Anticoagulation Reversal

Today I want to talk about anticoagulation reversal. I happened to be on Northside when a patient on dabigatran had an unwitnessed fall with some minor head trauma and got me thinking about my reversal agents, and here's the POTD. 


First it’s worth mentioning when to reverse anticoagulation. The first step to looking at anticoagulation is to determine why the patient is on it and recognizing that reversing the patient is putting them at some sort of risk. Usually within our patient population, patients are on AC for afib,  hx of strokes, though other considerations include any sort of hypercoagulable state. Reversing AC should be considered in life threatening bleeding in the ED. 


Anticoagulation: Warfarin (brand name Coumadin)

  • Can be evaluated by INR 

  • Intracranial hemorrhage: immediately give PCC 

  • Reversal: 

    • 10 mg IV Vitamin K over 30 minute + PCC or FFP 

      • Of note- PCC/FFP will only work for approximately 8 hours so please give with vitamin K 

    • For supratherapeutic INR with no life threatening bleeding, slowly treat: 

      • INR 3-5: 

        • hold warfarin 

      • INR 5-9: 

        • hold warfarin 

        • Vitamin K (1-2.5 mg PO or IV) if risk for bleeding 

      • INR >9: 

        • Hold warfarin 

        • Vitamin K 2.5-5 mg PO/IV 

Anticoagulant: Dabigatran 

  • Can be evaluated by PTT and thrombin time 

  • Reversal: 

    • Idarucizumab 5 g 

    • Dabigatran can be dialyzed out 


Anticoagulation: Factor Xa inhibitors (-xaban most commonly apixaban)

  • Can be evaluated through INR (normal INR goes against a significant drug level though does not exclude it entirely)

  • Reversal: 

    • 4 Factor PCC (KCentra) 

    • Adnexanet Alfa may be considered if available though v expensive 


Thrombolytic: tPA 

  • Order INR/PTT/fibrinogen though do not wait for results to reverse 

  • Reversal: 

    • Tranexamic acid: 

      • 1 g IV loading dose followed by 1 g infused over the next hour

      • Cryoprecipitate: start with 10 units 

    • Options: FFPs 2 units and platelet transfusions 


Anticoagulation: 

  • Heparin/LMWH: 

    • Measure with PTT

    • Reverse with protamine 

      • Dosing for protamine is quite intricate and depends on bolus, infusions and timing of both. I would recommend coordinating with pharmacy directly. 


Antiplatelet: 

  • Could consider TEG or platelet function assays 

  • Reversal: 

    • Desmopressin (DDAVP) 0.3-0.4 ug/kg infuse over 20-30 minutes 



Hopefully this helps as a quick reference, especially for those of us who will be sadly leaving Maimo and our beautiful anticoagulation orderset that makes reversing all of these things downstairs as painless as possible. 

https://emcrit.org/ibcc/reverse/


Aldhaeefi M, Badreldin HA, Alsuwayyid F, Alqahtani T, Alshaya O, Al Yami MS, Bin Saleh K, Al Harbi SA, Alshaya AI. Practical Guide for Anticoagulant and Antiplatelet Reversal in Clinical Practice. Pharmacy (Basel). 2023 Feb 11;11(1):34. doi: 10.3390/pharmacy11010034. PMID: 36827672; PMCID: PMC9963371.

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Terminating Adult and Pediatric Traumatic Arrests

This POTD is a sensitive one, it's one that I was actually asked to look into a week ago, but after the events of this weekend/this morning I felt it was even more appropriate to take a look at. I know that this may be too soon for some, I encourage you all to reach out to someone you trust, take some time for yourself, and take care of yourself. There is no one right way to process the tragedy we see on a regular basis especially after this weekend. If you need a listening ear, I am always here. 


Today’s POTD is talking about when to terminate the pediatric traumatic arrest. When we think about traumatic arrests we think about penetrating traumatic arrests vs blunt traumatic arrests. 


Blunt Traumatic: 

  • Injuries that occur from forceful impact without penetrating the skin

  • Examples: MVCs, falls, assault


Penetrating Trauma: 

  • Stab wounds, gunshots, impaled objects 


Pediatric traumatic cardiac arrests: 

  • Traumatic pediatric cardiac arrests accounts for 22% of all out of hospital cardiac arrests in pediatric patients 

  • It has become more of an acceptable practice to terminate adult traumatic arrests in the field, though one study showed that this occurred less than <1% of the time


Intervening In traumatic arrests, in adult traumatic arrests, we must consider when to further intervene. When thinking about these different traumas we think about how to intervene, including with hemorrhage control, usually this starts with chest tubes, and can progress to a thoracotomy.  Other hospitals also have REBOAs (resuscitative endovascular balloon occlusion of the aorta) which may also be used. At Maimo, we do not have REBOAs. With this in mind, a brief review of when to intervene for adult traumatic arrests: 

  • Penetrating Trauma

    • Cardiac arrest with: 

      • Signs of life (spontaneous respiratory effort, spontaneous motor function/movement, electric cardiac activity, blood pressure (palpable or measureable), carotid pulse palpable, pupillary response to light)

    • Cardiac arrest without signs of life and <15 minutes of CPR 

    • >1500 ml of blood from the chest tube with persistent hypotension 

    • Refractory shock despite adequate volume resuscitation 

  • Blunt Trauma: 

    • Cardiac arrest with at least one sign of life observed in the hospital or lost just prior to arrival at the hospital 

    • <10 minutes of pre-hospital CPR 

    • Refractory shock despite adequate volume resuscitation 

    • >1500 ml from chest tube 


Intervening for pediatric arrests: 

  • Looking at NYC EMS Protocols specifically for pediatric patients: CPR is required for pediatric patients with: 

  • Severe bradycardia (HR <60 bpm) AND signs of shock or AMS

  • CPR should be continued until any of the following: 

    • ROSC: return of spontaneous circulation

    • Resuscitative efforts have been transferred to equal or higher level of training

    • Qualified physician assumes responsibility

    • Present of valid DNR/MOLST


So all of this brings us to the original question- when should we terminate pediatric arrests in the field? 

  • A recent study looked at both neurological outcomes and ROSC in cases of out of hospital pediatric cardiac arrests. Poor neurological outcomes and termination of care were recommended when: 

    • Unwitnessed arrest 

    • Asystole 

    • Arrest not due to drowning or electrocution 

    • No sustained ROSC

    • No bystander CPR 

  • So is this really applicable to our population? 

    • Maybe? Terminating in the field should be considered with any obvious signs of death, extreme lividity, rigor mortis, tissue decompensation, obvious mortal injury, submersion >1 hour

  • For traumatic pediatric arrests: 

    • Most studies do not support a thoracotomy though will be at the discretion of the trauma attending 


With all things considered, it is possible and should be considered terminating pediatric arrests in the field. This should be done in conjunction with online medical control, the attending, and consideration of EMS who may stuck performing CPR/ALCS in front of crowds of strangers and loved ones who may not understand the nuance of stopping compressions in the field and why it may be necessary for their sakes to transport these patients.

Niemann M, Graef F, Hahn F, Schilling EC, Maleitzke T, Tsitsilonis S, Stöckle U, Märdian S. Emergency thoracotomies in traumatic cardiac arrests following blunt trauma - experiences from a German level I trauma center. Eur J Trauma Emerg Surg. 2023 Oct;49(5):2177-2185. doi: 10.1007/s00068-023-02289-7. Epub 2023 Jun 3. PMID: 37270467; PMCID: PMC10519862.


https://www.upstate.edu/surgery/pdf/healthcare/trauma/traumatic-arrest.pdf


https://www.jems.com/patient-care/cardiac-resuscitation/traumatic-cardiac-arrest-tca-maybe-we-could-do-better/


https://www.annemergmed.com/article/S0196-0644(19)30448-2/pdf


https://www.east.org/education-resources/practice-management-guidelines/details/emergency-department-thoracotomy-in-children-a-pts-wta-and-east-systematic-review-and-practice-manag


https://journals.lww.com/jtrauma/abstract/2023/09000/emergency_department_thoracotomy_in_children__a.21.aspx


https://nycremsco.org/wp-content/uploads/2024/07/2024-REMAC-Unified-Prehospital-Protocols-2024-01-004.pdf


https://umem.org/educational_pearls/4743/

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Syncope and ECG Changes

I was listening to CQI when a case of syncope came up, and the conversation turned to CDU syncope, and it got me thinking about serial ECGs and troponins in ECGs and eventually I started to think about why do we care about ECGs in syncope patients- and then we got to this POTD. So lets get chatting. 


Syncope is defined as a transient loss of consciousness that is self limited and accompanied by transient lose of tone. Approximately 50% of the time when a patient presents to the ED with syncope, there is an etiology determined, 50% of the time it is unclear why a patient syncopizes. Of that 50% of the time the reason is determined it is usually from a detailed history and physical exam, not often found from studies. 


What I wanted to focus on today was the 9.5-18% of the time when syncope is related to a cardiac cause. This is often due to the patient having an underlying cardiac etiology and is associated with a high rate of mortality and an elderly population. 


SO- you are looking at an ECG what should you be looking for in a patient with syncope? I normally am not a mnemonic person but thought this was a helpful one I came across: “ABCDE Left Right” 


A: AV Block: 

  • First start by looking at the PR interval: 

    • PR >200 ms: First Degree heart block, could be causing dizziness and syncope 

  • Notice a pattern between p waves and morphology: 

    • Dropped QRS complex with a normal P wave: Second Degree Mobitz type 1: (Wenckebach) 

    • Dropped QRS with a fixed PR interval: Mobitz type II 

  • Atrial and ventricular dissociation: Third Degree Heart Block


B: Brugada Pattern: 

  • Type 1: Coved pattern in leads V1/V2

  • Type 2: Saddleback appearance in the ST segment in V1/V2

  • Caused by a genetic mutation in the sodium channel of cardiac myocytes

  • Patient will have a family hx of sudden cardiac death


C: QTc Prolongation 

  • QTc is considered prolonged if it measures more than 440 ms in males/460 ms in females 

  • Should be measured from the end of the beginning of the QRS complex to the end of the T wave 

  • Typically measured in lead II or V5/V6 

  • Etiology to include a variety of electrolyte abnormalities: hypoK, hypoMg, hypCa, increased ICP, or medication induced, or genetic (Long QT Syndrome) 

  • In the case of genetic conditions, also consider if the patient has a family hx of sudden cardiac death


D: Delta Waves

  • A classic delta wave: shortened PR interval with slurred QRS upstroke is pathognomonic for Wolff Parkinson White Syndrome (WPW)

  • Caused by an electric conduction along an accessory pathway 

  • Look for these in limb leads and/or precordial leads 


E: Epsilon Waves 

  • Epsilon wave: inflection point between the QRS and the ST segment pathognomonic for arrhythmogenic right ventricular cardiomyopathy (ARVD)

  • Typically seen in leads V1 and/or V2

  • ARVD: is a genetic condition that presents with conduction impairment due to fatty fibrous deposits in the cardiac myocytes 

Left: 

  • Evidence of Left ventricular hypertrophy

  • Could represent any signs for left heart strain including HCOM, aortic stenosis, coarctation, aortic regur, mitral regurg 

  • Huge precordial R and S waves that overlap with adjacent leads 

  • LV strain pattern with ST depression and T wave inversions in I, aVL, and V5-6

Right: 

  • Evidence of right ventricular strain: ST segment depressions and T wave inversions in the right sided leads (V1-V4) and/or inferior limb leads II, III, AVF usually with right axis deviation 

  • Concern for right ventricular strain would be concerning for pulmonary embolism 

    • Must look for SIQ3T3 


TLDR: 

  • Syncope and ECGs, take a look at ABCDE Left Right:

    • AV Block: look at your PR interval and P and QRS morphology

    • Brugada: look at V1/V2 for saddleback deformities

    • QTc Prolongation: more than double the R-R is long! 

    • Delta wave: upswinging QRS in the precordial/limb leads

    • Epsilon wave: inflection at the QRS between ST segment at V1/V2 concerning for ARVD

    • Left heart strain: huge R and S waves

    • R heart strain: signs of strain in the right sided/inferior leads 

https://www.emdocs.net/ecg-pointers-7-cant-miss-ecg-patterns-of-high-risk-syncope-the-abcde-left-right-mnemonic/

https://litfl.com/left-ventricular-hypertrophy-lvh-ecg-library/

https://litfl.com/syncope/


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