A Case of Facial Nerve Palsy

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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 Physician, 84(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 Health, 13(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.Cureus, 11(3), e4339.
  4. Calhoun, J. H., & Manring, M. M. (2005). Adult Osteomyelitis.Infectious Disease Clinics of North America, 19(4), 765–786.
  5. Hogan, A., Heppert, V. G., & Suda, A. J. (2013). Osteomyelitis.Archives of Orthopaedic and Trauma Surgery, 133(9), 1183–1196.
  6. Pichichero, M. E., & Friesen, H. A. (1982). Polymicrobial Osteomyelitis: Report of Three Cases and Review of the Literature.Clinical Infectious Diseases, 4(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 Orthopaedics, 26(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 Diseases, 26(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 Care, 40(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 Radiology, 31(3), 464–472.
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Serum Sickness-Like Reaction

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Medical Student Pearl by Nicole Barry1 & Laura Harkness2

1. B.Sc., M.A., MD Candidate, Class of 2024, Memorial University

2.B.Sc., MD Candidate, Class of 2025, Dalhousie University

Reviewed by Dr. M McGraw & Dr. M Kovalik

Copy Edited by Dr. J Vonkeman

Pdf Download: EMSJ Serum Sickness-Like Reaction  NBarry & LHarkness

 

Case Overview 

History of Presenting Illness

A 5-year-old male arrives at the emergency department (ED) with his mother who is concerned her son is having an allergic reaction. She reported that the week prior, he presented to his family doctor’s office with general malaise and productive cough. He tested positive for Group A Streptococcal infection and was started on amoxicillin. The day prior to arriving at the ED, he developed a purpuric urticarial rash that covered his trunk and extremities which continued to progress. He complained of bilateral ankle pain and fatigue. The patient had no past medical history, was not on any other medications, his family history was unremarkable, and had no known allergies. There was no recent change in diet or environmental exposures.

Physical Exam

The patient had a temperature of 38.3 degrees. All other vital signs were normal. On exam, his gait was antalgic. His trunk and extremities had multiple large, erythematous, annular plaques. The lesions were pruritic, non-blistering, and non-photo sensitive (see Figure 1). His lips were erythematous, and cheeks appeared flush. His mucous membranes were spared. Head and neck exam was otherwise unremarkable. His ankles were swollen bilaterally, limited range of motion in all directions and non-tender to palpation. His knees were also swollen bilaterally, non-tender, positive patellar tap test. Wrist did not show signs of swelling, restricted motion, or pain.

Investigations

Based on the wheal-like rash, Lyme disease, Vasculitis and Kawasaki were ruled out. Reactive arthritis was unlikely with a lack of family history. Throat swab was collected to rule out post-streptococcal glomerulonephritis. Based on the age of the child, further blood work was held while throat swab was analyzed as to not cause distress. Renal function, CPR and Lyme anti-bodies may be indicated if the child was otherwise unwell with high degree of suspicious of a more severe diagnosis.

Diagnosis

Given the presentation, you consider serum sickness-like reaction as a diagnosis. You consult dermatology for their opinion.

The dermatologist on call confirms the diagnosis as serum sickness-like reaction.

 

Figure 1. Drug-induced urticaria in a pediatric patient (CincinattiChildren’s.org).

Serum Sickness-Like Reaction

Serum sickness was originally named due to the compilation of symptoms following injection of horse serum for treatment of scarlet fever and diphtheria1. Traditionally, the term serum sickness should be reserved for those reactions following a heterologous or chimeric protein therapeutic.

Other, similar acute inflammatory presentations are referred to as serum sickness-like reactions (SSLR), and classically present with a characteristic rash, fever, malaise, and polyarthralgia or polyarthritis one to two weeks after exposure to a causative agent2. If a patient has previously been exposed to the causative agent, the reaction may occur sooner. Serum sickness-like reaction is a type of hypersensitivity reaction following the administration of a substance, including vaccines or other medicines. Common antibiotics shown to result in SSLR are cefaclor, amoxicillin, and trimethoprim-sulfamethoxazole3-5. Serum sickness-like reaction is also highly associated with certain non-steroidal anti-inflammatory drugs, anti-cancer agents, and biologics4.  Serum sickness-like reaction can also occur following certain infections, particularly streptococcal infection, and hepatitis B6,7.

Normally self-limiting, SSLR most often subsides within weeks after discontinuing the responsible agent8. Onset of symptoms of SSLR is tri-phasic, with the first peak at day 5 post exposure, second peak at day 7 and third at day 1010. Although most seen in adults, SSRL are an increasingly common etiology of acute arthritis in children9,10.

The differential diagnosis for such reactions can include, but is not limited to:

  • Autoimmune diseases, including systemic lupus erythematosus, reactive arthritis.
  • Drug reactions, such as drug reaction with eosinophilia and systemic symptoms, Stevens-Johnson syndrome, drug-induced sweet syndrome.
  • Infectious diseases, including Epstein-Barr virus, Lyme disease, erythema multiforme, disseminated meningococcemia.
  • Vasculitis, including IgA vasculitis (Henoch-Schoenlein purpura), hypersensitivity vasculitis.

Diagnosis

The diagnosis of SSLR is typically based on the characteristic compilation of symptoms, including the typical urticarial-like lesions, arthralgias, with or without fever, secondary to, most commonly, drug exposure11. It’s important to rule out Steven-Johnson Syndrome/Toxic Epidermal Necrolysis in both pediatric and adult populations with lack of mucous membrane involvement8.

Pathophysiology

Serum sickness-like reaction is a Coombs type III/immune complex mediated hypersensitivity reaction. The formation of antigen-antibodies complexes, involving an antigen and coinciding antibody, are required for the reaction to occur. The immune complex formation of serum sickness is mediated by C3 and C5a complement proteins which recruit mast cells and neutrophils to release histamines resulting in vascular permeability (Figure 2). Normally excreted by phagocytes, they are unable to clear these complexes due to the overwhelming number of complexes formed or the under performance of the mononuclear phagocyte system. These immune complexes target certain organs in the body—why they target some and not others are not well understood. Typically, they will target joint spaces, presumed to be due to the fenestrations into the synovial fluid. Once deposited in areas of the body, these complexes will activate an inflammatory response12.

Figure 2. Type III immune complex mediated hypersensitivity mechanism of serum sickness.

 

Treatment

Serum sickness-like reactions resolve when the agent responsible is discontinued and cleared from the patient’s system. Most patients do not require additional treatment. Symptoms typically subside within two to three weeks, but in some cases may linger for up to three months. If required, arthralgias and fever can be treated with non-steroidal anti-inflammatory and analgesic medications11. For patients with severe symptoms, glucocorticoid medications can be prescribed. Intravenous immunoglobulin may be indicated for worsening or unresolving symptoms. Outcomes of serum sickness and SSLR are good, and prolongation of symptoms more than 40 days is uncommon10. Offending drug should be avoided in the future. In situations where the causative agent cannot be discontinued, treatment is highly dependent on the drug in question, and should be based on a case-by-case basis13.

Case Conclusion

While in the ED, the dermatologist on call recommended to discontinue the amoxicillin that the patient was taking for Group A Strep. Supportive measures were also recommended, as well as analgesics or NSAIDs for symptom management. The dermatologist agreed to follow up with this patient in the subsequent days to ensure resolution of symptoms and whether future treatment was needed.

References

  1. von Pirquet CF, Schick B. (Die Serumkrankheit). Serum Sickness, Schick B (Ed), Williams & Wilkins, Leipzig 1905 (translation Baltimore 1951).
  2. Vincent C, Revillard JP. Antibody response to horse gamma-globulin in recipients of renal allografts: relationship with transplant crises and transplant survival. Transplantation 1977; 24:141.
  3. Clark BM, Kotti GH, Shah AD, Conger NG. Severe serum sickness reaction to oral and intramuscular penicillin. Pharmacotherapy 2006; 26:705.
  4. Brucculeri M, Charlton M, Serur D. Serum sickness-like reaction associated with cefazolin. BMC Clin Pharmacol 2006; 6:3.
  5. Stricker BH, Tijssen JG. Serum sickness-like reactions to cefaclor. J Clin Epidemiol 1992; 45:1177.
  6. Hengge UR, Scharf RE, Kroon FP, Pfeffer K. Severe serum sickness following pneumococcal vaccination in an AIDS patient. Int J STD AIDS 2006; 17:210.
  7. Liang, Jake T. “Hepatitis B: the virus and disease.” (2009): S13-S21.
  8. Wener, Mark H., N. F. Adkinson Jr, and A. M. Feldweg. “Serum sickness and serum sickness-like reactions.” UpToDate. Wolters Kluwer Health, Philadelphia, PA (2013).
  9. Yorulmaz A, Akın F, Sert A, et al. Demographic and clinical characteristics of patients with serum sickness-like reaction. Clin Rheumatol 2018; 37:1389.
  10. Kunnamo I, Kallio P, Pelkonen P, Viander M. Serum-sickness-like disease is a common cause of acute arthritis in children. Acta Paediatr Scand 1986; 75:964.
  11. Del Pozzo-Magaña, Blanca R., and Alejandro Lazo-Langner. “Serum sickness-like reaction in children: review of the literature.” Dermatology 7 (2019): 106-111.
  12. Tolpinrud WL, Bunick CG, King BA. Serum sickness-like reaction: histopathology and case report. J Am Acad Dermatol 2011; 65:e83.
  13.  Bayraktar F, Akinci B, Demirkan F, et al. Serum sickness-like reactions associated with type III insulin allergy responding to plasmapheresis. Diabet Med 2009; 26:659.
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EM Journal Club – The BUCKLED Trial

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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

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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

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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 Physician, 84(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 Health, 13(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.Cureus, 11(3), e4339.
  4. Calhoun, J. H., & Manring, M. M. (2005). Adult Osteomyelitis.Infectious Disease Clinics of North America, 19(4), 765–786.
  5. Hogan, A., Heppert, V. G., & Suda, A. J. (2013). Osteomyelitis.Archives of Orthopaedic and Trauma Surgery, 133(9), 1183–1196.
  6. Pichichero, M. E., & Friesen, H. A. (1982). Polymicrobial Osteomyelitis: Report of Three Cases and Review of the Literature.Clinical Infectious Diseases, 4(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 Orthopaedics, 26(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 Diseases, 26(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 Care, 40(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 Radiology, 31(3), 464–472.
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Tips and Tricks on Assessing a Pediatric Hand Injury

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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.

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.

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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PoCUS For Maxillary Sinusitis

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PoCUS Clinical Pearl by Dr. Chew Kiat Yeoh

 

 

DalEM PoCUS Fellow

Reviewed by: Dr. David Lewis

 

 

 

Background

  • Acute rhinosinusitis is an inflammatory disease of nasal mucosa and paranasal sinuses. It is one of the most common ED presentations and fifth most common diagnosis for which antibiotics are prescribed (1).
  • It affects more than 30 million adult each year (2).
  • Accurate diagnosis of acute maxillary sinusitis based on clinical examination is unreliable (3) because the signs/symptoms are nonspecific.
  • Although radiographic imaging improves diagnostic accuracy, it is not recommended in uncomplicated sinusitis (4) due to radiation risk, additional costs, and time.

 

How accurate is PoCUS in identifying maxillary sinusitis?

  • Gold standard for diagnosing maxillary sinusitis is positive fluid culture obtained from sinus puncture (5). However, this method is invasive, unnecessary, and often not easily accepted by patient.
  • Ultrasound has been used to diagnose acute maxillary sinusitis as it is rapid, safe, and non-invasive.
  • Ultrasound is very sensitive in identifying fluid in sinus cavities, with accuracies more than 90% for the diagnosis of maxillary sinusitis have been reported in otolaryngology (ENT) practices.
  • While the result from ENT practices might not be applicable to the ED setting due to different patient demographic and severity of disease. When PoCUS performed by Emergency Physician compared to CT in ED patients with suspected maxillary sinusitis, the sensitivity and specificity are 81% and 89%, respectively, for diagnosis of maxillary sinusitis (7). The agreement between the two methods was 86%.
  • Study using MRI as gold standard, ultrasound was found to have 64% sensitivity and 95% specificity, compared to 73% sensitivity and 100% specificity for plain XR (6).
  • Overall – ultrasound is sensitive in detecting fluid in sinus cavities and highly accurate (>90%) in diagnosing maxillary sinusitis.

 

Scanning Technique

  • Position: sitting upright or lean slight forward to ensure sinus fluid if present, would layer out against the anterior wall.
  • Probe: High frequency (4 to 12 MHz) linear array transducer with adequate depth penetration (5-7cm) to visualize the entire sinus cavity Or phased-array probe if depth required.
  • Scan the maxillary sinus in between lateral nose and zygoma in at least two planes: transverse & sagittal (Figure 1).
  • Always scan the contralateral normal side is for comparison.

Ultrasound Features

Normal Ultrasound Appearance of Maxillary Sinus

 

 

The Ultrasound Appearance of Maxillary Sinusitis

  • If the sinus cavity is fluid filled (complete or partial), the ultrasound signal will be able to penetrate through the thin hyperechoic anterior wall, and the surrounding walls (posterior, medial, lateral) of the sinus will be visualized and seen as a bright echogenic line.
  • Positive Ultrasound finding : Presence of posterior wall echo >3.5 cm from the initial echo (3) (anterior maxillary wall)

 

Partially Filled: Partial Sinusogram

 

Completely Filled: Complete Sinusogram

 

 

The significance of the Pathology and how can PoCUS add value?

  • More than 1 in 5 antibiotics prescribed in adults are for sinusitis. It is the fifth most common diagnosis which antibiotics is prescribed.
  • Rhinosinusitis is a common disorder, however, only 50% of patients presenting to the acute care setting with sinus symptoms have acute bacterial sinusitis.
  • Although, ultrasound is not accurate as CT and MRI, it is a more practical adjunct bedside tool that can be rapidly, safely and routinely used to assess those with sinus symptoms and for diagnosing uncomplicated sinusitis in acute care settings and could potentially reduce unnecessary over prescription of antibiotic use.

 

Pearls and Pitfalls

  • Ultrasound is not helpful in differentiating between a viral and or bacterial sinusitis.
  • Positive sinusogram can also be caused by significant mucosal thickening, polyps, fluid-filled cysts, masses and blood from facial trauma or sinus fractures. All these can be mistaken for acute sinusitis.
  • Technical failure includes inadequate depth setting to properly visualize the posterior wall and improper position(supine).

 

References

  1. Summary E. Otolaryngology – Head and Neck Surgery Antimicrobial treatment guidelines for acute bacterial rhinosinusitis. 2004;130(January):1-45. doi:10.1016/j.otohns.2003.12.003
  2. Rosenfeld RM, Andes D, Bhattacharyya N, et al. Clinical practice guideline : Adult sinusitis. Published online 2007:1-31. doi:10.1016/j.otohns.2007.06.726
  3. Varonen H, Mäkelä M, Savolainen S, Läärä E, Hilden J. Comparison of ultrasound , radiography , and clinical examination in the diagnosis of acute maxillary sinusitis : a systematic review. 2000;53:940-948.
  4. Aring ANNM, Chan MM. Acute Rhinosinusitis in Adults. Published online 2011:1057-1063.
  5. Carolina S, Sur- N, Hospital HF, Cen- HM, Carolina S. Maxillary sinus puncture and culture in the diagnosis of acute rhinosinusitis : The case for pursuing alternative culture methods. Published online 2000:7-12. doi:10.1067/mhn.2002.124847
  6. Puhakka T, Heikkinen T, Makela MJ, et al. Validity of Ultrasonography in Diagnosis of Acute Maxillary Sinusitis. Arch Otolaryngol Head Neck Surg 126(12):1482–1486, 2000.
  7. Price D, Park R, Frazee B, et al. Emergency department ultrasound for the diagnosis of maxillary sinus fluid. Acad Emerg Med. 2006;13(3):363-4

 

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PoCUS Guided Nerve Blocks in EM

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Recommended resources  for PoCUS Guided Nerve Blocks in EM

This page is under maintenance – future updates will include a ‘Plan A‘ list of blocks with associated guides.

EMSJ Resources

Collection of our nerve block guidelines, clinical pearls and rounds

Fascia Iliaca Block

Serratus Anterior Plane Block

Dental Block

Regional Anesthesia of the Hand

Other Resources

Local Anesthetic Dose

LAST

Overview of Common Nerve Blocks in the ED

Recommended Nerve Block Resources

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Pancreatic Pseudocysts: An Uncommon Cause of Painless Jaundice

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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

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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
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