http://studywithgammakappa.yolasite.com/resources/CHEST%20GUIDELINES.pdf

Treatment and Prevention of Heparin-Induced Thrombocytopenia: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition)

Recombinant hirudin as an alternative for anticoagulation during cardiopulmonary bypass in patients with heparin-induced thrombocytopenia type II: a 1-year experience in 57 patients.

Hirudin as anticoagulant for cardiopulmonary bypass: importance of preoperative renal function.

H eparin-induced thrombocytopenia (HIT) is a major complication of surgery associated with the use of heparin. Two types of HIT have been distinguished: Type I HIT (HIT I) and Type II HIT (HIT II) (1–3). HIT I is thought to result from heparininduced microaggregation of platelets. Consequently, platelets may decrease within the first days after therapy with heparin. This thrombocytopenia is transient, self-limited, and asymptomatic. Platelet counts seldom decrease below 100 3 10/mL, and they usually recover even if heparin administration is continued (1–3). HIT I is solely a clinical diagnosis; heparindependent activation tests are negative. There is no specific treatment for HIT I and the main clinical importance of HIT I is to distinguish it from the more serious HIT II. HIT II is the result of a cascade of events related to the binding of heparin to platelet factor 4 (PF 4) (1). These complexes induce the formation of antibodies that bind to the complexes, thus stimulating platelet aggregation and a further release of PF 4 (1–6). Consequently, platelets are progressively consumed in the formation of thromboses and emboli (1,4–6). Rapid and pronounced decreases in platelet count (to levels below 30 3 10/mL) are frequently associated with HIT II; however, these decreases usually resolve after cessation of heparin exposure (1). HIT II-related thromboembolism has been observed in the absence of a decrease in platelet count (7). HIT II may be initiated by small, prophylactic doses of heparin, heparincontaining flush solutions and ointments, heparinbonded catheters, or systemic heparin administration (1,8). The condition is most often associated with unfractioned heparins (4,8,9). However, low-molecularweight heparins and heparinoids may also elicit an immunological cross-reaction with heparin-induced antibodies (8–10). The reported incidence of HIT II varies widely from 1% to 30% of surgical patients (11). HIT II was identified in 1% of patients undergoing cardiac surgery (12), although heparin antibodies were found in 19% (13) to 61% of these cases (14). HIT II is a clinical diagnosis, which is supported by laboratory tests (1). It can be identified from clinical criteria (i.e., a massive decrease in platelet count, thromboembolism, and resolution of thrombocytopenia after cessation of heparin), along with detection of heparin-dependent antibodies (1,15,16). Various laboratory tests can be used to verify the onset of HIT II (8,15,17): 1) the platelet C serotonin release assay; 2) the heparin-induced platelet aggregation assay (HIPAA); 3) the heparin-PF4 enzyme-linked immunosorbent assay (PF 4 ELISA); 4) platelet aggregation with simultaneous measurement of ATP release (lumiaggregometry); and 5) flow cytometric assays. However, in a recent study (17), none of these assays has been found to qualify as “gold standard.” The C serotonin release assay has a sensitivity of 94% and a specificity of approximately 100%, but the test is technically difficult and time-consuming, and requires the use of radioactive isotopes. Thus, the functional HIPAA, in which platelet aggregation is measured optically, and the PF 4 ELISA, which is an immunological test depending on the direct detection of heparin-induced antibodies, are increasingly being used. Both assays provide reliable results within 3–6 h (1,15,18,19) and are suitable for daily routine practice. The specificity of the HIPAA is more than 90% (15), and its sensitivity can approach 100% (15,20,21). At our institutions, the HIPAA is modified according to Accepted for publication October 15, 1999. Address correspondence and reprint requests to Fritz Mertzlufft, MD, PhD, Klinik fuer Anaesthesiologie und Intensivmedizin, Universitaetskliniken des Saarlandes, D-66421 Homburg-Saar, Germany. Address e-mail to mertzlufft@t-online.de.

Cardiovascular surgery without cardiopulmonary bypass in patients with heparin-induced thrombocytopenia type II using anticoagulation with recombinant hirudin.

https://www.annalsthoracicsurgery.org/article/S0003-4975(00)01511-3/pdf

Cardiopulmonary bypass in humans: bypassing unfractionated heparin.

Es wird von 6 Patienten mit einer Heparin-induzierten Thrombozytopenie und koronarer Herzkrankheit oder Aortenklappenstenose berichtet, die erfolgreich am Herzen operiert werden konnten, wobei rekombinantes (r) Hirudin als spezifischer und Cofaktoren-unabhangiger Thrombininhibitor fur den kardiopulmonalen Bypass (CPB) verwendet wurde. Ein intravenoser r-Hirudin-Bolus von 0,25 mg/kg Korpergewicht und eine Dosis von 0,2 mg/kg Korpergewicht ins Priming der Herz-Lungen-Maschine erwiesen sich als ausreichend fur eine effektive Antikoagulation wahrend CPB. Zusatzliche r-Hirudin-Boli von 5 mg (Gesamtdosis: 0,1–0,8 mg/kg Korpergewicht) wurden verabreicht, sobald der r-Hirudin-Plasmaspiegel unter 2,5 μg/ml abfiel. Bei 3 Patienten wurden koronare Bypassoperationen, bei den anderen 3 Patienten jeweils ein Aortenklappenersatz durchgefuhrt. Zum Monitoring der Antikoagulation wurden die Ecarinzeit (ECT) und die aktivierte partielle Thromboplastinzeit (aPTT) in Abstanden von 10 min bestimmt. ECT und aPTT-Werte korrelierten zuverlassig mit dem r-Hirudin-Plasmaspiegel. Die Perfusionszeit lag zwischen 83 und 180 min, die Aortenklemmzeit zwischen 0 und 83 min. Wahrend der Operation gab es keine Blutungs- oder thromboembolischen Komplikationen und der Einlasdruck am Oxygenator blieb konstant. Infolge der normalen Nierenfunktion kam es bei allen Patienten nach Ende des CPB zum zugigen Abfall des r-Hirudin-Plasmaspiegels und zur Normalisierung der Gerinnung. Bei einem Patienten konnte die r-Hirudin-Elimination mittels einer Hamofiltrationsphase von 15 min gegen Ende des CPB beschleunigt werden. Der postoperative Verlauf war bei allen Patienten unauffallig bis auf eine Rethorakotomie bei einem Patienten 6 h postoperativ wegen vermehrter Fordermenge aus den Thoraxdrainagen. Es fand sich eine chirurgische retrosternale Blutungsquelle, die durch Diathermie koaguliert wurde. Die ADP- und kollagen-induzierte Plattchenaggregation als Parameter fur die Thrombozytenfunktion war bei allen Patienten nach 60 min CPB-Zeit noch relativ gut erhalten. Die Ergebnisse zeigen, das r-Hirudin bei Patienten mit einer HIT erfolgreich als alternatives Antikoagulans wahrend CPB verwendet werden kann.

Rekombinantes Hirudin als Antikoagulans für den kardiopulmonalen Bypass in der Herzchirurgie: Klinische Erfahrungen

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Rekombinantes Hirudin als Antikoagulans für den kardiopulmonalen Bypass in der Herzchirurgie: Klinische Erfahrungen