Abstract:Premarin was administered prophylactically to every other patient in a series of 148 consecutive cases of open intracardiac surgery. Of these, 132 patients were matched to analyse the results of Premarin administration and postoperative blood loss. There were 67 patients who were given Premarin and 65 who did not receive this drug; both groups were identical in respect of age and sex. Matching was undertaken according to history of previous cardiac operations and anticoagulation, type of valve surgery or repa… Show more
“…Aprotinin (17,18), tranexamic acid, εaminocaproic acid (19,20), and premarin (a mixture of conjugated estrogens) (21) are less commonly used in these indications. However, there still is no validated concept of when to use these drugs or how to assess their effects before or during a surgical intervention.…”
mentioning
confidence: 99%
“…Tranexamic acid was effective in 12 of 16, aprotinin in 3 of 5, and factor VIII concentrates with vWF in all 4 pa-of vasopressin (8)(9)(10)(11)(12)(13)(14)(15)(16), has been shown to reduce blood loss and the need for blood transfusion in selected groups of surgical patients at an increased risk of bleeding due to platelet dysfunction. Aprotinin (17,18), tranexamic acid, εaminocaproic acid (19,20), and premarin (a mixture of conjugated estrogens) (21) are less commonly used in these indications. However, there still is no validated concept of when to use these drugs or how to assess their effects before or during a surgical intervention.…”
In a prospective study, 254 of 5649 unselected patients scheduled for surgery at our hospital were identified preoperatively as having either acquired (n=182) or inherited (n=72) impaired primary hemostasis (platelet dysfunction including von Willebrand disease). All patients were initially pretreated with desmopressin (DDAVP). Response to DDAVP or subsequent treatment(s) was defined as correction of any one of the abnormal PFA-100 platelet function tests. The non-responders were additionally treated with tranexamic acid or aprotinin; those with von Willebrand disease (vWD) received factor VIII concentrates with von Willebrand factor (vWF). Those still unresponsive to therapy received conjugated estrogens and, as a last attempt, a platelet transfusion. The administration of DDAVP led to a correction of platelet dysfunction in 229 of the 254 patients treated (90.2%). Tranexamic acid was effective in 12 of 16, aprotinin in 3 of 5, and factor VIII concentrates with vWF in all 4 patients with unresponsive to DDAVP. The remaining 6 patients were pretreated with conjugated estrogens, and 2 of these patients were additionally treated with platelet transfusion. The frequency of blood transfusion was lower, but not statistically significant (9.4% vs. 12.2%: p = 0.202) in preoperatively treated patients with impaired hemostasis than in patients without impaired hemostasis. In a retrospective group, the frequency of blood transfusion was statistically significant higher (89.3% vs. 11.3%: p < 0.001) in patients without preoperative correction of impaired hemostasis than in patients without impaired hemostasis. Preoperative correction of impaired primary hemostasis is possible in nearly all patients affected, and results in a reduction of homologous blood transfusions.
“…Aprotinin (17,18), tranexamic acid, εaminocaproic acid (19,20), and premarin (a mixture of conjugated estrogens) (21) are less commonly used in these indications. However, there still is no validated concept of when to use these drugs or how to assess their effects before or during a surgical intervention.…”
mentioning
confidence: 99%
“…Tranexamic acid was effective in 12 of 16, aprotinin in 3 of 5, and factor VIII concentrates with vWF in all 4 pa-of vasopressin (8)(9)(10)(11)(12)(13)(14)(15)(16), has been shown to reduce blood loss and the need for blood transfusion in selected groups of surgical patients at an increased risk of bleeding due to platelet dysfunction. Aprotinin (17,18), tranexamic acid, εaminocaproic acid (19,20), and premarin (a mixture of conjugated estrogens) (21) are less commonly used in these indications. However, there still is no validated concept of when to use these drugs or how to assess their effects before or during a surgical intervention.…”
In a prospective study, 254 of 5649 unselected patients scheduled for surgery at our hospital were identified preoperatively as having either acquired (n=182) or inherited (n=72) impaired primary hemostasis (platelet dysfunction including von Willebrand disease). All patients were initially pretreated with desmopressin (DDAVP). Response to DDAVP or subsequent treatment(s) was defined as correction of any one of the abnormal PFA-100 platelet function tests. The non-responders were additionally treated with tranexamic acid or aprotinin; those with von Willebrand disease (vWD) received factor VIII concentrates with von Willebrand factor (vWF). Those still unresponsive to therapy received conjugated estrogens and, as a last attempt, a platelet transfusion. The administration of DDAVP led to a correction of platelet dysfunction in 229 of the 254 patients treated (90.2%). Tranexamic acid was effective in 12 of 16, aprotinin in 3 of 5, and factor VIII concentrates with vWF in all 4 patients with unresponsive to DDAVP. The remaining 6 patients were pretreated with conjugated estrogens, and 2 of these patients were additionally treated with platelet transfusion. The frequency of blood transfusion was lower, but not statistically significant (9.4% vs. 12.2%: p = 0.202) in preoperatively treated patients with impaired hemostasis than in patients without impaired hemostasis. In a retrospective group, the frequency of blood transfusion was statistically significant higher (89.3% vs. 11.3%: p < 0.001) in patients without preoperative correction of impaired hemostasis than in patients without impaired hemostasis. Preoperative correction of impaired primary hemostasis is possible in nearly all patients affected, and results in a reduction of homologous blood transfusions.
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