An interesting derm case in the ED: Mycosis Fungoides

Mycosis Fungoides: A Medical Student Clinical Pearl

 

Nicholas Relja, B.Sc.(Hon), M.Sc.
Dalhousie Medicine New Brunswick
M.D. Candidate, Class of 2022

All case histories are illustrative and not based on any individual

Reviewed by Dr. Devon Webster

Copyedited by Dr. Mandy Peach

Case

A 55-year-old male presented to the ED after concerned family brought him in due to ongoing generalized weakness lasting approximately one month. On inspection he had erythematous, scaly, ulcerative lesions covering his entire body with only facial sparing. He mentioned burning-like pain originating from his ulcerative lesions. He had been previously diagnosed with T-cell lymphoma 30 years ago and had gone through multiple rounds of chemo and radiation therapy since that time.

Picture from: Denis D, Beneton N, Laribi K, Maillard H (2019). Management of mycosis fungoides-type cutaneous T-cell lymphoma (MF-CTCL): focus on chlormethine gel. Cancer Management and Research. Vol 11: 2241-2251

Differential for itchy, erythematous rash:

Condition
Atopic dermatitis
Contact dermatitis
Drug eruptions
Erythrodermic psoriasis
Psoriasis
Sezary syndrome
Various lymphomas

 

When reviewing the patient’s past medical history you see they were previously diagnosed with Mycosis Fungoides – a rare cutaneous form of T-cell lymphoma.

Epidemiology

Mycosis fungoides has an incidence of approximately 6 cases per million per year in the United States. It is more common in adults over 50 years of age, with a male to female ratio of 2:1. The disease is also more common amongst the Black population than in Caucasians or Asians.8,9

Etiology

The exact cause of mycosis fungoides is not known; however, there a variety of mechanisms that have been postulated:2

• Genetic and epigenetic abnormalities.3,4
• Environmental and occupational exposure to noxious substances and chemicals.5
• Human T-lymphotropic virus Type 1 – a suspected infection-type etiology.6
• Cytokines such as IL-2 and IL-4 due to their increased presence in patients with mycosis fungoides and Sezary syndrome.7

 

There are three stages of mycosis fungoides and therefore clinical presentation will vary depending on the stage of disease:

Patch stage: Erythematous, or brownish scaly patch, which may show some atrophy. It is possible to have one or multiple lesions develop in areas such as the gluteal region or on the proximal thighs. The likeness of this stage has been compared to “small-plaque” or “large plaque” parapsoriasis; however, the plaques are actually not plaques but patches instead.10

Plaque stage: This is the second stage – lesions will be larger, more numerous and will show infiltration. The lesions appear annular, are raised and have well-defined edges as well as asymmetry in terms of their distribution. Face and scalp involvement can also be seen starting at this stage.11

Tumor stage: The final stage – erythematous-purplish papules or nodules of larger diameter.12

There are other clinical variants of mycosis fungoides, but they are not as common, and some are quite rare.

Sezary syndrome:
In advanced form of the mycosis fungoides, Sezary syndrome may be present. This syndrome involves erythroderma with pruritus, lymphadenopathy and atypical circulating lymphocytes (referred to as Sezary or Lutzner cells).13

Evaluation in the ED

A detailed history and physical exam including checking for lymphadenopathy (most commonly cervical nodes) and organomegaly14,15 in addition to documenting the rash characteristics.

Labs: CBC, liver function tests, LDH

Radiological tests: depends on extent of lymphadenopathy and organomegaly. Can do a CXR in the ED for lung involvement, but otherwise advanced imaging can be decided upon by specialist consultant and may include CT, US, PET or MRI.

Biopsy: lymph nodes and rash – by consultants

Treatment and Management – refer to your friendly neighborhood dermatologist.

Early stage:

Treatment options include topical therapies such as corticosteroids and other agents, UV therapy, local radiation and systemic immunosuppressants 15,16,17.

Advanced Stage:

Treatment for the advanced stages of mycosis fungoides are directed at disease control and symptom relief. Localized radiation, targeted immunotherapy or chemotherapy. 15, 18

Prognosis

The prognosis of mycosis fungoides is variable but in general as the stage gets more advanced and with patients over the age of 60, the prognosis becomes poorer. Other poor prognostic factors include increased LDH, tumor distribution and organ involvement.2

Case Conclusion

The patient seen in hospital by the dermatologist on call and was deemed to be in the plaque stage. He was admitted due to the advancing course and and inability to manage his symptoms from home. Further care will involve palliation and a focus on quality of life.

 

References:

  1. Olisova, O. Y. et al. [Current possibilities of the differential diagnosis of plaque parapsoriasis and the early stages of mycosis fungoides]. Arkh. Patol. 81, 9–17 (2019).
  2. Lim, H. L. J. et al. Epidemiology and prognostic factors for mycosis fungoides and Sézary syndrome in a multi-ethnic Asian cohort: a 12-year review. J. Eur. Acad. Dermatol. Venereol. JEADV 33, 1513–1521 (2019).
  3. Bergallo, M. et al. DNA from Human Polyomaviruses, MWPyV, HPyV6, HPyV7, HPyV9 and HPyV12 in Cutaneous T-cell Lymphomas. Anticancer Res. 38, 4111–4114 (2018).
  4. Väisänen, E. et al. Cutavirus DNA in Malignant and Nonmalignant Skin of Cutaneous T-Cell Lymphoma and Organ Transplant Patients but Not of Healthy Adults. Clin. Infect. Dis. Off. Publ. Infect. Dis. Soc. Am. 68, 1904–1910 (2019).
  5. Slodownik, D., Moshe, S., Sprecher, E. & Goldberg, I. Occupational mycosis fungoides – a case series. Int. J. Dermatol. 56, 733–737 (2017).
  6. Blaizot, R., Ouattara, E., Fauconneau, A., Beylot-Barry, M. & Pham-Ledard, A. Infectious events and associated risk factors in mycosis fungoides/Sézary syndrome: a retrospective cohort study. Br. J. Dermatol. 179, 1322–1328 (2018).
  7. Fujii, K. New Therapies and Immunological Findings in Cutaneous T-Cell Lymphoma. Front. Oncol. 8, 198 (2018).
  8. Amorim, G. M., Niemeyer-Corbellini, J. P., Quintella, D. C., Cuzzi, T. & Ramos-E-Silva, M. Clinical and epidemiological profile of patients with early stage mycosis fungoides. An. Bras. Dermatol. 93, 546–552 (2018).
  9. Amorim, G. M., Niemeyer-Corbellini, J. P., Quintella, D. C., Cuzzi, T. & Ramos-E-Silva, M. Hypopigmented mycosis fungoides: a 20-case retrospective series. Int. J. Dermatol. 57, 306–312 (2018).
  10. Pimpinelli, N. et al. Defining early mycosis fungoides. J. Am. Acad. Dermatol. 53, 1053–1063 (2005).
  11. Burg, G., Dummer, R., Nestle, F. O., Doebbeling, U. & Haeffner, A. Cutaneous lymphomas consist of a spectrum of nosologically different entities including mycosis fungoides and small plaque parapsoriasis. Arch. Dermatol. 132, 567–572 (1996).
  12. Keehn, C. A., Belongie, I. P., Shistik, G., Fenske, N. A. & Glass, L. F. The diagnosis, staging, and treatment options for mycosis fungoides. Cancer Control J. Moffitt Cancer Cent. 14, 102–111 (2007).
  13. Lopez, A. T., Bates, S. & Geskin, L. Current Status of HDAC Inhibitors in Cutaneous T-cell Lymphoma. Am. J. Clin. Dermatol. 19, 805–819 (2018).
  14. Prince, H. M. & Querfeld, C. Integrating novel systemic therapies for the treatment of mycosis fungoides and Sézary syndrome. Best Pract. Res. Clin. Haematol. 31, 322–335 (2018).
  15. Wain, T., Venning, V. L., Consuegra, G., Fernandez-Peñas, P. & Wells, J. Management of cutaneous T-cell lymphomas: Established and emergent therapies. Australas. J. Dermatol. 60, 200–208 (2019).
  16. Dairi, M., Dadban, A., Arnault, J.-P., Lok, C. & Chaby, G. Localized mycosis fungoides treated with laser-assisted photodynamic therapy: a case series. Clin. Exp. Dermatol. 44, 930–932 (2019).
  17. Photiou, L., van der Weyden, C., McCormack, C. & Miles Prince, H. Systemic Treatment Options for Advanced-Stage Mycosis Fungoides and Sézary Syndrome. Curr. Oncol. Rep. 20, 32 (2018).
  18. Alpdogan, O., Kartan, S., Johnson, W., Sokol, K. & Porcu, P. Systemic therapy of cutaneous T-cell lymphoma (CTCL). Chin. Clin. Oncol. 8, 10 (2019).

 

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EM Reflections January 2021: TIA Review

 

Big thanks to Dr. Paul Page for leading discussions this month.

All cases are theoretical, but highlight important discussion points.

Authored and Edited by Dr. Mandy Peach

Case

A 69 yo male presents to the ED with dizziness that was ongoing 1 hour. His symptoms began when getting up from the couch and walking to the kitchen. He felt like he was going to ‘pass out’ and ‘couldn’t walk straight’. He also describes having a headache that began around the same time, but says he has headaches from time to time and wasn’t bothered by it. After 1 hour of feeling dizzy and off balance he called EMS. His symptoms resolved en route with EMS in the ambulance.

His vitals in triage are: 128/64, HR 89, RR 16 O2 95% on RA, T 36.3 Glucose 15

The nurse hands you his medication list and ECG

The ECG indicates atrial fibrillation. This is new from his previous ECG. His medications include ramipril, metformin and atorvastatin.

You suspect a transient ischemic attack (TIA), but what other mimics are on the differential1?

 

What are some important causes of TIA to consider? What features make TIA more likely1?

You feel your patient’s abrupt inability to walk straight certainly qualifies as lack of function. The onset was abrupt and symptoms have resolved. Your patient also has new atrial fibrillation, putting them at risk.

What if the patient didn’t have new atrial fibrillation? What other symptoms/features on clinical exam could suggest an alternative cause1?

Think “TIA and”…

TIA and neck pain: cervical artery dissection

TIA and new fever or heart murmur: endocarditis

You complete your physical exam. The patient is neurologically normal including cranial nerves, motor, sensory, reflexes, cerebellar, and gait. There is no new murmur, fever or neck pain. The patient has new a fib of unknown duration that is not anticoagulated. You suspect this is the cause.

Although the patient is normal now, you do wonder if they had objective signs initially with EMS, or with the first nursing assessment. As neuros can change so quickly you review the other documented exams

Of note EMS reports a GCS of 15 and the following description of symptoms:

“off balance, requiring support to walk”

“noticeable trouble speaking with slurred speech”

“patient reports feeling dizzy”.

The symptoms resolved en route. The patient walked unassisted from the ambulance bay to triage.

Nursing notes document a normal neuro exam in triage.

Is there a timeline involved in diagnosis TIA2?

TIA is now defined as a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction. The end point, stroke, is biologic (tissue injury) rather than an arbitrary timeline (≥24 hours).

Although the patient is now neurologically normal, this episode is a big red flag for stroke. To determine how urgent a work up is needed you decide to stratify the patient’s risk of stroke. The ABCD2 score likely comes to mind:

 

Is this tool accurate at predicting stroke3?

With the ABCD2 score physicians may misclassify up to 8% of patients as low risk. The sensitivity of the score for high risk patients was found to be only 31.6%3. This score also does not take into account neuroimaging findings – one study found up to 15% of patient’s with high grade carotid stenosis would be missed by using the ABCD2 score. Lastly an Australian study that used the ABCD2 score with ED patients all reported similar rates of strokes at the 30 and 90 day follow up, regardless of stratification using this tool.

Bottom line – ABCD2 is out.

So is there any tool I can use to predict risk of stroke4?

The Canadian TIA Score

This score was initially studied prospectively in over 7500 adult patients diagnosed with TIA in the ED or by a neurologist. The primary outcome was subsequent stroke in 7 days or prompt emergency carotid endarterectomy (CEA) to prevent stroke in less than 7 days. 1.4% of patients had a stroke and 1.0% had CEA in less than 7 days.

The score has recently been validated and is ready for clinical use8.

This score classifies patients as:

LOW risk: -3 to 3 points. Safely discharge following careful ED assessment with elective follow up

MEDIUM risk: 4-8 points. Undergo additional testing in the ED, have antithrombotic therapy optimized, be offered early stroke/neuro follow up

HIGH risk: ≥ 9 points. Fully investigate and manage ideally in consultation with a stroke specialist during the first ED visit.

Your patient is already at medium risk, before imaging is acquired. According to this tool your patient should be investigated with labs and imaging in the ED and offered urgent neuro follow up.

The acute nurse reminds you that it is 2330 and the CT tech leaves at midnight. You need to arrange urgent imaging – but what should you order6?

CT-angiography can be done at timing of non contrast CT and is the standard of care in neurovascular disease. It is well established that there is an association between vascular occlusion or high grade stenotic vessels and stroke recurrency and disability.

Angiography will show high grade stenotic lesions that are amendable to endarterectomy, as well as identify carotid or vertebral artery dissection as an alternative cause.

In high risk patients, CT-A should be the go to. This is based on Canadian Stroke Best Practice Guidelines.

 

Based on the Canadian TIA score my patient is medium risk. Could they still benefit from CT-A?

The Canadian TIA Score is not yet integrated with Stroke Management. According to Best Practice Guidelines high risk features are considered to be:

This patient had transient speech deficit – consider this a high risk feature and get a CT-A in your work up in the department.
You discuss this with your radiologist who agrees a CT-A is warranted.

Luckily a consultant neurologist is also on call and in house dealing with a patient in the neuro ICU. As this patient requires urgent neuro follow up he agrees to see post CT-A.

Your patient has 50% stenosis of the left vertebral artery. There is no sign of infarct or hemorrhage and no space occupying lesion.

The patient is assessed by neuro, while a trauma and STEMI roll into your department. You get back to work.

An hour later the neurologist speaks with you briefly after seeing the patient and agrees this is a TIA. Their plan is to initiate anticoagulation as they suspect a cardio-embolic source as the CT shows no infarct/dissection and the symptoms resolved within an hour. They plan to order an urgent echo and follow up with the patient this week and feel they can be discharged.

What would be a contraindication to starting anti-coagulation for A fib1?

Evidence of completed stroke on CT – these patients are started on anti-coagulation at a later date to prevent bleeding into infarct.

You wonder if the patient should be admitted as they had high risk features in their presenting TIA?

If the patient has a negative CT with no occlusion and no vessels amenable to endarterectomy then they can be discharged and followed-up within 48 hours1.

If there is an occlusion ameanable to endarterectomy, then admission is advisable. Urgent surgery can reduce the risk of stroke over 2 years from 26% to 9% (a 17% absolute risk reduction). If done within 2 weeks the absolute risk reduction is 30%1. This is generally the case for carotid stenosis.
Our patient has vertebral artery stenosis – which usually maximizes medical therapy before considering any surgical options7. If the patient had carotid stenosis, high grade stenosis of over 70% would warrant urgent consultation.

After this consideration you feel more comfortable with the plan and continue the rest of your shift.

You are reviewing the case with a student learner later in the shift and they ask what if the patient didn’t have A fib? What would have been the course of action1?

Investigations 1:
The patient would require holter and echo to assess for potential cardioembolic source from paroxysmal A fib. If admitted these would have beeen done as an inpatient. However, our patient was discharged. More urgent holter and echo is required for patients who:

“1. Patients with known heart disease including rheumatic heart disease, heart failure, severe valvular disease, severe CAD or history of MI.
2. Patients with no obvious cause of their TIA and no classic risk factors to identify an underlying cause of their TIA such as paroxysmal atrial fibrillation, severe valvular disease including endocarditis, PFO etc.”

Management 1:
Early dual antiplatelet therapy (DAPT) initiated within 24-72 hours and continued for 3 weeks decreases risk of stroke by up to 3.5% without increased risk of bleeding.

In the ED: load with ASA 160-325mg PO and Plavix 300mg PO
Discharge: on ASA 81 mg PO daily and Plavix 75mg PO daily x 3 weeks only

After the discussion with the neurologist the patient was discharged and given good advice on symptoms of CVA to return for. He left the ED.

 

1 week passes and you are working an evening shift. There is a stroke patient brought into the trauma bay to be urgently seen – you recognize the same 69 yo male you saw a week earlier with a TIA. On evaluation the patient has symptoms of a posterior circulation stroke. He is slightly dysarthric but can get out some slurred speech. You review his medication list and there is no anti-coagulant. You confirm with the patient he did not start any new medications after leaving the ED a week ago. When asked why he didn’t fill the prescription from the neurologist he communicates that he did not receive one.

What is the risk of stroke following TIA8?
Up to 10% of patients with TIA will have a CVA in 7 days, up to 12% in 90 days.

 

Patients in the ED are our patients, even when evaluated by a consultant and deemed well enough for discharge. In this situation confirming with the consultant who will be providing the prescription as well as confirming the patient has one in hand before leaving the department would have greatly benefited the patient.

 

 

References and further reading:

Helman, A, Himmel, W, Dushenski, D. TIA Update – Risk Stratification, Workup and Dual Antiplatelet Therapy. Emergency Medicine Cases. November, 2018. https://emergencymedicinecases.com/tia-update/. Accessed Feb 9, 2021

Furey & Rost. (2020). Initial evaluation and management of transient ischemic attack and minor ischemic stroke. Uptodate. https://www.uptodate.com/contents/initial-evaluation-and-management-of-transient-ischemic-attack-and-minor-ischemic-stroke?search=tia&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H3011236877. Accessed Feb 9, 2021

Long. Updates on TIA. emDocs. April 2016. http://www.emdocs.net/8538-2/. Accessed Feb 9, 2021

Helman, A. Morgenstern, J. Klaiman, M. Sayal, A. Perry, J, Reid, S. Rezaie, S. EM Quick Hits 18 – Conservative Management Pneumothorax, Microdosing Buprenorphine, Practical Use of CRITOE, Canadian TIA Score, Pediatric Surviving Sepsis Guidelines, Safety of Peripheral Vasopressors. Emergency Medicine Cases. May, 2020. https://emergencymedicinecases.com/em-quick-hits-may-2020/. Accessed Feb 10, 2021.

https://emergencymedicinecases.com/wp-content/uploads/2018/11/Canadian-Stroke-Guidelines-summary-2018-CJEM-1.pdf

American Heart Association (2018). Role of Brain and Vessel Imaging for the Evaluation of Transient Ischemic Attack and Minor Stroke. Stroke. Vol 49 (7) pg 1791-1795

Furie. (2019). Secondary prevention for specific causes of ischemic stroke and transient ischemic attack. Uptodate. https://www.uptodate.com/contents/secondary-prevention-for-specific-causes-of-ischemic-stroke-and-transient-ischemic-attack?sectionName=LARGE%20ARTERY%20DISEASE&search=tia&topicRef=1123&anchor=H2&source=see_link#H3. Accessed Feb 10, 2021

Perry et al. (2021). Prospective validation of Canadian TIA Score and comparison with ABCD2 and ABCD2i for subsequent stroke risk after transient ischaemic attack: multicentre prospective cohort study. BMJ 2021; 372:n49.

 

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PoCUS for Diverticulitis

Dal PoCUS Fellowship – Journal Club – Feb 2021

Dr. Mandy Peach  CCFP-EM

PoCUS Fellow

Dalhousie University Department of Emergency Medicine

 

A Prospective Evaluation of Point-of-Care Ultrasonographic Diagnosis of Diverticulitis in the Emergency Department Allison Cohen, MD*; Timmy Li, PhD; Brendon Stankard, RPA-C; Mathew Nelson

 

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Tube Thoracostomy

Saint John EM Rounds – February 2021

Dr Crispin Russell

Thoracic Surgeon, Dalhousie University, Saint John

 

 


 

Trauma Rounds Summary:  January 19 2021 “Chest Tube Management in Trauma – Insights from a Thoracic Surgeon”

Summary – Dr. Andrew Lohoar

Major take home points:

 

  • Most common complication with insertion is advancing tube too far.

  • Consider placing tube if pneumothorax is > 10%, lower threshold if transporting patient from peripheral hospital.

  • Use 28 French tube for most cases

  • Direction you puncture chest wall is generally direction chest tube will follow

  • Bigger skin incision may make procedure easier

  • “Corkscrewing” or twisting chest tube while placing it, helps ‘feel’ where it is in the chest cavity (avoids advancing too far)

  • Post-chest tube insertion CXR is critical to identify placement issues

  • Use large volume of local anesthetic (20+ cc) – try to infiltrate parietal pleura

  • Consider infiltrating prior to setting up your tray, allowing more time for anesthesia

  • Consider holding Kelly clamp with one hand when puncturing pleural, to protect from pushing tip to far into chest. Spread clamp parallel to ribs

  • 0 Silk is still preferred for securing chest tube

  • Consider tying an ‘air knot’ 1 cm above skin when securing tube, allows easier adjustment later

  • Secure chest tube connections with longitudinal taping – stronger and can see joint

  • U/S can be used to assist with placement

  • Always assess for chest tube functioning post-procedure

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Rounds and Reflections

All of our Grand Rounds, EM and Trauma Reflections.

 


SJ EM Rounds

All SJ Area EM Grand Rounds, Journal Club Rounds and PoCUS Rounds. Includes rounds videos and presentation pdfs where available.

PoCUS for Diverticulitis

Dal PoCUS Fellowship – Journal Club – Feb 2021 Dr. Mandy Peach  CCFP-EM PoCUS Fellow Dalhousie University Department of Emergency […]
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Original, peer reviewed, clinical articles authored by our medical students, residents, fellows and faculty.


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Short form case-based articles from our clerks and elective students.

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“The Mother’s Kiss”

A Tool in Nasal Foreign Body Removal in Pediatric Patients Melanie Johnston, PGY2 iFMEM Dalhousie University Saint John Reviewed by […]
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Fascia Iliaca Nerve Block

Hip Broke? Hip Block. Use of the fascia iliaca nerve block for analgesia in hip fractures. Resident Clinical Pearl (RCP) […]
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Point of Care Ultrasound pearls from our learners and faculty.

A Case of Ectopic Pregnancy

  Medical Student Clinical Pearl – December 2020 Marisa O’Brien @mbob58 MD Candidate, Class of 2021 Memorial University of Newfoundland […]
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Lisfranc Injury – We have PoCUS but do we still need the cavalry?

 

 

PoCUS Fellow Pearl

Dr. Melanie Leclerc, CCFP-EM

MSK PoCUS Fellow

Dalhousie University Department of Emergency Medicine

 

Reviewed & Edited by Dr David Lewis (@e_med_doc)

All case histories are illustrative and not based on any individual


 

Case Report

A 32 year old male presents to a rural Emergency Department with a complaint of traumatic left foot pain. He was playing recreational football this evening. While crouching, the patient was tackled by another player who landed on his hyper-plantar flexed left foot from behind. The patient had immediate onset of pain in the middle of his foot and was unable to weight-bear. 

On physical examination, you notice significant bruising and swelling of the mid-foot. There is tenderness to the medial mid-foot specifically at the 1st-2nd tarsal-metatarsal articulations. X-rays of the foot appear normal. You are concerned about the possibility of a ligamentous Lisfranc injury.

https://www.footandanklesurgery.com.au/lisfranc-injuries

 


 

Lisfranc injuries

Lisfranc injuries are those that involve the tarsal-metatarsal joints. A spectrum of injury exists from ligamentous to fracture-dislocation. Up to 20% – 40% of injuries to the Lisfranc complex are missed in the Emergency Department. Unrecognized and untreated injuries can lead to long-term instability through the midfoot. As this region of the foot is responsible for a significant load during weight bearing, instability can accelerate degenerative changes in the foot resulting in chronic pain and disability

The injury is named after Jacques Lisfranc de St. Martin, a French surgeon and gynecologist performed forefoot amputations at the tarsometatarsal joint on cavalrymen, during the 1815 Napoleonic wars. Although he didn’t specifically describe the injury, it has since been recognised in equestrians and occurring as a result of a trapped plantar flexed foot in the stirrup during a fall.

 

Other mechanisms have been described including high velocity injuries (sports injuries, foot on brake pedal MVA) and low velocity injuries (Stepping off a curb awkwardly). Low velocity injuries are more likely to be missed than high velocity injuries.

Further Reading – OrthoBullets


 

Anatomy

The Lisfranc ligament complex is comprised of 3 ligaments. The dorsal (red), interosseous (blue) and the plantar (green) Lisfranc ligaments. The  Interosseous ligament is the largest and the dorsal ligament is the smallest.

The first and second rays have unique ligamentous anatomy wherein no intermetatarsal ligaments exist, but extreme strength is imparted by dorsal, interosseous, and plantar bundles of ligament binding the lateral aspect of the medial cuneiform bone with the medial head of the second metatarsal bone—the Lisfranc ligamentous complex. Only the dorsal and plantar Lisfranc ligaments are accessible to ultrasound.

 

 



 

PoCUS of the Lisfranc joint and dorsal lisfranc ligament (DLL)

Lisfranc injuries are one of the most commonly missed orthopaedic injuries in the Emergency Department. Normal X-rays are often falsely reassuring to providers and patients are discharged with a diagnosis of “soft-tissue injury”. These injuries result in midfoot instability and often require definitive surgical management.

PoCUS has been studied as a method of early detection of these injuries. Specifically, assessment of the dorsal lisfranc ligament (DLL) between the second metatarsal (M2) and the medial cuneiform(C1). PoCUS also has the advantages of being significantly cheaper and more accessible than CT and MRI. Further investigation is needed to validate this method of diagnosis, however ultrasound findings of a disrupted DLL and a widened C1-M2 interval compared to the contralateral side may increase your suspicion when pre-test probability is high.


 

Technique

  1. Linear probe-MSK setting starting at a depth of 2cm
  2. Place probe in transverse orientation over the proximal aspect of the 1st-2nd metatarsals with the probe indicator to the patient’s right
  3. Slide the transducer proximally until you locate the medial cuneiform and identify the junction between the medial cuneiform (C1) and the 2nd metatarsal (M2)
  4. The medial cuneiform will have an angulated contour appearance in contrast to the round appearance of the metatarsals
  5. Sweep to identify the dorsal lisfranc ligament (DLL)
  6. Assess the DLL for a fibrillar pattern, normal echogenicity and contour
  7. Measure the DLL width and the C1-M2 distance compare to the contralateral side
  8. Measure the C1-M2 distance with weightbearing (if patient tolerates) to compare
  9. Apply colour doppler to assess for hyperemia


 

PoCUS Findings

Medial Cuneiform (C1), 2nd Metatarsal (M2)

Note the angulated contour of C1 and the smooth contour of M2 – this sectional plane is important when locating the dorsal Lisfranc ligament. The ligament appears hypoechoic with a fibrillar pattern, typical for other ligaments more commonly visualized with PoCUS e.g MCL, ATFL.

1. Normal image – Arrows = dorsal Lisfranc ligament

2. Normal Clip and annotated image. Note how the dorsalis pedis a. frequently overlies the dorsal Lisfranc ligament (yellow lines)

3. Normal clip. Note how there is no separation of C1/M2 while counterstressing the 1st and 2nd rays


 

4. Thickened, convex contour

5. DLL disrupted, wide joint space

6. Widening C1-M2 with weightbearing


Video Case


 

Limitations

  1. Anisotropy – Irregular dorsal contour of foot can result in difficult perpendicular imaging of doral Lisfranc ligament. Stand-off gel pad may help.
  2. History of prior trauma – chronic Lisfranc injury may result in joint widening
  3. Bilateral injuries – inability to compare sides to judge joint space widening

Application

Standard foot radiographs should be performed in all cases of suspicion for Lisfranc Injury. Weight bearing radiographs should also be performed if tolerated (the ability to fully weight bear is often limited in the acute setting)

HIgh velocity injuries result in significant soft tissue swelling, and although non-weight bearing radiographs may not be diagnostic, the index of suspicion for Lisfranc injury will be high. Immobilization +/- early CT and follow up with foot and ankle specialist is recommended. For these, high pretest probability injuries, PoCUS findings are unlikely to change management significantly. A clear Lisfranc ligament rupture on PoCUS may trigger a request for CT/MRI earlier than otherwise considered. In most cases advanced imaging and a clear diagnosis is not usually possible until the swelling has subsided.

In low velocity injuries, soft tissue swelling is less pronounced. in the acute presentation the ability to perform weight bearing radiographs is limited by pain. Index of suspicion for Lisfranc injury may be low-moderate and the decision to immobilize and refer for specialist follow up can be difficult. While there is limited published evidence for PoCUS test characteristics in Lisfranc injury, a positive scan (injury + disrupted ligament / widening of C1/M2) is likely to be highly specific. Patients with positive PoCUS findings should therefore be immobilized and referred for specialist follow up. In those with negative or inconclusive findings, management and disposition will depend on degree of clinical suspicion and correlated with radiographic findings.

In summary, PoCUS provides a useful additional piece of information that can be plugged into a bayesian diagnostic pathway. What is the pretest probability of a particular diagnosis? After reviewing radiographs and performing PoCUS is the diagnosis more or less likely?

More evidence is required to fully understand the test characteristics of PoCUS for Lisfranc injury. Would the addition of plantar views improve sensitivity?

Although the performing the scan takes only a few minutes, it is quite technically challenging for the novice. As with all MSK PoCUS, repeated practice in numerous patient presentations will increase operator speed and accuracy.


 

Finally, although we still need the cavalry, PoCUS can help us decide which regiment and how quickly we need them!

 


References

  1. Mayich DJ, Mayich MS, Daniels TR. Effective detection and management of low-velocity Lisfranc injuries in the emergency setting: principles for a subtle and commonly missed entity. Can Fam Physician. 2012;58(11):1199-e625. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3498011
  2. Woodward, S., Jacobson, J.A., Femino, J.E., Morag, Y., Fessell, D.P. and Dong, Q. (2009), Sonographic Evaluation of Lisfranc Ligament Injuries. Journal of Ultrasound in Medicine, 28: 351-357.
  3. Döring, S., Provyn, S., Marcelis, S., Shahabpour, M., Boulet, C., de Mey, J., De Smet, A., De Maeseneer, M. (2018). Ankle and midfoot ligaments: Ultrasound with anatomical correlation: A review. Eur J Radiol.107:216-226.
  4. Kaicker, J., Zajac, M., Shergill, R., & Choudur, H. N. (2016). Ultrasound appearance of the normal Lisfranc ligament. Emergency Radiology, 23(6), 609-614.
  5. DeLuca, M.K., Walrod, B. and Boucher, L.C. (2020). Ultrasound as a Diagnostic Tool in the Assessment of Lisfranc Joint Injuries. J Ultrasound Med, 39: 579-587.
  6. Marshall, J., Graves, N.C., Rettedal, D.D., Frush, K., Vardaxis. V. (2013). Ultrasound Assessment of Bilateral Symmetry in Dorsal Lisfranc Ligament. The Journal of Foot and Ankle Surgery, 52(3): 319-323.
  7. Rettedal, D.D., Graves, N.C., Marshall, J.J. et al. Reliability of ultrasound imaging in the assessment of the dorsal Lisfranc ligament. J Foot Ankle Res 6, 7 (2013).
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Well, that’s a pain – in the lower back: A case of back pain in the ED

Lower Back Pain: Medical Student Clinical Pearl

Grace Dao, CC4

MD Candidate

Class of 2021

Case Presentation

Mr. Payne Bach is a 54 yo male who presents to the emergency department via EMS with lower back pain.
He reports that he hurt his back this afternoon when he was picking up a heavy, antique chair. Immediately, he felt something “give out” in his back and reports a sharp 10/10 central lower back pain that radiates unilaterally to the left side. It did not radiate down his legs. He was unable to ambulate due to the pain and called EMS.

He received 975 mg Acetaminophen in the ambulance which did not alleviate his pain. Mr. Bach reports that before picking up the chair he was feeling well. He denies any history of back pain or activities of back overuse. He denies any history of trauma or injury to his back recently or in the past. In the emergency department he reports his pain remains at 10/10 and cannot sit up or move in bed due to the pain.

He denies any change in sensation or pain to his legs. He denies any change in sensation to his perineum or any bowel incontinence. He has not urinated since the incident. Incidentally when reviewing a past medical history he reports an unintentional weight loss of 15 lbs in the last 2 months. He denies any history of a prior cancer diagnosis. On review of systems he denies history of cough, fevers, night sweats, hematochezia or gross hematuria. Mr. Bach has a 20 pack year smoking history.

Mr. Bach had difficulty with the physical exam due to pain. He appeared very distressed. All vital signs were within normal limits. An order for IV opiods was ordered and he was reassessed 30 minutes later.

Physical exam

Inspection: there were no obvious deformities of the back, no scarring or bruising or abrasions. Mr. Bach continued to look uncomfortable but was no longer in any acute distress.
Palpation: Mr. Bach was tender to palpation over L4-5. There was tenderness to palpation of the paraspinal muscles at the same level.
ROM: Mr. Bach was very hesitant to move, thus, it was difficult to assess his range of motion.
Neuro: Reflexes at the knee and ankle were normal. Babinski was negative. Normal sensation throughout all dermatomes. 5/5 strength on flexion/extension at the hip, knee and ankle.
Special tests: Straight leg raise and Lasegue’s test were negative.

Back Pain

Back pain is an extremely common condition. It is estimated that 70-85% of people will experience back pain at some point in their life1. A recent study out of an emergency department in Halifax, found that 3.17% of patients presented with to the emergency department with a complaint of lower back pain2. Back pain is within the top 5 reasons for primary care visits3. The differential diagnosis for lower back pain ranges from mechanical lower back pain to critical conditions that need to be recognized 4. Due to its prevalence and potentially sinister causes it is important to have an evidence-based approach to lower back pain.

 

To Image or Not to Image-That is the Question

Choosing Wisely Canada has put out recommendations for both Family and Emergency physicians with regards to low back pain. For family medicine the recommendation is “don’t do imaging for lower-back pain unless red flags are present” 5. It has been found that imagining those without red flags before 6 weeks does not improve outcomes.5

Similarly, for emergency medicine the recommendation is “don’t order lumbosacral (low back) spinal imaging in patients with non-traumatic low back pain who have no red flags/pathologic indicators.”6

Red flags 6:

Cauda Equina Syndrome
Severe worsening pain, especially at night
Significant trauma
Weight loss
History of Cancer
Fever
Night sweats
Steroid use
IV drug use
First episode of back pain in age > 50, especially concerning if age > 65
Widespread neurological signs (loss of sensation, loss of motor function, loss of reflexes in the legs)

 

It is also important to remember that not all red flags are created equal and to include clinical judgement in the decision making process.8 A systematic review examining the predictive value of commonly assessed red flags found that for fracture older age, prolonged steroid use, severe trauma, and contusion/abrasion increased the probability of fracture to 10-33%, and if multiple red flags are present fracture risk increases to 42-90%.

When considering red flags that increase risk of malignancy, previous history of malignancy increased risk 7-33%; while older age, unexplained weight loss, and failure to improve after one month all were found to have post-test probabilities of less than 3% when predicting malignancy risk8.

Back to our case

Mr. Bach has red flags for both fracture and malignancy:

Severe, worsening pain
Age > 50
Weight loss

XRs of the lumbar spine were ordered and indicated several compression fractures, with one area suspicious for a metastatic lesion. Follow CT spine was ordered and confirmed metastatic disease. Mr. Bach was admitted to hospital for pain control, physiotherapy and a malignancy work up.

 

References
1. Andersson, G. B. (1999). Epidemiological features of chronic low-back pain. Lancet 354(9178):581-585. doi:10.1016/S0140-6736(99)01312-4
2. Edwards, J., Hayden, J., Asbridge, M., & Magee, K. (2018). The prevalence of low back pain in the emergency department: A descriptive study set in the Charles V. Keating Emergency and Trauma Centre, Halifax, Nova Scotia, Canada. BMC Musculoskeletal Disorders, 19(1), 306. https://doi.org/10.1186/s12891-018-2237-x
3. Finley, C. R., Chan, D. S., Garrison, S., Korownyk, C., Kolber, M. R., Campbell, S., Eurich, D. T., Lindblad, A. J., Vandermeer, B., & Allan, G. M. (2018). What are the most common conditions in primary care? Systematic review. Canadian family physician Medecin de famille canadien, 64(11), 832–840.
4. Patel, A.T., & Ogle, A.A. (2000). Diagnosis and management of acute low back pain. Am Fam Physician 61(6):1779-1790.
5. College of Family Physicians of Canada. Choosing Wisely Canada. Thirteen Things Physicians and Patients should question. July, 2019. Retrieved from: https://choosingwiselycanada.org/family-medicine/
6. Canadian Association of Emergency Physicians. Choosing Wisely Canada. Ten things Physicians and Patients Should Question. July, 2019. Retreived from: https://choosingwiselycanada.org/emergency-medicine/
7. Toward Optimized Practice (TOP). (2011). Guideline for the evidence-informed primary care Management of Low Back Pain. Retrieved from: https://portal.cfpc.ca/resourcesdocs/uploadedFiles/Directories/Committees_List/Low_Back_Pain_Guidelines_Oct19.pdf
8. Downie, A., Williams, C. M., Henschke, N., Hancock, M. J., Ostelo, R. W. J. G., de Vet, H. C. W., Macaskill, P., Irwig, L., van Tulder, M. W., Koes, B. W., & Maher, C. G. (2013). Red flags to screen for malignancy and fracture in patients with low back pain: Systematic review. BMJ, 347.

Copyedited by Dr. Mandy Peach

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