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Continuous renal replacement therapy. Keeping the circuit open: lessons from the lab.
Rob I Shulman1, Mervyn Singer, Jo Rock
1Pharmacy Department, Middlesex Hospital, London, UK. robert.shulman@uclh.org
Blood Purification
|February 28, 2002
Summary
Premature hemofiltration circuit clotting is linked to low antithrombin III (AT-III) levels, especially during inflammation. Supplementing AT-III or using alternative anticoagulants like danaparoid can maintain filter patency.
Area of Science:
- Nephrology
- Critical Care Medicine
- Hematology
Background:
- Hemofiltration requires anticoagulation to prevent membrane clotting.
- Understanding premature clotting mechanisms optimizes anticoagulation and filter patency.
Purpose of the Study:
- Investigate causes of premature hemofilter clotting.
- Highlight institutional approaches to anticoagulation management.
Main Methods:
- Analysis of premature clotting factors in hemofiltration circuits.
- Review of anticoagulation strategies, including standard heparin and alternatives.
Main Results:
- Low baseline antithrombin III (AT-III), heparin cofactor II, and tissue factor pathway inhibitor correlate with premature clotting.
- Clotting is preceded by increased thrombin-antithrombin complexes, indicating thrombin generation.
- AT-III levels decrease in sepsis and systemic inflammation.
Conclusions:
- Supplementing AT-III with fresh frozen plasma or aprotinin is effective when AT-III is consumed.
- Alternative anticoagulation for heparin-induced thrombocytopenia includes danaparoid, prostaglandins, and predilution.