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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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Unvexing the VExUS Score – An Overview

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Unvexing the VExUS Score – An Overview

 

PoCUS Clinical Pearl

Dr Steven Chen

DalEM PoCUS Elective

PGY2 Internal Medicine, University of Toronto

Reviewed: Dr David Lewis

Copyedited: Dr David Lewis

Introduction:

The pursuit of a rapid and objective measure of volume status has always been a vexing problem for clinicians as proper fluid management is pivotal for patient outcomes. In recent years, there has been increased attention towards the concept of “fluid-responsive” as liberal fluid boluses can often be associated with poor outcomes as a result of systemic congestion. 1

In the POCUS community, while Inferior Vena Cava (IVC) measurements have promise in assessing central venous pressure, the subsequent translation towards “volume responsiveness” has been met with many other limitations. For one, it did not account for venous congestion at other organ levels such as the pulmonary, renal, or hepatic systems. 2,3

Venous excess ultrasound (VExUS) is a growing bedside ultrasound-based approach that aims to provide a more comprehensive assessment of venous congestion. This was initially described by Beaubien-Souligny et al. (2020) from a post-hoc analysis correlating ultrasound grading parameters with risk in development of AKI in cardiac surgery patients.4 The protocol serves to assess multiple sites of venous congestion, including the IVC, hepatic veins, portal veins and intrarenal veins. By assessing congestion in these multiple sites, the VExUS score has gained attraction in providing a more comprehensive assessment of systemic congestion. 4,5

View Acquisition:

The VExUS protocol is composed of four main components outlined below:

  • IVC diameter
  • Hepatic Vein Doppler Assessment
  • Hepatic Portal Vein Doppler Assessment
  • Intrarenal Vein Doppler Assessment

This can be performed using either the curvilinear probe (preferred) or the phased array probe. The patient should be positioned flat and supine on the bed to acquire the views. The table below depicts some suggested views where larger regions of the veins may be accessible for pulse wave doppler gating in reference to standardized sonography protocols. 6,7

Note: Reviewing the basics of pulse wave doppler will be needed prior to completing VExUS scans (not covered in this article).

 

 

 

 

 

Interpretation:

Interpretation of the VExUS grading system is well summarized in diagram below (sourced from POCUS1018) and takes some practice to differentiate normal from abnormal waveforms. Pulse wave doppler assessment is pursued only if the inferior vena cava is found plethoric, defined as greater or equal to 2cm. 4,5

Each of the hepatic, portal and renal veins are subsequently examined and classified as normal, mildly congested, or severely congested. The VExUS system has four grades: Grade 0 represents no congestion in any organ, Grade 1 represents only mild congestive findings, Grade 2 represents severe congestive findings in only one organ, and Grade 3 represents severe congestive findings in at least two out of three organ systems. 4,5

Source: POCUS1018

Some sample waveforms are shown below with comments to help with distinguishing normal from abnormal waveforms.

 

Evidence:

VExUS has also been shown to be reliable and reproducible, with good interobserver agreement in trained individuals and correlation with other measures of volume status such as central venous pressure.4,5 As the technique is growing in the POCUS literature, below is a table summarizing several recent studies exploring its application across numerous settings.

Study Purpose Results
Beaubien-Souligny W, et al. (2020)4

 

Post-hoc analysis of a single centre prospective study in 145 patients

 

 

 

 Initial model of VExUS grading system looking at association in development of AKI in cardiac surgery population Association with subsequent AKI:

 

HR: 3.69 CI 1.65–8.24 p = 0.001;

+LR: 6.37 CI 2.19–18.50 when detected at ICU admission, which outperformed central venous pressure measurements

 
Bhardwaj V, et al. (2020)9

 

Prospective cohort study of 30 patients in ICU setting

 

 Prospective study on application of VExUS scoring on staging of AKI in patients with cardiorenal syndrome Resolution of AKI injury significantly correlated with improvement in VExUS grade (p 0.003).

 

There was significant association between changes in VExUS grade and fluid balance (p value 0.006).
Varudo R, et al. (2022)10

 

Case report of ICU patient with hyponatremia

 Application of VExUS in case report as rapid tool to help with volume status assessment in patient with complex hyponatremia Overall VExUS grade 2, prompting strategy for diuresis with improvement
Rolston D, et al. (2022)11

 

Observational study of 150 septic patients in single centre

 VExUS score performed on ED septic patients prior to receiving fluids with chart review done to determine if there is association with poorer outcomes Composite outcome (mortality, ICU admission or rapid response activation):

 

VExUS score of 0: 31.6% of patients

VExUS score of 1: 47.6% of patients

VExUS score >1: 67.7% of patients

(p: 0.0015)
Guinot, PG, et al. (2022)12

Prospective observational study of 81 ICU patients started on loop diuretic therapy

 Evaluation of multiple scores to predict appropriate diuretic-induced fluid depletion (portal pulsatility index, renal venous impedance index, VExUS) Baseline portal pulsatility index and renal venous impedance index were found to be superior predictors compared to VExUS.

 

The baseline VExUS score (AUC of 0.66 CI95% 0.53–0.79, p = 0.012) was poorly predictive of appropriate response to diuretic-induced fluid depletion.
Menéndez‐Suso JJ, et al. (2023)13

 

Cross-sectional pilot study of 33 children in pediatric ICU setting

 Association of VExUS score with CVP in pediatric ICU VExUS score severity was strongly associated with CVP (p<0.001) in critically ill children.
Longino A, et al. (2023)14

 

Prospective validation study in 56 critically ill patients

 Validation looking at association of VExUS grade with right atrial pressure. VExUS had a favorable AUC for prediction of a RAP ≥ 12 mmHg (0.99, 95% CI 0.96-1) compared to IVC

diameter (0.79, 95% CI 0.65–0.92).

Pitfalls:

It should be kept in mind that numerous factors may affect interpretation of VExUS gradings.

For the IVC component, increased intra-abdominal pressure can affect measurements independently of the pressure in the right atrium or may be affected by chronic pulmonary hypertension. The hepatic vein may not show significant changes even in severe tricuspid regurgitation if the right atrium can still expand and contract normally. In thin healthy people and those with arteriovenous malformations, the portal vein can have a pulsatile flow without venous congestion. It is also important to note that for patients with underlying disease renal or liver parenchymal disease, venous doppler recordings may be less reliable. 3-5

Outside of physiologic factors, another limitation is the need for adequate training and familiarity in performing and interpreting the technique. While VExUS is fairly well protocolized, it requires proficiency with pulse wave doppler to perform accurately. As with any new technique, there is a risk of variability in technique and interpretation. To avoid misinterpretation, it is important to consider repeat tracings to ensure consistency of results and to consider findings within the overall clinical context of the patient.

Bottom line:

VExUS is a non-invasive ultrasound method for assessing venous congestion across multiple organ systems. While there are several physiologic limitations and results need to be used in adjunct with the clinical picture, studies have shown promise for VExUS to be incorporated as part of a physician’s toolkit to help with clinical decision making. 3-5

References

  1. Atkinson P, Bowra J, Milne J, Lewis D, Lambert M, Jarman B, Noble VE, Lamprecht H, Harris T, Connolly J, Kessler R. International Federation for Emergency Medicine Consensus Statement: Sonography in hypotension and cardiac arrest (SHoC): An international consensus on the use of point of care ultrasound for undifferentiated hypotension and during cardiac arrest. Canadian Journal of Emergency Medicine. 2017 Nov;19(6):459-70.
  2. Corl KA, George NR, Romanoff J, Levinson AT, Chheng DB, Merchant RC, Levy MM, Napoli AM. Inferior vena cava collapsibility detects fluid responsiveness among spontaneously breathing critically-ill patients. Journal of critical care. 2017 Oct 1;41:130-7.
  3. Koratala A, Reisinger N. Venous excess doppler ultrasound for the nephrologist: Pearls and pitfalls. Kidney Medicine. 2022 May 19:100482.
  4. Beaubien-Souligny W, Rola P, Haycock K, Bouchard J, Lamarche Y, Spiegel R, Denault AY. Quantifying systemic congestion with point-of-care ultrasound: development of the venous excess ultrasound grading system. The Ultrasound Journal. 2020 Dec;12:1-2.
  5. Rola P, Miralles-Aguiar F, Argaiz E, Beaubien-Souligny W, Haycock K, Karimov T, Dinh VA, Spiegel R. Clinical applications of the venous excess ultrasound (VExUS) score: conceptual review and case series. The Ultrasound Journal. 2021 Dec;13(1):1-0.
  6. Mattoon JS, Berry CR, Nyland TG. Abdominal ultrasound scanning techniques. Small Animal Diagnostic Ultrasound-E-Book. 2014 Dec 2;94(6):93-112.
  7. Standardized method of abdominal ultrasound [Internet]. Japanese society of sonographers. [cited 2023Apr12]. Available from: https://www.jss.org/english/standard/abdominal.html#Longitudinal%20scanning_2
  8. Dinh V. POCUS101 Vexus ultrasound score–fluid overload and venous congestion assessment.
  9. Bhardwaj V, Vikneswaran G, Rola P, Raju S, Bhat RS, Jayakumar A, Alva A. Combination of inferior vena cava diameter, hepatic venous flow, and portal vein pulsatility index: venous excess ultrasound score (VExUS score) in predicting acute kidney injury in patients with cardiorenal syndrome: a prospective cohort study. Indian journal of critical care medicine: peer-reviewed, official publication of Indian Society of Critical Care Medicine. 2020 Sep;24(9):783.
  10. Varudo R, Pimenta I, Blanco JB, Gonzalez FA. Use of Venous Excess UltraSound (VExUS) score in hyponatraemia management in critically ill patient. BMJ Case Reports CP. 2022 Feb 1;15(2):e246995.
  11. Rolston D, Li T, Huang H, Johnson A, van Loveren K, Kearney E, Pettit D, Haverty J, Nelson M, Cohen A. 204 A Higher Initial VExUS Score Is Associated With Inferior Outcomes in Septic Emergency Department Patients. Annals of Emergency Medicine. 2021 Oct 1;78(4):S82.
  12. Guinot PG, Bahr PA, Andrei S, Popescu BA, Caruso V, Mertes PM, Berthoud V, Nguyen M, Bouhemad B. Doppler study of portal vein and renal venous velocity predict the appropriate fluid response to diuretic in ICU: a prospective observational echocardiographic evaluation. Critical Care. 2022 Dec;26(1):1-1.
  13. Menéndez‐Suso JJ, Rodríguez‐Álvarez D, Sánchez‐Martín M. Feasibility and Utility of the Venous Excess Ultrasound Score to Detect and Grade Central Venous Pressure Elevation in Critically Ill Children. Journal of Ultrasound in Medicine. 2023 Jan;42(1):211-20.
  14. Longino A, Martin K, Leyba K, Siegel G, Gill E, Douglas I, Burke J. Prospective Validation of the Venous Excess Ultrasound “(VExUS)” Score.

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Pediatric Hip Dislocation & Reduction

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Pediatric Hip Dislocation & Reduction

Resident Clinical Pearl (RCP) – November 2022

Dr. Nick Byers , R2 iFMEM, Dalhousie University, Saint John, New Brunswick

Reviewed/Edited by Dr. Brian Ramrattan

Case:
A 10 year old presents to the local emergency department after playing with their sibling. The child was “tackled” from behind. A history and physical exam inform you that the child has been healthy until now with a completely uneventful childhood. They are normal, healthy body habitus and laying on their right side, a pillow between their flexed left knee & hip, and straight right leg. This is the only position of comfort for the child. Neurovascular exam is normal and the child refuses to let you move the leg at all. Foot and ankle move normally. Xrays were obtained promptly. A dislocated hip was readily identified (note the arrow sign below).

Greater than 85% of traumatic pediatric hip dislocations are posterior. Male children are at a greater risk by a 4:1 ratio, and in younger patients, they often occur with minimal force, whereas older children tend to require much greater forces due to the strength of structures surrounding the joint. Fractures can be an associated injury, though it was not in this case. A general triad to consider when evaluating for posterior dislocation is an adducted, shortened, and internally rotated leg as seen below:

Treatment:

A simple dislocation should be treated with closed reduction under sedation, ideally within six hours of injury to reduce the risk of osteonecrosis of the femoral head.

Reduction techniques:

There are many reduction techniques discussed in the literature. Most involve in-line traction of the femur with abduction and external rotation as the leg lengthens, with counter-traction (or downward pressure) placed on the pelvis. This allows for the femoral head to enter the acetabulum gently.

A quick review of technique with attending staff present on shift included the following three options:

  1. The Allis maneuver (https://www.youtube.com/watch?v=zmk3vafjAd4): The physician stands on the stretcher with arms hooked under the flexed knee & hip (both at 90o) on the injured side and an assistant provides downward pressure on the pelvis. Hip extension and external rotation can be applied as the hip reduces.

2.  The Captain Morgan technique (https://www.youtube.com/watch?v=lQMWaFX-MeQ&t=6s): The physician flexes the injured hip and knee to 90o and places their foot on the stretcher at the injured hip of the patient, their knee under the patients. They then grasp the patient’s leg with one hand under the popliteal fossa and one at the ankle. With counter-traction/downward pressure on the pelvis by an assistant, the physician plantar-flexes their foot to put traction on the patient’s femur. External rotation and abduction can be applied with the lower leg as the hip is reduced.

3. The cannon technique: The stretcher is raised and the patient’s knee and hip are flexed to 90o with the popliteal fossa sitting directly over the physician’s shoulder, hands on the patient’s ankle (while facing the patients feet). An assistant stabilizes and provides downward pressure on the pelvis. The physician slowly stands up straight providing in-line traction on the femur until the hip is reduced.

Case Conclusion:

Once x-rays confirmed a posterior hip dislocation, closed reduction under sedation in the emergency department was performed by a resident and staff physician using the cannon technique. Post-reduction films and repeat neurovascular exams were normal and follow-up with orthopedics was in place before discharge home.

Post reduction film:

References:

https://www.merckmanuals.com/professional/injuries-poisoning/dislocations/hip-dislocations

https://www.emnote.org/emnotes/captain-morgan-hip-reduction-technique

CASTED course manual, Arun Sayal

Traumatic hip dislocation during childhood. A case report and review of the literature. American Journal of Orthopedics (Belle Mead, N.J.), 01 Sep 1996, 25(9):645-649

https://usmlepathslides.tumblr.com/post/64398003332/posterior-hip-dislocation-posterior-hip

https://posna.org/Physician-Education/Study-Guide/Hip-Dislocations-Traumatic

https://www.ochsnerjournal.org/content/18/3/242/tab-figures-data

https://coreem.net/core/hip-dislocation/

https://westjem.com/case-report/emergency-physician-reduction-of-pediatric-hip-dislocation.html

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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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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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A Summary of Bronchiolitis

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A Summary of Bronchiolitis: A review of bronchiolitis, evidence behind various treatment regimens, and suggested admission criteria – A Resident Clinical Pearl

 Melanie Johnston, R3

Integrated FMEM, Dalhousie

Reviewed by Dr. Patricia Dutton

Copyedited by Dr. Mandy Peach

Respiratory illnesses are the second most common ED presentation for paediatric patients, particularly during the winter months, in Canada. 1,2 These paediatric patients with respiratory pathologies are at risk of rapid clinical deterioration; a thorough history and exam with careful attention to respiratory evaluation is critical. Three of the most common paediatric respiratory complaints presenting to the ED include croup, asthma, and bronchiolitis. This pearl will focus on a review of bronchiolitis, its presentation, evaluation, and the evidence behind various treatments.

What is bronchiolitis:

Bronchiolitis is a viral lower respiratory tract infection. It is characterized by obstruction of small airways cause by acute inflammation, swelling/edema, and necrosis of the cells lining the small airways.2 Airways are further narrowed by increased mucous production. The most common causes are respiratory syncytial virus (RSV), influenza, rhinovirus, adenovirus, and parainfluenza.2 These viruses are transmitted by secretions from the nose/mouth and via respiratory droplets in the air. Co-infection with multiple viruses occurs in 10-30% of hospitalized children.2

Figure 1: Pathophysiology of Bronchiolitis.3

 

Epidemiology:
RSV season generally begins in November and persists until April. Bronchiolitis generally presents with a first episode of wheezing before the age of 24 months during the winter months.2 It is the most common reason for admission to hospital in the first year of life in Canada, and more than one-third of children will be affected by bronchiolitis in their first two years of life.2

Presentation:

Bronchiolitis may present with a wide range of symptoms from mild upper respiratory tract infection symptoms (cough, rhinorrhea, fever) to respiratory distress (tachypnea, wheeze, grunting, indrawing, abdominal breathing, and retractions).4 The peak severity of illness usually occurs on day 2-3 of the illness with resolution over 7-10 days.2,6 Cough can persist in infants for up to three weeks after onset.

Pediatric populations at risk for more serious illness include:
– Age <3 months
– Infants born prematurely (<35 weeks gestation)
– Chronic lung disease
– Congenital heart disease
– Chronic neurological conditions
– Immunodeficiency
– Trisomy 21

Patients with the above risk factors are at risk of rapid clinical deterioration even if presenting early in illness with mild symptoms.2,5

Diagnosis:


The diagnosis of bronchiolitis is considered to be clinical based on history and physical exam. The illness generally begins with a 2-3 day prodrome of mild URTI symptoms including cough, fever, rhinorrhea. This may progress to tachypnea, wheeze, and signs of respiratory distress.2 If respiratory distress is interfering with feeding, there may be signs of dehydration (delayed cap refill, dry mucous membranes, no tears produced with crying). Initial assessment should focus on overall appearance, breathing, and circulation. A tool to assist in establishing a general first impression of the paediatric patients stability is the paediatric assessment triangle. Abnormalities in any domain of the triangle (appearance, work of breathing, circulation) should be noted and factored into initial workup with potential to decompensate, with abnormalities in two domains indicative of potentially serious illness.

Figure 3: Pediatric Assessment Triangle.1

Signs of respiratory distress to note on exam include:

– Tachypnea
– Intercostal/subcostal retractions
– Accessory muscle use
– Nasal flaring
– Grunting
– Colour change or apnea
– Wheezing
– Low O2 saturation (<90%)

In stratifying the severity of illness in bronchiolitis, the Royal Children’s Hospital of Melbourne has proposed the following chart to assist with assessment:

Figure 4: Stratifying severity of illness in bronchiolitis, adapted from RCHM.5

Investigations

Bronchiolitis is considered to be a clinical diagnosis. As such, the majority of patients won’t require any additional investigations. If there is diagnostic uncertainty, then the following investigations may be considered:

Management:

Bronchiolitis is a self-limiting disease with peak severity generally at day 3-4 of illness.2,5,6 Most children have mild disease and can be managed with supportive care at home. For those ultimately admitted, focus in hospital is on supportive care with assisted feeding, nasal suctioning, and oxygen therapy as needed.

Disposition:

Most children do well and the symptoms will peak by day 3-5 of illness.

Criteria for safe discharge home include:
– O2 > 90-92%
– Adequate oral hydration
– Mild respiratory symptoms
– Access to reliable follow-up care if needed.2

Criteria for hospital admission include:

– Persistent oxygen saturation <92% and requiring supplemental oxygen AND/OR
– Unable to maintain oral hydration (fluid intake 50% of normal), requiring IV or NG fluids AND/OR
– Persistent moderate-severe respiratory distress
– Apnea (observed or reported)
– Children with risk factors for severe disease (see above).2

Admission or a period of observation in the ED can be used to document feeds and monitor vital signs/oxygen status. Other considerations for admission to hospital include social circumstances, comfort of caretaker in managing child at home, distance to healthcare facility in case of deterioration, and the phase of illness.

Resources:

1. Pediatric Respiratory Illnesses, Dr Allan Shefrin. Jan 30, 2020. Accessed at https://criticallevels.ca/2020/01/30/episode-3-paediatric-respiratory-illnesses-dr-allan-shefrin/

  1. Bronchiolitis: Recommendations for diagnosis, monitoring and management of children one to 24 months of age. Canadian Pediatric Society. Friendman, J., Rieder, M., Walton, J. et al. Nov 3, 2014. Accessed at https://emergencymedicinecases.com/wp-content/uploads/filebase/pdf/CPS-guidelines-bronchiolitis.pdf.3. Bronchiolitis. Cleveland Clinic. Accessed online at: https://my.clevelandclinic.org/health/diseases/8272-bronchiolitis
  2. Bronchiolitis, Bottom Line Recommendations. Trekk: Translating Emergency Knowledge for Kids. October 2020. Accessed online at: https://trekk.ca/system/assets/assets/attachments/502/original/2021-01-08-Bronchiolitis_v_3.0.pdf?16106625135. Bronchiolitis, Clinical Practice Guidelines. The Royal Children’s Hospital Melbourne. Accessed online at: https://www.rch.org.au/clinicalguide/guideline_index/Bronchiolitis/

    6. Bronchiolitis, Episode 59. Emergency Medicine Cases. Accessed online at https://emergencymedicinecases.com/episode-59-bronchiolitis/

    7. Bronchiolitis in children: diagnosis and management. NICE guideline. June 1, 2015. Accessed online at: https://www.nice.org.uk/guidance/ng9/resources/bronchiolitis-in-children-diagnosis-and-management-pdf-51048523717

    8. https://www.connectedcare.sickkids.ca/quick-hits/2019/8/29/volume6-efnk4-nyn48-max8h-rczlx (Pediatric assessment triangle)

    9. Bronchioitis, accessed online at: https://en.wikipedia.org/wiki/Bronchiolitis.

 

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A case of Herpetiform Keratitis- Clinical evaluation and important considerations.

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A case of Herpetiform Keratitis- Clinical evaluation and important considerations: A Resident Clinical Pearl

Bonnie He, PGY1

Ophthalmology, Dalhousie University

Reviewed by: Dr. Cherie Adams

Copyedited by: Dr. Mandy Peach

Case

A 68-year-old female presented to SJRH Emergency Department with a three-day history of atraumatic worsening of right eye pain, photophobia, and decreased vision. She denied any experience of flashing lights or “curtain falling”. She reported a long-standing history of glaucoma for which she was previously prescribed brimonidine (alpha-agonist) ophthalmic drops and was prescribed travoprost (prostaglandin) ophthalmic drops approximately one week prior to presentation. Additional ophthalmologic history revealed used of glasses, but not contact lenses, and bilateral cataract surgery two years previously. Of particular note, she recounted an episode of “sores from her upper lip along the side of her nose to right lower eyelid” in the past for which she was treated with oral valacyclovir. Further history positive for hypertension, for which she is prescribed ramipril, and type 2 diabetes mellitus, for which is is prescribed metformin. She is a retired schoolteacher, non-smoker, social drinker and denies any recreational drug use.
Visual acuity from 20 feet with spectacle correction revealed was 20/100 on the right (OD) and 20/30+1 on the left (OS). Her intraocular pressures were OD 17 and OS 19. Examination revealed mild upper and lower eyelid edema and moderate conjunctival injection. Fluorescein staining of the right cornea revealed four small dendritic epithelial defects (Figure 1) at about the 6 o’clock position. External and slit lamp examination of the left eye was normal. Fundoscopic examination to check the optic disc, macula, retinal vessels, and periphery were deferred.

Figure 1A: 4 small dendritic epithelial lesions can be seen at the 6’oclock position.

 

Figure 1B: Classic dendritic corneal epithelial lesions 17.

OPHTHALMOLGIC ASSSESSMENT:

Ocular complaints are common in emergency care settings. Yet, the quantity and quality of ophthalmology education varies significantly across Canada, with both medical students and residents report receiving insufficient ophthalmic medical education from medical education curricula.1-3
Proper history and physical examination taking skills are crucial to the appropriate management of patients with a red eye. The American Academy of Ophthalmology recommends the 8-point physical exam as a systematic approach to any eye problems:

  1. Visual acuity
    • Position the patient 20ft or 6m away from the Snellen chart to test for distance vision
    • Document whether it is their best corrected visual acuity, (ie. did they have their glasses or contact lens on at the time of the exam)
  2. Pupils
    • In dim room light, check for:
      1. Direct response by looking for pupil constriction in the eye being shined
      2. Consensual response by looking for pupil constriction in the other eye (eye that is not being shined)
  • Rapid Afferent Pupillary Defect (RAPD) with the swinging light test by shining light back and front between eyes
  1. Extraocular motility and alignment
    • Conduct a “H test” to test for the 9 cardinal positions of gaze by tracing out the letter “H” in the air while monitor their eyes for 3 S’s: speed, smoothness, and symmetry
    • Ask patient to follow your finger with their eyes while keeping their head still in the center and note for any double vision at certain gazes
  2. Intraocular pressure
    • The Icare tonometer requires no local anesthetic
    • Insert probe into tonometer and anchor the tonometer to the seated patient’s eyebrow.
    • Slowly bring tonometer probe towards patient light until the light turns green – now you’re ready to press the button that will automatically measure the patient’s intraocular pressure
  3. Confrontation visual fields
    • At about 1 arm’s-length away, test each eye individually by holding up 1 or 2 fingers and ask patient how many fingers they see
    • Ask patient to close their OS and fixate on your nose. Close your OS to assess with your open OD.
    • To check OS, ask the patient to close their OD and fixate on your nose. Close your OD to assess with your open OS.
  4. External examination
    • Assess for any obvious globe rupture, ecchymoses, deformities or lesions around the eye
    • Check to see if there’s any ptosis (lid drooping)
  5. Slit lamp examination (watch this video to learn how to perform a slit lamp exam: https://www.youtube.com/watch?v=gHW5OYj1Gf8
    • Assess for the following structures
    • Lids/lashes/lacrimal system: edema, erythema, lesions
    • Conjunctiva/sclera: injection, subconjunctival hemorrhage
    • Cornea: foreign body, fluorescein stain + cobalt blue light to assess corneal integrity (ie. corneal abrasions, herpetic dendrites), Seidel test (leakage of aqueous humour)
    • Iris: round (normal) vs. peaked (abnormal)
    • Anterior chamber: any hyphema, hypopyon, cells, flare
    • Lens: opacity
  6. Fundoscopic examination
    • In the emergency department, fundoscopy is typically undertaken in the undilated eye.
    • May consider dilating the eye with tropicamide (dilating drop) to visualize the back of the eye with the slit lamp or direct ophthalmoscope
    • Assess for the following structures:
      1. Optic nerve: cup-to-disc ratio, pallor, symmetry between eyes
      2. Macula: foveal light reflex
  • Vessels: Arteriovenous (AV) nicking, silver or copper wiring,
  1. Periphery: bleeding

DISCUSSION:

Given the patient’s endorsed history suggestive of ipsilateral V2 herpes zoster and classic dendritic corneal lesions, the leading differential diagnosis for her acute on chronic ocular pain in this case would be zoster keratitis, though herpes keratitis should also be considered, particularly in patients with identified history and recent episode of orolabial cutaneous HSV. Interestingly, she was started on travoprost for her glaucoma a week prior to her presentation. Topical ocular hypotensive agents, including travoprost, are known to have a myriad local and systemic side effects including: superficial punctate keratitis, corneal erosion, bradycardia, hypotension, and bronchoconstriction, are common.4,5 However, of particular interest in this case,  multiple clinical and animal studies have reported that topical prostaglandins for ocular hypertension are culprits  associated with herpes simplex virus (HSV) keratitis or varicella-zoster virus (VZV) keratitis.6-13 It is thought that prostaglandin analogues such as travaprost may induce the reactivation of HSV keratitis by releasing endogenous prostaglandins in the iris and ciliary muscles.9,14-16 Therefore it could also be very well possible that she may have developed HSV keratitis.

 

Irrespective of which differential was truly causing this patient’s symptoms the antiviral treatment for zoster ophthalmicus and HSV keratitis are the same: valocylcovir 1g TID PO x 7 days (or acyclovir 800mg po five times daily if cost of valcyclovir is prohibitive) and arrangements were made for next-day ophthalmologist consultation.

 

BOTTOM LINE:

Always take a thorough ophthalmologic history for patients with ocular complaints, including complete medication history.

Always ask about contact lens use in a history in any patient with a painful red eye.

Always conduct a complete physical exam for patients with ophthalmologic complaints using the AAO 8-point framework described above.


REFERENCES

  1. Sim D, Hussain A, Tebbal A, Daly S, Pringle E, Ionides A. National survey of the management of eye emergencies in the accident and emergency departments by senior house officers: 10 years on—has anything changed? Emerg Med J. 2008;25(2):76-77. http://emj.bmj.com/content/25/2/76.abstract. doi:10.1136/emj.2007.049999.
  2. Noble J, Somal K, Gill HS, Lam W. An analysis of undergraduate ophthalmology training in Canada. Canadian Journal of Ophthalmology. 2009;44(5):513-518. http://www.sciencedirect.com/science/article/pii/S0008418209801130. doi:https://doi.org/10.3129/i09-127.
  3. Gostimir M, Sharma RA, Bhatti A. Status of Canadian undergraduate medical education in ophthalmology. Canadian Journal of Ophthalmology. 2018;53(5):474-479. http://www.sciencedirect.com.ezproxy.library.ubc.ca/science/article/pii/S0008418216309553. doi:https://doi-org.ezproxy.library.ubc.ca/10.1016/j.jcjo.2017.11.015.
  4. Inoue K. Managing adverse effects of glaucoma medications. Clinical ophthalmology (Auckland, N.Z.). 2014;8:903-913. https://pubmed.ncbi.nlm.nih.gov/24872675 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4025938/. doi:10.2147/OPTH.S44708.
  5. Anwar Z, Wellik SR, Galor A. Glaucoma therapy and ocular surface disease: current literature and recommendations. Curr Opin Ophthalmol. 2013;24(2):136-143. doi:10.1097/ICU.0b013e32835c8aba [doi].
  6. Kroll DM, Schuman JS. Reactivation of herpes simplex virus keratitis after initiating bimatoprost treatment for glaucoma. Am J Ophthalmol. 2002;133(3):401-403. doi:S0002939401013605 [pii].
  7. Wand M, Gilbert CM, Liesegang TJ. Latanoprost and herpes simplex keratitis. Am J Ophthalmol. 1999;127(5):602-604. doi:S0002939499000501 [pii].
  8. Alm A, Grierson I, Shields MB. Side effects associated with prostaglandin analog therapy. Surv Ophthalmol. 2008;53 Suppl1:93. doi:10.1016/j.survophthal.2008.08.004 [doi].
  9. Soomro MZ, Moin M, Attaulla I. Latanoprost and Herpetic Keratitis. Pakistan Journal of Ophthalmology. 2011;27(4).
  10. Kothari MT, Mehta BK, Asher NS, Kothari KJ. Recurrence of bilateral herpes simplex virus keratitis following bimatoprost use. Indian J Ophthalmol. 2006;54(1):47-48. doi:10.4103/0301-4738.21617 [doi].
  11. Ekatomatis P. Herpes simplex dendritic keratitis after treatment with latanoprost for primary open angle glaucoma. Br J Ophthalmol. 2001;85(8):1008-1009. doi:10.1136/bjo.85.8.1007a [doi].
  12. Morales J, Shihab ZM, Brown SM, Hodges MR. Herpes simplex virus dermatitis in patients using latanoprost. Am J Ophthalmol. 2001;132(1):114-116. doi:S0002939401010121 [pii].
  13. Villegas VM, Diaz L, Izquierdo NJ. Herpetic keratitis in a patient who used two different prostaglandin analogue ophthalmic solutions: a case report. P R Health Sci J. 2008;27:348+. https://link.gale.com/apps/doc/A189052227/HRCA?u=anon~6a050068&sid=googleScholar&xid=2c140d29.
  14. Dios Castro E, Maquet Dusart JA. Latanoprost-associated recurrent herpes simplex keratitis. Arch Soc Esp Oftalmol. 2000;75(11):775-778.
  15. Gordon YJ, Yates KA, Mah FS, Romanowski EG. The effects of Xalatan on the recovery of ocular herpes simplex virus type 1 (HSV-1) in the induced reactivation and spontaneous shedding rabbit models. J Ocul Pharmacol Ther. 2003;19(3):233-245. doi:10.1089/108076803321908356 [doi].
  16. Kaufman HE, Varnell ED, Toshida H, Kanai A, Thompson HW, Bazan NG. Effects of topical unoprostone and latanoprost on acute and recurrent herpetic keratitis in the rabbit. Am J Ophthalmol. 2001;131(5):643-646. doi:S0002939400009107 [pii].
  17. Yu, Hubert (2019) Canadiem Medical Concepts: Approach to Corneal Disorders in the ED

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Cunningham Technique for dislocated shoulder reduction

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Cunningham Technique for dislocated shoulder reduction: A Resident Clinical Pearl

Rebecca Fournier, PGY1 

Family Medicine, Dalhousie University

Reviewed by Dr. Chris Doiron

Copyedited by Dr. Mandy Peach

Case

38yo woman presenting with right shoulder pain after falling on ice. Unable to adduct right arm across body. Pain is minimal when resting quietly. Xray confirms anterior dislocation. You recently read about a sedation sparing technique to reduce her shoulder and decide to attempt it.

The Cunningham technique has been shown to be an effective and simple method to reduce a dislocated shoulder. The technique is based on the theory that the humeral head remains outside the glenoid fossa due to tension in the muscles surrounding the shoulder, primarily the biceps. Without the use of sedation or analgesia, the Cunningham technique relaxes the muscles to encourage self reduction. When used as the first technique of choice, Puha et al (2016) found a success rate of 76.9 compared to more traditional methods at 87%+. However, attempting Cunningham technique first allowed avoidance of sedation and was not found to increase pain or duration of hospital stay.

Cunningham Technique

A. Patient Selection and Preparation

1. Ideal patient is calm, in minimal pain, able to take direction, understands and willing to participate in procedure.
2. May consider Ativan 0.5 to 1 mg prior to procedure with goal for calm, thoughtful patient able to participate in the reduction. In most cases, Ativan is not required for a successful reduction

B. Patient position

1. Performed with awake, seated patient. Encourage good posture to maximize success
2. Patient and examiner sit opposite one another eye to eye
3. Patients arm position

a. Held adducted at side: critical to success, may be limiting if patient uncomfortable in this position or body habitus restricts adduction at the side.
b. Elbow flexed to 90 degrees

4. Examiner position
a. Examiner rests one hand firmly on top of the patient’s dorsal forearm, applying downward pressure
b. Opposite hand will perform massage aspect of technique

C. Technique
1. Examiner applies gentle, steady pressure downward on dorsal forearm
2. With free hand, examiner massages upper extremity proximal muscles

a. Start at deltoid and trapezius
b. Move distally to biceps and triceps

3. As the patient’s musculature begins to relax, some may experience apprehension.

a. Patient positioning: an awake, seated patient. Encourage good posture with shoulders up and back + chest pushed forward to maximize success.

b. Gently reassure patient that this sensation indicates progress and continued relaxation is key to success
c. Premedication with Ativan prior to procedure may additionally facilitate this transition

4. Anticipate Shoulder to spontaneously relocate

a. May take as long as 15 minutes to relocate
b. Often times an audible “clunk” is not heard, check often to verify if reduction has been successful

5. Confirm reduction with post procedure xray

Take away points:

– Requires no sedation (requires awake patient!) or analgesia
– Pick the right patient! Must be calm, able to take direction, willing to participate, and trust provider
– Attempting Cunningham procedure first avoids risks of sedation and analgesia without increasing length of stay
– Cunningham method is all about positioning and relaxation; let the humeral head find its way back to the glenoid. Check out the videos for a step by step by visual.
– Confirm reduction with post procedure xray

 

References

Gudmundsson TH, Bjornsson HM. [Reduction of shoulder dislocation with the Cunningham method]. Laeknabladid. 2017 Sep;103(9):373-376. Icelandic. doi: 10.17992/lbl.2017.09.150. PMID: 29044033.

Puha B, Gheorghevici TS, Veliceasa B, Popescu D, Alexa O. CLASIC VERSUS NOVEL IN REDUCTION OF ACUTE ANTERIOR DISLOCATION OF THE SHOULDER: A COMPARISON OF FOUR REDUCTION TECHNIQUES. Rev Med Chir Soc Med Nat Iasi. 2016 Apr-Jun;120(2):311-5. PMID: 27483710

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A Peanut Problem or Pimple Popper Predicament

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 A Peanut Problem or Pimple Popper Predicament – A Resident Clinical Pearl

Grace Dao PGY1

Family Medicine, Dalhousie University

Saint John, NB

Reviewed by: Dr. Chris Vaillancourt

Copyedited by: Dr. Mandy Peach

 

Case Presentation

A 30-year-old otherwise healthy female presented to the ED with concerns about an “allergic reaction” to peanut butter. She reported that she woke 30 minutes prior to her presentation in the ED with a severely swollen red and disfigured lip. Her face had looked normal upon going to bed the evening prior. Her last meal was a peanut butter sandwich, which she eats frequently without difficulty. She described having some “wheezes” and “chest tightness” to the triage RN. When seen by writer, she denied any trouble breathing. She denied any issues the night prior before going to bed. She denied any GI upset, such as cramping, nausea, vomiting or diarrhea. Besides the swollen lip, she denied noticing any other skin changes; she denied any itchy sensation. Past medical history was unremarkable; she had no history of prior allergic reaction and no known allergies. She took no medications. Review of systems was negative, besides she noted that there was pimple at the base of her nose that she had “popped” yesterday.

On exam, all vitals were within normal limits besides a HR of 110. Respiratory exam revealed no obvious stridor or increased work of breathing; there was no swelling of the tongue or uvula on inspection of the mouth, clear air entry and exit were appreciated bilaterally. A faint wheeze was appreciated bilaterally. Cardiovascular and abdominal examinations were within normal limits. A skin exam revealed a diffusely red and swollen upper lip, with skin the above the vermillion border also showing swelling and redness. Increased erythema/pus at the R nostril sill was appreciated in the area of the previously popped pimple. The lip was tender and very warm to the touch.

With 2 system involvement (lip swelling and wheezes on respiratory exam); she was treated as anaphylaxis initially and given 0.5 mg Epinephrine IM, which did not lead to any change in her symptoms. However, it would be quite unusual for an IgE mediated reaction to present this late after ingestion. A peanut allergy especially, as most of these present before age 3.

Initial bloodwork showed a normal CBC, Cr and electrolytes. CRP was elevated at 67.1. Due to no change in symptoms with anaphylaxis treatment and concerns re an infectious etiology a CT facial bones was ordered after discussion with the radiologist on call. CT report showed a broad zone of cellulitis with an evolving central abscess. ENT was consulted who reported that incision and drainage was required, and that the infection likely came from the popped pimple. They performed an incision and drainage of the abscess in the ED, took wound cultures and started empiric antibiotics, and arranged for outpatient follow-up. In discussion with the ENT, it was noted that this presentation is typical of CA-MRSA cellulitis, and, thus, antibiotics to cover MSRA were required.

Anaphylaxis

While not the outcome in this case, it is important to be familiar with the various constellation of symptoms/signs that make anaphylaxis a likely and the initial management of this “can’t miss” diagnosis, which are outlined in the included figures1,2.

Lip Cellulitis and Abscess

Interestingly, after this case, a case study of a similar presentation was found in the literature where a MRSA lip infection was initially misdiagnosed as angioedema/anaphylaxis3. The diagnosis was discovered later, after the patient was unresponsive to anaphylaxis treatment and a history of a popping a pimple on their chin the day prior was elicited. Because Methicillin-resistant Staphylococcus aureus (MRSA) soft tissue infection also has a characteristic presentation of erythema, edema, and often, areas of fluctuance it can have a similar appearance to the typical angioedema that can be found in anaphylaxis.

See Reference 3. This CT was performed after incision and drainage; thus, no abscess is appreciated

While it is important to be vigilant towards the presentation of anaphylaxis, cellulitis is another diagnosis that it important not to miss4. Like other infections, complications of cellulitis include bacteremia, endocarditis, septic arthritis, osteomyelitis, metastatic infection, sepsis and toxic shock syndrome.  In patients with suspected erysipelas or cellulitis it is important to consider the possibility of an abscess, which requires incision and drainage. Findings in keeping with a skin abscess would be a painful, erythematous, fluctuant nodule.

The central face is not the most common area to develop cellulitis; however, it is an important area to recognize cellulitis. Untreated cellulitis in this area, can lead to septic cavernous thrombosis because the veins in this region are valveless.

Other diagnoses to consider for angioedema without history consistent with IgE mediated reaction or infection:

  1. Hereditary or acquired angioedema
  2. Mast cell disorder
  3. Idiopathic angioedema

 

Bottom Line: Always consider anaphylaxis in someone with apparent lip angioedema. However, it is also important to keep infection on the differential for a swollen lip, particularly if symptoms are not responding to therapy. Asking about prior injuries/skin lesions in the previous days can help clarify likelihood of infection. Also, as a personal takeaway, I should probably stop popping pimples.

References:

  1. Sampson, H. A. , Munoz-Furlong A., Campbell, R.L., et al. (2016). Second symposium on the definition and management of anaphylaxis: Summary report: Second National Institute of Allergy and Infectious Disease/Food Allergy and Anaphylaxis Network Symposium. J Allergy Clin Immunol 2006; 117:391. https://doi.org/10.1016/j.jaci.2005.12.1303
  2. Campbell, R.L. & Kelso, J.M. (2021). Anaphylaxis: Acute diagnosis. UpToDate. Retrieved December 30th, 2021 from : https://www.uptodate.com/contents/anaphylaxis-acute-diagnosis?search=anaphylaxis&topicRef=392&source=see_link#H1929228973
  3. Lucerna, A. R., Espinosa, J., & Darlington, A.M. (2015). Methicillin-resistant Staphylococcus Aureus Lip Infection Mimicking Angioedema. The Journal of Emergency Medicine 49 (1), 8-11 https://doi.org/10.1016/j.jemermed.2014.12.022.
  4. Spelman, D. & Baddour, L.M. (2021). Cellulitis and skin abscess: Epidemiology, microbiology, clinical manifestations, and diagnosis. UpToDate. Retrieved January 2nd, 2022 from: https://www.uptodate.com/contents/cellulitis-and-skin-abscess-epidemiology-microbiology-clinical-manifestations-and-diagnosis?search=cellulitis%20&source=search_result&selectedTitle=3~150&usage_type=default&display_rank=2#H1368100182

Cover image from: https://www.uptodate.com/contents/an-overview-of-angioedema-clinical-features-diagnosis-and-management?search=angioedema&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1

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Quadriceps Tendon Rupture

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Quadriceps Tendon Rupture – A Resident Clinical Pearl

Ida Szarics, PGY2

Dalhousie University

Reviewed by Dr. Paul Keyes

Copyedited by Dr. Mandy Peach

A 52 year old male presents to the ED with a right knee injury. He slipped while running, landing awkwardly on his right knee, with his foot caught behind him. He felt a “pop” and immediately had severe sharp right knee pain. He was unable to weight bear and states that his knee was swollen immediately afterwards. He denies any other injuries. He is otherwise healthy and is on no medications.

On exam, his vitals are within normal limits. There is obvious swelling of the right knee and has a palpable defect 2 cm above the patella which is extremely tender to palpation. He is unable to perform a straight leg raise. The remainder of the knee exam is non-contributory and he is neurovascularly intact.

He is clinically diagnosed with a quadriceps tendon rupture.

Above: Patients with complete quadriceps tendon ruptures will often present with a palpable defect within 2 cm above the patella. Image from: https://coreem.net/core/quadriceps-tendon-rupture/

 

Quadriceps tendon rupture: Mechanism

Quadriceps are the knee extensors, therefore rupture is most likely when the knee is flexed with simultaneous quadriceps contraction.1

-Age <40: Less common. Often occurs in athletes, particularly those who do not stretch activity, as a result of jumping and landing with the knee flexed. Patellar tendon rupture is more common in this age group

-Age >40: More common. Weaker tendons rupture more easily, so a fall onto a knee, or trying to prevent a fall onto the knees is typical.

 

Risk factors,2, 3

-Age (more common in patients >40 years of age)

-Male gender

-Type 2 Diabetes

-Renal disease

-Medications associated with tendon rupture (fluoroquinolones)

 

ABOVE: Anatomy of the muscles of the anterior thigh. Quadriceps tendon ruptures typically happen at the tendon’s insertion at the patella. Source: https://www.physio-pedia.com/Quadriceps_Tendon_Tear

 

Diagnosis

-Typically a clinical diagnosis, and is one of the “cannot miss diagnosis” in acute knee injuries.

-There is often a palpable defect ~2 cm above the patella where the tendon has been torn.

-Patients with a complete tear will be unable to perform a straight leg raise.

-Patients with a partial tear are unable to extend their knee against resistance – the ability to forcibly extend the knee against resistance is a critical part of the knee exam.

Investigations

XRays:

-May show a patella that is below expected anatomic position (patella baja). Of note, patella alta (or high-riding patella) can be a sign of patellar tendon rupture.

Ultrasound

-Can be a useful modality if diagnosis is uncertain. Often primary investigation available in the ED to supplement clinical exam findings.

MRI

-Best diagnostic modality, but cannot be obtained in the ED – this is typically a modality ordered by surgeons for surgical planning

ABOVE: Normal Knee XRay (left) and low-riding patella (right). The Insall Salvatti Index is the ratio of the patellar tendon length (red line) to the patellar length (yellow line). Normal is 0.8-1.2. Source: https://radiopaedia.org/articles/insall-salvati-ratio

 

Management

-Early surgical repair is important to maximize recovery, especially in complete tears. The distal tendon is avascular, so it will not heal well non-operatively.1

-Non-operative treatment (RICE, splinting, non-weightbearing) may be an option in partial tears or in patients with poor baseline mobility.

-Either way, orthopedic surgery should be consulted within a timely matter, usually within a week, to guide management. As time goes on difficulty of repair increases, as does probability of failed repair.  The ED physician should provide adequate analgesia as needed, immobilize the knee, and advise non-weightbearing while the patient is in the ED.

Back to our patient

Orthopedic surgery is contacted, and a plan is made to see the patient in clinic the following day to plan surgical repair. The patient’s knee is immobilized in extension, and an outpatient MRI is ordered. The patient undergoes surgical repair later that week.

References:

1Sharareh, Ben. (2021). Quadriceps Tendon Rupture. Orthobullets. https://www.orthobullets.com/knee-and-sports/3023/quadriceps-tendon-rupture

2 Von Fange, T.J., (last updated, 2021). Quadriceps Tendon and Muscle Injuries. UpToDate.

3 Nori, S., (2018) Quadriceps tendon rupture. J Family Med Prim Care. 7(1): 257–260.

 

 

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