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Deranged Physiology » Required Reading » Haematology and Oncology
Heparin resistance
ere are situations in which vast quantities of IV heparin fail to
increase the APTT in spite of your every effort. One might call this
"heparin resistance", or "heparin insensitivity". For some reason, this
issue seems to enjoy a significant amount of aention from the college:
estion 3.3 from the second paper of 2023
estion 13.2 from the first paper of 2012
estion 8.1 from the first paper of 2011
estion 6.2 from the second paper of 2008
Resistance to heparin therapy
ere are several reasons one might be resistant to heparin:
Increased heparin-binding protein levels (all of them
are acute phase reactants)
Low antithrombin-III levels (i.e. nothing for heparin
to bind)
Increased heparin clearance (eg. due to splenomegaly
in liver disease)
High Factor VIII levels
Factitious heparin resistance (eg. the heparin is not
UpToDate offers a good article about Antithrombin III
deficiency. Either you hereditarily fail to synthesise enough
of it, or your liver is so damaged that it cannot produce
enough. Or, it has been used up somehow, eg. in the context
of DIC, MAHA, or in a bypass circuit. Lastly, it is possible
that you are losing it along with other proteins via your
leaky nephrotic kidneys.
e management of AT-III deficiency is, predictably,
supplementation with AT-III.
If the expensive purified factor is not available, FFP will
suffice.
Effective coagulation of the heparin-
resistant patient
ere are several strategies one can employ. e specific
choice relies on what exactly is causing the heparin
resistance.
ere are some good articles on this. Most of them do not
touch upon the routne anticoagulation of some random
patient who happens to have escalating doses of heparin; I
suppose it is generally assumed that one will continue to
escalate the dose until such time as therapetic goals are met.
However, there are situations when anticoagulation is
 critically important, and one such scenario is the Hirsh, J., et al. "Heparin kinetics in venous thrombosis and
cardiopulmonary bypass circuit. pulmonary embolism." Circulation 53.4 (1976): 691-695.

• Change to low molecular heparin, instead of
unfractionated heparin
• Give cryoprecipitate and/or fresh frozen plasma (if
there is confirmed ATIII deficiency )
• Give antithrombin III concentrate
Or, you could consider using something else, such as a
direct thrombin inhibitor (hirudin or argobatran)
Beresford, C. H. "Antithrombin III deficiency." Blood
reviews 2.4 (1988): 239-250.
e PROTECT Investigators for the Canadian Critical Care
Trials Group and the Australian and New Zealand Intensive
Care Society Clinical Trials Group Dalteparin versus
Unfractionated Heparin in Critically Ill Patients N Engl J
Med 2011; 364:1305-1314April 7, 2011

Koster, Andreas, et al. "Management of heparin resistance

Previous chapter:
during cardiopulmonary bypass: the effect of five different
Intepretation of
anticoagulation strategies on hemostatic activation." Journal
abnormal ROTEM data
of cardiothoracic and vascular anesthesia 17.2 (2003): 171-
Next chapter: Heparin- 175.
Induced
Isil, Canan Tulay, et al. "Management of heparin resistance
rombocytopenia
in an emergency cardiac surgical patient." Indian journal of
anaesthesia 56.4 (2012): 430.

References

Anderson, J. A. M., and E. L. Saenko. "Editorial I Heparin

resistance." British journal of anaesthesia 88.4 (2002): 467-
469.

Young, E., et al. "Heparin binding to plasma proteins, an

important mechanism for heparin resistance." Thrombosis
and haemostasis 67.6 (1992): 639-643.
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