ARGATROBAN PRESCRIBING INFORMATION PDF

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HIGHLIGHTS OF PRESCRIBING INFORMATION. These highlights do not include all the information needed to use. Argatroban Injection safely and effectively. Page 4. PRESCRIBING INFORMATION. ARGATROBAN. Injection. DESCRIPTION. Argatroban is a synthetic direct thrombin inhibitor derived from L- arginine. ARGATROBAN (argatroban for injection) Product Monograph. Page 1 of PRODUCT SUMMARY PRODUCT INFORMATION.


Argatroban Prescribing Information Pdf

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ARGATROBAN (argatroban injection, solution). This product information is intended only for residents of the United States. for Health Care Professionals. Target is based on the prescribing information for argatroban which recommends targeting a steady state aPTT of to 3 times the baseline. • This is lower than. Given this information, argatroban can be effectively used in treating Keywords: argatroban, HIT, direct thrombin inhibitor. 51 to minutes), package insert recommendations provide guidance .. Download Article [PDF].

Update on argatroban for the prophylaxis and treatment of heparin-induced thrombocytopenia type II

The scheduled determination of endotoxins in the dialysate was always normal. In extracorporeal treatment, it is necessary to rule out air embolisms, haemolysis and acute anaemia. The visible area of the catheter was intact and no leaks were detected in the circuit. Situations inherent to patient pathology, such as pulmonary oedema, heart attack, embolism or pericardial tamponade, can be excluded in the clinical, biological and radiological context.

It is true that there was a certain amount of myocardial suffering in view of the increased cTnI figure, but there were no electrocardiographic changes.

The possibility of sepsis seems unlikely without a fever or leukocytes, and as such, procalcitonin was not determined. Bearing in mind the chronopathology of the event and following the parameters of the test mentioned Table 1 with a subjective score of 7, we decided to adjust to a presumptive diagnosis of HIT II, later supported by a positive ELISA test Table 2 , weighing up the risks and benefits.

Treatment We should not wait for diagnostic confirmation from laboratory tests when there is strong clinical suspicion. The first step is to discontinue heparin. The drugs indicated are thrombin inhibitors: lepirudin, bivalirudin and argatroban. The first has the disadvantage of causing anaphylaxis and it is excreted by the kidneys. Although it is not currently available, it has been successfully used in our setting6. Bivalirudin use is generalised in catheterisation laboratories due to its short half-life, however, it is also excreted by the kidneys Argatroban is not excreted by the kidneys and it therefore seems more suitable in Nephrology; it is acquired as foreign drug.

It has a short half-life, and as such, its effect disappears soon after it is discontinued. It is not immunogenic and does not require dose modification in renal failure. It is capable of inhibiting both free thrombin and clot-bound thrombin. It is metabolised in the liver and eliminated in bile and finally in faeces.

Equilibrium concentrations are achieved within between 1 and 3 hours and its effect disappears after it is discontinued. Liver and multiorgan failure require a dose reduction 0. Two prospective studies tested its efficacy and safety3,17 in terms of its anti-thrombotic power, without an increase in bleeding.

The often necessary transition from argatroban to dicoumarins must be carried out carefully, due to the risk of necrosis, gangrene and leg amputation brought on by the effect of dicoumarins in reducing protein S and C levels22, Thrombin inhibitors change the international normalized ratio INR values due to their high osmotic concentration.

Then argatroban is discontinued and a new INR test is carried out after 6 hours. If a patient is taking a dicoumarin anticoagulant and HIT II is observed, vitamin K should be administered in order to reverse a greater risk of thrombosis in this context.

In our case, the discontinuation of heparin and the administration of argatroban were safe and effective, and we achieved adequate dialysis as we waited for the patient to be transferred to the reference hospital for peritoneal dialysis, where they are continuing this treatment without any incidents.

In the differential diagnosis, we must consider all the details, which we did not do in our case because we forgot to check the manufacture information on methods of sterilisation and impregnation of the catheter with heparin.

Introduction

Conflicts of interest The authors declare that they have no conflicts of interest related to the contents of this article. Table 1.

Diagnostic probability of heparin-induced thrombocytopenia in haemodialysis three clinical factors and ELISA 7 Figure 1. Platelet count in relation to time and anticoagulant treatment.

Figure 2. Jugular vein thrombosis cross-sectional view.

Argatroban

Figure 3. During inset, the left flap was noted to have minimal dermal bleeding.

Arterial thrombosis was found in a 1- to 2-cm segment at the anastomosis. Following subsequent revisions, arterial thrombosis occurred twice more at 8 and 10 minutes following complete resection of the thrombotic segment and successful reanastomosis.

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Given a documented allergy to heparin products, midrange anticoagulation was initiated with Argatroban GlaxoSmithKline, Brentford, England. Approximately 40 minutes after administration, a fourth arterial anastomosis was performed.

This remained patent and resulted in a successful reconstruction. Argatroban is a synthetic direct thrombin inhibitor that has become standard treatment for heparininducted thrombocytopenia.

In the presence of hypercoagulability, goal partial thromboplastin time is generally two to three times the upper limit of normal partial thromboplastin time, 50 to 90 seconds.

Steady-state blood levels are achieved approximately 1 hour after initiation. Low- to mid-range anticoagulation may theoretically provide a systemic anticoagulant effect with a decreased risk of bleeding and hematoma compared with full therapeutic range anticoagulation.

A similar approach was taken in this case.

An initial infusion at full anticoagulation weight-based dosing was given for approximately 30 minutes to achieve a steady state level more rapidly. The reanastomosis was then performed and the dose was then decreased to half. Dosing was then titrated postoperatively to a goal partial thromboplastin time of 36 to 50 seconds normal range, 23 to 36 seconds. This was continued for 72 hours postoperatively, at which point the patient was transitioned to e a prophylactic dose of fondaparinux, 2.

The use of Argatroban for flap salvage in the setting of postoperative heparin-inducted thrombocytopenia has been reported previously. Although the impetus for thrombosis in this case is unclear and may have been technical, we felt the systemic anticoagulation was ultimately the key to success given the temporal relationship between maintenance of a patent anastomosis and administration of Argatroban.

Argatroban

Anticoagulation in free tissue transfer is often highly debated and based on surgeon preference.The effectiveness of anticoagulation was measured indirectly by the duration of dialysis filter use. Although it is not currently available, it has been successfully used in our setting6.

Dhillon S. After that, circuit coagulations disappeared and the performance of the same catheter was excellent. The data of the ARG and ARG investigations provide convincing evidence that argatroban enables rapid and effective anticoagulation in this condition and is an effective therapy for HIT-associated complications.

The antibody—antigen complexes also activate monocytes, leading to tissue factor production and endothelial injury, which contributes further to thrombosis.

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