DOES CONTINUOUS HEPARINIZATION INFLUENCE PLATELET-FUNCTION IN THE INTENSIVE-CARE PATIENT

Objective: To study the influence of continuous administration of hepa rin on platelet function in intensive care patients. Design: Prospecti ve, serial investigation. Setting: Clinical investigation on a surgica l and neurosurgical intensive care unit in a university hospital. Pati ents: The study included 45 patients: 15 postoperative with patients s epsis (Acute Physiology and Chronic Health Evaluation II score between 15 and 25), 15 trauma patients (Injury Severity Score 15 to 25), and 15 neurosurgical patients. Interventions: Management of the patients w as carried out according to the guidelines for modern intensive care t herapy. Sepsis and trauma patients received standard (unfractionated) heparin continuously [aim: an activated partial thromboplastin time (a PTT) approximately 2.0 times normal value; sepsis-heparin and trauma-h eparin patients], whereas neurosurgical patients received no heparin ( neurosurgical patients). Measurements and results: From arterial blood samples, platelet aggregation was measured by the turbidimetric metho d. Platelet aggregation was induced by adenosine diphosphate (ADP; 2.0 mu mol/l), collagen (10 mu g/ml), and epinephrine (25 mu mol/l). Meas urements were carried out on the day of diagnosis of sepsis or 12 h af ter hemodynamic stabilization (trauma and neurosurgery patients) (base line) and during the next 5 days at 12.00 noon. Standard coagulation p arameters [platelet count and fibrinogen and antithrombin III (AT III) plasma concentrations] were also monitored. Heparin 4-10 U/kg per h ( mean dose: approximately 500 U/h) was necessary to reach an aPTT of ab out 2.0 times normal. Platelet count was highest in the neurosurgical patients, but it did not decrease after heparin administration to the trauma and sepsis patients. AT III and fibrinogen plasma levels were s imilar in the three groups of patients. In the sepsis group, platelet aggregation variables decreased significantly (e.g., epinephrine-induc ed maximum platelet aggregation: -45 relative % from baseline value). Platelet function recovered during the study and even exceeded baselin e values (e.g., ADP-induced maximum platelet aggregation: +42.5 relati ve % from baseline value). Continuous heparinization did not blunt thi s increase of platelet aggregation variables. In the heparinized traum a patients, platelet aggregation variables remained almost stable and were no different to platelet aggregation data in the untreated neuros urgical patients. Conclusions: Continuous administration of heparin wi th an average dose of approximately 500 U/h did not negatively influen ce platelet function in the trauma patients. Recovery from reduced pla telet function in the sepsis group was not affected by continuous hepa rinization. Thus, continuous heparinization with this dose appears to be safe with regard to platelet function in the intensive care patient .