Antithrombin III supplementation reduces heparin requirement and platelet loss during hemodialysis of patients with fulminant hepatic failure

Langley, P. G.; Keays, Rick; Hughes, Robin D.; Forbes, Alastair; Delvos, U.; Williams, Roger

doi:10.1002/hep.1840140208

Cited by 40 publications

(14 citation statements)

References 17 publications

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“…If the underlying problem is deficiency of coagulation inhibitors that act with heparin, strategies to avoid this include the replacement of deficient factors [25] or the use of other anticoagulants. Loss of the haemofilter circuit is not merely a nuisance, but involves a significant delay before renal support can be reinstituted, wastes blood and, perhaps more importantly, platelets and clotting factors.…”

Section: Discussionmentioning

confidence: 99%

Continuous venovenous haemofiltration using polyacrylonitrile filters does not activate contact system and intrinsic coagulation pathways

Salmon

Cardigan

Mackie

et al. 1997

Intensive Care Medicine

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The contact system was not activated further by continuous venovenous haemofiltration using polyacrylonitrile filters in critically ill patients. Premature clotting of the haemofilter circuit was more common in patients with very low levels of antithrombin III and heparin co-factor II; although this was related to thrombin generation, the intrinsic coagulation pathway does not appear to be implicated.

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Section: Discussionmentioning

confidence: 99%

Continuous venovenous haemofiltration using polyacrylonitrile filters does not activate contact system and intrinsic coagulation pathways

Salmon

Cardigan

Mackie

et al. 1997

Intensive Care Medicine

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“…Critically ill patients and those with liver disease typically have low levels of AT, and increased extracorporeal circuit clotting typically occurs when anticoagulation with UFH is used in patients with antithrombin activity of 60% or less. Recombinant AT is now available, and a loading dose of 3000 IU at the start of hemodialysis typically provides normal AT levels for at least 4 hours . However, because of costs, AT is usually restricted to intensive care usage.…”

Section: Recombinant Antithrombin and Ufhmentioning

confidence: 99%

Optimization of heparin anticoagulation for hemodialysis

Davenport

2011

Hemodialysis International

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Unfractionated heparin remains the most commonly used anticoagulant for extracorporeal therapies worldwide due to cost, years of clinical experience showing effectiveness and safety for outpatient hemodialysis. Most centers administer unfractionated heparin as an initial bolus followed by a constant infusion, which is then stopped prior to the end of the dialysis session. Although the anticoagulant effect of heparin can be monitored at the bedside, most centers take a pragmatic stance for routine outpatient hemodialysis, and adjust bolus doses and infusion rates based on visual inspection of the dialyzer header and venous air detector chamber for clots, and stop the heparin infusion based on the time taken for needle puncture sites to stop bleeding at the end of the hemodialysis session. Heparin is negatively charged and can bind to plasma proteins, leukocytes, and plastic. As such, it is important to achieve adequate mixing of heparin with blood to optimize anticoagulation within the extracorporeal circuit, by administering an intravenous bolus a few minutes prior to connecting the patient to the circuit and ensuring thorough mixing of the heparin infusion.

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“…Although antithrombin may reduce platelet activation in terms of changes in peripheral platelet counts and beta thromboglobulin release, most clinical studies failed to show that a bolus of antithrombin failed to reduce PF 1 þ 2 or TAT production during intermittent hemodialysis [18]. Now that recombi-nant antithrombin is available, several studies have looked at the effect of administering both antithrombin and unfractionated heparin.…”

Section: Antithrombin and Heparinmentioning

confidence: 99%

Anticoagulation Options for Pediatric Hemodialysis

Davenport

2003

Hemodialysis International

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Blood coagulation in the extracorporeal hemodialysis circuit is one of the manifestations of bio-incompatibility that is related to the activation of monocytes, platelets, and the coagulation cascades. Compared to adults, in pediatric patients, the surface area of the extracorporeal circuit is increased relative to blood volume. This is due to the patient's smaller blood volume and the combination of the higher relative surface area of the dialyzer, smaller lumen lines, and small-bore vascular catheters, potentially increasing contact activation of coagulation proteins, platelets, and inflammatory cells. Although unfractionated heparin remains the most commonly used anticoagulant, low molecular weight heparin offers the advantages of a single bolus, less fibrin and platelet deposition in the dialyzer, and perhaps more importantly, less osteoporosis, hyperkalemia, and abnormal lipoprotein profile. Although regional anticoagulants are available, these are often prohibitively expensive or require increased complexity of the dialysis procedure (e.g., citrate), but have the advantage of reducing the risk of bleeding when compared to heparin. Thrombin inhibitors are now available, and with the advent of argatroban, which is metabolized in the liver, have become the anticoagulants of choice for the few patients who develop heparin-induced thrombocytopenia type II.

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Antithrombin III supplementation reduces heparin requirement and platelet loss during hemodialysis of patients with fulminant hepatic failure

Cited by 40 publications

References 17 publications

Continuous venovenous haemofiltration using polyacrylonitrile filters does not activate contact system and intrinsic coagulation pathways

Continuous venovenous haemofiltration using polyacrylonitrile filters does not activate contact system and intrinsic coagulation pathways

Optimization of heparin anticoagulation for hemodialysis

Anticoagulation Options for Pediatric Hemodialysis

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