How to switch from Coumadin to DOACs and vice versa

VKA to DOAC (upper panel)

  • If INR 2.0-2.5, DOAC can be started immediately of the next day.
  • If INR >2.5, actual INR value and half-life of VKA need to taken account to estimate when INR will drop into the range, then schedule a repeat INR at that time.

ehw05801.png

DOAC to VKA

  • measure INR before next intake of DOAC during concomitant administration
  • retest 24h after last dose of DOAC
  • monitor INR closely within 1st month until stable values attained

 

Reference:

Heidbuchel, H., Verhamme, P., Alings, M., Antz, M., Diener, H., Hacke, W., Oldgren, J., Sinnaeve, P., Camm, A. and Kirchhof, P. (2016). Updated European Heart Rhythm Association practical guide on the use of non-vitamin-K antagonist anticoagulants in patients with non-valvular atrial fibrillation: Executive summary. European Heart Journal, p.ehw058.

Advertisements

Perioperative Management of DOACs

Capture
Bold values deviate from the common stopping rule of ≥24 h low risk, ≥48 h high risk. Low risk: with a low frequency of bleeding and/or minor impact of a bleeding; high risk with a high frequency of bleeding and/or important clinical impact.

(a)Many of these patients may be on the lower dose of dabigatran (i.e. 110 mg BID) or apixaban (i.e. 2.5 mg BID), or have to be on the lower dose of rivaroxaban (i.e. 15 mg OD) or edoxaban (i.e. 30 mg OD).

 

Reference:

Heidbuchel, H., Verhamme, P., Alings, M., Antz, M., Diener, H., Hacke, W., Oldgren, J., Sinnaeve, P., Camm, A. and Kirchhof, P. (2016). Updated European Heart Rhythm Association practical guide on the use of non-vitamin-K antagonist anticoagulants in patients with non-valvular atrial fibrillation: Executive summary. European Heart Journal, p.ehw058.

Anticoagulation After Stroke

European Heart Association Guideline recommends:

  • 1 days after TIA
  • 3 days after mild stroke
  • 6 days after moderate stroke
  • 12 days after severe stroke

 

ehw05806

No strong evidence for this algorithm.

Another study showed that clinicians continue anticoagulation in most patients with acute stroke who use anticoagulation at amission except for those with severe neurological deficits (NIHSS >15).  Continuation of anticoagulation was not associated with a higher risk of bleeding.

 

 

References:

Groot, A., Vermeij, J., Westendorp, W., Nederkoorn, P., van de Beek, D. and Coutinho, J. (2018). Continuation or Discontinuation of Anticoagulation in the Early Phase After Acute Ischemic Stroke. Stroke, pp.STROKEAHA.118.021514.

Heidbuchel, H., Verhamme, P., Alings, M., Antz, M., Diener, H., Hacke, W., Oldgren, J., Sinnaeve, P., Camm, A. and Kirchhof, P. (2016). Updated European Heart Rhythm Association practical guide on the use of non-vitamin-K antagonist anticoagulants in patients with non-valvular atrial fibrillation: Executive summary. European Heart Journal, p.ehw058.

 

 

Low-Dose IV Heparin in aSAH?

Recent studies have shown potential benefit of UFH in preventing delayed neurologic deficit associated with aSAH.

UFH is the most negatively charged biological molecule known and can interfere with functioning of positively charged molecules.  It has been documented to interact with over 100 proteins.  IL, cytokines, receptors on endothelial cells are positively charged, and can be targeted by heparin.

Heparin has strong anti-inflammatory effects- binding to cell-surface glycosaminoglycans, preventing WBC migration, direct binding to chemokines and cytokines and inhibition of intracellular NF-κB.  Heparin can also modulate endothelin-1 activity and scavenge free radicals and upregulate superoxide dismutase.  Low-dose IV heparin provides anticoagulation effects, countering effects of SAH-induced microthrombi.

 

 

Recent study published in Journal of Neurosurgery used the following protocol for low-dose IV heparin:

Heparin 10-12 U/Kg/hr, start 12h after aneurysm treatment, until day 14 post-ictus, with routine PTT monitoring ensuring significant anticoagulation was not reached

Study was retrospective, non-randomized, with modest sample size, and suggests that the protocol is safe and has the potnetial to reduce cognitive outcomes in patients with aSAH.  See table below for results of the study:

Capture

Bottom line:  Not enough evidence to change practice, but promising.  Await the results of ASTROH Trial (aSAH Trial Randomizing Heparin) (ongoing Phase 2) for further clarification.

 

Reference:

James, R., Khattar, N., Aljuboori, Z., Page, P., Shao, E., Carter, L., Meyer, K., Daniels, M., Craycroft, J., Gaughen, J., Chaudry, M., Rai, S., Everhart, D. and Simard, J. (2018). Continuous infusion of low-dose unfractionated heparin after aneurysmal subarachnoid hemorrhage: a preliminary study of cognitive outcomes. Journal of Neurosurgery, pp.1-8.

 

QI Metrics for Stroke Neurointervention

Capture

 

Summary:

  • Treat those who meet inclusion criteria (90%)
  • Record process and outcomes data for all patients into institutional / national database (100%)
  • Image within 30 mins from time of arrival (75%); 12 mins for best centers
  • Imaging-to-puncture time <=110 mins (75%); <=50 mins for best centers
  • Door-to-puncture time (no imaging / OSH transfers) <=80 mins (75%)
  • mTICI 2b within 60 mins of puncture (70%)
  • mTICI scale is used to assess reperfusion
  • Achieve mTICI score 2b/3 (70%)
  • Image with CT/MRI within 36 hours of end of procedure (90%)
  • Review all sICH cases (100%), goal <10% sICH
  • goal <10% with new territory embolization
  • Review all mortalities that occurred within 72h of end of procedure (100%)
  • Document NIHSS score at discharge (100%), document 90-day mRS score (90%)
  • Achieve mRS score 0-2 (independent) at 90-days after treatment (30%)

 

In short:  Goal of endovascular team is to image within 12 mins of arrival, puncture within 50 mins after imaging, aiming for at least mTICI 2b within 60 mins of procedure, re-image within 36 hours of procedure, document all process and outcomes (including discharge NIHSS and 90-day mRS score), and review 72-h mortality and morbidity (sICH, new embolization, mortality) with an ultimate goal of having an independent patient (mRS score 0-2) at 90-days after treatment.

 

P-hew.

 

Reference:

Sacks, D., Baxter, B., Campbell, B., Carpenter, J., Cognard, C., Dippel, D., Eesa, M., Fischer, U., Hausegger, K., Hirsch, J., Hussain, M., Jansen, O., Jayaraman, M., Khalessi, A., Kluck, B., Lavine, S., Meyers, P., Ramee, S., Rüfenacht, D., Schirmer, C. and Vorwerk, D. (2018). Multisociety Consensus Quality Improvement Revised Consensus Statement for Endovascular Therapy of Acute Ischemic Stroke: From the American Association of Neurological Surgeons (AANS), American Society of Neuroradiology (ASNR), Cardiovascular and Interventional Radiology Society of Europe (CIRSE), Canadian Interventional Radiology Association (CIRA), Congress of Neurological Surgeons (CNS), European Society of Minimally Invasive Neurological Therapy (ESMINT), European Society of Neuroradiology (ESNR), European Stroke Organization (ESO), Society for Cardiovascular Angiography and Interventions (SCAI), Society of Interventional Radiology (SIR), Society of NeuroInterventional Surgery (SNIS), and World Stroke Organization (WSO). American Journal of Neuroradiology.

 

Sympathetic Storming

AKA:

  • paroxysmal sympathetic hyperactivity
  • central dysautonomia
  • paroxysmal autonomic instability with dystonia
  • diencephalic seizures

 

This syndrome is frequently seen in patients with TBI, (also after anoxic injury and stroke) is caused by dysfunctional autonomic regulation after brain injury.

Syndrome includes simultaneous motor and sympathetic activity, which is transient and episodic, in response to nonnoxious stimuli.

Incidence: ~30% of TBI patients

Signs and symptoms:

  • hyperthermia
  • tachycardia
  • hypertension
  • tachypnea
  • muscle rigidity
  • sweating

 

Associated with elevated levels of cortisol, norepinephrine, epinephrine and dopamine.

Patients with sympathetic storming tend to be younger (mean age 33) and predominantly men.

Diagnosis:

  • diagnosis is suggested by clinical context, episodic nature, simultaneity of symptoms
  • usually begin first week after injury, may continue into rehab setting
  • PSH-AM (paroxysmal sympathetic hyperactivity assessment measure) has been proposed to aid diagnosis

 

box 1

 

Treatment options: see below.

 

Box 2.JPG

 

Reference:

Abou El Fadl, M. and O’Phelan, K. (2018). Management of Traumatic Brain Injury. Neurosurgery Clinics of North America, 29(2), pp.213-221.

WAKE-UP TRIAL (MRI-Guided tPA)

Will patients with stroke with unknown time of onset and MRI showing recent infarction benefit from tPA?

 

Inclusion/Exclusion: 

  • All patients with unknown time of onset of stroke, no plans for thrombectomy
  • (+) ischemic lesion on DWI but no parenchymal hyperintensity on FLAIR

 

Results:

  • stopped early, ran out of funds
  • enrolled 503 of anticipated 800 patients
  • 254 given tPA, 249 given placebo
  • favorable outcome at 90d in 53.3% vs 41.8% in favor of tPA (95% CI 1.09-2.36, p=0.02)
  • median mRS score 1 in tPA, 2 in placebo (OR 1.62, 95% CI 1.17-2.23, p=0.003)
  • deaths 4.1% in tPA group,  1.2% in placebo (OR 3.38 95% 0.92-12.52, p=0.07)
  • rate of sICH 2% in tPA, 0.4% in placebo (OR 4.95, 95% 0.57-42.87; p=0.15)

Capture

Capture

Capture

Bottom line:  Patients with acute stroke of unknown time of onset and MRI evidence of recent infarction, IV tPA resulted in better functional outcome but more ICH at 90 days, and nonsignificant increase in 90-day mortality.  Trial was stopped early, which limits interpretation of safety results.  Higher rate of death in tPA group may become significant with a larger sample size.

 

 

References:

Ebinger, M., Scheitz, J., Kufner, A., Endres, M., Fiebach, J. and Nolte, C. (2011). MRI-based intravenous thrombolysis in stroke patients with unknown time of symptom onset. European Journal of Neurology, 19(2), pp.348-350.

Jovin, T. (2018). MRI-Guided Intravenous Alteplase for Stroke — Still Stuck in Time. New England Journal of Medicine.