Research Roundup: January 2021

 

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Brachial Plexus Injury After Shoulder Dislocation: A Literature Review

Olga G et al. Brachial Plexus Injury After Shoulder Dislocation: a literature review. Neurosurgical Review (2020) 43:407–423. https://doi.org/10.1007/s10143-018-1001-x

This literature review examined the neurological implications of shoulder dislocation. The authors analyzed the implications of brachial plexus injury, the incidence of neurological injuries in patients with shoulder dislocation, and proposed the algorithm for management.

 

Key Points
  • Traumatic anterior shoulder dislocation has an incidence estimated of 2% across the population.
  • 4-55% incidence of neurological complications after dislocations is reported in the literature.
  • Neurological complications are more prevalent with primary vs recurrent dislocations.
  • Brachial plexus injury (BPI) after dislocation is generally observed in two groups:
    • Dislocation from high energy impact (most often an MVA).
    • Dislocation from a fall (typically with no accompanying fractures).
  • BPI is more prevalent in populations sustaining a shoulder dislocation post-fall.
  • Neurological complications of shoulder dislocation include single nerve injuries and complex brachial plexus injuries.
  • Brachial plexus injury after shoulder dislocation is common among two patient groups:
    • Patients whose dislocation as the result of high-energy forces.
    • Patients with shoulder dislocation as the result of a simple fall.
  • Shoulder dislocation damages neural structures via different mechanisms:
    • Crushing of the nerve between the humeral head and the axillary border of the scapula.
    • Formation of a hematoma in the axillary region which leads to the compression of neural elements.
    • Vascular injury leading to the formation of a pseudoaneurysm of the axillary artery; this causes a delayed compression of neural structures, and deterioration of limb function.
    • Injury to vasa nervorum causing ischaemia of peripheral nerves resulting in impairment of their function.

  • Most injuries resulting from shoulder dislocation affect mostly the infraclavicular part of the plexus, in many cases extending up to the retro-pectoralis minor space.
    • This is likely because trauma in abduction causes injury to the lower part of the brachial plexus.
  • Position of the limb during dislocation influences site of nerve injury.
    • Medial cord when elbow and wrist are extended.
    • Medial and posterior cords when the elbow is flexed.
    • All cords when shoulder is in 90º abduction and full extension.
  • The posterior cord is the most likely to be injured.
  • Injury to the axillary nerve is most common, singly or in combination with other nerves.
  • Multiple nerve injuries are more common than singular nerve injuries after shoulder dislocation.
  • Short branches of the brachial plexus can also be injured, with the suprascapular nerve most commonly reported.
  • Clinically, axillary nerve and suprascapular nerve injuries may present similarly, and can also present together.
    • They may also present as shoulder instability and/or rotator cuff tears.
    • Nerve conduction studies are the only way to differentiate between axillary and suprascapular injuries.

  • A rare associated injury may be neurovascular injury to the axillary or subclavian arteries.

  • Spontaneous recovery will take > one year and make need surgical intervention.
  • Observed nerve injuries are most often neuropraxia or axonotmesis.
    • Complete disruption or avulsion is very rare.
    • Neurotmesis require nerve grafting occurred in 22.7-29% of cases.
  • Infraclavicular injuries require surgery significantly less often than supraclavicular injuries.
    • Timing of surgery is controversial, and there is yet no consensus.
  • Factors affecting surgical recovery include:
    • Age (less than 40 years).
    • Severity of nerve lesions.
    • Time between trauma and surgery.
    • Graft length.
    • Lateral cord recovers better than posterior or medial cord.
  • Elevated risk of neurological injury after shoulder dislocation is associated with variables such as:
    • Higher patient age
    • Male gender (due to a higher preponderance to be involved in high-energy collisions, not due to sex differences).
    • Increased time between dislocation and relocation.
    • Coexisting rotator cuff tear or greater tuberosity fracture.
    • Coexisting haematoma.

  • Infraclavicular injuries have a better prognosis for recovery.
  • Sensory recovery precedes motor recovery.

 

 Clinically: Pilates in Practice
  • Given that neurological sequelae may present similarly to instability and/or rotator cuff tears, it is important to continue to screen neurological signs and symptoms through injury management and recovery. 
  • Consider the mechanism of injury and the position of the upper limb during shoulder dislocation, for clues as to which cords may be compromised, and therefore which peripheral nerves may exhibit damage. 
  • Work to decompress the brachial plexus, especially the infraclavicular area: ACJ + SCJ and rib mobility are crucial. Hug a Tree on the Mat; Side Arm Press on the Cadillac. 
  • Posterior shoulder cuff engagement will support the stability of the shoulder and also facilitate anterior decompression: Hitch-Hiker and Single Arm Press on the Reformer; Triceps Press on the Wunda Chair (care not to over-stretch the subclavian vessels).
  • Integrate elbow, forearm, and wrist mobility within safe parameters for neurodynamic mobility. 

 

 

Long Term Outcomes Of Ventral Hernia Repair: An 11-Year-Follow-Up

Kadakia N, Mudgway R, Vo J, et al. (August 02, 2020) Long-Term Outcomes of Ventral Hernia Repair: An 11-Year Follow-Up. Cureus 12(8): e9523. DOI 10.7759/cureus.9523

This article is a comprehensive retrospective review of ventral hernia repair outcomes performed at one facility in the USA. The study was limited by a small sample size, facility treatment bias, retrospective review, and loss of information due to data extraction from paper charts; these are all acknowledged by the authors of the paper.

 

  • Ventral hernia repairs (VHR) may be performed through open or laparoscopic techniques, and with or without mesh.
  • Complication rates may be affected by various factors such as mesh placement and mesh position technique.

  • Mesh use is associated with a lower risk for recurrence and a higher risk of infections.
  • Laparoscopic repairs are associated with decreased quality of life, length of stay, and infection rates.
  • VHRs with mesh had lower rates of recurrence than suture repairs, and lower rates of complications, but these were not statistically significant.

  • Obesity, COPD, component separation technique, and prolonged operating time were associated with increased risk of complications.
  • Factors that contribute to post-operative complications after VHR in obese patients include:
    • Impaired visualization due to body habitus.
    • Defects in tissue structure.
    • Defects in tissue healing.

  • There is variability in outcomes for VHR with obesity and pre-existing hypertension.
    • Addressing these modifiable risk factors prior to surgery is recommended.

  • The primary outcome measure in this study was recurrence of hernia.

 

Clinically: Pilates in Practice
  • Begin with breathing.
  • Optimising breath biomechanics for someone with a compromised abdominal wall will decrease stress and strain into the surgical repair area.
  • Given that breathing is also altered in those conditions that are associated with increased risk of complications, early education is key.
  • Support the deep core cylinder with exercises focusing on the diaphragm, multifidus, psoas, and adductor-pelvic floor connections prior to anterior abdominal wall exercises.
  • Magic Circle Adductor Squeezes; Side lying segmental lumbar control; Reformer Footwork; Side lying Leg Lifts. 

 

 

New Developments in Our Understanding of Ankylosing Spondylitis Pathogenesis

Aniruddha V. and Paul B. New developments in our understanding of ankylosing spondylitis pathogenesis. 2020. Immunology, 161, 94–102.

The authors of this article reviewed data from animals and genetic studies highlighting the importance of Type 17 immune responses. The article comprehensively discusses the multifactorial pathogenesis of ankylosing spondylitis.

 

Key Points
  • Ankylosing spondylitis (AS) is an autoimmune inflammatory arthritis that is part of a larger class of spondyloarthropathies.
  • Complications of AS include iritis, an increased risk of osteoporosis, cardiovascular disease, and a high risk of spinal compression fractures.
  • Physiotherapy is the mainstay of treatment for AS along with pain management with analgesia and nonsteroidal anti-inflammatory drugs.

  • The risk of siblings or first-degree relatives of AS patients having AS is higher than that of the general population, and there is a high degree of concordance in twins.
  • The HLA-B*27 gene has the strongest genetic association with ankylosing spondylitis, followed by IL-23R and endoplasmic reticulum aminopeptidase (ERAP1).
  • The prevalence of ankylosing spondylitis in a population depends on the prevalence of HLA-B*27 in that population.
  • Multiple genetic loci have been linked to the pathogenesis of AS. However, only a quarter of the heritability of AS is currently accounted for by the genetic loci linked to the disease of which 20.1% is linked to the HLA-B*27 gene alone.
  • The IL-17-IL-23 axis and Type 17 immune responses are of particular relevance to the pathogenesis of AS.
    • IL-17 = interleukin 17.
    • The IL-17 protein consists of 150 amino acids.
    • Accumulated evidences have demonstrated that IL-17 is involved in ankylosing spondylitis, reactive arthritis, psoriatic arthritis, and other forms of spondyloarthritic conditions.1
  • There is a strong genetic association between ankylosing spondylitis and IL-23R polymorphisms with functional relevance in T cell immune response, indicating that genetic variations in the IL-23/IL-17 axis may influence the effector function of Th17 cells in patients with AS.2

  • Patients with AS have increased levels of circulating IL-17 and IL-23 compared with healthy controls.
  • Patients with AS have increased numbers of pathogenic TH17, TH22 cells and IL-17-secreting γδ cells in their peripheral blood and accumulating in their joints.
  • Th17 cells are a subset of T helper cells.
    • Th17 cells play a key role in the immune system’s defense against extracellular bacteria and fungi, as well as the development of autoimmune diseases.
  • TH22 cells are a subset of human T helper cells that are involved in the pathogenesis of inflammatory diseases.
    • Some studies have found that the frequencies of Th22 cells are elevated in patients with ankylosing spondylitis, thus implicating it in the pathogenesis of AS, and making it a reasonable cellular target for therapeutic intervention.3

  • There is a strong association between inflammatory bowel disease (IBD) and AS.
    • First-degree relatives of AS patients are three times more likely to have IBD, and up to 70% of AS patients have subclinical gut inflammation on endoscopic or histological examination.
    • Inflammatory bowel disease is not rare in ankylosing spondylitis, with its prevalence ranging from 6% - 14%.4
  • The pathophysiology of AS associated with IBD involves the so-called “gut-synovial axis” hypothesis, which implicates host factors and environmental factors.
    • Various environmental (gut bacteria-dysbiosis) and host factors (migration of activated gut-T cells and macrophages) leading to initiation of inflammation in genetically predisposed individuals may act as triggers of inflammatory responses against gut and joints components.5

  • Type 17 immune response is vital for the maintenance of mucosal barrier function, and AS patients are known to have elevated IL-23 levels.
    • IL-23 is indicated as the necessary mediator for organ-specific autoimmune diseases. 
    • It has been demonstrated that IL-23 can increase and stabilize the Th17 cells in disease models and humans.6
  • Genetic studies have demonstrated that interleukin-23 receptor (IL-23R) has a key role in various chronic inflammatory diseases including AS.7 
    • The results of these studies have led to the speculation that IL-23R gene is responsible for genetic predisposition to AS.8

 

References

1. Australo-Anglo-American Spondyloarthritis Consortium (TASC), J. D. Reveille, A. M. Sims et al., “Genome-wide association study of ankylosing spondylitis identifies non-MHC susceptibility loci,” Nature Genetics, vol. 42, no. 2, pp. 123–127, 2010.

2. I-Tsu Chyuan, Ji-Yih Chen, "Role of Interleukin- (IL-) 17 in the Pathogenesis and Targeted Therapies in Spondyloarthropathies", Mediators of Inflammation, vol. 2018, Article ID 2403935, 8 pages, 2018. https://doi.org/10.1155/2018/2403935

3. Zhang L, Li YG, Li YH, et al. Increased frequencies of Th22 cells as well as Th17 cells in the peripheral blood of patients with ankylosing spondylitis and rheumatoid arthritis. PLoS One. 2012;7(4):e31000. doi:10.1371/journal.pone.0031000

4. Stolwijk C, van Tubergen A, Castillo-Ortiz JD, Boonen A. Prevalence of extra-articular manifestations in patients with ankylosing spondylitis: a systematic review and meta-analysis. Ann Rheum Dis. 2015;74:65–73.

5. Fragoulis GE, Liava C, Daoussis D, Akriviadis E, Garyfallos A, Dimitroulas T. Inflammatory bowel diseases and spondyloarthropathies: From pathogenesis to treatment. World J Gastroenterol. 2019;25(18):2162-2176. doi:10.3748/wjg.v25.i18.2162

6. Langrish C, Chen Y, Blumenschein WM, Mattson J, Basham B, Sedgwick JD, McClanahan T, Kastelein RA, Cual DJ. IL-23 drives a pathogenic T cell population that induces autoimmune inflammation. The Journal of Experimental Medicine, 2005; 201(2): 233–240

7. Sung IH, Kim TH, Bang SY, m TJ, Lee B, Peddle L, Rahman P, Greenwood CM, Hu P, Inman RD.IL-23R polymorphisms in patients with ankylosing spondylitis in Korea. J Rheumatol, 2009; 36: 1003–1005

8. Rueda B, Orozco G, Raya E, Fernandez-Sueiro JL, Mulero J, Blanco FJ, Vilches C, González-Gay MA, Martin J. The IL23R Arg381Gln non-synonymous polymorphism confers susceptibility to ankylosing spondylitis. Ann Rheum Dis, 2008; 67: 1451–1454

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