacol. 1992; 32: 584 Hirsh J. Heparin. N Engl J Med. 1991; 32: 15651574. Hull RD, Raskob GE, Rosenbloom D, Lemaire J, Pineo GF, Baylis B, Ginsberg JS, Panjee AA, Brill-Edwards P, Brant R. Optimal therapeutic level of heparin therapy in patients with venous thrombosis. Arch Intern Med. 1992; 152: 1589 Hirsh J, Fuster V. Guide to anticoagulant therapy, part I: heparin. Circulation. 1994; 89: 1449 Levine MN, Hirsh J, Landefeld S, Raskob G. Hemorrhagic complications of anticoagulant treatment. Chest. 1992; 102: 352S363S. Cruickshank MK, Levine MN, Hirsh J, Roberts R, Siquenza M. A standard heparin nomogram for the management of heparin therapy. Arch Intern Med. 1991; 151: 333337. Raschke RA, Reilly BM, Guidy JR, Fontaine JR, Srinivas S. The weight-based heparin-dosing nomogram compared with a standard care nomogram. Ann Intern Med. 1993; 119: 874 Jordan N. How to improve heparin dosing by using a nomogram. Drug Utilization Rev. 1994; 21: 123125. Woloschuk D, Rubinger M. How to optimize heparin anticoagulation. Drug Info. 1994; 42: 16. Ansons J, Crowell RM. Cervicocranial arterial dissection. Neurosurgery. 1991; 29: 89 International Stroke Trial Collaborative Group. The International Stroke Trial IST ; : a randomised trial of aspirin, subcutaneous heparin, both, or neither among 19 435 patients with acute ischaemic stroke. Lancet. 1997; 349: 1569 Berge E, Abdelnoor M, Nakstad PH, Sandset PM. Low molecular-weight heparin versus aspirin in patients with acute ischaemic stroke and atrial fibrillation: a double-blind randomised study: HAEST Study Group: Heparin in Acute Embolic Stroke Trial. Lancet. 2000; 355: 12051210. Kay R, Wong KS, Yu YL, Chan YW, Tsoi TH, Ahuja AT, Chan FL, Fong KY, Law CB, Wong A. Low-molecular-weight heparin for the treatment of acute ischemic stroke. N Engl J Med. 1995; 333: 1588 Publications Committee for the Trail of Org 10172 in Acute Stroke Treatment TOAST ; Investigators. Low molecular weight heparinoid ORG 10172 danaparoid ; and outcome after ischemic stroke: a randomized controlled trial. JAMA. 1998; 279: 12651272. Miljic P, Colovic MD, Suvajdzic N. Thrombosis of lienal vein and acute consumptive coagulopathy following warfarin administration in a patient with severe protein C deficiency. Eur J Haematol. 2000; 64: 130 Pescatore P, Horellou HM, Conard J, Piffoux M, Van Dreden P, RuskoneFourmestraux A, Samama M. Problems of oral anticoagulation in an adult with homozygous protein C deficiency and late onset of thrombosis. Thromb Haemost. 1993; 69: 311315 and dantrolene.

COUNSEL, THAT ANY DISPUTE HEREUNDER BE RESOLVED BY A JUDGE APPLYING APPLICABLE LAW. Section 10.15 RECOVERY OF FEES BY PREVAILING PARTY. If any legal action, including, without limitation, an action for arbitration or injunctive relief, is brought relating to this Agreement or the breach or alleged breach hereof, the prevailing Party in any final judgment or arbitration award, or the non-dismissing Party in the event of a voluntary dismissal by the Party instituting the action, shall be entitled to the full amount of all reasonable expenses, including all court costs, arbitration fees and actual attorneys' fees paid or incurred in good faith. Section 10.16 SELLER DISCLOSURE SCHEDULE. The Seller Disclosure Schedule is hereby incorporated into this Agreement to the same extent as though fully set forth herein. Section 10.17 TIME OF THE ESSENCE. With regard to all dates and time periods set forth or referred to in this Agreement, time is of the essence. [SIGNATURES FOLLOW ON A SEPARATE PAGE] -52 and darifenacin.

Pain and tingling or numbness or weakness in fingers and sometimes hands. Several tendons and an important nerve the median nerve ; pass through the "carpal tunnel" a tunnel made of fibrous tissue between the arm and the hands ; at the wrist. Pressure on the nerve causes this condition. If the tendons or tendon sheaths become inflamed and swollen by tenosynovitis they can put pressure on the nerves running through the carpal tunnel.

The high prevalence of this incidence did not, however, have an impact on the refractive safety of the technique. The median BSCVA at 3 months postoperative for eyes that suffered any degree of DLK was not significantly different from the eyes that did not present with this syndrome. The complete absence of any other intra- or postoperative complications in the eyes operated on using IntraLase indicates a good level of safety for this device. Two new inflammatory conditions, TLSS and energyrelated DLK, appeared specifically related with the use of the femtosecond laser. From the results of our two studies, we concluded that although the femtosecond laser was a safe device for creating lamellar cuts for LASIK, the use of higher energy levels could induce a greater interface inflammatory reaction. Two strategies proved to be effective to reduce, at least in part, the incidence of TLSS and DLK: 1 ; adjusting the parameters of the femtosecond laser to reduce the amount of energy used to make the lamellar resection and 2 ; increasing the dose of steroids in the early postoperative period. Csar Albarrn-Diego practices in the Refractive Surgery Department, Centro de Especialidades Marqus de Sotelo, and Hospital NISA Virgen del Consuelo, in Valencia, Spain. Mr. Albarrn-Diego states that he has no financial interest in the products or companies mentioned. He may be reached at cesar.albarran gmail . Jorge L. Ali, MD, PhD, is Professor and Chairman of Ophthalmology, Miguel Hernandez University, Alicante, Spain, and Medical Director of VISSUM Corp., in Spain. Professor Ali states that he has no financial interest in the products or companies mentioned. He may be reached at + 34 515 00 25; jlalio vissum . Jaime Javaloy, MD, PhD, practices in the Department of Refractive Surgery, VISSUM Instituto Oftalmolgico de Alicante, and Division of Ophthalmology, Miguel Hernndez University, Medical School, in Alicante, Spain. Dr. Javaloy states that he has no financial interest in the products or companies mentioned. He may be reached at tel: + 34 96 515 00 25; fax: + 34 96 515 or jjavaloy coma . Gonzalo Muoz, MD, PhD, practices in the Department of Surgery, VISSUM Instituto Oftalmolgico de Alicante, Division of Ophthalmology, Miguel Hernndez University, Medical School, in Alicante, Spain, and Refractive Surgery Department, Centro de Especialidades Marque's de Sotelo and Hospital NISA Virgen del Consuelo, in Valencia, Spain. Dr. Muoz states that he has no financial interest in the products or companies mentioned. He may be reached at gon.munoz ono and deferasirox.

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