Use of Lepirudin in Patients with Heparin-Induced Thrombocytopenia and Renal Failure Requiring Hemodialysis

2001 ◽  
Vol 35 (7-8) ◽  
pp. 885-890 ◽  
Author(s):  
William E Dager ◽  
Richard H White

OBJECTIVE: To report two cases of successful lepirudin use in two patients with heparin-induced thrombocytopenia (HIT) and renal failure. CASE SUMMARY: Two patients with renal failure requiring hemodialysis developed HIT syndrome during intravenous heparin therapy. Anticoagulation was necessary to prevent recurrent, acute venous thrombosis in one patient and to prevent arterial thrombosis associated with the use of an intraaortic balloon pump in the second. Intravenous lepirudin was initiated at doses of 0.01 mg/kg/h and 0.005 mg/kg/h, respectively, and titrated based on the activated partial thromboplastin time (aPTT). Steady-state doses were 0.015 mg/kg/h to maintain aPTT values of approximately 60 seconds in one patient, and 0.005–0.008 mg/kg/h to achieve an aPTT of approximately 45 seconds in the other patient. DISCUSSION: Lepirudin is one of few anticoagulants that can be safely used in patients with HIT. Because it is eliminated through the kidneys, great care must be taken when administering lepirudin to patients with renal failure; in fact, its use is currently not recommended in patients requiring hemodialysis. Lepirudin effectively prevented acute thrombosis in both of our patients with documented HIT, with no bleeding complications. We describe how we selected the initial doses and report results of aPTT monitoring. CONCLUSIONS: In patients with renal failure who develop HIT, lepirudin is one available alternative to heparin despite its poor renal elimination pattern and subsequently prolonged half-life.

1993 ◽  
Vol 2 (1) ◽  
pp. 81-87 ◽  
Author(s):  
T Thomason ◽  
B Riegel ◽  
D Jessen ◽  
Smith SCJr ◽  
I Gocka ◽  
...  

OBJECTIVE: To evaluate the clinical safety of heparin titration and the procedural cost of anticoagulation measurement using bedside low-range activated clotting time. DESIGN: Quasi-experimental study using data gathered through retrospective record review. SETTING: Coronary care, medical intensive care and telemetry units of a community hospital. SUBJECTS: Sample of 102 patients undergoing elective percutaneous transluminal coronary angioplasty. INTERVENTION: Intravenous heparin therapy was titrated using low-range activated clotting time in 51 percutaneous transluminal coronary angioplasty patients. Data from this group were compared to a matched sample of 51 angioplasty patients whose intravenous heparin therapy was titrated using activated partial thromboplastin time. RESULTS: No differences in procedural, early or late complications were found between the groups. The cost of managing heparin therapy with low-range activated clotting time was less than with activated partial thromboplastin time. CONCLUSION: These results suggest that titrating heparin therapy based on bedside low-range activated clotting time for the angioplasty patients in this sample was as safe as with activated partial thromboplastin time. Use of bedside low-range activated clotting time saved money for the hospital.


2020 ◽  
Vol 2020 ◽  
pp. 1-4
Author(s):  
Ryo Kanamoto ◽  
Shinichi Hiromatsu ◽  
Tomoyuki Anegawa ◽  
Kanako Sakurai ◽  
Shohei Yoshida ◽  
...  

Heparin-induced thrombocytopenia (HIT) is a life-threatening adverse drug reaction of heparin therapy, which increases a patient’s risk of developing venous and/or arterial thromboembolism. HIT should be treated through discontinuation of heparin and administration of nonheparin anticoagulants such as argatroban. For long-term anticoagulation, parenteral nonheparin anticoagulants are generally converted to oral treatment with a vitamin K antagonist such as warfarin. Although administration of warfarin is recommended to overlap with a nonheparin anticoagulant for a minimum of 5 days, overlapping with argatroban and warfarin presents high risks of bleeding. We describe a case of HIT treated with edoxaban. A 78-year-old man underwent surgery for esophageal cancer and was administered heparin perioperatively. After surgery, he was diagnosed with HIT and venous thromboembolism. We immediately stopped heparin and initiated parenteral argatroban. The patient was subsequently started on edoxaban without any overlap between the two drugs. The treatment was successful. The treatment of edoxaban following argatroban for HIT could reduce bleeding complications and shorten the length of hospital stay. To the best of our knowledge, this is the first report of the use of edoxaban for HIT treatment.


1981 ◽  
Author(s):  
J A Caprini ◽  
C J Thorpe ◽  
S J Torkelson ◽  
J P Vagher ◽  
A Z Delos Reyes ◽  
...  

One hundred consecutive patients with thromboembolic disease were treated with subcutaneous heparin to prevent recurrence of deep venous thrombosis (70 patients), pulmonary embolus (21), or both deep venous thrombosis and pulmonary embolus (9). Thrombosis was documented by venography, doppler ultrasound, impedance plethysmography, V-P lung scanning, or pulmonary angiography. The hospitalized patients received intravenous heparin for an average of 12.3 days. Intravenous heparin was overlapped with the first dose of 5000 units of subcutaneous heparin which was then given every 12 hours. Fifteen patients had the subcutaneous dosage increased before discharge and 52 had changes in dosage at some point during therapy according to test results. Subcutaneous heparin therapy averaged 111 days per patient (range - 15 days to 16 months). No episodes of major bleeding occurred, although 5 patients had minor localized eccymosis or rash. Self-injection was well accepted and tolerated by the patients. Clinical examination, hematocrit platelet count, prothrombin time, activated partial thromboplastin time, fibrinogen, fibrin split products, and thrombelastography were performed every six weeks. Doppler and impedance plethysmography studies were repeated if clinical signs persisted or recurred. Two patients had recurrent nonfatal deep vein thrombosis 3 months after starting subcutaneous heparin therapy. Both of these patients originally had above knee thrombi.The results suggest that self-administered subcutaneous heparin injections titered to laboratory tests are effective in preventing recurrent thromboembolism without bleeding complications. This approach represents an effective alternative to oral anticoagulant therapy.


1975 ◽  
Vol 9 (10) ◽  
pp. 560-565
Author(s):  
Robert J. Ignoffo

The incidence of bleeding from heparin therapy in patients with diagnosed pulmonary embolism and deep vein thrombosis was evaluated in a university hospital. Major or minor bleeding episodes occurred in 32 percent of patients and of these 50 percent were major episodes requiring cessation of therapy and blood transfusion. Activated clotting times were not excessively prolonged during bleeding episodes nor was there any apparent association with the age or sex of the patient. It is felt that bleeding secondary to intermittent intravenous heparin therapy may be the result of the high degree of clotting inhibition from 15 minutes to 2 hours after injection. It is suggested that continuous intravenous infusion of heparin is as effective as intermittent heparin injections and yet appears to produce a lower incidence of both major and minor bleeding episodes.


2017 ◽  
Vol 86 ◽  
Author(s):  
Blanka Mahne ◽  
Mladen Gasparini ◽  
Matija Kozak

Background: Heparin-induced thrombocytopenia (HIT) is an immune-mediated disorder following heparin therapy presenting with thrombocytopenia and associated arterial or/and venous thrombosis (heparin induced thrombocytopenia with thrombosis–HITT). Unrecognised HIT can lead to severe complications like limb amputation and death.Case report: We report a case of a patient who presented with HIT-associated recurrent lower limb arterial thrombotic occlusions and popliteal venous thrombosis 29 days after coronary bypass graf surgery. The patient underwent urgent thrombectomy of superfcial femoral, popliteal and posterior tibial artery. Because of recurrent thrombotic occlusions of lower limb arteries three surgical revisions were performed. Te platelet count decreased from 124 × 109/l to 53 × 109/l on the fifth day after the first intervention. After clinical suspicion of HIT, heparin was discontinued and fondaparinux was started. Arterial thrombosis did not recur and the patient recovered without consequences.Conclusions: HIT occurs in 1–3 % of patients after cardiac surgery. Strict following of international guidelines regarding the frequency of platelet count monitoring, assessing probability for HIT and laboratory testing is mandatory in order not to miss the diagnosis of HIT. HIT can manifest clinically several days after the first exposure to heparin. If a patient presents with acute thrombosis and thrombocytopenia, HITT should be suspected. Postoperative HIT is associated with higher morbidity and mortality. Early recognition is crucial to prevent severe complications and death.


2020 ◽  
Vol 31 (2) ◽  
pp. 129-137
Author(s):  
Tanya Williams-Norwood ◽  
Megan Caswell ◽  
Barbara Milner ◽  
Joseph C. Vescera ◽  
Kelly Prymicz ◽  
...  

Background: The VA Northeast Ohio Healthcare System introduced a new nurse-driven anti–factor Xa (anti-Xa) protocol for monitoring unfractionated heparin to replace the previous activated partial thromboplastin time protocol. Objective: To design, implement, and evaluate the efficacy of the anti-Xa monitoring protocol. Methods: An interdisciplinary team of providers collaborated to develop and implement a nurse-driven, facility-wide anti–factor Xa protocol for monitoring unfractionated heparin therapy. The effectiveness of this protocol was evaluated by retrospective analysis. Results: We reviewed 100 medical records for compliance with the new anti-Xa monitoring protocol. We then evaluated 178 patients whose anticoagulation was monitored with the anti-Xa assay to determine the time to therapeutic range. We found that 80% of patients receiving the anti-Xa protocol achieved therapeutic anticoagulation within 24 hours, as compared with 54% of patients receiving the activated partial thromboplastin time protocol (P < .001). Protocol conversion also yielded a decrease in blood draws, dose adjustments, and potential calculation errors. Conclusions: Monitoring intravenous heparin therapy with the anti-Xa assay rather than activated partial thromboplastin time resulted in a shorter time to therapeutic anticoagulation, longer maintenance of therapeutic levels, and fewer laboratory tests and heparin dosage changes. We believe the current practice of monitoring heparin treatment with activated partial thromboplastin time assays should be reexamined.


2003 ◽  
Vol 37 (2) ◽  
pp. 229-233 ◽  
Author(s):  
Thuy N Nguyen ◽  
Peter Gal ◽  
J Laurence Ransom ◽  
Rita Carlos

OBJECTIVE: To describe a case of heparin-induced thrombocytopenia (HIT) in a premature infant and the doses of danaparoid and lepirudin needed to achieve appropriate therapeutic endpoints. CASE SUMMARY: A 30-week gestational age infant was diagnosed with HIT with heparin antibodies. Danaparoid 2.0–2.4 units/kg/h achieved anti-Xa levels of 0.2–0.4 U/mL, but thrombocytopenia failed to resolve. Lepirudin was started in place of danaparoid. Lepirudin doses of 0.03–0.05 mg/kg/h achieved target activated partial thromboplastin time values of 1.5–2.0 times baseline. DISCUSSION: Dosing information for danaparoid in neonates is limited, and information for lepirudin appears only in German literature at this time. HIT is well documented in newborns, and lepirudin use in these situations is likely to increase. This report provides some guidance for optimal dosing. It also provides some guidance for HIT evaluation in preterm infants, in whom blood volume for laboratory tests is a major issue. CONCLUSIONS: HIT is an important and potentially fatal problem in neonates. Lepirudin may be the drug of choice, especially since danaparoid is now unavailable. Initial lepirudin dosing should not exceed 0.05 mg/kg/h.


2000 ◽  
Vol 34 (5) ◽  
pp. 606-610 ◽  
Author(s):  
Deb S Sherman ◽  
Carrie L Kass ◽  
Douglas N Fish

OBJECTIVE: To report the use of fludrocortisone for heparin-induced hyperkalemia and to briefly review the available literature relating to heparin-induced hyperkalemia. CASE SUMMARY: A 34-year-old African-American man was admitted to the hospital for pneumococcal pneumonia and sepsis. His hospital course was complicated by the development of acute respiratory distress syndrome, severe sepsis, acute renal failure, placement of a tracheostomy, and recurrent nasopharyngeal bleeding. The patient also developed a subclavian vein thrombosis with extension to the cephalic and basilic veins secondary to placement of a pulmonary artery catheter; anticoagulation with heparin was required. On day 9 of heparin therapy, the patient developed symptomatic hyperkalemia refractory to conventional therapies. Oral fludrocortisone 0.1 mg/d was initiated with resolution of the hyperkalemia within 24 hours despite the continued administration of heparin. DATA SOURCES: A MEDLINE (1966–October 1999) search was performed to identify case reports and clinical trials discussing heparin-induced hyperkalemia or the use of fludrocortisone for hyperkalemia. DISCUSSION: Heparin has the potential to induce hyperkalemia by several mechanisms, including decreased aldosterone synthesis, reduction in number and affinity of aldosterone II receptors, and atrophy of the renal zona glomerulosa. Fludrocortisone promotes potassium excretion by its direct actions on the renal distal tubules. In this patient, fludrocortisone resulted in a significant and rapid decrease in serum potassium even with continued heparin administration and acute renal failure. CONCLUSIONS: This case suggests that fludrocortisone is a reasonable alternative therapy for patients with hyperkalemia secondary to heparin therapy when the continued administration of heparin is necessary.


1990 ◽  
Vol 63 (01) ◽  
pp. 016-023 ◽  
Author(s):  
A M H P van den Bessekaar ◽  
J Meeuwisse-Braun ◽  
R M Bertina

SummaryFive different APTT reagents, two amidolytic anti-ITa assays, one amidoiytic anti-Xa assay, and one coagulometric anti-Xa/ anti-IIa assay were used to assess the effect of heparin in patients treated for venous thromboembolic disease. Good correlations were observed between lug-transformed APYE> determined with the various reagents (correlation coefficients: 0.92-0.96).Nevertheless there were important differences in the slopes of the lines of relationship between the APTT reagents.Good correlations were observed between the anti-Xa and anti-IIa assay results (correlation coefficients: 0.92-0.97). However, the amidolytic anti-Xa activity was significantly higher (p <0.001) than the two amidolytic anti-IIa activities. Less good correlations were observed between the log-transformed APTTs and the anti-Xa or anti-IIa activities (correlation coefficients: 0.64-0.78). The correlations were improved by transforming the APTT into APTT-ratio, i.e. the ratio of the patient’s APTT to the same patient’s APTT after removal of heparin from the plasma sample by means of ECTEOLA-cellulose treatment. The correlation coefficients of log (AFTT-ratio) with anti-Xa or anti-IIa ranged from 0.76 to 0.87.For both APTT and amidolytic heparin assay, the response to in vitro heparin was different from the response to ex vivo heparin.Therefore, equivalent therapeutic ranges should be assessed by using ex vivo samples rather than in vitro heparin. Because of the response differences between the APTT reagents, it is not adequate to define a therapeutic range for heparin therapy without specification of the reagent.


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