[HSF] Unusual response to warfarin

Tea Acuff tacuff at swbell.net
Wed Jul 11 16:33:05 EDT 2007 

Thanks for additions. As you will notice all I am able to retain in my head are a few patterns...and they come out jumbled as some have noted...
tea



----- Original Message ----
From: Ben Bidstrup <benjamin.bidstrup at bigpond.com>
To: OpenHeart-L at lists.hsforum.com
Sent: Wednesday, July 11, 2007 5:14:10 PM
Subject: Re: [HSF] Unusual response to warfarin


It was Dieter Horstkotte who back calculated INRs from the PT or 
Quick times. He then looked at the incidence of TE and ACRH and 
suggested that St Jude valves could sustain an INR that was much 
lower than previously recommended (and indeed as is recommended even 
today. Horstkotte, D., H. D. Schulte, et al. (1994). "Lower intensity 
anticoagulation therapy results in lower complication rates with the 
St. Jude Medical prosthesis." J Thorac Cardiovasc Surg 107(4): 
1136-1145.

I agree with Bob that warfarin is one of the most difficult drugs to 
handle. It has so many interactions and such a variable response in 
the human. My personal view is that wherever possible, one of the 
point of care tests should be used. Whether it is self monitored or 
done say in a nearby family physician or other healthcare facility, 
it certainly provides tighter control and reduced AC related issues.
Vit K allows the liver to produce the relevant clotting factors. Oral 
is slow and a small dose of IV Vit K can return the levels in a few 
hours.

This is a paper in the Medical Journal of Australia that gives an 
overview of warfarin and reversal.

http://www.mja.com.au/public/issues/181_09_011104/bak10441_fm.html

Bob refers to the Gelia study - there are several others. This paper 
provides an overview of the subject of self monitoring.

http://eurheartjsupp.oxfordjournals.org/cgi/reprint/3/suppl_Q/Q44.pdf



The issue of levels of anticoagulation during CBP remain a subject of 
debate. We use a huge overdose of heparin mainly to avoid any 
possibility of clotting in the circuit.
For those who look at the history of things, the ACT level was based 
on a number plucked out of the air (sort of) and was 380 seconds. 
Young studied the ACT levels in monkeys (1978) and looked at the 
formation of fibrin monomers. When the ACT was <400 seconds  there 
was early formation and he recommended an ACT of >400.

Now there are numerous ways of measuring an ACT (Activated or 
Automated clotting time). Machine use different activating agents, 
e.g. celite and kaolin. The response of each of these depends on 
where it was mined. The end point detection system falling plunger, 
or small iron rod and there are many more also has an impact. So all 
ACTs ain't equal.
Further confusion with the use of aprotinin. Wildevuur's team made a 
rather bold statement that the prolonged ACT indicated better 
anticoagulation  and thus reduced heparin (de Smet 1990). It has 
subsequently been suggested that this is not the case.

I will dig out a few more references esp the older ones later and 
amplify my comments.



>I think Horskotte (or was it Grunkmeir ?) showed the lowest 
>thrombohemorrhagic rate to be at an INR of 2.2.
>Prasanna
>Tea Acuff wrote:
>>I think that there are probably patients who are quite "brittle" to 
>>borrow a word (sorry, Ben). The other thing to consider is the 
>>usefulness of home testing and patience. Even a mg or two a day 
>>when the patient is taking 10mg can make a difference.  There is a 
>>lag of around 48 hours or so before what ever you did is noticed. 
>>(I learned this  treating my daughter at home despite two decades 
>>of "managing coumadin" in my practice...all three points) What you 
>>describe is the same thing with the hypersenitive and heavy handed 
>>yet diligent nurse (or anesthesiologist, anyone but us) pushing the 
>>BP from 60 to 200 and back to 60 with drips in the ICU. Bet you 
>>have seen that, too.
>>The last thing to remember (for which i would like confirmation 
>>from our experts) is that our targets (much like our "best 
>>practices") are misleading as are my analogical thoughts. As in the 
>>ACT on CPB higher is not necessarily "more" anticoagulated or more 
>>to the point, less thrombotic, right Ben?, but decreases the 
>>frequency of drop to below anticoagulated. I was told by another 
>>expert that an INR over 2 is all that is needed, but a level of 
>>2-2.5 means that the patient spends frequent time below 2. (See 
>>above.)
>>tea
>>
>>
>>----- Original Message ----
>>From: john pj <john_pj15 at yahoo.com>
>>To: OpenHeart-L at lists.hsforum.com
>>Sent: Tuesday, July 10, 2007 4:07:42 PM
>>Subject: [HSF] Unusual response to warfarin
>>
>>
>>We have difficulty in managing  warfarin dosing for a patient. 
>>Twice she was admitted for embolic episodes and twice with bleeding 
>>episodes. We suspected inadequate compliance and hospitalised  for 
>>long periods  and realised it not a problem with compliance.
>>   It takes long time for INR to come up and then it shoots up.INR 
>>remains high for long times even with out warfarin. She underwent 
>>multiple admissions to manage over and under anti coagulation.
>>   
>>   We did not try to change over to acitrom or phenindione as they 
>>are not available through public health system.
>>   
>>Any suggestions?
>>
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-- 
Ben Bidstrup FRACS FRCSEd FEBCTS
Consultant Cardiothoracic Surgeon
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