Hematology & Anticoagulation

5,000/microL for every unit, usually you give platelets as a 6-pack of platelets which should raise the count 30,000/microL.

right away, they don't have to do anything and you are giving them right into the blood so you can check right away.

It begins with the juxtaposition of the great depression in North America (1920s) and the fiscal
inability of farmers to purchase additional cattle feed when the usual sweet clover feed had become moldy. Cattle eating the spoiled sweet clover predictably began hemorrhaging 15 days later, with fatal hemorrhage within 30 to 50 days of ingestion.
The disease was named ‘‘sweet clover disease.’’ In February 1933, one distraught rancher who had lost many cattle and doubtful of his local veterinarian’s ‘‘sweet clover
disease’’ explanation was referred to the ‘‘local agricultural experimental station.’’ He
loaded his truck with a dead heifer, 100 pounds of spoiled sweet clover, a milk can of unclotted blood, and drove 190 miles in a blizzard to present the truckload to a scientist,
Karl Link, and his senior student, Wilhelm Schoeffel.

It was entitled WARFARIN because the study was founded by the Wisconsin Alumni Research Foundation.

Notably and early in its development before adequate clinical efficacy evidence,
President Eisenhower was treated with warfarin following his acute myocardial infarction in 1955 and initial heparin anticoagulation

The demonstration of warfarin’s effectiveness early in its development was
hampered by highly variable laboratory assays. The development of the international
normalized ratio (INR) system in the mid-1980s helped reduce laboratory assay variability
and introduced an internationally standardized method for monitoring warfarin’s effect. One must remember that INRs are reproducible between laboratories for only those patients who are stably anticoagulated (ie, at least 6 weeks of VKA
therapy). It is speculated that this unique interlaboratory reproducibility of INRs is related to the presence of proteins induced by VKAs

One small cautionary note: because the INR is derived from the measured PT, one
must know if the PT reagent is sensitive to the presence of heparin. Some PT reagents
are sensitive to heparin and if both heparin and warfarin are simultaneously present,
may yield disproportionately long PT INRs, thereby unnecessarily decreasing anticoagulant
dosing, and increasing the risk of clotting

The more serious form (heparin-induced thrombocytopenia, type II; HIT-II) is an immune-mediated disorder characterized by the formation of antibodies against the heparin-platelet factor 4 complex. This disorder has also been called heparin-associated immune thrombocytopenia, heparin-associated thrombocytopenia and thrombosis (HITT), and white clot syndrome [1,2]. White clot syndrome refers to platelet-rich arterial thrombosis (rather than fibrin-rich venous thrombosis), which occurs with high frequency in patients who develop this disorder

A critical assessment of immune-mediated HIT suggests a frequency of 0.2 to 5.0 percent in patients exposed to heparin for more than four days [10-15], with an overall incidence of 2.6 percent noted in a meta-analysis [10]. The incidence is closer to 0.2 percent for those treated with unfractionated heparin (UFH) for less than four days

There are three factors in addition to longer duration of therapy that are most strongly associated with the development of HIT.

*Use of unfractionated heparin (UFH) rather than low molecular weight heparin (LMWH)

*Surgical rather than medical patients

*Female rather than male patients

*You can, there are reported cases with just the use of heparin flushes.

Immune-mediated HIT is associated with a fall in the platelet count of >50 percent that typically occurs 5 to 10 days after the initiation of heparin therapy.

So it usually starts about a week after therapy is inititated unless there was prior heparin exposure recently and the patient will develop it sooner. Patients rarely get platelet levels less than 20,000 and therefore don't usually get spontaneous bleeding.

*skin necrosis

It is actually a prothrombic agent in vivo but it gets its name from its in vitro effect which is to prolong the aPPT making it look like a patient is more prone to bleed.

The lupus anticoagulant is an immunoglobulin against certain phospholipids and it is thought to bind to part of the platelet phospholipid layer promoting clot formation

The initial workup of a prolonged PTT is a mixing test whereby the patient's plasma is mixed with normal pooled plasma and the clotting is re-assessed. If a clotting inhibitor such as a lupus anticoagulant is present, the inhibitor will interact with the normal pooled plasma and the clotting time will remain abnormal. However, if the clotting time of the mixed plasma corrects towards normal, the diagnosis of an inhibitor such as the lupus anticoagulant is excluded; the diagnosis is a deficient clotting factor that is replenished by the normal plasma.