Recurrent early filter clotting in regional citrate anticoagulated continuous venovenous hemodialysis due to undetected antibodies to heparin-platelet factor 4 complexes
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Abstract
Introduction
We recently published a citrate anticoagulated continuous venovenous hemodialysis
(citrate-CVVHD) protocol with variable treatment dose. The protocol was safe and easy
to handle and the mean filter lifetime was 61.5 hours [1]. We here report five cases
with unexplained recurrent early filter clotting beside effective citrate anticoagulation
due to undetected antibodies to heparin-platelet factor 4 complexes (hep-PF4 ab).
Methods
Regionale citrate anticoagulation was performed with variable treatment dose using
the MultiFiltrate™ CRRT device (Fresenius, Germany) in CVVHD mode. Between May 2008
and August 2009 we detected five cases on the ICU. All had acute kidney injury with
need for RRT. Underlying diseases were: three sepsis, one cardiac surgery, one abdominal
surgery. All patients were anticoagulated with heparin or fractionated heparin for
more than 10 days before initiation of citrate-CVVHD. At the time of initiation of
citrate-CVVHD, none of the patients had clinically evident signs of thomboembolism.
Results
The mean filter lifetime before diagnosis of hep-PF4 ab was 8 (range 1.3 to 14) hours.
Postfilter ionized calcium concentrations were always in the demanded range (mean
0.28, range 0.24 to 0.35 mmol/l). The mean thrombocyte count was 160/nl (range 48
to 215) at time of initiation of citrate-CVVHD. Thrombocyte counts fell to a mean
114/nl (range 36 to 177) within 5 days. Mean time to testing for and diagnosis of
hep-PF4 ab was 6 (range 3 to 12) days. After positive testing (HIPA) for hep-PF4 ab,
heparin was stopped and all patients received argatroban with a mean PTT of 83 (range
48 to 119) seconds. Under systemic anticoagulation with argatroban, the filter lifetime
of citrate-CVVHD increased to a mean 58 (range 18 to 96) hours. Within 14 days after
initiation of citrate-CVVHD, three patients had a diagnosis of a clinically significant
thrombembolic event.
Conclusions
In patients on the ICU with moderate-low thrombocyte count and without clinically
evident signs of thomboembolism, often sepsis or the state of critical illness is
assumed as the cause for decreasing platelet counts and tests for hep-PF4 ab are not
performed. In cases of undetected and untreated hep-PF4 ab, filter clotting can occur
beside effective citrate anticoagulation in CVVHD. In cases of unexplained recurrent
early filter clotting in citrate-CVVHD, patients should be carefully examined for
underlying hep-PF4 ab and heparin-induced thrombocytopenia.