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In a previous study we tried to assess the clinical usefulness of platelet count (PlC) to confirm whether postoperative pulmonary embolism could be suspected early. Unexpectedly, the 19 patients who subsequently developed pulmonary embolism had significantly lower mean PlC levels even before surgery. In an attempt to discover whether the preoperative PlC levels were associated with a different incidence of postoperative blood loss, we decided to retrospectively study the relationship between preoperative PlC levels and the consequences of blood loss. There were 459 consecutive patients undergoing hip surgery. After excluding 5 patients who died during the first 3 postoperative days, and 16 patients who bled from a definitive anatomic site, there were 438 patients. Blood loss was considered to be excessive when two or more of the following conditions were present: (1) total transfusion requirements exceeding 1,000 ml whole blood or 2 units of packed red cells; (2) a drop in hemoglobin level of 5 g/dl or more, and (3) a hemoglobin level below 8 g/dl at any moment during the first 8 postoperative days. Blood loss was considered to be excessive in 91 patients. Preoperative PlC levels were significantly lower in these patients as compared to patients without the condition (204 +/- 52 vs. 236 +/- 79 x 10(9) liter-1; p = 0.0002). When patients were classified according to the quartiles of preoperative PlC, the odds ratio of developing excessive blood loss was 0.69 (95% CI: 0.38-1.26) in patients in the second quartile; 0.57 (95% CI: 0.30-1.06) in the third quartile, and 0.27 (95% CI: 0.13-0.57) in patients in the highest quartile. After adjusting for age, sex, type of surgery and type of prophylaxis, the preoperative PlC levels maintained a statistically significant inverse correlation with postoperative blood loss.

We have prospectively studied a large series of patients with acute venous thromboembolism, trying to correlate pulmonary embolism (PE) recurrences to a number of clinical variables, and platelet count behavior. A baseline lung scan was obtained initially in every patient. Repeated chest X-ray and lung scans were obtained routinely 8 days after heparin onset. The primary trial endpoint was confirmed, clinically apparent recurrent PE; in addition, laboratory evidence of subclinical PE at the repeat scan was also considered. PE recurrences were found in 26/180 patients, and 3 out of these patients died because of massive, recurrent PE. No significant differences were found in age and sex distribution, or in the degree of deep vein thrombosis proximity between patients who did or did not develop recurrences. There were, however, differences between groups in platelet count: No differences were found in baseline counts, but mean values were significantly lower by the 8th day when recurrences had appeared (229 +/- 86 x 10(9) liters-1 versus 314 +/- 129 x 10(9) liters-1; p < 0.005). The sensitivity, specificity, positive predictive value and negative predictive value for platelet count decrease were 52, 71, 21 and 91%, respectively. Thus, platelet count cannot be reliably used for individual cases, but our findings add to the pathophysiological picture of the disease.

In a randomized, blind study, both the antithrombotic efficacy (reduction of thrombus weight) and potency (anti-Xa activity) of several commercially available low-molecular-weight heparins (LMWHs) were compared with those of unfractioned heparin (UFH) and placebo. Three different thrombogenic challenges were used: venous thrombosis was induced by direct endothelial damage in 60 New Zealand rabbits (group I), intracarotid injection of bovine thrombin in an additional series of 60 rabbits (group II), or after inferior-vena-cava ligature in 60 Wistar rats (group III). The drugs were administered subcutaneously 2 h before surgery in a blind fashion. The doses recommended for clinical practice were used (adjusted by body weight), except in group II animals, in whom doses were doubled. No differences were found between UFH and most LMWHs in terms of reduction of thrombus weight in group I animals. But UFH showed a weaker antithrombotic efficacy in the other two models. Similarly, one of the LMWHs used (Clexane) proved to be not as effective as the remainder. However, only clinical studies will provide enough information to verify these differences. Additionally, our findings confirm that the antithrombotic efficacy of a given drug differs according to the stimulus used to induce venous thrombosis.