Tag Archives: med student pearl

A Case of Facial Nerve Palsy

Posted on by

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.
Continue Reading

Serum Sickness-Like Reaction

Posted on by

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.
Continue Reading

Osteomyelitis

Posted on by

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.
Continue Reading

Tips and Tricks on Assessing a Pediatric Hand Injury

Posted on by

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.

Continue Reading

Pancreatic Pseudocysts: An Uncommon Cause of Painless Jaundice

Posted on by

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
Continue Reading

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

Posted on by

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.
Continue Reading

A Case of Boerhaave Syndrome

Posted on by

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/
Continue Reading

A Meeting with the Curb: Review of Lip Laceration Repair

Posted on by

Medical Student Pearl by Nick Ellingwood

MD Candidate, Class of 2024

Dalhousie University

Reviewed by Dr. B Ramrattan

Copy Edited by Dr. J Vonkeman

Pdf Download:  EMSJ NEllingwood Review of Lip Laceration Repair

Case Presentation

A 68-year-old female presents to the ED with facial trauma. She tells you that she was walking in a parking lot trying to remember where she parked when she suddenly tripped over a curb and scraped her face on the asphalt. She remembers the event and did not lose consciousness. She denies any nausea/vomiting, headache, or blurry vision. She arrived at the ED by EMS who say that her GCS has remained 15. She tells you that she is a healthy individual other than her diabetes for which she takes Metformin and Ozempic. She does not smoke or drink alcohol. She tells you numerous times during your history that she is very worried about her lip injury and how it will look after it heals.

On exam, she is alert and oriented to person, place, and time. She has an abrasion over her nasal bridge and a laceration at the midline of her lower lip which is approximately 1.5cm deep extending all the way through the vermillion. Her upper right incisor is chipped. She is tender over her nasal bone. Her pupils are equal and reactive, and she has normal extra-ocular movements. She has normal facial sensation and strength and there is symmetrical rise of the uvula. There is no battle sign, hemotympanum, or periorbital bruising. You quickly test her sensation and strength is all her extremities which is normal.

Figure 1: Similar lip laceration as the patient in this case. (Benjamincousinsmd.com)

Associated Injuries

Before repairing a lip laceration, associated injuries must be considered. Common associated injuries include dental fractures, LeFort fractures, nasal bone fractures and jaw fractures.1 Much less common, but can’t miss, associated injuries include intracranial bleed, basal skull fracture, or orbital floor fractures.

Impression/Plan

Given that she is older than 65 years old, you can’t rule out a head injury based of the Canadian CT Head Rule. However, given the mild mechanism of injury and the lack of signs/symptoms of intracranial pathology you decide to forego a CT head and turn your attention to the lip laceration.

Background

When repairing a lip laceration, extra vigilance is needed to ensure proper cosmetic appearance and to preserve the functionality of the lips. It is often one of first facial features people look at when talking to someone and therefore, minimal scarring and good aesthetic are often very important to patients presenting with these lacerations. The lips are also important in tactile sensation, phonation, and mastication.

Evaluation

Lip lacerations are almost always repaired with primary closure because of the difference in aesthetic outcome between primary and secondary closure. Secondary closure may be appropriate in patients with a delayed presentation, signs of infection (erythema, drainage of pus), or contamination in the wound.1 Evaluation of the laceration includes location, length, depth, involvement of the vermillion border and presence of contamination or foreign bodies. Make sure to examine the internal and external lip as partial thickness without vermillion border involvement could be managed conservatively.

Figure 2: Anatomy of the superficial and deep structures of the lips (UpToDate, 2023)1

Anesthesia

Local anesthesia is often avoided in lip lacerations as it can cause swelling which will contort the laceration making it more difficult to maximize the cosmetic appearance. In young children, conscious sedation is needed as they will not stay still for the repair even if they are anesthetized. In adults, infraorbital nerve blocks are used for upper lips lacerations and mental nerve block are used for lower lip lacerations. These nerve blocks provide excellent anesthesia and the landmarking for these blocks are relatively simple. The supraorbital foramen, infraorbital foramen and mental foramen are lined up in a midsagittal plane (See figure 3). Another way to landmark the mental foramen is to find the midpoint between the alveolar crest of the second premolar and the inferior border of the mandible.2 When the mental foramen is located, inject 2-3cc of 1% lidocaine with epinephrine and bicarbonate approximately 1cm under the skin towards the mental nerve. If your laceration is at the midline, then bilateral mental nerve blocks will be needed. Next, wait 15-20 minutes to allow for the anesthetic to take full effect before starting the repair.

Figure 3: Anatomical location of the supraorbital foramen, infraorbital foramen, and mental foramen. (Can J Anesth/J Can Anesth 56, 704–706 (2009).)2

Laceration Repair

Once the laceration is fully anesthetized, you can irrigate the wound and thoroughly examine the laceration. You need to rule out any foreign bodies in the lip through palpation as teeth fragment may not be initially visualized. If in doubt, a lateral XRay may rule out any teeth fragments in the lips as they are radiopaque. You may need to get an extra set of hands to help evert the lip when closing the inner lip portion of the laceration. The most important suture in this repair is the suture at the vermillion border as lining up the vermillion border perfectly will yield the best cosmetic result.3,4Some clinicians prefer to close the inner and outer fibrofatty junction before the vermillion border, whereas some will put their first suture at the vermillion border before closing the deeper tissues. After these steps, you simply need to bring the rest of the lacerations back together. Most clinicians will use either 4-0 or 5-0 absorbable sutures for their deep sutures then 5-0 or 6-0 absorbable sutures for the superficial sutures depending on the anticipated tension on the wound when closed.

Aftercare

The main considerations for aftercare of wounds are tetanus, prophylactic antibiotics, and follow-up.

  • A tetanus booster should be given to patients who are unsure as to when their last dose was or if it has been greater than 5 years since their last Tdap.
  • The evidence of prophylactic antibiotic treatment for lip lacerations is lacking. One study by Steele et al showed that there may be a benefit to prophylactic antibiotics in full thickness lip lacerations such as our case, but their results were not statistically significant.5 The face in general is such a highly vascularized area that if the patient is healthy and not taking any immunosuppressants medications, then the risk of infection is low, and antibiotics are not needed. Irrigation with salt water 2-3x/day is sufficient.
  • Lastly, simple lip lacerations that were repaired in the ED with satisfactory results don’t need Plastics follow-up. If the lip is quite disfigured and you are worried about the cosmetic results, then these patients should be seen by Plastics either in the ED or within 24 hours. Follow-up after several days or more should be avoided as the laceration will already be in the healing stage. This would make any revision and/or alteration to cosmetic results difficult.

References

  1. Hollander, J., &amp; Weinberger, L. (2022, September). Assessment and management of lip lacerations. UpToDate.
  2. Tsui, B.C.H. Ultrasound imaging to localize foramina for superficial trigeminal nerve block. Can J Anesth/J Can Anesth 56, 704–706 (2009).
  3. Espinosa MC, Hohman MH, Sivam S. Oral and Maxillofacial Surgery, Facial Laceration Repair. [Updated 2023 May 26]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-.
  4. Armstrong, B. Denise. “LACERATIONS OF THE MOUTH.” Emergency medicine clinics of North America 18.3 (2000): 471–480. Web.
  5. Steele, Mark T et al. “Prophylactic Penicillin for Intraoral Wounds.” Annals of emergency medicine 18.8 (1989): 847–852. Web

 

Continue Reading

Understanding Urachal Anomalies

Posted on by

 

Medical Student Pearl by Alexander MacPherson

MD Candidate, Class of 2024

Dalhousie University New Brunswick

Reviewed by Dr. B Ramrattan

Copy Edited by Dr. J Vonkeman

Pdf Download: EMSJ Understanding Urachal Anomalies by AMacpherson

 

Case Presentation

17-year-old male presents to the emergency room with what he tells you is a pop bottle amount pus-like fluid discharging from his belly button. He appears well and said that this has happened before, but it was never in this amount. He and his family members are, however, concerned as to what may be causing this unusual presentation. Patient denies any past abdominal surgeries or piercings.

Physical Exam

  • Vitals: HR 70, BP 118/78, RR 14, T 37.3°C
  • Tenderness in the periumbilical region
  • Discharge of whitish, mucus-like liquid.
  • Red, dome shaped swelling at centre of umbilicus.

Differential Diagnosis [1]

  1. Urachal anomaly
  2. Abscess
  3. Benign lesion (hamartomas, pyogenic granulomas etc.)
  4. Primary malignancy (urachal adenoma, melanoma, squamous cell carcinoma and basal cell carcinoma).
  5. Metastatic lesion
  6. Omphalitis

Common Clinical Findings of Urachal Anomalies [1]

Urachal anomalies when found in children typically present with:

  • Umbilical drainage
  • Abdominal pain
  • Abnormal appearance of the umbilicus, with a palpable mass
  • Infection
  • Incidental finding

Urachal anomalies when found in adulthood typically present with:

  • Hematuria
  • Pain
  • Dysuria
  • Incidentally

Investigations

  • The primary investigation for a urachal anomaly is through Imaging.
    • Most urachal remnants are diagnosed via abdominal ultrasonography.
    • CT abdomen, MR abdomen and Voiding Cystourethrography (VCUG) are also used to detect and diagnose urachal anomalies and to confirm that there are no associated genitourinary tract abnormalities. [1,2].
  • Our patient received an ultrasound and went on for a CT abdomen to confirm the diagnosis of urachal cyst.

Treatment

  • Surgical resection seems to be the most definitive way to manage and prevent the return of symptoms. It is also important to note that adults presenting with urachal anomalies are at a considerable progressive risk for cancer and if not removed should undergo routine screening.
  • Early removal of urachal remnants at first diagnosis are deemed to be best at preventing future morbidity by some studies, while others recommend that children who are experiencing asymptomatic lesions do not benefit from prophylactic excision [1,2,3]
  • Our patient was referred to general surgery and the urachal cyst was excised.

Background on Urachal Anomalies

During embryologic development the allantois has a connection to the apex of the fetal bladder. This connection is called the urachus and allows for fetal bladder emptying [4]. In a normally developing fetus, the bladder descends into the pelvis. This decent of the bladder stretches the urachus and its lumen is eventually obliterated. The now obliterated urachus is a fibrous cord that is called the median umbilical ligament and continues to be connected to the umbilicus and the bladder. This process, like any other, can be disrupted [5].

The disruption can be divided into several urachal anomalies based on the amount of and where the residual tissue is located (Figure 1):

  1. Patent urachus: A complete failure of closure of the lumen forming a tubular connection between the bladder and umbilicus. Allows for urine to drain through the umbilicus.
  2. Bladder diverticulum: Extra tissue present at the bladder end but does not continue to the umbilicus.
  3. Umbilical polyp: Extra tissue and patency at the umbilical end that does not continue to the bladder.
  4. Urachal cyst: An area of patency in between the bladder and umbilicus that does not communicate with either [1,4].

Figure 1. Urachal anomaly types. Accessed from UpToDate [6]

An Important Note on Malignancy

  • Although there have been no reports of urachal adenocarcinoma in the urachal anomalies resected from children a longitudinal study by Ashley et al (2007) found that 51% of those resected from adults showed evidence of malignancy. It was also determined that age >55 and hematuria were the strongest predictors for malignancy [2].
  • A comprehensive review performed by Gleason et al (2013) however determined that urachal anomalies are more common that previously reported and that the number needed to excise to prevent one case of urachal adenocarcinoma was 5,721 [3]

References

  1. Palazzi, D. L., & Brandt, M. L. (2021, August 27).Care of the umbilicus and management of umbilical disorders. UpToDate. Retrieved April 16, 2022, from https://www.uptodate.com/contents/care-of-the-umbilicus-and-management-of-umbilical-disorders
  2. Ashley RA, Inman BA, Routh JC, Rohlinger AL, Husmann DA, Kramer SA. Urachal anomalies: a longitudinal study of urachal remnants in children and adults. J Urol. 2007 Oct;178(4 Pt 2):1615-8. doi: 10.1016/j.juro.2007.03.194. Epub 2007 Aug 16. PMID: 17707039.
  3. Gleason JM, Bowlin PR, Bagli DJ, Lorenzo AJ, Hassouna T, Koyle MA, Farhat WA. A comprehensive review of pediatric urachal anomalies and predictive analysis for adult urachal adenocarcinoma. J Urol. 2015 Feb;193(2):632-6. doi: 10.1016/j.juro.2014.09.004. Epub 2014 Sep 16. PMID: 25219697.
  4. Briggs KB, Rentea RM. Patent Urachus. [Updated 2021 Jun 9]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK557723/
  5. Naiditch, Jessica A.; Radhakrishnan, Jayant; Chin, Anthony C.(2013). Current diagnosis and management of urachal remnants. Journal of Pediatric Surgery, 48(10), 2148–2152.        doi:10.1016/j.jpedsurg.2013.02.069
  6. Retrieved from: https://www.uptodate.com/contents/image?imageKey=PEDS%2F79324&topicKey=PEDS%2F5009&search=urachal+cyst+infection&rank=1%7E150&source=see_link

Continue Reading

Could it be Kawasaki Disease?

Posted on by

 

Medical Student Pearl by Farhad Hossain

MD Candidate, Class of 2024

Dalhousie University

Reviewed by Dr. M McGraw

Copy Edited by Dr. J Vonkeman

Pdf Download: EMSJ Could it be Kawasaki Disease FHossain

 

 

 

Case Presentation

A 6-year-old female presents to the Emergency Department with a history of a fever over 5 days. She had initially visited the ED a few days ago, where croup was suspected, and she was administered a dose of dexamethasone with minimal improvement. On the day she was brought in for the second time her fever had peaked. Her mom reports increased fatigue and decreased PO intake over the duration, as well as rash.

On physical exam vitals were stable aside from an elevated temperature. Mucosal changes were observed inside her mouth and on her tongue, a non-pruritic rash was present over most of her body, and she had enlarged cervical nodes and an otitis media of the right ear. Further examination showed no pharyngitis, no conjunctivitis, lungs were clear, and heart sounds were normal.

Aside from previous croup and infections, she is otherwise healthy.

Labs yielded elevated CRP and WCC.

Given the clinical picture you consider Kawasaki Disease.

Kawasaki Disease

Kawasaki disease (KD) is an acute systemic vasculitis that mostly affects small and medium size vessels.1-3 It is typically self-limited and usually presents in those under the age of 5.1 Kawasaki disease is now the most common cause of acquired heart disease in children in developed countries due involvement of the coronary arteries.4,5 There are no pathognomonic tests, so diagnosis is dependent on key clinical signs and exclusion of other diagnoses on the differential. A differential can include the following:

  • Scarlett fever
  • Peritonsillar abscess
  • Group A Strep
  • Rheumatic fever
  • Measles

Etiology and Pathophysiology

While several theories have been proposed to explain the cause of KD, none have been definitively proven. Evidence suggests that genetic factors increase the predisposition of KD as siblings are more likely develop it than the general population, as well as those of Japanese descent.3,4 The trigger for the disease has also been believed to be some viral or bacterial antigen that enters the body through mucosal surfaces such as the lung as roughly 40% of children diagnosed with KD tested positive for a viral pathogen.1-4 Various cytokines and immune cascades lead to myocarditis and arteritis, eventually this may cause weak spot in the vessel that predisposes the formation of aneurysms.2,4

Diagnosis

The diagnosis of KD is clinical and requires the presence of fever that has persisted for 5 or more days that is not better explained by another cause and 4/5 of the following:1,3-6

  • Extremity changes such as erythema of the palms/soles and desquamation of the fingers/toes
  • An erythematous rash that is commonly a maculopapular eruption, but urticarial and multiforme-like rashes have been seen. The rash is usually diffuse and affects the trunk and extremities.
  • Bilateral bulbar conjunctival injection with uveitis often observed.
  • Changes to the oral mucosa include erythema, fissuring, strawberry tongue (erythema and prominent fungiform papillae), and diffuse erythema of the oral mucosa.
  • Cervical adenopathy is usually unilateral and confined to the anterior cervical triangle but is the least common clinical finding observed.

Patients can meet the definition of typical or classical KD, but those who do not meet the set criteria can be diagnosed with incomplete KD based off of clinical, laboratory, and echocardiographic findings.6 The following figure shows the evaluation of suspected KD:6

Figure 1: Algorithm for the evaluation of typical Kawasaki Disease. Figure obtained from UpToDate.

 

Aside from measuring CRP, additional lab findings are assessed in those with incomplete KD. The evaluation of suspected incomplete KD is shown in the below figure:1

 

Figure 2: Algorithm for the evaluation incomplete Kawasaki Disease. Figure obtained from McCrindle et al.

People with either complete or incomplete KD should receive an echocardiogram to assess for coronary artery aneurysm in the acute phase of the disease, as well as other cardiac abnormalities.1 It is common for initial echocardiography to be normal, but it does establish a baseline for sequential scans.

Treatment

Treatment for KD should be initiated immediately if clinical criteria are met. It is treated with intravenous immunoglobulin (IVIG) and high dose aspirin.1-6 The maximum dose of IVIG is 2 g/kg and it has been shown that increasing dose (up 2 kg/kg) reduces risk of CA aneurysms and duration of fever.1,5 Aspirin, usually 30 to 100 mg/day divided into 4 doses, modifies the risk in KD leading to lower risk of thrombosis.1,3,5 Studies have demonstrated that combining IVIG with corticosteroids has better effect on reducing coronary artery abnormalities in those who are refractory to initial therapy.1,4 Disease modifying anti-rheumatic drugs and antibodies have been used to treat KD, but there is not enough evidence to recommend their use as treatment.3 Patients often start seeing improvements in 36 to 48 hours. Long term management depends on the patient and the risk of coronary events reaches a peak at 5 to 6 weeks after the acute phase.

Case Conclusion

The patient was started on amoxicillin 500 mg tid down in the Emergency Department for the otitis of the right ear and within 12 hours showed improvement. It was determined she met 3 of 5 criteria for KD along with the fever that persisted for 5 days, so an echocardiogram was ordered. Upon review of the echocardiogram there were no findings suggestive of KD. The patient was discharged with a script of amoxicillin and instructed to follow up with her family doctor if conditions worsen.

References

  1. McCrindle BW, Rowley AH, Newburger JW, et al. Diagnosis, Treatment, and Long-Term Management of Kawasaki Disease: A Scientific Statement for Health Professionals From the American Heart Association. Circulation. 2017;135(17). doi:10.1161/CIR.0000000000000484
  2. Noval Rivas M, Arditi M. Kawasaki disease: pathophysiology and insights from mouse models. Nat Rev Rheumatol. 2020;16(7):391-405. doi:10.1038/s41584-020-0426-0
  3. Ramphul K, Mejias SG. Kawasaki disease: a comprehensive review. Arch Med Sci Atheroscler Dis. 2018;3(1):41-45. doi:10.5114/amsad.2018.74522
  4. Owens AM, Plewa MC. Kawasaki Disease. In: StatPearls. StatPearls Publishing; 2023. Accessed March 30, 2023. http://www.ncbi.nlm.nih.gov/books/NBK537163/
  5. Galuppo J, Kowker A, Rolfs J, Nicholas J, Schmidt E. Kawasaki disease: Shedding light on a mysterious diagnosis. J Am Acad Physician Assist. 2020;33(7):18-22. doi:10.1097/01.JAA.0000668792.41976.f2
  6. Sundel R. Kawasaki disease: Clinical features and diagnosis. Post TW, ed. UpToDate.Waltham, MA: UpToDate Inc. UpToDate.com (Accessed on March 30, 2023)

Continue Reading

An EM Approach to Syncope in Adults

Posted on by

 

Medical Student Pearl

Samarth Fageria

Med 3

Memorial University of Newfoundland Class of 2024

Reviewed by Dr. J Gross

Copy Edited by Dr. J Vonkeman

Pdf Download: EMSJ An EM Approach to Syncope by SFargeria

 

Case

A 60-year-old male presented to the ED after experiencing recurrent episodes of syncope. The first episode occurred at a convenience store in an upright position. He denied prodrome and exertional activity at the time of syncope. After a transient loss of consciousness, he woke up confused with urinary incontinence. He felt nauseous and had emesis in the ambulance on the way to ED. He had two more episodes of syncope over the span of two hours. On assessment in the ED, he endorsed a past history of light-headedness preceded by laughing and holding his breath. He denied dyspnea and chest pain. He had no significant past medical history. There was no family history of cardiovascular disease and syncope, and social history was unremarkable.

 

On examination, he was alert and oriented. He had a minor laceration on his forehead from the fall. His respiratory and cardiovascular exams were unremarkable, neurological exam was normal. In the ED, his blood work was unremarkable. He was placed on telemetry when he had two more episodes of syncope. The monitor showed 20-second-long sinus pauses corresponding with the syncopal episodes. Cardiology was consulted and he was temporarily placed on intermittent transcutaneous pacing.

 

 

Differential Diagnosis of Syncope2

True Syncope

1. Reflex (autonomic hypersensitivity)

  • Vasovagal, carotid sinus hypersensitivity, situational

2. Orthostatic hypotension

  • Volume depletion, autonomic failure

3. Cardiac

  • Valvular (aortic stenosis, mitral stenosis), dysrhythmias (bradyarrhythmia, ventricular tachyarrhythmia, supraventricular tachyarrhythmia), mechanical (pacemaker dysfunction), cardiomyopathy, infiltrative (eg. hemochromatosis, sarcoidosis, amyloidosis), acute MI, ARVC, cardiac tamponade, acute aortic dissection

Other Causes

1. Medication/ Drug-induced

  • Anti-hypertensives, QT prolonging meds, insulin, alcohol, anti-depressants, anti-glycemic agents, diuretics, anti-anginal agents, etc

2. Transient Loss of Consciousness (TLOC)

    • Traumatic brain injury, seizure disorders, intoxications, hindbrain TIA, conversion disorders and metabolic abnormalities

 

Background

Syncope is defined as a brief, sudden, transient loss of consciousness due to cerebral hypoperfusion1. The three broad categories of syncope are reflex, orthostatic and cardiac syncope. The most common cause of cardiac syncope includes dysrhythmias1. A good past medical history of cardiovascular disease is important as it is 85-94% sensitive and 64-83% specific in predicting a cardiac etiology of syncope1.

Diagnostic Workup

Diagnostic workup for syncope requires a thorough history, physical exam, and a 12-lead ECG. Cardiac monitoring is necessary in patients that present to ER with an acute presentation of syncope, and a strong suspicion for cardiac etiology2. History should consist of identifying high-risk features that warrant a prompt cardiology consult2. A detailed HPI should consist of asking about an absence of a prodrome, exertional or supine syncope, concomitant trauma, past medical history of cardiovascular disease and family history of sudden cardiac death (<50 years)2. Low-risk features include presence of a prodrome, specific triggers (eg. dehydration, stress, laughter), syncope while upright and the absence of cardiovascular disease2. Vital signs and a cardiac exam should be completed2. If cardiac causes of syncope cannot be ruled out on first assessment, a 12-lead ECG should be placed to assess for dysrhythmias or conduction disease, and serial troponin values should be collected2.

 

Though there are multiple clinical decision rules for syncope, the following have been externally validated: Evaluation of Guidelines in Syncope Study (EGSYS), San Francisco Syncope Rule and Osservatorio Epidemiologico sulla Sincope nel Lazio (OESIL)1. Patients that are stratified as high risk require admission for further evaluation. EGSYS predicts the probability of cardiac syncope at two years based on abnormal ECG findings (eg. BBB, sinus bradycardia), heart disease (eg. ischemic, structural), palpitations before syncope, as well exertional and positional syncope, symptoms of prodrome (nausea/vomiting) and predisposing/precipitating factors1. An admission is warranted if the patient scores a three or higher as there is a 21% mortality risk at two years1. The OESIL risk score estimates a 1-year all-cause mortality in patients presenting with syncope1. The factors include age (>65), history of cardiovascular disease, lack of prodrome and abnormal ECG characteristics (eg. BBB, AV conduction disorders and hypertrophy)1. Admission is warranted for one or more variables1. The Canadian Syncope Risk Score can be used in patients presenting to ER with syncope to predict a 30-day serious adverse events2.  It consists of factors such as abnormal QRS axis, corrected QT interval >480 ms, elevated troponin (>99th percentile of normal population) and ED diagnosis based on evaluation to stratify patients into risk categories: very low (-3 to -2), low (-1 to 0), medium (1 to 3), high (4 to 5) and very high (6 to 11)2.

The Canadian Journal of Cardiology recommends a disposition algorithm for patients presenting to ER with syncope that is based on history of a serious medical condition and high-risk features3. Figure 1 illustrates an approach to disposition from the ER. Patients that have an unclear etiology and intermediate risk should be considered for an urgent cardiology assessment.

 

Figure 1: A disposition plan for patients presenting to the ER with syncope (Canadian Cardiovascular Society 2020).

Best Practice for Treatment

Given the benign course, treatment for vasovagal syncope is based on lifestyle modification, education and reassurance2. Lifestyle modification consists of educating patients on identifying and managing prodromes early and managing triggers (eg. dehydration, defecation, micturition, laughing, coughing and crowded environments)2.

Treatment for orthostatic syncope also relies on lifestyle modification, education and reassurance2. Lifestyle modification consists of re-adjusting diuretics, ACE-inhibitors, angiotensin receptor blockers, calcium channel and beta blockers to ensure optimal blood pressure and hydration control2.

Managing cardiac syncope requires addressing the underlying etiology through antiarrhythmic medications (eg. tachyarrhythmias), cardiac pacing (eg. bradyarrhythmias), catheter-directed ablation and ICD insertion1. Cardiac pacemaker therapy is indicated for patients that have intermittent sinus node disease if correlation is identified between sinus pauses on ECG and syncope3. Selected patients that are diagnosed with the bradycardia-tachycardia form of sick sinus syndrome, can benefit from a percutaneous cardiac ablative technique3.  Dual-chamber pacing is recommended for patients with sinus node dysfunction provided there is an increased risk of AV block4.

Case continued

The patient was admitted and had no further asystole after receiving atropine and intermittent transcutaneous pacing. He was accepted for a dual-chamber pacemaker insertion and was discharged with the diagnosis of syncope with sinus arrest and vagal overtones.

Take Home Points

  1. Patients presenting to the ER with new-onset syncope require a thorough history and physical exam to rule out cardiogenic causes.
  2. Validated clinical decision-making tools can be helpful to supplement clinical judgement for assessing the risk of a future cardiac event, identifying the need for a cardiology consult and creating a disposition plan.

References

  1. Runser LA, Gauer RL, Houser A. Syncope: Evaluation and Differential Diagnosis. Am Fam Physician. 2017;95(5):303-312. https://www.aafp.org/pubs/afp/issues/2017/0301/p303.html#:~:text=A%20standardized%20approach%20to%20syncope,%2C%20physical%20examination%2C%20and%20electrocardiography
  2. UpToDate. www.uptodate.com. https://www.uptodate.com/contents/syncope-in-adults-clinical-manifestations-and-initial-diagnostic-evaluation
  3. Sandhu RK, Raj SR, et al. Canadian Cardiovascular Society Clinical Practice Update on the Assessment and Management of Syncope. Can J Cardiol. 2020;36(8):1167-1177. doi:10.1016/j.cjca.2019.12.023 https://www.onlinecjc.ca/article/S0828-282X(19)31549-1/fulltext
  4. Brignole M, Moya A, de Lange FJ, et al. 2018 ESC Guidelines for the diagnosis and management of syncope. Eur Heart J. 2018;39(21):1883-1948. doi:10.1093/eurheartj/ehy037https://academic.oup.com/eurheartj/article/39/21/1883/4939241?login=false
  5. Dakkak W, Doukky R. Sick Sinus Syndrome. In: StatPearls. Treasure Island (FL): StatPearls Publishing; July 18, 2022. https://www.ncbi.nlm.nih.gov/books/NBK470599/

Continue Reading

Approach to Inguinal and Femoral Hernias in the Emergency Department

Posted on by

Medical Student Pearl

Julia Short

Med 2

DMNB Class of 2025

Reviewed by Dr D Lewis

Copy Edited by Dr. J Vonkeman

PDF Download: EMSJ Approach to Inguinal and Femoral Hernias in the ED by JShort

Case

A 52-year-old male patient presents in the ER with a lump in their right groin. The lump protrudes when they cough and when laying on their left side, although it re-enters the abdomen on its own. You wonder if it could be a femoral or an inguinal hernia, and how to go about differentiating between the two.

Introduction

A hernia is defined as an organ, or part of an organ, that protrudes through the body wall in which it is normally contained. The etiology of a hernia can be due to congenital anatomical malformations or from acquired weakening of the body wall tissues. There are various subtypes of abdominal hernias, while groin hernias consist of inguinal and femoral hernias. Throughout their lifetime, males have a 27 to 43% chance of developing a groin hernia, while females have a 3 to 6% lifetime prevalence1. Although it is much more likely that a groin hernia is inguinal in nature (they account for 96% of groin hernias), it is clinically useful to identify and distinguish between the types of groin hernias. Additionally, there are important clinical features that must not be overlooked when characterizing a groin hernia.

Distinguishing inguinal from femoral hernias

An important landmark in determining the hernia origin is the inguinal ligament. Inguinal hernias protrude superior to the inguinal ligament, while femoral hernias present inferior to the inguinal ligament (Figure 1). This is because femoral hernias protrude from the femoral ring, located medial to the femoral vein. As a result, in males, femoral hernias will never course into the scrotum. Femoral hernias also present more lateral than inguinal hernias and may be difficult to differentiate from lymph nodes. Although they account for only 3% of all groin hernias, 40% of femoral hernias present as urgent due to bowel strangulation or incarceration1. Females are more likely to develop femoral hernias, while males are more likely to develop inguinal hernias.

Figure 1. Groin anatomy © 2023 UpToDate7

Distinguishing between direct and indirect inguinal hernias

Direct inguinal hernias originate medially, near the pubic tubercle and external inguinal ring. They protrude through Hesselbach’s triangle as a result of weakness in the floor of the inguinal canal. On exam, a bulge near the external (superficial) inguinal ring is suggestive of a direct inguinal hernia. In contrast, indirect inguinal hernias protrude near the midpoint of the inguinal ligament, at the internal (deep) inguinal ring (Figure 2). In males and females respectively, the internal inguinal ring is where the spermatic cord and round ligament exit the abdomen. A bulge in this area therefore suggests an indirect inguinal hernia. This type of hernia is the most common in all ages and sexes, accounting for approximately two thirds of all inguinal hernias2. In males, the indirect hernia often courses into the scrotum, which can be palpated if the patient strains or coughs. In contrast, it is rare for a direct hernia to course into the scrotum.

Figure 2. Anatomical comparison of direct and indirect inguinal hernias © 2020 Dr. Vaibhav Kapoor8

Clinical Approach

General considerations for investigating groin hernias include assessing the symptoms at presentation as well as any “red flag” physical findings. Patients commonly complain of dull or heavy types of discomfort when straining, which resolves when straining stops. Most groin hernias occur on the right side. Common physical findings include a bulge in the groin, which can indicate the type of hernia based on location relative to the inguinal ligament (Figure 3). However, in female or obese patients, the layers of abdominal wall may make the hernia more difficult to locate. In these cases, ultrasound or other imaging is needed to detect hernias. Clinicians should also determine if the hernia is reducible, or if the herniated bowel can be returned to the abdominal cavity when moderate pressure is applied externally.

Figure 3. Locations of femoral and inguinal hernias on examination © 2023 UpToDate7

 

Physical examination has a 76 to 92% sensitivity and 96% specificity for diagnosing groin hernias, although imaging may also be required1,2. Nausea, vomiting, fever, moderate-to-severe abdominal pain, localized tenderness, or bloating may indicate more sinister pathology such as bowel incarceration (when the hernia contents cannot return to the abdominal cavity), strangulation (when the blood supply to the involved bowel section is compromised) or necrosis.

Figure 5. CT images of A) femoral hernia (courtesy of Chris O’Donnell9 and B) inguinal hernia (courtesy of Erik Ranschaert10)

Management

Uncomplicated or asymptomatic hernias in males can be monitored through watchful waiting. Surgical repair is a definitive treatment for inguinal hernias and should be considered for symptomatic or complex hernias. If repair is needed for an uncomplicated inguinal hernia, a laparoscopic repair is recommended. Watchful waiting is not recommended for femoral hernias – these patients should have a laparoscopic repair (when anatomically feasible).

Manual reduction of the hernia can be performed by following the GPS Taxis technique. Taxis is a non-invasive technique for manual reduction of incarcerated tissues in a hernia to the original compartment5. “GPS” is an acronym to remind clinicians to be gentle, be prepared, and be safe when performing taxis5. Conscious sedation with intravenous diazepam and morphine is recommended for the procedure. Consider having an anesthetist present for the procedure if the patient is frail. Provide appropriate early resuscitation by monitoring vital signs, administering oxygen therapy and establishing IV access. Place the patient in Trendelenburg position. Begin the GPS Taxis technique by palpating the fascial defect around the base of the hernia and gently manipulating hernia contents back into the abdominal cavity. Use gentle manipulation pressure over 5-10 minutes until a gurgling sound is heard (indicating successful reduction of bowel).

 

Taxis guided by ultrasound may increase success rates for reduction.

https://sjrhem.ca/taxis-reduction-of-inguinal-hernia/

Figure 4. Colourized clip demonstrating PoCUS assisted Taxis reduction of an inguinal hernia11

 

It should be noted that the major contraindication to performing GPS Taxis is bowel strangulation within the hernia. A rare but serious complication of manual reduction is reduction en masse, when a loop of bowel remains incarcerated at the neck of the hernia after manual reduction6. This can lead to early strangulation, intestinal necrosis, sepsis, organ failure and death. Femoral hernias and indirect inguinal hernias are at higher risk of reduction en masse from manual reduction attempts.

References:

  1. UpToDate – Classification, clinical features, and diagnosis of inguinal and femoral hernias in adults
  2. Hammoud M, Gerken J. Inguinal hernia. StatPearls. 2022 Aug 15.
  3. UpToDate – Overview of treatment for inguinal and femoral hernia in adults
  4. Bates’ Guide to Physical Examination and History Taking, 12th ed. (pdf). Chapter 13: Male Genitalia and Hernias
  5. Pawlak M, East B, de Beaux AC. Algorithm for management of an incarcerated inguinal hernia in the emergency settings with manual reduction. Taxis, the technique and its safety. Hernia, 25, 1253-1258. 2021 May 25.
  6. Yatawatta A. Reduction en masse of inguinal hernia: a review of a rare and potentially fatal complication following reduction of inguinal hernia. BMJ Case Rep. 2017 Aug 7.
  7. UpToDate – Classification, clinical features, and diagnosis of inguinal and femoral hernias in adults
  8. Kapoor, V. Difference between and inguinal and umbilical hernia. 2020. Retrieved from: https://www.drvaibhavkapoor.com/difference-between-inguinal-and-umbilical-hernia.html
  9. Patel, MS. Femoral hernia. Radiopaedia. 2022 Dec 28. Retrieved from: https://radiopaedia.org/articles/femoral-hernia
  10. Fahrenhorst-Jones, T. Inguinal hernia. Radiopaedia. 2022 Apr 12. Retrieved from: https://radiopaedia.org/articles/inguinal-hernia
  11. PoCUS assisted Taxis reduction of an inguinal hernia. Video obtained courtesy of Dr. David Lewis.

Continue Reading