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PubMed2001

Anticoagulation management in a patient with an acquired antithrombin III deficiency.

We report a case of heparin resistance and its management during cardiopulmonary bypass (CPB). A 63-year-old, 96 Kg female with a posterior myocardial infarction (MI) with previous deep venous thrombosis was treated with intravenous (IV) heparin infusion for 7 days before myocardial revascularization surgery. The patient required 1200 IU/Kg of beef lung heparin to extend the activated clotting time (ACT) in order to initiate CPB. A total of 1562 IU/Kg of heparin was administered throughout the procedure. This acquired heparin resistance was attributed to an antithrombin (AT III) deficiency, and was treated with fresh frozen plasma (FFP) to restore adequate anticoagulation. The patient's heparinized ACTs ranged between 368 seconds and 387 seconds before FFP administration as opposed to 626 seconds to 1329 seconds after treatment with FFP and additional heparin once on CBP. The patient experienced an uneventful postoperative course. Future treatment with AT III concentrate rather than FFP may reduce heparin requirements that will, in turn, reduce protamine reversal dose, postoperative bleeding attributable to heparin rebound, and its associated complications.

Anticoagulants↗
PubMed1981

[L-asparaginase, antithrombin III deficiency and thromboses (author's transl)].

In 2 children treated for acute lymphoblastic leukemia (ALL), sural phlebitis followed treatment with L-asparaginase. The latter was responsible for a decreased synthesis of antithrombin III (AT III) resulting in low plasma activity. Treatment with heparin was not successful and only fresh plasma led to recovery. The activity of AT III, a progressive inhibitor of thrombin and cofactor of heparin, is always below 50% after L-asparaginase. However, since the risk of thrombosis is very low, interruption of treatment and fresh frozen plasma are needed only when additional risk factors are present.

Adolescent↗
PubMed1984

[Treatment of deep venous thrombosis in the presence of a congenital antithrombin III deficiency. Apropos of the use of purified concentrates].

The authors report the case of an active 32 year old man who developed right leg DVT. Before heparinisation, he was discovered to have a low antithrombin III level (biological activity (B) 60%, immunological level (I) 50) and a further inquiry showed the same abnormality in 4 members of the family, leading to a diagnosis of a congenital deficit: a 35 year old sister with a bilateral post-DVT changes had antithrombin III levels of 70% (B) and 45% (I); two nephews, sons of the affected sister: the one aged 5 years was asymptomatic despite antithrombin III levels of 50% (I) and 70% (B); the other had experience DVT at the age of 2 and, on oral anti-vitamin K drugs, had antithrombin III levels of 55% (I) and 67% (B) at the age of 15 years; the patient's brother died at the age of 29 of cerebral vein thrombosis after pulmonary embolism. The recurrence of local signs of DVT after 12 day's heparin therapy with AT III levels (B) of 40%, led to a change in management with infusion of purified AT III concentrate at a dose of 40 U per kg (2 500 U per hour). This induced a rise in AT III activity to over 100% and enabled early introduction of anti-vitamin K therapy. The patient remains asymptomatic after 6 months follow-up. This case illustrates the value of determining AT III activity in all patients who developed DVT without obvious reason.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗