Back to School – Back-to-Back Asthma Attacks


Resident Pearl by Dr. Rosario Hernandez Barba

FM PGY1

Dalhousie University

Reviewed by Dr. B Ramrattan

Copy Edited by Dr. J Vonkeman

Pdf Download: EMSJ Back to School – Back-to-Back Asthma Attacks – RHernandezBarba


Background

Asthma is a common chronic respiratory condition characterized by reversible airway inflammation and bronchoconstriction. Asthma affects people of all ages, but often is diagnosed in childhood from as early as 12months of age. Key symptoms include coughing, wheezing, shortness of breath, and chest tightness (Trottier et.al, 2021). Acute asthma exacerbations in children and youth are frequent presentations in the emergency department. Triggers for asthma exacerbations include: pollutants, allergens, respiratory infections, exercise, and cold air. (Trottier et.al, 2021). Appropriate and rapid assessment of respiratory distress in the emergency department can guide efficient treatment for patients of all ages.


Evaluation

  • Vital signs
  • PRAM score
  • +/- bedside spirometry ( FEV)

 

PRAM – a rapid assessment of asthma symptom severity (Ducharme, 2008)

  • 5 criteria 12-point scoring tool
  • Watch then listen!
  1. Vitals – O2 saturation
    • Measured with the patient on room air.
  2. Suprasternal retractions
    • Visible indrawing

  1. Scalene muscle retraction
    • Palpable contraction of deep cervical muscles on lateral neck.

  1. Air entry – Lung fields matter
    • Determine rating using the most severely affected lung.
    • Lung fields: Right anterior, right posterior, left anterior, left posterior.
  1. Wheezing – Lung auscultation zones matter
    • Determine rating with least 2 affected auscultation zones. Use the 2 most severely affected.
    • Auscultation zones: RUL, RML, RLL, LUL, LLL

 

Other indicators of severity include: (Trottier et. al, 2021)

  • Nasal flaring
  • Reduced activity level
  • Inability to speak in full sentences, inability to feed (infant)
  • Decreased level of alertness
    • Clinical features of cerebral hypoxemia
    • Sign of impending respiratory failure

 

Bedside Spirometry (Trottier et.al, 2021)

  • Can be used as an objective measure of airway obstruction and severity of exacerbation to guide management.
  • Although recommended by the Canadian Pediatric Society, it requires patient cooperation for reliability.
  • FEV1 is often not measured before initiation of bronchodilators.

 


Management

 

Critical Bedside Actions (Ducharme, 2008)

  1. Ensure oxygenation.
    • Goal is to keep oxygen saturation >92%
  2. Administer bronchodilators:
    • Salbutamol (SABA) +/- Ipratropium (SAMA)
  3. Systemic corticosteroids to relieve inflammation.
    • Mild exacerbation: Corticosteroids are optional.
    • Consider oral steroids if risk factors for severe asthma.
  4. Serial reassessments to monitor response to therapy.

Clinical Pathways

  • Use a clinical pathway for management according to severity. Order the pediatric asthma order set for correct dosing based on age. (Lewis, 2021)
  • See Clinical Pathways for Asthma Exacerbation for management according to severity

Medical Management (Trottier, et.al, 2021)

  1. Oxygen – treat hypoxemia urgently with facemask or nasal cannula.
  2. Bronchodilator – Short acting beta2-agonist: Salbutamol
    • A metered-dose inhaler (MDI) with an aero chamber is the more efficient than a nebulizer for bronchodilator delivery.
    • The dose and frequency of therapy depends on the severity of the presentation and the response to treatment.
    • In Severe presentations – continuous administration may have a better bronchodilator effect than intermittent therapy. Used if response to conventional treatment is poor.
    • Side effects: are generally well tolerated.
    • Inappropriately escalating doses can cause increased lactic acid and compensatory hyperventilation which can be confused with asthma deterioration.
  3. Bronchodilator – Short acting anticholinergic: Ipratropium
    • If Moderate-Severe: Adjunctive therapy to Salbutamol
    • Reduces hospital admission rates, risk of nausea and tremor, and improves lung function.
  4. Corticosteroids PO/IV: methylprednisolone
    • If Moderate-Severe: ALL patients should receive steroids as part of their initial treatment.
    • Mild: no clear evidence to support routine use of oral corticosteroids. Use clinical picture and patient history of repeated salbutamol doses to guide management.
  5. Magnesium Sulphate IV
    • If Moderate-Severe: patients with incomplete response to conventional therapy during the first 1-2 hours
    • Side effects: hypotension and bradycardia
      • Initiation requires consultation with a pediatrician.
      • Cardiorespiratory monitoring

Reassess

  • While initiating management, obtain a focused asthma history from caregivers including:
    • Triggers
    • Current medications
      • Amount of rescue inhaler use
      • Systemic steroid use
    • Previous events and admissions, including ICU and intubation.
    • Comorbidities
  • Reassess after 1 hour if mild, more frequently if moderate- severe
  • Communicate with parents.

 

Figure 5 Medications and dosages for acute asthma treatments for children > 1y (CPS.ca)

Management of Impending Respiratory Failure: (Trottier, et.al, 2021)

  • Confused, lethargic, cyanotic, decreasing respiratory effort.
  1. CALL FOR HELP: PICU, anesthesia (or best provider for intubation if needed)
    • Cardiopulmonary monitors
    • Start IV lines x2.
    • Labs: CBC, lytes, VBG
  2. Oxygen – 100% non-rebreather mask
    • Support ventilation if required.
  3. Bronchodilators – nebulized salbutamol and ipratropium
  4. Corticosteroids – IV/IM
  5. Magnesium Sulfate – IV
  6. Consider other medications with pediatric consultation:
    • IV salbutamol
    • Heliox
    • Ketamine
    • Anesthetic gases.
  7. Consider non-invasive ventilation until help arrives.
  8. CXR if possible – r/o other causes of respiratory failure
  9. Be ready for rapid sequence intubation.
  10. Reassess and COMMUNICATE
  • Try to avoid intubation unless the patient becomes bradycardic and pCO2 is HIGH
  • ALWAYS chat with peds ICU before intubating

 


Bottom Line

  • Assess the severity of the asthma exacerbation using PRAM scores.
  • Initiate treatment promptly to relieve bronchoconstriction.
    • Regardless of severity, salbutamol is first line to relieve bronchoconstriction.
    • When in doubt, take the blue puffer out.
  • Know when to call for help!
  • Continuous reassessment and monitoring are key throughout their stay to adjust treatment.
  • Communicate with children and their parents throughout.

 


References

  1. Ducharme, F. M., Chalut, D., Plotnick, L., Savdie, C., Kudirka, D., Zhang, X., Meng, L., & McGillivray, D. (2008). The Pediatric Respiratory Assessment Measure: A Valid Clinical Score for Assessing Acute Asthma Severity from Toddlers to Teenagers. The Journal of Pediatrics, 152(4), 476–480.e1. https://doi.org/10.1016/j.jpeds.2007.08.034
  2. Lewis,D. (2021, March). Emergency Medicine Saint John. Asthma Pediatrics | Department of Emergency Medicine | Saint John (sjrhem.ca)
  3. Trottier, E. , Chan,K., Allain,D., Chavin-KImoff,L. (2022, May). Managing an acute asthma exacerbation in children. Canadian Paediatric Society. Managing an acute asthma exacerbation in children | Canadian Paediatric Society (cps.ca)
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A Focus on Knee PoCUS


Resident Pearl by Dr. Iain McPhee

iFMEM PGY2

Dalhousie University

Reviewed by Dr. D Lewis

Copy Edited by Dr. J Vonkeman

 


Ultrasonography is a non-invasive imaging modality that has numerous uses in the Emergency Department, including assessment of musculoskeletal injuries. This Resident Pearl includes an approach to ultrasound examination of the knee, some high yield knee POCUS findings, as well as an approach to ultrasound-guided knee arthrocentesis.


Case 

A patient presents to your emergency department with a painful, swollen knee.


Part 1: What is your approach? 

History

  1. History of Presenting Illness
    • Have a discussion with the patient and discern key elements of the history including;
      • Mechanism?
        • If traumatic or mechanical in nature, obtaining a step by step, walk through will allow you to better understand the mechanism. Typically, the more specific the story, the better diagnostic value.
        • Determine how the injury took place will help narrow your differential. Was this trauma?  Sport related? Idiopathic? Any infectious symptoms?, etc.
    • Medical history
      • Gather the past medical history, medications, allergies, habits, and a review of systems
  2. Location of pain
    • The knee is a complex joint with several potential structures that can be damaged. As such, determining where the patient is experiencing the most pain will also help narrow the differential and will guide you on where to begin your POCUS investigations in a specific quadrant.

PoCUS Knee Quadrants (1) – Anterior Knee Approach

 

  • Patient positioning: Supine position
  • Knee positioning: 20-30° of knee flexion (can place pillow under the knee if needed)
  • Transducer positioning: transverse and longitudinal views

 

Relevant structures:

 

a. Quadriceps Tendon

  • Observe the multilevel appearance to the tendon, representing the distal union of the three tendon layers arising from the quadriceps muscles.

 

Video 1 Quadriceps Tendon – Short Axis View

 

Video 2 Quadriceps Tendon – Long Axis View

 

Figure 1 Quadriceps Tendon

 

b. Suprapatellar Recess

  • Observe the suprapatellar fat pad – found under distal 1/3 of quadriceps tendon superior to the patella, and the pre-femoral fat pad
  • The suprapatellar recess lies deep to the quadriceps tendon and the suprapatellar fat pad and superficial to the pre-femoral fat pad. This recess is a common site of effusion.

 

Video 3 Suprapatellar Recess in the Long Axis

 

Figure 2 Suprapatellar Recess

 

c. Parapatellar Recess

  • Assess lateral and medial sides of the quadriceps tendon as fluid can accumulate on lateral and medial sides of the suprapatellar recess.

Video 4 Medial Parapatellar Recess in the Short Axis

 

Figure 3 Parapatellar Recess (medial)

 

d. Femoral Trochlea

  • Examine in transverse plane with knee in full flexion

 

Video 5 Trochlea visualized in the Short Axis

 

Figure 4 Trochlea

 

e. Patellar Retinacula and Patellar Medial Articular Facet

  • Visualized in transverse plane on either side of the patella (medial shown below)
  • Extend the knee, apply pressure with your hand to the lateral aspect of the patella and hold the transducer in the transverse plane to view the Medial articular facet. Stress movement is seen in video. The lateral articular facet cannot be visualized.

Video 6 Patellar Retinaculum – Medial Aspect. With stress and no stress

 

Figure 5 Patellar Retinaculum

 

f. Patellar Tendon

  • Examine tendon, from cephalad origin to distal insertion, in both long and short axis.
  • Deep to the patellar tendon, inferior to the patella, is the Hoffa fat pad
  • Appreciate the deep infrapatellar bursa that is deep to the distal patellar tendon and anterior aspect of the tibial epiphysis

 

Video 7 Patellar Tendon viewed in the Long Axis

 

Figure 6 Patellar Tendon in the Long Axis

 

Video 8 Patellar Tendon viewed in the Short Axis

 

Figure 7 Patellar Tendon in the Short Axis

 


PoCUS Knee Quadrants (1) – Medial Knee Approach

 

  • Patient positioning:  Supine
  • Knee positioning: Maintain 20-30° of knee flexion, rotate leg externally
  • Transducer positioning: Oblique- long axis of ligaments

 

Relevant structures:

 

a. Medial Collateral Ligament (MCL) and Pes Anserinus

  • Examine entire length. Add valgus stress to assessment of MCL integrity
  • Follow to distal MCL, then rotate the transducer counter clockwise by 5-10 degrees to visualize the pes anserinus tendon.

 

Video 9 MCL visualized in Long Axis

 

Video 10 Pes Anserinus visualized in the Long Axis

 

 

Figure 8 a) Medial Collateral Ligament (MCL) and b) Pes anserinus

 


PoCUS Knee Quadrants (1) – Lateral Knee Approach

 

  • Patient positioning:  Supine
  • Knee positioning: Maintain 20-30° of knee flexion, rotate leg internally
  • Transducer positioning: Oblique- long axis of ligaments

 

Relevant structures:

 

a. Iliotibial Band

  • Located between the anterior and middle third of the lateral aspect of the knee and oriented along the major axis of the thigh

 

Video 11 Iliotibial Band visualized in the Long Axis

 

Figure 9 Iliotibial Band

 

b. Lateral Collateral Ligament (LCL)

  • Obtain long axis view. Transducer should be oriented with the major axis of the lower leg

 

Video 12 LCL in the Long Axis of the Lower Leg

 

Figure 10 Lateral Collateral Ligament (LCL)

 


PoCUS Knee Quadrants (1) – Posterior Knee Approach

  • Patient positioning:  Prone
  • Knee positioning: knee extended
  • Transducer positioning: Transverse and longitudinal

 

Relevant structures:

 

a. Medial Tendons

  • Examine in Transverse (Short axis)
  • From medial to lateral  Sartorius (muscle), gracilis tendon and semitendinosus tendon

 

Video 13 Medial Tendons in the Short Axis

 

Figure 11 Medial Tendons

 

b. Semi-Membranous-Gastrocnemius Bursa

  • Site where popliteal (Baker’s) cyst arises
  • Envelopes the Semitendinosus tendon and Sartorius muscle

Video 14 The Semi-Membranous-Gastrocnemius Bursa in the Short Axis

 

Figure 12 Semi-Membranous-Gastrocnemius Bursa

 

c. Popliteal Neurovascular Bundle and Intercondylar Fossa

  • The popliteal neurovascular bundle is superficial to the popliteal artery (deep) and popliteal vein (intermediate)
  • Can appreciate the Posterior Cruciate Ligament (PCL) here with transducer in oblique longitudinal plane

 

Video 15 The Popliteal Neurovascular Bundle in the Short Axis

 

Figure 13 Popliteal Neurovascular Bundle

 

Video 16 The Posterior Cruciate Ligament in the Long Axis

 

d. Posterolateral Corner of the Biceps Femoris

  • In longitudinal plane, can visualize the biceps femoris tendon

 

 

Video 17 Posterior Biceps Femoris viewed in the Long Axis

 

Figure 14 Posterior Biceps Femoris

 

e. Peroneal Nerve

  • Examine in short axis. Begin on posterolateral aspect of leg and advance around fibular head.
  • The Peroneal nerve is found posterior to the biceps femoris

 

Figure 15 Various views of the Peroneal Nerve

 

Videos 18-21 Various views of the Peroneal Nerve 

 


Part 2: High Yield Knee PoCUS Findings

 

1. Knee Effusion

Background:

  • A knee effusion refers to an increased volume of fluid in the synovial compartments of the knee and can arise from acute or chronic conditions 2,3.
  • Small, asymptomatic effusions can occur in healthy individuals, while larger joint effusions usually indicate underlying pathology 3.

What to look for:

  • Knee effusions are best visualized with a linear transducer, and placed in the long axis over the medial joint line, positioned over the suprapatellar recess 4.
  • An effusion will appear as an anechoic fluid that displaces but remains constrained by the hyperechoic joint capsule 4. Of note, It is important to assess both knees to establish true asymmetry and thus abnormality between knees 4.

 

2. Haemarthrosis

Background:

  • Haemarthrosis is an articular bleeding into the joint space and represents a type of joint effusion.
  • The most common mechanism of knee haemarthrosis is forced twisting in a loaded joint resulting in ligamentous and/or meniscal damage 5.
  • Tearing the anterior cruciate ligament (ACL) represents ~70% of post traumatic haemarthrosis of the knee 5.

What to look for:

  • A haemarthrosis may be more hypoechoic due to potential clotting when compared to other effusion fluids.

 

3. Medial Collateral Ligament Tear

Background:

  • The Medial Collateral Ligament (MCL) is the most commonly damaged ligament of the knee in situations of direct trauma and is usually a result of valgus stress. Using POCUS to evaluate soft tissue of the knee has become more common 6, however, ligaments are small in size and usually in close proximity to bone, making visualization difficult 4.

What to look for:

  • MCL’s are generally dense, hyperechoic in appearance, however may appear darker given their proximity to bone cortex and fascia.
  • An abnormal exam includes a thickened MCL and is typically more heterogeneously hypodense in appearance 17

 

Figure 17 Longitudinal view of the MCL. a) normal MCL. b) abnormal MCL. F: Femur, T: Tibia, s: superficial portion of MCL, d: deep portion of MCL. 18

4. Patellar Tendonitis

Background:

  • Tendons are best viewed with a linear transducer in both the long and short axis, and appear hyperechoic. Tendons are particularly susceptible to anisotropic artefact, that being, the tendon will become more hypoechoic as the transducer angulation changes 4.
  • Patellar tendinitis accounts for 10% of clinical knee diagnoses 9, and is particularly common in athletes whose sport involves frequent jumping ex. basketball, volleyball or running 10.

What to look for:

  • In patellar tendonitis, a clinician can expect to see a thickened patellar tendon with a loss of normal fibrillar pattern, characteristic of a normal tendon 4.
  • There may also be signs of hyperechoic calcifications and/or patchy hypoechoic zones 10.
  • Comparison with the other (asymptomatic) knee is often helpful in visualizing this change.

Figure 18  (a) and (c) represent normal patellar tendons, where (b) and (d) represent patellar tendinopathy. 10,11

5. Osgood Schlatter

Background:

  • Apophysitis is a term used to indicate inflammation and stress injury where a tendon attaches to a growth plate of bone 12.
  • Osgood-Schlatter disease (OSD) is a traction apophysitis of the tibial tuberosity (site of patellar tendon insertion on the tibia) due to repetitive strain.
  • Contraction of the quadriceps muscle is transmitted through the patellar tendon which results in the avulsion of the anterior surface of the tibial tuberosity 13.
  • This usually occurs in young boys between the ages of 10-15 14.

What to look for:

  • Best visualized with a linear probe, look first at the region of the tibial tuberosity.
  • A fragmented hyperechoic lesion surrounded by hypoechoic cartilage will be visualized.
  • There will also be a thickening of the distal patellar tendon and evidence of infrapatellar bursitis – represented by an anechoic collection deep to the patellar tendon 13.

Figure 19 a) Osgood-Schlatter anatomy. b) Ultrasound image of Osgood-Schlatter. Arrow: highlighting fragmented lesion of the tibial tuberosity. Ultrasound image obtained from ultrasoundcases.info.

6. Meniscal Injury

Background:

  • The meniscus of the knee is a wedge shaped piece of fibrocartilage that plays the role of shock absorber between the distal femur and proximal tibia.
  • There are two menisci, lateral and medial, and they play an important role in knee stabilization 15.
  • An injury to the meniscus typical occurs with internal or external twisting of the upper leg while the foot is securely planted.
  • Ultrasound has been shown to be an effective initial diagnostic modality 16.

What to look for:

  • Best observed with the linear probe in the long axis of the affected side of the knee (medial or lateral side).
  • The meniscus will be a triangular “wedge” between the hyperechoic tibia and femur.
  • Pertinent positive for a torn meniscus include anechoic regions of the wedge representing a tear or fluid accumulation.

Figure 20 a) Normal Medial Meniscus. (b/c) Arrow: Medial Meniscus Tear. Ultrasound images from ultrasoundcases.info.


Part 3: Ultrasound Guided Arthrocentesis of the Knee – A Suprapatellar Approach (7,8)

 

Anatomy

  • A basic understanding of knee anatomy is required
  • Knee – composed of 4 major bones: the distal femur, proximal tibia, proximal fibula and the patella.
  • Three articulations: Femorotibial, patellofemoral and tibiofibular

Common pathologies

  • Arthritic conditions (Osteoarthritis, rheumatoid arthritis, crystal arthropathies)
  • Trauma (sports injuries and MVA)
  • Infectious (synovitis)

Equipment

  • Ultrasound machine with linear array transducer (<4cm depth)
  • 22-18 gauge 1.5-2 inch needle for aspiration (Can consider spinal needle- 20 gauge)
  • 10-20ml syringe – for small effusions
  • 30-60ml syringe – for large effusions
  • Local anesthetic – Lidocaine
  • Sterile transducer cover
  • Sterile ultrasound gel
  • Sterile towel
  • Sterile gloves

Procedure:

  • Patient position – Supine
  • Knee positioning – Knee flexed to 30° with either a towel/pillow under the affected knee
  • Clinician position – positioned on the side of the affected knee
    • Note: Ensure the ultrasound machine screen and the knee are in the same line of sight
  • Needle position – Long axis – In-plane, lateral to medial approach

Step-by-step

  • Prep and clean the skin
  • Drape the knee, leaving the suprapatellar region exposed
  • Numb the skin and needle track with local anesthetic
  • Prep the U/S machine for sterility
  • Place the transducer superior to the patella in transverse orientation (short axis to the quadriceps tendon)
  • Advance your aspiration needle from lateral to medial until you reach the anechoic suprapatellar recess.

 

USK Medial Arthrocentesis

 

Video 22, 23 Medial approach to suprapatellar ultrasound guided arthrocentesis in the long axis.

 


   

References

  1. Martinoli C. Musculoskeletal ultrasound: technical guidelines. Insights Imaging. 2010;1 (3): 99-141. doi:10.1007/s13244-010-0032-9
  2. Li TY. Sonography of Knee Effusion. Journal of Diagnostic Medical Sonography. 2020;36(6):545-558. doi:1177/8756479320944848
  3. Gerena, L. A., Mabrouk, A., & DeCastro, A. (2022). Knee Effusion. In StatPearls. StatPearls Publishing.
  4. Atkinson, Paul, and others (eds), Point of Care Ultrasound for Emergency Medicine and Resuscitation, Oxford Clinical Imaging Guides(Oxford, 2019; online edn, Oxford Academic, 1 Apr. 2019), https://doi.org/10.1093/med/9780198777540.001.0001
  5. Lombardi, M., & Cardenas, A. C. (2023). Hemarthrosis. In StatPearls. StatPearls Publishing.
  6. Ahmadi O, Heydari F, Golshani K, Derakhshan S. Point-Of-Care Ultrasonography for Diagnosis of Medial Collateral Ligament Tears in Acute Knee Trauma; a Diagnostic Accuracy Study. Arch Acad Emerg Med. 2022 Jun 9;10(1):e47. doi: 10.22037/aaem.v10i1.1480. PMID: 35765618; PMCID: PMC9206825.
  7. Josh Hackel, Todd Hayano, John Pitts, Mairin A. Jerome, 21 – Knee Injection Techniques, Editor(s): Christopher J. Williams, Walter. L Sussman, John Pitts, Atlas of Interventional Orthopedics Procedures, Elsevier, 2022, Pages 366-427, ISBN 9780323755146, https://doi.org/10.1016/B978-0-323-75514-6.00021-2.
  8. Avila, Jailyn. Knee arthrocentesis and injections. Core ultrasound. 2023. https://www.youtube.com/watch?v=tf5hF0QflDI
  9. Rosen, A.B., Wellsandt, E., Nicola, M., and Tao, M.A., 2022. Clinical Management of Patellar Tendinopathy.Journal of athletic training, 57(7), pp.621–631.
  10. Sports Medicine Ultrasound Group. Case study – patellar tendinopathy. 2023. https://www.ultrasoundtraining.co.uk/case-study-patella-tendinopathy/
  11. Abat, F., et al. “Patellar tendinopathy: diagnosis by ultrasound and magnetic resonance imaging. Conservative and surgical management alternatives.” Rev Esp Artrosc Cir Articul En1 (2022): 13-20.
  12. Mark Riederer, MD and Neeru Jayanthi, MD. American medical society for sports medicine
  13. Siddiq MAB. Osgood-Schlatter Disease Unveiled Under High-frequency Ultrasonogram. Cureus. 2018 Oct 4;10(10):e3411. doi: 10.7759/cureus.3411. PMID: 30538899; PMCID: PMC6281446.
  14. Indiran, V., & Jagannathan, D. (2018). Osgood-Schlatter Disease. The New England journal of medicine378(11), e15. https://doi.org/10.1056/NEJMicm1711831
  15. Alaia M, Wilkerson R, Fischer S. Meniscus tears. American Academy of Orthopaedic Surgeons: 202. https://orthoinfo.aaos.org/en/diseases–conditions/meniscus-tears/
  16. Ahmadi, O., Motififard, M., Heydari, F. et al.Role of point-of-care ultrasonography (POCUS) in the diagnosing of acute medial meniscus injury of knee joint. Ultrasound J14, 7 (2022). https://doi.org/10.1186/s13089-021-00256-0
  17. Lee, J. I., Song, I. S., Jung, Y. B., Kim, Y. G., Wang, C. H., Yu, H., Kim, Y. S., Kim, K. S., & Pope, T. L., Jr (1996). Medial collateral ligament injuries of the knee: ultrasonographic findings. Journal of ultrasound in medicine : official journal of the American Institute of Ultrasound in Medicine15(9), 621–625. https://doi.org/10.7863/jum.1996.15.9.621
  18. Chiang, Yi-Pin & Wang, Tyng-Guey & Lew, Henry. (2007). Application of High Resolution Ultrasound for Examination of the Knee Joint. Journal of Medical Ultrasound. 15. 203-212. 10.1016/S0929-6441(08)60038-7.
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One Pill Can Kill – Single Dose Pediatric Toxicology


 

Medical Student Clinical Pearl by Marlise O’Brien

MD Candidate, Class of 2024

Dalhousie University

Reviewed by Dr. P Dutton

Copy Edited by Dr. J Vonkeman

Pdf Download: EM One Pill Can Kill – Single Dose Paediatric Toxicology MO’Brien

 


Case 

A three-year-old, 14kg boy is brought to your emergency department by his distressed mother. The child is crying but otherwise appears well on first glance. The mother rapidly explains to you that while she was making dinner, he reached a pill case that was on a sofa table and opened it. She found him minutes later sitting on the ground, surrounded by an assortment of unmarked pills and the empty case. She was able to discard some but doesn’t know which or how many pills he may have consumed. The pill case belonged to a relative who has been asked to provide a list of their prescriptions as soon as possible.

You examine an assortment of pills – you think you might recognize a few but can’t be certain. You enter the room to assess the child and see the following vitals:

 

You identify that this child is bradycardic and hypotensive for now, with a reassuring pediatric assessment triangle. You are concerned about a toxic overdose of unknown substances. You wonder if a pill or two could really be that bad. After all, it wasn’t the whole bottle…

You plan to call the regional poison centre for advice, then remember that pediatric toxic overdoses for some medications can occur with very small doses, sometimes a single pill. You come up with a list of potentially toxic one-pill medications while a colleague works to identify some of the pills at hand.


Approach to Pediatric Toxicology

Pediatric toxicology differs from adults in many ways. Children have different body surface area, more total body water, smaller glycogen stores, immature livers and kidneys for drug elimination, more sensitive hemodynamics, and more permeable blood brain barriers3. Given that the average toddler weighs between 10-15kg5, toxic drug doses can be achieved with a single pill of adult dosing.

Suspected overdose history:

  • Time of ingestion?
  • Substances, doses, and co-ingestions?
  • Immediate reactions?
  • Weight of child?2

Initial investigations:

  • ECG
  • CBC, Electrolytes, Creatinine
  • Blood Gas
  • Liver enzymes and function
  • Blood toxicology panel3.

Assess for common toxidromes and consider the possibility of co-ingestions with household products in addition to medications (i.e. methanol, ethylene glycol, caustics); investigate as necessary.


“One Pill Can Kill” Medications

You draw up a list of medications you know can cause significant harm to children in small doses.

Table 1 is by no means a comprehensive list of medications causing toxic overdoses in children (more exhaustive lists have been included in Further Reading4). They are, however, commonly prescribed medications that you may encounter in overdoses. Always consult your regional poison control center, making use of the expertise of toxicologists to determine the best course of action. Many infographics and mnemonics exist highlighting different medications that can be harmful, as seen below.


Case Continued

You are given a prescription list by the mother and identify amlodipine and gliclazide as potentially harmful. Given that the child is exhibiting bradycardia and hypotension, you initiate a fluid bolus and continue to monitor his hemodynamics. You recheck their POC glucose, and they are now mildly hypoglycemic. Given that they are still awake and alert, you encourage PO intake of juice and food and provide a dose of activated charcoal mixed in chocolate milk.

You call the Atlantic Canada Poison Control Center at 902-470-8161 and they reinforce your decision to treat. Your pediatric colleagues agree to admit the child for monitoring. The next morning, you are pleased to hear that the child’s blood sugar stabilized, and they did not develop any significant hemodynamic compromise.

 

 


Treatment

Some methods of treating toxic overdoses have fallen out of favour and are now rarely used, including gastric lavage and total bowel irrigation. The cornerstone of overdose management in pediatrics is supportive care and early intervention with specific antidotes, once ingestants have been identified. Activated charcoal may be recommended in specific ingestions but is not required for all.

The child ingested a potentially toxic amount of calcium channel blocker. Though he was able to be treated conservatively with IV fluids, some cases of calcium channel blocker overdose may require high-dose insulin euglycemic therapy (HIET). Insulin release is dependent on calcium flux into pancreatic cells, which is impeded in CCB overdoses8. Additionally, calcium channel blockers alter cardiac myocyte metabolism making glucose use by the heart more challenging8. High dose insulin therapy provides a boost to cardiac myocyte metabolism and a positive inotropic effect8. For interest, a standard HIET protocol has been included below.

 


Disposition

The disposition of children following ingestion depends on the substances in question, doses, and stability. All children should be monitored for at least 4-6 hours, while others will require admission to the inpatient pediatric service for close monitoring. Some medications, such as opioids or sulfonylureas, can have symptom recurrence after initial treatment. The same principle applies to extended or sustained release formulations of medications with long half-lives.

A common example is the need for repeat doses of naloxone in treating opioid overdoses. IV naloxone dosing for pediatric patients is weight based. See Table 2 for details on dosing details10.

 


Conclusion

Toxic overdoses pose a challenge for many clinicians as history can be uncertain and close monitoring is required to adjust treatments for prolonged exposures. Appropriate use of resources can greatly improve patient care in these situations. Of interest, technology may be very helpful in cases of unknown ingestions. Using provincial prescription medication databases to access prescription lists can help in identifying what medications were ingested. Many apps and websites also have pill identification databases allowing you to search pills by shape/colour/inscription. Consult with colleagues liberally, including pharmacy and regional toxicology centers.

Another challenge with pediatric overdoses is the consideration for neglect, abuse, and child safety. When taking a history, pay particular attention to details of how the child accessed the substances and if the story and presentation align. Do not disregard to possibility of purposeful misadministration of medications. At minimum, parents should be provided with education about proper medication storage and handling for safety in the home. The IWK Regional Poison Center has several excellent resources for families about poisoning prevention and medication safety, included in Further Reading1.


References, Resources and Further Reading:

  1. WK Regional Poison Centre Medication Safety handout https://atlanticcanadapoisoncentre.ca/Documents/PDF/medicationsafety.pdf
  2. Bigham, B. One Pill Can Kill: Advancing Your Knowledge of Pediatric Toxicity. EMS World, 2020. Retrieved from: https://www.hmpgloballearningnetwork.com/site/emsworld/article/1224498/one-pill-can-kill-advancing-your-knowledge-pediatric-toxicology
  3. Davis, T. Toxicology – A crash course in accidental overdoses. Don’t Forget the Bubbles, 2019. Retrieved from: https://doi.org/10.31440/DFTB.17991
  4. Euwema, M., Swanson, T. Deadly Single Dose Agents. StatPearls, 2023. Retrieved from: https://www.ncbi.nlm.nih.gov/books/NBK441849/
  5. Knight, K., Ziebers, L. One Pill Killers. Pediatric FOAMed, N.D. Retrieved from: https://www.paediatricfoam.com/2018/08/one-pill-killers/
  6. Max, P., Erdman, A., Chyka, P. et al. Beta Blocker Ingestion: An Evidence-Based Consensus Guideline for Out-Of-Hospital Management. Clinical Toxicology, 2005. Doi: 10.1081/CLT-62475
  7. Nickson, C., and Little, M. Early use of high-dose insulin euglycemic therapy for verapamil toxicity. The Medical Journal of Australia, 2009.
  8. Nickson, C. High-Dose Insulin Euglycaemic Therapy. Life in the Fast Lane, 2020. Retrieved from: https://litfl.com/high-dose-insulin-euglycaemic-therapy/
  9. Richardson, N., Kopec, K. ToxCard: Pediatric Toxicology – One Pill/Taste Can Kill. EmDOCS, 2019. Retrieved from: http://www.emdocs.net/toxcard-pediatric-toxicology-one-pill-taste-can-kill/
  10. Shenoi, R. and Timm, N. Drugs Used to Treat Pediatric Emergencies. Committee on Drugs and Committee on Pediatric Emergency Medicine. Pediatrics, 2020.
  11. Bar-Oz, B. Levichek, Z., Koren, G. Medications That Can Be Fatal For a Toddler With One Tablet or Teaspoonful A 2004 Update. Pediatric Drugs, 2004.

 

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Approach to Simple Corneal Foreign Body Removal


 

Resident Clinical Pearl by Dr.Khoi Dao

FM PGY1

Dalhousie University

Reviewed by Dr. B Ramrattan

Copy Edited by Dr. J Vonkeman

Pdf Download: EMSJ Simple Corneal FB Removal

**Special thanks to Dr. Luke Taylor

 


Case 

A 30yo male presents to the ED complaining irritation to his right eye. He is a sheet metal worker/fabricator and was cutting steel the day prior. Although he was wearing protective goggles and a face shield at the time, he noticed his right eye started to tear and become red. He couldn’t sleep through the night due to eye irritation whenever he closed his eye. He denies any vision changes, headache, or any focal neuro symptoms. Otherwise, he is relatively healthy with no medications or known allergies.

On examination, his acute visual examination is normal. On inspection of his eyes, there is a 0.5mm in diameter foreign body visualized on his cornea at approximately the 7 o’clock position of his iris. There are no signs of hyphema. There is epiphora, or excessive tearing, and conjunctival injection of his right eye. His pupils are equal, round, and reactive to light. His extraocular movements are normal.

After the exam, you decide that the foreign body needs to be removed. You apply two drops of 0.5% tetracaine and get your equipment ready.


Key Point #1: Always perform a Visual Acuity and PenPoint Light Exam. 

 

  • It is essential to exclude penetrating trauma or signs of hyphema
  • If present, these findings warrant prompt ophthalmologic consultation. 1,2

Key Point #2: Prepare your Equipment.


Key Point #3: Proper Patient Positioning

  • If the patient’s affected eye is the same side of your dominant hand, then the
    • Position the patient to look straightforward towards the slit lamp.
  • If the patient’s affected eye is the opposite side of your dominant hand
    • Tilt the patient’s head turn toward the dominant hand as much as the patient can tolerate.

Key Point #4: Removing the Foreign Body.

  • Attach the needle to the syringe.
    • The syringe is used as a shaft for the needle.
  • Focus the slit lamp on the foreign body.
  • With your dominant hand, hold the syringe between your thumb and index finger.
    • With your other fingers, stabilize your dominant hand on the patient’s zygoma.2,3
  • Position the needle’s bevel away from the patient.
  • Move the needle toward the visual field of the microscope until you see the needle within the visual field.
  • Move the needle’s bevel toward the foreign body; hold the long shaft of the needle near parallel to the patient’s eye and face.3
    • Quick Tip: you can also bend 1 to 2 mm of the tip of the needle with a needle driver at 90 degrees, so that the needle tip is perpendicular to the corneal surface, making the procedure safer.3
  • Like a spoon, use the needle to scoop out the foreign body with light force. Be gentle.
    • Quick Tip: Provide reassurance to the patient during the procedure. No one likes needles this close to their eye!
  • If the foreign body falls away from visual field, use the cotton swab to wipe under the lower lid.
    • In most cases, the foreign body could be found here.

 

  • Once the foreign body is removed reassess the area for a residual rust ring.
    • Rust rings can develop after two hours.
    • An Algerbrush can be used to remove it.
    • If left, it could cause scarring and necrosis of the cornea.
    • Minimal rust ring can be left, but if any uncertainty, the patient should be referred to ophthalmology for follow up.
  • Once the foreign body and rust ring are removed, complete a Fluorescent Eye Stain and Seidel Test to assess for other corneal abrasions and rule out full-thickness deficit in cornea.
    • Quick Tip: It is essential to document all ocular findings, especially a negative Seidel Test

Key Point #5: Post-Removal Eye Care 

  • Topical antibiotic use is controversial, but most will recommend their use to prevent the possibility of superinfection, for clinical symptomatic relief secondary to lubrication, and to aid with corneal regeneration.
    • They are recommended for 3 to 5 days as cornea recovers quickly.2,4,5
  • Oral NSAIDs are recommended for pain control.
  • Topical anesthetic use for pain control is somewhat controversial.
    • However, there may be a role for short term use for simple corneal abrasion.
    • They can be given up for 48 hours.1,4,5
  • There is no evidence for tetanus vaccination or eye patching.

Quick Tip for Instrumentation Use

  • Hang a small fruit (cherry or grape), with some dirt on it, in front of the slit lamp microscope.
  • Another option is to put some dirt/sand on an inflated balloon.
  • Practice removing the dirt without damaging the fruit or popping the balloon to be comfortable.

Case Conclusion 

  • Since the foreign body was on the right eye, the patient was positioned toward the right dominant hand.
  • The foreign body was removed with a 25G needle.
  • The cornea was reassessed for rust ring, and rust ring was removed as much as possible.
  • A fluorescent eye stain was performed to assess for any other corneal abrasions and rule out full thickness corneal defect.
  • The patient was given a short 5-day course of topical antibiotics and counselled on OTC NSAID use for pain management.

References

  1. Jacobs, D. Corneal abrasions and corneal foreign bodies: Management.com, 2023. [Online]. Available: https://www.uptodate.com/contents/corneal-abrasions-and-corneal-foreign-bodies-management?search=foreign%20body%20eye&source=search_result&selectedTitle=2~122&usage_type=default&display_rank=2#H7154937
  2. Wipperman, J.L., John, D.N. Evaluation and Management of Corneal Abrasions. 2013. AFP 87(2):114-120
  3. Beyer, H., Cherkas, D. Corneal foreign body removal using a bent needle tip. 2010. The American Journal of Emergency Medicine 30(3):489-490.
  4. Ahmed, F., House, R.J., & Feldman, B.H. Corneal Abrasions and Corneal Foreign Bodies. 2015. Prim Care Clin Office Pract 42:363-375.
  5. Shipman, S., Painter, K., Keuchel, M., & Bogie, C. Short-Term Topical Tetracaine Is Highly Efficacious for the Treatment of Pain Caused by Corneal Abrasions: A Double-Blind, Randomized Clinical Trial. 2021. Annals of Emergency Medicine 77(3), 338–344.

 

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A Case of Facial Nerve Palsy


Medical Student Clinical Pearl by Livia Clarke

 

MD Candidate, Class of 2024

Dalhousie University

Reviewed by Dr. M McGraw

Copy Edited by Dr. J Vonkeman

Pdf Download: EMSJ A Case of a Facial Nerve Palsy

 


Case 

A 45-year-old male presents to the Emergency Department with muscle paralysis of the left side of his face. That morning, he experienced some difficulty eating his breakfast and noticed that the left side of his face was immobile when looking in the mirror. He is also experiencing paresthesia of the left side of his face. He is an otherwise healthy individual with no past medical history and not taking any medications.

On examination, he is vitally stable and in no apparent distress. He has left sided facial paralysis involving the upper and lower portions of the face, suggesting impairment of cranial nerve VII, as well as paresthesia. The rest of the cranial nerve exam is normal. Upper and lower extremity muscle tone and strength are normal. Sensation is normal. Cerebellar testing with finger-to-nose, heel-to-shin, and rapid alternating movements is normal. Gait is normal.


Differential Diagnosis of Facial Nerve Palsy (1,3)

  • Peripheral Causes:
    • Lyme disease
    • Otitis media
    • Ramsey Hunt syndrome
    • Guillain-Barre syndrome
    • Cholesteatoma or tumor of parotid gland
    • Bell’s Palsy
    • Leukemia
  • Central causes:
    • MS
    • Neoplasm
    • Stroke

Bell’s Palsy

Bell’s Palsy is a common idiopathic condition that results from the peripheral paralysis of the seventh cranial nerve causing unilateral facial paralysis4. It is thought to be caused from inflammation causing compression of the facial nerve at the geniculate ganglion3,4. The exact cause of this inflammation is unknown, but suspected causes include viral infections such as Herpes simplex virus1.

 

Figure 1: Anatomy of the facial nerve (American Family Physician)

 

Patients often present with sudden onset (over several hours and up to 72 hours) of unilateral facial paralysis that involves the upper and lower face1,4. Commonly patients cannot close the affected eyelid, experience eyebrow sagging, loss of the nasolabial fold, and drooping of the affected corner of the mouth1,4. Patients may also experience impairment in taste and decreased tearing of the eye1,4.

 

Figure 2: Presentation of a left Bell’s Palsy. A) Inability to raise left eyebrow. B) & C) Inability to close left eye or raise left corner of mouth (UptoDate).

 

The involvement of both upper and lower portions of the face is important because facial weakness originating from central causes (i.e., stroke, tumor) results in a pattern of facial weakness restricted to the lower region of the face that spares the forehead3.

Figure 3: (A) a facial nerve lesion. (B) a supranuclear lesion with forehead sparing (American Family Physician).

The risk of Bell’s Palsy is three times greater during pregnancy, with the highest risk in the third trimester and during the first week postpartum. Hypertension has also been associated with an increased risk in some studies1. Other risk factors include diabetes, preeclampsia and obesity4.


Diagnosis

Bell’s Palsy is a diagnosis of exclusion and is diagnosed clinically1. If there are atypical features, the patient should be evaluated for central causes. During the assessment of a patient presenting with Bell’s Palsy it is important to assess for a patient’s ability to completely close the affected eye.


Treatment

In most cases, Bell’s Palsy will resolve without treatment4. Oral corticosteroids are often prescribed to reduce the inflammation of the facial nerve. Prednisone 60-80 mg/day for one week is recommended2. Often an antiviral will also be prescribed, but its effectiveness is not proven. Valacyclovir 1000mg three times daily for one week or acyclovir 400mg five times daily for 20 days are popular choices for those with severe symptoms2. If the patient is unable to completely close the affected eye, they must be cautioned to apply hydrating solutions (i.e. artificial tears) during waking hours as well as artificial tears ointment and taping the eyelid shut during sleep to prevent corneal injury5.


Prognosis 

Bell’s Palsy has a favorable prognosis. Approximately 70% of patients will completely recover without treatment by 3-6 months2. With glucocorticoid treatment, 80-85% of patient are expected to completely recover2. 7-15% of patients will experience recurrent Bell’s Palsy either on the same or opposite side2.


Case Continued 

The patient’s symptoms were classic for Bell’s palsy, and he did not have any atypical features. He was provided a prescription of an oral corticosteroid and an antiviral and discharged home.


References

  1. Hatzenbuehler, J., & Pulling, T. J. (2011). Diagnosis and Management of Osteomyelitis.American Family Physician84(9), 1027–1033.
  2. Chiappini, E., Mastrangelo, G., & Lazzeri, S. (2016). A Case of Acute Osteomyelitis: An Update on Diagnosis and Treatment.International Journal of Environmental Research and Public Health13(6), 539.
  3. Yuschak, E., Chase, S., Haq, F., & Vandever, C. (2019). Demographics and Length of Stay for Osteomyelitis in Opioid Drug Users: A Unique Population with High Healthcare Costs.Cureus11(3), e4339.
  4. Calhoun, J. H., & Manring, M. M. (2005). Adult Osteomyelitis.Infectious Disease Clinics of North America19(4), 765–786.
  5. Hogan, A., Heppert, V. G., & Suda, A. J. (2013). Osteomyelitis.Archives of Orthopaedic and Trauma Surgery133(9), 1183–1196.
  6. Pichichero, M. E., & Friesen, H. A. (1982). Polymicrobial Osteomyelitis: Report of Three Cases and Review of the Literature.Clinical Infectious Diseases4(1), 86–96.
  7. Momodu, I.I., & Savaliya, V. Osteomyelitis. ]. StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan. Updated 2023 May 31.
  8. Arnold, S. R., Elias, D., Buckingham, S. C., Thomas, E. D., Novais, E., Arkader, A., & Howard, C. (2006). Changing Patterns of Acute Hematogenous Osteomyelitis and Septic Arthritis: Emergence of Community-associated Methicillin-resistant Staphylococcus aureus.Journal of Pediatric Orthopaedics26(6), 703–708.
  9. Parikh, M. P., Octaria, R., & Kainer, M. A. (2020). Methicillin-Resistant Staphylococcus aureus Bloodstream Infections and Injection Drug Use, Tennessee, USA, 2015-2017.Emerging Infectious Diseases26(3), 446–453.
  10. Best, K., Hussien, S., Malik, A., Patel, S., & Michael, M. B. (2022). Suprapubic Osteomyelitis in an Intravenous Drug User: A Case Report. InCureus (Vol. 14, Issue 1, pp. e21312–e21312).
  11. Lauri, C., Tamminga, M., Glaudemans, A. W. J. M., Juárez Orozco, L. E., Erba, P. A., Jutte, P. C., Lipsky, B. A., IJzerman, M. J., Signore, A., & Slart, R. H. J. A. (2017). Detection of Osteomyelitis in the Diabetic Foot by Imaging Techniques: A Systematic Review and Meta-analysis Comparing MRI, White Blood Cell Scintigraphy, and FDG-PET.Diabetes Care40(8), 1111–1120.
  12. Schirò, S., Foreman, S. C., Bucknor, M., Chin, C. T., Joseph, G. B., & Link, T. M. (2020). Diagnostic Performance of CT-Guided Bone Biopsies in Patients with Suspected Osteomyelitis of the Appendicular and Axial Skeleton with a Focus on Clinical and Technical Factors Associated with Positive Microbiology Culture Results.Journal of Vascular and Interventional Radiology31(3), 464–472.
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EM Journal Club – The BUCKLED Trial

Presenter: Dr. Casey Jones (RCPSC EM PGY1)
Host: Dr. David Lewis 


Ultrasonography or radiography for suspected pediatric distal forearm fractures

Snelling et al., for the BUCKLED trial group

NEJM, 2023; 388:2049-2057.


PICO

  • Research Question: Is ultrasonography non-inferior to X-ray with respect to ..
  • Population: Children and adolescents between 5–15 years old presenting to an ED with an isolated, acute, clinically non-deformed distal forearm injury
  • Intervention: Randomization to either POCUS by a trained ED practitioner or radiography for injury evaluation
  • Comparison: POCUS vs Radiography
  • Outcome: Self-reported physical function of affected arm at 28 days

 

Background

  • Forearm fractures represent 40-50% of all childhood fractures
  • Distal third of forearm accounts for ~75% forearm fractures and 20-25% of all pediatric fractures
  • Most fractures are buckle fractures, treated conservatively with a wrist splint
  • Other pediatric fracture patterns include greenstick, Monteggia, Galeazzi, and Salter-Harris fractures
  • POCUS for distal forearm fractures is accurate, timely, and confers no radiation.
  • Ultrasonography may be more accessible in low and middle-income countries.
  • Is POCUS just as good as x-ray in diagnosing distal forearm fractures in pediatric patients?

 

Methods

  • Bedside Ultrasound Conducted in Kids with Distal Upper Limb Fractures in the Emergency Department (BUCKLED) trial
  • Study Design: Multi-center, open-label, noninferiority, randomized controlled trial
  • Setting: Four centers in Queensland, Australia (large tertiary pediatric hospital, two large mixed academic hospitals with dedicated pediatric treatment areas within their emergency departments, and one mixed hospital without a dedicated pediatric treatment area)
  • Inclusion criteria
    • Age 5-15
    • Distal forearm injury requiring radiological evaluation
    • Ability to follow up (distance from centre, telephone, internet access)
  • Exclusion criteria – many, but namely:
    • Obvious angulation
    • Injury sustained >48 hr prior to presentation
    • Compound / open fracture, neurovascular compromise, known bone disease
    • Suspicion of non-accidental injury, additional injuries
  • Imaging modalities
    • X-Ray – minimum 2 views performed by radiography. Classified by treating clinician (not radiologist) into either: no fracture, buckle fracture, other fracture
    • POCUS – 6-view forearm POCUS protocol with assessment of secondary signs (Snelling et al., 2020, BMJ)

 

  • POCUS credentialling
    • Scans in the study were done by either: nurse practitioner, physiotherapist, or emergency physician
    • Training course – 2 hour simulated course with lectures and staged learning (scanning)
    • 3 proctored scans on actual patients
    • Logbook of total 20 patients with a mix of at least 10 buckle and cortical breach fractures, then image interpretation quiz
  • Outcome measures:

  • Statistical analysis

    • Assumed true between-group difference in PROMIS score of 0 at 4 weeks, with noninferiority margin of 5 points (chosen by experts from trial group)
    • Power: 300 participant enrollment  outcome data for 224 participants (112 per group)  90% power with one-sided alpha of 0.025
    • Primary outcome of PROMIS score at 4 weeks was analyzed for noninferiority of ultrasonography to radiography
    • Primary analysis was with linear regression modeling to assess noninferiority of POCUS to radiography

Results

  • Participant characteristics (Table 1)
    • Well randomized groups for ultrasound and radiography (n=135 each group)
  • Primary outcome:
    • PROMIS (physical function score) at four weeks showed no difference between ultrasonography and radiography

  • Secondary outcomes:
    • No difference in physical function scores at week 1 or 8 between POCUS/X-ray
    • Parent / caregiver-reported satisfaction (5-point likert scale) appeared to be greater in POCUS group vs X-ray at 4 weeks (0.19 points) and 8 weeks (0.20 points)
    • Patients in POCUS group had shorter length of stay in the ED (median difference: 15 minutes), and shorter treatment time (median difference: 28 minutes) versus X-ray group
    • No substantial difference between groups in number of follow-up radiography films obtained up to week 8

 

Authors Discussion and Conclusions

  • The authors show that point-of-care ultrasound can be used as an initial diagnostic test in distal forearm injury in pediatric patients, with XR reserved for features suggestive of a diagnosis that leads to casting and follow-up (i.e. POCUS best suited for diagnosing buckle fractures)
  • Reduced initial radiography at initial ED presentation, especially in patients with buckle fracture or no fracture.
  • A diverse group of health care practitioners (physicians, nurse practitioners, physiotherapists) were trained to use ultrasound for this purpose
  • “The present randomized trial examined the feasibility, safety, acceptability, and timeliness of using an ultrasonography-first approach to the diagnosis of clinically non-angulated distal forearm injury in children and adolescents who presented to the emergency department.”

Discussion at journal club

Strengths

  • Well powered trial to study their question of non-inferiority of POCUS to XR
  • Feasible approach to imaging distal radius, and transferrable to many health professions
  • Showed that simple fractures can be initially imaged with POCUS only

Weaknesses

  • Children with features of a more concerning fracture (i.e. anything more than a buckle) received x-ray anyway (122 films were obtained in POCUS group vs 375 in XR group)
    • To that end, does this study show that POCUS may only be appropriate for simple fractures?

Bottom Line

This was a well-designed and executed study by this group in Australia. This method of diagnosing distal forearm injuries would be helpful in rural or resource-limited settings that don’t have readily accessible X-ray. I will certainly be using this more at the bedside in children with this injury pattern!


Further Reading

Quick Take NEJM Video

View the author’s webinar here

 

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EMSJ – Transesophageal Echo (TEE) Protocol

Please refer to our TEE introduction and video guides in the resources at the bottom of this page


EMSJ MD Protocol

Download (PDF, 2.16MB)


Information for Nursing and Respiratory Therapy

Download (PDF, 741KB)


Reminders:

  • Please ensure the probe is sent for sterilization at the end of the procedure
  • Please ensure it is returned to the Walmart HEPA cupboard when it returns (usually takes 1 hr)
  • Please save the clips to Path and ensure it is coded as a TEE – for our database

Pearls:

  • Resuscitative TEE requires 2 MDs. One to run the code, the other to exchange the EMS airway for an ETT and perform the TEE
  • The TEE probe only works with the XPORTE
  • Attach TEE probe and place the XPORTE at the head of the bed before the patient arrives
  • Exchange Intubate the patient during first pulse check, immediately followed by passing the TEE
  • Laryngoscopy can assist with directing TEE posterior to ETT, but the blade will need to be removed prior to advancing into esophagus (it gets in the way)
  • Stand at the head of the bed to control the probe.
  • Advance probe until the first view is obtained (ME4C)
  • Follow protocol
  • Defibrillation can be done with probe in situ
  • Communicate findings with the team


Videos

Introduction to TEE Guide

Introduction to Transesophageal Echo – Basic Technique

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Osteomyelitis


Medical Student Clinical Pearl by Jared Mullen

 

MD Candidate, Class of 2024

Dalhousie University

Reviewed by Dr. R Goss

Copy Edited by Dr. J Vonkeman

Pdf Download: EMSJ Osteomyelitis JMullin

 

 


Case Overview 

A 40-year-old man presents to the ER with falls and new confusion. His vitals signs are BP of 110/72, HR 135, RR 28, Temp 39.4, and GCS 14.

History of Presenting Illness

He is 2 months post-operative for ORIF of a significant R tibial plateau fracture that led to an extended hospital stay. Post-operative course was complicated by compartment syndrome requiring fasciotomy and persistent soft tissue infections that required treatment with IV antibiotics followed by PO step down after discharge. Collateral history from his wife indicates that he had been doing well at home on his PO antibiotics with daily wound dressing changes, but his status began deteriorating 2 days ago following completion of his antibiotics. He had several falls at home in the 24 hours leading to his ER presentation and his wife noted new confusion and difficulty in conversation. His leg had been looking “good” until stopping the antibiotics.

Physical Exam

On exam he appears unwell, lethargic, and he has difficulty cooperating in the assessment due to confusion. He has clear lungs, normal heart sounds, and equal and reactive pupils. Notably, his right leg is swollen, erythematic, tender, and hot to the touch from the level just above the patella to the midfoot. There are four wounds draining purulent discharge and one of the wounds has a significant sinus tract 4cm in depth with a bony endpoint.

Investigations & Initial Management

Wound swabs are obtained, and arthrocentesis of the right knee joint shows serosanguinous fluid pending analysis. Initial orders include chest x-ray, urinalysis + culture, blood cultures, routine labs + ALkPhos and CRP. Empiric antibiotics (IV cefazolin + IV vancomycin) and IV fluids are initiated.


Background

Osteomyelitis is an infection of the bone (most often bacterial) that can be broadly categorized as acute or chronic.

  • Acute osteomyelitis generally occurs following hematogenous spread and less often following direct inoculation (e.g., trauma/surgery)1. More than 50% of cases occur in children < 5 years of age2. IV drug use (IVDU) is a common cause acute osteomyelitis through hematogenous spread most often affecting the vertebral bodies3. Acute osteomyelitis presents with local clinical findings such as erythema, tenderness, edema, and warm skin.
    • Systemic findings such as fever, tachycardia, and hypotension may also be present.
    • The non-specific signs and symptoms of osteomyelitis make it difficult to differentiate from conditions such as cellulitis, septic arthritis, and even crystalline arthropathies.
      • Cellulitis is more likely to present in association with a preceding wound and findings of erythema and edema radiating from the focus of the infection/wound. In contrast, these findings in osteomyelitis are more diffuse and circumferential to the affected bone.
      • When osteomyelitis presents close to a joint it is difficult to rule-out a septic or crystalline arthropathy clinically, however, arthrocentesis and synovial fluid analysis/culture can clarify this.
  • Chronic osteomyelitis is far more common in adults and the most common mechanism is contiguous spread of infection from adjacent tissues (e.g., from a diabetic ulcer)4. It is associated with conditions and lifestyle factors that contribute to poor limb perfusion and wound healing including peripheral vascular disease, diabetes, renal/hepatic failure, EtOH abuse, and IV drug use3,5. In these populations, hematogenous spread accounts for only 20% of cases.
  • Chronic osteomyelitis should be suspected in patients who have non-healing ulcers, persistent soft tissue infections/failed antibiotic course, and draining sinus tracts5. Chronic osteomyelitis has been reported to be polymicrobial in 30 – 60% of cases with polymicrobial infections accounting for 5% of acute infections6.

In both acute and chronic, the most common offending organisms include Staphylococcus aureus (incl. methicillin-resistant Staphylococcus aureus [MRSA]), Staphylococcus epidermidis, Streptococcus species, Enterococcus species, and Pseudomonas species7. An increasing number of cases of osteomyelitis are caused by MRSA with MRSA accounting for more than one-third of infections in numerous studies7,8. IVDU is associated with an increased incidence of osteomyelitis caused by MRSA9,10.


Diagnosis

Diagnosing osteomyelitis clinically is difficult for several reasons including its overlap in presentation with other common conditions and because the presenting complaints might be non-specific with no external exam findings.

Laboratory findings such as leukocytosis, thrombocytosis, and increased CRP and ESR support the diagnosis of osteomyelitis but are non-specific5. It can take up to 2 weeks for radiographic evidence of osteomyelitis to appear (features include periosteal reaction, focal bone lysis/cortical loss, and regional osteopenia). X-rays have a reported sensitivity of 14-54% and a specificity of 68-70%1,4. With MRI, sensitivity is improved to 78-90% and specificity to 60-90%1.

In systemically unwell patients it is reasonable to do a broad infectious work-up. Blood cultures are positive in 50% of acute osteomyelitis cases but do not rule-out the diagnosis when negative1,4. A probe-to-bone test is supportive of the diagnosis of osteomyelitis and the test is positive when a blunt metal probe can be passed through a sinus tract directly to bone without intervening soft tissue. Care should be taken with the probe-to-bone test so that existing tracts are not extended deeper through soft tissues. Advanced imaging including a white blood cell (WBC) scan can be performed to visualize WBC infiltration to bone; this may also be used to determine treatment success with a reported sensitivity of 91% and specificity of 92%11. The gold standard for definitive diagnosis of osteomyelitis is bone biopsy (generally image guided) with culture and histologic examination. In osteomyelitis, CT-guide percutaneous needle bone biopsy (CTNBB) is reported as having a sensitivity of 43.0-64.6% and a specificity of 71.9-93.1%12.


Management

Initial management of osteomyelitis is with empiric antibiotics followed by targeted antibiotic selection based on culture and susceptibility testing.

  • Empiric therapy with vancomycin and Gram-negative coverage (ceftriaxone, cefepime, ciprofloxacin, etc.) is appropriate1,3.
  • Alternatives to vancomycin include daptomycin, TMP-SMX, and clindamycin.
  • Initial parenteral administration is appropriate with step-down to PO antibiotics after clinical stability, but PO can be considered alone in otherwise well patients.
  • A 4-week course and a 6-week course of antibiotics is typical for acute osteomyelitis in pediatric and adult populations, respectively5. Chronic osteomyelitis may require up to 8 weeks with several weeks of parenteral antibiotics to begin.

A surgical approach may be required in patients who fail antibiotic therapy alone, have implanted hardware, and those with tissue necrosis1.

  • Surgery primarily involves drainage and debridement of necrotic tissue, but extensive disease may cause instability that must be corrected with surgical fixation.
  • The Cierny-Mader classification of osteomyelitis can help provide insight into which patients require surgery (Figure 1)4. In this classification patients are first designated a type based on radiographic/anatomic findings followed by classification according to clinical status based on pre-existing systemic/local risk factors. Type III and IV often require surgical intervention to address “deadspace” from debrided necrotic bone (type III and IV) and to restore stability (type IV).

 


Case Conclusion 

Investigations come back with a normal chest x-ray, normal urinalysis with negative cultures, and normal arthrocentesis. Blood cultures are positive for Gram-positive cocci in clusters suggestive of Staphylococcus species (likely S. aureus). Labs show CRP elevated at 227, LKC 16.6, HGB 103, and otherwise unremarkable. X-ray series of the right leg shows several lytic lesions in the proximal third of the tibia with apparent bone resorption surrounding the implanted hardware. He is admitted to the orthopedics service pending urgent I&D and hardware removal. He is maintained on IV cefazolin and vancomycin pending culture and susceptibility testing of bone and tissue samples collected intraoperatively.


References

  1. Hatzenbuehler, J., & Pulling, T. J. (2011). Diagnosis and Management of Osteomyelitis.American Family Physician84(9), 1027–1033.
  2. Chiappini, E., Mastrangelo, G., & Lazzeri, S. (2016). A Case of Acute Osteomyelitis: An Update on Diagnosis and Treatment.International Journal of Environmental Research and Public Health13(6), 539.
  3. Yuschak, E., Chase, S., Haq, F., & Vandever, C. (2019). Demographics and Length of Stay for Osteomyelitis in Opioid Drug Users: A Unique Population with High Healthcare Costs.Cureus11(3), e4339.
  4. Calhoun, J. H., & Manring, M. M. (2005). Adult Osteomyelitis.Infectious Disease Clinics of North America19(4), 765–786.
  5. Hogan, A., Heppert, V. G., & Suda, A. J. (2013). Osteomyelitis.Archives of Orthopaedic and Trauma Surgery133(9), 1183–1196.
  6. Pichichero, M. E., & Friesen, H. A. (1982). Polymicrobial Osteomyelitis: Report of Three Cases and Review of the Literature.Clinical Infectious Diseases4(1), 86–96.
  7. Momodu, I.I., & Savaliya, V. Osteomyelitis. ]. StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan. Updated 2023 May 31.
  8. Arnold, S. R., Elias, D., Buckingham, S. C., Thomas, E. D., Novais, E., Arkader, A., & Howard, C. (2006). Changing Patterns of Acute Hematogenous Osteomyelitis and Septic Arthritis: Emergence of Community-associated Methicillin-resistant Staphylococcus aureus.Journal of Pediatric Orthopaedics26(6), 703–708.
  9. Parikh, M. P., Octaria, R., & Kainer, M. A. (2020). Methicillin-Resistant Staphylococcus aureus Bloodstream Infections and Injection Drug Use, Tennessee, USA, 2015-2017.Emerging Infectious Diseases26(3), 446–453.
  10. Best, K., Hussien, S., Malik, A., Patel, S., & Michael, M. B. (2022). Suprapubic Osteomyelitis in an Intravenous Drug User: A Case Report. InCureus (Vol. 14, Issue 1, pp. e21312–e21312).
  11. Lauri, C., Tamminga, M., Glaudemans, A. W. J. M., Juárez Orozco, L. E., Erba, P. A., Jutte, P. C., Lipsky, B. A., IJzerman, M. J., Signore, A., & Slart, R. H. J. A. (2017). Detection of Osteomyelitis in the Diabetic Foot by Imaging Techniques: A Systematic Review and Meta-analysis Comparing MRI, White Blood Cell Scintigraphy, and FDG-PET.Diabetes Care40(8), 1111–1120.
  12. Schirò, S., Foreman, S. C., Bucknor, M., Chin, C. T., Joseph, G. B., & Link, T. M. (2020). Diagnostic Performance of CT-Guided Bone Biopsies in Patients with Suspected Osteomyelitis of the Appendicular and Axial Skeleton with a Focus on Clinical and Technical Factors Associated with Positive Microbiology Culture Results.Journal of Vascular and Interventional Radiology31(3), 464–472.
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Tips and Tricks on Assessing a Pediatric Hand Injury


Medical Student Clinical Pearl by Borum Yang

 

MD Candidate, Class of 2024

Dalhousie University

Reviewed by Dr. B Ramrattan

Copy Edited by Dr. J Vonkeman

Pdf Download: EMSJ Tips and Tricks on Assessing a Pediatric Hand Injury

 


Presentation 

You’ve just arrived for your shift in the emergency department, when your preceptor says, “How about you go see this 6-year-old in room 12?”.

As a 3rd year clerk, you pick up the chart and read: “6yr old, hand injury.”


What Will Be Your Approach to History Taking? 

A mnemonic a cool R1 taught you last week pops into your head: HAND 1

H: How

You recall that knowing the context and mechanism of injury will help guide your physical exam and generate a list of differential diagnosis2. Was it a FOOSH? Laceration with a potential tendon injury? High pressure injection injury increasing the risk of compartment syndrome?

H: Hobbies

Sports and activities are important to note in pediatric hand injuries, as it will impact management. Kids can be less compliant with non use or being protective of their injured hand. We don’t want lack of immobilization to be the cause of malunions and dehisced wounds3.

A: Altered sensation

Ask about paresthesia or numbness as it can indicate a nerve injury.

N: Needle/tetanus shot

Vaccinations up to date? Because if they were rolling in the dirt or got into a fight with the neighbour’s dog, you may need to grab that tetanus shot.

N: Non-accidental injury/ Child abuse

While most childhood fractures are caused by accidental trauma, it is important to always have this in the back of your head. Be on the lookout for red flags and inconsistencies in history including unwitnessed injury, or recurring fractures. Look for presence of other injuries and bruising and /or fractures at various stages of healing4.

D: Dominant hand

From the history, it seems like the kid was playing basketball, and at one point the flying ball landed directly on the kid’s outstretched fingers. They have been complaining of pain ever since.


What Will Be Your Approach to Physical Examination? 

You quickly realize that the physical exam will be a challenge, as the kid is distracted and guarding their painful hand. Inspection alone can go along way with peds exams. You quickly go through the SEADS in your head:

On inspection, there is an obvious swelling and bruising of the right small finger. You quickly glance at the rest of the hand to check for other abnormalities or deformities. Nail beds and nail folds intact? Normal creases of the hands and fingers? Any areas of laceration or open wounds?  Unusual skin changes, color changes, or atrophy of the thenar and hypothenar eminence? Don’t forget to compare findings with the non-injured hand.

Next, you test sensation of the median, ulnar and radial distribution by asking if the kid can feel touch over their thumb, small finger and back of their hand.

Now determine active and passive range of motion. If the kid is not capable of following directions, asking the kid to play ROCK PAPER SCISSORS 5 is a good way to quickly glance at the motor function and integrity of tendons. Being able to straighten out all fingers without evidence of extensor lags. Making a full fist makes you less suspicious of a flexor tendon injury. Being able to cross fingers or manipulate them makes you less suspicious of an ulnar nerve injury.

Next, you want to check for any evidence of displaced or rotated fractures by observing the cascade of the fingers. A trick is to ask the kid to totally relax the hand, and you put the wrist in passive flexion. All fingers should passively extend. Then, you put his wrist in passive extension. All fingers should passively flex and for the most part point towards the base of the thumb. This is called the tenodesis exam and is helpful in looking for tendon injuries independent of nerve or muscle function.

Lastly, you keep chatting with the child while you gently palpate the wrist, carpal bones including the snuff box, PIP, DIP, MCP joints to rule out any other injuries.

There is normal capillary refill, and focal tenderness on palpation at the base of the proximal phalanx.

You report back to your preceptor and decide to order a hand x ray.

Figure 1: PA radiograph showing minimally displaced oblique Salter Harris type II fracture of the proximal phalanx of the right small finger6.

 

Upon discussion, the right hand is immobilized in an ulnar gutter to ensure proper immobilization. The time window for intervention maybe shorter in children than adults due to faster healing times. A call to a hand surgeon at the time of presentation is never a bad idea if you are unsure of the management. The kid is discharged with a follow up with the plastic surgeon as an outpatient within a week.


Summary

 

  1. Assessing hand injuries in pediatric patients can be challenging due to ability or willingness to cooperate. It can be helped with thorough observation, and use of familiar gestures and “games”
  2. The complete hand exam includes assessment of the skin, vascularity, sensation, motor function and the underlying skeleton.
  3. Management of pediatric hand fractures differ from adult fractures due to differences in anatomy, rate of healing and patient compliance.

Helpful Videos from Boston Children’s Hospital on the Pediatric Hand Examination


References

  1.  

    1. Fox, S. (2023, May 16). Finger injuries: Basics and bones. Don’t Forget the Bubbles. https://dontforgetthebubbles.com/finger-injuries-basics-and-bones/
    2. Taghinia, A. H. (2020, May 18). 39 Pediatric Hand Trauma. Plastic Surgery Key: Fastest Plastic Surgery & Dermatology Insight Engine. Retrieved June 15, 2023, from https://plasticsurgerykey.com/39-pediatric-hand-trauma/
    3. Helman, A. (2023). Ep 178 Hand Injuries – Pitfalls in Assessment and Management. Emergency Medicine Cases. https://emergencymedicinecases.com/hand-injuries-assessment-management/
    4. Chauvin-Kimoff L, Allard-Dansereau C, Colbourne M. The medical assessment of fractures in suspected child maltreatment: Infants and young children with skeletal injury. Paediatr Child Health. 2018;23(2):156-160. doi:10.1093/pch/pxx131
    5. Marsh AG, Robertson JS, Godman A, Boyle J, Huntley JS. Introduction of a simple guideline to improve neurological assessment in paediatric patients presenting with upper limb fractures. Emerg Med J. 2016;33(4):273-277. doi:10.1136/emermed-2014-204414
    6. Wahba G, Cheung K. Pediatric hand injuries: Practical approach for primary care physicians. Can Fam Physician. 2018;64(11):803-810.

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Pancreatic Pseudocysts: An Uncommon Cause of Painless Jaundice


Medical Student Clinical Pearl by Thomas Camp

 

MD Candidate, Class of 2024

Dalhousie University

Reviewed by Dr. J Vonkeman

Copy Edited by Dr. J Vonkeman

Pdf Download: EMSJ Pancreatic Pseudocysts: An Uncommon Cause of Painless Jaundice

 


Introduction

It’s 6:30 pm on a Monday evening, and a 52-year-old man presents to the ER with overt jaundice. He says that he’s been feeling great and that he only came in because his coworkers have been teasing him about his changing skin colour.


History and Physical

The patient reports that his skin has been turning yellow for the past week. He denies abdominal pain, nausea, vomiting, weight loss, fever, and fatigue. He also denies any pruritus, bruising, gastrointestinal bleeding, abdominal distension, or mental status changes. On further questioning, he reveals that his stool was pale this morning and that his urine has been unusually dark. Last year he was admitted to hospital for acute pancreatitis, which was thought to be induced by heavy alcohol consumption.

He is unaware of any other medical conditions and does not take any regular medications or herbal supplements. The patient denies any alcohol consumption since his previous admission, any history of IV drug use, and any history of international travel or blood transfusions. He smokes two packs of cigarettes per and there is an extensive family history of gastric cancer.

Physical examination reveals a thin, overtly jaundiced man with scleral icterus and a strong scent of tobacco. His lungs are clear, and his heart sounds are normal. His abdomen is soft and nontender, and there is no evidence of organomegaly or extra hepatic manifestations of liver disease (Figure 1). Ultrasound reveals a distended gallbladder and biliary tree without stones.


Approach to Jaundice

Jaundice is the result of excessive bilirubin levels in the blood, and bilirubin is a product of heme catabolism.2 The differential diagnosis for jaundice is broad but, conceptually, can be divided into pre-hepatic, intra-hepatic, and post-hepatic causes (Figure 2).3

  • Pre-hepatic jaundice is the result of excessive unconjugated bilirubin production, which overwhelms the liver’s ability to conjugate it for excretion. Hemolysis is the most common cause of pre-hepatic jaundice.
  • Intra-hepatic jaundice is the result of either decreased bilirubin uptake or impaired bilirubin conjugation within the liver’s hepatocytes,4 leading to impaired secretion in the bile. Common causes include viral hepatitis, drug toxicity, alcoholic hepatitis, and any of the many conditions leading to cirrhosis.
  • Post-hepatic jaundice is the result of biliary obstruction, which impairs the flow of bile into the duodenum. Gallstones and cancer are the most common cause, but pancreatic pseudocysts, primary sclerosing cholangitis, and bile duct strictures are also possible etiologies.

The distention of the biliary tree, the presence of acholic stools, and dark urine suggests post-hepatic jaundice in this patient.  These are characteristic findings of post-hepatic jaundice because the lack of bilirubin entering the duodenum results in pale stools, and at the same time conjugated bilirubin is water soluble, giving urine a dark colour.3 His age, sex, smoking status, and family history are also significant risk factors for pancreatic cancer, which commonly presents with jaundice.5

 


Work Up

Laboratory investigations reveal conjugated hyperbilirubinemia with a large increase in ALP and a mild increase in ALT. This is a cholestatic pattern of liver injury, which is characterized by a fourfold or greater increase in ALP and absent or mild elevations in the aminotransferases.6,7 In contrast, a hepatocellular pattern of liver injury is characterized by elevated aminotransferases and normal or mildly elevated ALP.6,7

INR and albumin levels are normal, suggesting that synthetic liver function is preserved. Normal hemoglobin levels (that are also stable when compared to the patient’s historical baseline) help exclude hemolysis from the differential. Elevated lipase is worrying for pancreatic cancer but could be explained by obstruction of the pancreatic duct by another cause, for example, gallstones not appreciated on ultrasound.

An urgent CT scan is ordered, and the radiologist comments that there is a complex cystic mass arising from the head of the pancreas that is causing obstruction of the common bile and pancreatic ducts. He notes that underlying malignancy cannot be excluded, and endoscopic retrograde cholangiopancreatography (ERCP) is recommended for further investigation. The patient is referred to gastroenterology and discharged home.


Conclusion 

A week later, ERCP confirms that the mass is in fact a pancreatic pseudocyst. Pancreatic pseudocysts are collections of fluid with a well-defined wall that lack the epithelium required to be classified as true cysts. Classically, they form after an episode of acute pancreatitis, but they are also seen in chronic pancreatitis, in obstruction of the pancreatic duct, and after pancreatic trauma.8 The cyst is drained endoscopically, a technique that is now considered preferable to a percutaneous approach due to its excellent rates of resolution (82-94%).9 The patient’s jaundice resolves over the following weeks and repeat laboratory investigations normalize within two months.


Key Points

  • Categorizing jaundice as pre-hepatic, intra-hepatic, or post-hepatic can provide a useful framework for formulating a differential diagnosis.
  • A fourfold or greater increase in ALP with mild or no elevation in the aminotransferases is characteristic of post-hepatic jaundice.
  • Consider pancreatic pseudocysts in patients presenting with post-hepatic jaundice, especially if they have a recent history of acute pancreatitis.

References

  1. Scott L Friedman M. Clinical manifestations and diagnosis of alcohol-associated fatty liver disease and cirrhosis. In: Post TW, ed. UpToDate. Wolters Kluwer; 2023. https://www.uptodate.com/contents/clinical-manifestations-and-diagnosis-of-alcohol-associated-fatty-liver-disease-and-cirrhosis
  2. John S, Pratt DS. Jaundice. In: Loscalzo J, Fauci A, Kasper D, Hauser S, Longo D, Jameson JL, eds. Harrison’s Principles of Internal Medicine, 21e. McGraw-Hill Education; 2022. http://accessmedicine.mhmedical.com/content.aspx?aid=1197684641
  3. Beckingham IJ, Ryder SD. ABC of diseases of liver, pancreas, and biliary system. Investigation of liver  and biliary disease. BMJ. 2001;322(7277):33-36. doi:10.1136/bmj.322.7277.33
  4. Wolkoff AW. The Hyperbilirubinemias. In: Loscalzo J, Fauci A, Kasper D, Hauser S, Longo D, Jameson JL, eds. Harrison’s Principles of Internal Medicine, 21e. McGraw-Hill Education; 2022. http://accessmedicine.mhmedical.com/content.aspx?aid=1190492793
  5. Freelove R, Walling AD. Pancreatic cancer: Diagnosis and management. Am Fam Physician. 2006;73(3).
  6. Moseley RH. EVALUATION OF ABNORMAL LIVER FUNCTION TESTS. Medical Clinics of North America. 1996;80(5):887-906. doi:https://doi.org/10.1016/S0025-7125(05)70472-7
  7. Bethea ED, Pratt DS. Evaluation of Liver Function. In: Loscalzo J, Fauci A, Kasper D, Hauser S, Longo D, Jameson JL, eds. Harrison’s Principles of Internal Medicine, 21e. McGraw-Hill Education; 2022. http://accessmedicine.mhmedical.com/content.aspx?aid=1190492731
  8. Habashi S, Draganov P V. Pancreatic pseudocyst. World J Gastroenterol. 2009;15(1):38-47. doi:10.3748/wjg.15.38
  9. Piraka C, Chen YK. Pseudocyst Drainage: ERCP and EUS Approaches. Tech Gastrointest Endosc. 2007;9(3). doi:10.1016/j.tgie.2007.05.002
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A Case of Spaghetti Wrist: Approach to an Extensive Volar Forearm Laceration in the ED


Medical Student Clinical Pearl by Krystal Stewart

 

 

MD Candidate, Class of 2024

Dalhousie University

Reviewed by Dr. F MacKay

Copy Edited by Dr. J Vonkeman

Pdf Download: EMSJ A Case of Spaghetti Wrist: Approach to an Extensive Volar Forearm Laceration in the ED

 


Case Presentation

A 13-year-old male presents to the Emergency Department by ambulance, with a deep laceration to his distal volar forearm. The injury occurred at a friend’s house, after tripping on a bong with the shattered glass lacerating his left wrist. The patient was intoxicated by cannabis at the time of arrival and experienced bouts of age regression while attempting to assess and treat him. He is otherwise healthy, with no significant past medical history and is not taking any regular medications. This was an isolated injury; no other lacerations were found on the body, and blood loss at the site of injury was well controlled by the time of arrival at the ED.

On physical examination, pertinent findings consist of the ulnar arterial pulse not being palpable, no sensation throughout the ulnar nerve distribution of the hand, and the flexor carpi ulnaris tendon is visibly torn. Capillary refill was normal, with perfusion being provided solely by the radial artery – which remains intact. Motor examination of the hand was difficult to assess due to patient’s intoxicated state and pain level. The patient felt he was unable to move his hand but was able to wiggle his thumb and index finger.

The on-call plastic surgeon was consulted to assess the defect. The wound was washed out with saline and briefly explored under local anesthetic by the surgeon. Subsequently, the wound was closed with simple interrupted sutures and a volar slab splint was placed on the hand and forearm for temporary stability. The patient was admitted overnight to the pediatric floor to await further exploration in the OR and reparation of the ulnar artery, ulnar nerve, and several flexor tendons.


Anatomical Context

Figure 1: Carpal tunnel anatomy of the volar wrist.1


Clinical Approach

A deep laceration of the distal volar forearm may otherwise be known as the “spaghetti wrist,” due to the number of potential structures that could require repair, including tendons, nerves, and vessels. This term came about from the appearance of lacerated tendons overlying the red background of muscle.2 There lacks a unified classification system for this term in the literature, thus defining a volar forearm laceration and its level of severity as a spaghetti wrist injury is more subjective – with an arbitrary sum of structures lacerated.3

First begin by assessing the patient for hemodynamic instability, if bleeding – apply direct pressure, if it continues a temporary tourniquet may be needed.2 It is important to evaluate for hemorrhagic shock and resuscitation prior to assessment of the hand.2

Vascular status of the hand can be assessed with capillary refill or Doppler ultrasound to each fingertip.2 If the hand is considered well perfused and bleeding is well controlled, surgical exploration can be delayed, as it will take several days for cut tendons, nerves, and vessels to retract.2 If there is concern for arterial laceration, palpation for radial and ulnar pulses would be valuable.

The next important assessment is a focused sensory and motor examination of the hand. Lightly touch at the three sensory areas that represent the cutaneous radial, median ulnar innervation of the hand as demonstrated in Figures 2 and 3.2 Evaluating the extrinsic and intrinsic hand muscle innervation requires a focused motor examination, as demonstrated in Figure 4.2 Have the patient demonstrate a series of hand gestures, the “OK” sign using the index finger and the thumb represents the muscles innervated by the median nerve.2 By abducting the digits, this represents the muscles innervated by the ulnar nerve.2 Lastly, demonstrating a “thumbs up” sign represents the muscles innervated by the radial nerve.2 If there is lack of sensation at a particular sensory distribution and/or lack of ability to demonstrate those representative hand gestures for extrinsic and intrinsic muscle innervation, it should be noted that the associated nerve(s) may be damaged.

To evaluate for any associated injuries to bone, muscle, tendon or ligament, gentle manipulation and palpation is required, along with assessing passive and active range of motion.2 It may also be valuable to assess if there is any ulnar or radial deviation of the wrist.2

 

 

Figure 2: Cutaneous innervation of the volar hand.2

 

Figure 3: Cutaneous innervation of the dorsal hand.2

 

Figure 4: Motor examination of the hand. I: Median nerve, II: Ulnar nerve, III: Radial nerve.2


Management 

Important information to gather on clinical history include the use of anticoagulants, diagnosis of advanced liver disease or diabetes. As the former two impair hemostasis, and the latter may impair wound healing.2 Broad spectrum IV antibiotics may be warranted if the wound is largely contaminated or extensive in size.2 There is a potential risk of contracting tetanus based on the mechanism of injury, thus it is important that the patient has tetanus prophylaxis.2,4An X-ray of the hand and forearm may be necessary if suspicion of a bony fracture.

A consult should be sent to the Plastic Surgery service for further management, including surgical exploration and reparation of any lacerated nerves, tendons, and vessels. These structures begin to retract after injury; thus, it is important that reparation is done within two weeks of injury. If plastic surgeon on call is planning to see the patient in clinic, have the forearm and wrist dorsally splinted at the position of safe immobilisation – wrist in 0-30 degree of extension, MCP joints in 70-90 degrees of flexion and IP joints in full extension.5,6 Once the repair is completed and appropriate hand immobilization has been achieved, the patient should see a designated occupational hand therapist for further patient education and hand rehabilitation.


Prognosis 

The road to recovery largely depends on the patient’s willingness to undergo post-operative rehabilitation and adhere to the regimens set forth by the surgeon and the occupational hand therapist. Age and smoking status may also impact neurologic recovery.5 Nerve regrowth from the site of laceration is a slow process, with approximately 1 mm in growth daily.5 Recovery tends to be functional, with less emphasis on perfection. Ulnar innervation tends to be less predictable in regrowth of intrinsic muscles.5 Possible long-term sequelae include stiffness, neuropathic pain, and cold intolerance.5


Key Points

  • If the hand is de-vascularized, immediate emergency surgery is essential.5
  • If the injury was self-inflicted, a consult to psychiatry is recommended once medically cleared.5
  • Negative prognostic factors include increasing age, low education level, presence of a crush injury.7

Complications

With complex volar forearm lacerations there is the risk of developing acute compartment syndrome post-injury. Diagnosis of acute compartment syndrome is achieved clinically, with signs of swollen and taut muscle compartment(s), pain out of proportion to the injury, or severe pain with passive digital extension.2 Neurological deficits present as a late feature of the syndrome, including paresthesia, paresis and then paralysis.2 Paresthesia is an indicative feature of early nerve ischemia.2 The intra-compartmental absolute pressure may also be measured if suspicious of compartment syndrome – an emergent forearm fasciotomy should be done if greater than or equal to 30 mmHg.2

Post-operative complications may include major deformity of hand due to clawing, ‘anesthetic hands,’ as well as neuromas – being the most cited complication.3 The former two are most likely due to the initial injury rather than a complication from the surgery itself.3 The term ‘clawing’ refers to an ulnar nerve palsy, where the hand will resemble that of a claw hand.8

 


Conclusion

While the Spaghetti Wrist terminology does not have a severity scale, it is intuitively known to be an emergent case with the need for prompt management. Whether the cause of injury was accidental or self-inflicted, the same steps must be taken to ensure that the function of the hand can be salvaged – as the impact on the patient’s physical function and psychological health could be enormous if not managed correctly.


References

  1. Hansen JT, Netter FH. Netter’s Clinical Anatomy. 2nd Philadelphia, PA: Saunders/Elsevier; 2010.
  2. Thai JN, Pacheco JA, Margolis DS, et al. Evidence-based Comprehensive Approach to Forearm Arterial Laceration.West J Emerg Med. 2015;16(7):1127-1134. doi:10.5811/westjem.2015.10.28327
  3. Koshy K, Prakash R, Luckiewicz A, Alamouti R, Nikkhah D. An Extensive Volar Forearm Laceration – The Spaghetti Wrist: A Systematic Review.JPRAS Open. 2018;18:1-17. Published 2018 Jul 11. doi:10.1016/j.jpra.2018.06.003
  4. Bae C, Bourget D. Tetanus. In:StatPearls. Treasure Island (FL): StatPearls Publishing; August 19, 2022.
  5. Meals CG, Chang J. Ten Tips to Simplify the Spaghetti Wrist.Plast Reconstr Surg Glob Open. 2018;6(12):e1971. Published 2018 Dec 12. doi:10.1097/GOX.0000000000001971
  6. Dobson P, Taylor R, Dunkin C. Safe splinting in hand surgery.Ann R Coll Surg Engl. 2011;93(1):94. doi:10.1308/003588411×12851639108033
  7. De M, Singhal M, Naalla R, Dave A. Identification of Prognostic Factors in Spaghetti Wrist Injuries.J Hand Surg Asian Pac Vol. 2021;26(4):588-598. doi:10.1142/S2424835521500569
  8. Lane R, Nallamothu SV. Claw Hand. In:StatPearls. Treasure Island (FL): StatPearls Publishing; January 8, 2023.
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A Case of Boerhaave Syndrome


Medical Student Clinical Pearl by Jillian Allan

MD Candidate, Class of 2024

Dalhousie University

Reviewed by Dr. R Goss

Copy Edited by Dr. J Vonkeman

Pdf Download: EMSJ JAllan A Case of Boerhaave Syndrome

 


Case Presentation

44-year-old male presents to the ER with a 5-hour history of retrosternal chest pain and recent onset shortness of breath. He was out drinking the previous night and has been profusely vomiting since 5am.


Differential Diagnosis

A variety of conditions may present in this fashion:

  • GERD/Gastritis/ Esophagitis/Gastric ulcer
  • Pneumothorax
  • Aortic dissection
  • Acute pancreatitis
  • ACS/MI
  • Cannabis hyperemesis syndrome
  • Esophageal rupture

History and Physical

Upon arrival to the ER, he is hemodynamically unstable: tachycardic (125), hypotensive (90/58) and febrile (38.2 C). His O2 sats are 86% on RA. He has no history of gastroesophageal reflux or other relevant medical conditions. He does not use cannabis.

On examination, his abdomen is soft, he is tender in the left upper quadrant and diffusely across his chest wall. Breath sounds are decreased on the leftIn addition, he has bilateral supraclavicular crepitus on palpation and a positive Hamman’s crunch (mediastinal crackling, synchronous with the heartbeat) on auscultation. His neck is becoming increasingly distended, and you have noticed a change in phonation since his arrival.


Etiology 

Boerhaaves syndrome is most commonly caused by profuse vomiting but can also be the result of anything that increases esophageal pressure such as weightlifting, seizures, abdominal trauma, locally invasive cancers/infections, childbirth, or compressed air injuries.7


Pathophysiology 

  • Esophageal perforations are classified into 3 groups:
    • Cervical esophagus: can present with neck tenderness, dysphagia, or dysphonia
    • Thoracic esophagus: presents with severe back pain, pleuritic, chest or epigastric pain, inability to lie supine. Most common area for perforation.
    • Intra-abdominal esophagus: Peritonitis

 

  • Severity of perforation tends to depend on the location of rupture, with intrathoracic esophageal ruptures leading to more devastating outcomes.
    • Intrathoracic rupture results in contamination of the thoracic cavity with gastric contents, which can lead to chemical mediastinitis, infection and mediastinal necrosis.6
    • Barogenic rupture of the cervical esophagus has a more benign course, as the spread of contamination to the mediastinum is slow and attachments of the esophagus to the prevertebral fascia limit the lateral dissemination of esophageal flora.6


Evaluation

  • Diagnosis is established through a computed tomography (CT) scan of the chest or contrast enhanced esophagram. Contrast should be water soluble (gastrografin) to avoid mediastinal contamination with barium contrast.
    • CT: Findings suggestive of esophageal rupture include esophageal wall edema and thickening, peri-esophageal fluid, mediastinal widening, and free air/fluid within the pleural spaces, retroperitoneum, or lesser sac.6
    • Radiography: Plain films may also demonstrate air in the soft tissues of the prevertebral space. Other indications can include pleural effusion, hydropneumothorax, mediastinal widening or subdiaphragmatic air.6 While thoracic and cervical radiography can aid in diagnosis, they cannot exclude or confirm esophageal rupture and should not routinely be performed to diagnose this condition. However, a plain radiograph may be performed, and mediastinal air found incidentally when the diagnosis had not been suspected.
    • Esophagram: Reveals the location and extent of perforation of the esophagus by the extravasation of the contrast medium.6
  • Endoscopy should be performed with caution due to the risk of further esophageal damage.

Case Continued

Laboratory results showed elevated leucocytes at 12.9 x 109/L (normal 4.5-11.5) and an elevated C-reactive protein level but were otherwise unremarkable.

An erect chest radiograph and urgent CT was done, which showed the “V” sign of Naclerio, a V shaped collection of air along the mediastinum and diaphragm, indicating pneumomediastinum (Fig.1a).2 An urgent contrast CT confirmed the radiograph findings, showing pneumomediastinum and left hydropneumothorax (Fig. 1b).2

 

Figure 1. Boerhaave syndrome in a 44-year-old man. (A) Chest radiograph showing Naclerio’s V sign, demonstrating air outlining the mediastinal borders (arrows), indicating pneumomediastinum. (B) Chest CT showing pneumomediastinum and left hydropneumothorax.2

  

Esophageal perforation was confirmed with a contrast esophagram, which showed leakage from the lower esophageal sphincter into the left pleural space.

 

Figure 2. Contrast esophagram showing esophageal rupture at lower esophageal sphincter with leakage into the left pleural space.1


Treatment and Management

  • Mainstay of treatment includes volume resuscitation, broad-spectrum antibiotic coverage, and surgical evaluation.
  • 3 treatments options: conservative, endoscopic, or surgical
    • Conservative: typically reserved for small or contained ruptures.
    • Endoscopic: stent placement to prevent fistula formations or seal esophageal leaks.
    • Surgical: primary esophageal repair via open thoracotomy vs VATS (video-assisted thoracoscopic surgery) with fundic reinforcement- which is the gold standard of treatment if within 24 hours.7

Case Conclusion

The patient underwent an emergency VATS procedure which revealed a small tear in the lower esophagus, which was successfully repaired with sutures and a pleural patch. The patient made an uneventful recovery and was discharged on postoperative day 6.


Summary of Key Points


References

  1. Calvin S.H. Ng, Wilfred L.M. Mui and Anthony P.C. Yim. Barogenic esophageal rupture: Boerhaave Syndrome. CAN J SURG December 01, 2006 49 (6) 438-439;
  2. Chew, Fatt Yang; Yang, Su-Tso. Boerhaave Syndrome. CMAJ 2021 September 27;193:E1499. doi:10.1503/cmaj.202893.
  3. Kassem MM, Wallen JM. Esophageal Perforation And Tears. [Updated 2022 Aug 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK532298/
  4. Kukuruza K, Aboeed A. Subcutaneous Emphysema. [Updated 2022 Jul 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK542192/
  5. Rawla P, Devasahayam J. Mallory Weiss Syndrome. [Updated 2022 Oct 9]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK538190/
  6. Triadafilopoulos, G. Boerhaave Syndrome: Effort rupture of the esophagus. In: UpToDate, Waltham, MA. (Accessed on October 29th, 2022).
  7. Turner AR, Turner SD. Boerhaave Syndrome. [Updated 2021 Dec 15]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK430808/
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