Journal Club – Diagnostic Accuracy of ECG for Acute Coronary Occlusion resulting in MI

Presenter: Dr. Nick Byers (iFMEM R2)

Host: Dr. Colin Rouse

Article:

Research question/PICOD

  • Question:
    • Does shifting from a STEMI/NSTEMI paradigm to a new approach (ACO-MI/ non-ACO-MI) result in better identification of the patients who need acute reperfusion therapy?
  • Population:
    • Adult ED patients with ACS Symptoms
  • Intervention/Comparison:
    • STEMI/NSTEMI vs ACOMI/NACOMI
  • Outcome:
    • Composite ACO defined as one of:
      • A) Total occlusion or presence of culprit lesion on angiography with a peak troponin I level equal to or greater than 1.0 ng/mL plus an at least 20% rise within 24 h
      • B) A highly elevated peak troponin (greater than 5.0 ng/mL), which was shown to be correlated with ACO
      • C) Cardiac arrest before any troponin rise has been documented with supporting clinical evidence of possible ACO
    • All cause in hospital mortality
    • All cause long term mortality
  • Secondary Outcomes: 
    • Time from ECG to coronary angioplasty or CABG
    • The sensitivity and specificity of current criteria in diagnosing ACO
    • The sensitivity and specificity of ECG without ST-segment elevation to diagnose ACO (accuracy of ECG interpretation of acute coronary occlusion without STEMI criteria)
    • The specificity of ECG with STEMI criteria (correct ECG interpretation of false positive STEMI criteria)
    • The sensitivity of ECG with STEMI criteria (correct ECG interpretation of false negative STEMI criteria)
    • The outcome according to ECG subclassifications (outcomes of the patients who are labeled as STEMI and the patients who are labeled as having NSTEMI but have acute coronary occlusion)
  • Design:
    • Single center, retrospective case-control study in Turkey

Results

Authors conclusions

“We believe that it is time for a new paradigm shift from the STEMI/non-STEMI to the ACOMI/non-ACOMI in the acute management of MI”

 

Discussion at Journal Club

Strengths

  • 3000 patients included, 1000 per arm
  • Reviewers were blinded, disagreements were resolved by a 3rd independent reviewer
  • EKGs were reviewed again 3 months later to decrease inter-observer variability
  • Consecutive patients with an initial diagnosis of MI (i.e. not a convenience sample)
  • All patients received guideline-recommended medical treatment
  • There were documented criteria of ECG findings to classify the ECGs

Weakness

  • This was a retrospective study and at a single centre.
  • When troponins were taken was not controlled for/accounted for in any way
  • Control group age, medical comorbidities, and cardiac risk factors were much less
  • Their results suggest 17% of patients in N-ACOMI (N-STEMI Subgroup B) with angiographic ACO were missed (slide 16 results)
  • Study wasn’t powered enough to indicate modest benefit of early intervention over late
  • Extrapolating results to the real world may be difficult because ecg interpretation

 

Bottom line/suggested change to practice/actions

  • This single center retrospective chart review suggests that considering coronary occlusion vs. just ST elevation on ekg decreases long-term mortality, and has a better sensitivity, specificity, PPV, and NPV.
  • This could be a great way of getting patients better access to PCI for occlusive lesions, though inter-operator variability and time constraints are likely to be difficult to implement

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Transfusion Troubles: A review of transfusion reactions and management

Transfusion Troubles: A review of transfusion reactions and management- A Resident Clinical Pearl

Author: Dr. Victoria Landry (iFMEM R2)
Copyedited by Dr. Mark McGraw CCFP EM


Case: A  70 year old female presents to the emergency department via EMS with chest pain and weakness. Her systolic pressure is in the 90s with a MAP of 68. She is placed in a monitored bed. She recently had a STEMI and was successfully thrombolysed but also found to have an LV thrombus. She was discharged on Plavix and warfarin.

Today her bloodwork shows a hemoglobin of 50 and INR 11.6. In the ED she was given 5mg of IV vitamin K. She was typed and crossmatched for three units of blood which were initiated at 85ml/hr. An hour into transfusion she is noted to have temperature of 38.1°C.

You review the differential of transfusion reactions presenting with fever and their features….

  • Acute intravascular hemolytic reaction
    • Cause: recipient antibodies induce hemolysis of donor’s RBCs, usually due to ABO incompatibility (resulting from clerical error) 1
    • Presentation: fever, chills, hemoglobinuria, pain (transfusion site, low back, headache), hypotension, nausea/vomiting, dyspnea, renal failure, DIC, flushing, tachycardia, pulmonary edema, bleeding, bronchospasm1
  • Febrile nonhemolytic transfusion reaction1
    • Cause: recipient antibody vs donor WBCs, release of cytokines produced during storage1
    • Presentation: fever within 4hrs of transfusion, chills, rigors, nausea/vomiting, hypotension, headache, myalgias, dyspnea, tachycardia, chest pain usually mild but can be life threatening if tenuous cardiopulmonary status 1
    • *Consider using leukocyte reduced blood products in the case of recurrent febrile transfusion reactions 1
  • Delayed extravascular hemolytic reaction (FNHTR) 2
    • Cause: in previously sensitized patient, recipient antibodies have delayed reaction to RBC antigens1, may occur with transfusion-transmitted malaria and babesiosis2
    • Presentation: 3 days to 2 weeks2 after transfusion hemolytic anemia occurs with low grade fever or entirely asymptomatic, rarely causes hemodynamic instability1
  • Bacterial sepsis/contamination2
    • Cause: contamination during storage or processing1
    • Presentation: variable based on underlying source, occurs more common in platelets due to storage temperature 20-24°C 2

You consider your next steps….

  • Stop the transfusion1,2
  • Send remaining donor blood and post-transfusion recipient blood specimen for repeat type and cross-match (blood bank will determine if syndrome was due to transfusion reaction)1
  • Send infectious work up:2
    • Bacterial cultures and gram stain of transfusion unit and attached IV solutions
    • Blood culture on patient taken from different IV site
    • Post transfusion urine culture
  • If transfusion-associated sepsis suspected, give broad-spectrum antibiotics immediately1
  • Send hemolytic work up1
    • Direct and indirect coombs test (DAT)
    • CBC, Cr, PT, aPTT
    • Haptoglobin, bilirubin, LDH, plasma free Hgb, urine hemoglobin
  • Treat acute intravascular hemolytic reaction and febrile nonhemolytic transfusion reaction the same as initially can’t distinguish between the two1
    • Maintain renal blood flow and urine output with IV fluids, mannitol, furosemide
    • Cardiorespiratory support (vasopressors) as needed
    • Manage hemorrhage and DIC
    • Acetaminophen, meperidine 25-50mg IV for severe rigors if no contraindications2


Case continued: You re-assess your patient and find her to be asymptomatic aside from having chills and mild rigors.  You stop the transfusion, notify the blood bank and send the remaining blood back to them, send a hemolytic work up, and draw patient blood cultures as well as send a urine culture. You give her acetaminophen. Since she remains otherwise asymptomatic with unchanged stable vitals and negative hemolytic work up, you determine this was a febrile nonhemolytic reaction. You make a note in her chart so that next time she receives blood products she can be pre-medicated with acetaminophen.

 

 


After successfully managing this patient, your review other possible transfusion reactions.

 

If the patient had urticaria, you would consider….

  • Allergic reaction: immune response to transfused plasma proteins1
    • Presentation: urticaria, +/- mild upper respiratory symptoms (cough, wheeze), nausea vomit, cramps, diarrhea2
    • Treatment: stop transfusion, diphenhydramine/antihistamines, notify blood bank, restart transfusion slowly if symptoms resolve/are very mild1
  • Anaphylaxis: 5% of transfusion related fatalities; reaction within 45min to 1hr after start of transfusion2
    • Presentation: urticaria, dyspnea, bronchospasm, hypotension, tachycardia, shock, stridor, wheeze, chest pain, anxiety, nausea, vomiting1
    • Treatment: stop transfusion, epinephrine, steroids, diphenhydramine, H2 blockers, bronchodilators, vasopressors PRN, do NOT restart transfusion1
    • Note: those with IgA deficiency may have severe reactions to IgA in donor products (minimized by washing plasma from RBCs) 1

If the patient had dyspnea, you would consider….

  • TACO (transfusion-associated circulatory overload): most common cause of death from transfusion2
    • Presentation: dyspnea, hypoxia, pulmonary edema, orthopnea, cyanosis, tachycardia, increased venous pressure, hypertension2
    • To mitigate, transfuse slowly (2-4ml/kg/hr) in those at risk (age >70yrs, infants, Hgb <50, renal impairment, fluid overload, cardiac dysfunction) 2
    • Treatment: stop transfusion, diuretics&O2 PRN, can consider restarting transfusion at reduced rate if clinical status allows1
  • TRALI (transfusion-related acute lung injury):
    • Cause not fully understood; donor anti-leukocyte antibodies produce polymorphonuclear leukocyte degranulation in lung1
    • Definition: acute lung injury (acute onset hypoxemia with bilateral lung infiltrates/pulmonary edema on CXR and no evidence of circulatory overload) within 6hrs of completion of transfusion, and no other risk factors for acute lung injury (ALI) 2 (“possible TRALI” if ALI risk factors present)
    • Presentation: dyspnea, hypoxemia, fever, hypotension, may be followed by acute transient leukopenia2
    • More common with plasma, RBCs, platelets1
    • Treatment: stop transfusion, resolves in 24-72hrs with supportive care1
      • mechanical ventilation required in 72% of cases, death in 5-10%2
      • distinguish from TACO, as aggressive diuresis in TRALI can cause rapid deterioration; steroids not helpful1
      • notify blood bank to perform special donor and recipient testing2

*ALI risk factors: aspiration, pneumonia, toxic inhalation, lung contusion, near drowning, severe sepsis, shock, trauma, burn injury, acute pancreatitis, cardiopulmonary bypass, drug overdose2

If the patient develops hypotension (>30mmHg drop in systolic or diastolic BP; pediatric: >25% drop in systolic BP) 2, you would consider….

  • Acute hemolytic transfusion reaction
  • Bacterial sepsis
  • Severe febrile non-hemolytic transfusion reaction
  • Bradykinin mediated hypotension (ACE breaks down bradykinin, usually pt takes ACEi)
  • TRALI
  • Anaphylaxis

Complications of massive transfusion (>10u of RBCs in 24hrs) 2

  • Independent risk factor for multi-organ failure2
  • Dilutional coagulopathy: monitor with q1h bloodwork, transfuse to keep 2
    • platelets >50 x109/L (>100 in head injury)
    • INR <1.8
    • Fibrinogen >2.0 g/L
    • Give 1g IV TXA bolus then 1g IV over 8 hrs
  • Hypothermia: higher risk with >5 units blood; mortality inversely related to core temperature2
    • low temperature increases blood loss and causes cardiac arrhythmias, platelet dysfunction, reduced citrate clearance, decreased cardiac output, hypotension, decreased coagulation factor activity2
    • Maintain core temp >36°C2
  • Citrate (anticoagulant in blood components) accumulation due to liver metabolism of citrate to bicarbonate being overwhelmed 1
    • Hypocalcemia: citrate binds calcium2
    • Hypomagnesemia: citrate binds magnesium2
    • Hypokalemia: Excess bicarbonate generated by metabolism of citrate, causing alkalemia and driving potassium into cells1
  • Hyperkalemia: Potassium in blood increases during storage (neonates and those with renal insufficiency at most risk) 1
  • Metabolic acidosis (rare; from acid pH of blood products) 2

 

Other complications

  • Cytopenias After Transfusion2
  • Hemolysis not related to RBC alloantibodies2
    • Use of hypotonic IV solutions with RBC transfusions
    • Medical device-related (ex: cell saver or blood warmer malfunction)
    • Overheating of RBCs due to improper storage
    • Freezing of RBCs
    • Transfusion under pressure through small bore needle
    • Outdated RBCs

See – EM Cases – Massive Hemorrhage Protocols


Concluding thoughts….

 

Transfusion pearls1

  • Complications occur in 20% of all transfusions – most are minor, life-threatening reactions are rare
  • Watch for unexpected changes in patient status to identify reactions
  • First steps in all transfusion reactions:
    • Stop transfusion immediately
    • Contact blood bank (the transfusion physician is a valuable resource)
    • Draw new specimen to re-type and cross-match to resume transfusion
  • Do NOT abandon all transfusion! Typically the reaction is due to interaction between individual patient and individual unit – thus is safe if appropriately matched

References

 

  1. Coil C.J., & Santen S.A. (2020). Transfusion therapy. Tintinalli J.E., & Ma O, & Yealy D.M., & Meckler G.D., & Stapczynski J, & Cline D.M., & Thomas S.H.(Eds.), Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw Hill. https://accessmedicine-mhmedical-com.ezproxy.library.dal.ca/content.aspx?bookid=2353&sectionid=221179053

 

  1. Callum, J. L., Ontario Regional Blood Coordinating Network Staff, Pinkerton, P. H., Lima, A., Lin, Y., Karbouti, K., Lieberman, L., Pendergrast, J. M., Robitaille, N., & Tinmouth, A. T. (2016). Bloody Easy 4: Blood Transfusions, Blood Alternatives and Transfusion Reactions. Ontario Regional Blood Coordinating Network. https://books.google.ca/books?id=6G1ZDQEACAAJ

 

  1. Helman, A. EM Cases Episode 152: The 7 Ts of Massive Hemorrhage Protocols. February 9, 2021. https://emergencymedicinecases.com/7-ts-massive-hemorrhage-protocols/

 

 


 

 

Figure 2: Red Blood Cell Pre-Transfusion Checklist (Bloody Easy 4) 2

EM Cases – Massive Hemorrhage Protocols

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Congratulations Dr. Rob Dunfield – Iype/Wilfred Resident Award Winner!

Congratulations Dr. Rob Dunfield – Iype/Wilfred Resident Award Winner!

 

Our own Dr. Rob Dunfield is the recipient of the 2022 Iype/Wilfred Resident Award. The New Brunswick Medical Society awards this honor to residents who have demonstrated outstanding achievements during their residency training in New Brunswick. More specifically this award recognizes achievements in research, professionalism, compassion and caring.

Dr. Dunfield is a third year resident in our local Integrated Family Medicine Emergency Medicine program. He previously served as the program’s chief resident and has already been recognized during residency for his award winning research. 

We are proud of Dr. Dunfield and can’t wait to see what he achieves next!

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Congratulations Dr. Melanie Johnston – Resident Research Award Winner

Congratulations to our own Dr. Melanie Johnston, a second year resident in the FMEM Program here in Saint John. Dr. Johnston was the recipient of The Dr. Douglas E. Sinclair Award in Emergency Medicine Research for her research project entitled “- Impact of shift Trial on Overnight Patient Flow at the Saint John Regional Emergency Department.” This award is presented by the Dalhousie Department of Emergency Medicine to the most significant research project presentation at the annual Emergency Medicine Research Day.

It is judged on the following criteria: background and research methodology, overall presentation, critical appraisal and appropriateness to emergency medicine and clinical practice.

Congratulations Dr. Johnston!

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Congratulations to Dr. Rob Dunfield – CAEP Resident Research Award Winner!

CAEP 2021 Resident Research Award Winner – Dr. Rob Dunfield

A big congratulations goes out to our very own resident researcher, Dr. Rob Dunfield! Dr. Dunfield is a second year resident in the FMEM Program here in Saint John. He is one of seven residents recognized nationally for their excellent research abstract submissions to the annual CAEP conference. Dr. Dunfield’s research project is a secondary study from the SHOC-ED group and is entitled:  “Does IVC Ultrasound independently predict fluid status in spontaneously breathing, undifferentiated hypotensive patients? SHOC-IVC”.

Congratulations again, Dr. Dunfield!

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Congratulations to Dr. Kavish Chandra!

Congratulations to Dr. Kavish Chandra – recipient of the Iype/Wilfred Resident Award!

Dr. Chandra, a PGY3 in the Integrated Family Medicine/Emergency Medicine program, was one of 3 recipients of the prestigious Iype/Wilfred award. This is awarded annually by the New Brunswick Medical Society to residents who have demonstrated outstanding achievements during their residency training in New Brunswick. Recipients are recognized as being leaders in research and professionalism, and who do so while showing compassion and caring towards patients and colleagues.

This award will be presented to Dr. Chandra at the Celebration of Medicine ceremony hosted by the New Brunswick Medical Society on May 26, 2018.

Congratulations, Dr. Chandra!

Far right: Dr. Chandra in a simulation training session

 

This post was copy edited by Mandy Peach

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