I'm a little behind on my reading and just saw an excellent Q&A by Dr. John Olson on critical values for prothrombin time (PT) coumadin monitoring. In our Quick Question on the subject we didn't include the option some laboratory managers select, which is to assign the critical value to the PT result in seconds rather than the INR. Please have a look at Dr. Olson's answer linked here. Go down to the second question in the link.

Here is a question on how to develop the PTT therapeutic range using the Brill-Edwards method in a low-volume facility. This is from Michael D. Blechner, MD, Assistant Professor of Pathology and Laboratory Medicine, University of Kentucky Medical Center:

George,
Here at UK (University of Kentucky) we use plenty of unfractionated heparin (UFH) and it is relatively easy to identify 30+ specimens from patients on UFH with which to establish a PTT range by comparing the PTT values with anti-Xa results.
UK has recently purchased a smaller hospital across town and I have been consulted about how to establish their RR when they switch PTT reagent lots. There is very little UFH used there, making it very difficult to identify enough patients to compare PTT and anti-Xa in ex vivo samples. What is the recommended approach? Spiking? Thanks for any help.
Mike Blechner

By the way, I found a post from you from 1997 while searching the MEDLAB-L listserv on this topic...

A question about the chromogenic factor X assay from Eryn Cramer:

I am working as a student in an anticoagulation clinic and we are looking for information on the frequency of chromogenic factor X (CFX) monitoring before returning to INR monitoring for patients with antiphospholipid syndrome (APS).  Are there any recomendations for CFX test frequencies?  Also, it appears that the CFX varies depending on the reagents used.  How does that allow for a correlation to the INR, since INR is standardized?

I sent Eryn's question to Dave McGlasson, who has published a great deal of research on the CFX:

In follow-up to her initial posting and Dave McGlasson's follow-up comment, Judy Davis wrote:

Are either of you aware of the data from the American College of Chest Physicians evidence-based  antithrombotic and thrombolytic therapy clinical practice guidelines - 8th ed published in Chest in June indicating that INR intervention ranges need to be decreased significantly due to risk of bleeding?  That's the reference our pharmacists are citing re the need to lower INR critical values.

Here is an interesting note about INRs from my long-time colleague and friend, Judy Davis:

I'm working with the pharmacists in our healthcare system on the new Joint Commission National Patient Safety Goal related to anticoagulation.  We are just beginning to standardize laboratory services at our hospitals but are investigating standardizing our INR upper critical values.  Since our INR critical values are currently not the same, I would be interested in knowing the criteria other systems have used to determine which critical value to adopt in similar situations.  I've learned a great deal from the pharmacists who use our coagulation data and also would like more information on changes other laboratories are implementing in response to the NPSG.

Judy Davis
Manager, Laboratory Quality & Compliance
Saint Thomas Health Services
Nashville, TN

Here is a question from new member Patricia Doleski:

I oversee the activated clotting time (ACT) program at two hospitals that use the Response RxDx System. One has no problem reaching the calculated heparin target (480s). They are using 5,000-unit heparin preparations.
 
The second hospital is having a problem using the RxDx calculation on certain patients. They are using 1,000-unit heparin. I know we anticipate 10% expected variability in the strength of heparin from what is labeled. Is there an "industry standard" strength of heparin used for cardiac surgery or perfusion?

Here's a summary of our September 22 Quick Question:

What is your upper critical value for low molecular weight heparin therapy using the chromogenic anti-Xa heparin assay?

Answers...

I have a provocative question about the activated clotting time (ACT) assay from my friend and one-time student Jeanine Walenga PhD, at Loyola University Medical Center in Maywood, IL. I don't know a lot about iSTAT's ACT so am posting this for general feedback.

Dr. Walenga writes: We are validating the iSTAT kaolin ACT hospital-wide. All clinical sites will change from the Hemochron 801, Signature Jr, or HemoTec ACT II to the iSTAT, which means most will convert from a celite- to a kaolin-based ACT. We are running patient samples at each clinical site for comparison of clot times between current system and iSTAT. Not surprisingly, the paired values throughout the heparinization period do not match.

My questions/concerns are the following:

• Has your hospital made a switch from celite to kaolin for the ACT?
• If so did you have any issues during with the conversion?
• Did the clinical decision-making threshold points of the ACT differ?  For example, did the clot times for high heparin levels during the procedure; or low heparin levels at the time to pull sheaths different between kaolin and celite ACTs?
• Did the doctors have any issues with the conversion?

Dave McGlasson posted this question on Medlab_L and gave me his permission to paraphrase and copy it here:

What do you use for critical heparin values when notifying providers about hemorrhage risk? It seems there is no standardization on this issue.  Chest 2008;133, Antithrombotic and  thrombolytic Therapy: American College of Chest Physicians Evidenced-Based Clinical Practice Guidelines (8th edition) does not seem to offer guidelines other than for elevated PTTs in standard unfractionated heparin monitoring.  Manufacturers of heparinoids also are strangely non-committal when asked these questions.

I have a couple of comments in follow-up to Dave's question...

Presenter: Marisa B. Marques, MD
Panelists: Dorothy Adcock-Funk, MD, Kandice Kottke-Marchant, MD, PhD, John D. Olson, MD, PhD
Moderator: George A. Fritsma, MS MT (ASCP)

Precision BioLogic Laboratory Medicine Roundtable, June 20 and 21, 2008, Dartmouth, Nova Scotia

I’d like to thank Wendy Porteous, Steve Duff, Michael Scott, and all the Precision BioLogic Inc. participants who organized our June round-table discussion. I’d especially like to acknowledge researchers Balwant Bhullar and Diane Jette who participated in this discussion.

Heparin-induced thrombocytopenia (HIT) is a menacing prothrombotic syndrome caused by antibodies to platelet factor 4 (PF4)-heparin complexes that develop during exposure to heparin, mostly commonly when it is used intravenously. IgG-isotype antibodies predominate and bind platelet membrane Fc receptors, activating them, causing thrombocytopenia and, in a minority of cases, potentially lethal venous and arterial thrombosis.