Author Archives: Mark McGraw

Transfusion Troubles: A review of transfusion reactions and management

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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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EMSJ CPD Recommendations – September 2022

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Dr Mackenzie Howatt MD FRCPC, Director of CPD

External CPD Activities

I’ve listed below a few external CPD activities for your perusal. I’m hoping to be able to update you monthly on upcoming activities both internal and external to our department to make sure everyone is aware of at least some of the myriad activities out there. I have no involvement/personal stake in any of the listed activities.

 

Clinical:

  1. CAEP CPD – There is an upcoming Geriatric ER course on Oct 27 12-4 (eastern) 400$ for members. Course is mix of pre-recorded videos along with the 4 hour live virtual event. https://caep.ca/cpd-courses/
  2. CAEP CPD – “Pump  it up: updates on POCUS, Risk Stratification, and new meds for ED patients” – FREE online webinar – Oct 19 at 1 pm eastern. Need to Register via CAEP. https://caep.ca/cpd-courses/
  3. Dalhousie CPD – “Community Hospital Programs.” – Is a series of CPD events across NS, most of which has a virtual component. Is free to register. Many topics are primary care, but given current realities are presentations we are being asked to manage in the ED. Some appear relevant, some not. held from 7-8 pm on Tues-Thurs. https://medicine.dal.ca/departments/core-units/cpd/programs/nova-scotia-community-hospital-program.html
  4. Critical Care – Recorded lectures from a conference in the spring held in montreal are available “The Hospitalist and Resuscitationist”. You can “rent” the entire library for 375 for a years worth of access. Have not attended so can’t attest to quality, but have heard positive things. https://thinkingcriticalcare.com/

 

Leadership:

  1. CAEP CPD – Virtual leadership series Nov 3, 10, 17, 24 from 3-430 (eastern). 400/550 (member non member).
  2. NBMS – Foundations of Leadership certificate – multi week commitment for a 4 module leadership course. Free registration. Need to apply by Sept 19. 30 participant max. application can be found on NBMS website.

 

Faculty Development:

  1. Dalhousie CPD office puts on frequent Fac Dev topics that are available to us. They seem to have reasonable registration fees if affiliated with Dalhousie. Topics are on the page linked. https://medicine.dal.ca/departments/core-units/cpd/faculty-development.html

Administration:

  1. EDAC Nov 7 – Fully virtual. Based out of Toronto. Full day course on ED administration (For current or wanna-be admins). 500 dollars for the day
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Peritonsillar Abscess Considerations and Treatment

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Flimsy on Quinsy: Considerations and procedures to help diagnose and treat peritonsillar abscess  

Author: Iain McPhee- PGY1

Case study:

A 30 y.o. female presented to the emergency department with a 2-3 day history of sore throat, a unilateral, right sided oral pain that was worsening, and mild right ear ache. Although she was able to swallow food and liquid with discomfort, she reported an increased pooling of saliva in her mouth. She became more concerned when she noticed voice changes and decided to come to the hospital. 

On exam, she looked well and her vitals were within normal limits. On examination of the oral cavity there was a noted mild deviation of the uvula to the left. There was clearly demarcated erythema of both the hard palate and soft palate on the right side. Her right tonsil was only mildly enlarged and the presence of tonsillar stones were appreciated bilaterally. There was very mild fluctuance when palpating the junction between the hard and soft palate. There was an obvious dysphonia (Hot potato voice).

Background:

Peritonsillar abscess (PTA) (Quinsy) and peritonsillar cellulitis (PTC) are often indistinguishable, sharing similar clinical signs and symptoms (1). As management differs depending on the condition, several aspects warrant consideration in the differentiating process

Considerations: 

  1. Assess for severe upper airway obstruction
    • Look for signs of trismus, suprasternal retractions and anxious appearance. If present consider airway management.
  2. Computed tomography of the neck
    • Consider if you suspect signs of deep neck infection like a retro or parapharyngeal abscess. The CT scan should be obtained with contrast to help identify an abscess (4)
  3. Ultrasound guided exam 
    • Intraoral ultrasound has been shown to be a superior method to both diagnose and assist in the execution peritonsillar abscess drainage when compared to classic landmark-based needle aspiration (2,3). 
  4. Time
    • In the absence of a significant/apparent fluctuating mass in the mouth, consideration of the amount of time the symptoms have been present can help distinguish between the two conditions. Peritonsillar cellulitis is considered a transition phase of peritonsillar inflammatory process which leads to abscess formation (1). Look for 1-2 day history of symptoms as peritonsillar cellulitis, Abscesses are more likely to form between 2-8 days.

Algorithm: Approach to diagnosis and treatment of peritonsillar abscess in the emergency department

https://www.uptodate.com/contents/image?csi=59e98f58-4a45-4ff2-b021-31528346c088&source=contentShare&imageKey=EM%2F112062

Intraoral Ultrasound approach to drainage (as described on emdocs)

http://www.emdocs.net/unlocking-common-ed-procedures-peritonsillar-abscess-drainage/

  1. Use intracavitary probe with cover (Fig 1).
    • Examine affected area and locate abscess 
    • Also locate depth of carotid artery and any potential vascular anatomy anomalies (Fig 2).

      Figure 1: Intracavitary Probe with cover

      Figure 2: Anechoic abscess and carotid artery highlighted in red

       

  2. Analgesia/anesthesia
    • Consider IV analgesia, anxiolytics
    • Anesthetize oral cavity using topical spray like cetacaine or nebulized lidocaine
    • Inject lidocaine with epinephrine into the area of abscess with 18g needle with cut sheath (Fig 3).

      Figure 3 : Scalpel with taped guard and

  3. Optimize Abscess visualization 
    • Insert laryngoscope blade to a depth that is comfortable for the patient. Ask patient to hold laryngoscope (Fig 4)

      Figure 4: Laryngoscope blade optimizing view

  4. Drainage
    • Once adequate visualization is achieved, approach superior pole of abscess with sheathed spinal needle and continuously aspirate when advancing until pus is reached (Fig 5).
    • Consider incision with scalpel with protective guard and used 
    • Insert curved hemostat into abscess space to break up remaining loculations

      Figure 5: Anatomical picture showing superior pole

 

References

  1. Mohamad I, Yaroko A. Peritonsillar swelling is not always quinsy. Malays Fam Physician. 2013 Aug 31;8(2):53-5. PMID: 25606284; PMCID: PMC4170468.
  2. Costantino TG, Satz WA, Dehnkamp W, Goett H. Randomized trial comparing intraoral ultrasound to landmark-based needle aspiration in patients with suspected peritonsillar abscess. Acad Emerg Med. 2012 Jun;19(6):626-31. doi: 10.1111/j.1553-2712.2012.01380.x. PMID: 22687177.
  3. Froehlich MH, Huang Z, Reilly BK. Utilization of ultrasound for diagnostic evaluation and management of peritonsillar abscesses. Curr Opin Otolaryngol Head Neck Surg. 2017 Apr;25(2):163-168. doi: 10.1097/MOO.0000000000000338. PMID: 28169864.
  4. Galioto NJ. Peritonsillar abscess. Am Fam Physician. 2008 Jan 15;77(2):199-202. PMID: 18246890.

Procedures and Algorithms

  1. http://www.emdocs.net/unlocking-common-ed-procedures-peritonsillar-abscess-drainage/
  2. https://www.uptodate.com/contents/image?imageKey=EM%2F112062&topicKey=EM%2F6079&search=peritonsillar%20cellulitis&rank=1~19&source=see_link

 

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