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Approach to Foot Radiographs

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Resident Pearl by Dr. Sarah Belbraouet

Diagnostic Radiology PGY2

Dalhousie University

Reviewed by Dr. R Goss

Copy Edited by Dr. J Vonkeman

Pdf Download: EMSJ SBelraouet An Approach to Foot Radiographs

Foot XRs in the ED

Foot Radiographs are often requested in the emergency department. Indicated in cases of trauma, infection, or pain for instance, it is essential to have an efficient and structured approach to reading these studies.

Using a consistent approach to any radiograph is key to overcoming common pitfalls and blind spots in imaging. This resident clinical pearl will provide a systematic approach that can be molded into personal preferences (1).

1. Adequacy (2)

A standard foot radiograph includes an AP or anteroposterior view (also called DP view or dorsoplantar), a lateral view and an oblique view.

  • AP view: all metatarsal bones should be appropriately visible.
  • Oblique view: taken with a 30-40 degree medial angulation of the foot.
  • Lateral view: includes a projection of the ankle. Here, the base of the 1st, 2nd and 3rd metatarsal should align with the three cuneiforms.

 

 Figure 1: Foot series

 

Figure 2: Foot Anatomy

2. Soft Tissue

Assess for soft tissue swelling and/or effusion; these findings can guide you to an underlying pathology (i.e.: fracture).

3. Bone (1)

Outline the cortex of each bone to assess for fractures.

  • Beware that subtle and frequently missed fractures usually occur at the base of the metatarsal bones.
  • An unattached bone may represent a bone fragment, an avulsion fracture, or an accessory ossicle in which case, could be normal variant anatomy.

4. Cartilage and Joints (2)

Always look out for a Lisfranc injury located at the Lisfranc joint complex which is best seen on the AP and oblique views. The Lisfranc ligament stabilizes the foot therefore, a missed injury can lead to great damage to the foot cartilage. Arthritis and collapse of the arch are complications of a missed Lisfranc injury.

  • The Lisfranc ligament complex consists of a dorsal, interosseous, and plantar ligament (see Figure 3).
  • The medial borders of the 2nd metatarsal and 2nd cuneiform, also named intermediate cuneiform, should be aligned on the AP view. The medial border of the 3rd metatarsal and 3rd cuneiform should align on the oblique view.
  • If there is any disruption or widening of the 1st-2nd metatarsal space, a Lisfranc injury should be suspected.
  • This injury typically results from an axial load to a plantarflexed foot or a crush injury.

 

Figure 3: The Lisfranc ligament complex. Red: Dorsal ligament, Blue: Interosseous ligament, Green: Plantar ligament (6)

 

Examine the midtarsal joints for good alignment to assess for appropriate integrity of the corresponding ligaments.

 

Figure 4: Midtarsal joints (5)

 

5. Additional View Needed?

  • Weight bearing foot AP or lateral view if a Lisfranc injury is suspected. Some institutions will acquire a foot CT instead as it is more sensitive for this type of injury and could also unveil subtle findings that would be missed on a plain radiograph.
  • Os calcis view if there is suspicion for a calcaneal fracture.
    • Around 60% of tarsal bone fractures are associated with the calcaneus.

The Bohler’s angle is used on plain radiographs to assess the presence and severity of these fractures. This angle is measured on the lateral view and results from an initial line drawn from the highest point of the anterior process of the calcaneus and the posterior articular facet (line 1) followed by a line joining the highest point of the posterior articular facet with the calcaneal tuberosity as shown in figure 5. A normal Bohler’s angle ranges between 20 and 40 degrees, any value below should raise suspicion for a calcaneal fracture.

 

Figure 5: Bohler’s angle (6)

 

Pitfall

Apophysis of the proximal 5th metatarsal: Appears from age 10 and 12 in girls and boys, respectively and generally fuses within 2-4 years. This apophysis is located laterally and oriented parallel to the shaft as seen in Figure 6. Do not mistake this with an avulsion fracture or an os peroneum (accessory bone) which are often oriented transversally.

 

Figure 6 : Apophysis of the proximal 5th metatarsal (4)

Figure 7 : Avulsion fracture of the 5th metatarsal (9)

 

Bottom Line

Foot radiographs are often utilized in clinical practice and especially in the emergency department. Research shows that having a systematic approach improves the diagnosis accuracy and therefore can reduce the incidence of inappropriate management of foot injuries (8).

 

References

  1. https://radiopaedia.org/articles/foot-radiograph-an-approach
  2. https://www.aliem.com/emrad-foot-x-ray/
  3. https://www.researchgate.net/figure/Oblique-radiographs-of-a-Lisfranc-injury-and-normal-right-foot-The-rotation-and-loss-of_fig1_262265287
  4. https://radiopaedia.org/articles/apophysis-of-the-proximal-5th-metatarsal?lang=us
  5. https://radiopaedia.org/articles/midtarsal-joint?lang=us
  6. https://radiopaedia.org/articles/bohler-angle-2?lang=us
  7. https://radiologyassistant.nl/musculoskeletal/wrist/foot-1#foot-case-1-distortion
  8. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1964112/
  9. https://www.mdedge.com/familymedicine/article/100121/pain/twisted-ankle

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A Case of Bilateral Internuclear Ophthalmoplegia (INO)

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Resident Pearl by Dr. Saly Halawa 

iFMEM PGY2

Dalhousie University

Reviewed by Dr. B Ramrattan

Copy Edited by Dr. J Vonkeman

Pdf Download: EMSJ Bilateral INO SHalawa

 

Case Presentation

A 42yo male presents to the Emergency Department with abrupt onset right-sided facial numbness and double vision. His facial numbness quickly improved but he continued to have diplopia and gait ataxia. He denied headache, nausea or photophonophobia. The patient had a history of sickle cell disease and diabetes. His medications included hydroxyurea and insulin. On physical examination, he was unable to adduct his eyes bilaterally on lateral gaze with abducting nystagmus. His power, tone, reflex, and sensation were all normal.

Internuclear Ophthalmoplegia (INO)

Internuclear ophthalmoplegia (INO) is a neurologic condition characterized by impaired control of conjugate eye movements (1). It is caused by a lesion of the medial longitudinal fasciculus (MLF) in the brainstem. The MLF is the pathway containing internuclear neurons connecting cranial nerve nuclei that control conjugate eye movements. These include the nucleus of the abducens nerve (CN VI) in the pons and the contralateral nucleus of the oculomotor nerve (CN III) in the midbrain supplying the medial rectus (1). Together CNIII and CN VI allow for adduction and abduction of the eye, respectively. For instance, interneurons of CNVI on one side project across the midline to the contralateral MLF which ascends to CNIII to control the medial rectus on that side, allowing the lateral and medial rectus to move the eyes together (1). In this way, the MLF coordinates eye movements between both eyes allowing for conjugate gaze. Patients with INO have an adduction deficit on the ipsilateral side with associated contralateral nystagmus of the abducting eye.

INO is named with respect to the side of the adduction deficit, which is the side of the MLF lesion. A R sided INO is due to a lesion of the R MLF. Patients may also present with bilateral INO as in the case presented here.

 

Figure 1: Adduction Defects produced by Internuclear Ophthalmoplegia (1)

Patients with INO often experience horizontal diplopia due to dysconjugate gaze or they may report vertical-oblique diplopia due to associated skew deviation (1). Patients may also present with difficulty in tracking fast-moving objects as a result of a mismatch in saccadic movements between the eyes.

Differential

The differential diagnosis for INO is broad (1). The most common causes of bilateral INO include multiple sclerosis in younger patients, often younger than 50 yrs old, or due to brainstem infarction in older patients. Other causes of INO include infection, toxicity to medications including amitriptyline, benzodiazepines or ethanol, chiari malformations or trauma. In the present case, bilateral INO was the first presentation of MS due to demyelination of the MLF.

Prognosis

Prognostically, INO symptoms do improve over time, often resolving spontaneously after an average of 2 months, but up to 12 months (2). Associated neurologic symptoms such as vertigo, ataxia, sensory or speech deficits are poor prognosticating factors. Those with cerebrovascular etiology have less favorable recovery as well.

Figure 2: Internuclear Ophthalmoplegia caused by lesion at the Medial Longitudinal Fasciculus (4)

Video link: https://www.youtube.com/watch?v=eL3_6yYJdUA&ab_channel=MoranCORE

 

Case Conclusion

CT angiography of the brain demonstrated no evidence of acute infarction. MRI showed periventricular white matter hyperintensities which was also seen in the corpus callosum, suspicious for multiple sclerosis. He was given a five-day trial of methylprednisolone.

Bottom Line

Though uncommon, internuclear ophthalmoplegia points to a brainstem lesion with a wide variety of causes. Multiple sclerosis should be suspected in a young patient presenting with bilateral INO.

References

  1. Toral M, Haugsdal J, Wall M. Internuclear Ophthalmoplegia. EyeRounds.org. posted June 8, 2017; Available from: http://EyeRounds.org/cases/252-internuclear-ophthalmoplegia.htm
  2. Eggenberger E, et al. Prognosis of ischemic internuclear ophthalmoplegia. Ophthalmology. 2002; 109(9):1676-8.
  3.  https://www.youtube.com/watch?v=eL3_6yYJdUA&ab_channel=MoranCORE
  4. https://sketchymedicine.com/2013/12/internuclear-opthalmoplegia/

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Under pressure: Anorectal abscesses… to drain or not to drain?

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Resident Clinical Pearl

Victoria Landry

iFMEM R3

Reviewed by Dr. J Mekwan

Copy Edited by Dr. J Vonkeman

PDF Download: EMSJ Anorectal Abscess by VLandry

Case

A 57yo male presents to the emergency department with complaints of a lump near his rectum and pain with sitting which developed over the past week. He is afebrile with normal vital signs. He tells you that about 6 months ago this same thing occurred and drainage was attempted in the ED but was unsuccessful. A colorectal surgeon subsequently drained it successfully under local anesthetic in clinic later the same day. He has had no recurrence of symptoms until the past week. He smokes and has hypertension controlled with medication but is otherwise healthy.

He denies pain with defecation and has not had any rectal bleeding nor changes in bowel habits. He feels otherwise well and denies fevers or chills.

On exam you find a tender firm mass in the subcutaneous tissue lateral to his rectum on the left side. There is minimal overlying erythema and no fluctuance.

Key Point #1: Always do a Digital Rectal Exam

  • Palpate in all directions to localize area of tenderness1
  • Should be unremarkable after you get past the anal verge2 – if tenderness, mass, induration past anal verge, do a CT scan to assess for deeper abscess

You think back to your perirectal anatomy and recall the spaces where abscesses can develop.

Figure 1: Transverse anorectal anatomy3

Figure 2: Longitudinal anorectal anatomy3

 

  Perianal Ischiorectal Intersphincteric Supralevator Postanal
Incidence 40-45% 20-25% 20-25% <5% 5-10%
Location Outside anal verge, red, swollen, fluctuant, easily palpable at anal verge Between rectum and ischial tuberosity, outside sphincters, palpable through rectal wall or lateral to anal verge on buttocks Lower rectum, between sphincters, inferior to levator ani (tender indurated mass in rectum) Above levator ani (tender indurated mass in rectum) Posterior to rectum, Deep to external sphincter, inferior to levator ani
Symptoms Painful perianal mass Buttock pain Rectal fullness, throbbing, worse with defecation Perianal and buttock pain Rectal fullness and pain near coccyx
Fever, ↑WBC No Possibly Possibly Yes Yes
Fistula formation ++ + +++ +++ –
ED I&D Yes Possibly: I&D/needle aspiration only if abscess is superficial and fluctuant No No:

Consult surgery for urgent drainage

 No

Table 1: Types of abscesses3

** caution as mass may be bigger/deeper than anticipated – prudent to defer to surgery for their expertise

Figure 3: Anorectal abscess locations4

Key Point #2: Get a CT scan to define the abscess for any of the following2

  • Unable to see the abscess superficially
  • Patient is unable to tolerate the DRE due to significant pain
  • Induration, bogginess or tenderness in the supralevator space (above the sphincter muscle)
  • If the extent of the abscess is uncertain4

Note: can use POCUS to evaluate location of abscess, but caution against false reassurance as to extent/depth, and safer to rely on palpable fluctuant mass to determine if I&D is safe

 

Figure 4: Perianal abscess on CT1

Management5

  • Simple, isolated, fluctuant perianal abscess4
    • Bedside I&D
    • Goal is to relieve the pus under pressure2
  • Ischiorectal abscess2
    • Can consider I&D only if superficial, but prudent to get a CT first
    • Consult surgery for their expertise
  • Intersphincteric, Supralevator, Postanal
    • CT to define the abscess
    • Consult surgery

Key Point #3: Err on the side of caution

Only do I&D in the ED if the following criteria are met3 [3]

  • Perianal abscess (+/- ischiorectal) is small and superficial
  • Patient
    • Is Well-appearing
    • Is Cooperative
    • Has no complicating factors (DM, immune compromise etc.)

Incision and Drainage of simple perianal abscess2

  • Local anesthetic – lidocaine with epinephrine
    • Infiltrate superficial skin where you will poke with needle
    • occasionally procedural sedation is needed3
  • Needle poke +/- aspiration (18guage) or pinpoint incision over painful region to localize purulent pocket4
  • Inject more local anesthetic2
  • Enlarge the incision
    • Make incision as close to anal verge as possible to minimize the length of any potential fistula2,5,6
    • Cruciate (with trimming of the flaps) or elliptical incision over fluctuant part of abscess is preferred over a linear incision to keep incision open and draining without painful packing2
    • If linear only, will need packing to prevent premature closure
    • Note: loop drainage technique not recommended for I&D in the ED7
  • Break up loculations with finger (increased tactile feedback and better control) or hemostat +/- irrigation with saline7
  • Cover with bulky dressing4
  • Ideally, close follow up until complete healing (up to 8wks) to monitor for recurrence and for fistula formation5
  • Uncomplicated perianal abscesses do not require antibiotics after successful drainage2.

Figure 5: Cruciate incision4

Instruct the patient to WASH8

  • W – warm water sitz baths 5-10min BID-QID PRN, with Epsom salts (start the day after I&D)
    • Water >40°C helps decrease anal canal pressure
  • A – analgesics (NSAIDs, topical 1-2% lidocaine gel)
  • S – stool softeners (PEG, senna)
  • H – high fiber diet +/- fiber supplement
  • Uncomplicated perianal abscesses do not require antibiotics after successful drainage2.

Indications for antibiotics (+/- tetanus +/- admission to hospital with surgical consult)4

  • Surrounding cellulitis
  • Immune compromise
  • Valvular heart disease
  • Diabetes
  • Systemic symptoms (Fever, ill appearing, leukocytosis)
  • Elderly

Note: Send off a wound culture before giving antibiotics

Antibiotic choice5:

  • Systemic: piperacillin-tazobactam
  • Oral: Amoxicillin-clavulanate or Metronidazole + ciprofloxacin

A word on fistulas

  • Fistulas are a connection between two epithelium-lined surfaces, characterized by persistent or recurrent anal drainage. They are seen in Crohn’s, TB, cancer, FB reactions, and as a complication of anorectal abscesses. Treatment is surgical3
  • ~50% of anorectal abscesses form a fistula overtime2
  • Suggest surgical consultation after drainage of perianal abscess as fistula formation is common4
  • Fistulas may be missed on CT scan; MRI is more sensitive for diagnosis2     

Take home points: 

  1. Always do a rectal exam as part of the initial evaluation
  2. Have a low threshold to get a CT scan to define the abscess
  3. Reserve I&D in the ED for perianal abscesses that are visible, superficial and fluctuant

References

  1. Farah, Jennifer, Mason, Jessica, and Werner, Jessie, “Perirectal Abscess & Pilonidal Cyst.” [Online]. Available: https://www.emrap.org/episode/gastro/perirectal
  2. Jhun, Paul and Cologne, Kyle, “Anorectal Infections,” HIPPO EMRAP, vol. 15, no. 9, pp. 17–18, Sep. 2015.
  3. Parrillo, “Anorectal Emergencies,” presented at the EMRAP, Temple University Hospital EM Residency, Feb. 2004. [Online]. Available: https://www.emrap.org/episode/september2004/anorectal
  4. Berberian J.G., & Burgess B.E. Tintinalli J.E., & Ma O, & Yealy D.M., & Meckler G.D., & Stapczynski J, & Cline D.M., & Thomas S.H.(Eds.), “Anorectal disorders,” in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e, McGraw Hill, 2020. [Online]. Available: https://accessmedicine-mhmedical-com.ezproxy.library.dal.ca/content.aspx?bookid=2353&sectionid=219642697
  5. Streitz Matthew, Long Brit, “Anorectal Disease,” in CorePendium, Burbank, CA: CorePendium, LLC, 2022. [Online]. Available: https://www.emrap.org/corependium/chapter/reclLjrt5HvPGSIDv/Anorectal-Disease#h.d78nqbylr3x
  6. Bleday, Ronald, Perianal and perirectal abscess. uptodate.com, 2022. [Online]. Available: https://www.uptodate.com/contents/perianal-and-perirectal-abscess
  7. Cavanaugh, Megan and Ormon, Rob, “Anorectal Disorders.” [Online]. Available: https://www.emrap.org/episode/april2011/anorectal
  8. Lipp, Chris, “Anorectal Disorders.” [Online]. Available: https://canadiem.org/crackcast-e096-anorectal-disorders/

 

 

 

 

 

 

 

 

 

 

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

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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

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

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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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