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A. Risk Assessment
i. PREDICTION OF BLOOD LOSS IN CPB BY PCFTM
 Although
several hemostatic abnormalities may contribute to bleeding after
surgery, acquired platelet dysfunction has been reported to be
responsible for more than 90% of non-surgical bleeding after Cardiac
Pulmonary Bypass (CPB) surgery.
This figure shows the change in PCFTM over the course of CPB
procedures. During the procedure, PCFTM
values drop to essentially zero reflecting the inhibition of platelet
activity by Heparin. After the reversal of Heparin with Protamine
Sulfate, patient PCFTM
values recover to an average of 45% of their preoperative levels with
some.
The degree to which a patient’s PCFTM recovers to its preoperative
level correlates very strongly with the amount of postoperative blood
loss. This figure shows a plot of blood loss at 24 hours versus PCFTM . The outlying patient (open
circle) was later found to have von Willebrand’s disease.
This data suggests that PCFTM may be a useful method for
predicting and differentially diagnosing postoperative bleeding loss,
leading to more targeted use of blood products and reduced need for
reoperation.
ii. PCFTM AND GLANZMANN’S THROMBASTHENIA
Glanzmann’s Thrombasthenia is an inherited, severe
abnormality of platelet function, which causes significant bleeding
problems. The term “thrombasthenia” means weak platelets. Although they
contained normal numbers of platelets, these clots behaved as if they
contained no platelets. In this figure, PCFTM in samples from three such patients are compared
to a group of normals. The decrease in PCFTM is significant.
iii. DECREASED PCFTM IN ACUTE RENAL FAILURE
The qualitative platelet disorder known as Uraemia results in decreased
primary hemostatic capacity, which can result in significant blood loss
during invasive procedures. Treatments of the disorder tend to be
empirical and include measures such as aggressive dialysis, conjugated
oestrogens, and use of DDAVP.
These figures illustrate the case of a uraemic patient with massive
gastrointestinal haemorrhage whose haemostatic defect was best
demonstrated by deficient PCFTM
during clot retraction. The therapeutic effect was also mirrored by
improved force development.
B. Drug Monitoring
DOSE
DEPENDENT EFFECTS OF NOVOSEVEN ON PCFTM
Since development of PCFTM is a thrombin dependent
process, PCFTM production is delayed or reduced if thrombin
is inhibited or its generation is delayed. PCFTM is abnormal in blood
obtained from patients with factor VIII deficiency and factor IX deficiency
and from patients with inhibitors to factor VIII. This figure shows
dose dependent improvements of PCFTM by NovoSeven (rVIIa) on blood from a patient
with factor VIII deficiency and a factor VIII inhibitor.
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