INR of 5.2 what is best way to reduce INR, along with vitamin K?

[ALCapshaw2]

the reading is from a finger stick device, and it was only taken once so there was no verification. It is my understanding that the risks of stroke/internal bleeds etc. go syk high from 3 to 4 to 5 INR.

Where did you get that (mis)information? The recommended range for people with mechanical valves in the Mitral Position is 2.5 to 3.5 and with ANY sign or history of Stroke Risk (TIA's etc) that range is raised to 3.0 to 4.0

Before the INR type of testing (which came along in the 1990's), managing Coumadin dosing and Prothrombin Time was a very INEXACT science due to variation in reagents. This is probably where a lot of the Horror stories about Coumadin come from. With an INR of 5.2 from a Finger Stick Instrument, you should have had a re-test, at least with another instrument or (maybe) better, a Lab Draw, just to be sure.

Yes, there can be a stroke risk at VERY HIGH INR levels from bleeding in the brain, but to my mind, the Bigger Risk is from clotting if your INR drops below 2.0

A Long Time Ago, someone posted a graph which showed Stroke Risk rising rapidly below 2.0 and showed Bleeding Risk Rising above 5.0 We have had MANY people report INR's of 5.0 or so with NO BLEEDING and they returned to range simply by skipping ONE Dose and returning to their normal dose. Some have even reported NO Bleeding with an INR as high as 8 but there is no guarantee at that range.

As was said before, taking Vitamin K for an INR of 5 is like using a Sledge Hammer to pound in a Tack, and it will only prolong the time it takes for your INR to stabilize.

Did you look at the Guidelines from the Family Practice Physicians Journal? Those should be similar to AL Lodwick's Dosing Guide.

Re: Buying your own Home Test Instrument, QAS has been known to 'negotiate' a lower price for individuals who wish to purchase one out of their own pocket. It doesn't hurt to ask!

'AL Capshaw'

 

[Karlynn]

Thanks for all of your help, I couldn't get the website www.warfarinfo.com to load. I am reticent to start the K especially when I might be traveling to MA for a surgery, however I was curious if here are any vitamin K dosing instructions out there on vitamin K. The RX I have for 5 times 5 mg a day for 2 days does seems a bit high, but I dont have a medical doctorate. All in all it seems to make a bit more sense to go into the hospital where I could be bridged with coumidan from Heprin if they are to start the K.

I really dont think that medicare and insurance will cover the INR/PT moniter so I might just have to bite the bullet and buy one myself.

Are you now speaking of doing the Vit. K prior to the surgical procedure - or to lower you 5.3 INR?

If I were you, I'd call your doctor and just tell him that from what you have read, taking Vit. K in the dosages he is providing will drop your INR too low and tell him you'd like to lower it by adjusting your warfarin dose since you are not bleeding. I have not heard of using Vit. K to lower an INR for a planned surgical procedure. Lovenox or Heparin are used for this.

Or - you can go ahead and do his instructions, and learn just what that amount of Vit. K will do to your INR for the next 3 or 4 weeks. I'm not being snide, just hinting that some of us have acquired our knowledge the hard way. And sometimes that's the only way.

I know you have many medical issues that affect what you must decide to do, but I'm very uncomfortable with the doctor you have handling your warfarin. It appears he's over-reactive and is operating off of old myth and information.

If you are talking about going to the hospital to start heparin in order to take Vit. K to lower your 5.3, that just isn't necessary.

If you skipped a dose last night, you're already on your way back down, so you don't need to be scared. The question is now "What is your weekly dose?" as you go forward.

I'm curious as to what you did since yesterday. Did you skip your dose? Take the Vit. K?

 

[KristyW]

Not sure what to tell you

Not sure what to tell you

Frank,

I see that you have a complicated health history with the MS and a cerebral bleed in the past. You said that the bleed occurred when your INR was only slightly elevated. What was your INR at the time & what caused the bleed? The cause of the bleed is as important as what your INR was. An elevated INR DOES NOT cause a bleed, but it does make you bleed longer once you start.

About 5 years ago I had a kidney stone (post AVR), and when I got to the hospital my INR was 8.0. I did not bleed extraordinarily, but the hospital sure panicked! I have had INR's of 6.8 and such at least 2 other times in the last 5 years and they were all brought down by skipping 1 dose, and then taking 1/2 dose the next day. I resumed my regular weekly dose after that and things were ok.

I know several others have asked you what your weekly warfarin dosing is, but I haven't seen your reply. Has your anti-coagulation manager been fiddling with your dose? Have you been taking any other medications that may have caused your INR to spike? Prednisone or other steroid for an exacerbation? (Those can definitely cause and increase in your INR.)

I think that you have received excellent advice here. Please check into things. Vitamin K is a POWERFUL antidote & not easily reversed.

 

[warrenr]

graph

graph

Where did you get that (mis)information? The recommended range for people with mechanical valves in the Mitral Position is 2.5 to 3.5 and with ANY sign or history of Stroke Risk (TIA's etc) that range is raised to 3.0 to 4.0

Before the INR type of testing (which came along in the 1990's), managing Coumadin dosing and Prothrombin Time was a very INEXACT science due to variation in reagents. This is probably where a lot of the Horror stories about Coumadin come from. With an INR of 5.2 from a Finger Stick Instrument, you should have had a re-test, at least with another instrument or (maybe) better, a Lab Draw, just to be sure.

Yes, there can be a stroke risk at VERY HIGH INR levels from bleeding in the brain, but to my mind, the Bigger Risk is from clotting if your INR drops below 2.0

A Long Time Ago, someone posted a graph which showed Stroke Risk rising rapidly below 2.0 and showed Bleeding Risk Rising above 5.0 We have had MANY people report INR's of 5.0 or so with NO BLEEDING and they returned to range simply by skipping ONE Dose and returning to their normal dose. Some have even reported NO Bleeding with an INR as high as 8 but there is no guarantee at that range.

As was said before, taking Vitamin K for an INR of 5 is like using a Sledge Hammer to pound in a Tack, and it will only prolong the time it takes for your INR to stabilize.

Did you look at the Guidelines from the Family Practice Physicians Journal? Those should be similar to AL Lodwick's Dosing Guide.

Re: Buying your own Home Test Instrument, QAS has been known to 'negotiate' a lower price for individuals who wish to purchase one out of their own pocket. It doesn't hurt to ask!

'AL Capshaw'

Here is the link for the inr graph. The graph is on page 2.
https://openaccess.leidenuniv.nl/bitstream/1887/1672/1/303_183.pdf

 

[frank10b]

Well, been an eventfull day, to sum it up I did not take the vitamin K, worried about the half life even though my doctor was not at all worrried about the half life and aftereffects of the K. Also, found out that my digi level was high so I guess I am to hold that for like ........forever. I guess it is all due to liver congestions because of my Mitro Stenosis. While I feel better today the MS looks to be getting worst.

I am on 5 mg of coumidan, once a day.

I was an advocate of more frequent testing of the INR however, now it will be checked tomorrow and Thurs. And no it was not re-checked the same day, wish I had thought of that at the time. Good suggestion. I have been eating more leafy green veggies to help the anemia and serium protein levels rathen than do the K thing. If my coumidan levels were on a upward trend I guess it would make sense to try and halt it with K and maybe I would need something stronger than jsut holding the coumidan to halt the increasing INR, esp given the liver congestion and all the coumidan that is backed up in there and still getting metobilized. But I didnt take the K, b/c I really dont want to start something that will also be something I cant stop and will loose control over like the K reaction in my body. Tomorrow I guess I will know the results of the INR.


Guess I am crazy, but since I felt like eating today that is what I did. And to top it all off the drain in my bedroom bathroom pluged up and flooded the shower floor with crap from the tolet flush! Boy I hope I dont get sick from all those germs! Got someone to fix it real quickly however- God bless my plumber!

 

[frank10b]

Found this though it as interesting:

Warfarin and Other Oral Anticoagulants
from Southern Medical Journal

Congestive Heart Failure
While further study is needed, it appears that some patients with decompensated CHF have an increased responsiveness to oral anticoagulants.[6,8,24-33] One possible mechanism for this interaction is CHF-induced hepatic congestion. In 1949, Stats and Davison[24] evaluated the effect of CHF on dicumarol. The researchers studied 23 patients with right-sided CHF and 48 control patients. Prothrombin times were evaluated at baseline and on 3 successive days after a single 150 mg dose of dicumarol. Results of the study showed a greater prolongation of the PT in patients with moderate to severe right ventricular failure as compared with control patients and those with only mild cardiac disease. Patients with more severe cardiac disease also had a more gradual decline in PT. Liver congestion induced by CHF was mentioned as one likely mechanism for this effect on dicumarol. Similar results were reported by Killip and Payne[25] in a review of the effects of heart disease on hepatic function.
Reisner et al[8] described the response of 100 men to a single 100 mg dose of dicumarol. Of the 33 patients with CHF, 42% showed a significant depression of prothrombin activity to <60% of normal. Although the researchers did not attempt to correlate the response to severity of cardiac disease, 3 patients did have evidence of concomitant liver disease.

Plasma volume expansion during CHF may be another mechanism for the interaction with oral anticoagulants. This theory is supported by studies that show diuresis can decrease the response to warfarin.[26,27] O'Reilly et al[26,27] believe the decreased response to warfarin is caused by an increased concentration of clotting factors due to plasma volume reduction.

Although the mechanism(s) for the effect of CHF on oral anticoagulants remains scarcely studied, additional reports have documented the increased risk of excessive anticoagulation and hemorrhage. In 1958, Peyman[28] reported that hemorrhage developed in 25% of patients with CHF (n = 31) during coumarin treatment compared with 14% of patients without CHF who received coumarin (n = 149).

In 1998, Oates et al[29] conducted a two-phase study in outpatients to evaluate an algorithm for starting warfarin therapy. In the first phase (n = 107), factors that may affect the final maintenance dosage of warfarin were defined and used to build a decision tree and dosage algorithm. In the second phase (n = 106), the algorithm was tested. It was concluded that right ventricular failure was an important risk factor associated with increased warfarin response.

The mere presence of stable CHF does not consistently increase the risk of excessive anticoagulation or hemorrhage. Petitti et al[30] retrospectively studied the significance of risk factors, including CHF, for bleeding complications in patients receiving warfarin. They concluded that the relative risk for major hemorrhage in patients with treated CHF was 2.5 times greater than in patients without CHF. However, the relative risk was reduced to 1.4 after controlling for age and sex. Similar results were found by Doecke et al.[31] No increased risk of excessive anticoagulation or hemorrhage was detected in a retrospective study by Brigden et al.[12]

While stable CHF may not increase the risk of excessive anticoagulation with oral anticoagulants, exacerbations of CHF with concomitant hepatic congestion or edema appear likely to alter anticoagulant response. Caution should be exercised in the use of anticoagulants in patients with CHF, especially those with decompensated disease.

 

[Nancy]

I am not at all surprised by the article. My husband "lived" the article. He had severe CHF and was on tons of diuretics. He also had liver and at times spleen congestion with his ascites.

His Coumadin management was a nightmare. It was all over the place, and in the 2 years before his death, he was being tested sometimes three times per week, and that included weekends. He did not want to get a home testing unit, so we schlepped to the doctor's office or to the hospital lab.

I guess the variation in his levels was related to whether his CHF was congested or whether it was in a better mode.

He was often on Zaroxolyn to try to keep things cleared out. And he was also on an extremely low sodium diet.

I don't know what the answer is. CHF should be kept as minimal as possible short of kidney failure.

Coumadin management can become a real juggling act in folks with severe CHF.

Prior to his developing severe CHF, his Coumadin management was quite easy and rarely out of range.

 

[frank10b]

Clearly Nancy you know your stuff, to bad you had to learn it the hard and difficult way. I really appreciate the great contribution you bring to these fourms.


Good news this morning INR........ 2.4 peeerrrrfeeccttt. Now how do keep it there long enough for me to get on that aeroplane! Going to test again tomorow evening 5-6 PM. Then maybe Fri if I can convince the doctor, or unless I breakdown and buy a machine to avoid another sleepless night

 

[Ross]

Testing more then twice a week is wasting a test. It takes Coumadin 3 days to show up in a test and one week only has 7 days.

 

[Nancy]

In a normal situation I would agree with only twice a week testing. The last couple of years prior to Joe's death, I was taking care of him at home as if he were in the hospital. And when he was in the hospital, he was tested daily. They were looking more for trends in the levels, rather than waiting for final results. I don't know how to explain it, except to say it was not an ordinary situation at all. And he was a great deal sicker than I ever mentioned here.

Early on, when his Coumadin levels were ordinary and about what was expected, he sometimes only had testing every 2 weeks.

But not when he got sicker. He also had his metabolic profiles done about once a week. Everything became a huge critical balancing act.

But quite frankly, it all worked to keep him alive several more years than what was expected. It was an enormous effort by his doctors, they really tried.

Looking back now, everything revolved around the CHF, and the CHF had multiple heart related origins.

I am hoping that your doctors will do their best to keep you on an even keel until such time as you can get in and have whatever surgery you need, Frank. It does take an interested doctor who is willing to bend over backwards to try to work things out.

It is also very necessary that you micromanage your own symptoms, you have the background. You should be able to spot things early on like not urinating as much as you had been, more shortness of breath, bigger girth, more weight, slight confusion, etc. If you have a good relationship with your doctor, maybe you can head off some of the nasty stuff.

I was fortunate that one of Joe's cardiologists assigned his RNP to Joe's case, and allowed me to call her whenever I felt I needed to. We did just about everything on the phone, micromanaging the smallest things. There were standing orders in place for Metabolic profiles and other necessary bloodwork, so whenever she told me to bring him into the hospital lab for a draw, it was not a hassle, it just got done. And she would call me with any adjustments to potassium, Lasix, Zaroxolyn, sodium, dig levels, blood count levels and even ammonia levels if needed. His Coumadin was managed by his Internist.

Maybe you can get a similar arrangement, since you have a medical background.

I hope that once you have your surgery, things will straighten out for you. Just keep working at keeping things as even as possible until you have selected a surgeon.

Don't ever give up, make the system work for you.

 

[frank10b]

Thank you for your words of encouragement, however after trying to set up appointments etc, I see that it is going to be extremely dificult to keep me stabel while I wait for the earliest surgery dates in begining to mid Feb. To be honest I really dont now how I am going to make it.

 

[Nancy]

You ARE going to make it. Now, keep your wits about you. Keep checking your symptoms and call your cardiologist for necessary changes in your diuretics and related meds. You know what to do, make your doctors be responsive to your needs at this time, or have some of your visiting nurses ride herd on them. Don't ever let them think you are giving up on yourself, 'cause then they will too.

It is not that far away, February, just have to hang in there for a while longer.

I have faith in you and your training. Stay strong!