POTD: Supratherapeutic INR

I’ve maybe had to think about this twice during residency and both times was like ??? so I figured I should at least learn a little about it.

 

Although slowly dying out in terms of popularity, some providers STILL put their patients on warfarin. One of the last conditions where warfarin is indicated over a DOAC is in the setting of a mechanical valve, which can be a clue into the patient’s past medical history if you see it on their medication list (or that their PCP is old school). And even this may change as data on DOAC’s continues to evolve. There are multiple reasons why warfarin is a very annoying drug to work with.

 

1)    Narrow therapeutic window – for most indications the target INR is between 2-3

2)    Variable dose response

3)    Multiple drug-diet and drug-drug interactions

4)    Requiring bridging therapy

 

The main benefit of warfarin is that in the event of bleeding or hemorrhage, there are easy and effective reversal agents.

 

So, what happens if you shotgun labs on a patient (as one does) and their INR returns at a higher level? Like 4? 7? 10?? It depends on the scenario.

 

Significant or Life-Threatening Bleeding – very obvious, no thought involved. Obviously do not wait for confirmatory testing before treating.

-       Stop warfarin

-       Give Vitamin K 10mg IV over 20-60min. Some considerations…

o   Vitamin K works by helping the body produce more coagulation factors (no, I won’t go over the mechanism). This takes more than a few hours and does not help immediately

o   If started on vitamin K the patient will usually be refractory to warfarin for some time, but this is less of a problem as a different (and likely better) anticoagulant can be started in the interim

-       4-factor prothrombin complex concentrate (PCC) – Kcentra (what we have at Maimonides). I think this will end up institution specific, but we do…

o   Fixed approach – does not depend on INR. After a lovely discussion with pharmacy, studies appear to show that it is just as effective but lowers cost as overall doses are lower. Preferred if you have a choice.

§  GI/ENT/life-threatening hemorrhage – 1500 IU

§  ICH – 2000 IU 

o   INR-based approach – start off with 1500 IU empirically then add SUPPLEMENTAL dose…

§  INR 2-4: total 25 IU/kg (max 2500)

§  INR 4-6: total 35 IU/kg (max 3500)

§  INR > 6: total 50 IU/kg (max 5000)

-       If no Kcentra, consider FFP (but it honestly sounds like you should never really consider FFP). Per UpToDate…

o   2U FFP. Check INR 15 min after infusion, if >1.5 give another 2IU. Repeat until INR < 1.5.

o   Consider Lasix if infusing large amounts

 

Luckily, the order set reflects this at Maimonides, and we don’t have to think about it here.

 

Not really a debate anymore, but Kcentra vs FFP? Kcentra…

-       Is more rapid and effective at correcting INR - ~30 min

-       Can be infused faster with less volume  less likely leading to fluid overload

-       Shorter preparation time

-       Does not require blood-type matching

-       FFP is cheaper though….      +1

 

For Urgent/Emergent procedures

-       Treat as above in discussion with surgeon or proceduralist

-       If it can wait, don’t need to treat as aggressively

 

Minor Bleeding (like epistaxis) – very complicated, decided by many factors and heavily decided by physician judgement. Some things to consider

-       Extent of bleeding and risk of progression

-       Previous bleeding history

-       Comorbidities (CKD, HTN)

-       Concomitant anti-platelet therapy

-       INR level

-       Thromboembolic risk of the patient (prosthetic valve, atrial fibrillation, history stroke/DVT/PE, etc.)

-       Therapy will range from holding warfarin, giving vitamin K, and treating as above

 

Now on to why I actually decided to make this POTD.

 

Asymptomatic Elevated INR – based on INR

-       INR > 10: oral vitamin K 2.5-5mg  response in 24-48 hours

o   Hold warfarin

o   No role for Kcentra or FFP

o   INR should be checked daily or every other day, repeat oral vitamin K as needed

-       INR 4.5-10

o   Hold warfarin (1-2 doses)

o   Can consider low dose oral vitamin K – 1 - 2.5mg. Again, consider SEVERAL factors

§  Risk of bleeding – older age, prior bleeding, higher INR  consider oral vitamin K

§  Risk of thrombosis

-       INR <4.5

o   Hold next dose of warfarin (or reduce dose, this is generally on the PCP though)

o   Needs more frequent INR checks in the immediate future

 

Does anyone NEED to be admitted for management of supratherapeutic INR? Likely not. Fortunately, or unfortunately, depends on our clinical judgement. Off the top of my head…

-       Consider calling PCP to ensure follow-up / PCP comfort

-       Consider risk of bleeding vs. risk thrombosis

-       Patient ability to follow up

-       The thousand other things we think about when deciding whether to admit or discharge patients

 

What about an elevated INR in a liver patient?

-       Do not treat like warfarin-induced elevated INR

-       Patients are usually at baseline PRO-THROMBOTIC from low levels of protein C and S (anticoagulation factors)

-       Nothing to really do for elevated INR in the cirrhotic patient – per UptoDate appears that most attempts to correct lead to adverse events (thrombosis, etc.)

 

TL;DR

-       Ensure proper patient follow-up for cases of asymptomatic supratherapeutic INR

-       INR > 10 – hold warfarin, consider 2.5 – 5mg oral vitamin K

-       INR 4.5-10 – hold warfarin, consider 1 – 2.5mg oral vitamin K

-       INR < 4.5 – hold a single dose and recheck INR (not in ED)

 

https://www.nuemblog.com/blog/supratherapeutic-inr

https://www.uptodate.com/contents/management-of-warfarin-associated-bleeding-or-supratherapeutic-inr#H21790898

http://www.emdocs.net/em-cases-liver-emergencies/

 

 

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Transfusion Reactions. The facts (and opinions)

Welcome to Tuesday. POTD. 

Question: Why do nurses use red pens? ---- answer at the bottom of this e-mail.

Have you ever been sickle to your stomach about consenting patients about the risks of transfusions? Well today we're going to iron out all the details about transfusion reactions 

Facts about transfusions

  • ~20,000,000 units of pRBC's are transfused in the US per year

  • In 2011, 8,000,000 people in America received a transfusion

  • There were 51,000 reported transfusion reactions (0.64% of transfusions)

  • 317 of them required pressor support, intubation, or ICU care

  • While screening techniques have reduced the risk of viral transmission, they still exist. in 2010, the risks of viral transmission were estimated:

    • HIV: 1:1,467,000 units

    • Hep C: 1:1,149,00 units

    • Hep B: 1:357,000 units

The initial therapy for ALL transfusion reactions is to STOP THE TRANSFUSION

Types of transfusion reactions and therapies:

  • Acute Hemolytic Reaction

    • most severe, easiest to prevent

    • due to ABO compatibility 2/2 human/lab error ---> patient antibodies attack donor blood

    • presentation:

      • within minutes of transfusion initiation

      • fever, agitation, tachycardia, hypotension, diffuse pain

        • can progress to jaundice and bleeding 2/2 coagulopathy and DIC

    • intervention

      • STOP the TRANSFUSION

      • IVF to maintain renal perfusion, loop diuretics to maintain urine output, pressors for refractory hypotension

    • work up

      • notify blood bank, send a type and screen from the patient AND the bag of donor blood to the blood bank

      • send labs

        • peripheral smear, LDH, haptoglobin, bilirubin, direct coombs to assess for hemolysis

        • repeat CBC, BMP, UA

        • fibrinogen, D-dimer, coags if concerned for DIC

  • Febrile non-hemolytic transfusion reaction (FNHTR)

    • most common, usually due to recipient antibodies against donor leukocytes

    • STOP the TRANSFUSION

      • while FNHTR is a benign process, more severe reactions must be ruled out

    • assess the patient to ensure a more severe reaction isn't occurring (monitor vital signs, assess for pain indicative of acute hemolytic reaction)

    • Tylenol is the mainstay of treatment

    • patient's with a history of this can receive leuko-reduced or washed cells for future transfusions

  • Allergic reactions/anaphylaxis

    • within minutes the patient will have symptoms of a typical allergic reaction: rash, urticarial, itching. Can progress to an anaphylactic reaction with hypotension, angioedema, and respiratory distress

    • Treat as an allergic reaction with H1-blockers, adding epinephrine if signs of anaphylaxis are present

    • If no signs of anaphylaxis, can continue the transfusion

  • Transfusion-associated Circulatory Overload (TACO)

    • typically within 6 hours of transfusion initiation, due to fluid overload

    • may show signs similar to a CHF exacerbation: crackles, peripheral edema, B-lines on US, infiltrate on CXR, hypoxia

    • obtain an EKG to assess for ACS

    • positioning (sit upright), diuresis, nitrates, respiratory support as needed

    • BNP can be helpful if a pre-transfusion BNP was drawn 

    • prevent this by transfusions SLOWLY in at risk patients (Heart failure, renal failure patients)

  • Transfusion Related Acute Lung Injury (TRALI)

    • Similar presentation to TACO, within the same 6 hour timeframe

    • both present with dyspnea, crackles, hypoxia, bilateral infiltrates on CXR 

    • TRALI is non-cardiogenic pulmonary edema due to donor antibodies attacking recipient leukocytes causing cytokine release --> increased permeability in pulmonary capillary membranes -- > ARDS

    • so will not have signs of cardiogenic fluid overload = NO peripheral edema, normal cardiac function

    • STOP the transfusion

    • manage as an ARDS patient

      • respiratory support

      • if intubation is required, use lung protective ventilation strategies

      • diuretics are NOT helpful. but if there is concern for an underlying cardiac problem you may administer them 

  • Sepsis

    • due to bacterial contamination of donor blood

    • will show signs of septic shock. 

    • can be confused with early stages of acute hemolytic reaction --> send the appropriate labs to rule that our

    • send cultures from patient and from donor blood

    • manage sepsis as per usual, broad antibiotic coverage

    • IVF, sepsis protocols, get your eyes on that lactate measuring and re-measuring 

There are also several delayed reactions

  • Graft Versus Host Disease (GVHD)

    • 7-10 days after transfusion

    • due to donor lymphocytes attacking an immunocompromised patient’s cells or when immunologically similar lymphocytes are transfused and not recognized as donor/foreign cells by the patient’s immune system

    • fever, jaundice, pancytopenia, transaminitis

    • prevented by using irradiated blood products in high-risk populations (immunocompromised

    • supportive treatment, though nearly 100% fatality rate

    • immunosuppressants, steroids, cytotoxic agents, and stem cell transplantation rescue have been used, though with questionable efficacy

  • Delayed hemolysis

    • 5-10 days after transfusion

    • less severe form of acute hemolytic reaction due to antibodies against minor RBC antigens

    • typically minor hemolysis and progressive anemia

    • supportive care, transfuse as necessary; discuss with blood bank 

And a brief word on effects of massive transfusion

  • Coagulopathy can occur from dilutional effect of administering pRBC alone without clotting factors. prevent by using MTP

  • Hypothermia can result form using cold blood products. Prevent by warming products

  • hypocalcemia can result from citrate binding. Can administer empiric calcium gluconate

  • hyperkalemia can result. monitor potassium levels and treat accordingly 

  • Acidosis can result from large amounts of lactic acid in stored blood

Why do nurses use red pens?

---

---

Because they draw blood!!!!

Thank you Ankit and Rebecca of our pharmacy department for your insight into today's Pearl. 

-Elly

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Indications for use of Tranexamic Acid (TXA)

Indications for use of Tranexamic Acid (TXA)

Trauma

 

Trial Name: CRASH 2 (Positive trial)

Trial Type: Multicenter, double-blind RCT

Sample size: 20,211

Dose/Route of TXA: Loading dose 1g over 10 min, then infusion of 1g over 8hr

Primary outcome: All-cause mortality within 4 weeks of injury

Secondary outcome: Vascular occlusive events (AMI, stroke, PE, and DVT), surgical intervention, receipt of blood transfusion, and units of blood products transfused

Results:  Reduced All-cause mortality p 0.0035, death due to hemorrhage p 0.0077, no significant vascular occlusion p 0.96

Risk of thrombotic events: No increase in risk

Take home point: The use of TXA in trauma patients with “significant bleeding” reduces all-cause mortality without an increase in thromboembolic events.  This effect seems to be greatest in the subset of patients with severe shock (SBP ≤70mmHg) and when given ≤3 hours from time of injury 

 

Shakur H et al. Effects of Tranexamic Acid on Death, Vascular Occlusive Events, and Blood Transfusion in Trauma Patients with Significant Haemorrhage. Lancet 2010. PMID: 20554319

 

Trial Name: MATTERs (Positive trial)

Trial Type: Single center, retrospective, observational study

Sample size: 896

Dose/ route of TXA: 1 g initially, 2nd dose per MD discretion

Primary outcome: 24hr mortality, 48hr mortality, and 30-day mortality

Secondary outcome: Transfusion requirements and rate of thromboembolic complications.

Results: Not significantly decreased 24 hr p >0.05, Significantly decreased 48hrs p 0.004 and 30 day mortality p 0.03

Risk of thrombotic events: Increased overall VTE p 0.001 but patients who had a VTE also had higher burden of injury

Take home point:  Patients with penetrating injuries, requiring blood transfusions within 1hr of presentation the use of TXA reduced overall mortality

 

Morrison JJ et al. Military Application of Tranexamic Acid in Trauma Emergency Resuscitation (MATTERs) Study. Arch Surg 2012. PMID: 22006852

 

 

ICH

 

Trial Name: Meta-Analysis of TXA for Traumatic Brain Injury- negative trial

Trial Type: Meta-analysis and systematic review of RCTs or quasi-RCTs 

Sample size:  510

Outcome: Mortality, neurological function, hematoma expansion

Results: statistically significant reduction in ICH progression with TXA non-statistically significant improvement of clinical outcomes in ED patients with TBI.

Risk of thrombotic events: No adverse effects reported

Take home point: Did not lead to a statistically significant mortality benefit or improved neurological functional status. Further evidence is required to support its routine use in patients with TBI.

 

Zehtabchi S et al. Tranexamic Acid for Traumatic Brain Injury: A Systematic Review and Meta-Analysis. Am J Emerg Med 2014. PMID: 25447601

 

 

Trial Name: Tranexamic Acid for Hyperacute Primary IntraCerebral Haemorrhage (TICH-2)- Negative

Trial Type: International, randomized, double-blind, placebo-controlled, parallel group

Sample size:  2325

Dose of TXA used: 1g IV TXA bolus followed by an 8hr infusion of 1g of TXA 

Outcome:  Functional Status at Day 90, Hematoma Expansion at Day 2, Mean Hematoma Volume Expansion from Baseline to 24hr, Death by Day 7, Death by Day 90

Results: No difference in neurological impairment (mean NIHSS score at day 7), 90-day functional outcomes, length of hospital stay, discharge disposition, venous thromboembolic events, or arterial occlusions

Risk of thrombotic events: None

Take home point: TXA was given >3hrs after stroke onset, patients had more severe strokes, and larger hematoma volumes (>60mLs) than prior studies. Possible benefit if given to a subset of patient within 3 hours with smaller strokes but cannot be recommended at this time in clinical practice for spontaneous ICH based on the results of these trials

 

Sprigg N et al. Tranexamic Acid for Hyperacute Primary IntraCerebral Haemorrhage (TICH-2): An International Randomised, Placebo-Controlled, Phase 3 Superiority Trial. Lancet 2018. PMID: 29778325

 

 

Post Partum Hemorrhage

 

Trial Name: WOMAN trial – Negative trial

Trial Type: Randomized, double-blind, placebo-controlled trial,

Sample size:  20,060 ≥16 years of age with post-partum hemorrhage after vaginal delivery or caesarean section 

Dose of TXA used: 1 g IV vs matching placebo, If bleeding continued after 30 minutes or stopped and restarted within 24hrs, a second dose of 1g of TXA or placebo was given

Outcome: Initial outcome of all-cause mortality and/or hysterectomy within 42 days of giving birth

Final Primary Outcome: Death from PPH

Results: No difference in all cause mortality or hysterctomy

Risk of thrombotic events:

Take home point: It is difficult to draw definitive conclusions from this trial as the NNT was still large (i.e. ≈250) and the study had a fragility index of 0. Data showed a consistent association of delayed administration of TXA with no benefit

WOMAN Trial Collaborators. Effect of Early Tranexamic Acid Administration on Mortality, Hysterectomy, and Other Morbidities in Women with Post-Partum Haemorrhage (WOMAN): An International, Randomised, Double-Blind, Placebo-Controlled Trial. Lancet 2017. PMID: 28456509

 

UGIB

 

Trial Name: Cochrane review

Trial Type: Systematic review and meta-analysis of 8 RCTs

Sample size:  1700

Dose of TXA used: Total daily dose of TXA ranged from 4 – 8g and ranged from 2 – 7 days with both PO and IV adminsteration

Outcome: Primary: all-cause mortality and adverse events

Secondary: Rebleeding and surgery

Results: All-Cause Mortality p 0.007, rebleeding P = 0.07

Risk of thrombotic events: No difference in thromboembolic events (only evaluated in 4 trials)

Take home point: May benefit in higher risk patients but better RCTs required to confirm or refute evidence. HALT IT trial underway currently with N of 12000

 

Bennett C et al. Tranexamic Acid for Upper Gastrointestinal Bleeding (Review). Cochrane Database Syst Rev 2014. PMID: 25414987

 

 

Epistaxis

 

Trial Name: Zahed et al 2017 – Positive study

Trial Type: Randomized, parallel group clinical trial

Sample size:  124 on antiplatelets

Dose of TXA used: topical TXA (500mg in 5mL) or anterior nasal packing.

Outcome: Primary outcome resolution at 10 minutes. Secondary outcomes were re-bleeding rate at 24hours and one week, ED length of stay, and patient satisfaction

Results: epistaxis treatment with topical application of TXA resulted in faster bleeding cessation (NNT 2) , less re-bleeding at 1-week, shorter ED LOS, and higher patient satisfaction as compared with anterior nasal packing.

Risk of thrombotic events: not evaluated

Take home point: Do it!

Zahed R et al. Topical Tranexamic Acid Compared With Anterior Nasal Packing or Treatment of Epistaxis in Patients Taking Antiplatelet Drugs: Randomized Controlled Trial. Acad Emerg Med 2017. PMID: 29125679

 

Post-Tonsillectomy Bleeding

 

Trial Name: Meta-Analysis 2012

Trial Type: Systematic review and meta-analysis

Sample size:  7 studies with 2,444 patients

Dose of TXA used: 250mg for children <25kg, 500mg for children >25kg

Outcome: mean volume of blood loss

Results: TXA led to a significant reduction of tonsillectomy blood loss volume but had no impact on the rate of patients with post-tonsillectomy hemorrhage.

Risk of thrombotic events: Not evaluated

Take home point:  In patients with minor post-tonsillectomy bleeding consider using nebulized TXA to reduce or stop bleeding.  

Chan CC et al. Systematic Review and Meta-Analysis of the Use of Tranexamic Acid in Tonsillectomy. Eur Arch Otorhinolaryngol 2013. PMID: 22996082

 

Heavy Menstrual Bleeding

 

Trial Name: Cochrane Review

Trial Type: Systematic review and metanalysis

Sample size:  1312 in 13 RCTs

Dose of TXA used: majority of studies used regular dose TXA (ranging from 3 g/day to 4 g/day), Four other studies used low‐dose TXA (ranging from 2 g/day to 2.4 g/day) 

Outcome: Volume of blood loss, Quality of life

Results:  Appears effective for treating HMB compared to placebo, NSAIDs, Oral luteal progestogens, ethamsylate or herbal remedies but less effective than levonorgestrel intrauterine system

Risk of thrombotic events: Not studied in most RCTs

Take Home point: Antifibrinolytic treatment (such as TXA) appears effective for treating HMB compared to placebo, NSAIDs, oral luteal progestogens, ethamsylate, or herbal remedies. There were too few data for most comparisons to determine whether antifibrinolytics were associated with increased risk of adverse events, and most studies did not specifically include thromboembolism as an outcome.

 

Bryant-Smith AC, Lethaby A, Farquhar C, Hickey M. Antifibrinolytics for heavy menstrual bleeding. Cochrane Database of Systematic Reviews 2018, Issue 4. Art. No.: CD000249. DOI: 10.1002/14651858.CD000249.pub2

 

Hemoptysis

Trial Name: Inhaled TXA RCT 2018

Trial Type: Prospective, double-blind, placebo-controlled randomized controlled trial 

Sample size:  47

Dose of TXA used: nebulized TXA (500mg/5mL

Primary outcome: rate of complete resolution of hemoptysis during first 5 days from admission, difference in daily volume of expectorated blood

Secondary outcome: rate of interventional bronchoscopy, rate of angiographic embolization, rate of surgery, mean hospital LOS

Results: Resolution of hemoptysis within 5 days of admission, NNT = 2, P<0.0005. Statistically shorter LOS, less invasive procedures

Risk of thrombotic events: not studied

Take home point: Although this was a small study, the advantages of inhaled TXA vs placebo in patients with non-massive hemoptysis included faster resolution of hemoptysis, shorter hospital LOS, fewer invasive procedures, and although not statistically significant, a trend toward improved 30d mortality.

 

Wand O et al. Inhaled Tranexamic Acid for Hemoptysis Treatment: A Randomized Controlled Trial. Chest 2018. PMID: 30321510

 

References:

See above

RebelEM

 

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